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CHAPTER
1
•
i
Plastic Surgery:
The Problem-Solving Specialty
STEPHEN J. MATHES, MD
CREATIVITY
THE 2005 EDITION OF PLASTIC SURGERY
Format
Content and Contributors
STAYING AHEAD: MAJOR INNOVATIONS IN PLASTIC
SURGERY
What Is Plastic Surgery?
CREATIVITY
The deformities requiring operations of this class
are necessarily so dissimilar in different cases, every-
one becomes a separate study to the surgeon and
opens a fresh field for the exercise of his mind in
restoring the lost or deformed parts.
—Joseph Pancoast*
Plastic surgery is a problem-solving specialty. It is
special among surgical disciplines in that every patient
presents with a challenging problem requiring a
unique solution. This problem may be a result of a
congenital abnormality, an accident, a disease, or the
aging process. The scope of the problem, which often
dictates timing of surgical intervention, varies; but for
our purposes, it may be divided into three types: life-
threatening, limb-threatening, or contour and func-
tional abnormality. Regardless of etiology, location, or
type, the solution must be based on an analysis of the
anatomy of the defect and the requirements for repair
or reconstruction. In plastic surgery, the solutions are
rarely based on protocols and often vary widely as each
procedure performed is tailored to the specific require-
ments of the individual patient.
Plastic surgery is also unique in that there are no
anatomic barriers to our involvement in care of the
patient. Plastic surgery requires manipulation of skin,
soft tissue, and bone—from head to toe. With broad
training in the surgical sciences and a tradition of inno-
vation in problem solving, the plastic surgeon maybe
consulted by both patients and medical colleagues for
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Dr.Mustafa D.
Observing the Master Surgeon
Observing the Master Teacher
Observing Anatomy
PROFILE FOR INNOVATION
JOY OF SURGERY
*)
all types of congenital and acquired deformities regard-
less of location, etiology, and severity. Because of our
diversity of interest, plastic surgeons work closely with
other surgical and medical specialties in the quest to
find the best possible solution for each individual
patient. Frequently, the patient requires a multidisci-
plinary approach for optimal treatment.
The techniques used for correction of the multi-
tude of problems encountered by the plastic surgeon
are constantly evolving. From a historical perspective,
the plastic surgeon has been characterized as an inno-
vator who is willing and ready both to introduce and
to accept new ideas. Furthermore, innovations are not
limited to the academic centers—all plastic surgeons
are united in their search for creative solutions. When
a good idea is revealed by presentation and publica-
tion, plastic surgeons are quick to incorporate these
new techniques or technique modifications into their
practice.
Innovation is the key to the current success of plastic
surgery and must continue for the future of the spe-
cialty. Unique and innovative solutions introduced by
plastic surgeons influence other surgical and nonsur-
gical specialties and are readily incorporated into their
armamentarium for patient management. However,
plastic surgeons are never satisfied with the current
solutions. We are continually compelled to use our
surgical skills and imagination to continue to im-
prove the management of congenital and acquired
deformities.
The new edition of Plastic Surgery is designed to
cover the scope of this specialty and to provide current
2 I • GENERAL PRINCIPLES
data on the best and most reliable approaches to
problem solving. In view of the rapid changes occur-
ring in plastic surgery, historical perspectives are
included to remind us of how we got to where we are
in patient management and to provide us with moti-
vation to continue evolving. Although a great deal of
effort has been made to include all current solutions
in dealing with the scope of problems relevant to the
practice of plastic surgery, the data presented really
represent the launch pad for innovation. Every treat-
ment can and should be improved by creative assess-
ment of the requirements for repair and reconstruction
to develop new and safer techniques to restore and reju-
venate each patient to a healthy and happy state.
By way of introduction to this eight-volume text,
there are several areas that require amplification. First
is a discussion of the format of this new edition and
how it has changed from the two Converse editions
of Reconstructive Plastic Surgery (1964 and 1977)2,3 and
the McCarthy edition of Plastic Surgery.4 The changes
that have occurred in these volumes to a large extent
reflect the evolution of our specialty, and it is most
interesting to observe and reflect on the past as well
as to anticipate the current and future directions of
our specialty. Second, a discussion of the major inno-
vations that have occurred during the last 15 years,
and how the wide variety of changes have affected our
management of congenital and acquired deformities,
is in order. It is exciting to see all of this information
in one place for both reconstructive and cosmetic
surgery and reassuring to know such a comprehen-
sive work will be to the benefit of our patients. Finally,
the key to the growth and respect of plastic surgery
by our colleagues and patients is the creativity exhib-
ited by surgeons within the specialty. A look at profiles
for innovation may help each of us focus on the
advancement of the principles and approaches for the
multitude of problems covered in the eight volumes
in the text. Patients as well as surgical and nonsurgi-
cal practitioners consult the plastic surgeon with
hope and confidence in our ability not only to resolve
difficult problems but also to restore and rejuvenate
to an optimal level. As one may observe from the many
descriptions of techniques covered throughout these
volumes, we can currently provide excellent solutions
for many challenging problems. However, each of the
219 chapters also covers problems that require new
approaches. The profile for innovation will serve as a
stimulus for the reader to turn to basic and clinical
research and review outcomes to develop original, fresh
approaches and techniques that may be incorporated
into the practice of plastic surgery. The efforts of the
293 contributors of this text will be well rewarded by
the innovations stimulated as a result of the infor-
mation contained in their respective chapters. For this
is the essence of the specialty of plastic surgery: observe,
read, innovate, treat, and teach.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
THE 2005 EDITION OF
PLASTIC SURGERY
Format
The goal for the new edition of Plastic Surgery is to
cover the scope of the specialty. The current body of
knowledge necessary to treat all the problems encoun-
tered by plastic surgeons has increased as reflected in
the number of pages contained in the four texts: Con-
verse (1964), 2255 pages; Converse (1977), 3970 pages;
McCarthy (1990), 5556 pages; and Mathes (2005), more
than 7000 pages. The text has been divided into volumes
to allow the reader to use the text with more ease. Con-
verse (Fig. 1 -1), in the Preface to the 1964 edition, states,
"For the convenience of the reader, the text has been
published in five volumes. Ernest Hemingway once
stated that no book should be so large that it could not
be read in bed, and it is hoped that the reader will find
these volumes easier to handle than the originally pro-
jected two large volumes."5
The initial text published by Converse in 1964
entitled Reconstructive Plastic Surgery1 comprises
five volumes (2255 pages) divided into seven parts by
specific subjects: Volume 1 contains Part 1: General
Principles; Volume 2 (emphasis on trauma) and
Volume 3 (emphasis on congenital defects and one
chapter entitled "The Aging Face") contain Parti: The
Head and Neck; Volume 4 contains Part 3: The Hand
and Upper Extremity (edited by J. William Littler) and
Part 4: The Lower Extremity; and Volume 5 contains
Part 5: The Trunk, Part 6: The Genitourinary System
and Anorectal Malformations, and Part 7: Tissue Trans-
plantation and Burn Shock. This last part contained
Joseph Murray's "Transplantation of the Kidney,"
Blair O. Rogers and Fritz H. Bach's "Genetics as Applied
to Tissue Transplantation," and Clifford Snyder and
Robert P. Knowles' "Autotransplantation of Limbs."
The recognition of the importance of the science of
transplantation is captured in this statement by Con-
verse in the Preface to the 1964 edition:
The plastic surgeon, that daily transplanter, must consider
himself akin to the transplantation biologist. Transplanta-
tion biology is at the forefront of the phenomenal advances
in surgery of recent years. Transplantation of tissues and
replacement of structures and organs, physiologically worn
out, resected for disease or amputated in accidents, will be
one of the major tasks of the surgeon of the future. The plastic
surgeon, because of his experience in transplantation in his
clinical practice, his ability to perform delicate and intricate
techniques, is admirably suited by temperament and train-
ing to play a leading role in the development of transplan-
tation surgery. The teaching of transplantation biology should
become an integral part of the teaching of the plastic surgery
resident.5
The next edition of Reconstructive Plastic Surgery,
also edited by Converse, was published in 1977,
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1 • PLASTIC SURGERY: THE PROBLEM-SOLVINC SPECIALTY
FIGURE 1 - 1 . John Marquis Converse (1909-1981), editor of Reconstructive Plastic Surgery and Reconstructive Plastic
Surgery, second edition.
contained 3970 pages, and included seven volumes. 3
As in the previous edition, volumes are further divided
into parts by specific subjects. Volume 1 contains Part
1: General Principles. In this edition, General Princi-
ples now included B. M. O'Brien and J. W. Hayhurst's
"Principles and Techniques of Microvascular Surgery."
Volumes 2, 3, 4, and 5 contain Part 2: The Head and
Neck. Volumes 2 and 3 deal largely with acquired defor-
mities, and Volume 4 is primarily focused on congenital
deformities. The increase in space devoted to man-
agement of congenital and acquired deformities of the
face is reflected in this statement by Converse that
appeared in the first chapter of the 1977 edition:
Wc have taken for granted that each human face is differ-
ent, that no human face has ever been reduplicated among
the millions that surround us and the billions that have pre-
ceded us. Not even a facial feature has ever been reproduced.
The uniqueness of the individual, which extends to the sub-
cellular level, is the clue to the diversity of the facial features
of man, his facial expression with its infinite variants, the
timbre of his voice,his posture, his movements, and the entire
mysterious psychosomatic complex that constitutes the per-
sonality of a human being.6
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
Many aspects of craniofacial surgery are introduced
in chapters within Volume 4 of this edition, including
Blair O. Rogers' "Embryology of the Face and Intro-
duction to Craniofacial Anomalies"; John Marquis
Converse, Joseph G. McCarthy, Donald Wood-Smith,
and Peter J. Coccaro's"Craniofacial Microsomia"; Blair
O. Rogers' "Mandibulofacial Dysostosis"; and John
Marquis Converse, Joseph G. McCarthy, and Donald
Wood-Smith's "Principles of Craniofacial Surgery."
Volume 5, also included in Part 2, covers head and neck
tumor management. In this volume, greater empha-
sis is placed on head and neck reconstruction after
tumor ablation in several chapters, including John C.
Gaisford and Dwight C. Hanna Ill's "Oromandibular
Tumors: Reconstructive Aspects," Ian A. McGregor s
"Reconstruction Following Excision of Intraoral and
Mandibular Tumors," and Vahram Y. Bakamjian and
Peter M.Calamel's"Oropharyngeo-esophageal Recon-
structive Surgery." Rather than coverage under Part 1:
General Principles, a comprehensive chapter entitled
"Tumors of the Skin" with five separate sections cov-
ering "A Dermatologist's Viewpoint" "A Plastic
Surgeon's Viewpoint" "Malignant Melanoma,"
"Superficial Forms of Cancer," and "Chemosurgery"
age
4 I • GENERAL PRINCIPLES
is included. Volume 6, containing Part 3: The Hand
and Upper Extremity, was again edited by J. William
Littler. This volume contains a chapter by Vincent R.
Hentz and J.William Littler entided "The Surgical Man-
agement of Congenital Hand Anomalies." Vincent R.
Hentz, who was working with Dr. Littler at that time,
has now become the editor for the volumes covering
the hand and upper extremity for this edition. Volume
7 contains Part 4: The Lower Extremity, Part 5: The
Trunk, and Part 6: The Genitourinary System.
Joseph G. McCarthy (Fig. 1-2) changed the title of
the new edition in 1990 to Plastic Surgery.4 This text
includes eight volumes and is 5556 pages in length.
Volume 1 of this edition is entitled General Principles.
A number of new principles are covered in chapters
that appeared in this volume, including G. Ian Taylor,
John H. Palmer,and Douglas McManamnyV'The Vas-
cular Territories of the Body (Angiosomes) and Their
Clinical Applications." Stephen Mathes and Issa
Eshima's "The Principles of Muscle and Musculocu-
taneous Flaps" covers new concepts in flap design based
on vascular anatomy in the human. Louis C. Argenta
and Eric D. Austad's "Principles and Techniques of
Tissue Expansion" describes wound closure with use
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Dr.Mustafa D.
of local tissue made possible by the process of tissue
expansion. Volume 2, The Face (Part 1), concentrates
on trauma, and Volume 3, The Face (Part 2), is largely
dedicated to acquired facial deformities. Volume 4, Cleft
Lip and Palate and Craniofacial Anomalies, provides
in-depth coverage of advances in craniofacial surgery
in chapters such as Joseph G. McCarthy, Charles H.
M. Thorne, and Donald Wood-Smith's "Principles of
Craniofacial Surgery: Orbital Hypertelorism" and
Joseph G. McCarthy, Fred J. Epstein, and Donald
Wood-Smith's "Craniosynostosis." In Volume 5, Tumors
of the Head and Neck and Skin, David B. Apfelberg and
Morton R. Maser's chapter, "Laser Therapy," introduces
the new interest in the use of lasers in treatment of
skin abnormalities. Volume 6 is entitled The Trunk and
Lower Extremity, and Volumes 7 and 8 are entitled The
Hand (Part 1) and The Hand (Part 2). Volumes 7 and
8 are edited by James W. May Jr. and J. William Littler.
The space devoted to hand treatment is enlarged to
two volumes and partially reflects the impact of
microsurgery in hand management. These volumes
include Harry J. Bunckc's "Thumb and Finger Recon-
struction by Microvascular Second Toe," Leonard A.
Sharzer's "Free Flap Transfer in the Upper Extremity,"
 image...
1 • PLASTIC SURGERY: THE PROBLEM-SOLVING SPECIALTY
TABLE 1-1 • PLASTIC SURGERY, 2 0 0 5
New chapter topics 67
Technique chapters 25
Secondary chapters 7
Total chapters 219
Contributors 293
Michael G. OrgePs "Innervated Free Flaps and Free
Vascularized Nerve Grafts in the H a n d " Ralph T.
Manktelow's "Functioning Muscle Transfer for Recon-
struction of the Hand " James W. May Jr.'s "Microvas-
cular Great Toe to Hand Transfer for Reconstruction
of the Amputated T h u m b " and Wayne A. Morrison's
"Thumb Reconstruction by the Wrap-Around
Technique."
The 2005 edition of Plastic Surgery includes eight
volumes and is now more than 7000 pages in length.
As in the past, authors for each chapter are selected on
the basis of specific expertise in their respective sub-
jects. In this edition, changes in format include new
chapter topics that reflect the increasingly diverse body
of knowledge required for effective patient manage-
ment in the daily practice of plastic surgery, chapters
primarily focused on the performance of specific recon-
structive and cosmetic techniques, and, finally, chap-
ters designed to comprehensively present the various
techniques and approaches necessary in the manage-
ment of patients requiring secondary surgery
(Table 1-1).
NEW CHAPTER TOPICS
New topics that reflect changes in the scope of the spe-
cialty of plastic surgery, with an emphasis on the unique
and innovative techniques currently used in both
reconstructive and cosmetic surgery, have been added
to this edition. Although many of the subjects have
been discussed in previous editions, they were not
covered independently. It is hoped that the additional
division of general concepts into more specific areas
of practice will enable the plastic surgeon to address
the needs of a diverse and steadily increasing popu-
lation of patients. In the 15 years since the publica-
tion of the previous edition of Plastic Surgery, there
has been a proliferation of interest in and publica-
tions on breast surgery, contour procedures (especially
after bariatric surgery), skin care and skin resurfac-
ing, facial rejuvenation, and diagnostic functional
studies for the hand and upper extremity. Many areas
of increased interest required new chapter topic
assignments to cover the significant advances and inno-
vations in the specialty of plastic surgery.
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Dr.Mustafa D.
TECHNIQUE CHAPTERS
Overview chapters, as in previous editions of Plastic
Surgery, have been written by established authors on
important topics in the specialty of plastic surgery.
Technique chapters are added to complement the
overview chapters. Overview chapters are designed to
cover the scope of diagnostic and therapeutic tech-
niques useful in current practice. Historical references
within each topic are limited to events or techniques
that directly influenced present-day patient manage-
ment. The technique chapters are written by recog-
nized experts in a particular area of plastic surgery and
are meant to accompany and augment the overview
chapters, especially in areas in which techniques may
be difficult or controversial. Each technique chapter
is meant to provide specific "how-to" information
required to safely and effectively perform reliable tech-
niques for specific problems in both reconstructive and
cosmetic patients. Although similar data are likely to
be covered in the comprehensive overview chapter, the
information provided by the technique chapter allows
the reader to verify the reliability of a specific approach
and, perhaps, obtain a different viewpoint as to how
to execute the procedure.
SECONDARY CHAPTERS
The initial procedure selected does not always accom-
plish the cosmetic or reconstructive goals to establish
form and function. In the past editions edited by Con-
verse and McCarthy, only one chapter was designated
specifically to review secondary surgery in the area
of rhinoplasty. In our practices today, patients often
present with failure of the primary procedure or
dissatisfaction with the result. Therefore, secondary
chapters have been added to most reconstructive and
cosmetic surgery topics. Again, experts have been
selected who are experienced in the management of
secondary patients in the assigned topic. Even if the
plastic surgeon does not intend to become involved in
secondary surgery, a review of these chapters provides
useful data on pitfalls in selection of patients, tech-
nique selection for specific problems, and technical
errors that may result in unsatisfactory results.
Content and Contributors
All of the chapters in this edition are carefully edited,
and many are revised to follow the concise format
required to cover key aspects of the essential topics
in eight manageable volumes. As in all the prior
editions of Plastic Surgery, the contributors (293 in
this 2005 edition) were generous in their time and
efforts, and all have provided accurate, insightful, and
timely coverage of their assigned subjects. All of the
contributors are successful, busy surgeons who gave
VtJWH^aelcrKf image...
6 I • GENERAL PRINCIPLES
of their precious time to provide comprehensive
information related to their respective areas of
expertise.
The 2005 edition of Plastic Surgery, like the 1990
edition, includes eight volumes but has increased to
more than 7000 pages in length. Volume I, General Prin-
ciples, has been expanded to include 13 new chapters
that reflect the continued evolution and expansion of
the practice of plastic surgery. Robert A. Chase, a sur-
gical leader and outstanding teacher, states the following
regarding the importance of surgical principles:
The education of a plastic surgeon does not consist of fur-
nishing his mind with facts and techniques but rather it con-
sists of setting a milieu in which he learns how to discipline
himself to use his own powers within a broad array of prin-
ciples. The same brainpower used to memorize and recall
details could better be used in learning to understand the
determinants of outcome after surgical refurbishing or alter-
ing biological systems. The general principles provided in
this volume provide the necessary guidelines to practice
plastic surgery and to empower the creativity within each
plastic surgeon toward problem solving.7
New subjects introduced in this volume include
ethics in plastic surgery, liability: legal issues, liability:
insurance issues, advances in prosthetics, management
of exfoliative disorders, pharmacologic and mechan-
ical management of wounds, management of complex
wounds, and principles of endoscopic surgery. Specific
subjects on the horizon of advancement in plastic
surgery include tissue engineering, fetal surgery,
telemedicine, and robotics (Table 1-2).
Wound care centers are now available at both major
medical centers and community hospitals. The chapter
entitled "The Pharmacologic and Mechanical Man-
agement of Wounds" provides the essentials for
objective wound management. The chapter entitled
"Problem Wounds and Principles of Closure" provides
a systemic approach to complex wound management
TABLE 1-2 • VOLUME I: GENERAL
PRINCIPLES
Ethics in Plastic Surgery
Liability Issues in Plastic Surgery: A Legal Perspective
Liability Issues in Plastic Surgery: An Insurance
Perspective
Prostheses in Plastic Surgery
Exfoliative Disorders
Pharmacologic and Mechanical Management of Wounds
Problem Wounds and Principles of Closure
Principles of Endoscopic Surgery
Tissue Engineering
Fetal Surgery
Telemedicine
Robotics in Plastic Surgery
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
and coordinates basic science principles with tech-
niques for complex wound closure.
Endoscopic surgery has been used in plastic surgery
for both reconstructive and cosmetic procedures to
provide unique visualization of deep structures that
require surgical manipulation and to minimize or elim-
inate objectionable scar to achieve improvements in
aesthetic outcomes. The chapter entitled "Principles
of Endoscopic Surgery" provides an overview of the
principles of instrumentation and the mechanics of
use for this innovation in plastic surgery.
The future direction of our specialty will be deter-
mined by principles directly or indirectly derived from
basic science, experimental surgical projects, and
innovations in technology that continue to geomet-
rically increase the scope and magnitude of all prac-
titioners with the medical field. New chapters focused
on the horizon of discovery in plastic surgery include
"Tissue Engineering," "Fetal Surgery," and "Tele-
medicine." The chapter entitled "Robotics in Plastic
Surgery" not only covers advances in prosthetics but
also includes a discussion of robotic systems that are
currently used for surgical assistance throughout
the world. With the changes in reimbursement for
medical care and the need to provide care at the local
level, areas such as telemedicine and robotics, which
are being developed concurrently with innovative
imaging systems, offer unique solutions to improve
efficiency in the delivery of health care both locally
and remotely. Although the chapter entitled "Repair
and Grafting of Bone" has appeared in prior editions
of Plastic Surgery, it has been expanded to include
principles involved in bone distraction with additional
scientific data to support this new method of recon-
struction for patients with congenital facial bone
abnormalities.
Volume II, The Head and Neck (Part 1), is pri-
marily dedicated to aesthetic surgery. To provide an
accurate assessment of preoperative and postopera-
tive results, when available, figures are presented in
color. To reflect the increasing number of cosmetic
surgery procedures performed in the head and neck
region, there is a corresponding increase in coverage
related to contour, functional improvements, and facial
rejuvenation within this and other volumes. Nineteen
new chapters have been introduced covering subjects
that are largely focused on the performance of specific
techniques for both primary and secondary cosmetic
patients (Table 1-3).
This volume begins with a unique and compre-
hensive discussion of a subject often overlooked
in plastic surgery literature, "Anthropometry and
Cephalometric Facial Analysis."The reader is provided
with useful information as well as practical tools to aid
in clinical examinations with the techniques described.
The chapter entitled "Analysis of the Aesthetic Surgery
Patient" gives practical and important advice
 image...

1 • PLASTIC SURGERY: THE PROBLEM-SOLVING SPECIALTY

TABLE 1-3 • VOLUME II: THE HEAD AND NECK (PART 1)

Topics Techniques Secondary Techniques

Anthropometry and Cephalometric
Facial Analysis
Analysis of the Aesthetic Surgery
Patient
Pharmacologic Skin Rejuvenation
Facial Skeletal Augmentation
Aesthetic Reconstruction of the
Nose
Aesthetic Orthognathic Surgery
Rejuvenation of the Upper Face: Secondary Rejuvenation of the
Current Techniques Face
Face Lift (Midface): Current Techniques Secondary Aesthetic Periorbital
Surgery
Face Lift {Lower Face): Current Secondary Blepharoplasty:
Techniques Current Techniques
Face Lift (Neck): Current Techniques
Aesthetic Periorbital Surgery
Open Rhinoplasty: Concepts and
Techniques
Closed Rhinoplasty: Current Techniques,
Theory, and Applications

regarding the appropriate management of this ever-
increasing population of patients.
The principles of face lift are fully covered in the
overview chapter entitled "Aging Face and Neck." Again,
to provide further in-depth coverage of this impor-
tant field in plastic surgery, the components of face lift
are also divided into upper face, midface, lower face,
and neck to give the reader an opportunity to obtain
additional data on decision-making and techniques
specific to the regions of the face. The chapter "Face
Lift (Lower Face): Current Techniques" includes a
section on injectable fillers widely used in this as well
as in other regions for facial rejuvenation and to reduce
the appearance of scars and objectionable contour
defects. Together, these five chapters on face lift will
allow comparison of techniques and assist the plastic
surgeon in decisions regarding management of the
component parts of the total face lift.
As in previous editions, periorbital rejuvenation
procedures are covered in an overview chapter. "Aes-
thetic Periorbital Surgery"provides complete and com-
prehensive coverage on this important subject. Again,
an additional chapter has been introduced that focuses
on specific aesthetic techniques in periorbital surgery.
These two chapters provide the reader with an in-depth
discussion of selection of patients, techniques, and out-
comes of primary periorbital aesthetic procedures.
The chapter entitled "Pharmacologic Skin Rejuve-
nation" is introduced in this edition as a separate and
unique discussion of a rapidly growing area. The non-
operative rejuvenation of facial skin or management
of facial skin disease is of interest to a wide variety of
surgical and nonsurgical specialists.
Plastic surgeons still debate the advantages and dis-
advantages of open versus closed rhinoplasty tech-
niques. Although the general subject of rhinoplasty is
covered in"PrimaryRhinoplasty,"both open and closed
techniques are examined separately in "Open Rhino-
plasty: Concepts and Techniques" and "Closed Rhino-
plasty: Current Techniques, Theory, and Applications"
to give the reader an opportunity to review and compare
the advantages and disadvantages.
As the specialty evolves, the boundaries of aesthetic
surgery are widened to include patients with defects
that may have often remained untreated in the past,
to their social and emotional detriment. For this reason,
the subject of "Aesthetic Genital Surgery" now deserves
a separate chapter because of increased public aware-
ness of and interest in aesthetic genital procedures.
Additional chapters concerning reconstructive proce-
dures of both congenital and acquired defects of the
genitalia are included in Volume VI.
The other additions to this volume reflect the
emphasis placed on secondary surgery. These chap-
ters address the potential failures of techniques in
aesthetic surgery and provide unique solutions for
prevention, avoidance, and repair of difficult prob-
lems. In addition to "Secondary Rhinoplasty," which
also appeared as a separate chapter in the previous
edition of Plastic Surgery* there are three new sec-
ondary surgery chapters included in Volume II: "Sec-
ondary Rejuvenation of the Face,""Secondary Aesthetic
Periorbital Surgery" and "Secondary Blepharoplasty:
Current Techniques." Astley Paston Cooper, in his lec-
tures on surgery, states,"... the best surgeon, like the
best general, is he who makes the fewest mistakes."8
When failure of a procedure does occur, experts in
their respective fields of plastic surgery have provided
detailed descriptions of reliable techniques to correct
the deficiencies observed from the primary procedure.
Three areas involving skeletal surgical contour and
functional alterations to restore or to enhance facial
appearance are now included in Volume II. These chap-
ters include"Facial Skeletal Augmentation,""Aesthetic

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
8 I • GENERAL PRINCIPLES
TABLE 1-A • VOLUME III: THE HEAD AND
NECK (PART 2)
Facial Trauma: Soft Tissue Injuries
Endoscopic Facial Fracture Management: Techniques
Endoscopic Mandible Fracture Management: Techniques
Acquired Cranial Bone Deformities
Acquired Facial Bone Deformities
Scalp Reconstruction
Forehead Reconstruction
Subacute and Chronic Respiratory Obstruction
Mandible Reconstruction
Neck Reconstruction
Reconstruction of the Nose," and "Aesthetic Orthog-
nathic Surgery."
Volume III, The Head and Neck (Part 2), is pri-
marily devoted to reconstruction of this region. A
tradition of emphasis in this area throughout previ-
ous editions of Plastic Surgeryand Reconstructive Plastic
Surgery has been maintained with 10 subjects added
to provide the reader with additional insights into this
integral, diverse, and continually expanding area of
reconstructive surgery (Table 1-4). New chapters and
independent areas of coverage include"FacialTrauma:
Soft Tissue Injuries" "Endoscopic Facial Fracture
Management: Techniques" "Endoscopic Mandible
Fracture Management: Techniques,""Acquired Cranial
Bone Deformities," "Acquired Facial Bone Defor-
mities" "Scalp Reconstruction" "Forehead Recon-
struction," "Subacute and Chronic Respiratory
Obstruction," "Mandible Reconstruction," and "Neck
Reconstruction."
Volume IV, Pediatric Plastic Surgery, contains a vast
array of classic as well as new concepts in the body of
knowledge related to craniofacial surgery in the pedi-
atric patient (Table 1 -5). This comprehensive overview
is presented for plastic surgeons as well as the multi-
ple surgical and medical disciplines involved in the care
of patients afflicted with congenital anomalies affect-
ing the head and neck region. In this 2005 edition, the
tradition of offering a separate volume for this impor-
tant subject area has been not only maintained but
also augmented with the addition of five new chap-
ters in pertinent areas related to reconstructive tech-
niques and innovations. The new chapters include
TABLE 1-5 • VOLUME IV: PEDIATRIC PLASTIC
SURGERY
Nonsyndromic Craniosynostosis
Reconstruction: Facial Clefts
Reconstruction: Craniofacial Syndromes
Reconstruction: Craniofacial Microsomia
Hemifacial Atrophy
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Dr.Mustafa D.
TABLE 1-6 • VOLUME V: TUMORS OF THE
HEAD, NECK, AND SKIN
Tumors of the Lips, Oral Cavity, and Oropharynx
Tumors of the Mandible
Benign Tumors of the Skin
Malignant Melanoma
Local Flaps for Facial Coverage
Management of Nonmelanoma Skin Cancer
Management of Regional Metastatic Disease of the
Head and Neck: Diagnosis and Treatment
"Nonsyndromic Craniosynostosis " "Reconstruction:
Facial Clefts," "Reconstruction: Craniofacial Syn-
dromes,""Reconstruction: Craniofacial Microsomia "
and "Hemifacial Atrophy."
In Volume V, Tumors of the Head, Neck, and Skin,
seven topics identified as new or newly independent
subject areas have been added to provide an in-depth
discussion of tumor management in this region (Table
1 -6). These new chapters provide an overview of man-
agement and include"Tumors of the Lips, Oral Cavity,
and Oropharynx,""Tumors of the Mandible,""Benign
Tumors of the Skin," "Malignant Melanoma," "Local
Flaps for Facial Coverage," and "Management of Non-
melanoma Skin Cancer." The last chapter addresses all
current modalities, including micrographic surgery,
regarding techniques and effectiveness in management
of basal and squamous cell carcinoma. Finally, a new
chapter is included to assist the reader in both diag-
nosis and treatment of metastatic disease in the head
and neck entitled "Management of Regional Metasta-
tic Disease of the Head and Neck: Diagnosis and
Treatment."
Volume VI, Trunk and Lower Extremity, has
increased markedly in size because of efforts to include
technique and secondary chapters in areas where plastic
surgeons have become increasingly involved in patient
management. Although most topics identified as new
chapters have been addressed in the past editions of
Reconstructive Plastic Surgery and Plastic Surgery, the
increasing interest, innovations, and participation of
plastic surgeons in trunk, breast, and lower extremity
reconstruction require multiple new chapters
specifically focused on topics required to effectively
participate in both aesthetic and reconstructive surgery
of this region. This volume now contains 34 additional
chapters to accompany the traditional overview chap-
ters presented in past editions (Table 1-7). The new
and newly independent topics covered as separate chap-
ters include "Breast Augmentation" and "Breast Aug-
mentation Techniques." The latter chapter follows the
overview chapter and provides the reader with a thor-
ough discussion of indications and techniques required
to achieve optimal results in breast enhancement. Again,
the technique chapter is designed to provide the reader
image...

1 • PLASTIC SURCERY: THE PROBLEM-SOLVING SPECIALTY

TABLE 1-7 • VOLUME VI: TRUNK AND LOWER EXTREMITY

Topics Techniques Secondary Techniques

Breast Augmentation Breast Augmentation Techniques Secondary Breast

Mastopexy
Reconstruction of the Back
Congenital Anomalies of the
Chest Wall
Breast Reduction
Reconstruction of Female Genital
Defects: Congenital
Reconstruction of Acquired Vaginal
Defects
Surgery for Gender Identity Disorder
Reconstructive Surgery: Skeletal
Reconstruction
Foot Reconstruction
Vascular Insufficiency of the Lower
Extremity: Lymphatic, Venous,
and Arterial
Reconstructive Surgery: Lower
Extremity Coverage
Augmentation
Abdominoplasty Techniques Secondary Liposuction
Body Contouring: Large-Volume Liposuction Secondary Reconstructive
Surgery: Mastopexy and
Reduction
Body Contouring: Trunk and Thigh Lifts Secondary Breast
Reconstruction
Liposuction of the Trunk and Lower
Extremities
Body Contouring: Upper Extremity
Vertical Reduction: Techniques
Inferior Pedicle Reduction: Techniques
Immediate Postmastectomy Reconstruction:
Latissimus Flap Techniques
Immediate Postmastectomy Reconstruction:
TRAM Transposition Techniques
Postmastectomy Reconstruction; Free
TRAM Flap Techniques
Postmastectomy Reconstruction:
Expander-Implant Techniques
Delayed Postmastectomy Reconstruction:
TRAM Transposition Techniques
Delayed Postmastectomy Reconstruction:
Free TRAM Techniques
Delayed Postmastectomy Reconstruction:
Latissimus Flap Technique
Perforator Flaps for Breast Reconstruction
Postmastectomy Reconstruction:
Alternative Free Flaps
Reconstruction of the Nipple-Areola
Complex

with another author's perspectives on this popular pro-
cedure. Although mastopexy has been covered in the
past within overview subjects related to breast surgery,
"Mastopexy" is now provided as a separate chapter
to thoroughly address this important area of current
clinical practice.
The overview chapter on abdominoplasty provides
a comprehensive study of abdominoplasty procedures.
The technique chapter that accompanies this sub-
stantial review, "Abdominoplasty Techniques," is
focused on providing additional information, related
to both experience and innovation, on technique to
achieve optimal superior results in body contour pro-
cedures in the abdominal region.
The overview chapter "Body Contouring: Suction-
Assisted Lipectomy" covers the entire subject of body
contour and provides the essential principles and tech-
niques required to perform body contour by liposuc-
tion. The increasing interest in body contour proce-
dures reflects the rapidly growing population of
patients eager to benefit from this exceptional tech-
nology. In addition to the overview chapter, four addi-
tional chapters have been introduced in this volume
to provide additional data and include "Body Con-
touring: Large-Volume Liposuction" "Body Con-
touring: Trunk and Thigh Lifts," "Liposuction of the
Trunk and Lower Extremities," and "Body Contour-
ing: Upper Extremity." In addition to insights regard-
ing techniques and technique selection, these chapters
also provide information concerning selection of
patients.
The chapter entitled "Reconstruction of the Back"
includes a discussion of noncomplex as well as complex
wounds of the back. The chapter "Congenital Anom-

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TeWR^aacTKf image...
10 I • GENERAL PRINCIPLES
alies of the Chest Wall" is included as a separate chapter
because of the unique needs of this distinct group made
up of both adult and pediatric patients.
The three chapters on breast reduction have been
separated into"Breast Reduction ""Vertical Reduction:
Techniques," and "Inferior Pedicle Reduction: Tech-
niques" to provide an overview of the subject as well
as a separate discussion with emphasis on techniques
related to the two approaches most commonly used
to accomplish breast reduction.
The following 10 chapters represent new chapters
addressing approaches to breast reconstruction on an
immediate or delayed basis after mastectomy. These
chapters follow the overview chapter, which in addi-
tion to in-depth coverage and comparison of tech-
niques in breast reconstruction also now provides
extensive coverage of oncologic principles related to
management of the patient with breast cancer. Plastic
surgeons have been responsible for many of the inno-
vations in approaches to mastectomy as well as post-
mastectomy reconstruction and frequently perform
prophylactic mastectomy. Because the plastic surgeon
is now an essential component of the breast manage-
ment team, a review of diagnostic and therapeutic prin-
ciples in breast cancer management is essential. The
following is a listing of chapters related to techniques
of postmastectomy reconstruction: "Reconstruction of
the Nipple-Areola Complex," "Immediate Postmas-
tectomy Reconstruction: Latissimus Flap Techniques,"
"Immediate Postmastectomy Reconstruction: TRAM
Flap Transposition Techniques," "Postmastectomy
Reconstruction: Free TRAM Flap Techniques," "Post-
mastectomy Reconstruction: Expander-Implant Tech-
niques" "Delayed Postmastectomy Reconstruction:
TRAM Transposition Techniques" "Delayed Post-
mastectomy Reconstruction: Free TRAM Techniques,"
"Delayed Postmastectomy Reconstruction: Latissimus
Flap Technique ""Perforator Flaps for Breast Recon-
struction," and "Postmastectomy Reconstruction:
Alternative Free Flaps."
There is increasing involvement in repair of ventral
hernias and complex abdominal wall reconstruction
by plastic surgeons. Also, with increasing use of the
abdominal wall as a source of transposition or free flaps,
the plastic surgeon must have current knowledge of
the anatomy and repair of abdominal wall defects.
For this reason, the chapter "Reconstruction of the
Abdominal Wall" is now independent of the overview
chapter.
These two chapters have been separated from the
overview of female genital reconstruction as the
approach is quite different for congenital and acquired
defects, and there are additional options as well as
specifications for each. As public awareness and accept-
ance of corrective surgery in this region have increased,
development of a wider array of surgical options has
ensued. It is hoped that both"Reconstruction of Female
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Genital Defects: Congenital" and "Reconstruction of
Acquired Vaginal Defects" will provide the reader with
useful information in managing these defects.
In 1965, Johns Hopkins established the first Gender
Identity Clinic in the United States in Baltimore, Mary-
land. Milton Edgerton was the founding director
and later wrote, "The 'gender identity movement' has
brought together such unlikely collaborators as sur-
geons, endocrinologists, psychologists, psychiatrists,
gynecologists, and research specialists into a mutually
rewarding arena."9 This field continues to evolve in
regard to indications, techniques, and outcomes. The
chapter "Surgery for Gender Identity Disorder" is pro-
vided to assist the reader in managing this particular
group of patients.
Four new chapters related to management of defects
in the lower extremity have been added. Two chapters
have been separated from the overview of lower
extremity reconstruction to reflect the different
approaches required on the basis of type, size, and extent
of the defect (skin and soft tissue coverage versus skele-
tal reconstruction).These two chapters include"Recon-
structive Surgery: Lower Extremity Coverage" and
"Reconstructive Surgery: Skeletal Reconstruction."
Maintaining an ambulatory status is the goal for every
patient with a foot injury or vascular disease. "Foot
Reconstruction" addresses the current options avail-
able and their rationale for use in the management
of foot defects. "Vascular Insufficiency of the Lower
Extremity: Lymphatic, Venous, and Arterial" addresses
the complexity of vascular insufficiency problems in
the lower extremity and describes treatment options
that offer hope to patients with functional defects of
the lower extremity.
An emphasis has been maintained on secondary
surgery for the trunk and lower extremities. Four new
chapters, "Secondary Breast Augmentation," "Sec-
ondary Liposuction" "Secondary Reconstructive
Surgery: Mastopexy and Reduction," and "Secondary
Breast Reconstruction," describe both causes for and
prevention of aesthetic and reconstructive failures,
provide recommendations for managing the additional
needs of these patients, and offer technical solutions
when secondary surgery is indicated.
Volumes VII and VIII are TheHandand Upper Limb
(Part 1) and TheHandand UpperLimb(Part 2).These
two volumes are edited by Vincent R. Hentz. As in the
McCarthy edition in 1990, the hand and upper extrem-
ity chapters are contained in two volumes to cover the
extensive principles and techniques involved in the
management of congenital and acquired deformities.
Each of these volumes has been further separated into
sections. Volume VII includes "Introduction and
General PrincipIes,""Acquired Disorders—Traumatic"
and "Acquired Disorders—Nontraumatic." Volume
VIII includes three sections, "Congenital Anomalies,"
"Paralytic Disorders," and "Rehabilitation."
 1 • PLASTIC SURGERY: THE PROBLEM-SOLVING SPECIALTY
TABLE 1-8 • VOLUME VII: THE HAND A N D
UPPER LIMB (PART 1)
Plastic Surgery: Contributions to Hand Surgery
Anatomy and Biomechanics of the Hand
Diagnostic Imaging of the Hand and Wrist
Arthroscopy of the Wrist
Principles of Internal Fixation as Applied to the Hand
and Wrist
Reconstructive Surgery of Individual Digits (Excluding
Thumb)
Adult Brachial Plexus Injuries
Obstetric Brachial Plexus Palsy
Disorders of Musicians' Hands
In keeping with the multiple innovations and new
areas of interest, these two volumes also include 22
new chapters (Tables 1-8 and 1-9): "Plastic Surgery:
Contributions to Hand Surgery" "Anatomy and Bio-
mechanics of the Hand," "Diagnostic Imaging of the
Hand and Wrist," "Arthroscopy of the Wrist" "Princi-
ples of Internal Fixation as Applied to the Hand and
Wrist," "Reconstructive Surgery of Individual Digits
(Excluding Thumb) ""Adult Brachial Plexus Injuries"
"Obstetric Brachial Plexus Palsy" "Disorders of
Musicians' Hands," "Embryology of the Upper Limb,"
"Classification of Upper Limb Congenital Differences
and General Principles of Management ""Management
of Transverse and Longitudinal Deficiencies (Failure
of Formation)" "Management of Disorders of Sepa-
ration—Syndactyly," "Constriction Ring Syndrome "
"Disorders of Duplication," "Failure of Differentiation
and Overgrowth," "Hypoplastic or Absent T h u m b "
"Pediatric Upper Extremity Trauma," "Hand Man-
agement for Patients with Epidermolysis Bullosa,"
"Effect of Growth on Pediatric Hand Reconstruction,"
"Hand Therapy," and "Upper Limb Aesthetic and Func-
tional Prosthetics."
TABLE 1-9 • VOLUME VIII: THE HAND AND
UPPER LIMB (PART 2)
Embryology of the Upper Limb
Classification of Upper Limb Congenital Differences and
General Principles of Management
Management of Transverse and Longitudinal
Deficiencies (Failure of Formation)
Management of Disorders of Separation—Syndactyly
Constriction Ring Syndrome
Disorders of Duplication
Failure of Differentiation and Overgrowth
Hypoplastic or Absent Thumb
Pediatric Upper Extremity Trauma
Hand Management for Patients with Epidermolysis
Bullosa
Effect of Growth on Pediatric Hand Reconstruction
Hand Therapy
Upper Limb Aesthetic and Functional Prosthetics
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Dr.Mustafa D.
11
In the past editions of Reconstructive Plastic Surgery
and Plastic Surgery-, brachial plexus injuries were
included in one overview chapter. This challenging
subject has been divided into two chapters to provide
more discussion and review of management techniques
and procedures. The subject of congenital anomalies
of the hand and forearm has been subdivided into eight
new chapters, and the final section, "Rehabilitation,"
is entirely new with three informative chapters on this
important area of upper limb management.
SUMMARY
This eight-volume text contains the standard subjects
traditionally included in the scope of plastic surgery.
Each chapter is written by a specialist in the subject
area who has provided an up-to-date overview cov-
ering the state of the art on the assigned topic. As noted,
in each of the eight volumes, new chapters and topics
have been included. Some of the topics covered indi-
vidually in this edition were previously part of an
overview chapter, but continued growth and interest
in this area now require an individual chapter to prop-
erly cover the subject. In other instances, new subjects
have been identified that reflect innovation within our
specialty, but areas that were not formerly considered
part of the scope of practice of the plastic surgeon are
also included. All chapters contained in this edition,
which appears almost 15 years after the previous
edition in 1990, have been completely revised. Apart
from titles that are similar to those in the previous
edition, chapters in this edition bear little or no resem-
blance to their predecessors. The changes in our spe-
cialty are rapid, and although some classical approaches
are still currently used for the management of patients,
many have evolved to include significant advancements
described within these pages. In addition, cutting edge
techniques and technologies, beyond the realm of
imagination and possibility in 1990, are now part of
the plastic surgeon's armamentarium and have thus
been included in this new, comprehensive edition. As
noted in the initial section of this introductory chapter,
innovations and accelerated changes are part of the
mindset of the specialty of plastic surgery.
STAYING AHEAD: MAJOR
INNOVATIONS IN PLASTIC
SURGERY
What Is Plastic Surgery?
John Marquis Converse, in his introductory chapter
to the first edition of Reconstructive Plastic Surgery,
defined the specialty as follows: "Plastic surgery is a
specialized branch of surgery devoted to the treatment
of deformities of the face and of other areas of the body,
notably the hand Because of the special nature of
plastic surgery, it is largely concerned with form, as is
12 I • GENERAL PRINCIPLES

implied in the term plastic"10 Webster, in his foreword

to the textbook by Gillies and Millard, The Principles
and Art of Plastic Surgery,11 quotes from Aristotle's On
the Parts ofAnimals,"Art> indeed, consists in the con-
ception of the result to be produced before its realiza-
tion in the material."12 Perhaps this quality is the most
essential component of a plastic surgeon; it is the quality
that distinguishes the artist from the technician.

Observing the Master Surgeon

From the earliest time, medicine has been a
curious blend of superstition, empiricism, and that
kind of sagacious observation, which is the stuff
out of which ultimately science is made. Of these
three strands—superstition, empiricism, and
observation—medicine was constituted in the days
of the priest-physicians of Egypt and Babylonia;
of the same three strands it is still composed. The
proportions have, however, varied significantly; an
increasingly alert and determined effort, running
through the ages, has endeavored to expel super-
stition, to narrow the range of empiricism, and
to enlarge, refine, and systematize the scope of
observation.
—Abraham Flexner"

As Flexner states, observation is the key to progress in
medicine. In plastic surgery, observation has allowed
us to progress from the initial surgical procedures for
nasal and earlobe reconstruction in ancient India as
recorded in the writings of Sushruta (circa 800 BC),
to the advancement flaps described by Celsus in
Roman times, to the discovery of the skin graft by
Reverdin, Oilier, Thirsch, and Wolfe between 1869 and
1875. Gillies observed Morestin in Paris, and soon the
tubed pedicle flap was described by Filatov (1917) and
Gillies (1918). Converse mentions the surgeons who
influenced an entire generation practicing between
World War I and World War II, such as Vilray Blair,
R. H. Ivy, V. H. Kazanjian, Ferris Smith, Eastman
Sheehan, and Sterling Bunnell in the United States and
the "Big Four" in the United Kingdom, including Sir
Harold D. Gillies (Fig. l-3),Thomas Kilner,Archibald
Mclndoe, and Rainsford Mowlem (Fig. 1-4). Obser-
vation of these master surgeons who were presented
with the uniquely difficult wounds sustained by sol-
diers in two wars during a new era of devastating
weaponry allowed plastic surgery to establish a firm
foundation in the management of both acquired and
congenital deformities.14 D. Ralph Millard, Jr., a master
surgeon who trained with Harold D. Gillies and con-
tinued the line of surgical expertise and innovation
into present times, states in his text Principlization of
Plastic Surgery, "Know the ideal beautiful normal.
Diagnose what is present, what is diseased, destroyed,
displaced, or distorted and what is in excess. Then
FIGURE 1-3. Sir Harold Delf Gillies, 1916. (Courtesy
of the Gillies Archive.)
guided by the normal in your mind's eye, utilize what
you have to make what you want—and when possi-
ble, go for even better than what would have been."15
Christian Albert Theodor Billroth in The Medical Sci-
ences in the German Universities, part l,"The Early
Universities," states the following regarding observa-
tion of the masters:
It is quite correct to distinguish between medical science and
the physician's art. A person may have acquired from books
a vast amount of medical knowledge, he may even have mem-
orized from books the technic of its application; such aperson
has much knowledge, and yet with it all he is no physician.
He must see and hear a master's diagnosis, prognosis, and
treatment of disease. He must witness the master's skill in
action, in order to himself become a practitioner.16
Observing the Master Teacher
The great possession of any university is its great
names ... not its wealth nor the number of its
schools, not the students who throng its halls—
but the men who have trodden in its service the
thorny road through toil.
—William Osier17

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image..

1 • PLASTIC SURGERY: THE PROBLEM-SOLVING SPECIALTY 13

FIGURE 1-4. British Association of Plastic Surgeons Council 1946-1947. Left to right, standing, A. B.Wallace,
M. C. Oldfield. W. Hynes. Left to right, sitting, R. Mowlem, J. N. Barron, Sir Harold Gillies, Prof. T. P. Kilner,
R. P. Osborne. (From The History of the British Association of Plastic Surgeons, Commissioned by the Council
of the British Association of Plastic Surgery, November 1986.)

William Osier identifies the ideal professor as one who
"thinks, talks, and works." The great teacher imparts
the following to his students: "enthusiasm, a full and
personal knowledge of the medical field, and a sense
of obligation to contribute to the medical field."17
Growth in our specialty is a direct byproduct of the
great teachers who have attracted the brightest stu-
dents to enter into our specialty. Looking at a list of
past presidents of the American Association of Plastic
Surgeons, one is presented with a multitude of exam-
ples of master teachers who have provided the stim-
ulus for future innovators to enter and enrich the art
and science of plastic surgery. Certainly, there are many
stimuli to attract the receptive student to such an inno-
vative, challenging, and rewarding discipline. However,
the most powerful, motivating force to enter the field
of plastic surgery is the opportunity to observe the
master surgeon and teacher.
Observing Anatomy
A single word embodies the entire foundation of
Western Medicine. Its three letters set the tone for
a distinctive worldview of healing and for the
science upon which it is based. They differentiate
the structure we have come variously to call ortho-
dox medicine, allopathic medicine, and most
recently biomedicine from every other system of
caring for the sick that the world has ever known.
That word is see.
—Sherwin B. Nuland18
Galen (Fig. 1-5), a Greek physician who wielded pro-
found influence on the practice of medicine for 1500
years, was born in Pergamon in Asia Minor (modern-
day Bergama, Turkey) around AD 129. He went on to
become the foremost physician in Rome, where numer-
ous honors, including the position of court physician,
were bestowed on him by the emperor Marcus Aure-
lius. Because of social and culture boundaries against
the use of human cadavers for medical study, most of
his anatomic observations were based on animal
experimentation with the resultant errors regarding
the structure and function of internal organs and
circulation (ebb and flow thesis through veins) in
humans. Galen also elaborated on the four fundamental

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14 I • GENERAL PRINCIPLES

FIGURE 1 - 5 . Galen of Pergamon (circa 129-200). (From

Asimovl: Biographical Encyclopedia of Science and Tech-
nology; the Lives and Achievements of 1510 Great Sci-
entists from Ancient Times to the Present, Chronologically
Arranged, rev. ed. New York, Avon, 1976:108.)

humors: phlegm, blood, yellow bile, and black bile.

However, in spite of his errors, Galen's experience as
a physician to the gladiators in Pergamon, and his
powers of observation, allowed him to contribute to
surgical practice. He stated,

All the operations in surgery fall under two heads, separa-

tion and approximation. Approximation has to do with the
reduction and dressing of fractures, reduction of disloca-
tion of the joints, reductions of prolapsed intestines, uterus,
or rectum, suture of the abdomen and restoration of tissue
deficiencies, as in the nose, lips, and ears. Division is con-
cerned with simple incision, circumcisions, elevations of skin,
scalping, excision of veins, amputation, cauterization, scrap-
ing, smoothing, excisions with the saw.

Galen's writings remained unchallenged through

the Middle Ages, awaiting further elucidation as to the
mysteries of human anatomy. 11
Andreas Vesalius was born in Brussels from a long
line of physicians (Fig. 1-6). He studied at the Uni-
versity of Paris and later at the medical school of Padua
in northern Italy, where he later became a teacher. He B A S I L S AB«

published his primary work and ultimate masterpiece, FIGURE 1-7. Title page of Vesalius' De Humoni Cor-
De Humani Corporis Fabrics in 1543 (Figs. 1-7 and poris Fobrico, Basel, 1543.

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 1 • PLASTIC SURCERY: THE PROBLEM-SOLVING SPECIALTY 15

Another stimulus resulting from Vesalius* brilliant

powers of observation was the publication of Novum
Organum: Aphorisms Concerning the Interpretation of
Nature and the Kingdom of Man (1620) by Francis
Bacon21 (Fig. 1-12). In this text, the new "instrument"
presented was the process of observation, hypothesis,
and experimentation, which yielded a resultant theory.
In other words, this text describes the scientific method
that was increasingly used through the 17th century
and continues to thrive in our modern era of medi-
cine. M Francis Bacon wrote, "Empiricists are like ants,
they collect and put to use; but rationalists, like spiders,
spin threads out of themselves" 21

Nature herself must be our advisor; the path she

chalks must be our walk. For as long as we confer
with our own eyes, and make our ascent from lesser
things to higher, we shall be at length receivedinto
her closet-secrets.
—William Harvey20

Certainly, anatomic research paved the way for the

expansion of our understanding of skin, muscle, and
fascia circulation, which provided the basis for the
development and evolution of current flap concepts
and design (Fig. 1-13). As a result, we now have a vast
array of restorative solutions, increased by the use of
microsurgical techniques, provided by muscle, mus-
culocutaneous, fascial, fasciocutaneous, and perfora-

FIGURE 1-8, Plate 44, De Humoni Corporis Fabrica,

Basel, 1543.

1 -8). t 9 Although it was highly controversial at the time

because of the direct challenge it posed to the accepted
principles published by Galen, De Hutnani Corporis
Fabricawas a stimulus for future physicians who would
continue the process of observation regarding func-
tional anatomy.
The 17th century marked the Age of Scientific Rev-
olution, when the process of observation provided
significant insights into human anatomy and physi-
ology. Foremost of the physician discoveries was that
of William Harvey (Fig. 1-9), who discovered the con-
tinuous circulation of the blood within a contained
system (Fig. MO). His most famous published work,
Exercitatio Anatomica de Motu Cordis et Sanguinis in
Animalibus [An Anatomical Exercise on the Motion of
the Heart and Blood in Animals]20 (Fig. 1-11), repre-
sents one of the most important books in medicine
and biology. Of interest, although Harvey was edu-
cated in Cambridge, he later studied in Padua and
there established a direct historical link with
Vesalius.14 FIGURE 1-9. William Harvey (1578-1657).

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image...

16 I • GENERAL PRINCIPLES

Digestive canal

Portal vein

HVC Hepatic vein

SVC Superior
vena cava

IVC Inferior
vena cava
Right auricle
(fermentation
of new blood)

Distribution of
blood from the
aorta
Renewal and
purification of
the blood

FIGURE 1-1 0. A, The circulatory system of the blood as taught by William Harvey in the 17th
century. RV, LV, right and left ventricles; RA, LA, right and left auricles.

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Vtsmtf'SdCf'Kf image..

1 • PLASTIC SURCERY: THE PROBLEM-SOLVING SPECIALTY

^*>'
Upper half of body

/
Independent terminations
of the two currents

\
\
\

\ \
• \
\
i
i

(b) Digestive canal

(EJ Portal vein

Chylic blood
vc Trunk of
vena cava
Ascending
vena cava
Descending
DVC
vena cava
Aerated blood

CD Ascending artery
Descending
artery

Pulmonary vessels

(ED* Trachea and

bronchi

VA: Venous artery

« Arterial vein

Lower half of body

FIGURE 1 - 1 0 , c o n t ' d . B, The traditional system of the movements of the blood as taught by
Galen in the 2nd century AD. (From Chauvois L: William Harvey: His Life and Times, His Discov-
eries, His Methods. New York, Philosophical Library, 1957:21.)

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image...

18 I • GENERAL PRINCIPLES

knowledge. Knowledge is limited. Imagination

eXF.RCITATIO encircles the world.
ANATOMICA DE —Albert Einstein22

MOTV CORDIS ET SAN- Half of these school boys are already published. I
* GVINIS IN A N I M A L I - cannot waste time with these classes. These books,
BVS,
mesmerizing the weaker assumptions of lesser
qytLIELMI HAKVEI A,NGLI,
mortals. I need to look through, to the governing
:V r •* i^UmmtnM Ldnduwji dynamics, find a truly original idea. It is the only
way I will distinguish myself.
—John Nash2'

Plastic surgery has never stood still. As one practices

surgery on a daily basis, it may seem that the skills
and solutions have stood the test of time. Like being
in a boat traversing a lake, progress seems slow stand-
ing on the bow. However, when you turn toward the
stern and look back, much to your amazement, you
have traveled a long distance. Plastic surgery is in a
constant state of evolution toward problem solving.
It is the essence of our specialty and the reason we
currently flourish. We treat skin and its contents with
F KJXCOFrXTT, no anatomic boundaries and are called on by all sur-
SmnpdburfGVIUELMI FITZERI. gical specialties for consultation and collaboration. If
ASSO X. DC xxntL we ever lose this talent for innovation, our specialty
will most likely be absorbed within the multiple dis-
FIGURE 1 - 1 1 . Title page of Harvey's Exercitatio
Anatomica de Motu Cordis et Sanguinis in Animolibus [An ciplines limited to specific organ systems or anatomic
Anatomical Exercise on the Motion of the Heart and Blood regions.
in Animals}.

tor flaps (Figs. 1-14 to 1-16). Angiosomes and vascu-

lar territories were identified as a result of anatomic
observation, which further identified the vascularity
of bone (Fig. 1-17; see also Chapter 15). Anatomic
studies have also provided fascial planes for use in facial
rejuvenation (Color Plate 1-1). There is still much to
learn through observation in anatomy and physiol-
ogy. In Exercitatio Anatomica de Motu Cordis et San-
guinis in Animalibus, Harvey states, "I profess to both
teach and learn anatomy not from books but from
dissections; not from the position of philosophers, but
from the fabric of nature." 20 The ability to "see," that
is, to sincerely observe, remains the key to medical dis-
covery. The outstanding contributors responsible for
producing the information contained in this com-
prehensive text certainly embody both the spirit and
practice of "seeing." Each chapter exemplifies the power
of observation and will give the reader the basis to see
the art and science of plastic surgery.

PROFILE FOR INNOVATION

/ am enough of an artist to draw freely upon my
imagination. Imagination is more important than FIGURE 1-12. Sir Francis Bacon (1561-1626).

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Dr.Mustafa D.
image...

1 • PLASTIC SURGERY: THE PROBLEM-SOLVING SPECIALTY 19

fS^ms^
r*« ••
. * -_ •

.V>: *
-**'*- V A

9&/. WT»I n w r n •-

B
FIGURE 1-13. A, Illustration from the celebrated 1794 "Letter to Editor" responsible for the Western
spread of the "Indian method" for total nasal reconstruction. B, Plate VIII illustrating the bandaging. [A
from B.L: Letter to Editor. Gentleman's Magazine 1794;October:891. 6 from Tagliacozzi C: De Curtorum
Chirurgia per Insitionem. Venice, Gaspare Bindoni, 1597.)

WHAT Is THE BASIS FOR SUCCESS IN INNOVATION?
The likely answer is found in the previous section on
the amazing master surgeons who preceded us and the
teachers who have captured the interest of the bright-
est students and provided the principles necessary to
bring creativity to our specialty. Difficult problems are
also an important motivating factor in eliciting our
creativity. World Wars I and II produced massive soft
tissue and bone injuries requiring innovative solutions
and yielding principles that are now applied in more
peaceful times. Genitourinary congenital anomalies
attracted the plastic surgeons to establish surgical treat-
ments that now are mostly used by our pediatric
urology colleagues but represent the creative efforts of
a generation of plastic surgeons. Craniofacial defor-
mities begged for solutions, and plastic surgeons
developed inventive methods of manipulating both
bone and soft tissue in the head and neck region that
today amaze both physicians and patients. Milton
Edgerton, a surgical leader and teacher, in 1957 regard-
ing management of head and neck cancer stated, "It
is time for all surgeons who conscientiously treat oral
cancer to draw together any and all methods that lead
to fewer recurrences, less deformity, and better func-
tion in that increasing fraction that remain well."24
Plastic surgeons responded with multiple innovations,
initially including the array of muscle and musculo-
cutaneous flaps and subsequently the microvascular
transplantation of skin, bone, functional muscle,
and innervated skin to restore the patient after tumor
extirpation.
As life expectancy is extended, interest in facial and
body rejuvenation procedures is likely to increase in
an aging population. Plastic surgeons have been at the

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image...

20 I • GENERAL PRINCIPLES

T A F E L IX.
Uebersichtsschema der Hautarteriengebieie.
FJgur A. Fisur B,
Hautgebiet der A. cpigastn'ca auperficialis superior. Hautgebiet der Rr. dorsales aua den Aa. iotercojtsles.
Hautgebiet <l«r A. cpigastrica auperficialis inferior. Hautgebiet der Rr. doi atea aus deu Aa. lumbalca.
Hautgebiet der Aa. epigaatrica superior und inferior, Hautgebiet der Rr. dorsales aus den Aa. sacrales.
Haulgcbict der Aa. pudendao cxternae. Hautgebiet der Rr. perforantes posleriores derAa. in-
Hautgebiet der Aa. dorsales penis, tcrcostales.
Hautgebiet der Rr. pcrforantes aus den Aa. intcrcostalcs. Hautgebiet der Rr. perforantes posleriores d. A; lumbales.
Hautgebiet der Rr. perforautes aus den Aa. lumbales. Hautgebiet des Truocus tliyreocervicalis.
Hautgebiet der A. circumflexa ilium supcrficialis. a der A. cervicaiis superficial is.
liautgebiet der A. profunda fcnjori8(Aa. circumll. femor.). h der A. transversa scapulae.
10 Hautgebiet der A. feraoralis. c der A. transversa colli,
11 Hautgebiet des Rctc auperficiale genu, Hautgebiet der A. deltoidea subcutanea posterior.
12 Hautgebiet der A. tibialis antica. S Hautgobiet der A. circumflexa scapulao supcrficialis.
der A. tibialis postica. Hautgebiet der A. collateralis radialis inferior.
13 Hautgebiet der A. poplitea (Aa. eurales). 9
14 Hautgebiet der Aa. tboracicae. 10 Hautgebiet der A. collateralis ulnaria superior.
15 Hautgebiet der A. tboracico-acromialia. It Hautgebiet dea Rete cubitale.
15a Hautgebiet der Rr. perforantes dor A. mammaria interna, 12 Hautgebiet der A. radialis.
1G Hautgebiet dee Truncus tliyreocervicalis. 13 liautgebiet der A. ulnaris.
14 Hautgebiet der A. interoaaea externa und interna.
17 Hautgebiet der A. thyreoide* superior, 15 Hautgebiet der A. glutaca.
18 Hautgebiet der A. deltoidea aubculanea anterior, 10 Hautgebiet der A. ischiadica.
19 Hautgebiet der A. brachialia. 17 Uuutgebiet der A. pudenda interna.
20 Hautgebiet der A. collatcralia ulnaris superior, IS Hautgebiet der A. obturatoria.
21 Hautgebiet der A. radialis. 19 Hautgebiet di»r Rr. perforantes der A. profunda fcraoria
22 Hautgebiet der A. mediana. 20 Hautgebiet der A. poplitea.
23 Hautgebiet der A. ulnaria.
21 Hautgebiet 21 Hautgebiet der A. tibialis antica und poatica.

FIGURE 1-14. Anatomic territories were demonstrated by Carl Manchot in Die Houtarterien
des menschlichen Korpers (1889), based on results of his dissections of the human integument.

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image...

<

1 • PLASTIC SURGERY: THE PROBLEM-SOLVING SPECIALTY 21

FIGURE 1-1 5. A, Reproduction of Plate 70 from Michael Salmon's Arteries de la Peau (1936). B, Repro-
duction of Plate 71 from Salmon's book. (From Cormack CC, Lamberty BGH: The Arterial Anatomy of Skin
Flaps. Philadelphia, Churchill Livingstone, 1986.)

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22 I • GENERAL PRINCIPLES

700 BC Susruta f graft or pedicled flap

1595 Tagliacozzi pedicled random flap

1797 Carpue. Graofe
Dieffenbach random cutaneous
1842 Mutter
1887 Gersunny i
1900 1913 Trotter delayed flaps
1917 Filatov
1918 Esser tube pedicles
1920 Gillies I
I
1

1950 1950 Wookey

i
axial cutaneous pedicled flap > musculocutaneous pedicled flap
1951 Edgerton
1955
1957
Owens
Zovickian
p 1 ___-
1960 Conley
1960 1963 myo-osteo-cutaneous
M c Gregor
1965
1967
1967
Bakamjian
Littlewood
Wilson ij r no further basic
types defined

Ger
Orticochea
Serafin O
M c Craw
Dibbel cutaneous pedicled flaps muscle flaps
Mathes musculocutaneous flaps
Vasconez
Jurkiewicz
Nahai !
Maxwell musculocutaneous free flaps
Bostwick
Ariyan I cutaneous free flaps muscle free flaps
myo-osteo-cutaneous free tissue transfers
Taylor

1980
Daniel t
Hayhurst
Ohmori
O'Brien fasciocutaneous flaps
Ponien
Song
Corma ck/Lam berty
various types including
osteo-fascio-cutaneous

FIGURE 1 - 1 6 . The historical development of the present concept of flaps. (From Cormack GC, Lamberty
BGH: The Arterial Anatomy of Skin Flaps. Philadelphia, Churchill Livingstone, 1986:3.)

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image...

1 • PLASTIC SURGERY: THE PROBLEM-SOLVING SPECIALTY 23

A B
FIGURE 1-17. Following reviews of the works by Manchot and Salmon (see Figs. 1-14 and
1-15), and with total body studies of the blood supply to the skin and underlying tissues, it was
possible to segregate the body anatomically into three-dimensional vascular territories termed
angiosomes. Each angiosome can be subdivided into matching arteriosomes (arterial territo-
ries) and venosomes (venous territories). A, The cutaneous perforators with their choke con-
nections are depicted. B, The origin of the perforators from their underlying source arteries and
their muscle branches is shown. The vascular territories of each source artery are illustrated in
the integument (A) and deep tissues (B) by lines drawn through the choke connecting vessels.
Note that the territories correspond to those two layers and how they appear as sectors in the
limbs. (From Taylor CI, Palmer JH: The vascular territories [angiosomes] of the body: experi-
mental study and clinical applications. Br J Plast Surg 1987;40:113.)

forefront of the development and refinement of aes-
thetic procedures that have provided a reliable means
of delaying the visible effects of the aging process in
our older but healthy population. The current rise in
obesity has led to widespread interest in bariatric
surgery. We have responded with innovative procedures
designed to return the body to normal, appropriate
proportions. In the future, plastic surgeons will no
doubt continue to lead creative efforts toward unique
solutions, including basic science research, in areas such
as fetal surgery, composite tissue transplantation, and
tissue engineering.
WHAT QUALITIES ARE ESSENTIAL TO SUCCESSFUL
INNOVATION? Traits that may play a role in the profile
for innovation include intelligence, curiosity, drive,
desire, imagination, and health (Table 1-10). Each year
since 1974, the American Association of Plastic Sur-
geons selects a recipient for the James Barrett Brown
(JBB) Award, given for the best publication for the
year by a plastic surgeon based on membership voting.
A look at the list of titles and recipients of this award
summarizes the many innovations that have affected
the course of our specialty. Also, the American Asso-
ciation of Chairmen of Academic Programs, composed
of the program directors for the American Council
for Graduate Medical Education's approved residency
programs in the specialty of plastic surgery, is a driving
force in cultivating a profile of innovation in the res-
idents under their supervision. In a questionnaire sent

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Dr.Mustafa D.
24 I • GENERAL PRINCIPLES

TABLE 1-10 • QUALITIES ESSENTIAL TO projects: college, 40%; medical school, 69%; residency
SUCCESSFUL INNOVATION (general surgery), 83%; residency (plastic surgery),
86%; fellowship, 49%; present, 86%. Mentor was listed
Traits Factors in the top three most important factors for successful
innovation by the JBB prize winners and the program
Intelligence Environment directors. When the JBB Award respondents were asked
Curiosity Time to define the significant mentor supporting their
Drive Mentor creativity, the list included the following based on
Desire Collaborator
Resources percentage of the respondent: friend, 4%; professor—
Imagination
Luck college, 4%; professor—medical school, 17%; faculty
Health
(plastic surgery), 36%; colleague—plastic surgeon,
Other Traits or Other Traits or 17%; colleague—basic science, 12%; other, 10%.
Factors (JBB) Factors (PD)
The urge to form partnership, to link up in col-
Persistence Promotion requirement
Persistence laboration arrangements is perhaps the oldest,
Honesty
Self-motivation Leaving legacy strongest, and most fundamental force in nature.
Aggressiveness —Lewis Thomas27
Belief
Collaboration has been foremost in the clinical and
JBB, recipients of James Barrett Brown Award (senior authors); PD, plastic research activities of plastic surgery. Because our spe-
surgery program directors. cialty has the strongest background in surgical science
and has no anatomic boundaries, we work with other
fields of medicine on a daily basis. This constant col-
in 2002 regarding the most important factors for inno- laboration serves to open our minds to problems and
vation, the senior authors of the JBB Award (26 of to the expertise of our colleagues and allows us to ask
28 winners responded) and the individual program new questions and begin the process of innovation
directors in the United States were asked to list the together with our medical colleagues. When specifically
above-mentioned traits for innovation in order of asked the value of collaboration to their scientific
importance. 25 The JBB Award recipients listed the top publications, 69% of JBB Award respondents to the
three as curiosity, imagination, and drive. The program previously mentioned questionnaire indicated that
directors listed the top three as drive, desire, and curios- collaboration was vital to the contribution. The field
ity. Factors that may be important in the profile for of endeavor of the collaborators was listed as follows:
innovation include environment, time, mentor, col- anatomy, 19%; plastic surgery, 26%; pediatric surgery,
laborator, resources, and luck (Table 1-10). The JBB 16%; biochemistry, 7%; other, 32%.
Award recipients listed the top three as environment, Program directors who responded to the ques-
resources, and mentor. The program directors listed tionnaire (39) conduct research (97%) and have a
the top three as mentor, resources, and collaborator. research laboratory in the program (77%). Of the pro-
Each questionnaire allowed the participant to list other grams, 77% have extramural funding, 66% employ
traits or factors that may influence creativity. Exam- a technician, and 5 1 % conduct a regular research
ples for the JBB Award recipients included persistence, seminar. Collaboration is used on a regular basis by
honesty, self-motivation, aggressiveness, and belief. 90% of the program director respondents. Fields of
Examples included by program directors were pro- endeavor of the collaborators include the following:
motion requirement, persistence, and leaving legacy. general surgery, 8%; physiology, 6%; biochemistry, 8%;
Obviously, all these traits and factors are key to a profile anatomy, 6%; molecular biology, 8%; and other, 65%.
for innovation. Other categories in the responses of the JBB Award
recipients and the program directors included 31 and
Genius, in fact, involves significant energy and 80 separate fields, indicating the wide range of con-
passion to question assumptions that have been tacts used by a plastic surgeon in collaborative efforts,
taken for granted over long periods. which speaks to the diversity of talent available in the
—David Bohm26 university and communities in which we work and
reside.
Commitment to research is an important aspect in the
profile for innovation. Each JBB Award winner was Scientists who consider themselves cooperative tend
asked to indicate exposure to research in the course to have more published articles than their com-
of the educational process toward the profession of petitive colleagues Not surprisingly, coopera-
plastic surgery. The response included the following tion increases creativity.
percentages indicating involvement in research —Perry Buffington2*

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TekPt'tf'SelCiW image...
1 • PLASTIC SURGERY: THE PROBLEM-SOLVING SPECIALTY
Innovation is our hallmark. To foster our c o m m i t m e n t
to creativity, a plastic surgeon should work with medical
colleagues for the advancement of health care. Accord-
ing to No Contest a u t h o r Alfie Kohn, 29 competition has
downsides, which include the following: competition
promotes conformity; competition p r o m o t e s risk
aversion; c o m p e t i t i o n distracts from creativity.
Although we must direct o u r patients to physicians
w h o are best able to provide t h e state of t h e art in
problem solving, there is much to benefit a profile of
innovation by collaboration.
JOY OF SURGERY
A surgeon attempts to alter certain physical rela-
tionships within the organism so as to restore
or improve function. He may excise diseased or
unwanted tissues; he may reorganize and reshape
tissue, he may transplant or implant tissues or
organs. Whichever of these he is doing, his goal is
normality, or perhaps the improvement of func-
tion, through effective physical relations between
the organs, tissues or cells of the patient.
—H. Bendy Glass"
In a lecture delivered at Surgical Grand Rounds at the
University of California, San Francisco, entitled "Joy
of Surgery," Maurice Jurkiewicz traced his experience
as a surgeon and teacher and described the excitement
and rewards of delivery of care to his patients with
congenital and acquired deformities. T h e opportunity
to treat life- and limb-threatening problems and at the
same time restore function and contour is unique to
t h e specialty of plastic surgery. As a relatively small
specialty, we k n o w o u r fellow plastic surgeons, are
abreast of innovations, and are quick to use new ideas
to the benefit of our patients. As we progress through
our career, we have the joy of seeing our patients
progress through their lives with renewed spirits, in
part from the benefit derived from o u r surgical skills
used to correct their congenital or acquired deformity.
It is hoped that this new edition of Plastic Surgery will
serve as a source of joy for each reader as well as a tes-
tament to the astounding progress of the art and science
of plastic surgery and the c o m m i t m e n t and skills of
the contributors who m a d e this text possible. Finally,
it is hoped that this text will serve as a foundation for
future innovations by o u r readers through individual
efforts and collaboration with others.
REFERENCES
1. Pancoast J: A Treatise on Operative Surgery Comprising a
Description of the Various Processes of the Art Including All
the New Operations; Exhibiting the State of Surgical Science in
Its Present Advanced Condition. Philadelphia, Carey and Hart,
1844.
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Dr.Mustafa D.
25
2. Converse JM: Reconstructive Plastic Surgery. Philadelphia, WB
Saunders, 1964.
3. Converse JM: Reconstructive Plastic Surgery, 2nd ed. Philadel-
phia, WB Saunders, 1977.
4. McCarthy JM: Plastic Surgery. Philadelphia, WB Saunders,
1990.
5. Converse JM: Preface. In Converse JM,ed: Reconstructive Plastic
Surgery. Philadelphia, WB Saunders, 1964:vii.
6. Converse JM: Introduction to plastic surgery. In Converse JM,
ed: Reconstructive Plastic Surgery, 2nd ed. Philadelphia, WB
Saunders, 1977:3.
7. Chase RA: Epilogue (or after shock). In Millard RD: Princi-
plization of Plastic Surgery. Boston, Little, Brown, 1986:649.
8. Cooper AP: Surgical Essays; written with Benjamin Travers
(1783-1858). London, Cox & Son, 1818-1819.
9. Edgerton MT: The role of surgery in the treatment of trans-
sexualism. Ann Plast Surg 1984; 13:473.
10. Converse JM: Introduction to plastic surgery. In Converse JM,
ed: Reconstructive Plastic Surgery. Philadelphia, WB Saunders,
1964:3.
11. GiIliesHD,MilIardRD:ThePrinciplesandArtofPlasticSurgery.
Boston, Little, Brown, 1957.
12. Aristotle: On the Parts of Animals fDe Partibus Animalium],
350 BCE.
13. Flexner A: Medical Education in the United States and Canada:
A Report to the Carnegie Foundation for the Advancement of
Teaching. The Carnegie Foundation, Bulletin No. 4,1910.
14. Lyons AS, Petrucilli RJ: Medicine, An Illustrated History. New
York, Harry N. Abrams, 1978.
15. Millard RD: The plastic surgeon's creed. In Millard RD:
Principlization of Plastic Surgery. Boston, Little, Brown,
1986:648.
16. Billroth CAT: Ober das Lehren und Lernen der medicinischen
Wissenschaften an den Universitaten der deutschen Nation nebst
allgemeincn Bemerkungen iiber Universitaten. Vienna,
1876. English translation by William Henry Welch (1850-1934):
The Medical Sciences in the German Universities: A Study in
the History of Civilization. New York, Macmillan, 1924.
17. Osier W: Principles and Practice of Medicine. New York, Apple-
ton, 1894.
18. Nuland SB: The Mysteries Within: A Surgeon Explores Myth,
Medicine, and the Human Body. New York, Simon & Schuster,
2001.
19. Vesalius A: De Humani Corporis Fabrica. Basel, 1543.
20. Harvey W: Exercitatio Anatomica deMotu Cordis et Sanguinis
in Animalibus [An Anatomical Exercise on the Motion of the
Heart and Blood in Animals]. Frankfurt, 1628.
21. Bacon F: Novum Organum: Aphorisms Concerning the Inter-
pretation of Nature and the Kingdom of Man, 1620.
22. Viereck GS: What life means to Einstein: an interview. The
Saturday Evening Post, October 26,1929.
23. Nasar S: A Beautiful Mind: The Life of Mathematical Genius
and Nobel Laureate John Nash. New York, Simon 8c Schuster,
2001.
24. Edgerton MT, Desprez JD: Reconstruction of the oral cavity in
the treatment of cancer. Plast Reconstr Surg 1957;19:89.
25. Mathes SJ: Profile for Innovation Study. Presented at the Amer-
ican Association for Plastic Surgery, 2002.
26. Bohm D: On Dialogue. Nichol L, ed. New York, Routledge,
1998.
27. Thomas L: The Lives of a Cell. New York, The Viking Press,
1974.
28. Buffington P: Creative Problem-Solving Personality. Lecture
Series.
29. Kohn A: No Contest: The Case Against Competition. Boston,
Mariner Books, 1992.
30. Glass HB: Genetics and surgery. The Ravidin Lecture. Bulletin
of the American College of Surgeons, 1972.
CHAPTER
U
Historical Perspectives
WILLIAM D. MORAIN, MD
What we know today as plastic surgery dates to anti-
quity. The earliest known procedures were described
in an Indian publication, the Samhita, about 600 BC.
In the book, Sushruta, a member of the caste of potters,
described reconstructions of the nose and earlobes with
use of tissue transfer techniques. In his nasal recon-
struction, known yet today as the Indian method,
Sushruta transposed skin from the forehead to replace
missing skin of the nose (Fig. 2-1). He and his fellow
potters had ample opportunity to perform the proce-
dure because of the frequency of nasal amputation as
a humiliating punishment at the time.
A Greco-Roman tradition in plastic surgical prac-
tice developed in the first century AD. Celsus described
the advancement flap and a form of subcutaneous
island flap. Continuing through the Classical period,
the procedures reached their apogee in the seventh
century with Paulus Aegineta, whose spectrum of
surgery extended from facial fractures to hypospadias.
It is likely that Paulus provided a link between the
Western surgical traditions and those of the Indian and
Arab schools through his many travels.
Although the coming of the Dark Ages extinguished
most of Western scholarship, the traditions of learn-
ing flourished through Islamic scholarship across the
Arab world. As a result, plastic surgery benefited from
the fortuitous geography of a religion that bridged East
and West. The result was the translation and trans-
mission of the experience of Indian surgeons to the
Latin world.
The legacy of that linkage came to highest fruition
in the Renaissance of the 15th century when the Branca
family in Sicily began reapplying the Indian method
to nasal reconstruction. They soon found it advanta-
geous, however, to substitute flap skin from the arm
as a superior donor site for facial and ear reconstruc-
tion. This new method spread across much of south-
ern Italy during the next century and was broadly
applied to sizable numbers of dueling deformities and
other mutilating injuries.
Such was the background for the remarkable tech-
nical achievements of Gaspare Tagliacozzi (1545-
1599) of Bologna, whose copiously illustrated De
Curtorum Chirurgia per Insitionem (1597) endures as
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Dr.Mustafa D.
a landmark in the history of plastic surgery (Fig. 2-2).
Tagliacozzis elaborate description of the delayed arm
flap for nasal reconstruction demonstrated a maturity
of surgical judgment and observation that would not
be surpassed for more than 2 centuries.
The rebirth would come, as before, from India,
or at least it would be reintroduced to the Western
world from India, never having in fact disappeared
there over the centuries. The impetus arose out of a
letter from an Englishman appearing in the Gentle-
man's Magazine in London in October 1794, describ-
ing a forehead flap nasal reconstruction that had been
performed on a mutilated soldier. Joseph Carpue,
a 30-year-old London surgeon, was intrigued by the
article and spent 2 decades researching the tech-
nique. In 1814, Carpue at last faced his own patient
without a nose and performed the operation in just
37 minutes, following precisely the method of the
Indian potters.
In the meantime, von Graefe, Surgeon General of
the Prussian Army in the Napoleonic Wars, reported
three nasal reconstructions. One used the Indian
method, a second the tagliacotian, and the third a mod-
ified tagliacotian without a delay procedure and with
a shortened period of arm attachment. Von Graefes
publication stimulated renewed interest in plastic
surgical techniques on the continent.
The first half of the 19th century built on the work
of Carpue and von Graefe in a number of important
areas. Dieffenbach extended the work of his German
colleague beyond the face into many reconstructive
challenges; von Langenbeck established many of the
principles of modern cleft lip and palate surgery.
In France, Labat and Blandin were the first to write
works on plastic surgery. Their colleague Serre pio-
neered important work on facial reconstruction,
especially as father of the advancement flap procedure
(today known as the French method of nasal recon-
struction). Dupuytren contributed much to this
growing field of surgery, in particular to the delineation
of the pathology and correction of palmar fibromatosis
and the classification of burns according to their skin
depth. Velpeau and Malgaigne contributed important
textbooks in plastic surgery.
27
28 I • GENERAL PRINCIPLES
FIGURE 2 - 1 . Illustration from the celebrated 1794
"Letter to Editor" responsible for the Western spread of
the "Indian method" for total nasal reconstruction. (From
B.L: Letter to Editor. Gentleman's Magazine 1794;
October:891.)
Elsewhere, Sabbatini described the first lip switch-
ing operation in his comprehensive Italian treatise on
the history of plastic surgery. In the United States, a
variety of reconstructive procedures were described
by Pancoast, Mutter, Mott, Post, and Buck.
The early 19th century was especially important for
the development of skin grafting. In 1804, Baronio pub-
lished his experimental work on skin grafts in sheep.
In 1817, Sir Astley Cooper performed the first successful
human skin graft, covering the stump of an ampu-
tated thumb with skin from the amputated part. Full-
thickness grafts were successfully transplanted in other
regions by Warren in Boston.
It was in the second half of the 19th century, however,
that a more significant development occurred in skin
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Dr.Mustafa D.
FIGURE 2-2. Plate VIII illustrating the bandaging.
(From Tagliacozzi G: De Curtorum Chirurgia per Insitionem.
Venice, Gaspare Bindoni, 1597.)
grafting. The partial-thickness graft was first applied
by Reverdin in 1869, followed by Oilier in 1872 and
Thiersch in 1874. Such grafts, in which the donor area
would quickly resurface itself, offered the opportunity
to cover large open areas for the first time. At the same
time, specialized full-thickness grafts for critical areas
such as the eyelid were perfected by Wolfe, Krause, and
others.
The two greatest advances in the history of surgery—
anesthesia and asepsis—were developed during the
19th century as well. Without them, plastic surgery
would have remained an occasional hazardous curios-
ity rather than the ubiquitous offering it has become
today. Morton's famous introduction of ether at the
Massachusetts General Hospital in 1842 is known to
all surgeons. Lister's antiseptic principles, so slow to
be adopted in the United States, would soon make
primary healing the rule rather than the exception.
All of these 19th century advances became prologue
to the epidemic of mayhem arising in the European
trenches of 1914. In World War I, an appalling host of
infantrymen were wounded, with maxillofacial wounds
reaching unprecedented numbers. The Parisian recon-
structive surgeon Morestin was noted for his distin-
guished work with these injuries early in the conflict.
A young New Zealand otolaryngologist, Harold Gillies,
was sufficiently inspired by what he saw of Morestin's
techniques that he established his own unit at the
image...
FIGURE 2-3. Harold Dell Gillies.
Aldershot Military Hospital in England to treat such
wounds (Fig. 2-3). However, when the overwhelming
numbers of facial injuries demanded a larger treat-
ment center, it was necessary for Gillies to move his unit
to a major facility at Queen Mary Hospital in Sidcup.
Sidcup would become for plastic surgery what
Vienna had been for psychiatry—a fountainhead from
which the specialty arose and flourished. Those who
apprenticed the craft there included Ferris Smith from
the United States, Pickerill and Newland from New
Zealand and Australia, and Risdon and Waldron from
Canada.
On the continent, a separate approach to maxillo-
facial injuries was developed near Boulogne-sur-Mer
under the leadership ofVarastad H. Kazanjian, a Boston
dental surgeon. Kazanjian based his approach on his
background in prosthetic dentistry, devising ingenious
methods for stabilizing jaw fractures in preparation
for delayed wound closure. Kazanjian's meticulous
record keeping became the basis for the comprehen-
sive instruction of those who followed.
It could be said that plastic surgery had been per-
formed frequently during the 19th century but that
the world knew few "plastic surgeons" at the time—
and certainly not in the United States. Thus, there was
no trained corps on which Surgeon General Gorgas
could call when the United States entered Europe's
trenches in 1917. Adopting the regionaThead and neck"
model of Gillies and Kazanjian, Gorgas appointed
Vilray P. Blair of St. Louis to direct a military subsec-
tion for the treatment of maxillofacial injuries. Blair
had recently published the first edition of his Surgery
and Diseases of the Mouth andjawsthat included several
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2 • HISTORICAL PERSPECTIVES 29
innovations of his own. He established teams consist-
ing of a surgeon and a dentist who were to combine
their respective skills. The teams were trained through
concentrated educational programs at American denial
and medical schools as well as through visits to the
evacuation hospitals of Gillies and others.
American maxillofacial casualties, initially treated
and stabilized on the continent, were soon transported
to military maxillofacial centers in the United States.
These included facilities at Fort McHenry, Baltimore;
Cape May, New Jersey; Walter Reed General Hospital,
Washington, DC; and others. All would serve as the
foundation for a new specialty that was taking shape
out of the crucible of wartime necessity.
International conferences and publications served
to systematize and disperse the techniques and clini-
cal experiences of the batdefield, and the residual defor-
mities of the wounded continued to provide a basis
for expanding the knowledge as each was sequentially
improved in civilian operating theaters over the years.
Blair's earlier book on maxillofacial surgery went
through two greatly expanded editions that incorpo-
rated his wartime experience, and Gillies summarized
the Sidcup activities in his landmark Plastic Surgery of
the Face in 1920.
The war gave birth to a number of technical inno-
vations. Gillies developed the tubed pedicle flap and
explored its limits on many wounded patients, only to
discover later that the Russian surgeon Filatov had pre-
ceded him by a few months. The delay procedure was
widely popularized and perfected. Kazanjian's many
dental and maxillofacial appliances revolutionized the
treatment of facial skeletal fractures.
After World War I, the dispersion of plastic surgi-
cal knowledge was notable for two circumstances. The
first was the shift of focus from post-traumatic defor-
mities to more aesthetic concerns. The most notable
figure in this field was Jacques Joseph, a Berlin ortho-
pedic surgeon, who developed many of the modern
techniques and instruments for corrective rhino-
plasty. Among those who observed and emulated his
work were Gustave Aufricht and Joseph Safian, whose
trainees in the United States would make the methods
universally available to future apprentices.
The second circumstance was the method by which
the techniques were transmitted to the next genera-
tion of surgeons. Rather than in university-based pro-
grams of education, the new specialty grew largely
through informal arrangements whereby those who
wished to learn observed in the operating rooms of
senior surgeons for varying periods. Some, like Gillies,
made teaching a regular part of their practice and
organized regular demonstration clinics. Others were
more protective of their knowledge and would permit
observation but with little accompanying explanation.
For the most part, university surgical programs
in the United States, functioning in the austere
image...

30 I • GENERAL PRINCIPLES

ML
FIGURE 2-4. First annual meeting of the American Board of Plastic Surgery held in Galveston, Texas, February
2, 1938. From left to right, standing: William S. Kiskadden, George Warren Pierce, Ferris Smith, William E. Ladd,
Fulton Risdon, Robert H. Ivy, John Staige Davis, Harold L. D. Kirkham, and Jerome P. Webster. Seated: George M.
DorranceandVilray Papin Blair. (From Converse JM: Plastic surgery: the 20th century. The period of growth [1914-
1939]. Surg Clin North Am 1967;47:261.)

halstedian tradition, wanted little to do with plastic
surgeons. Those who professed to perform the proce-
dures were often marginalized by powerful chiefs of
surgery and encouraged to shift to more traditional
surgical work. John Staige Davis at Johns Hopkins
found acceptance to be especially difficult. Among the
first to devote his entire practice to the new specialty,
he was granted little support within his department
despite publication of his landmark textbook, Plastic
Surgery—Its Principles and Practice.
Despite the growing maturity and dispersion of the
specialty through the 1920s and 1930s, the public and
(too often) professional image of plastic surgery was
that of a cadre of cosmetic dilettantes. It was clear that
an umbrella of legitimacy would have to be established
under which reputable practitioners could maintain
respectability and distinguish themselves from those
whose ethics and skills were marginal. Blair persevered
with his general surgery colleagues to promote the
concept of an organized board for this purpose. The
American Board of Plastic Surgery was formed in 1937
(Fig. 2-4). In addition to Blair, the founding members
included Davis, Robert Ivy, George Pierce, Ferris
Smith, Jerome Webster, William Kiskadden, William
Ladd, Fulton Risdon, Harold Kirkham, James Barrett
Brown, Sumner Koch, Gordon New, John Wheeler, and
George Dorrance.
Despite the imprimatur of the Board, plastic surgery
education did not soon become a dominant force in
university programs. The majority of those seeking
training in the specialty continued to do so in one-on-
one preceptorship arrangements if they were fortu-
nate or through varying periods of mere observation
if they were not. Several preceptors protected their own
interests by forcing their trainees to sign agreements
that prevented them from establishing practices within
the city or region in which they had trained. In time,
however, formal residency programs were established
in major centers such as New York, Philadelphia, and
St. Louis.
The fountainhead of plastic surgical education in
the United States would soon become Barnes Hospi-
tal in St. Louis. There, under Vilray Blair's guidance,
the specialty forged its place as an integral component
of the department of surgery. Blair recognized the
common threads that bound plastic and general
surgery together and worked to strengthen those bonds.
In time, the Barnes faculty of Blair, Brown, Louis Byars,
and Frank McDowell seeded the nation's universities
with professors whose students, in turn, formed the

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 image...
CHAPTER
42
•
Analysis of the Aesthetic
Surgery Patient
GILBERT P. GRADINCER, MD •
SOCIETAL INTEREST IN AESTHETIC SURGERY
A PRACTICAL APPROACH TO THE AESTHETIC
SURGERY PATIENT
Initial Contact
Consultation
Psychological Effects of Plastic Surgery
Limitations and Complications
SOCIETAL INTEREST IN
AESTHETIC SURGERY
According to the most comprehensive survey to date
of U.S. physicians and surgeons conducted by the
American Society for Aesthetic Plastic Surgery, there
were nearly 8.3 million surgical and nonsurgical
cosmetic procedures performed in 2003.' Surgical
procedures represented 78% of the total; nonsurgical
procedures represented 22% of the total (Fig. 42-1).
From 1997 to 2003, there was a 293% increase in the
total number of cosmetic procedures. Surgical proce-
dures increased 87%; nonsurgical procedures increased
471% (Fig. 42-2). In 2003, women had nearly 7.2
million cosmetic procedures (87% of the total), and
men had approximately 1.1 million (13% of the
total). The number of cosmetic procedures for men
increased 3 1 % from 2002.
There can be no doubt as to the rapidly increasing
and widespread interest in aesthetic plastic surgery pro-
cedures. Generalized public approval and acceptance
of plastic surgery have also increased in the last
decade. A survey by the American Society for Aesthetic
Plastic Surgery of 1000 American households in 2003
indicated that more than half (54%) of all Americans
approve of cosmetic plastic surgery, and nearly one
quarter (24%) say diey would consider having cosmetic
surgery either now or in the future. 2
Whether people are married or unmarried has little
to do with whether they would consider cosmetic
surgery; 24% of married Americans and 25% of
'Deceased.
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Dr.Mustafa D.
EUGENE H. COURTISS, M D f
Scheduling Surgery
Preoperative Appointment and the Anesthesia
Consultation
The Surgical Experience
Postoperative Communication and Office Visits
Unsatisfactory Results
CURRENT RESEARCH ON THE "SCIENCE OF BEAUTY-
unmarried Americans said they would consider cos-
metic surgery.2 Although women (30%) are more likely
than men to contemplate cosmetic surgery, almost 18%
of men said they were considering having a proce-
dure. Many of those who might not want surgery them-
selves say it has nothing to do with what others might
think. More than three quarters (77%) of all women
and 74% of all men said that if they had cosmetic
surgery, they would not be embarrassed if other
people knew about it.2 The top surgical procedure for
both sexes is liposuction (Figs. 42-3 and 42-4).'
Even though approval of cosmetic surgery among
people younger than 35 years is high (56%), younger
people are more likely than older Americans to want
to keep their cosmetic surgery a secret. Of 18- to 34-
year-olds, 24% said they would not want people outside
their family and close friends to know they had under-
gone cosmetic surgery, compared with only 8% of
55- to 64-year-olds. 2
The age group with the most procedures performed
ranges from 35 to 50 years. In 2003, patients within
this age range had 3.7 million cosmetic procedures per-
formed, accounting for 45% of the total number of
procedures.The patients within this age group are gen-
erally classified as baby boomers. Liposuction is the
most popular surgical procedure within this group,
and Botox injection is the most popular nonsurgical
procedure. 1
The top five aesthetic plastic surgery procedures in
2003 were liposuction (384,626, up 3% from 2002),
breast augmentation (280,421, up 12%), eyelid surgery
(267,627, up 17%), rhinoplasty (172,420, up 10%),
and breast reduction (147,173, up 17%). The top five
31
32 • THE HEAD AND NECK

10,000,000 -
8,470,363 8,251,994
CD
>-
8,000,000 - 6,889,531
o
2 5,741,154/
Q. 6,000,000 -
o
4,606,954^^^^
^J-'
XJ
E 4,000,000 -
2 2,774,942/^
2,098,173^a<
2,000,000 -
"T~ T~ r~
1997 1998 1999 2000 2001 2002 2003
FIGURE 4 2 - 1 . Total numbers of surgical and nonsurgical cosmetic procedures performed,
1997-2003. (Data from the American Society for Aesthetic Plastic Surgery.)

2003- 1,819,485

2002 - 1,620,736

1997- 972,996

2003- 6,432,509

2002 - 5,268,795 FIGURE 4 2 - 2 . Total numbers of surgical

(top) and nonsurgical [bottom] cosmetic pro-
cedures performed, 1997-2003. (Data from
1997-" ] 1,126,177 the American Society for Aesthetic Plastic
Surgery.)

Liposuction 322,975

Breast augmentation 280,401

Eyelid surgery 216,829

Breast reduction* 147,173

FIGURE 4 2 - 3 . Top cosmetic sur-
geries for women. In 2003, women
had 87% of the nearly 8.3 million
cosmetic procedures performed in Rhinoplasty 119,047
the United States. {Data from the
American Society for Aesthetic Plastic
Surgery.)

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 image...

42 • ANALYSIS OF THE AESTHETIC SURGERY PATIENT 33

Liposuction 61,646

Rhinoplasty 53,376

Eyelid surgery 50,798

Reduction of enlarged breasts

22,049
FIGURE 4 2 - 4 . Top cosmetic surger-
ies for men. In 2003, men had 13% of
the nearly 8.3 million cosmetic proce- Hair transplantation
dures performed in the United States. 14,891
(Data from the American Society for
Aesthetic Plastic Surgery.)

nonsurgical cosmetic procedures in 2003 were Botox A PRACTICAL APPROACH TO THE

injection (2,272,080, up 37% from 2002), laser hair
removal (923,200, up 25%), microdermabrasion
(858,312, down 17%), chemical peel (722,248, up
46%), and collagen injection (620,476, down 21%)
(Figs. 42-5 and 42-6).
Within the rapidly growing market of aesthetic
surgery candidates, it is important to discern which
patients are truly the best candidates for specific pro-
cedures. The American Society for Aesthetic Plastic
Surgery, working with an independent research firm,
compiled data for procedures performed from 1997
to 2003 by multiple specialists and was able to quan-
tify the best candidates for specific procedures as well
as standard fees, length of procedure, number of treat-
ments, results, and length of time before a patient
normally returns to work (Table 42-1).'
AESTHETIC SURGERY PATIENT
From initial contact to postoperative care to ongoing
cosmetic maintenance, a dedicated team of profes-
sionals assembled to ensure excellence in care of patients
through the entire process of evaluation is essential.
Because aesthetic surgery patients are usually respon-
sible for all or most of the fees involved in their care,
they have considerable expectations for high-quality
treatment and continued care.
Initial Contact
The patient forms an indelible impression of the office
as a result of the initial telephone call for information
and to make an appointment. If the telephone

Liposuction 384,626

Breast augmentation 280,401

Eyelid surgery 267,627

Rhinoplasty 172,420

Breast reduction* 147,173

FIGURE 4 2 - 5 . Top surgical cosmetic procedures. In 2003, 22% of the nearly 8.3 million
cosmetic procedures performed in the United States were surgical. (Data from the American
Society for Aesthetic Plastic Surgery.)

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 *
TABLE 42-1 • AMERICAN SOCIETY FOR AESTHETIC PLASTIC SURGERY PROCEDURE QUICK FACTS

Physician-
Surgeon Length of Number of Back to
Procedure Best Candidate Fees* Procedure Treatments Results' Work

Abdominoplasty Protruding abdomen; excess fat and skin; $4,477 2-5 hours One Permanent 1 -3 weeks
(tummy tuck) weak abdominal muscles
Botox Frown lines and crow's-feet $413 30 minutes Repeat Temporary No downtime
treatments
4-6 months
Breast augmentation Small, disproportionate breasts $3,257 1-2 hours One Permanent; 1 -2 weeks
possible
implant
replacement
Breast lift Sagging, poorly shaped breasts $4,616 1V2-3V2 hours One Long-lasting 1 -2 weeks
Breast reduction Large, heavy, pendulous, or $5,183 2-4 hours One Permanent 1-2 weeks
disproportionate breasts
Buttock lift Sagging skin, excess fat, weakened muscles $4,616 2 hours One Long-lasting 10-14 days
in thigh/buttocks area
Cellulite treatment Dimpled thighs and buttocks $503 30-45 minutes Ongoing Temporary No downtime
(mechanical roller
massage therapy)
Cheek implants $2,376 2 hours One Permanent 1 -2 weeks
Chemical peel (ranges Sun-damaged or unevenly pigmented skin $831 Va hour-3 hours; One or multiple; Long-lasting Depends on
from light to deep) depends on depends on type of peel
type of peel type of peel
Chin augmentation Receding chin $1,735 1 hour One Permanent 1 -2 weeks
Dermabrasion Acne, wrinkles around mouth, sun-damaged <$ 1,367 A few minutes to Multiple sessions Long-lasting 7-10 days
skin 1V2 hours
Ear surgery Protruding or disproportionate ears $2,589 2-3 hours One Permanent 5 days
Eyelid surgery Excess fat, wrinkled, drooping skin of upper $2,510 1 -3 hours One Long-lasting Within 10 days
eyelids; bags, puffiness under eyes
Face lift Loose skin, deep lines, wrinkles, jowls $5,622 2-3 hours One Long-lasting Within 2 weeks
Fat injection Frown lines, crow's-feet, nasolabial folds $1,065 30 minutes- May require Temporary Minor: 1-4 days
1 hour reinjection Extensive:
in 3-18 months 7-14 days

Forehead lift Sagging, low eyebrows; forehead creases; $2,779 1-2 hours One Long-lasting Within 10 days
frown lines
Gynecomastia Enlarged male breasts $2,894 2 hours One Permanent 1 week
treatment

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 3
w
to

Hair transplantation Hair loss with the availability of healthy hair $3,580 Several hours Multiple sessions Permanent Several days
in donor areas over 1-2 years
Laser hair removal Unwanted hair on face or body $423 1-2 hours; Multiple sessions Ongoing No downtime
depends on
area
Laser skin resurfacing Fair, nonoiiy skin; sun-damaged facial skin, $2,250 Variable, up to One or multiple, Long-lasting Variable, up to
wrinkles around mouth and eyes, acne 1 '/ a hours depending on 14 days
scars on laser and
skin condition
Laser treatment of Very small spider veins $427 30 minutes- Multiple sessions Permanent No downtime
leg veins 1 hour
Lip augmentation Thin lips $1,487 1 hour One Permanent Within 1 week
(surgical)
Lipoplasty Normal weight with isolated fatty areas $2,425 45 minutes- One Permanent 1 -2 weeks
(liposuction) 2 hours
Lower body lift Skin laxity without significant fat deposits $5,833 Up to 8 hours One Long-lasting Up to 4 weeks
Microdermabrasion Fine lines, crow's-feet, age spots, acne scars $201 Multiple sessions, Temporary No downtime
2- to 3-week
intervals
Rhinoplasty Nose too large, wide, or tip needs reshaping $3,745 1-2 hours One Permanent 7-10 days
Sclerotherapy Spider veins $273 30 minutes- 3-4 injections Permanent No downtime
1 hour
Soft tissue fillers
Autologous fat Nasolabial folds, lips, frown lines, and facial $1,270 1 hour, Highly variable, Temporary Minor: 1-4 days
recontouring depending on repeat Extensive 7-14
the sites treatments days
Calcium Nasolabial folds, frown lines, crow's-feet, $1,169 Less than 1 hour Repeat Temporary No downtime
hydroxyapatite and lips treatments
(Radiance) 2 years or
longer
Collagen Frown lines, crow's-feet, nasolabial folds $381 Less than 1 hour Repeat Temporary No downtime
treatments
3-6 months
Hyaluronic acid Nasolabial folds, forehead wrinkles, smile $552 Less than 1 hour Repeat Temporary No downtime
(Hylaform, lines, and lips treatments 4
Restylane) months-1 year
Thigh lift Loose, excess skin $4,078 2 hours One Long-lasting 2-4 weeks
Upper arm lift Excess skin and fat on underside of arm $3,056 2 hours One Long-lasting 1 -2 weeks

"National average; surgeon fees are based on ASAPS 2003 statistics. Fees vary considerably by geographic region.
•With any surgical procedure, a revision or touch-up may sometimes be necessary.
© Copyright 2003 The American Society for Aesthetic Plastic Surgery. All rights reserved.

cn

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36 II • THE HEAD AND NECK
Botox injection
Laser hair removal 923,200
Microdermabrasion 858,312
I
Chemical peel 722,248
Collagen injection
1620,476
FIGURE 4 2 - 6 . Top nonsurgical cosmetic procedures. In 2003, 78% of the nearly 8.3
million cosmetic procedures performed in the United States were nonsurgical. (Data
from the American Society for Aesthetic Plastic Surgery.)
receptionist is welcoming, the patient is encouraged
to proceed. The opposite is equally true. All person-
nel who answer the phone must be skilled in making
the patient want to come to the office. Of course, the
most important skill is courtesy. However, office per-
sonnel must also be knowledgeable about the aesthetic
surgery procedures performed by the plastic surgeon
and be able to give the prospective patient general and
specific information about a consultation. Setting up
the initial appointment, information relating to the
costs of consultation, and payment expectations and
estimated costs for the procedure in which the patient
is interested are part of the initial telephone contact.
The telephone receptionist must also be adept at triage
of potential patients.
Consultation
Common courtesy requires that the patient be received
and seen in a friendly, timely manner. Each office needs
a procedure for scheduling patients in a realistic way
so all commitments can be met. No one likes to be
kept waiting for an extended period after the sched-
uled appointment. Although it is true that patients
have been "trained" to expect many physicians to be
unavoidably late, one must never forget that the
patient's time should be considered valuable. It is the
responsibility of the receptionist to inform patients if
there is a delay, to tell them approximately how long
they may have to wait, and to offer to reschedule the
appointment. There should also be a method in place
to determine how patients wish to be addressed (first
name, Mr. or Mrs.). The information needs to be
transmitted to "back office" personnel and ultimately
to the physician.
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2,272,080
Each office has its routine in regard to the consul-
tation. The patient fills out an information sheet
including medical history and personal data (Fig. 42-
7). The nurse or resident typically completes the
medical history and records vital signs and informa-
tion about the patient's interest in aesthetic surgery
procedures.
General information about the patient typically
includes name, address, telephone, date of birth,
marital status (including name of spouse), social secu-
rity number, name of party responsible for payment
of bill, name of employer, name of referring party, and
health insurance information. Although some of the
information is not relevant or necessary for aesthetic
surgery, it is important to have in case of emergency
or unforeseen medical problems.
Some cosmetic surgery patients wish to withhold
information (e.g., age, name of spouse, previous
plastic surgeries, occupation). If the information that
they withhold is not necessary for rendering proper
medical care, their decision can be respected. However,
if it is necessary or strongly advisable that the infor-
mation be shared, it is the surgeon's responsibility to
tell the patient. If, for example, the patient has had
previous surgery that relates to the surgery being
requested, it is wise to obtain the previous surgeon's
name and permission to request a copy of the oper-
ative note. Patients who keep secrets from their
surgeons or need to be secretive about their surgery
may have a suspicious degree of guilt concerning the
prospective procedure. 3 The reason may, on the other
hand, be a straightforward privacy request.
The consultation should be more than an evalua-
tion of a condition amenable to aesthetic plastic
surgery. It should be a time when the patient and
1*e**>ttf<ascme image...

42 4- ANALYSIS OF THE AESTHETIC SURGERY PATIENT 37

MEDICAL HISTORY INFORMATION

Name of Family Physician:. Patient Height:. Weighlrm

Drug sensitivities or allergies; if yes, which drugs Yes No
Problems with anesthesia Yes No
Local Yes No
General Yes No
Do you bruise easily? Yes No
Do you have a bleeding tendency? Yes_ No
Breathing or lung problems Yes No
Heart disease Yes No
High blood pressure Yes No
Diabetes Yes No
Kidney disease Yes No
Glaucoma, cataracts, or "dry eye" Yes No

Psychiatric problems Yes No

Epilepsy Yes No

Present medications (list)

Past illnesses and surgeries (list)

FOR OFFICE USE ONLY

Blood Pressure Pulse Temperature

FIGURE 42-7. Medical history information form.

surgeon evaluate one another. Patients are often won-
dering whether the physician is right for them and if
they feel comfortable. The physician is determining
whether the patient's goals are realistic in terms of what
can be achieved and if the patient will be happy with
the result.
Goin and Goin4 state that at the end of the first inter-
view, the surgeon should know the answers to the
following questions:
• How long has the patient been dissatisfied with
the relevant body part? For example, if the patient

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TeWftf«aatfW image...

38 I • GENERAL PRINCIPLES

Prospective Cohort Study

]
(^ Risk Factor Absent (e.g., smoking) L j ; Cases of Lung Cancer
Risk Factor Present (e.g., smoking) Study Cohort

Risk factors collected Outcomes assessed

Present Future

Time
i ri I T ii.

Cohort at Risk Cohort with outcomes identified

FIGURE 3-3. Prospective cohort study. In the prospective cohort study, the investigator develops a
hypothesis about variables that may affect the outcome under investigation, collects data about those
risk factors, and then follows the cohort for development of the outcome of interest. For example, when
the association between smoking and lung cancer was suspected, a prospective study design increased
the strength of that causal association. Although prospective studies lend credence to causal associa-
tions, they are expensive and generally require years of follow-up.

of which are flawed compared with prospective data
collection. Data collected in this manner are more likely
to be incomplete, inaccurate, inconsistent, or subject
to recall bias. On the other hand, the major advantages
of retrospective studies are that they can be done in a
relatively short time frame and are much less costly
than prospective studies.
Case-Control Studies
Case-control studies (Fig. 3-5) differ from cohort
studies in that two distinct groups of subjects are inves-
tigated. The first group (case) is selected by the pres-
ence of disease and the second (control) by its absence.
In contrast, a single population at risk for disease is
studied in a cohort design. Like cohort studies, the case-
control design may be prospective or retrospective.
The major strength of the case-control study is in the
investigation of rare conditions or outcomes. Its weak-
ness lies in the inability to assess incidence or preva-
lence of disease, and it has an increased susceptibility
to bias. Controls may be concurrent or historic,
matched (on key variables such as age and sex), or
unmatched.
Case Series and Case Reports
Cases are simply a collection of subjects who havebeen
identified by the presence of a disease or condition. In
our literature, these are frequently reported on the basis
of a specific intervention. If the collection of subjects
is large and consecutive (case series), it may provide
valuable information about indications and con-
traindications for surgery and expected outcomes. If

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42 • ANALYSIS OF THE AESTHETIC SURGERY PATIENT
patient's employment may also depend on appearance.
For many patients, looking healthy, alert, and attrac-
tive may be necessary to advance in their career, or
they may be competing with younger people for their
job. 3 In most instances, however, patients are usually
happier with the result if their motivation for the
surgery is for the effect it will have on them rather than
the effect it will have on others (e.g., employer, co-
workers, friend, lover, spouse, family).
PHOTOGRAPHY
Appropriate photographs should be taken (or arrange-
ments made to have them done by a professional) at
the time of the initial consultation. This practice
ensures that they can be reviewed with the patient at
a subsequent visit. This allows more objectivity when
surgical goals are discussed. The photographs can be
used to point out asymmetry and to analyze the defect
of concern to the patient. Alerting a patient to asym-
metry before surgery is performed is far superior to
having to explain that a suboptimal result is due to a
condition that existed preoperatively. A reversal mirror
can be a valuable preoperative aid in establishing
the patient's awareness of asymmetry. In the reversal
mirror, the patient sees a reversed image of what is
normally seen on looking in the mirror.
It is preferable for surgeons to take their own pho-
tographs. One may often discern a defect through the
lens in a limited field that was not apparent during
examination of the patient. Preoperative photographs
should always be in the patient's chart before surgery
is performed.
Showing photographs of other patients is contro-
versial.5 It is, however, a widespread practice. Propo-
nents think it helps inform patients of what kind of
improvement they can expect. Skeptics think it is unfair
commercialism, and the surgeon is likely to select only
the very best results, thereby implying and warrant-
ing the improvement to be expected.
Digital imaging with computer-generated modifi-
cation of the patient's own photographs is widely used
to show patients the physical changes that are being
requested. Care must be taken to emphasize that no
guarantee can be made that the goal will be realized.
Patients need to understand that surgery is an inexact
art form. A realistic goal of improvement must be
stressed and the expectation of perfection dismissed.
Psychological Effects of
Plastic Surgery
In the classic book Changing the Body—Psychological
Effects of Plastic Surgery, Goin and Goin 4 stress the
importance of understanding the psychological effects
of plastic surgery. Plastic surgeons need an under-
standing of body image to help interpret the positive
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Dr.Mustafa D.
39
and negative changes that patients often experience
subsequent to a plastic surgery procedure.
Body image is the mental representation an indi-
vidual has of his or her body at any one moment. 8 A
negative body image can be realistic or unrealistic. It
is probably fair to say that if a person's body image is
totally positive, he or she would not be seeking aes-
thetic surgery improvement. Postoperatively, patients
need to adjust to their new body image. They need
time for their mental representation to change to match
the altered postoperative reality.
Body dysmorphic disorder is a preoccupation
with an imagined defective appearance, the magni-
tude of which may be underestimated by the plastic
surgeon. The plastic surgeon needs to be cautious in
dealing with the monosymptomaticaily obsessed
patient, the delusional patient, and the polysurgical
patient (especially individuals who move from pre-
occupation with one body part to another). In addi-
tion, one should be especially wary of patients with
a psychiatric history or exaggerated, unrealistic
surgical expectations. 9
Limitations and Complications
All procedures have limits. The known limitations
should be discussed in great detail with the patient pre-
operatively. One should stress to the patient that the
body heals by making scars and that all surgical scars
are permanent. Potential complications of the con-
templated surgery constitute the major component of
counseling of patients and therefore of informed
consent. 5
Scheduling Surgery
A key position in every plastic surgery office is that of
surgery coordinator. This is the person who is respon-
sible for
• helping the patient select the date, time, and site
(office surgery, freestanding facility, hospital) of
the procedure;
• discussing fees, facility charges, and all other
expenses related to surgery and arranging for the
patient's payment of these fees (most often in
advance of cosmetic surgery); Courtiss 5 states that
"when the procedure has been paid for previously,
a major area for conflict is eliminated and the
patient is more satisfied with the results";
• identifying and arranging for any necessary lab-
oratory work (e.g., mammogram, electrocardio-
gram, complete blood count);
• obtaining the patient's signed photography and
operative consent forms;
• distributing to the patient printed forms that
describe preoperative preparation, transportation
40 II • THE HEAD AND NECK

needs to and from surgery, and instructions for
postoperative care; and
• scheduling an appointment for a follow-up post-
surgical office visit.
This person must be patient, understanding, and
gentle. Very often, the patients come to look on the
coordinator as a friend and confidant. Patients fre-
quently share information, questions, and concerns
previously withheld. Establishment of a trusting
relationship cannot be rushed and is usually followed
by one or more phone calls. A typical surgery sched-
uling form is used in most offices (Fig. 42-8). There
are other forms that the coordinator reviews with
the patient. Three forms require the patient's
signature:
A statement that clearly addresses fiscal respon-
sibility for expenses incurred as a result of treat-
ment of postoperative complications (Fig. 42-9).
Without such an understanding, a dispute about
who pays the bills is common. This statement
clearly outlines the surgeon's commitment as well
as the patient's responsibility. Although aesthetic
surgery is not paid for by health insurance,
expenses related to complications may some-
times be covered. Surgeons may purchase insur-
ance at a reasonable cost that pays medical and
surgical expenses incurred in the treatment
of complications that follow cosmetic surgery
procedures.
A photographic and peer review consent form
(Fig. 42-10). This allows not only the taking of

Surgery Scheduling Checklist

Name Age.
Home phone. Work Cell
Surgery date/time Length of surg..
Anesthesia: local, .general Hospital
Outpatient In patient
Diagnosis
Procedure
Assist Confirmed.
Referring MD. Phone Advised
Pt. advised to arrive. Info sheet
Photos taken Photo consent.
Surgery consent. Laboratory
IA date noted Fee quote* (IA) By.
IA billed
IA rec'd.
Post-op appt.. Post-op Rx.
Other

*IA after fee quote indicates M.D. told patient the fee and that it is payable in advance of surgery.

FIGURE 42-8. Surgery scheduling checklist. Highlighted areas are typically completed by the physician.

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TSWTtf'Seicrtee image...

42 • ANALYSIS OF THE AESTHETIC SURGERY PATIENT 41

To my patients:

Prior to surgery, you will have paid my fee, as well as other costs. Although they are very
unusual, complications requiring additional surgery, consultation, hospital or other
services can occur. There will be no additional charges for any service performed by my
office staff or me. Any other doctor, hospital, or related expenses are your responsibility.

Healing after surgery is usually a predictable process leading to a good result; however,
occasionally, a surgical revision is necessary to help achieve this result. Whereas there
will not be a charge for my services, there will be a facility charge if it is done in our
office. If it is done at the hospital, there will be charges for which you are responsible.

-, M.D.

I understand and accept the above statements.

Patient Signature:. Date:.

Witness: Date:

FIGURE 42-9. Statement of fiscal responsibility for payment of expenses incurred as a result of treat-
ment of postoperative complications.

photographs but also the use of the photographs
for purposes of medical education medical
publication, and education of patients. The peer
review portion allows record review necessary
for the maintenance of quality care.
3. The surgical consent form, which provides for
the administration of sedation and local anes-
thesia and performance of necessary surgery
(Fig. 42-11).
Preoperative Appointment and
the Anesthesia Consultation
This appointment should be scheduled as close to the
day of surgery as possible, preferably the day before.
This proximity allows one to perform any necessary
surgical markings on the patient for breast, torso, or
extremity surgery. This is particularly important for
body contour and liposuction. It involves the patient
in decisions that, made jointly, help avoid postopera-
tive disappointment. This appointment should also be
used to perform and dictate the preoperative surgical
note, including history and physical examination
(unless this was previously done by the patient's
primary physician). One may engage in further dis-
cussion about the surgery and answer any outstand-
ing questions. At this time, preoperative photographs
of the surgical markings are taken.
If the surgery will be performed at a hospital facil-
ity under general anesthesia, a hospital-based anes-
thesiologist sees the patient before the day of surgery
at the hospital. In most offices, if the general anes-
thesia is administered in the office surgery suite, the
anesthesiologist calls the patient at home at a pre-
arranged time the evening before surgery. The anes-
thesiologist should have received the patient's pertinent
medical information. This allows the anesthesiologist
to feel comfortable that the venue selected for the
patient is appropriate. The patient, in turn, feels com-
fortable with the plans for anesthesia.

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42 • THE HEAD AND NECK

Photographic and Peer Review Consent

To Whom It May Concern:

I hereby give my consent to. ., M.D., and/or his associates or

assistants, to take preoperative, intraoperative and postoperative photographs for the
medical record of .

understand that these photographs are the property of Dr.. and

authorize him to use them for professional medical purposes deemed appropriate,
including the showing of these photos or slides for purposes of medical education,
medical publication, and patient education.

In addition, I hereby give permission to Dr.. and/or his associates to

perform a review of my medical records for the purposes of insuring the delivery of the
highest quality of care.

Patient Signature:. Date:.

Witness: Date:

FIGURE 42-10. Photographic and peer review consent form.

The Surgical Experience Postoperative Communication and

It is important that all of the medical personnel
involved with the patient's care have a positive atti-
tude about aesthetic surgery. This is controllable if the
surgery is performed on an outpatient basis in an
accredited office surgical suite. The anesthesiologist
and the operating room, recovery room, and office
personnel are chosen by the surgeon. In a hospital or
freestanding surgical environment, this control lies
with the institution. Employees who are indifferent to
or have negative feelings about aesthetic surgery do
not help foster an environment conducive to a posi-
tive experience for the patient. This environment
should be positive and supportive from the moment
the patient walks through the front door to the time
the patient is delivered by wheelchair to the caregiver.
Caregivers need to be educated in person by the nurse
who is discharging the patient to their care.
Office Visits
It is a sound, considerate practice to call the patients
home the evening of surgery to check on the patient's
well-being. This practice is also appreciated by patients.
If the call is made by the surgeon, it is especially appre-
ciated. It is preferable not to tell patients to expect a
call so they are either pleasantly surprised when it
comes or not disappointed if it does not. At any rate,
it is reassuring to patients and family to know they
are in the thoughts of the surgical team. The caregiver
needs to be instructed, even encouraged, to call if there
is any concern that things are not going well. A list of
adverse reactions to look for should always be given
to the caregiver.
Arrangements are usually made for postoperative
visits before surgery. This may be 1 day or 1 week after
surgery, depending on the nature of the procedure. It

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Dr.Mustafa D.
 42 • ANALYSIS OF THE AESTHETIC SURGERY PATIENT 43

Surgical Consent

I hereby give permission to. j M.D., to administer the necessary

sedation and perform any and all operations as may be deemed necessary and/or
advisable to his patient.

It is understood that although good results are expected, this cannot be guaranteed, nor
can it be guaranteed that there will be no untoward results of surgery.
I understand the surgical prodedure(s) and terminology as discussed, described, and as
listed hereon.

Surgery(ies):

Patient Signature:. Date:.

Witness: Date:

FIGURE 4 2 - 1 1 . Surgical consent form.

is advantageous to have a second office entrance for
patients who have just undergone facial cosmetic
surgery. The advantages of a second entrance include
the following: it ensures the patient is seen promptly
by being taken directly to the treatment room; it elim-
inates embarrassment for the patient, who thinks the
appearance is unsightly; and it protects other patients
in the waiting room from feelings of fear, shock, or
revulsion caused by seeing another patient's swollen,
bruised face.
After appropriate examination and treatment, the
patient can exit by the same route with the next
appointment card in hand. The office personnel need
to support the patient in every way possible through
the recovery period. Surgery is physically and emo-
tionally exhausting for the patient. Encouragement that
things are going well and extra care when progress is
slow are required. Patients must be told before surgery
that healing is a long process. This statement will sub-
sequently have to be reinforced repeatedly after surgery.
Patients frequently experience postoperative "blues"
even when things are going well. They need to be
advised that this is to be expected. Understanding office
personnel can help a patient get through this difficult
time more easily. The light at the end of the tunnel
appears when patients realize they look better, their
surgical goal has been met, and they are glad they had
the surgery.
Unsatisfactory Results
These are the three possible combinations of sub-
optimal results:
1. The patient is happy, the surgeon is unhappy.
This can be chalked up to good fortune. The goal
of surgery is for the patient to be happy with the
results.
2. Both the patient and the surgeon are unhappy.
• If the tissues have healed, the problem is not
resolving, the patient wants it fixed, and the
surgeon thinks it can be improved, then one
should undertake secondary or revision
surgery, provided an appropriate amount of
time has passed. Procrastination is difficult for
both the patient and the surgeon.
• If honest appraisal is that time alone will lead
to significant improvement, it is best to refrain
from any additional procedures. Help the
patient to be patient.
• If the problem needs to be fixed and the
surgeon does not think he or she will be able

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Dr.Mustafa D.
44 II • THE HEAD AND NECK
to revise it appropriately, the patient should
be referred to another surgeon who has the
skills to improve the result. If the problem
cannot be fixed, it is best to try to get the patient
as much information as possible to assist the
patient in accepting the result.
3. The surgeon is happy, the patient is unhappy.
This is the worst combination. It means the
surgeon had no chance to succeed because
the patient and the surgeon had different
goals. Try to appease the patient, but do not do
surgery that most likely will not be successful in
making the patient happier with the result. It
may mean referring the patient to another
surgeon.
CURRENT RESEARCH ON THE
"SCIENCE OF BEAUTY"
Although the sharp rise in aesthetic surgical proce-
dures is uniquely modern, the pursuit of beauty is and
always has been an integral part of every known human
culture. 10 Studies in the early 1990s by Langlois and
colleagues"' 12 concluded that empirical evidence sup-
ported the notion that the most attractive faces in a
given population favored characteristics close to the
mean of the population. It was reasoned that selec-
tion favored normative features adaptive for survival
within the local environment. This theory, which is
based on natural selection, offers a plausible expla-
nation for why average faces may be considered attrac-
tive, how these preferences could have been acquired,
and why cultural differences would occur. However,
subsequent experiments have challenged this theory,
and new data suggest that the most "attractive" faces
vastly differ from the average in a systematic and repro-
ducible manner.13'*5
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Dr.Mustafa D.
In a study using computer technology known as
FacePrints, Johnston and Franklin14 developed com-
posite, "evolved," computer-generated faces that were
deemed most attractive to white participants. Anthro-
pometric measurements of these composite faces
were compared with measurements of random female
faces within the population. The study revealed that
the most attractive female faces were by no means
average or arbitrary but were composed of specific
features (e.g., full lips) with specific proportions (e.g.,
chin length) that were significantly different from the
average face (Fig. 42-12). These results were confirmed
by subsequent studies14 and suggest that the theory of
sexual selection, first proposed by Darwin in 1871,
is likely to account for the evolution of nonaverage
displays of attractiveness.16,17
In terms of "darwinian" sexual selection, charac-
teristics that are considered most attractive in men
and women should be sex specific and occur as a result
of sex hormones, occur at puberty, and reflect bio-
logic attributes that are beneficial to the reproductive
success of the opposite sex (e.g., fertility, immuno-
competence). Experimental evidence provides strong
support for this theory.18 Thus, a strong jaw related to
the presence of generous amounts of testosterone is
considered attractive in men. In women, a lower than
average testosterone exposure leads to a shorter,
narrower lower jaw and wider eyes, traits that are
consistently seen as attractive by test subjects.'9,20 In
addition, lip fullness (also consistently considered
attractive) parallels fat deposits on the hips and breasts
during later puberty, indicating higher than average
estrogen exposure during this time. 20
The age-old maxim that "beauty is in the eye of the
beholder" is called into question as both event-related
potential and functional magnetic resonance imaging
recordings indicate that male brains show a rapid
FIGURE 4 2 - 1 2. Major significant
differences between an average (left)
and attractive (right) female face.
(From Johnson VS, Solomon CJ,
Gibson SJ, Pallares-Benjamin A:
Human facial beauty: current theo-
ries and methodologies. Arch Facial
Plast Surg 2003:5:371.)
T-ekPttf^eicMee image...
42 •
e m o t i o n a l response and activation of t h e nucleus
accumbens, an effect closely associated with reward,
on exposure to attractive, evolved female faces gener-
ated to convey specific characteristics based on sexual
selection criteria. 21,22 Examination of women's pref-
erences for male faces also supports the sexual selec-
tion theory. 23 It is therefore not surprising that even
in the animal k i n g d o m , o n e sees secondary charac-
teristics related to sexual competition for mates in the
evolution of stag antlers, tails of peacocks, bird songs,
frog croaks, and extravagant colors of many bird feath-
ers. 2 4 C u r r e n t theoretical and empirical findings
suggest that what is considered "beautiful" is cued on
visual, vocal, and chemical characteristics that signify
health, including developmental and reproductive
health. T h e conclusion is stated in Evolutionary Aes-
thetics as follows: "Beauty is a promise of function in
the e n v i r o n m e n t . . . survival and reproductive success
in evolutionary history. Ugliness is the promise of low
survival and reproductive failure." 17
It is possible that technology will allow the devel-
o p m e n t of an imaging system to produce a three-
dimensional variation of a patient's face, by use of
anthropometric data (a " 10-point"beauty scale known
as principal components analysis has been developed 25 )
standardized for m a x i m u m "attractiveness," for use as
a clinical decision-making tool to mutually define
desired surgical goals. 26 Experts agree that making this
technology available to clinicians is still m a n y years
away. However, similar technology is currently being
used for many automated facial recognition systems. 27,28
CONCLUSION
There has been a sharp rise in both societal interest in
plastic surgery and the n u m b e r of procedures being
performed. Current research suggests that beauty is
vital in terms of mate selection and competitiveness
within society. T h e availability of aesthetic surgery
offers many patients a chance to correct congenital
aesthetic defects as well as defects brought on by
aging and environmental factors.
T h e aesthetic surgery process is unlike any other
medical experience for the patient. The patient is
healthy before treatment and temporarily sick as a result
of surgery. At t h e same time, t h e aesthetic s u r g e o n s
office is different from other medical offices. It must
be capable of providing integrated care in a personal-
ized manner, with a goal of making things as easy as
possible for the patient. T h e result should be a patient
w h o is pleased with the overall experience as well as
the improved appearance.
REFERENCES
1. American Society for Aesthetic Plastic Surgery: Cosmetic
Surgery National Data Bank 2003 Statistics. Available at:
http://www.surgery.org/press/statistics-2003.php.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
ANALYSIS OF THE AESTHETIC SURGERY PATIENT 45
2. The American Society for Aesthetic Plastic Surgery:
Consumer Attitudes Survey 2003. Available at:
http://www.surgery.org/prcss/statistics-2003.php.
3. Gorney M: Patient selection criteria. In Gradinger G, Kaye B,
eds: Symposium on Problems and Complications in
Aesthetic Plastic Surgery of the Face. St. Louis, Mosby,
1984:12.
4. Goin JM,Goin MK: Changing the Body—Psychological Effects
of Plastic Surgery. Baltimore, Williams & Wilkins, 1981.
5. Courtiss EH: Patient counseling. In Gradinger G, Kaye B, eds:
Symposium on Problems and Complications in Aesthetic
Plastic Surgery of the Face. St. Louis, Mosby, 1984:15.
6. Goldwyn RM: Patient selection: the importance of being
cautious. In Courtiss EH, cd: Aesthetic Surgery: Trouble,
How to Avoid It and How to Treat It. St. Louis, Mosby,
1978:15.
7. Musgrave R: learning to say no. In Gradinger G, Kaye B, eds:
Symposium on Problems and Complications in Aesthetic
Plastic Surgery of the Face. St. Louis, Mosby, 1984:4.
8. Goin MK: Psychiatric considerations on aesthetic surgery. In
Courtiss EH, ed: Aesthetic Surgery: Trouble, How to Avoid It
and How to Treat It. St. Louis, Mosby, 1978:22.
9. Hanes K: Body dysmorphic disorder and the plastic surgeon.
Plast RcconstrSurg 1996;97:I082.
10. Johnson VS, Solomon C], Gibson SJ, Pallares-Benjamin A:
Human facial beauty: current theories and methodologies. Arch
Facial Plast Surg 2003;5:371.
11. Langlois JH, Roggman LA: Attractive faces are only average.
Psychol Scil990;l:115.
12. Langlois JH, Roggman LA, Musselman L: What is average and
what is not average about attractive faces? Psychol Sci 1994;5:214.
13. Alley TR, Cunningham MR: Average faces are attractive, but
very attractive faces arc not average. Psychol Sci 199I;2:123.
14. Johnston VS, Franklin M: Is beauty in the eye of the beholder?
Ethol Sociobiol 1993;14:183.
15. Perrett DI, May KA, Yoshikawa S: Facial shapes and judgments
of female attractiveness. Nature 1994;368:239.
16. Darwin C: The Descent of Man, and Selection in Relation to
Sex. London, John Murray, 1871.
17. Voland E, Grammar K: Evolutionary Aesthetics. New York,
Springcr-Verlag, 2003.
18. Johnston VS: Why We Feel: The Science of Human Emotions.
Reading, Mass, Perseus Press, 1999.
19. Farkas LG: Anthropometric Facial Proportions in Medicine.
Springfield, III, Charles C Thomas, 1981.
20. Singh D: Adaptive significance of female physical attractiveness:
role of waist-to-hip ratio. J Pers Soc Psychol 1993;65:293.
21. Johnston VS, Oliver-Rodriguez JC: Facial beauty and the late
positive component of event-related potentials. J Sex Res
1997;34:188.
22. Aharon I, Etcoff N, Ariele D, et al: Beautiful faces have variable
reward value: MRI and behavioral evidence. Neuron 2001;
32:537.
23. Johnston VS. Hagel R, Franklin M, et al: Male facial attractive-
ness: evidence for hormone mediated adaptive design. F>ol Hum
Behav2001;22:251.
24. Moller AP, Swaddle JP: Asymmetry, Developmental Stability,
and Evolution. Oxford, Oxford University Press, 1997.
25. Jolliffe IT: Principal Component Analysis. New York, Springer-
Verlag, 1986.
26. Cootes TF, Edwards GJ, Taylor CJ: Active appearance models.
In Burkhardt H, Neumann B, eds: Proceedings of European
Conference on Computer Vision, vol 2. New York, Springer-
Verlag, 1998:484.
27. Turk M, Pentland A: Eigenfaces for recognition. J Cogn
Neuroscil991;3:71.
28. Moghaddam B, Pentland A: Probabilistic visual learning for
object representation. IEEETrans Pattern Analysis Machine Intell
1997; 19:696.
46 • GENERAL PRINCIPLES

Review: Tamoxifen for early breast cancer

Comparison; 01 Adjuvant tamoxifen v e r s u s control
Outcome: 02 Mortality (death f r o m any cause)
Study Tamoxifen Control Peto Odds Ratio 9 9 % CI Weight % Peto Odds Ratio 9 9 % CI

03 Tamoxifen for average of 3 or more (median: 5) years

CRFB Caen 002 33 / 2 5 0 38 / 244 0.6 0.85 [0.46,1.58]
CRFB Caen C5 post 57 / 8 9 64 / 9 0 0.9 0.82 [0.50,1.34J
FASG GFE A 02 68 /37S 104 / 368 1.3 0.61 [0.41.0.92]
GROCTA I lt«ly ER+ 57 / 1 7 1 86 / 1 6 8 1.1 0.51 [0.33.0.80]
Marseille post 15 / 3 7 8 /34 0.2 1.94(0.63. 5.93]
NSAB? 6-14 N- ER+ 248 /1439 278 / 1453 4.2 0.88 10.70,1.11 J
Osaka 10/53 12/55 0.2 0.82 [0.27, 2.47]
Scottish 305 /666 3S4 / 657 4.9 0.74 [0.60,0.91]
Stockholm B post(5) 263 /1104 300 / 1096 4.4 0.84 [0.67.1.05]
Subtotal ( 9 5 % CI) 1056 /4184 244 / 4165 17.7 0.78(0.72. 0.85J
Test tor heterogeneity chi-square«15.86 df=8 p '0.0445
Test for overall effect Z=-5.68 p-0.00

Total (95% CI) 6346/18565 7030/18534 100.0 0.85(0.82.0.89]

Test for heterogeneity chi-square=55.88 df=54 p=0.4041
Test for overall effect Z--8.69 p-0.00

0.2 0.5 X 5
Tamoxifen better Tamoxifen worse

FIGURE 3-9. Meta-analysis of randomized controlled trials evaluating the impact of adjuvant tamoxifen on survival
risk among women with early breast cancer/'* Multiple studies have been included, with the findings of each plotted
on the central axis. Data are represented as an odds ratio. (Odds ratio, similar to relative risk, reports the proportion
of an occurrence to a nonoccurrence.) The summary analysis, which incorporates data from these studies, appears at
the bottom of the vertical axis and suggests a benefit for the use of adjuvant tamoxifen in early breast cancer.

disease or infirmity."46 This broader view of health
requires new approaches with foundations in sociol-
ogy, psychology, and economics. Many physicians will
initially be suspicious of these trends, expecting such
measures to produce only soft findings and not hard
data. Once it is understood that the scientific rigor used
in conducting studies of well-being meets or exceeds
our traditional biologic measures, only then will
progress be made in understanding global health. This
shifts the focus away from disease and treatment and
toward well-being and prevention.
Negative Outliers Versus Best
Practices
This shift in emphasis is also reflected in our approach
to improving patient care. In the past, we have focused
on negative outliers; in the future, our focus should

TABLE 3-6 • WHAT THE FUTURE HOLDS

Past Future

Focus on disease and treatment Focus on well-being and prevention

Emphasis on negative outliers Emphasis on best practices
Reliance on expert opinion and case series Reliance on randomized controlled trials and
large cohort studies
Use of ad hoc surveys Use of validated and standardized questionnaires
Individual data collection and analysis Collaborative data collection and aggregate
analysis for benchmarking
Physician profiling done by external forces (e.g., Confidential physician profiling provided by our
insurers or government agencies) or professional national organizations with useful practice
organizations (e.g., ABPS) and not shared with physicians feedback and national benchmarks
Surgery location driven by consumer choice and convenience Outcome-driven regionalization of surgery
Critical mass of physicians without computer access or Critical mass of physicians with computer access
computer skills; software/hardware cost-prohibitive and computer skills; software/hardware
affordable and widely available

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Tew 8*90 CTKf image...

3 • OUTCOMES RESEARCH: THE PATH TO EVIDENCE-BASED DECISIONS IN PLASTIC SURGERY 47

be on the best practices. The Northern New England
Cardiovascular Disease Study Group, a voluntary
regional consortium, includes all cardiothoracic
surgeons and interventional cardiologists as well as
nurses, anesthesiologists, perfusionists, administrators,
and scientists associated with six medical centers. Since
1987, the group has met regularly to identify best prac-
tices based on best outcomes. This has led to 293 fewer
deaths than the 868 expected.47 By focusing on best or
ideal outcomes, this group has made a major impact
on overall quality of care in the region. This study high- for individual surgeons to analyze their cases with a
lights the growing emphasis on collaborative data
collection, benchmarking, team approach to care, and
identification of best practices. Studies such as this willis based on the experience of individual physicians or
serve as a model for future efforts aimed at improv-
ing patient care.
Expert Opinion and Case Series
Versus Randomized Trials and
Large Cohort Studies
Our traditional model of learning through appren-
ticeship has long focused on the mentoring relation-
ship that is the core of residency training. The mentor
serves as the expert and directs knowledge acquisition
on the basis of his or her prior experiences. We now
understand that this style of learning is limited by the
quality of evidence implicit in expert opinion. New
and higher standards have been adopted by many
specialists, who now routinely incorporate evidence
from randomized trials into everyday medical deci-
sion-making. This higher standard is not widely avail-
able in our plastic surgery literature. Two randomly
selected issues of Plastic and Reconstructive Surgery from improved patient outcomes.
2001 were evaluated for the levels of evidence as pre-
sented in Table 3-1. Of the 46 clinical articles, 72%
qualified for level V, 11% for level IV, 4% for level III, External Versus Internal
and 13% for level II evidence. There were no articles
with level I evidence. In part, this reflects the nature
of our specialty. We are a small group of specialists
performing a wide range of procedures often for rel-
atively rare conditions. Nonetheless, it is reasonable to not shared with the surgeons. Therefore, they cannot
expect that our clinical decision-making in the future
will be supported by stronger evidence than in the past.
Ad Hoc Surveys Versus Validated
and Standardized Questionnaires
One area that would be simple to improve is in the use
of standardized surveys, rather than ad hoc question-
naires for each new study. Without standardization and
the use of validated questionnaires, each study must
stand alone. A common currency is needed to allow
systematic reviews and meaningful aggregation of data.
This is particularly true in our specialty, in which we
treat many rare conditions and each surgeon or
practice may encounter only a handful of cases in a
lifetime. There are now many well-validated ques-
tionnaires for almost any area of interest (see Table
3-2). There are also excellent compilations of existing
questionnaires that provide both summaries of the
instruments and analysis of their merits.13
Individualized Versus Collaborative
Data Collection and Analysis
The traditional approach to data collection has been
view to publication. For this reason, much of the current
evidence for medical decision-making in plastic surgery
practices. What further confounds this issue is the fact
that those who publish are typically the high-volume
surgeons and academic medical centers. A number of
studies have shown that volume and academic status
have a significant impact on outcome.30 Therefore, the
experiences of these high-volume surgeons and aca-
demic centers do not accurately reflect the outcomes
that might be expected by a typical surgeon in
practice.
What becomes obvious is that collecting evidence
individually is like blind men describing an elephant.
Each will perceive only a portion of the truth. A more
effective approach is to pool resources and begin to
see the big picture more clearly. The compelling trend
for the future will be collaborative data collection. Only
in this way can we generate a higher level of evidence,
a feat that is impossible for a single surgeon or prac-
tice to accomplish. Among other uses, these aggregate
data will allow improved decision-making and thus
Physician Profiling
Surgeons may be surprised to learn that many insur-
ers use their administrative databases for physician
profiling. In most instances, however, this profiling is
benefit from potential evidence that might help them
make practice improvements. Even the few clinical data
that are collected nationally, such as at the time of board
examination, are not converted to feedback informa-
tion to the individual practitioner. This is a missed
opportunity. For many years, the American Society of
Plastic Surgeons has surveyed a small sampling of prac-
tices about the surgical procedures performed. This
has served as the basis for procedural statistics within
the specialty. Simultaneously, the American Board of
Plastic Surgery collects procedural information for its
oral examination process and will soon be collecting
similar data for its recertification program. The Resi-
dency Review Committee collects procedural infor-
mation from trainees, which is analyzed to accredit

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Dr.Mustafa D.
48 I • GENERAL PRINCIPLES
training programs. The American Association for
Accreditation of Ambulatory Surgical Facilities also
requires surgical logs to be completed. Curiously, all
these data collection efforts are predominantly one-
way streets. The practitioner t ypically collects the data
and sends the data off into a black box, never to be
seen again. In the future, collaborative data collection
efforts will benefit individual physicians and practices
by providing them with a confidential practice profile
with accompanying national benchmarks. These data
may be used for negotiating managed care contracts,
understanding referral patterns, identifying areas in
need of further analysis, assessing satisfaction of
patients, and identifying best practices on the basis of
best outcomes.
Surgery Location: Consumer
Choice Versus Regionalization
of Care
On the basis of the known association between pro-
cedure volume and clinical outcomes, large-scale pur-
chasers and some professional societies are considering
regionalizing health care.48 Leapfrog, a powerful con-
sortium of Fortune 500 companies, has designated
selected procedures for referral to high-volume centers
(see Table 3-5).32 The American College of Surgeons
has established regional trauma networks and encour-
ages referral of severely injured patients to designated
centers meeting volume criteria.49 The Health Care
Financing Administration is exploring contracts with
"centers of excellence" for cardiac surgery and joint
replacement for Medicare patients. Leaders of large,
integrated health plans may follow suit and require
referrals to high-volume centers or those shown to
be more cost-effective while maintaining quality
outcomes.
Whereas the first procedures to come under scrutiny
are those with high mortality, it is reasonable to assume
that many other procedures will come under scrutiny,
both for better medical outcomes and for cost-effec-
tiveness. As this trend evolves, it will be important for
specialists to have their own resources for bench-
marking their practices. It is likely that consumer choice
will continue to play a role in location for surgery. One
study has shown that when patients are given a choice
between local and regional surgery, 45 of 100 patients
would theoretically prefer local care despite knowing
that the operative mortality risk locally is twice the
regional risk (6%).50 Providing patients with accurate
data may become an important force in their selec-
tion of health care options.
Technology Now and Then
One of the obstacles to collaborative data collection
has been the cost involved in such large-scale efforts.
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Dr.Mustafa D.
Few groups, other than the collaborative cancer trial-
ists with national funding, have been successful at car-
rying out such efforts. However, with the evolution of
computer technology and the Internet, the feasibility
of carrying out these studies has become much more
affordable, practical, and realistic. Several specialty soci-
eties have hired consultants to design data collection
Web sites. In many instances, these data will be used
for a variety of purposes, such as physician feedback,
benchmarking, improvement of care, credentialing,
and certification.
CONCLUSIONS
This chapter would be incomplete without emphasiz-
ing three key take-home messages. First, you cannot
make good decisions without good evidence. Maxi-
mizing patient care and surgical outcomes will require
continuous efforts to identify information needs and
to produce the best evidence to fulfill these needs.
Second, outcomes research offers a broad spectrum of
methods by which to obtain good evidence, and these
have been insufficiently leveraged by our specialty. Mea-
suring outcomes is not just about the final result of
our interventions but a means by which we gather
evidence to improve decision-making, the processes
of care, and the systems in which we work. Third, col-
laborative data collection is imperative to generate
meaningful information for medical decision-making.
Our decisions need to be based on the highest quality
evidence and not the accumulated experience of a single
surgeon, even if that surgeon is truly expert in the field.
Our new strategy should be to work together, to iden-
tify the best among us, and to strive to become as good
as the best. Future trends will, it is hoped, see a national
collaborative effort to develop standards of quality and
safety and then to provide mechanisms for surgeons
to implement and monitor these standards in their
practice.
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14. Kaplan RM, Alcaraz JE, Anderson JP, Wcisman M: Quality-
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21. Bennett KJ, Torrance GW: Measuring health state preferences
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nomics in Clinical Trials,2nd cd. Philadclphia.Lippincott-Raven,
1996:253-265.
22. Chang WT, Collins ED, Kerrigan CL: An Internet-based utility
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23 Kerrigan CL, Collins ED, Knccland TS, ct al: Measuring health
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24 Froberg DG, Kane RL: Methodology for measuring health-state
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delivery. Science 1973;182:1102-1108.
28. Wennbcrg J, Gittelsohn A: Variations in medical care among
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29. Naylor CD: Assessing processes and outcomes of medical care.
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30. BcggCB, Cramer LD, Hoskins WJ, Brennan MF: Impact of hos-
pital volume on operative mortality for major cancer surgery.
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31. Roohan PJ, Bickell NA, Baptiste MS, et al: Hospital volume dif-
ferences and five-year survival from breast cancer. Am J Public
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32. The Leapfrog Group for patient safety. Available at:
http://www.lca pfroggroup.org. Accessed December 19, 2001.
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quality of hospital care. Pitfalls and potential of ICD-9-CM
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34. Mark DHi Race and the limits of administrative data (letter;
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38. Boice JD Jr, Persson I, Brinton LA, et al: Breast cancer follow-
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43. Kassirer JP, Pauker SG: The toss-up [editorial]. N Engl J Med
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aboutwho/en/definition.html. Accessed July 30,2001.
47. Malenka DJ, O'Connor GT: The Northern New England Car-
diovascular Disease Study Group: a regional collaborative effort
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Joint Commission J Quality Improvement 1998;24:594-600.
48. Birkmeyer JD: High-risk surgery—follow the crowd. JAMA
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49. American College of Surgeons Committee on Trauma: Resources
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American College of Surgeons, 1998.
50. Finlayson SR, Birkmeyer JD, Tostcson AN, Nease RF Jr: Patient
preferences for location of care: implications for regionaliza-'
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51. Ware J£: SF-36 Physical and Mental Health Summary Scales: A
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54. Harris DL, Carr AT: The Derriford Appearance Scale (DAS59):
a new psychometric scale for the evaluation of patients with
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55. Kerrigan CL, Collins ED, Striplin DT, et al: The health burden
of breast hypertrophy. Plast Reconstr Surg 2001; 108:1591 -1599.
image...
CHAPTER
4
•
Genetics
DEEPAK NARAYAN, MS, MD, FRCS (Eng), FRCS (Edin)
MENDELIAN INHERITANCE
Autosomal Inheritance
Sex-Linked Inheritance
NONMENDELIAN INHERITANCE
Imprinting
Uniparental Disomy
Mitochondrial Inheritance
MALFORMATIONS, DISRUPTIONS, AND
DEFORMATIONS
TECHNIQUES IN GENETIC ANALYSIS
Chromosomal Analysis
Nucleic Acid Analysis
The recent success of the Human Genome Project will
fundamentally change the practice of medicine in the
years to come. The molecular pathology of disease, the
design of "rational drugs," and the classification of dis-
eases arc but a few of the areas that will be revolu-
tionized as a result of this success.
The implications for practitioners of medicine are
profound. Therefore, given the increasing importance
of genetics in daily practice, one should have at least
a passing familiarity with the vocabulary, techniques,
and implications of recent discoveries in this fasci-
nating area. Although a detailed discussion of all the
facets of genetics pertaining to plastic surgery is
clearly beyond the scope of this chapter, an attempt
is made to highlight those aspects that are most clin-
ically important and relevant.
MENDELIAN INHERITANCE
Mendelian inheritance or unifactorial inheritance
refers to the classic genetic paradigm, first postulated
by Father Gregor Mendel,1 in which one gene is respon-
sible for one trait. This may take the form of autoso-
mal inheritance or sex-linked inheritance. However,
the inheritance of many human traits and disorders
like diabetes and hypertension is a melding of the effects
of numerous genetic and nongenetic factors and is
properly termed multifactorial. A brief description of
the common unifactorial inheritance patterns is given
in the following sections.
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Dr.Mustafa D.
Southern and Northern Blots
Polymerase Chain Reaction
Microarray Analysis
ANALYSIS OF SELECTED GENETIC SYNDROMES
Craniosynostosis and the Fibroblast Growth Factor
Receptors
Nevoid Basal Cell Carcinoma Syndrome (Gorlin
Syndrome)
GENETICS AND ETHICS
Autosomal Inheritance
The autosomes are the 22 pairs of chromosomes other
than the X and Y chromosomes. Traits that are carried
by the autosomes can be inherited in a dominant or
recessive fashion.
An autosomal dominant disease is one that mani-
fests itself in a heterozygous state, that is, in the com-
bined presence of a normal gene and a mutant gene
in an individual. A child born to a person affected by
an autosomal dominant disorder has a 1 in 2 chance
(50%) of being affected. A person with an autosomal
dominant disorder can be the first affected person in
the family because of a new dominant mutation. An
autosomal recessive disorder manifests itself when the
mutant gene is present in a double dose, that is, the
person is homozygous for the disorder. Offspring of
parents who are both heterozygous for a disorder have
a 1 in 4 (25%) chance of being homozygous for the
mutant gene and thus of manifesting the disease (Fig.
4-1). Examples of autosomal dominant disorders
include Apert syndrome, achondroplasia, and Stickler
syndrome. Examples of autosomal recessive dis-
orders include Meckel syndrome and Bardet-Biedl
syndrome.
Codominance refers to two traits that are both
expressed in the heterozygous state. A good example
of codominance is the inheritance of the AB blood
group, in which it is possible to demonstrate both A
and B blood group antigens on red blood cells, so that
the loci for A and B are said to be codominant. Some
51
52 I • GENERAL PRINCIPLES
individuals, despite being heterozygous for an auto-
somal dominant disorder, do not manifest features
of the disorder. Colloquially, the disease is said to
have "skipped a generation," a phenomenon formally
referred to as lack of penetrance or nonpenetrance.
This can result from various modifying influences, both
genetic and environmental, and can be a confound-
ing factor in genetic counseling. The variations in the
degree of expression of the phenotype among patients
with the same disease is termed expressivity.
Sex-Linked Inheritance
Sex-linked inheritance refers to the pattern of inher-
itance of the genes located on the sex chromosomes,
that is, the X and Y chromosomes. X-linked inheri-
tance or Y-linked inheritance is the term used to specify
the sex chromosome involved.
The most famous of the X-linked disorders is the
X-linked recessive disorder hemophilia (Fig. 4-2).
X-linked recessive traits almost exclusively affect
males, although there are some exceptions. In hemo-
philia, males with a single mutant gene on their
single X chromosome manifest the disease because a
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Dr.Mustafa D.
FIGURE 4 - 1 . A, Autosomal domi-
nant pattern. B, Autosomal recessive
inheritance pattern. (From Cohen
MM: Dysmorphology, syndromology,
and genetics. In McCarthy JC, ed:
Plastic Surgery. Philadelphia, WB
Saunders, 1990:105, 106.)
compensating normal gene can be carried only by
another X chromosome, which males lack.
X-linked dominant disorders are much rarer and
bear a resemblance to an autosomal dominant inher-
itance in that both the daughters and sons of an affected
female have a 1 in 2 (50%) chance of being affected
(see Fig. 4-2). The major difference between the two,
however, resides in the fact that in an X-linked dom-
inant trait, an affected mate can never transmit the trait
to his sons, but all his daughters will bear the trait. An
example of an X-linked dominant trait that plastic sur-
geons might encounter is vitamin D-resistant rickets,
which may produce cranial vault deformities.
Y-linked inheritance implies that the disease or trait
affects only males because by definition only males
carry the Y chromosome. The H-Y histocompatibil-
ity antigen is a good example of Y-linked inheritance.
NONMENDELIAN INHERITANCE
The well-ordered world of mendelian genetics has
undergone vast changes in the last decade with the
discovery of new forms of inheritance, such as
imprinting, uniparental disomy, and mitochondrial
TtSWt^aeltfW image...
«^i
FIGURE 4 - 2 . A, X-linked dominant
pattern, fi, X-linked recessive
pattern. (From Cohen MM: Dysmor-
phology, syndromology, and genet-
ics. In McCarthy JC, ed: Plastic
Surgery. Philadelphia, WB Saunders,
1990:107, 109.) A
inheritance, all of which are classified together under
the rubric of nonmcndelian inheritance.
Imprinting
The conventional teaching of the inheritance of genes
on homologous chromosomes was that they were
expressed equally. In other words, if one inherited a
gene located on an autosome or the X chromosome,
it would have the same effect if it were inherited from
the mother or the father. However, it is now under-
stood that a small number of genes are expressed dif-
ferently, depending on which parent contributed the
gene. This "parent of origin" effect is termed genomic
imprinting. 2 A gene that is imprinted is not expressed.
When the maternally derived gene is inactive, it is
said to be maternally imprinted. The mechanism of
imprinting is unclear, but methylation has been touted
as a possible cause.
Uniparental Disomy
Uniparental disomy is a term given to individuals who
have inherited both copies of a chromosome pair from
the same parent instead of one copy from each parent.
This can give rise to a situation akin to that seen in
imprinting, in which the genes from one parent are
preferentially inactive.
A classic example of imprinting is found in the
Prader-Willi and Angelman syndromes. 3 Prader-Willi
syndrome is characterized by obesity, hypogonadism,
short stature, and learning difficulty; Angelman syn-
drome is characterized by microcephaly, epilepsy,
ataxia, and mental retardation. Approximately 75%
of patients with the Prader-Willi syndrome can be
shown to have an interstitial deletion in the proximal
portion of the long arm of chromosome 15. In almost
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Dr.Mustafa D.
4 • CENETICS 53
IZFr©
Dill
all individuals with this syndrome, the segment of chro-
mosome that is missing is on the paternally derived
chromosome. In the Angelman syndrome, the same
deletion can be demonstrated, but on the maternally
derived chromosome.
In Prader-Willi syndrome, the critical disease-
causing region contains several imprinted genes,
including the small nuclear riboprotein N gene
(SNftPN), which is maternally imprinted. Thus, a dele-
tion in the paternal chromosome, which contains the
only functioning copy of the gene, leads to a complete
absence of gene activity. In the Angelman syndrome,
the UBE3A gene, which belongs to the ubiquitin family,
is paternally imprinted in the brain. Thus, deletion of
the maternal chromosome 15 copy of UBE3A results
in Angelman syndrome.
Mitochondrial Inheritance
It is perhaps not generally known that mitochondria
have their own DNA, which is distinct from that present
in the nucleus. Mitochondrial DNA is almost exclu-
sively inherited from the mother and has, in general,
a higher rate of mutation than that of nuclear DNA.
It has been proposed that some of the somatic effects
of aging are in part due to an accumulation of muta-
tions in mitochondrial DNA. Some examples of
mitochondrially inherited diseases are chronic pro-
gressive ophthalmoplegia and aminoglycoside-induced
deafness.
MALFORMATIONS, DISRUPTIONS,
AND DEFORMATIONS
The concepts of malformation, deformation, and dis-
ruption are of practical importance to the surgeon
because they provide an easily applicable method
54 I • GENERAL PRINCIPLES
for the classification of birth anomalies. Such a
classification does not in any way imply that the fun-
damental pathologic basis of the defects is well under-
stood. Although such a distinction may be useful for
clinical purposes, the three classes of anomalies are
interrelated, and it is not always possible to assign an
anomaly to one single class.
Spranger et al4 define a malformation as a mor-
phologic defect of an organ, a part of an organ, or a
larger area of the body resulting from intrinsically
abnormal development. Cleft palates and syndactyly
are representative of abnormal morphogenesis result-
ing in malformations. Malformations in general are
nonspecific and may occur in isolation or as part of
a constellation of defects that constitute a syndrome.
A deformation maybe defined as an abnormal form
or position of a part of the body caused by nondis-
ruptive mechanical forces. The mechanical forces may
be extrinsic, such as unicornuate uterus or uterine
tumor (e.g., leiomyoma), or intrinsic, such as that
resulting from renal agenesis or hypoplasia. A classic
example of a deformation is the Potter sequence. A
defect in the anatomic structure of the urinary tract
decreases the fetal urinary output, which in turn
decreases the quantity of amniotic fluid. The result-
ing oligohydramnios can cause a direct pressure effect
against the face, resulting in the flattened face and the
low-set ears that are characteristic of the Potter facies.
The amniotic band syndrome is the archetype of
a disruption, which is a morphologic defect of an organ,
a part of an organ, or a larger region of the body result-
ing from a breakdown of or interference with origi-
nally normal development. Amputations of fingers in
utero and ring constriction of fingers are disruptions
resulting from aberrant tissue bands (Fig. 4-3). Dis-
ruptions, in contrast to malformations and deforma-
tions, tend to be sporadic events.
In this context, it is useful to highlight the role of
minor anomalies as indicators of a more serious struc-
tural defect, since plastic surgeons are often called on
to treat these problems. Mongolian spots, auricular
tags, and epicanthic folds are minor anomalies, which
in and of themselves are not of serious medical
import. It is estimated that single minor anomalies
are found in 15% of all newborns. However, Marden
et al5 point out that 90% of all newborns with three
or more minor anomalies have major malformations,
such as those involving the cardiac or the genitouri-
nary system.
TECHNIQUES IN GENETIC
ANALYSIS
The plastic surgeon has been assailed by a variety of
genetic techniques that have made their way from the
laboratory to the clinical arena, a phenomenon that
has been more marked in recent years. The plastic
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Dr.Mustafa D.
surgical literature also reflects these trends, in a dis-
tinct departure from the norm that existed a decade
ago. To be an informed clinician, it is imperative that
the surgeon understand the principles that underlie
these tests. A brief review of some important, clinically
relevant techniques is given in the following sections.
Chromosomal Analysis
Chromosomal analysis serves as a screening test to
detect alterations in number, shape, size, or form of
chromosomes in diseases in which the genetic causes
are unknown. 3 These techniques have proved extremely
useful in focusing the geneticist's attention on specific
chromosomes associated with a disease process and,
as a result, on the genes that are potentially implicated.
The term karyotype refers to the chromosomal con-
stitution of an individual. Whereas any nucleated cell
capable of growing in culture can be analyzed, for logis-
tical reasons, lymphocytes derived from peripheral
blood are the most commonly used. Phytohemagglu-
tinin is used to stimulate lymphocyte division, and
colchicine is used to produce "metaphase arrest" or a
metaphase spread for maximum visualization of the
chromosomes. The identity of specific chromosomes
is established by chromosome banding, whereby
special stains are used to produce a unique banded
staining pattern for each chromosome. The most
frequent banding technique is G banding (Giemsa
banding). One to 20 cells are commonly studied and
the banding patterns of individual chromosomes are
analyzed, resulting in a karyogram, a formal presen-
tation of the representative banded chromosomes in
descending order of size (Fig. 4-4). A normal male
karyotype is designated 46,XY; the female karyotype
is designated 46,XX. Loss or gain of a single gene cannot
be visualized on a standard chromosomal analysis.
Therefore, a normal chromosomal study does not rule
out the presence of a genetic disorder.
A classic example of an abnormality detected by a
karyotype study is trisomy 21, which produces Down
syndrome, in which three copies of chromosome
21 are present. Plastic surgeons may occasionally
encounter other examples of such disorders that can
be diagnosed by karyotype analysis, such as the Kline-
felter syndrome (47,XXY) in association with gyneco-
mastia or Turner syndrome (45,X) associated with
webbing of the neck. Patients with the Klinefelter syn-
drome have an extra X chromosome; those with Turner
syndrome, which affects only females, are missing one
X chromosome.
The identification of the chromosome and its
component parts has reached a higher degree of res-
olution with fluorescent in situ hybridization 6 (Fig. 4-
5). Briefly, the procedure involves the labeling of a
fragment of DNA with a fluorescent dye (the probe)
and allowing it to hybridize (bind to) the patient's
image...
* • • -
A B
FIGURE 4 - 3 . A and B, Constriction bands of the finger and hand. (Photograph courtesy of J.G. Thomson, MD,
Yale University.)
denatured chromosomes in a metaphase spread.
Hybridization is a process by which the labeled frag-
ment attaches itself to that part of the chromosome
that matches its sequence. The slide is then examined
under a fluorescent microscope, and the location of
the tagged DNA is identified. Thus, if the patient lacks
a part of the chromosome that corresponds to the
probe, no signal will be seen. Alternatively, if the patient
has a translocation of genetic material to a different
chromosome, the probe ends up hybridizing in the
new location. The new site can easily be identified
because there are chromosome-specific fluorescent
markers that are unique to the 23 pairs.
Whole chromosome paint probes, which consist
of a mixture of probes corresponding to different parts
of an entire chromosome, can be used en masse in a
single hybridization to produce a detailed picture of
the anatomy of the chromosome. 7 This is extremely
useful for identifying complex rearrangements or
subtle translocations that are easily missed by the older
banding techniques. Newer techniques whereby the
chromosome is essentially unwound and then probed
promise to yield even higher degrees of resolution.
This technique can theoretically identify deletions of
a single gene.
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4 • GENETICS 55
The increasing use of these techniques has identified
microdcletions, a term that refers to submicroscopic
areas of chromosomes that are missing (and generally
contain more than one gene), resulting in a group of
disorders called the microdeletion syndromes. Of inter-
est to plastic surgeons is a report that identifies an
increased incidence of chromosome 22ql 1 microdele-
tions in patients with velopharyngeal insufficiency in
the absence of clefting.8
Nucleic Acid Analysis
The analysis of DNA forms the cornerstone of genetic
testing. This can be done at varying degrees of com-
plexity ranging from Southern blots to sequencing of
a gene in its entirety.
Southern and Northern Blots
The Southern blot, 9 named for its inventor, Edward
Southern, is a method of analyzing DNA based on the
differential migration of DNA fragments through an
agarose gel driven by an electric field (Fig. 4-6). In the
analysis of clinical samples, the fragmentation of the
sample of a patients DNA is achieved through the use
56 I • GENERAL PRINCIPLES

K »
u n " » " J* si 8 10 11 12

** U M * *
: t II
13 14 15 16 17 18

• t.
19 20 X Y 21 22

FIGURE 4 - 4 . Karyogram of Down syndrome showing additional chromosome 21 (47.XY + 21). (From Cohen MM:
Dysmorphology, syndromology, and genetics. In McCarthy JC, ed: Plastic Surgery. Philadelphia, WB Saunders,
1990:102.)

of special enzymes termed restriction enzymes that

have the ability to cleave DNA in specific patterns based
on the sequence of the DNA. The DNA pattern is trans-
ferred to a nylon membrane (which is more robust
than the gel) and probed with a labeled (usually
radioactively) DNA fragment of interest. If the patient's
DNA is not cleaved by the restriction enzyme (e.g.,
because of a mutation), a different pattern thus helps
identify an aberrant result. The Northern blot refers
to the analysis of RNA in a similar fashion and is useful
in studying the expression of various genes.

FIGURE 4-5. Visualization of genes by fluorescent in Polymerase Chain Reaction

situ hybridization showing probe localization (arrows).
Inset: Excess copies of the RBI gene and cyclin D1 gene
are demonstrated in human breast cancer cells. (From
Sinclair A: Genetics 101: cytogenetics and FISH. CMAJ
2002:167:373.)
The polymerase chain reaction is one of those tech-
niques that truly merits the appellation "revolution-
ary" and won its inventor, Kary Mullis, a well-deserved
Nobel Prize.10,11 The basis of the versatility of its

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!*&**> K^aeldW image...

A • GENETICS 57

RNA or DNA- Solution passes through

gel and filter to paper towels

Migration
^P-labeled
Paper towel Sponge
','ie markers

Gel

Salt
solution Nitrocellulose
ilter

DNA
transferred
Hybridize with unique
to filter
nucleic acid probe

Filter in
"Seal-a-Meal'
bag

Remove
unbound Probe hybridized
probe to complementary
sequence
FIGURE 4 - 6 . Analysis of DNA and RNA by gel electrophoresis and
blotting. DNA cleaved with restriction enzymes or RNA isolated from
cells is applied to an agarose gel and electrophoretically separated by
size. The nucleic acids in the gel are transferred to a nitrocellulose filter
to make a precise replica of the gel. This is usually done by placing the
gel atop a sponge sitting in a tray of buffer. The filter is laid over the
gel and covered with a stack of paper towels that act as a wick, pulling
buffer up through the sponge, gel, and filter. DNA or RNA fragments Expose to
from the gel are carried up onto the filter, where they stick tightly. The x-ray film
filter is removed and hybridized with a radioactively labeled probe.
Hybridization specifically tags the sequence of interest, even though it
may constitute only a minute fraction of the nucleic acids on the filter.
This is the basis of the exquisite selectivity of the method. The unbound
probe is washed off, and the filter is exposed to x-ray film. The posi-
tion of a DNA or RNA fragment complementary to the probe appears
Autoradiogram
as a band on the film. This procedure is termed Southern blotting when
DNA is transferred to nitrocellulose, Northern blotting when RNA is
transferred. (From Watson JD, Gilman M, Witkowski J, Zoller M: Recom-
binant DNA, 2nd ed. New York, Scientific American, 1992:129.)

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58 I • GENERAL PRINCIPLES
applications is the amplification of a minute quantity
of the starting material, DNA, needed for the reac-
tion. Some of the uses of this reaction that are of
relevance to plastic surgeons include detection of
melanoma cells in sentinel lymph nodes and sequenc-
ing mutations in craniofacial syndromes (Fig. 4-7).
The enormous sensitivity of the technique is also
a drawback. Even minute levels of contamination,
such as those resulting from skin cells shed by the inves-
tigator, can have an impact on the result. However,
the sensitivity and specificity of the reaction are
improved by the use of heat-stable polymerase, such
as the Taq polymerase (derived from the bacterium
Thermits aquaticus), which is relatively stable even at
temperatures above 90°C, and by careful attention to
technique.
Microarray Analysis
Microarrays are a recently developed tool that allow
the analysis of thousands of genes in a single reac-
tion.12,13 Currently, the most commonly used arrays
are those that use labeled cDNA (complementary
DNA) to perform the analysis. Arrays are particularly
useful in comparing the expression profile of normal
versus abnormal tissue of any kind. Briefly, the arrays
themselves are constructed by robotically spotting a
number of unique gene sequences to either a glass slide
or a nylon membrane. RNA from the samples to be
compared (i.e., normal versus abnormal) is initially
extracted from the specimens. The RNA from the
samples is then treated with reverse transcriptase,
an enzyme that converts the RNA into cDNA; cDNA
is so termed because the sequence of the DNA exactly
matches the RNA sequence, hence the term comple-
mentary DNA. This step yields a more stable and easily
manipulated form of nucleic acid than RNA, without
altering the content of the message. The cDNA from
the two different samples is then labeled with two
different fluorescent dyes and cohybridized on the array,
and the data are analyzed (Fig. 4-8). Depending on
the intensity of the binding reaction, genes that are
overexpressed or underexpressed can be identified.
Microarrays have also been used to create expression
profiles of tumors such as melanomas 14 and lym-
phomas 15 that, when correlated with clinical data, have
profound consequences for methods of classification,
prognosis, and treatment of these tumors. Currently,
data obtained from microarrays need to be confirmed
by other means.
ANALYSIS OF SELECTED
GENETIC SYNDROMES
In this section, selected genetic disorders of interest
to plastic surgeons are analyzed. The underlying
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molecular pathology and the implications for clinical
care are highlighted. These examples serve to under-
line the increasing importance of the molecular mech-
anisms of disease and how the study of relatively rare
diseases can have profound implications in the man-
agement of more common disorders.
Craniosynostosis and Fibroblast
Growth Factor Receptors
Fibroblast growth factors (FGFs) are a large family of
multifunctional growth factors that are involved in a
wide range of developmental processes, events that are
initiated by their binding to fibroblast growth factor
receptors (FGFRs). There are four known FGFRs (1
to 4), and strong evidence for the existence of a fifth
receptor (FGFR5) has been presented. 16 A great deal
of interest has centered on these molecules because
several craniofacial syndromes have been linked to
mutations in their coding sequences. The demonstra-
tion of mutations of FGFRs in gastric and colorectal
cancers underscores the pleiotropic activity of these
receptors. 17
The most common craniosynostosis syndromes
caused by FGFR mutations are the Apert, Crouzon (Fig.
4-9), Pfeiffer, Jackson-Weiss, and Muenke syndromes. 18
The clinical features that characterize these conditions
are discussed elsewhere in this book.
These receptors are typically single trans-membrane
proteins that have three extracellular, immunoglobulin-
like structural motifs (Fig. 4-10). These motifs are linked
by a trans-membrane region to the intracellular com-
ponent, which is made up of a split tyrosine kinase
domain and a - C O O H tail. Located in the interval
between the first and second immunoglobulin domain
are a series of acidic residues termed the acid box, a
heparin-binding region, and a cell adhesion molecule
domain. Signal transmission is mediated by binding
of FGF to an FGF receptor. This automatically causes
the binding of an additional FGF receptor to this
complex, a process termed dimerization of the recep-
tor. The proximity of these two receptor molecules
results in the self-phosphorylation of tyrosine residues
on the cytoplasmic end of the receptor, which in
turn initiates a further signal transmission cascade
downstream.
The mutations in FGFRs tend to be highly local-
ized, specific, and, on occasion, highly recurrent.18,19
The mutations affecting FGFRs are mainly caused by
a specific gain of function of the mutated protein, in
effect a "hyperfunctioning protein." Different muta-
tions in the same gene can give rise to different
phenotypic manifestations as exemplified by those
affecting FGFR2, which is associated with Crouzon, 20
Apert, and Pfeiffer syndromes.19,21 Some mutations are
highly specific, such as the Pro250Arg mutation of
 image...

4 • GENETICS 59

Denature DNA sample Original target

to separate DNA strands double-stranded D N A
(94°C, 5 min) 5' 3'

Primers bind to Separate strands

DNA strands and anneal primers
(30-65X 30 s) 5' 3'
lb] Primer 2^- Primer 1
3' 5'
Denature to separate
DNA strands Polymerase synthesizes Extend primers
(94°C, 30 s) new DNA strands
(65-75X 2-5 min) 5' 3'
(el / W W W W W V A ^ i
Complementary
Complementary
to primer 2 to primer 1

Separate strands
and anneal primers

id) ^- New primers —.^

5' • • » / \ / \ / \ / \ / \ / \ / \ / \ / \ / \ / \ / \ 3'

Extend primers

FIGURE 4 - 7 . A, The polymerase chain reaction cycle. Variable-length

The DNA sample is heated to separate the DNA strands Unit-length
strands
(initial denaturation), and then the reaction mixture goes strands
through repeated cycles of primer annealing, DNA syn-
thesis, and denaturation. The target sequence doubles in • • k A A A A A A A A A A A A A y
concentration for each cycle. B, Amplification of target
sequence, (a) The starting material is a double-stranded Separate strands
DNA molecule, (b) The strands are separated by heating and anneal primers
the reaction mixture. It is then cooled so that the primers
anneal to the two primer binding sites that flank the target
region, one on each strand, (c) Taq polymerase synthe- II)
5' • • » / \ / \ / \ / \ / \ / \ / \ / \ / \ / \ / 3'
sizes new strands of DNA, complementary to the tem- Complementary )
v
-f/ Complementary
plate, that extend a variable distance beyond the position to primer 2 to primer 1
of the primer binding site on the other template, (d) The 3'
reaction mixture is heated again; the original and newly
synthesized DNA strands separate. Four binding sites are Extend primers
now available to the primers, one on each of the two orig-
inal strands and the two new DNA strands. (To simplify
the diagram, subsequent events involving the original
strands are omitted.) (e) Taq polymerase synthesizes new
complementary strands, but the extension of these chains lg)
is limited precisely to the target sequence. The two newly
synthesized chains thus span exactly the region specified
by the primers, (f) The process is repeated, and primers
anneal to the newly synthesized strands (and also to the Desired fragments
variable-length strands, but these are omitted from the [variable-length strands not shown}
figure), (g) Taq polymerase synthesizes complementary
strands, producing two double-stranded DNA fragments
that are identical to the target sequence. The process
is repeated. (From Watson JD, Cilman M, Witkowski J,
Zoller M: Recombinant DNA, 2nd ed. New York, Scientific A n d so on
American, 1992:81,82.)
B

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60 I • GENERAL PRINCIPLES

Test Reference
DNA clones , r - ,

Reverse
transcription
and label

0000©©©©© I00000000©
©0©©®®®©© J000000000
®0®©©®®«© 0©0©0©©©0
®0®©®©0©© !0®®©®0©0©
®0®®©®®©® i®00®©©©©© FIGURE 4 - 8 . Diagrammatic representation of a
Computer
cDNA microarray. Aliquots of cDNAs of interest are
analysis^ gridded on a glass template by a computer-controlled
robot. The test and reference RNA samples that are
labeled with different-colored fluorochromes by
O OO reverse transcription are mixed and allowed to
O OO hybridize with the cDNAs on the microarray. The tem-
O O plates are exposed to laser light, and the excitation
pattern generated is compared, identifying genes that
show differences in expression between the refer-
Identification of clones ence and test samples. (From Mueller RF, Young ID:
showing differential Emery's Elements of Medical Genetics, 11th ed.
expression London, Churchill Livingstone, 2001:324.)

FGFR3 associated with Muenke syndrome22,23 (Figs.
4-11 and 4-12).
CLINICAL IMPLICATIONS
What does all this mean to a practicing clinician? First
and foremost, molecular genetic testing allows an accu-
rate diagnosis to be made. A good example is that of
the Muenke syndrome, the nonspecific features of
which lend to a variety of diagnoses ranging from
Crouzon syndrome to isolated multifactorial cra-
niosynostosis. The demonstration of the specific and
easily detectable Pro250Arg FGFR3 mutation clarifies
the situation in clinically ambiguous cases. The tighter
clinical definition also helps measurably in estimating
recurrence risks during genetic counseling.
The identification of molecular mutations opens
up an avenue for an entirely new and more rational
method of classification of craniosynostosis disorders.18
Such clarity of classification helps in the development
ofbetter communication between researchers and cli-
nicians as well as in improved epidemiologic studies
to further define the pathology of these complex
disorders.

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 image...

4 • CENETICS 61

FIGURE 4 - 9 . Crouzon syndrome in

mother and son. Note brachycephaly,
proptosis, maxillary hypoplasia, and
beaked nose. (From Cohen MM: Dys-
morphology, syndromology, and genet-
ics. In McCarthy JG, ed: Plastic Surgery.
Philadelphia, WB Saunders, 1990:86.)

The molecular definition of these disorders also
allows accurate prenatal diagnosis. However, such
knowledge must be tempered by the difficulty in
predicting, with any degree of certainty, the actual
severity of the disorder. Recurrent craniosynostosis
in a child previously operated on with a diagnosis
of a nonsyndromic sutural stenosis should alert
the surgeon to the possibility of a genetic diathesis
and necessity of a more detailed work-up. Along
the same lines, the presence of a borderline head
shape in an individual from a family with docu-
mented craniosynostosis may lead to the erroneous
impression that the proband is affected. A demon-
stration that the person has not inherited the

A Igllla | Iglllb

AC
I
Icjl

I
igii -] Igllla
Up
Iglllc
—r m TK1 H TK2

FIGURE 4-1 0. Structure of fibroblast growth factor receptors. The FCFR consists of three extra-
cellular immunoglobulin-like domains (Igl, Igll, and Iglll), an acid box (A), a cell adhesion mole-
cule homology domain (C), a transmembrane domain (TM), and an intracellular split tyrosine
kinase domain (TK1 and TK2). The Iglll domain may contain the Igllla-lglllb or Igllla-lglllc vari-
ants. The cell membrane is denoted by the dashed lines. (From Wilkie AOM: Molecular genetics
of craniosynostosis. In Lin K, Ogle RC, Jane J, eds: Craniofacial Surgery: Science and Surgical
Technique. Philadelphia, WB Saunders, 2002:43.)

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image...

62 • GENERAL PRINCIPLES

FGFR1 —[
H3 H
s s s s s

FGFR2 H
S~ s S s s

k
FGFR3 K K} H
I i
Pfeiffer(FGFRI) | splice site mutations
Apert o Jackson-Weiss
Muenke
Crouzcn/Pfeiffoc (FGFR2)

F I G U R E 4 - 1 1 . Schematic representation of locations of mutations in the FGF receptors. Impor-

tant or distinctive recurrent missense mutations are indicated by symbols of different shapes.
The bar denotes the region of the Igllla and Iglllc in FGFR2 that is subject, in Crouzon and
Pfeiffer syndromes, to numerous recurrent missense mutations and a small number of in-frame
insertions and deletions. (From Wilkie AOM: Molecular genetics of craniosynostosis. In Lin K,
Ogle RC, Jane J, eds: Craniofacial Surgery: Science and Surgical Technique. Philadelphia, WB
Saunders, 2002:46.)

mutation will prevent unnecessary
intervention.
Nevoid Basal Cell Carcinoma
Syndrome (Corlin Syndrome)
Nevoid basal cell carcinoma syndrome or the epony-
mously named Gorlin syndrome was delineated nearly
40 years ago.24,25 This disorder, inherited in an auto-
somal dominant fashion, belongs to an important
group of hereditary cancer syndromes. Multiple basal
cell carcinomas, medulloblastomas, and ovarian
fibromas are frequently present; rarer tumors may
include cardiac fibromas, fibrosarcomas, meningiomas,
and rhabdomyosarcomas. In addition, a unique con-
stellation of malformations associated with the syn-
drome include palmar or plantar pits, bifid ribs,
keratocysts of the jaw, dysgenesis of the corpus callo-
sum, and a characteristic coarse fades. 26
The putative Gorlin syndrome gene was mapped
to 9q22-31. On the basis of the similarity of defects
seen in the mutations of the Drosophila patched
gene, mutations in the human equivalent of this
gene were identified as the principal cause of this
disorder.27,28
THE HEDGEHOG PATHWAY AND
GORLIN SYNDROME
Hedgehog is a 45-kd secreted protein that plays an
important role in the differentiation of various tissues
surgical during development and binds to the cell membrane
receptor patched. Hedgehog undergoes self-cleavage
and modification to give a 20-kd N-terminal fragment
that is covalently bound to cholesterol. The addition
of cholesterol may play a role in the spatial distribu-
tion of its effects.29 Three vertebrate homologues
(equivalents) of the Drosophila gene have been
identified and termed Sonic hedgehog (SHH)t Desert
hedgehog (DHH), and Indian hedgehog (JHH). SHH
is the most widely distributed and is thought to mediate
a major effect on the development of the neuraxis and
the limbs 30 (Fig. 4-13).
Hedgehog binds to a receptor complex on the cell
membrane comprising Patched and Smoothened.
The latter is a 115-kd protein that resembles an impor-
tant group of proteins called the G protein-coupled
receptors.31 Several homologues of the human patched
gene have been identified in contrast to a single human
smoothened gene (SMO). It is currently believed that
the binding of Hedgehog to the inactive Patched-
Smoothened membrane complex alters the inhibitory
effect of Patched on Smoothened (possibly through a
conformational effect), allowing Smoothened to trans-
duce the downstream signaling pathway.
In Gorlin syndrome, mutations in the patched gene
result in a loss of its inhibitory effect on smoothened,
which in turn results in a constitutive activation of
the downstream process causing tumorigenesis. 32
Analysis of the patchedgene in Gorlin syndrome reveals
mutations that are scattered throughout the length of
the gene and do not correlate to the phenotype.

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image...

4 • GENETICS 63

igi
igii
Igllla dill
Iglllc

OH
TK
OH

Iglllb [

FIGURE 4 - 1 2 . Proposed mechanisms of FCFR activation in craniosynostosis syndromes. A, Normal FCF-depen-

dent activation. The example illustrates a cell that normally expresses the isoform containing the Iglllc exon
(shaded) of FCFR2 on its surface. The cell membrane is shown as a pair of dashed lines; the extracellular region
containing immunoglobulin domains is uppermost. In the absence of FGF (left), FCFRs exist as monomers that
are inactive because the tyrosine -OH groups in the intracellular TK domain are unphosphorylated. In the pres-
ence of specific FGFs (right), binding to FGFR promotes formation of dimers. This causes approximation of the
TK domains, which leads to tyrosine phosphorylation. Note that only two of the FGFs illustrated (shaded verti-
cally) are able to bind to the Iglllc isoform. Heparan sulfate proteoglycan, an important cofactor for binding, is
omitted for clarity. B, Mechanisms of FGFR activation in craniosynostosis. Left, The -SH 2 groups of unpaired cys-
teine residues in the immunoglobulin domains can form covalent, constitutively activated dimers in the absence
of FGF. This is the major mechanism of Crouzon syndrome mutations. Center, A mutation in the linker between
the Igll and Igllla domains (denoted *) enhances the surface area of contact with the FGF, leading to increased
FGF binding affinity. This is the major mechanism of action of the Ser->Trp and Pro^Arg mutations in the Igll-
Iglll linker region. Right, Abnormal splitting of the Iglllc exon to generate FCFR containing the Iglllb exon (checker-
board pattern) generates a different receptor isoform able to bind a different repertoire of FGFs (shadedhorizontally).
This is proposed to cause additional limb abnormalities in some patients with Pfeiffer syndrome and, rarely, Apert
syndrome. (From Wilkie AOM: Molecular genetics of craniosynostosis. In Lin K, Ogle RC, Jane J, eds: Craniofa-
cial Surgery: Science and Surgical Technique. Philadelphia, WB Saunders, 2002:48.)

BASAL CELL CARCINOMA,
THE HEDGEHOG PATHWAY, AND
CLINICAL SIGNIFICANCE
Since the identification of the causative mutation of
Gorlin syndrome, prenatal screening has been avail-
able for clinical use.32 Absence of detectable mutations
offers a high degree of certainty that the conceptus is
free of the disease.
Basal cell carcinomas are the most common malig-
nant neoplasm in the United States and account for
nearly a third of all cancers diagnosed annually. A sur-
prising finding was that the patched gene was mutated
in a high number of the "garden variety" or sporadic

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64 I • GENERAL PRINCIPLES
TARGET GENES
| Wnt Family
Nucleus
f TGF/BMP Family
f Patched (PTCH)
basal cell carcinomas. Minute basal cell carcinomas
are just as likely as large lesions to have mutations,
as do all histologic subtypes, whether primary or
recurrent.
Analysis of the mutations of the patched gene in
sporadic basal cell carcinomas suggests that factors
other than ultraviolet B, the principal carcinogenic
component of sunlight, may play an etiologic role.
Ultraviolet B typically causes the formation of pho-
todimers that result in GC or AT transitions opposite
dipyrimidine sites. Because less than 50% of sporadic
basal cell carcinomas have this characteristic signature,
other possible carcinogens, such as ultraviolet A or
cosmic rays, may play a role in the etiology. This obvi-
ously has an impact on a clinician's advice on the use
of sunscreen and the effect of photodamage on the
skin.
Mutations in Sonic hedgehog have been shown to
occur in holoprosencephaly.34 Investigations of preg-
nant sheep with a high incidence of holoprosencephaly
in their progeny identified the culprit as an alkaloid
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FIGURE 4 - 1 3 . The Hedgehog pathway.
Hedgehog binds to Patched, releasing
Smoothened to transduce the signal. A
complex composed of Fused, Suppressor of
Fused, Costal2, and CLi disassociates, and
an active form of GLi translocates to the
nucleus, where it switches on the transcrip-
tion of target genes.
found in a certain type of lily that the pregnant sheep
had been known to ingest while grazing. The alkaloid,
dubbed "cyclopamine " was shown to act by inhibit-
ing the Hedgehog pathway. A study has shown that
the oncogenic effects of mutations of patched and
smoothened can be reversed by cyclopamine. 35 This,
coupled with the knowledge that adult sheep suffer no
ill effects from the ingestion of the alkaloid, opens up
the exciting possibility that this agent can be used in
the treatment of basal cell carcinomas and other tumors
associated with patched and smoothened mutations.
GENETICS AND ETHICS
The frenetic technological advances that have brought
genetics to the forefront of human scientific endeavor
have added controversy to an already contentious field.
A significant part of this problem has resulted from
the speed of these changes that has prevented the cre-
ation of a coherent moral and philosophical platform
of practical and ethical guidelines.
TeWttf'fceldW image...
Whereas the fundamental ethical principles of
autonomy, consent, and confidentiality are generally
accepted as a patient's right, these very features may
come into direct conflict with a provider's principles
and clinical j u d g m e n t (e.g., parents d e m a n d i n g a ter-
mination of pregnancy on a prenatal diagnosis of a
cleft lip). A more practical dilemma results from obtain-
ing a molecular diagnosis of a disease for which no
therapy exists. Such findings may be c o m p o u n d e d by
the very real fear that insurance companies will use
the knowledge of these tests to discriminate against
those individuals who have tested positive for a m u t a -
tion. Genetic testing has implications beyond its
immediate impact on the patient. For instance, a molec-
ular diagnosis of Huntington disease, an incurable, late-
onset neurodegenerative disorder, has p r o f o u n d
implications for t h e close antecedent relatives w h o m a y
not wish to delve into their disease status. Appropri-
ate genetic counseling is therefore vital before embark-
ing on a potentially hazardous course of genetic
testing. This is particularly important for plastic sur-
geons to remember because the repair of congenital
defects often thrusts them into the role of primary care-
giver and advisor.
The commercial implications of genetic testing and
patenting of disease-causing genes add another layer
of complexity to the debate. Biotechnology enterprises
have argued that the e n o r m o u s investment of financial
resources entitles t h e m to protect their intellectual
property in the form of patents on disease-causing
genes or the products derived thereof.
Diametrically opposed to this view is the more ide-
alistic one that holds the information originating from
the H u m a n G e n o m e Project and other allied genetic
research represents the heritage of m a n k i n d and as
such cannot be patented. The clash between commerce
and ethics vis-a-vis the identification of disease-
causing genes is exemplified by the Icelandic genomics
company DeCODE, which sold the potential rights to
a dozen genes associated with c o m m o n complex dis-
eases to Hoffman-La Roche for $200 million, thereby
trumping the assent of an entire population w h o were
the unwary contributors to its database.
Gene therapy, despite many promises, has yet to
deliver any substantial results. However, given the
pace of current research, it is not inconceivable that
such manipulation of the g e n o m e will become a part
of medical practice in the not too distant future. A
concern of opponents of gene therapy has been the
specter of germline manipulation or the introduction
of genes into the e m b r y o to produce desired charac-
teristics (which has a particular resonance with aes-
thetic surgery) rather than the original intent of gene
therapy, which focused on somatic cell therapy as a
means of curing an inherited disease. Issues such as
these will be the focus of intense debate in the years
to come.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
4 • GENETICS 65
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naturforschenden Vereins. Abhandlungen Brunn 1866;4:3-
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2. Hall JG: Genomic imprinting: review and relevance to human
disease Am J Hum Genet 1990;46:857.
3. Mueller RF, Young ID: Emery's Elements of Medical Genetics,
11 th ed. London, Churchill Livingstone, 2001.
4. Sprangcr JW, Benirschke K, Hall JG, et al: Errors of morpho-
genesis: concepts and terms. J Pediatr 1982;100:160.
5. Marden PM, Smith DW, McDonald MJ: Congenital anomalies
in the newborn infant including minor variations. J Pediatr
1964;64:357.
6. Lichter P, Boyle AL, Cremer T, et al: Analysis of genes and chro-
mosomes by nonisotopic in situ hybridization. Genet Anal Tech
Appll991;8:24.
7. Jalal SM, Law ME: Utility of multicolor fluorescent in situ
hybridization in clinical cytogenetics. Genet Med 1999;1:
181.
8. Boorman JG, Varma S, Ogilvie CM: Velopharyngeal incom-
petence and chromosome 22ql 1 deletion. Lancet 2001;357:
774.
9. Southern EM: Detection of specific sequences among DNA
fragments separated by gel electrophoresis. J Mol Biol 1975;
98:503.
10. Saiki RK, Gclfand S, Stoffel SJ, et al: Primer directed enzymatic
amplification of DNA with a thermostable DNA polymerase
Science 1988;239:487.
11. Mullis KB: The unusual origin of the polymerase chain reac-
tion. Sci Am 1990;262:56.
12. Brown PO, Botstein D: Exploring the new world of the genome
with DNA microarrays. Nat Gent 1999;21:33.
13. Geschwind DH: Sharing gene expression data: an array of
options. Nat Rev Ncurosci 2001;2:435.
14. Bittner M, Meltzer P, Chen Y, et al: Molecular classification of
cutaneous malignant melanoma by gene expression profiling.
Nature 2000;406:536.
15. Alizadeh AA, Eisen MB, Davis RE, etal: Distinct types of large
B-cell lymphoma identified by gene expression profiling. Nature
2000;403:503.
16. Slceman M, Fraser J, McDonald M, et al: Identification of a
new fibroblast growth factor receptor, FGFR5. Gene 2001;
271:171.
17. JangJH.Shin KH, Park JG: Mutations in fibroblast growth factor
receptor 2 and fibroblast growth factor receptor 3 genes asso-
ciated with human gastric and colorectal cancers. Cancer Res
2001;61:3541.
18. Wilkic AOM: Molecular genetics of craniosynostosis. In Lin K,
Ogle RC, Jane J, eds: Craniofacial Surgery: Science and Surgi-
cal Technique. Philadelphia, WB Saunders, 2002:46.
19. Passos Bueno MR, Wilcox WR, Jabs EW, et al: Clinical spec-
trum of fibroblast growth receptor mutations. Hum Mut
1999;14:115.
20. Muenke M, Schell U: Fibroblast growth factor receptor
mutations in human skeletal disorders. Trend Genet 1995;
11:308.
21. Neilson KM, Friescl RE: Constitutive activation of fibroblast
growth factor receptor-2 by a point mutation associated with
Crouzon syndrome. J Biol Chem 1995;270:26037.
22. Muenke M, Gripp KW, McDonald-McGinn DM, et al: A unique
point mutation in the fibroblast growth factor receptor 3 gene
(FGFR3) defines a new craniosynostosis syndrome. Am J Hum
Genet 1997;60:555.
23. Plotnikov AN, Schlessinger J, Hubbard SR, et al: Structural
basis for FGF receptor dimcrization and activation. Cell
1999:98:641.
24. Gorlin RJ, Goltz RW: Multiple nevoid basal cell epithelioma,
jaw cysts and bifid rib. A syndrome. N Engl J Med 1962;262:
908.
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25. Howell B, Caro MR: The basal cell nevus: its relationship to
multiple cutaneous cancers and associated anomalies of devel-
opment. Arch Dermatol I959;79:57.
26. Kimonis VE, Goldstein AM, Pastakia B, et al: Clinical features
in 105 persons with nevoid basal cell carcinoma syndrome. Am
J Med Genet 1997;69:299.
27. Gailani MR, Bale SJ, Lefell DJ, et al: Developmental defects in
Gorlin syndrome related to putative tumor suppressor gene on
chromosome 9. Cell 1992;69:111.
28. Hahn H, Wicking C, Zaphiropolous PG, et al: Mutations of the
human homolog of Drosophila patched in the nevoid basal cell
carcinoma syndrome. Cell 1996;85:841.
29. Porter JA, Young KE, Beachy PA: Cholesterol modification of
hedgehog signaling proteins in animal development. Science
1996;274:255.
30. Chiang C, Littingung Y, Lee E, et al: Cyclopia and defective axial
patterning in mice lacking sonic hedgehog gene function. Nature
1996;383:407.
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31. Van der Heuvel M, Ingham PW: Smoothcned encodes a
receptor-like serpentine protein required for Hedgehog
signaling. Nature 1996;382:547.
32. Bale AE, Yu K: The hedgehog pathway and basal cell carcino-
mas. Hum Mol Genet 2001;10:757.
33. Gailani MR, Stahle-Backdahl M, Lefell DJ, et al: The role of the
human homologue Drosophila patched in sporadic basal cell
carcinomas. Nat Genet 1996;14:78.
34. Belloni E, Muenke M, Roessler E, et al: Identification of Sonic
hedgehog as a candidate gene responsible for holoprosencephaly.
Nat Gent 1996;14:353.
35. Taipale J, Chen JK, Cooper MK, et al: Effects of oncogenic muta-
tions in Smoothened and Patched can be reversed by
cyclopamine. Nature 2000;406:1005.
image...

CHAPTER

5•
Psychological Aspects of
Plastic Surgery
U U R I E STEVENS, MD • MARY H. MCGRATH, MD, MPH

BODY IMAGE AND PU\STIC SURGERY The Self-Destructive Denier

Defining Body Image The Entitled Demander
Body Image Determines Emotional Response and Manipulative Help-Rejecting Complainers
Behavior SURGICAL PROCEDURES AND RELATED
Four Stages of Body Image Development PSYCHOLOGICAL ISSUES
How Plastic Surgery Changes Body Image Aesthetic Facial Surgery
PERSONALITY AND CHARACTER FORMATION Rhinoplasty
Defense Mechanisms Augmentation Mammaplasty
PERIOPERATIVE PSYCHOLOGICAL REACTIONS Reduction Mammaplasty
THE PHYSICIAN-PATIENT RELATIONSHIP: Trauma: Acquired Defects
TRANSFERENCE, COUNTERREACTION, AND Cancer and Reconstruction
COUNTERTRANSFERENCE PLASTIC SURGERY IN CHILDHOOD
Acquired and Congenital Defects: General
PERSONALITY STYLES AND PERSONALITY DISORDERS Considerations
Obsessive-Compulsive Personality and Personality Craniofacial Anomalies
Disorder Aesthetic Surgery in Teenagers
Narcissistic Personality and Personality Disorder
Dependent Personality and Personality Disorder SELECTION OF PATIENTS: DANGERS AND PITFALLS
Paranoid Personality Disorder General Risk Factors
Histrionic Personality and Personality Disorder Psychiatric Syndromes of Concern to Plastic
Borderline Personality Disorder Surgeons
STRATEGIES FOR MANAGEMENT OF THE DIFFICULT STRATEGIES FOR MANAGEMENT OF THE
PATIENT DISSATISFIED PATIENT
The Hateful Patient
The Dependent dinger

Plastic surgeons deal with the psychological needs and
responses of their patients on a daily basis. To deter-
mine whether a person is a suitable candidate for the
requested surgical procedure, plastic surgeons must
have a keen eye and intuitive sense, know the right
questions to ask, and have the good judgment to learn
from their past experiences, especially those in which
errors were made. The aim of this chapter is to provide
the plastic surgeon with tools to determine the appro-
priateness of patients* requests, to assess their capac-
ity to tolerate the requested procedure, and to predict
the likelihood that they will be satisfied with the
surgical results.
For a plastic surgeon to understand how psycho-
logical processes may affect a patient's reactions to
plastic surgery, the foundation lies in understanding
the psyche-—how it is formed and how it works. Per-
sonality structure affects a patient's experience of
surgery and its accompanying alterations in body
image; awareness of this is essential to good commu-
nication and rapport with a patient.
BODY IMAGE AND
PLASTIC SURGERY
Defining Body Image
Although it is mentioned casually and widely, the term
body image actually describes a complex psychologi-
cal abstraction. Real physical appearance is only a part
of it, and body image has been defined as the mind-
body relationship, the subjective perception of the body
as seen through the mind's eye, or the psychological
effects of what a person looks like.1 In 1935, Schilder,
one of the first to study body image, described it as a
tridimensional scheme of one's own body involving

67

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Dr.Mustafa D.
68 I • GENERAL PRINCIPLES
interpersonal, environmental, and temporal factors.11
Within his construct, body image is a result of what
our bodies look like, what people say about how we
look, our reactions to this input, the circumstances
and community in which we grow up, and when key
life events occur. Within this frame of reference,
consider two examples.
In the first instance, there is a large muscular girl
with small breasts. If she also has a championship tennis
serve and is part of an active, close-knit, sports-minded
family that celebrates her triumphs, her feelings about
her breasts may be quite different from those of a girl
of the same age who stands out as the least feminine
and shapely member of her socially prominent,
appearance-conscious family.
In a second example, an individual is told contin-
ually that he has his grandfather's rather large and
prominent nose. This may be welcome news if he was
a legendary fellow known for his charisma and
respected for his business and political successes. The
feeling might be different if he was a solitary, ill-
tempered failure disliked and avoided by his children.
Thus, the possession of certain physical character-
istics is colored by feelings about their value, and a
person's reaction to having familial, ethnically nor-
mative, or culturally popular features is influenced by
personal perceptions. Because of this, body image is
necessarily subjective. We cannot know someone else's
feelings about his or her body by an external evalua-
tion of his or her actual appearance. It follows that
changing someone's appearance for the better is a
positive event only if the person considers it an
improvement.
Body Image Determines Emotional
Response and Behavior
Perceptions of body image affect emotional response
and drive behavioral changes. Let us look at how this
important sequence occurs and then consider how this
cause and effect make plastic surgery a profound and
life-altering event for many patients.
When a person looks and thinks about himself or
herself, a body image is formed. Individuals appraise
themselves on the basis of this image of their physi-
cal and mental abilities and their relative success in
the environment. This produces a psychological effect
with varying amounts of confidence or anxiety. These
feelings of self-confidence or inadequacy will then
influence their ability to perform. Thus, in dealing with
other people and with life's challenges and problems,
one's body image influences the amount of success
that can be realized. Repeating this process over and
over on a daily basis, we learn what can be accom-
plished and then use this information to direct our
behavior. Goal-oriented patterns develop as we
learn to avoid situations in which we are not effective
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Dr.Mustafa D.
and seek out those that reward our efforts. As we do
this, others learn our strengths and weaknesses, and
this further determines their response and behavior
toward us. 2
Four Stages of Body
Image Development
EARLY CHILDHOOD
Beginning in the earliest months, children learn how
to think about themselves from those around them.
As a child's parents proffer approval and love or, alter-
natively, show a lack of attention or disapproval, the
child learns about his or her attractiveness and value
to others. In a warm and loving environment, a child
will develop feelings of self-worth, and these become
the foundation of a positive body image.
STARTING SCHOOL
The second stage of body image development begins
at the age of 5 or 6 years, when the child leaves the
security of the family to begin school and encounters
outside competition with peers. If the child is attrac-
tive to others and capable of projecting qualities desir-
able to the other children, the child will be well
accepted. Reinforced by positive feedback, the child
will grow in confidence and be ready to invest further
in rewarding behaviors, and patterns of thinking about
himself or herself are further established.
ADOLESCENCE
With puberty, the child's physical appearance changes
dramatically. There are changes in height; facial fea-
tures enlarge; secondary sex characteristics develop;
and the adolescent must deal with body hair, acne,
and odor. The changes are not equal among adoles-
cents in terms of when they occur or the endpoints
they reach, and with all of this comes great vulnera-
bility to the opinion of others. As physical changes
occur, the teenager will respond to the objective
changes with impressions that will be tested repeat-
edly against the opinion of peers. In gauging the reac-
tions of others, a self-picture will emerge and engender
an unusually strong emotional response in this age
group. Assaulted with feelings of insecurity, inade-
quacy, or depression, the adolescent may respond with
behavioral changes that alter social interaction
and introduce a negative pattern of body image
development.
AGING
With the passage of time and concomitant changes in
physical appearance, body image again undergoes
adaptation. Now, as one appears less vigorous and fresh,
competitors respond by granting less authority to the
image...
5 • PSYCHOLOGICAL ASPECTS OF PLASTIC SURGERY
older individual. Faced with this response, the phys-
ically older person starts to show weakening of body
image and retreats from situations in which he or she
was comfortable previously.
How Plastic Surgery Changes
Body Image
Plastic surgery is effective and useful to many patients
because it changes body image. As long as this change
is perceived by the patient as an enhancement, there
will be resultant positive changes in his or her emo-
tional life and behavioral patterns and, thus, improved
quality of life. It is significant that plastic surgery tends
to be undertaken at the time of one of the four stages
of body image development discussed in the preced-
ing section.3"5
Plastic surgery maybe undertaken in the child with
a congenital deformity or a physical defect that could
cause others to withdraw emotional or physical contact
with the child. Even if the deformity is of trivial pro-
portions, its correction will eliminate a factor that
might cause early rejection. The second period, when
a child enters school, is the usual time to correct pro-
truding ears, webbed toes, scars, small hairy nevi, and
other problems that will mobilize the attention of and
draw comments and criticisms from the child's peers.
The teenage years are a time for correction of recently
developed unattractive features, such as a large nasal
hump, or humiliating conditions, such as gyneco-
mastia. The aging person seeks plastic surgery to correct
deficiencies associated with maturation (e.g., wrin-
kling, a worn and tired appearance).
Given that the motivation to have aesthetic and
reconstructive plastic surgery may often be psycho-
logical and involves body image, the key to achieving
success is selection of patients. The core value of the
surgery lies not in the objective beauty of the visible
result but in the patient's opinion of and response to
the change. Recognition and understanding of
psychological issues begin with identification of the
personality traits that determine human interactions.
PERSONALITY AND
CHARACTER FORMATION
Much has been written about how personality or char-
acter develops in human beings. We all have person-
ality traits that characterize who we are and how we
interact with the world. These traits govern how we
perceive and relate to our environment and ourselves.
These traits are consistent and stable despite outside
stimuli and influences.
The ego is the chief executive of the mind, in charge
of balancing the internal and external influences
that confront it. These influences include memories,
drives, anxieties, perceptions, and external needs. To
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69
function smoothly, the ego has to have a set of auto-
matic operations that deal with these influences.
These operations are called defense mechanisms.
Defense Mechanisms
We use defense mechanisms to cope with the stresses
of our internal and external worlds. These mechanisms
are not under our conscious control and develop in
response to our early life experiences. Our repertoire
of defenses contributes to our character formation and
enables us to forget painful experiences, to minimize
or deny anxiety-provoking situations, and to evade
unwanted impulses (sexual and aggressive).6 For pur-
poses of understanding plastic surgical patients and
their response to surgery, the defense mechanisms of
regression, denial, projection, repression, distortion,
somatization, intcllectualization, rationalization, and
sublimation are discussed.
Regression is a return to a previous stage of func-
tioning or development to avoid anxiety or conflict.6
Regression may be seen in both healthy and unhealthy
adaptations to illness. Patients have to undergo some
degree of regression to allow themselves to be cared
for when they are ill and to be in a dependent posi-
tion. However, regression may get to a pathologic level
when the patient acts in an infantile and helpless
manner and is unable to participate as a partner in the
medical care.
Denial is being consciously unaware of a painful
aspect of reality. Through denial, patients invalidate
unpleasant or unwanted bits of information and act
as though they do not exist/' Denial, like regression,
can be adaptive or maladaptive in the medical setting.
For example, a certain degree of denial can function
to allow a patient to cope with an overwhelming feeling
of helplessness or hopelessness in response to a diag-
nosis of terminal cancer. Denial becomes maladap-
tive when it interferes with a patient's ability to
participate in medical care. Denial need not be con-
fronted when a patient is accepting appropriate
medical treatment and participating in care. Denial
can reach psychotic proportions in psychiatrically ill
individuals.
Projection is when one attributes one's unac-
knowledged feelings to others. 6 Projection maybe dis-
played by falsely attributing or misinterpreting
attitudes, feelings, or intentions of others (e.g., "I'm
not angry at her; she's angry at me").
Repression involves keeping unwanted memories,
thoughts, or feelings from conscious awareness.6 The
patient who "forgets" unpleasant news that the physi-
cian tells her or him is likely to be repressing the
disturbing thoughts or feelings.
Distortion occurs when patients grossly reshape
external reality to suit their inner needs, including
magical beliefs and delusional thinking. 7
TWttf'aeldW image...
70 I • GENERAL PRINCIPLES
Somatization is when patients convert their psychic
conflicts and conflicted feelings into body symptoms. 7
The most common presentation of somatization is
hypochondriasis.
Intellectualization is when the patient controls anx-
ieties and impulses by excessively thinking about them
rather than experiencing them. 7 These thoughts are
devoid of affect or feeling.
Rationalization is when the patient justifies his or
her attitudes, beliefs, or behavior that might be unac-
ceptable by inventing a convincing fallacy.7
Sublimation is the transformation of drives,
feelings, and memories into healthy and creative
outcomes. 7
PERIOPERATIVE PSYCHOLOGICAL
REACTIONS
Even when the surgeon has preoperatively considered
a patient to be a suitable candidate for surgery, it does
not mean that he or she should cease to look for signs
of psychological disturbance in the patient in the post-
operative period. Transient episodes of anxiety or
depression that last days to weeks after surgery have
been reported in studies by Edgerton 8 and Meyer.9 A
patient may experience psychiatric side effects to
various medications used preoperatively, intraopera-
tively, and postoperatively. The sudden onset of a new
psychiatric symptom should suggest a medication-
induced psychiatric side effect. Perhaps one of the most
profound reactions seen is lidocaine-induced delir-
ium after regional limb surgery in which a local anes-
thetic block was used. This can happen if there is an
inadvertent intravenous injection of the anesthetic
agent.
Mood improvement has been reported in a variety
of cosmetic surgery patients postoperatively.10*15 Even
the so-called high-risk patients, those thought most
likely to have a poor psychological outcome, may show
benefit after cosmetic surgery.16 These findings have
led to the conclusion that cosmetic surgery can be psy-
chologically beneficial even to patients with psychi-
atric conditions, assuming that they are properly
managed by their physician and psychiatrist.17
In the discussions that follow, different personal-
ity styles and disorders are discussed relative to how
they respond to surgery and recovery.
THE PHYSICIAN-PATIENT
RELATIONSHIP: TRANSFERENCE,
COUNTERREACTION, AND
COUNTERTRANSFERENCE
Surgeons are invested with strong emotions by patients
who are entrusting them with their bodies and lives.
Patients may develop special feelings for their surgeons
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Dr.Mustafa D.
that are similar to those associated with figures of
authority from their past.' 8 This may account for the
idealization of the surgeon as the "miracle worker" or
"savior" as well as for some of the unwarranted angry
feelings toward the surgeon. This is a phenomenon
known as transference. The nature of the physician-
patient relationship is extremely important to the
success of the treatment of the seriously ill patient.
Although many physicians are uncomfortable with the
patients who develop feelings about them, it is impor-
tant to recognize the phenomena of transference,
counterreaction, and countertransference.
Transference can be described as recreating, in the
physician-patient relationship, a conflicted relation-
ship with a childhood figure. The transference maybe
of a paternal or a maternal nature, but this is not nec-
essarily the case. Grandparent, aunt or uncle, and
sibling transferences can also occur. When transfer-
ence is present, the patient will react to the physician
as if the physician were the transferential figure; in
other words, feelings about that figLire become "trans-
ferred" onto the physician. If the transference is pos-
itive, it generally does not need to be addressed.
However, if the transference is negative, it does need
evaluation.
An example of negative transference is the patient
who treats the physician as if he or she were sadistic,
uncaring, cold, and heartless when the physician is
trying his or her best to be empathic, warm, and caring.
The patient is acting in an overly exaggerated fashion
out of proportion to the real interaction. Oftentimes,
the transference is not a total distortion of the real
relationship between the physician and patient; the
patient may have picked up on some aspect of the
physician's personality or behavior that has served as
the foundation for the development of transferential
feelings.
The physician's emotional reaction to the patient's
expression of transferential feelings is termed coun-
terreaction. For example, when the patient becomes
angry with the physician, the physician wishes to with-
draw or may feci anger in response. Instead, the physi-
cian should try to figure out how best to respond to
the patient's feelings and behavior without personal-
izing them. This is easier said than done, as physicians,
like their patients, are only human and are prey to
their own feelings and those of others toward them.
Counterreaction, which is a common or "normal"
response to the patient's emotions or behaviors, needs
to be differentiated from countertransference.
Countertransference is the physician's reaction to
the patient based not on the real circumstances but
on issues or conflictual relationships in the physician's
own life—if you will, a "neurotic" response to a patient's
transference. When these feelings occur, they may
be intense for both the patient and the physician.
Recognition of these feelings and their origins is an
 5 • PSYCHOLOGICAL ASPECTS OF PLASTIC SURGERY
important insight and a good tool to have to improve
relationships with patients and to avoid pitfalls in the
treatment relationship, including the selection of spe-
cific interventions.
PERSONALITY STYLES AND
PERSONALITY DISORDERS
There are various personality types or styles that all
physicians treat in clinical practice. This section focuses
on the personality styles and disorders most commonly
encountered by the plastic surgeon, the typical reac-
tions to surgery or alterations of body image, and the
medical management of these.
When personality traits become inflexible and
maladaptive and cause either significant impairment
in social or occupational functioning or subjective dis-
tress, they constitute a personality disorder.19 Person-
ality disorders are generally apparent by late childhood
or adolescence, continue throughout most of an indi-
vidual's adult life, and may become exaggerated in the
older years.
There are four characteristics that all personality
disorders share. They are (1) an inflexible and mal-
adaptive response to stress, (2) a disability in working
and loving that is generally more serious and always
more pervasive than that found in neurosis, (3) elic-
itation by interpersonal conflict, and (4) a peculiar
capacity to "get under the skin" of others. 20 Patients
with personality disorders see the rest of the world,
rather than themselves, as having a problem. They have
little insight into their own behavior or its impact on
others around them.
Obsessive-Compulsive Personality
and Personality Disorder
Many individuals with an obsessive-compulsive per-
sonality arc highly successful and productive members
of the community. This personality style lends itself
to efficiency, effectiveness, and goal-directed behav-
ior. These persons tend to deal with feelings by using
intellectualization; are preoccupied with details, organ-
ization, and schedules; tend to be perfectionistic; are
scrupulous about matters related to morality and
ethics; have trouble delegating tasks to others; and can
be rigid, stubborn, and miserly.21
When obsessive-compulsive patients become
anxious, they can quickly decompensate and become
overly invested in routines or seemingly trivial infor-
mation. These patients can overwhelm the physician
with questions and occupy enormous physician and
staff time, leading to resentment by caretakers. It is
important to reassure these patients and to address
their fears and anxieties; sometimes the surgeon
should try to determine what may be making them
anxious or fearful and provide appropriate comfort.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
71
These patients are often unaware of their feelings,
and providing them with detailed medical explana-
tions can be helpful to them. Giving them tasks to
perform makes them feel like a partner in their ther-
apeutic treatment and in decision-making. This could
take the form of having them change dressings,
measure their fluid intake and output, or care for scars
with topical moisturizers. Even if these measures are
not strictly necessary, they will help these patients
manage their anxiety.
•PATIENT EXAMPLE
Ms. A. is an overly neat 43-year-old successful
business executive who underwent a blepharo-
plasty. After surgery, she barraged the surgeon's
office with endless questions and details and
occupied excessive amounts of staff time on the
telephone. The surgeon, Dr. B., had Ms. A. come
in for an extra postoperative visit and instructed
her to prepare, in advance, a list of questions she
needed answered. After answering her questions,
Dr. B. addressed her anxiety about the eventual
outcome, reassuring her that this was a normal
concern, and tried to determine how best to con-
tinue to reassure her. She was given a scheduled
daily call-in time, limited to 5 minutes, during
which she could ask her questions and receive
support and reassurance.
Narcissistic Personality and
Personality Disorder
Narcissistic patients have an excessive need for admi-
ration, an exaggerated sense of self-importance, and
grandiose notions of their beauty and power. They
have a sense of entitlement, can be exploitative of others
to achieve their own ends, lack empathy toward
others, can be envious of others or feel that others are
envious of them, and may be arrogant and haughty
in their behaviors and attitudes. 21
Because these patients place such value on their
physical appearance, surgery to alter their appearance
will naturally generate some anxiety. They generally
find the physical effects of aging on their appearance
unacceptable. Similarly, they find distressing any sur-
gical complication or even the typical swelling and
bruising that are the sequelae of surgical procedures.
These patients need to be educated as much as pos-
sible about the process of healing and recovery and
offered reassurance along the way about common post-
operative events. They respond to being treated like
equal, independent partners in their care.
Plastic surgeons should take care not to be taken in
by the narcissistic patient's idealization of them (e.g.,
"You're the best plasticsurgeon in the country"). These
72 I • GENERAL PRINCIPLES
patients can quickly switch to profound devaluation
of the surgeon if the surgeon displeases them or causes
them discomfort. These patients tend to become
demanding when they are physically uncomfortable
and anxious, and they respond best to empathic
reassurance.
Dependent Personality and
Personality Disorder
These patients exhibit clinging and submissive behav-
ior, seemingly needing endless reassurance and
support. They have great difficulty making daily deci-
sions without an excessive amount of advice and reas-
surance. They want others to assume responsibility
for their major decisions. They experience difficulty
initiating actions because of a lack of self-confidence
in their judgment and abilities. They often find it dif-
ficult to disagree with others because they fear rejec-
tion or disapproval. Dependent personalities have great
discomfort when they are alone and are fearful that
they cannot take care of themselves.21
This translates in the surgical situation to the
dependent patient's becoming clinging and fearful after
surgery, in part facilitated by the regression initiated
by being taken care of while ill. This behavior can
sometimes alienate health care providers and bring
about the very thing the dependent personality fears,
to be alone and abandoned. The physician should try
to recognize these fears and provide reassurance to
the patient that he or she will not be abandoned. Warm
support should be offered, but firm limits must be
set on undue neediness and manipulativeness.
Paranoid Personality Disorder21
Paranoid patients have a pervasive mistrust and sus-
picion of others. They fear that motives are ill-inten-
tioned and they suspect, with an insufficient basis in
fact, that others are trying to harm, exploit, or injure
them. They may attribute a malevolent intent to inno-
cent remarks. They are unforgiving and bear grudges,
even to seemingly benign slights. They perceive others
as attacking their character or reputation and may
respond angrily and with vindictiveness.
These patients experience surgery as an "intrusion"
and attack on their bodies. They find it difficult to
establish a therapeutic alliance with health care
providers. Their lives sometimes appear to be without
direction, "drifters." They have few friendships and
few social interactions. Their occupational choices are
most successful when they choose professions in
which they have little contact with others and can work
in relative isolation.
Under stress, paranoid individuals can develop brief
psychotic episodes. It is preferable not to perform elec-
tive cosmetic surgery on such an individual. If the
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paranoid patient requires reconstructive surgery or
other nonelective cosmetic surgery, it is important to
respect the patient's distance and interact with the
patient in a professional manner, not attempting to
get too close or friendly, because this behavior may
be viewed with suspicion. The surgeon should be direct
and answer questions in a candid and honest fashion.
Any distortions by the patient that are noted by the
surgeon should be addressed and discussed openly.
Accusations should be neither disputed nor confirmed
but explained as coming from illness rather than from
any attempt to injure the patient. 22
Histrionic Personality and
Personality Disorder21
Histrionic patients tend to be excessively emotional
and exhibit attention-seeking behavior. Although they
are often lively, flirtatious, and dramatic, they con-
tinually demand to be the center of attention. If they
feel the spotlight move away from them, they may do
something dramatic to refocus attention on themselves
(e.g., make a scene on the floor, call patient relations).
They are highly suggestible and easily influenced by
others and current fads. The plastic surgeon should
take care in assessing this patient to ascertain the real
reasons for seeking surgery.
Histrionic persons may be overly trusting, especially
of physicians, whom they see as magically solving their
problems. They tend to view the therapeutic relation-
ship as more intimate than it actually is and may develop
romantic fantasies about their physicians. Individuals
with histrionic personality disorder are at an increased
risk for suicidal gestures and may make threats to get
attention and coerce better caregiving.
The surgeon should adopt a professional manner
with these patients and give the appropriate amount
of attention to them. The surgeon must be very careful
not to become too friendly or to be drawn into their
seductive behavior. Certainly, one should not be flir-
tatious or seductive in response. Firm limit setting with
regard to the nature of the therapeutic relationship and
the physician's role in the patient's life is necessary.
Borderline Personality Disorder21
Borderline patients have a pattern of unstable inter-
personal relationships. They may have an identity dis-
turbance characterized by shifting and changing senses
of self, goals, values, and aspirations. Likewise, feeling
states or moods can also show wild swings and vari-
ability. Borderline patients can be impulsive and often
have trouble controlling their anger and emotions.
Their behavior can be self-destructive and manipula-
tive. They may engage in gambling, excessive money
spending, binge eating, substance abuse, unsafe sex,
or reckless driving. At the extreme, they may perform
VSWt^SelcriSP image...
5 •
self-mutilating acts (cutting or burning) or suicidal
behavior. Completed suicide occurs in 8% to 10% of
such patients. During periods of extreme stress, tran-
sient paranoid ideation or dissociative symptoms
(e.g., depersonalization) may occur but generally do
not persist.
Such patients are best handled with strict limit
setting. The physician should make every attempt to
be consistent and attentive but not respond to manip-
ulative behavior. The patient should be given a sched-
ule for visits and follow-up plans to limit fears of
abandonment.
These patients generally respond best to the cor-
rective experience of developing a trusting, stable rela-
tionship with the physician who does not retaliate in
response to their angry and disruptive behaviors. 23 Use
of the resources of other health care providers, such
as a psychiatric consultant for psychotherapy and psy-
chopharmacotherapy or a nurse practitioner to "spread
the transference" can help make these patients feel ade-
quately attended to and cared for. However, it is impor-
tant for the surgeon to continue to care for them in
the usual fashion because these other relationships are
not a substitute for the surgeon's relationship with them.
STRATEGIES FOR MANAGEMENT
OF THE DIFFICULT PATIENT
The Hateful Patient
The "hateful patient" is a term coined by James E.
Groves in his seminal article in the New England Journal
of Medicine.24 These are patients who often inspire
dread in their physicians when they see their names
on the appointment schedule. These patients often
make a provider feel angry and helpless, leading to
possible retaliation or confrontation. Who are these
individuals? It is helpful to recognize these patients,
to understand why they inspire negative feelings, and
to manage their treatment on the basis of specific prin-
ciples. One cannot pretend that negative feelings do
not exist because failing to acknowledge these feelings
can lead to suboptimal medical care.
The Dependent Clinger24
Dependent dingers range from having mild requests
for reassurance to demanding requests for many dif-
ferent forms of attention (such as analgesics, long expla-
nations, caring, affection). These patients may be
experienced as "bottomless pits" of neediness, and
avoidance behaviors on the part of the physician may
ensue.
The warning signs of the dependent clinger are the
overly grateful patient who idealizes the physician, pro-
fesses undying "love" and admiration, and behaves
in a seductive manner. The physician becomes "the
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PSYCHOLOGICAL ASPECTS OF PLASTIC SURGERY 73
inexhaustible mother"; the patient becomes the
"unplanned, unwanted, unlovable child."24
• P A T I E N T EXAMPLE
Ms. T., a 24-year-old woman who is seeking aug-
mentation mammaplasty, places several telephone
calls before her surgery, asking for more informa-
tion and needing reassurance about the upcom-
ing surgery. Her plastic surgeon gives her the time
she seems to need to make her feel comfortable
about the procedure. Several days postoperatively,
she starts to place phone calls to the office, esca-
lating in frequency and urgency. She is requesting
office visits despite little objective need for a visit
outside of the usual postoperative follow-up. She
also starts to ask for analgesic medications and to
request reassurance about her breast size and her
discomfort. The plastic surgeon stops answering
her phone calls and lets his nurse field the ques-
tions and calls. As a result of not being able to
reach the surgeon directly, she starts to page him
in the evenings, telling his service that it is an
emergency.
The best management of this patient is to set firm
limits relative to appointments and telephone contacts.
The physician needs to kindly but clearly state to the
patient that the physician has human limitations and
cannot be an inexhaustible resource to the patient,
available at any time of day or night. Regular office
visits should be scheduled, during which time the
patient can see the physician and ask questions. The
surgeon's nurse can also schedule visits in between visits
to the physician to provide reassurance. These actions
should give the patient the contact needed without
disrupting the office and the physician's life. Enlisting
the help of a psychiatric consultant can be helpful in
providing additional support to the patient and
spreading the transference.
The Self-Destructive Denier24
All physicians have patients who deny their illnesses.
Denial is pathologic when it interferes with the
patient's ability to accept proper medical care for the
illness. Otherwise, denial can be adaptive in coping
with illness.
However, there is a group of patients who are self-
destructive deniers. Unlike the adaptive deniers, these
patients are fundamentally dependent on others and
seem to revel in their self-orchestrated destruction.
They appear to their physicians as taking great pleas-
ure in putting obstacles in the path to delivery of
optimal care.
74 I • GENERAL PRINCIPLES
• P A T I E N T EXAMPLE
Mr. B., a 49-year-old man, is an intravenous drug
abuser. He has a long history of drug-related
medical problems and hospitalizations. Despite
multiple attempts to get him to pursue drug
treatment, he has resisted attending any pro-
grams. He was admitted to the hospital with
bacterial endocarditis and given intravenous
antibiotics for 6 weeks. Shortly after discharge, he
was readmitted with cellulitis from a fresh intra-
venous heroin injection site. The plastic surgeon
was consulted to provide skin flaps for coverage
after skin loss followed the cellulitis. After that
treatment and discharge, he was readmitted
with recurrence of the endocarditis and required
additional skin grafting for breakdown due to
new soft tissue infections. Two months later, he
was admitted with sepsis and died in the
hospital.
Self-destructive deniers make their physicians feel
angry, helpless, used, and abused. They engender rescue
fantasies, especially in younger physicians, but may also
lead their physicians to have negative feelings toward
them. Physicians often feel guilty about their hateful
feelings toward such patients.
The best management is to see the patient's pattern
of self-destructive denial and to set realistic expecta-
tions relative to the patient s ability to get well. It may
be helpful to think of the patient as having a degener-
ative or terminal illness for which there is no medical
treatment and to set the goal of providing supportive
care and alleviating suffering.
The Entitled Demander 24
The entitled demander is fundamentally similar to the
dependent dinger in neediness; however, the presen-
tation is quite different. These patients are demand-
ing, devaluing, and intimidating. These are the patients
who threaten lawsuits or contact patient relations rep-
resentatives when the medical staff does not fulfill their
demands as they require.
Their primary feeling state is one of entitlement.
This is actually a defense against fears of loss of control
and helplessness. However, when a physician is at the
other end of the angry demands and entitled behav-
ior, it is easy to understand how one could become
enraged with this patient. They also make the physi-
cian feel fearful of their threats. The usual reaction to
these patients is to let them know, in no uncertain
terms, how undeserving they are of what they demand.
This usually docs not work with this population.
Groves24 speaks eloquentiy about how to handle such
a patient:
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I know you're mad about this . . . and at the other doctors.
You have reason to be mad. You have an illness that makes
some people give up and you're fighting it. But you're fight-
ing your doctors too. You say you're entitled to repeated tests,
damages for suffering and all that. And you are entitled—
entitled to the very best medical care we can give you. But
we can't give you the good treatment you deserve unless you
help. You deserve a chance to control this disease; you deserve
all the allies you can get. You'll get the help you deserve if
you'll stop misdirecting your anger to the very people who are
trying to help you get what you deserve—good medical care.
This strategy allows the patient to fulfill the under-
lying wish to receive "the best" medical care and, it is
hoped, will enlist the individual as an ally in the treat-
ment. It enables the physician to tactfully address the
entitled, demanding behavior in a constructive way
rather than to respond with rage or retaliation.
Manipulative Help-Rejecting
Complainers 24
No matter to what lengths the physician may go to
help them, this is the group of patients who will try
to thwart the help. They express their hopelessness that
any physician can help them. They return to the physi-
cian's office week after week to affirm that the
recommended treatment failed once again. When one
physician "fails" them, they shop for the next.
Like the dependent dinger and the entitled deman-
der, they may tend to have no limits to their need.
They do not seem to wish to get well; instead, they
seem to wish an "undivorceable marriage" with their
health care provider. When one symptom resolves,
another appears to replace it. These patients often suffer
from undiagnosed and untreated depression.
• P A T I E N T EXAMPLE
Ms. S. is a 30-year-old sales associate with
intractable hand pain. She has gone for consulta-
tions all over the country and has received
numerous diagnoses, including causalgia, reflex
sympathetic dystrophy, and carpal tunnel syn-
drome. She has had hundreds of diagnostic pro-
cedures, but (fortunately) she has refused to have
surgery when it was recommended. She had a 14-
day hospitalization at a pain treatment center,
during which time her hand pain diminished
with a combination of antidepressants, relaxation
therapy, behavioral therapy, and occupational and
physical therapy. However, after discharge, she failed
to follow any of the recommendations, and the
pain recurred. She is now angry that the pain center
failed to cure her and is determined to find a phy-
sician who can find the "real cause" of her pain.
image...
5 • PSYCHOLOGICAL ASPECTS OF PLASTIC SURGERY
This group of patients makes physicians worry that
they may have overlooked a correctable illness and
makes them feel anxious and uncertain about their
clinical skills- It is usually not constructive to confront
this patient with his or her behavior or neediness. It
is important to realize that the ultimate goal of the
patient is to never be abandoned and to always be con-
nected to the physician. However, he or she is fearful
of real closeness with the physician.
A good strategy for the physician is to communi-
cate to these patients that he or she may not be able
to help them and to share their pessimism that they
can be "cured." Instead, the physician could suggest
treatments that may provide "some" relief (but not
enough that the patient will be cured, thereby engen-
dering fear in the patient of losing the physician). This
technique was used by Ms. S.'s physician, who also
treated her depression and offered behavioral strate-
gies to alleviate her pain while telling her that he did
not think that the techniques could be more than
50% helpful. Ms. S. was satisfied with this approach,
which allowed her to hold onto her symptom and to
her relationship with her physician simultaneously
but also permitted her to become more functional
in her daily life. Psychiatric consultation can be
helpful but not as a replacement for the primary
physician; it must be presented as an adjunctive
treatment.
SURGICAL PROCEDURES AND
RELATED PSYCHOLOGICAL
ISSUES
Aesthetic Facial Surgery
Our society seems to value youth and to associate the
physical changes of aging with weakness and loss of
worth. Surgery to rejuvenate the face can be of enor-
mous benefit to the person with an aging appearance.
It may allow the person to feel better and acquire
acceptance, to feel sexually attractive to others, and to
be viewed as more vibrant, strong, and youthful. There
are clear economic, psychological, and social benefits
to having a more youthful appearance.
Surgery of the aging face is done for the purpose
of restoring a previously existing appearance or pre-
existing image of the face. This type of surgery seems
to require no dramatic body image readjustment 25
because the aging face does not appear to be fully incor-
porated into the body image over time. This opera-
tion is generally successful and psychologically
beneficial to the individual.
Procedures to rejuvenate the face are generally per-
formed in the middle to later ages of life. This is a time
of potential loss—of loved ones, of career, of friends
and family, menopause, baldness, the empty nest left
by children's emancipation. In a study of face lift
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75
patients older than 50 years, Webb et al'° found that
90% had lost an important person in the 5 years before
surgery. Dunofsky26 found the study population of
women who had facial cosmetic surgery to be more
narcissistic and to have more problems with separa-
tion-individuation than the control group but to have
no differences in self-esteem and social anxiety. Edger-
ton et al27 found that 74% of face lift patients had been
diagnosed with a psychiatric disorder.
Sarwer and Crerand 28 looked at the various pre-
operative studies in the literature and found that clin-
ical interview-based investigations identified a higher
incidence of psychopathology in the cosmetic surgery
population. However, when preoperative studies using
standardized psychometric testing as part of the
assessment were evaluated, little psychopathology was
uncovered.
There have been various studies that alluded to
greater psychological difficulties in male than in
female face lift patients.27,29 However, the percentage
of men having face lifts has increased during the past
20 years with no clear increase in psychological diffi-
culties postoperatively.
In Goin's study,30 the motivations for face lift surgery
were related to feelings about aging in 70% of the
patients, and most were satisfied with the results even
when they had some unrealistic expectations. The study
ofLeistetal 31 revealed that about 13% of patients were
dissatisfied with their surgical results.
Postoperatively, face lift patients may experience
some hypoesthesia or paresthesias of the face and neck.
They may experience some sleep disturbance caused
by physical discomfort. Those individuals who par-
ticularly prize their autonomy and independence may
find it difficult to manage the postoperative period of
physical discomfort and incapacity. However, psy-
chological reactions are usually short-lived, and
patients are generally satisfied with their results,
experiencing a sense of enhanced attractiveness and
self-esteem.
Aging face patients who seek face lift surgery
appear to be motivated by the desire to restore their
previous youthful visage. Rhinoplasty patients, on
the other hand, are seeking to change their basic
appearance.
Rhinoplasty
The literature is filled with articles and studies about
the patients who seek rhinoplasty. In general, older
studies of this group of patients suggested a great deal
of psychopathology. In 1975, Gibson and Connolly 32
studied rhinoplasty patients 10 years postoperatively
and found a high level (38%) of psychopathology,
including schizophrenia. They compared this group
with a trauma and disease group, in which they found
only 8% with a psychological disorder. Wright and
76 I • GENERAL PRINCIPLES
Wright found a high level of psychopathology based
on psychological testing measures (Minnesota Mul-
tiphasic Personality Inventory) in their controlled study
of rhinoplasty patients. Compared with the control
group, patients seeking rhinoplasty were more self-
critical, more sensitive to others' opinions of them,
and more restless. The most consistent personality
diagnosis was "inadequate personality" which prob-
ably translates into "dependent personality" by today's
diagnostic nomenclature. Hay's 1973 study15 of 45
rhinoplasty patients demonstrated psychological dis-
turbance in about 58% of the study group. Micheli-
Pelligrini and Manfrida's study34 as well as Linn and
Goldman's study 35 also revealed a high incidence of
psychopathology.
There has been much focus in the plastic surgery
literature on the so-called minimal defect rhinoplasty
patient. The 1960 study of Jacobson et al36 looked at
20 consecutive men requesting cosmetic surgery for
"minimal defects." The most requested procedure was
rhinoplasty. All but two of the patients (those two
refused psychological evaluation) were found to have
psychiatric diagnoses. Seven were found to have psy-
chosis; four were found to be neurotic; seven had per-
sonality disorders. Half of the patients underwent the
procedure, and more than 50% of these surgical
patients had postoperative psychological problems,
including one suicide attempt.
However, not all studies have supported a link
between rhinoplasty and psychopathology, and in
actual practice, a great majority of rhinoplasty patients
seem to benefit from the surgery. The patients
described by Linn and Goldman 35 reacted with
"elation" after the surgery and shortly afterward were
no longer preoccupied with their nose and were pleased
with the cosmetic results. They found an overall
improvement in the patient's level of adjustment. They
hypothesized that the anatomic changes made to the
nose and subsequent change in others' behavior
toward the patient led to a release of the psychic energy
attached to the nose. Goin and Goin's study37 of rhino-
plasty patients who were simultaneously in psy-
chotherapy supported Linn and Goldman's hypothesis.
Goin and Goin asserted that the loss of self-
consciousness achieved after the rhinoplasty led to
greater self-confidence, which led others to behave dif-
ferently toward the patient, enabling the patient's self-
esteem to grow with this reinforcement. In this group,
33% showed no detectable psychological changes
postoperatively, and most were happy with their sur-
gical results. On balance, a substantial number of
studies seem to demonstrate psychological and
psychosocial benefit from rhinoplasty surgery.
Several studies during the last decade have shown
that the psychological benefits of rhinoplasty surgery
are greater in female than in male patients.38,39 Slator
and Harris 40 found that male patients show more
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symptoms of anxiety and depression than do their
female counterparts preoperatively, but they found no
evidence to support earlier suggestions that requests
for rhinoplasty may be early symptoms of severe psy-
chiatric illness.
Several writers have urged plastic surgeons to be
cautious about drastically altering the appearance of
the patient. Some patients experience a sense of a"loss
of identity."6 In a series of more than 5000 rhinoplasty
patients, Bruck41 reported that older patients often
poorly tolerate drastic changes in their appearance.
He warns against "type changing" rhinoplasty in
patients older than 35 years. Other authors looking at
dissatisfaction of the patient in the setting of multi-
ple rhinoplasty procedures may have been seeing cases
of body dysmorphic disorder, which at the time of the
papers was not a recognized psychiatric entity.
Rhinoplasty patients, especially men, may experi-
ence some concerns relative to their sexual identity in
the postoperative period. These concerns appear to
be connected to feelings about the size and shape of
their nose. Consequently, to avoid psychiatric distur-
bances in the postoperative period, the plastic surgeon
needs to try to ferret out the presence of sexual iden-
tity disturbances before deciding to operate. Likewise,
psychotic patients should be identified and surgery
avoided in this population because their psychotic
thinking or delusions may be exacerbated by the
surgery.
Augmentation Mammaplasty
In general, augmentation mammaplasty patients are
happy with their plastic surgical result. Even in the
presence of scarring and capsular contractures, most
augmentation mammaplasty patients are satisfied
with their aesthetic appearance and the psychologi-
cal benefits derived from the surgery.42 The groups of
women most commonly seeking augmentation
mammaplasty are small-breasted women who have
always been unhappy with the appearance of their
breasts and seek the surgery for psychological reasons,
women whose breasts have undergone involution post
partum or with nursing and who wish to restore their
previous size and appearance, and those who seek the
surgery for occupational reasons (such as actresses,
models, and nude dancers).
In general, the first group is the least psychologi-
cally healthy group before surgery. There appears to
be a higher than normal incidence of depressive dis-
orders, 43 ' 45 with one study by Edgerton et al report-
ing the percentage to be up to 60%. These patients
often have poor self-esteem and feelings of inadequacy.
They may feel a diminished sense of femininity and
sexual attractiveness. Sexual functioning may be
impaired by inhibitions about not wanting their
breasts viewed or fondled during sexual play.
image..
5 • PSYCHOLOGICAL ASPECTS or- PLASTIC SURGERY
After augmentation mammaplasty, patients will
report enhanced self-esteem, greater feelings of attrac-
tiveness and femininity, fewer inhibitions during
sexual activity, and improved mood. Studies by
Kilmann et al46 and Schlebusch and Mahrt 47 have
reported improvement in body image after breast
augmentation. The patients rapidly integrate their
augmented breasts into their body image. Druss 44
explained this remarkable change in behavior, outlook,
and self-esteem from a psychoanalytic perspective. He
stated that a woman seeks augmentation mammaplasty
in an effort to repair chronic and deep-seated intrapsy-
chic conflicts. In his study group, he found that the
patients had problematic identification with their
mothers, secondary to the mother's being emotion-
ally unavailable. This failure of identification led to
poorly formed self-images as women and doubts about
femininity. Druss' observations may help explain why
not all small-breasted women seek augmentation
mammaplasty and many seem content with their breast
size.
Interestingly, in light of the breast implant con-
troversy and litigation during the 1990s, many women
with augmented breasts chose to have explantation
of their silicone implants because of their fears.
Although many of these women felt less fearful after
explantation, many also felt depressed when they had
to return to their original breast size. Some chose to
be reimplanted with saline implants to restore the pos-
itive feelings captured by the original augmentation
procedure.
Reduction Mammaplasty
Many women who seek reduction mammaplasty
experience significant physical discomfort from their
heavy and pendulous breasts and report restrictions
in activities, especially sports. Finding clothing that
fits properly is a problem. They describe feelings of
unease wearing bathing suits. iMany feel self-conscious
about the size of their breasts and state that people,
especially men, look at their breasts before looking at
their faces. They may avoid social interactions and
sexual encounters because of their discomfort and wear
bras and clothing that minimize their breast size.
Studies of the psychological issues in breast reduc-
tion surgery are not numerous. Goin et al H showed
preoperative evidence of depression in a small sample;
Hollyman et al48 also found a higher incidence of
depression and anxiety compared with control sub-
jects, also in a small sample. Sarwer et al49 reported
that breast reduction patients experience greater dis-
satisfaction with their overall body image, worry and
embarrassment about their breasts in public and social
situations, and avoidance of physical activity.
Postoperatively, this is a satisfied group of patients.
They quickly integrate their smaller breasts into their
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77
body image. They are often more self-confident and
feel more feminine and sexually attractive. On occa-
sion, patients are more satisfied with their surgical
results than are their surgeons. Despite visible aesthetic
problems postoperatively with scarring and the fre-
quency of some loss of nipple-areola sensibility,
patients are generally satisfied.
Jones and Bain50 reviewed the literature of outcome
studies that demonstrated a high degree of satisfac-
tion of patients (78% to 95% being very or moder-
ately satisfied) and improvement in body image and
psychological well-being. Chadbourne et al51 per-
formed a review of the literature and meta-analysis of
published studies and found that although quality of
life parameters of physical function were statistically
improved, measures of psychological function were not.
Other studies did document psychological and emo-
tional benefits after reduction mammaplasty. 52
However, one study by Guthrie et al56 described this
population of patients, compared with a control group
of large-breasted women not seeking reduction surgery,
as having greater psychological and physical difficul-
ties, with higher levels of anxiety and depression as
well as poorer self-esteem, body image, and interper-
sonal functioning.
Patients may occasionally experience a sense of loss
and require readjustment to their new body. There
may be some social and sexual disturbances now that
they no longer feel the need to isolate themselves
because of their self-consciousness. They may need
encouragement to become more socially active and
less withdrawn.
Trauma: Acquired Defects
HAND TRANSPLANTATION
Accompanied by much media interest and public
debate, the first hand transplants were reported in 1998
and 1999. It was clear that the transplantation of cadaver
hands to the forearm amputation stumps of living
patients was technically possible. What was less clear
was the appropriateness of consigning the recipients
to a lifetime of immunosuppressive therapy for a
non-life-threatening condition. 57
In the discussions that followed, it was mentioned
frequently that for the patient who has lost a hand,
transplantation offers the potential psychological
benefit of restoring body image as well as improving
function. This consideration was used to defend the
level of risk accompanying transplantation, but it
has not yet been established. Of the original four
recipients of a hand transplant, three are reported
to be pleased with the results at 2 years and to have
incorporated the transplanted hand into their
self-image. The fourth patient was enthusiastic
initially, but the hand was later amputated at his
request. 58
78 I • GENERAL PRINCIPLES
Whereas the psychological status of the patients
themselves remains to be studied over time, informa-
tion has come forward from the discourse of these cases
about the psychology of decision-making. 59 Those,
physicians and patients alike, struggling with the advis-
ability of performing hand transplantation andlooking
at the risk-to-benefit ratio can come to very different
conclusions. Work from the field of decision-making
analysis has shown that physicians and patients proceed
from different frames of reference and prioritize
values differently in making medical decisions. Patients
tend to show a large preference for a risky alternative
that has a chance of erasing a loss and of return to the
previous status quo, and they tend to think of imme-
diate rather than long-term risks (e.g., immunosup-
pression). 60 These and other irrational factors, such as
denial of the possibility that they will have a severe
complication, need to be made explicit in the deci-
sion-making process, particularly with a procedure as
uncertain as hand transplantation.
BURNS
Burn patients must initially face the issues concern-
ing survival, the pain caused by the burn itself, and the
need to often undergo multiple procedures (e.g., skin
grafts,dressing changes).They are then faced with issues
concerning scarring caused by the burn and the
deforming nature of these scars. The anatomic loca-
tion of the scarring is relevant because those scars that
are more obvious to others (e.g., on the face) lead to
discomfort in their presence and increased self-
consciousness. Often, plastic surgical procedures are
performed in stages during a protracted period, which
delays the return to preinjury functioning. The chronic-
ity of treatment can pose psychological difficulties, as
is true with any chronic illness.
Psychological difficulties seen in the burn popula-
tion include depression, helplessness, frustration,
hopelessness, diminished self-image, self-conscious-
ness, social isolation, and despair. There is a greater
likelihood that burn patients will discontinue treat-
ment and lose contact with their physicians and other
caretakers.61 This avoidance may be reflective of anxiety
with repeated surgeries, permanent scarring, and loss
of hope that their disfigured appearance can ever be
changed.
In general, a multidisciplinary approach is the most
helpful in the burn population. The team should
include the surgeon, primary care physician, mental
health professional, nursing staff, physical therapist,
occupational therapist, and support group therapy.
Family members may also benefit from supportive
therapy, individually or in a group. Close attention
should be paid to the patient's mental state, mood,
and degree of demoralization. Medical personnel
sometimes make the mistake of dismissing a clinical
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Dr.Mustafa D.
depression. Pain management is extremely important,
and mood stabilizers and antidepressants may also be
helpful. Staff should try to look past the disfigured
appearance to see the person inside. Having a normal
conversation with the patient about daily life, sports,
or current events will be reassuring as it indicates
the person is still intact internally and can be inter-
esting to others and accepted by them. Staff can
empathize with the patient's self-consciousness, but
it is important to emphasize the person's strengths
and assets and help him or her return as soon as pos-
sible to activities that previously gave pleasure and
self-esteem.
Cancer and Reconstruction
BREAST CANCER: LUMPECTOMY,
MASTECTOMY, AND RECONSTRUCTION
The treatment of breast cancer has undergone a
remarkable evolution during the past 20 years, both
from a medical standpoint and from the psychologi-
cal perspective. Cancer treatment has been revolu-
tionized by new chemotherapeutic agents and surgery
sparing the breast and nipple, which have enhanced
the psychological well-being of women with breast
cancer. The survival rates have also improved with early
detection and improved treatment.
A woman's reaction to loss of her breast is related
to how she felt about her breasts and their role in
her sexuality and self-image before the diagnosis of
cancer. Common reactions after mastectomy are
depression,62,63 diminished self-esteem,64'66 feelings
of being "less of a woman," and fears related to
recurrence.67,68
When postmastectomy breast reconstruction
became accepted in the 1970s, it was hypothesized that
a woman would have to live for a time without a breast
to be happy with an imperfect, reconstructed breast.
However, various researchers showed that immediate
reconstruction at the time of mastectomy offers the
patient with breast cancer a higher quality of life after
mastectomy67,69 and better integration of the "new"
breast into the body image.70"72 In addition, regardless
of timing, breast reconstruction offers the opportu-
nity to minimize feelings of disfigurement, deformity,
mutilation, sexual unattractiveness, and loss of
femininity.
Reconstruction does not interfere with the griev-
ing process initiated by mastectomy. Women are able
to properly mourn the loss of the breast while feeling
"whole,""symmetric," and feminine after reconstruc-
tion. They still have to face the fact that they have cancer
and need appropriate follow-up treatment and care.
Reconstruction sometimes gives women who had been
dissatisfied previously with their breast size the oppor-
tunity to reduce or augment their breasts. Nipple-areola
reconstruction completes the cosmetic result.
image...
5 •
Many women with breast cancer choose lumpec-
tomy, a breast-sparing surgery, rather than mastec-
tomy for aesthetic and psychological reasons. Not all
lumpectomy patients are happy with their surgical
results, related to the quantity and location of the tissue
excised. The breast sometimes looks misshapen,
causing distress for the patient and interfering with
her comfort with her sexuality and being unclothed
with her sexual partner or in locker rooms. Even though
the defect may not be readily apparent to others, some
patients will later request reconstructive breast surgery.
They wish to restore the symmetry and shape of their
breasts to minimize feelings of disfigurement and to
benefit their self-image and psychological and sexual
functioning.
HEAD AND NECK CANCER
Head and neck cancer precipitates a loss of function
and loss of form of the face and oral cavity that can be
devastating to both the patient and the family. Facial
expression (controlled by the facial muscles), speech,
and ability to eat and drink in a socially acceptable
fashion with one's friends and family are of vital impor-
tance.73 Any disfigurement of the face may lead to social,
interpersonal, and occupational handicaps.
In the preoperative period, patients must prepare
themselves for the likely disfigurement and dramatic
change in their face. In the early postoperative period,
the patient experiences a great deal of anxiety. This
results from a difficulty with communication and
speech, especially if there is a tracheostomy or naso-
gastric tube in place, and the need for frequent lengthy
dressing periods for wound and flap care.74 Many
patients have a severe reactive depression during this
time. They often feel fearful, abandoned, and intensely
alone because of their inability to speak or difficulty
with communication.
Pain management may be necessary. The combi-
nation of analgesic agents and antidepressant med-
ication is often effective. Because overuse of alcohol
may be a factor in this population of patients,
the surgeon should be alert for signs of alcohol with-
drawal. Later in the recovery period, the patient next
has to grapple with the change in appearance and body
image. Simultaneously, the patient is also becoming
aware of difficulties with swallowing, speech, and
dribbling.
In addition to functional changes, there are reac-
tivity and adjustment to the diagnosis as well as con-
sideration of the prognosis of cancer, which may
include the potential need for adjuvant cancer treat-
ment. All of these experiences may engender chronic
depression, social withdrawal, loss of self-esteem,
anxiety, and feelings of loss and grief in the patient.
Family relationships may be disrupted, leading to
further distress. Patients may not be able to return to
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PSYCHOLOGICAL ASPECTS OF PLASTIC SURGERY 79
their previous occupation, and this may be devastat-
ing, especially if their career was an important factor
in their self-esteem. When they are out in public,
strangers may stare at their disfigured face, fostering
hurt and humiliation. Discharge planning should
include the initiation of important treatment services,
such as speech, physical, and occupational therapy, as
well as education concerning wound care and psy-
chological support for the patient and caregivers.
PLASTIC SURGERY
IN CHILDHOOD
Acquired and Congenital Defects:
General Considerations
An overt physical defect does not have a direct rela-
tionship to the degree of a person's response to a hand-
icap.75 Some patients cope well with a major deformity,
whereas others decompensate psychologically when
they are faced with a minor scar. Castelnuevo-Tedesco76
remarked, "when an individual acquires a defect in
contrast to someone who is born with one, he always
feels a sense of loss; loss of hope, loss of his future,
loss of normality and the rich experiences that go
with it." However, when a defect is perinatal or con-
genital, the individual grows up maintaining lower
expectations about what he or she will expect in life,
and the sense of loss is hardly present as a psycho-
logical issue.77 Children born with congenital defects
do have an awareness of having had an experience that
is out of the ordinary, different from that of others.
Craniofacial Anomalies
Anecdotal reports have led to the impression that chil-
dren with craniofacial deformities are either shunned
or overprotected by family and others. Clifford78
described negative initial maternal reactions after the
birth of a deformed child. However, good clinical
studies have not borne out initial impressions and anec-
dotal reports in the literature.
Pertschuk and Whitaker 79 studied 51 patients
several months before reconstructive surgery for cra-
niofacial deformities. They reported that on the whole,
the younger children were remarkably well adjusted.
They were often outgoing and had regular friends.
Their appearance did not, according to the children,
pose great difficulties in their daily lives. Although they
did report teasing at school, they seemed to manage
adequately in the school setting. These children were
being referred for surgery by their parents, who were
concerned about future problems with vocational pur-
suits and teenage socialization. The most frequently
reported problems in this younger group were in the
behavioral realm. A small minority were socially iso-
lated, inhibited, or aggressive. The authors suggest that
whatever psychological trauma these children may
80 I • GENERAL PRINCIPLES
experience from the deformity, it is manifested in
behavioral rather than in personality problems. In con-
trast, older patients with craniofacial deformities do
not cope well with their deformities. There are prob-
lems with dating and sexual relationships) although
there does not seem to be substantial difficulty with
same-gender friendships. Self-esteem and self-image
are adversely affected in this older group, and they arc
self-conscious about their defect.
As a result, the younger population seems to func-
tion better than the older one, presumably because they
use the defense mechanism of denial to cope. It also
seems that facing dating and sexual situations produces
anxiety, fear, self-consciousness, and self-doubt in the
older child.
These data have bearing on the question of timing
of reconstructive surgery in this population of patients.
The results support the contention that there are psy-
chological advantages to performing surgery earlier
in life, definitely before the onset of adolescence.
Pertschuk and Whitaker's postoperative results show
that a younger group has better behavior, reduced
anxiety, and perhaps improved socialization, even
allowing for their better psychosocial adjustment pre-
operatively.79 In both younger and older groups, the
majority of patients and parents express satisfaction
with the surgical results. The satisfied patients expe-
rience a positive impact on their behavior, personal-
ity, and self-esteem. In disappointed patients and
parents, there is little psychosocial change noted post-
operatively. Their work generally confirms Macgre-
gor's finding that patients with more major deformities
are more satisfied with whatever surgical changes can
be effected, even if they are slight.80
Often in craniofacial reconstructive surgery, the pro-
cedure can only hope to transform a grossly unattractive
person into a milder, less conspicuously unattractive
person. Patients need to be carefully counseled about
what to expect postoperatively to minimize disap-
pointment. It may sometimes be better to under-
estimate potential gain to avoid arousing unrealistic
expectations; when the gains are more than expected,
the patient and family are likely to be happier with the
surgical results.
The best measure of the success of craniofacial
surgery is the psychosocial adjustment of the patients
after surgery. Are they less fearful in social or dating
situations? Do they feel free to pursue their occupa-
tional goals and leisure activities? Do they take pleas-
ure in their friendships and relationships? Are they able
to participate in daily life without significant self-
consciousness or inhibition?
Aesthetic Surgery in Teenagers
Body image development occurs in stages, and puberty
stands out as a particularly sensitive time as the teenager
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undergoes major changes in his or her physical appear-
ance and does this at a time of heightened vulnera-
bility to the opinion of others. Physical change occurs
in almost every area of the body. The mouth widens,
the nose becomes prominent, and the chin is the last
to increase in size. Body hair appears and darkens,
breasts develop, sweat glands become active, voice
quality changes, and complexion and acne problems
arise.
As these physical changes are occurring, the ado-
lescent's cognitive abilities expand. Thinking becomes
more abstract, multidimensional, complex, and subtle.
Adolescents become more self-aware and develop the
capacity for self-reflection and reflection on the
thoughts of others, using others as an audience to val-
idate and evaluate themselves. They depend heavily
on what others think, are vulnerable to peers for
validation, and respond with complex emotional
reactions. 2
In this context, plastic surgery to correct a truly
unattractive feature can be remarkably successful in
changing the teenager's body image in a positive way.
By making what the adolescent and his or her peers
see as an improvement in appearance, self-perception
is altered, and the youngster grows in comfort and
confidence and feels a greater sense of well-being.
Plastic surgery is remarkably free of conflict in this
population, and teenagers undergo a rapid reorgani-
zation of self-image after plastic surgery with subse-
quent positive changes in behavior and interpersonal
interactions.
In 2002, teenagers represented about 3% of the total
number of patients having plastic surgical procedures
in the United States (Table 5-1).81 For these patients,
plastic surgery is taking place when they have the great-
est concerns about becoming attractive, competent,
and acceptable to other people. Compared with other
age groups, plastic surgery in teenagers produces very
TABLE 5-1 • PLASTIC SURGERY PROCEDURES
ON PATIENTS 18 YEARS AND
YOUNGER
No. of Patients 18
Procedure Name* Years and Younger
Rhinoplasty 40,696
Otoplasty 3,919 (age 13-18 only)
Suction-assisted lipectomy 3,002
Male breast reduction 2.008
(gynecomastia)
Breast augmentation 3,095
Mastopexy 497
Chin augmentation 1,316
"Numbers for reduction mammaplasty were not included in the statistics.
Data from NationalClcaringhouse of Plastic SurgeryStatistics, 2003 Report.
American Society of Plastic Surgeons. Available at: www.plasticsurgery.org
 image...
5 •
little anxiety and emotional conflict, and this is dif-
ferent from their response to other invasive procedures,
such as intra-abdominal surgery or repair of facial lac-
erations. Studies investigating this apparent lack of con-
flict have looked at teenage rhinoplasty, which is by
far the most frequently performed operation in this
group. It has been suggested that this event, when it
is affirmed by parental acceptance, represents an area
of agreement and common thinking between parent
and child at a time when almost every other issue has
become a source of conflict. Some of the affirmation
may flow from the parent's own narcissistic wish for
a more beautiful child or from parental guilt; the
teenager may be relieved that the narcissistic aspira-
tions are shared. For the youngster, a plastic surgery
operation is a gift and requires no effort at a time when
he or she is being challenged to achieve in academic,
athletic, and social realms. There may also be under-
tones of magical transformation, as in the childhood
stories in which the ugly duckling becomes a beauti-
ful swan rising above its critical peers—again through
no effort on the part of the duckling.9'82
Teenage patients seem to undergo rapid reorgani-
zation of their self-image after rhinoplasty. A previ-
ous overawareness of the body part disappears; they
tend to forget what they used to look like, and the fact
of the surgery itself is recalled only casually. The
patients harbor little sense of invasion and in general
tend to be more pleased and satisfied than are older
patients having the same operation. Feelings of infe-
riority may be replaced with self-confidence, and
anxiety and self-consciousness in social situations
tend to diminish. Gifford82 comments on the "major
changes in behavior, body awareness, or identity" after
rhinoplasty.
•PATIENT HISTORY
A 16-year-old boy felt that his large beaked nose
made him look ugly, mean, humorless, and
unathletic. His family reassured him that he
looked fine, but he continued to feel insecure and
self-conscious with his classmates and considered
himself unattractive to girls. After much discus-
sion, he underwent a rhinoplasty in which the
dorsum was lowered and the hump eliminated.
He was happy with the result, went to college, and
did well. Ten years later, he was studied with in-
depth psychiatric interviews and expressed pleas-
ure that he had gone forward with the surgery
and given himself an "edge." He recognized the
surgery as positive and useful and said it freed
him from a preoccupation with his appearance,
which let him then focus on working on other
issues in his life.
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PSYCHOLOGICAL ASPECTS OF PLASTIC SURGERY 81
For this patient, as for most plastic surgery patients,
the surgery was successful, not because the plastic
surgeon did a nice job on the nose but because the
surgery was done on a patient who then felt more pos-
itive about himself. The surgery treated a body image
discomfort that lay at the heart of the young man's
sense of identity.83
Not every teenager who seeks surgery is well suited
for an operation. Emotional maturity is required to
understand the limitations of plastic surgery and the
complications that can occur. In addition, the teenager
needs to have reached certain growth milestones or
physical maturity, depending on the surgical proce-
dure. The American Society of Plastic Surgeons devel-
oped a position statement about surgery in teenagers,
and this cites important characteristics of the teenage
patient.84
• The adolescent must initiate and reiterate
his or her own desire for the plastic surgery
improvement.
• There must be realistic goals and appreciation of
the benefits and risks.
• There must be sufficient maturity to tolerate the
discomfort and temporary disfigurement of a
surgical procedure.
The position statement cautions against plastic surgery
in teens who are prone to mood swings or erratic
behavior, who are abusing drugs or alcohol, or who
are being treated for clinical depression or other mental
disease.
SELECTION OF PATIENTS:
DANGER AND PITFALLS
General Risk Factors
It is generally known that patients with major psy-
chiatric illnesses or with vague, unrealistic expecta-
tions of plastic surgical procedures are more likely to
be dissatisfied with their surgical results. However, there
are no definable criteria by which to distinguish the
patients who will be satisfied with their postoperative
results and those who will be dissatisfied. Careful assess-
ment during initial evaluation should be conducted
to ascertain the patient's viability as a surgical candi-
date (Table 5-2).
There are populations of patients, such as those
with body dysmorphic disorder, who, after objectively
successful cosmetic surgery, may be dissatisfied, bring
litigation against the surgeon, commit suicide, or even
present a danger to the surgeon with homicidal ideas
and impulses. Plastic surgeons and psychiatrists have
the unhappy distinction of being the victims of homi-
cide and assault more often than physicians in other
specialties.
82 I • GENERAL PRINCIPLES

TABLE 5-2 • ASSESSMENT OF THE PLASTIC SURGERY PATIENT

Important questions to ask the patient and information for the surgeon to ascertain during a plastic surgical
evaluation include the following:

The patient's ability to be realistic about expectations regarding the surgical results: Are the expectations
unrealistic? Can education make them more realistic?
The objective assessment of the identified defect and a realistic appraisal of the deformity by the surgeon: Is the
patient's complaint out of proportion to the nature of the defect ("minimal" defect)?
History of prior cosmetic procedures and degree of satisfaction: How does the patient feel about previous
surgeons? Is the patient a "doctor shopper"?
If the patient is satisfied or dissatisfied, did the focus shift to a new body part?
Is the patient seeking a "perfect" result? Will the patient be able to tolerate a scar?
Indication of an ulterior motive, for example, expecting that the surgery will result in a job promotion or magical
improvement of a troubled marriage: Does the patient place the success of the surgery on the realization of that
motive?
History of whether the patient has prior psychiatric illness or treatment: Is there a history of depression, anxiety,
substance abuse, obsessive-compulsive disorder, social phobia, or impulse control disorders?
Is there a history of litigation?
The degree of functional impairment: What is the patient's occupational, social, and interpersonal functioning and
marital status?
Is there a history of hair or skin pulling/picking? How much time is spent daily thinking about the "defective" body
part or mirror gazing? How much time is spent daily on grooming?
History of eating disorder symptoms (anorexia, bulimia, binging and vomiting, laxative abuse): Does the patient
have a body image disturbance (such as thinking he or she is too fat when objectively not overweight)?
Is there any avoidance behavior? Does the patient avoid situations that would expose or exacerbate the perceived
defect? Is the patient housebound?
Is there a history of suicidal behavior or self-mutilation?
Is the patient being pressured by others to have the requested surgery?
Do significant others (spouse, family, close friends) think that the requested surgery is unwarranted or do they
disagree with the decision?
Is there any evidence of post-traumatic stress syndrome (especially in the reconstructive population)? Did the
patient experience a profound physical and psychological trauma, such as a life-threatening injury (e.g., burn)?

Psychiatric Syndromes of Concern been reports of depressive symptoms, if not full-blown

to Plastic Surgeons
DEPRESSION
Why is it important to obtain a history of mood dis-
orders and to determine whether the patient is
depressed or has suffered from depression? Studies in
psychoneuroimmunology have shed light on the neg-
ative effects of depression on the course of healing and
postoperative recovery and on its impact on morbid-
ity and mortality. Natural killer cell activity, helper
(CD4) and suppressor (CD8) cell activity, numbers of
T lymphocytes, and lymphocyte mitogen response have
been shown to be negatively affected by depression.85
Similarly, these changes are found in patients with a
significant life stress, such as work-related stress,
divorce, bereavement, or caring for a patient with
Alzheimer disease.85 As a consequence, the plastic
surgeon should attempt to avoid performing an elec-
tive procedure on a depressed individual.
The prevalence of all depressive disorders is between
9% and 20% of the U.S. population (Table 5-3). The
incidence of major depression is higher in medically
ill patients and in separated or divorced individuals
compared with the general population.86 Major depres-
sion is present in up to 18% of preadolescents and
approximately 5% of adolescents, although there have
depression, in up to one third of adolescents in this
country.87 Depression is associated with an increased
use of medical services.88
As many as 50% of depressions may be "masked,"
that is, not obvious or easily recognized.21 A masked
depression is suspected if the patient is having a higher
level of marital or family conflicts, increased alcohol
use, problems with job performance or excessive
absenteeism, truancy from school or poor school per-
formance, social withdrawal, or a seeming lack of moti-
vation. Increased irritability or exaggeration of the
usual personality traits may sometimes be a clue to
this possibility.
If the surgeon suspects a depressive disorder, he or
she should refer the patient for a psychiatric consul-
tation, explaining to the patient how healing and recov-
ery could be adversely affected by the presence of
depression. The patient is advised that after appro-
priate treatment and recovery from the depression,
surgery can be reconsidered.
GENERALIZED ANXIETY AND
PANIC DISORDERS
Anxiety disorders are the most common psychiatric
illnesses (Table 5-4). When assessing a patient, the

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Tewttf^eicrw image...

5 • PSYCHOLOGICAL ASPECTS OF PLASTIC SURGERY 83

TABLE 5-3 • MAJOR DEPRESSIVE EPISODE: DSM-IV DIAGNOSTIC CRITERIA

A. Five (or more) of the following symptoms have been present during the same 2-week period and represent a
change from previous functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of
interest or pleasure.
Note: Do not include symptoms that are clearly due to a general medical condition, or mood-incongruent
delusions or hallucinations.
(1) depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad or
empty) or observation made by others (e.g., appears tearful). Note: In children and adolescents, can be
irritable mood.
(2) markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as
indicated by either subjective account or observation made by others)
(3) significant weight loss when not dieting or weight gain (e.g., a change of more than 5% of body weight in a
month), or decrease or increase in appetite nearly every day. Note: In children, consider failure to make
expected weight gains.
(4) insomnia or hypersomnia nearly every day
(5) psychomotor agitation or retardation nearly every day (observable by others, not merely subjective feelings
of restlessness or being slowed down)
(6) fatigue or loss of energy nearly every day
(7) feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not
merely self-reproach or guilt about being sick)
(8) diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or
as observed by others)
(9) recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a
suicide attempt or a specific plan for committing suicide
B. The symptoms do not meet criteria for a mixed episode.
C. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas
of functioning.
D. The symptoms are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication)
or a general medical condition (e.g., hypothyroidism).
E. The symptoms are not better accounted for by bereavement, i.e., after the loss of a loved one, the symptoms
persist for longer than 2 months or are characterized by marked functional impairment, morbid preoccupation
with worthlessness, suicidal ideation, psychotic symptoms, or psychomotor retardation.

Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Copyright 2000. American Psychiatric Association.

TABLE 5-4 • GENERALIZED ANXIETY DISORDER: DSM-IV DIAGNOSTIC CRITERIA

A. Excessive anxiety and worry (apprehensive expectation), occurring more days than not for at least 6 months,
about a number of events or activities (such as work or school performance).
B. The person finds it difficult to control the worry.
C. The anxiety and worry are associated with three (or more) of the following six symptoms (with at least some
symptoms present for more days than not for the past 6 months). Note: Only one item is required in children.
(1) restlessness or feeling keyed up or on edge
(2) being easily fatigued
(3) difficulty concentrating or mind going blank
(4) irritability
(5) muscle tension
(6) sleep disturbance (difficulty falling or staying asleep, or restless unsatisfying sleep)
D. The focus of the anxiety and worry is not confined to features of an Axis I disorder, e.g., the anxiety or worry is
not about having a panic attack (as in panic disorder), being embarrassed in public (as in social phobia), being
contaminated (as in obsessive-compulsive disorder), being away from home or close relatives (as in separation
anxiety disorder), gaining weight (as in anorexia nervosa), having multiple physical complaints (as in somatization
disorder), or having a serious illness (as in hypochondriasis), and the anxiety and worry do not occur exclusively
during post-traumatic stress disorder.
E. The anxiety, worry, or physical symptoms cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
F. The disturbance is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication)
or a general medical condition (e.g., hyperthyroidism) and does not occur exclusively during a mood disorder, a
psychotic disorder, or a pervasive developmental disorder.

Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Copyright 2000. American Psychiatric Association.

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84 I • GENERAL PRINCIPLES

surgeon must try to distinguish between the typical EATING DISORDERS

anxieties that patients experience in anticipating
surgery and an anxiety disorder. Typical anxieties are
worries about the anesthesia, concerns about the degree
of pain, and fears regarding loss of control. 89
Anxiety reaches pathologic proportions when there
is excessive worrying that the patient finds difficult to
control. The worrying may be accompanied by easy
fatigability, difficulty concentrating, irritability, sleep
disturbance, restlessness, and generalized muscle
tension. 21 The anxiety or associated physical symp-
toms may be interfering with occupational, social, or
interpersonal functioning.
Panic attacks, a form of anxiety disorder, are
described as discrete periods of intense fear or dis-
comfort, developing suddenly and peaking in a 10-
minute period. Patients will report any or all of the
following physical sensations: palpitations, sweating,
shaking, sensation of shortness of breath, chest pain
or discomfort, nausea or abdominal distress, light-
headedness, derealization (feeling unreal) or deper-
sonalization (feeling outside of one's body), fear of
losing control or dying, numbness and tingling, and
chills or hot flushes.
If the surgeon identifies anxiety symptoms, it is
important to address them and treat them in advance
of the surgery. The typical anxieties previously dis-
cussed can usually be allayed with explanation and
reassurance. When an anxiety disorder exists, psychi-
atric consultation should be obtained, and the psy-
chiatrist can partner with the plastic surgeon in
making a decision about the timing of surgery
and observe the patient postoperatively if surgery is
undertaken.
Eating disorders are illnesses characterized by distur-
bances in eating behavior and perceptions about food
and eating. Anorexia nervosa is an illness character-
ized by refusal to maintain a minimally normal body
weight and a significant disturbance in an individual's
perception of the body's shape or size (Table 5-5).2l
These patients usually accomplish weight loss through
reduction in total food intake but may also purge (self-
induced vomiting or the misuse of laxatives or diuret-
ics) or engage in increased or excessive exercise. Some
anorexic patients will have the physical signs and symp-
toms of semistarvation or starvation, including amen-
orrhea, constipation, abdominal pain, cold intolerance,
lethargy or excess energy, hypotension, hypothermia,
bradycardia, and skin dryness. Some will develop
lanugo, a fine downy body hair on the trunk. Bulimia
nervosa is characterized by binge eating and inap-
propriate compensatory methods to prevent weight
gain (Table 5-6).21 The hinging usually occurs in secrecy
and continues until the individual is physically uncom-
fortable. Individuals with bulimia nervosa may employ
self-induced vomiting, laxatives, and diuretics to com-
pensate for the binging. Patients with bulimia nervosa
are typically in the normal weight range, although they
may be slightly underweight or overweight. In both
syndromes, there may also be mood disorders. In those
who induce vomiting, dental enamel may be eroded.
Electrolyte imbalances and hematologic abnormali-
ties can also be found.
The overwhelming majority of patients with eating
disorders are female, and when they seek plastic
surgery, they usually inquire about breast surgery or

TABLE 5-5 • ANOREXIA NERVOSA: DSM-IV DIAGNOSTIC CRITERIA

A. Refusal to maintain body weight at or above a minimally normal weight for age and height (e.g., weight loss
leading to maintenance of body weight less than 85% of that expected: or failure to make expected weight gain
during period of growth, leading to body weight less than 85% of that expected).
B. Intense fear of gaining weight or becoming fat, even though underweight.
C. Disturbance in the way in which one's body weight or shape is experienced, undue influence of body weight or
shape on self-evaluation, or denial of the seriousness of the current low body weight.
D. In postmenarchal females, amenorrhea, i.e., the absence of at least three consecutive menstrual cycles. (A
woman is considered to have amenorrhea if her periods occur only following hormone, e.g., estrogen,
administration.)

Specify type:

Restricting Type: during the current episode of anorexia nervosa, the person has not regularly engaged in binge-
eating or purging behavior (i.e., self-induced vomiting or the misuse of laxatives, diuretics, or enemas).
Binge-Eating/Purging Type: during the current episode of anorexia nervosa, the person has regularly engaged
in binge-eating or purging behavior (i.e., self-induced vomiting or the misuse of laxatives, diuretics, or
enemas).

Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Copyright 2000. American Psychiatric Association.

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VtJWt^aelcrtSf image...

5 • PSYCHOLOGICAL ASPECTS OF PLASTIC SURGERY 85

TABLE 5-6 • BULIMIA NERVOSA: DSM-IV DIAGNOSTIC CRITERIA

A. Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following:
(1) eating, in a discrete period of time (e.g.. within any 2-hour period), an amount of food that is definitely larger
than most people would eat during a similar period of time and under similar circumstances
(2) a sense of lack of control over eating during the episode (e.g., a feeling that one cannot stop eating or
control what or how much one is eating)
B. Recurrent inappropriate compensatory behavior in order to prevent weight gain, such as self-induced vomiting;
misuse of laxatives, diuretics, enemas, or other medications; fasting; or excessive exercise.
C. The binge eating and inappropriate compensatory behaviors both occur, on average, at least twice a week for 3
months.
D. Self-evaluation is unduly influenced by body shape and weight.
E. The disturbance does not occur exclusively during episodes of anorexia nervosa.

Specify type:

Purging Type: during the current episode of bulimia nervosa, the person has regularly engaged in self-induced
vomiting or the misuse of laxatives, diuretics, or enemas.
Nonpurging Type: during the current episode of bulimia nervosa, the person has used other inappropriate
compensatory behaviors, such as fasting or excessive exercise, but has not regularly engaged in self-induced
vomiting or the misuse of laxatives, diuretics, or enemas.

Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Copyright 2000. American Psychiatric Association.

suction-assisted lipectomy. However, by virtue of BODY DYSMORPHIC DISORDER:

their body image disturbance, patients with eating
disorders usually do not benefit from plastic sur-
gery. The surgery can never match the body image
they fantasize will be the cosmetic result. For the
sake of these patients, it is appropriate to defer aes-
thetic surgery and refer them to a psychiatric
consultant.
SUBSTANCE ABUSE
Information about substance abuse is not elicited rou-
tinely by physicians, especially when there is no
explicit evidence to suggest a problem. In addition,
there are varying opinions about what constitutes
"abuse." The three-martini lunch may be alarming to
some physicians but not to others.
There are several good reasons why the plastic
surgeon should make an inquiry about the patient's
use of drugs and alcohol. Most important, the patient
could develop signs of alcohol or drug withdrawal in
the postoperative period; if the physician does not have
the information or index of suspicion to consider with-
drawal, diagnosis and treatment would be delayed,
which carries its own morbidity and mortality. Second,
substances like alcohol can have a negative impact on
the recovery and rehabilitation process.90,91 Third, sub-
stance dependence, especially drugs such as opiates,
has a direct impact on pain management postopera-
tively. Last, the dependency may be a symptom of an
underlying psychiatric condition, such as depression
or anxiety.
"IMAGINED UGLINESS" 92
Body dysmorphic disorder (BDD) is a psychiatric dis-
order in the spectrum of obsessive-compulsive disor-
ders (Table 5-7). Afflicted individuals perceive
themselves to be ugly, despite having a normal appear-
ance, and present to plastic surgeons for aesthetic
surgery without perceiving the psychological under-
pinnings of their concerns. They perform repetitive,
compulsive behaviors, such as frequent mirror check-
ing, excessive grooming, and skin picking.93 Patients
with BDD often have little or no insight into their illness,
and some are frankly delusional, convinced that the
imagined defect is real.94 The imagined body defects
are focused mostly on the face but may also be focused
on the hair, hands, feet, and sexual body parts.
TABLE 5-7 • BODY DYSMORPHIC DISORDER:
DSM-IV DIAGNOSTIC CRITERIA
1. A preoccupation with a slight or imagined defect in
appearance. If a slight physical anomaly is present,
the person's concern is markedly excessive.
2. The preoccupation causes clinically significant
distress or impairment in social, occupational, or
other important areas of functioning.
3. The preoccupation is not better accounted for by
another mental disorder (e.g., dissatisfaction with
body shape or size characterizing anorexia nervosa).
Reprinted with permission from the Diagnostic and Statistical Manual of
Mental Disorders, Copyright 2000. American Psychiatric Association.

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Dr.Mustafa D.
86 I • GENERAL PRINCIPLES
The preoccupation, anxiety, and self-consciousness
connected to BDD may lead to interference with daily
functioning (occupational,social, and interpersonal),
and a significant percentage of patients with BDD may
become housebound. 95 These patients may have exces-
sive preoccupation with their imagined physical defects
to the level of delusional or psychotic thinking; some
of these patients may have suicidal ideation or may
have attempted suicide in the past.96
There is strong evidence that patients with BDD do
not benefit from aesthetic surgery. Phillips and Diaz97
reported in their study that 8 3 % of procedures per-
formed on patients with BDD led to an exacerbation
or no change in BDD symptoms. A study by Veale98
revealed that 76% of patients with BDD who under-
went cosmetic surgery reported dissatisfaction with
the postoperative result.
With repeated cosmeticsurgeries, patients with BDD
may actually become worse, often developing a rather
grotesque surgically altered appearance. This fosters
the vicious circle of seeking more surgery. With esti-
mates that between 50% and 88% of patients with BDD
have undergone cosmetic procedures,99 it is enormously
important to detect signs of BDD. Whether a prospec-
tive plastic surgery patient has BDD is not always clear.
Judgments about beauty and ugliness and whether a
defect should be categorized as "slight" are inherently
subjective. Only if the preoccupation with the slight
or imagined defect is excessive compared with the objec-
tive appearance is the diagnosis of BDD easily made.
There has been some work attempting to differ-
entiate the patient with BDD from other cosmetic
surgery patients. A study by Aronowitz et al100 looked
in a controlled fashion at the differences between
patients with BDD and other plastic surgery patients.
They found patients with BDD more likely to report
preoccupation for longer than 1 hour daily; greater
associated anxiety, depression, and obsession; greater
disagreement with others regarding the defect;
greater associated functional impairment; and greater
fixed belief in the reality of the defect. The patients
tended to seek multiple consultations with plastic sur-
geons and dermatologists until they found one to
provide the treatment they requested.
As well as considering their defects more serious,
patients with BDD worry about a larger number of
body defects than do other cosmetic surgery patients
and feel less satisfaction with past surgeries. After cos-
metic procedures, patients with BDD may shift pre-
occupation to other body parts or aspects of their
appearance or even increase their preoperative level
of dissatisfaction, since it may not match their ideal-
ized image of how they think their revised body part
should look. Because there is a gross distortion of the
body image to begin with, a cosmetic change is
unlikely to correct this distortion. Even when there is
an objectively satisfactory outcome, the patient with
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Dr.Mustafa D.
BDD may introduce a lawsuit or become violent toward
the surgeon or harmful to himself or herself. Some
patients with BDD may self-mutilate to try to alter their
appearance.
If the surgeon evaluating a patient suspects that he
or she may have BDD, psychiatric consultation should
be sought and strongly encouraged. The surgeon may
confront great resistance in suggesting psychiatric
consultation; the surgeon should not perform the
requested surgery on the patient.
Psychiatric treatment is available for the patient with
BDD. Psychotherapy, especially cognitive-behavioral
techniques,101 may be helpful, and it is often used in
conjunction with psychopharmacotherapy. These
techniques attempt to restructure distorted thinking.
Clomipramine, a potent serotonin reuptake inhibitor,
has been shown to be effective and superior to
desipramine, a selective norepinephrine reuptake
inhibitor, in ameliorating the symptoms of BDD.102 In
addition, other serotonin reuptake inhibitors like flu-
oxetine, citalopram, fluvoxamine, sertraline, and parox-
etine may be helpful, but they may need to be
administered at higher doses and for longer duration
than is typical in the treatment of depression.
BDD in men is an underrecognized disorder.103,104
A study by Garner105 found that the percentage of men
who are dissatisfied with their overall appearance is
43%, a number that has tripled during the past 25
years, and that men appear to be similar to women in
their levels of dissatisfaction with how they look. Like-
wise, BDD appears to affect men as well as women.
Mayville106 found that 2.8% of females and 1.7% of
males in a community sample of 566 adolescents ful-
filled the criteria for BDD. Some investigators have
found a higher proportion of men than of women
with BDD, and the largest published sample of patients
with BDD revealed 5 1 % to be male.97
Muscle dysmorphia is a newly described disorder
characterized by a preoccupation with the idea that
one's body is not sufficiently lean and muscular.107 It
involves a body image disturbance similar to that seen
in anorexia. This preoccupation can interfere with
important areas of functioning; the patients often have
a compulsive need to maintain their workout and diet
schedule, may use performance-enhancing substances
despite knowledge of adverse psychological or phys-
ical consequences, and often shy away from showing
their bodies in public. In a 1997 study of 156 unse-
lected weightlifters, 10% perceived themselves to be
less muscular than they were objectively.108 Another
study in 1997 of 193 men and women with BDD
demonstrated that 9.3% had muscle dysmorphia. 109
VIOLENT BEHAVIOR
Violence is something that all physicians correctly fear.
The ability to predict that a patient is or will be violent
 image...

5 • PSYCHOLOGICAL ASPECTS OF PLASTIC SURGERY 87

is not ensured. The role of psychopathology and vio-
lence is a subject of long debate. There is evidence that
certain categories of psychiatric patients are overrep-
resented in groups of violent patients. Patients with
psychotic disorders, like paranoid schizophrenia, pose
a higher risk of violent behavior.110 However, nonpsy-
chotic disorders are also often associated with violent
behavior, 111 particularly borderline and antisocial
personality disorders.
Alcohol and drugs are often associated with vio-
lence. The violence may be purposeful, for the purpose
of procuring drugs or money. It may be related to
the lowering of inhibitions against violent or antiso-
cial behavior caused by the substances or decreased
cognitive alertness, resulting in impaired judgment.
For this reason, screening for the presence of sub-
stance abuse as well as for severe personality and
psychotic disorders should be an essential part of
the plastic surgical evaluation of a potential
patient.
STRATEGIES FOR MANAGEMENT
OF THE DISSATISFIED PATIENT
There are many discussions in the literature about why
patients may be dissatisfied with the results of their
plastic surgery. Hoopes and Knorr112 concluded that
patients whose chief motivation is to resolve difficul-
ties in interpersonal relationships and whose chief
expectation is that others will change their behavior
toward them have the greatest dissatisfaction with their
surgery and the highest incidence of postoperative
problems.
Linn113 asserts that the "chief preoperative problem
with these patients is not a psychiatric one," but rather
that the surgeon has made a poor decision about
whether a correctible deformity exists. Certainly, as the
syndrome of body dysmorphic disorder has been better
understood, it is likely that many dissatisfied patients
may have suffered from this disorder that has slipped
by, undiagnosed by the plastic surgeon.
Gifford82 wonders "why there are so many favor-
able results even in patients with neurotic motivations
and severe psychopathology, and why there are such
emotionally malignant reactions in the rare failures."
He opines that "all serious emotional sequelae cannot
be predicted and prevented without refusing opera-
tion to many patients who would probably have an
uneventful course." He also suggests that severe char-
acter pathology (e.g., borderline personality disorder)
is often present in the dissatisfied patient.
Reich114 found that the existence of psychopathol-
ogy is not a contraindication to plastic surgery but that
it should be viewed in relation to two criteria, (1)
whether the expectations for the surgery are realistic
and (2) the ability of the patient to tolerate an imper-
fect result.
One of the most significant decisions the plastic
surgeon makes is whether to perform the requested
surgical procedure. Satisfaction of the patient is not
necessarily predictable, even by a careful psychiatric
examination. 115 However, several psychological factors
that often present at initial evaluation should be con-
sidered contraindications to plastic surgery (Table
5-8). The feature underlying most dissatisfaction in
plastic surgery is a breakdown in rapport and com-
munication between patient and surgeon. Breakdown
in communication between patient and surgeon can
lead to a vicious circle, described by Gorney.116 A
patient's disappointment, anger, or frustration gener-
ates the surgeons reactive hostility,defensiveness,and
arrogance, which deepens the patient's anger, leading
to eventual litigation. The dissatisfied patient must be
handled carefully to avoid this circle (Table 5-9).
CONCLUSION
The need for a thoughtful interview of the patient who
requests a plastic surgical procedure, whether for aes-
thetic or reconstructive reasons, cannot be overstated.
The plastic surgeon can be guided to make sound deci-
sions about whether to offer a requested surgery to a

TABLE 5-8 • PSYCHOLOGICAL CONTRAINDICATIONS TO PLASTIC SURGERY

The patient is uncertain as to which aspect of the appearance he or she would like to change.
The patient is unable to contemplate an imperfect result.
The patient has an unstable personality disorder or an untreated major psychiatric illness.
The patient has unrealistic expectations about the surgery that are not modifiable by education.
The patient is under emotional stress during the consultation or at the time of the planned surgery.
The patient complains of the opposition of others in his or her life, such as family members, to the planned surgery.
The patient is motivated to have the surgery at the request of or because of pressure by others.
In the case of a revision of a previous surgery, the surgeon thinks the previous result is reasonable despite the
patient's vocal complaints and dissatisfaction about the result.
The patient is a "doctor shopper" and dissatisfied with the results of prior multiple procedures.
The patient pins the success of the surgery on realization of a particular goal (e.g., the resolution of marital
problems or a job promotion).

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88 I • GENERAL PRINCIPLES

TABLE 5-9 • MANAGING THE DISSATISFIED PATIENT

Remember that the patient's dissatisfaction is often transitory and related to postoperative psychological changes.
Be supportive and understanding and let the patient ventilate his or her feelings.

See dissatisfied patients frequently and offer concern and compassion. Allow the patient to see that you are an ally
in resolving the problem.

Do not get angry with the patient. Anger will create an adversarial situation and make the patient feel abandoned
and isolated. The patient will respond with angry defensiveness, and this may increase the likelihood of litigation.

Consider an offer to revise an operation if you concur with the patient's complaints and dissatisfaction, but only if
you think that you can better the appearance.

Suggest a "waiting period" before performing any additional surgery to allow the patient to live with the current
appearance and integrate it more fully into the body image.

Sit with the patient and have a frank discussion of the complaints. Respond to them, one by one, and express the
problems you are experiencing with caring for the patient, including what obstacles you think he or she may be
placing in the way of receiving optimal care. Always take the position of being an ally and partner in obtaining
satisfaction but acknowledge when you cannot meet expectations. If you conclude that the expectations are
unrealistic, try patiently to educate the patient, using photographs and whatever data you think will accurately
portray a reasonable surgical result.

If the patient is terminally enraged with you or you with him or her, and there does not seem to be any positive
working relationship, simply state that the relationship can no longer be productive for the patient and refer the
patient to several of your colleagues for consultation, offering to help the patient make the transition to the new
surgeon as smoothly as possible.

patient by being attentive to psychological motivations
and body image concerns and alert for psychiatric dis-
orders and warning signs of a problem patient. Failing
to pay attention to potential pitfalls and one's intuitive
sense about a patient may result in a dissatisfied patient.
Calling on a psychiatric consultant to help evaluate
the patient and to work collaboratively through the
preoperative and postoperative period (if the decision
is made to operate) is often helpful. Presenting the psy-
chiatric consultant as a member of the surgical team
to assist with body image adjustment and other psy-
chological issues may encourage compliance and allow
the patient to feel more comfortable with the consul-
tation. Even if the patient is lost by the suggestion of
a psychiatric referral, it is better not to operate on a
patient who may not be satisfied with the results.
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65. Jamison K, Wellisch DK, Pasnau RO: Psychological aspects of
mastectomy. 1. The woman's perspective. Am J Psychiatry
1978;135:432-436.
66. Polivy IJ: Psychological effects of mastectomy on a woman's
feminine self-concept. J Nerv Ment Dis 1977;154:77-87.
67. Stevens LA, McGrath MH, Druss RG, et al: The psychological
impact of immediate breast reconstruction for women
with early breast cancer. Plast Reconstr Surg 1984;73:619-
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69. Teimourian B, Adham MN: Survey of patients' responses to
breast reconstruction. Ann Plast Surg 1982;9:321-325.
70. Levinson J: Breast reconstruction: a patient's view (letterl. Plast
Reconstr Surg 1984;73:703.
71. Goldberg P, Stolzman M, Goldberg HM: Psychological con-
siderations in breast reconstruction. Ann Plast Surg 1984; 13:38-
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72. Wellisch DK, Schain WS, Noone RB, Little JW 3rd: Psychoso-
cial correlates of immediate versus delayed reconstruction of
the breast. Plast Reconstr Surg 1985;76:713-718.
73. Liggett J: The Human Face. London, Constable, 1974.
74. David DJ, Barritt JA: Psychosocial implications of surgery
for head and neck cancer. Clin Plast Surg 1982;9:327-
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75. Castelnuevo-Tedesco P: Psychological consequences of phys-
ical defect: a psychoanalytic perspective. Int Rev Psychoanal
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76. Castelnuevo-Tedesco P: Ego vicissitudes in response to replace-
ment or loss of body parts. Certain analogies to events during
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77. Castelnuevo-Tedesco P: The psychological consequences of
physical illness or defect and the relationship to the concept
of deficit. Psychoanal Study Child 1997;52:76-88.
78. Clifford E: Psychological aspects of the craniofacial surgical
experience. In Converse JM, ed: Symposium on Diagnosis and
Treatment of Craniofacial Anomalies. St. Louis, CV Mosby,
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79. Pertschuk MJ, Whitaker LA: Craniofacial deformity. Clin Plast
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80. Macgregor FC, Abel TM, Bryt A, et al: Facial Deformities
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81. National Clearinghouse of Plastic Surgery Statistics, 2003
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82. Gifford S: Cosmetic surgery and personality change: a review
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vorable Result in Plastic Surgery. Boston, Little, Brown,
1972:11-33.
83. McGrath MH, Mukerji S: Plastic surgery and the teenage patient.
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84. Plastic Surgery for Teenagers. Plastic Surgery Briefing Paper,
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IL 60005.
85. Stein M, Miller AH, Trestman RL: Depression, the immune
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ined ugliness. Am J Psychiatry 1991; 148:1138-1149.
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sional and non-delusional body dysmorphic disorder in 100
cases. Psychopharmacol Bull 1994;30:179-186.
95. Hollander E, Cohen L, Simeon D: Body dysmorphic disorder.
Psychiatr Ann 1993;23:359-364.
96. Phillips KA: Body dysmorphic disorder: the distress of imag-
ined ugliness. Am J Psychiatry 1991;148:1138-1149.
97. Phillips K, Diaz S: Gender differences in body dysmorphic
disorder. J Nerv Ment Dis 1997;185:570-577.
98. Veale D: Outcome of cosmetic surgery and "DIY" surgery in
patients with body dysmorphic disorder. Psychiatr Bull
2000;24:218-221.
99. Phillips KA, Dufresne RG Jr: Body dysmorphic disorder: a guide
for dermatologists and cosmetic surgeons. Am J Clin Derma-
tol 2000;1:235-243.
100. Aronowitz BR, Simeon D, Hollender E, et al: A survey of
body dysmorphic disorder in plastic surgery patients. Presented
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101. Wilhelm S, Otto MWf Lohr B, et al: Cognitive behavior group
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102. Hollander E, Allen A, Kwon J, et al: Clomipramine vs.
desipramine crossover trial in body dysmorphic disorder. Arch
Gen Psychiatry 1999;56:1033-1039.
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facing the man in the mirror. Primary Psychiatry 2001;8:32-
36.
104. Phillips KA: Body dysmorphic disorder: diagnostic contro-
versies and treatment challenges. Bull Menninger Clin
2000;64:18-35.
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prevalence of body dysmorphic disorder in an ethnically
diverse group of adolescents. J Child Fam Studies 1999;8:357-
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them all? Features and phenomenology of muscle dysmor-
phia. Harv Rev Psychiatry 2001;9:254-259.
108. Pope HG Jr, Gruber AJ, Choi P, et al: Muscle dysmorphia. An
under recognized form of body dysmorphic disorder. Psycho-
somatics 1997;38:548-557.
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anabolic/androgenic steroid use: a controlled study of 160
athletes. Arch Gen Psychiatry 1994;51:375-382.
110. Humphreys MS, Johnstone EC, MacMillan JF, et al: Danger-
ous behaviors preceding first admission for schizophrenia. Br
J Psychiatry 1992;161:501-505.
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5 • PSYCHOLOGICAL ASPECTS OF PLASTIC SURGERY 91

111. Binder RL, McNeil DE: The relationship of gender to violent
behavior in acutely disturbed psychiatric patients. I Clin Psy-
chiatry 1990;51:110-114.
112. Hoopes IE, Knorr NJ: Psychology of the flat chested
woman. In Masters FW, Lewis JR, eds: Symposium on Aes-
thetic Surgery of the Face, Eyelid, Breast. St. Louis, Mosby, 1972.
113. Linn L: Psychiatric aspects of plastic surgery. In Bellack L, ed:
Psychology of Physical Illness. New York, Grune & Stratton,
1952.
114. Reich J: The surgery of appearance: psychological and rela-
tional aspects. Med J Aust 1969;2:5-13.
115. Reich J: The interface of plastic surgery and psychiatry. Clin
Plast Surg 1982;9:367-377.
116. Gorney M: Claims prevention for the aesthetic surgeon: prepar-
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2002;18:135-142.

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
TtJWftS^dd'fee image...
CHAPTER
6•
Ethics in Plastic Surgery
THOMAS J. KRIZEK, MD, MA (HON)
DESCRIPTION OF ETHICS
HISTORY OF PLASTIC SURGERY ETHICS
ETHICAL THEORIES
Unsystematized Ethical Theories
Systematized Ethical Theories
Professionalism and Virtue-Based Ethics
APPLICATION OF ETHICAL THEORIES
Principlism and Rules-Based Ethics
Casuistry
Ethics of Care (Feminist Ethics)
• SCENARIO: LOST
AND FOUND
A young woman comes to a plastic surgeon several
years after a bilateral augmentation mammaplasty with
silicone gel implants. She has severe fibrous capsule
formation on one side; the other side is soft and
aesthetically pleasing. Concerned about silicone, she
requests that both implants be replaced with saline
implants as part of the correction of the capsular
contraction.
An outpatient procedure is accomplished under
general anesthesia. The surgeon encounters a gauze
sponge, which is removed. The anesthesiologist is con-
centrating on the management of the patient and the
scrub nurse is momentarily distracted, so there are no
apparent witnesses to the presence of and removal of
the sponge. The operation is completed satisfactorily.
Issues of morality, the expression of right and wrong,
present themselves on a daily basis. Most persons,
invoking principles of self-determination and the right
to pertinent information, would assume that the
patient should be told the entire truth about the find-
ings. Many will assume there is a long tradition of truth
telling in medicine. Yet, this example raises less appar-
ent considerations and questions. Would it matter, for
instance, whether the sponge was found on the side
that did MO? have fibrous capsule formation? Would it
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
ETHICAL PROCESSES
. Impartiality
Consistency
Precedent Setting
ETHICS FOR PLASTIC SURGERY
Aesthetic Surgery for the Healthy Patient
Professionalism
CODES OF BEHAVIOR
Code of Ethics of the American Society of Plastic
Surgeons
TRUTH TELLING
matter that the patient was emotionally distraught and
such information might worsen her overall condition?
Would the situation be different if the present surgeon
were not the original surgeon? Concerns arise about
litigation, possible compensation, regulations about
reporting, and possible limitations of privileges and
licensing. These are examples of conflicting interests
and rights that influence our decision-making. The
answers to these questions are not clear or unequiv-
ocal. Standards of behavior must guide the practice
of plastic surgery in relationships with patients, col-
leagues, and society at large; they involve determina-
tions of right and wrong behavior. Ethics is the study
and understanding of these standards.
Ethics is the discipline devoted to the study of the
principles and processes for determining right and
wrong behavior. Ethics is the consideration of good
and bad, in the context of moral duty and obligation.
Although the fundamentals of right and wrong are
learned early in life, professional ethics are incorpo-
rated as part of the development of a professional iden-
tity. In the development of surgical professionalism,
character can be shaped, nurtured, developed, and
solidified; on occasion, its absence can be exposed.
Character is important to being a professional,
whether it is a plastic surgeon or, for example, an
athlete. Camus' wrote, "Yes, there was the sun, and
poverty. Then sports, from which I learned all I know
about ethics." Sport has been described by Simon 2 as
the "mutually acceptable quest for excellence through
competition." Playing fair, within the rules of the game,
93
94 I • GENERAL PRINCIPLES
is intrinsic to sport, and although it is possible to cheat,
cheating violates the very integrity of the game and it
ceases to be sport. Plastic surgery also involves a quest
for excellence and also has established "rules" that are
embodied in the ethics of medicine and in the code
of behavior established by our specialty. Although it
is possible for an individual to violate the rules, such
violation debases the "good," the very integrity of the
profession. Fundamental in one's responsibilities to
patients, society, and self is the question Why should
1 be ethical?
The ethics of professionalism has both intrinsic and
extrinsic characteristics. The intrinsic values of pro-
fessionalism are part of what it means to be a good
and moral physician in general and a plastic surgeon
in particular. These internal characteristics of good
behavior, sometimes called internal goods or virtues,
include empathy, honesty, courage, prudence, tem-
perance, and practical wisdom. Some of these char-
acteristics are learned early, and a disposition is
brought by the student to medical school and resi-
dency. There, they are shaped just as surgical skills are
learned and realized. Some of these characteristics are
personal, and psychoanalysts would say that the source
of these virtues is the superego. Others would call them
conscience and would attribute them to religious expe-
riences. Others would observe that these qualities are
philosophical and secular and are merely the quali-
ties of being a good person. According to Deverette,3
"Ethics is an effort to discover in each of our chal-
lenges in our profession what feelings, habits and
behavior will give us the best chance of living a happy
life."
Such a "happy life" is not merely doing what seems
to bring pleasure at any given moment but a sense
of fulfillment, contentment, and serenity, which are
the rewards of a life lived morally. Part of the goal of
ethical behavior is personal accomplishment and
satisfaction.
Other aspects of professionalism are codified in the
form of rules or guidelines that shape one into doing
right by patients, protecting them from harm, and
respecting their autonomy. These codes also define our
role as surgeons in dealing with colleagues and society
at large. The reason for following these rules and codes
is more obvious in that deviation can lead to disap-
proval or discipline, and all professionals—surgeons,
lawyers, ministers, and athletes—are subject to temp-
tations by the external goods of the world. These worldly
goods involve the pursuit of power, prestige, and wealth.
None of these external goods adds to the skills of a
surgeon or increases ability to render excellent care of
patients.
The surgeon faced with the dilemma of what to
tell the patient about the sponge in the wound must,
almost in an instant, make the ethical decision. The
surgeon must balance honesty, integrity, and learned
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
ethics against the real consequences, including the
possibilities of loss of prestige, litigation, and limita-
tion of privileges and license to practice. Like skilled
athletes and trained warriors in battle who must react
almost intuitively to challenges, the ethically aware
plastic surgeon must also learn to react promptly and
properly.
DESCRIPTION OF ETHICS
Surgical textbooks approach clinical issues from a
scientific point of view. Science makes observations
about the world and then, on the basis of patterns of
outcomes, derives generalizations and judgments.
Although plastic surgery involves much that is artis-
tic and imaginative, most of one's work is based on
scientific principles such as asepsis, blood clotting, and
healing of wounds. It is believed that the appropriate
placement of incisions will predictably lead to healing
and inconspicuous scars. Even new approaches and
techniques are based on and evolve from known prin-
ciples. Abelson4 observed that science is "descriptive
and provides us with hypotheses for predicting what
will happen." Ethical theory, in contrast to science, is
based on commonsense facts that are known to every-
one. From common observation, ethics formulates prin-
ciples and standards whose function is not to predict
outcome, as in science, but to guide our choices and
actions. Ethical principles do not lend themselves to
the precision of scientific observation. Traditionally,
humans have called on religion and philosophy for
guidance about morals and ethics.
From earliest times, people shared stories about
important issues of life and death; these are referred
to as religious myths and described what was and what
ought to be. Certain behavior was believed to lead to
favorable outcomes, to fertility, health, and prosper-
ity. To ensure good outcomes, such correct or right
behavior evolved into rites or rituals. The shared myths
and rituals constituted the earliest forms of religion,
and as larger and larger groups gathered together, early
religions became more formalized. Judaism, Chris-
tianity, and Islam share a fundamental belief in a single,
all-knowing, and all-powerful god. Western medicine
has also developed its shared beliefs around myths and
rituals that have emanated from the early teachings of
Hippocrates (Table 6-1 and Fig. 6 - l ) . w The staff of
Aesculapius with the entwined serpent is the symbol
of healing power, and the Hippocratic Oath is the most
time-honored code of behavior.
Western religions are historical and linear, begin-
ning at birth and ending at death, with guidelines for
leading a good and proper life along the way.7 The
very fundamental issues of when life begins and when
life ends are religious rather than medically or
scientifically defined. In many Eastern societies, the
world view was and is more holistic. End-time is not
ItJWR^aaciW image...
TABLE 6-1 • HIPPOCRATICOATH
Classical Version
i swear by Apollo Physician and Asclepius and Hygieia
and Panaceia and all the gods and goddesses, making
them my witnesses, that I will fulfil according to my
ability and judgment this oath and this covenant:
To hold him who has taught me this art as equal to my
parents and to live my life in partnership with him, and
if he is in need of money to give him a share of mine,
and to regard his offspring as equal to my brothers in
male lineage and to teach them this art—if they desire
to learn it—without fee and covenant; to give a share of
precepts and oral instruction and all the other learning
to my sons and to the sons of him who has instructed
me and to pupils who have signed the covenant and
have taKen an oath according to the medical law, but
no one else.
I will apply dietetic measures for the benefit of the sick
according to my ability and judgment; I will keep them
from harm and injustice.
I will neither give a deadly drug to anybody who asked
for it, nor will ! make a suggestion to this effect.
Similarly I will not give to a woman an abortive remedy.
In purity and holiness I will guard my life and my art.
I will not use the knife, not even on sufferers from
stone, but will withdraw in favor of such men as are
engaged in this work.
Whatever houses I may visit, I will come for the benefit
of the sick, remaining free of all intentional injustice, of
all mischief and in particular of sexual relations with
both female and male persons, be they free or slaves.
What I may see or hear in the course of the treatment
or even outside of the treatment in regard to the life of
men, which on no account one must spread abroad, I
will keep to myself, holding such things shameful to be
spoken about.
If I fulfil this oath and do not violate it, may it be
granted to me to enjoy life and art, being honored with
fame among all men for all time to come; if! transgress
it and swear falsely, may the opposite of all this be my
lot.
Translation from the Greek by Ludwig Edelstein: The Hippocratic Oath:
Text, Translation, and Interpretation. Baltimore, Johns Hopkins Press, 1943.
well defined, and death often represented a new begin-
ning, a reincarnation. Much of the Eastern world has
developed world views based on harmony and balance,
and the goal of medicine is to restore balance. In con-
trast, for most of us in the West, disease is viewed as
a visitation from without, and rather than an imbal-
ance, it is the result of an external agent that must be
prevented or excised.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
6 • ETHICS IN PLASTIC SURGERY 95
Modern Version
I swear to fulfill, to the best of my ability and judgment,
this covenant:
I will respect the hard-won scientific gains of those
physicians in whose steps 1 walk, and gladly share such
knowledge as is mine with those who are to follow.
I will apply, for the benefit of the sick, all measures
which are required, avoiding those twin traps of
overtreatment and therapeutic nihilism.
I will remember that there is art to medicine as well as
science, and that warmth, sympathy, and
understanding may outweigh the surgeon's knife or the
chemist's drug.
I will not be ashamed to say "I know not," nor will I fail
to call in my colleagues when the skills of another are
needed for a patient's recovery.
I will respect the privacy of my patients, for their
problems are not disclosed to me that the world may
know. Most especially must I tread with care in matters
of life and death. If it is given me to save a life, all
thanks. But it may also be within my power to take a
life; this awesome responsibility must be faced with
great humbleness and awareness of my own frailty.
Above all, I must not play at Cod.
I will remember that I do not treat a fever chart, a
cancerous growth, but a sick human being, whose
illness may affect the person's family and economic
stability. My responsibility includes these related
problems, if I am to care adequately for the sick.
I will prevent disease whenever I can, for prevention is
preferable to cure.
I will remember that I remain a member of society, with
special obligations to all my fellow human beings, those
sound of mind and body as well as the infirm.
If I do not violate this oath, may I enjoy life and art,
respected while I live and remembered with affection
thereafter. May I always act so as to preserve the finest
traditions of my calling and may I long experience the
joy of healing those who seek my help.
Written in 1964 by Louis Lasagna, Academic Dean of the School of Med-
icine at Tufts University, this is the version used in many medical schools
today.
Patients may have a point of view different from
that of the surgeon. Communication about sensitive
and personal issues the patient presents to the surgeon
must be clearly understood.
Much of Western philosophy began in Ancient
Greece and was centered in a person's relationship to
the polis, the city-state in which one lived.8 Socrates
evolved a method of exploring important issues
96 I • GENERAL PRINCIPLES
FIGURE 6 - 1 . Hippocrates as envisioned in an engrav-
ing by Paulus Pontius (1603-1658) after a drawing by
Peter Paul Rubens from an ancient marble bust. (Cour-
tesy of the National Library of Medicine, Bethesda, Md.)
that involved the dialectic and exploration of words
and concepts. The Socratic method remains in-
grained in much of the teaching methods in plastic
surgery. Socrates would have framed a discussion of
the sponge under the broad rubric of truth and what
truth would contribute to the good life of those
involved. Aristotle then codified ethics and good cit-
izenship on the basis of virtue. Good citizens would
possess wisdom that would dispose them to the other
virtues, such as courage, prudence, discretion, and
temperance.
The enlightenment and scientific revolution began
when society learned that the earth was not the center
of the universe. Philosophers began to seek and
attempt to explain the important issues on the basis
of rationality. Human reason has largely replaced the
authority of religion or the authority of kings. To resolve
complicated ethical issues in a pluralistic community
with multiple religious beliefs and varying ethnic and
cultural backgrounds, the United States has established
authority on the basis of law.
This background in religion and philosophy has
led medical ethics to be divided into two major cate-
gories, those relating to the individual behavior of pro-
fessionals and those aspects of ethics that relate to
others. The virtues of Aristotle identified some of the
personal virtues for behavior; the code of ethics from
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
the Hippocratic school formed the basis for how physi-
cians should act toward patients.
HISTORY OF PLASTIC
SURGERY ETHICS
For more than two millennia, physicians and surgeons,
patients and society were comfortable with the two
major tenets of the Hippocratic Oath: to do good,
beneficence, and to keep patients from harm,
nonmaleficence. Curiously, Hippocrates was largely
silent about the salient issue of the scenario of the found
sponge, that is, truth telling. The issue of truth is not
mentioned in the Oath or, except indirectly, in his other
writings. In Decorum, as described by Katz,9 Hip-
pocrates said,"Perform your duties calmly and adroitly,
revealing nothing of present or future conditions to
your patient." This is hardly a call for candor. Plato is
said to have recommended that you prescribe nothing
for a patient until you convince the patient that it will
be effective. Others have observed that without the
physician's right to make decisions for the patient, there
would be no such thing as medicine. The relationship
of the physician to patient was paternalistic, and it was
assumed that the physician would tell the patient what-
ever the patient needed to know, as determined by the
physician. Since almost everyone assumed that the
physician always would act in the patient's best inter-
est, nothing more specific was needed. This was not
unreasonable because, until the last century, physicians
were woefully ill-equipped to alter the outcome of most
diseases. Surgeons were limited in their success to
amputations, drainage of abscesses, and removal of
stones. Hippocrates dismissed surgeons, excluding us
from the Oath: "I will not use the knife, not even on
sufferers from stone, but will withdraw in favor of such
men as are engaged in this work."5
It is only since the availability of anesthesia, asepsis
and antisepsis, and blood transfusions that surgery has
achieved its modern level of respectability. Surgeons
have had to strive for recognition in professional circles.
Despite sometimes being marginalized, plastic sur-
geons should remain proud of our heritage. Nasal
reconstruction was performed in India at about the
same time as Hippocrates walked the countryside of
Greece. Gaspar Tagliacozzi transferred soft tissue from
the arm to the face for nasal reconstruction in the 16th
century. 10 The procedure was sought by the disfigured
who accepted the surgery performed without anes-
thesia, aseptic technique, antibiotics, or even the most
basic hygienic measures common in our modern
society. Tagliacozzi's work remains testimony to the
dedication to an idea. It also reveals that patients are
willing to undergo such procedures for the purpose
of appearance only and confirms that disfigurement
has profound human significance. To some, the very
act of operating on persons perceived to be normal
for the primary purpose of changing appearance is
Tt?W>ttf<aelcrt# image...
unethical. Even surgery to correct the ravages of defor-
mity, from birth defects or scarring from burns, is con-
sidered by some to be unnecessary and a misuse of
society's valuable resources.
• S C E N A R I O : C L E F T S
A N D E V I L S P I R I T S
An otherwise healthy newborn has a bilaterally com-
plete cleft of the lip and palate. The parents, newly
arrived immigrants to the United States, determine that
the child has been invaded by an evil spirit and must
be allowed to die. Their other three children are normal
and seem to have received good care.
Many will argue that all ethical questions are
relative (relativism) to the attitudes and customs of
various societies and that answers will vary from time
to time. For much of history and for most parts of the
world, the parents' decision about a child with a cleft
would have been not only accepted but also perhaps
mandated. Infanticide, particularly the killing of
deformed newborns at the time of Hippocrates and
for centuries later, was not considered to be morally
wrong.11 In desperate societies, one more mouth to
feed made support of a child disfigured with a cleft
lip or palate, for instance, inappropriate. Unwanted
children, particularly the deformed, were either killed
outright or, in more sophisticated societies, aban-
doned. 12 Oedipus, one of the most famous abandoned
children, had his feet punctured and bound to deform
him, and he derived his name from his "swollen foot."
Attention to facial deformity, particularly surgery to
correct cleft lips, has been almost unprecedented in
history. It is true that the morality of a society may be
judged by how well it treats those who are disfigured,
deformed, infirm, simply too old, or unable to care
for themselves for whatever reason. Fuchs 13 predicted
the ethical dilemmas of today, in which the resources
to render total care for all persons will not be avail-
able, and that society will have to decide "who shall
live and who shall die." Most plastic surgeons would,
of course, argue that the child with the cleft lip and
palate must be treated, the lip and palate repaired, and
the parents' concerns about evil spirits respectfully
heard but not accepted. What might have been accept-
able in another time and place is not acceptable in our
society at this time.
Throughout history, there have been examples of
behavior we would find offensive today. Such exam-
ples are called normative in that they must be consid-
ered wrong no matter when they occurred. Slavery in
the United States was a national tragedy; in other parts
of the world, slavery continues to be a moral tragedy.
The treatment of Native Americans bordered on geno-
cide, and the Holocaust was the single greatest horror
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Dr.Mustafa D.
6 • ETHICS IN PLASTIC SURGERY 97
of recent generations. There is fairly widespread agree-
ment throughout the civilized world that slavery, geno-
cide, torture, rape, and murder are wrong. Most would
agree that such wrongs represent evil. That wrongs con-
tinue to occur and social attitudes in some cultures
allow it demonstrate the problem with ethical rela-
tivism. Female circumcision and infibulation may be
socially acceptable or even of religious significance in
some parts of the world, but such practices would be
considered wrong in our society. Simply because such
behavior happens to be the custom of a society does
not mean that it is acceptable. There may be differ-
ences of opinion about some behavior, but it does not
confirm that there is no right or wrong moral action.
A serious approach to ethics demands a search for nor-
mative or objective standards that apply to everyone.
Although the fundamental concepts contained
within the Oath of Hippocrates have been accepted
by most of medicine, standards of professional behav-
ior have continued to evolve. Prominent among these
are codes of behavior promulgated by the American
Medical Association and the American College of Sur-
geons and the Code of Ethics of the American Society
of Plastic Surgeons. Although many of the earlier codes
involve descriptions of physician behavior that were
as much matters of etiquette as issues of morality, these
codes survive the boundaries of time, geography,
culture, and religion.
ETHICAL THEORIES
It would be convenient if one were able to reduce ethical
understanding to a few simple rules and some illus-
trative scenarios. A meaningful approach to ethics
requires understanding of theories, processes, and
applications, as do clinical issues facing plastic surgeons
in practice (Table 6-2).
Unsystematized Ethical Theories
To some in present society, all morality should be a
matter of individual choice, and whatever produces
pleasure and avoids pain should be acceptable. This
hedonistic approach implies that if an action feels good,
one may do it. Accordingly, if an action does not
adversely affect other parties, it should be acceptable.
This approach grants primacy to individual liberties,
and morality becomes a matter of individual rights.
However, it is not always apparent that seemingly indi-
vidual decisions affect those other than the individ-
ual. Sexual activity, for instance, although involving
only two persons, may have devastating consequences
for others. Possible unplanned pregnancy or the trans-
mission of a sexually transmitted disease involves
others. Second, to decide important issues on the basis
of individual emotions eliminates any predictability
as to what would be determined to be right or wrong.
One would feel most insecure entering a courtroom
98 I • GENERAL PRINCIPLES

TABLE 6-2 • ETHICAL THEORIES Systematized Ethical Theories

Unsystematized
Emotivism Moral judgments are based on
personal preference, expressions
of attitudes, or feelings.
Systematized
Utilitarianism Actions are right in proportion to
their tendency to promote
happiness and wrong in their
tendency to produce unhappiness.
Deontology The "principles" one acts on are the
decisive moral factor and should
stem from good will rather than
self-interest or avarice. In
addition, one should not act in a
certain way unless it can be
universally applied to all situations
in the same category.
Authoritarianism Morality is determined by a ruling
authority (usually religious).
Professionalism/Virtue-Based Ethics
Internal goods A coherent, complex form of socially
established cooperative activity
that produces internal goods in
the participants striving to excel in
the activity, such as honesty,
integrity, prudence, temperance,
and practical wisdom
External goods The temptations that challenge and
interfere with excellence in
professions and practices
presided over by a judge who based decisions on per-
sonal emotions and preferences.
Alasdair Maclntyre,14 a contemporary philoso-
pher-ethicist, condemned these early unsystematized
theories and argued that, absent shared religious
belief, "All evaluative moral judgments and more
specifically all moral judgments are nothing but
expressions of preference, expressions of attitude or
feelings, insofar as they are moral or evaluative in char-
acter" This he termed emotivism. He argued that when
morality was based on religious belief, it had the shared
objective reality provided by shared religious tenets,
and what was good or bad and what was right and
wrong were clearly specified. It was not all relative and
not merely a matter of preference, and it was certainly
not limited to that which felt good. But in modern
societies, particularly in countries that allow religious
pluralism, there is difficulty in gaining agreement about
norms for behavior. If hedonism and emotivism were
the only ethical standards, all reasoning would become
circular and arguments would be only about whether
one approves of this or that, not whether it is, in its
essence, good or bad.
Efforts to design a secular system of morality have been
based on several theories.
UTILITARIANISM
Utilitarianism is the "greatest happiness principle."
Jeremy Bentham and John Stuart Mill are credited with
developing the principle that "actions are right in pro-
portion as they tend to promote happiness; wrong as
they tend to produce the reverse of happiness."15 Hap-
piness is more than immediate pleasure; rather, it is
longer term well-being such as peace, security, and even
serenity. Utilitarianism enjoins persons to act in
certain ways: tell the truth, do not steal, and do not
harm others. The Tightness of these actions depends
largely on the consequences of the action. Actions may
have unintended consequences that detract from
the goal of happiness. Furrow'6 uses the example of a
person lending a sum of money to another with the
expectation that it is a loan to be repaid. The recipi-
ent decides instead that a greater happiness will result
to more people if that money is given, without the
person's permission, to the poor and needy. Utilitar-
ianism, for the perceived greater good, may fail to rec-
ognize obligations and debts and for a perceived greater
good may ignore more individual rights. The goals of
utilitarianism can lead to a tyranny of the majority at
the expense of the minority; a limitation of utilitari-
anism is failure to address justice. This is true in health
care, where resources are limited. The wishes of the
majority may dictate that complicated and expensive
treatments be withheld. The majority may also decide
to ignore the needs of the disfigured, the deformed,
the very young and the very old, and those who can
no longer care for themselves. The values of a major-
ity may become distorted and lead to the dehuman-
ization of the disadvantaged and are only another form
of emotivism or matters of preference.
DEONTOLOGY
Deontology refers to one's duty to act in certain ways.
Immanuel Kant (1724-1804) argued that the conse-
quences of an act do not make the act right or wrong,
but rather it is the principles on which an agent acts
that are decisive.15 Perhaps this principle is understood
best from the simple maxim that "the ends do not
justify the means."
• SCENARIO:
RESIDENT'S DILEMMA
A patient presents to the resident-training clinic for
an abdominal contouring procedure. There is only a
vague suggestion of periumbilical weakness. Neither

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Dr.Mustafa D.
TeWttf^adW image...
the resident nor supervising surgeon stands to gain
financially from performing the procedure. The patient
cannot afford the procedure unless it is coded as an
umbilical hernia repair.
The question is whether a greater good is achieved
by providing the patient with the operation and the
resident with the experience, even though the means
to the end involve deception. The decision obviously
brings several "duties" into conflict: the duty to educate
residents, the duty to try to do the best for the patient,
and the duty to society and those who must pay for
the procedure. According to deontology, acts should
spring from good will and be governed by moral prin-
ciples. The desire to perform this procedure may, in
fact, arise from good will rather than self-interest or
avarice. The question, however, is not merely good will
and inclination but morality. Kant would say that some
actions are ethically neutral, such as the use of our
intelligence and surgical skills. Accordingly, deontol-
ogy would dictate that if the surgeon's skills were
applied to eradicate illness and to improve the well-
being of a patient, they are good actions. The same
skill used to defraud an insurance company or the
taxpaying public is wrong.
Categorical Imperative
This principle broadly states that one should not act
in a certain way unless the action can be universally
applied to all situations in the same category. Kant
referred to these rules as maxims. Accordingly, in the
situation of the resident abdominoplasty, a decision
to deceive the carrier to obtain coverage for the pro-
cedure could be applied similarly in other compara-
ble situations in the future. It does not matter that
there is no specific financial gain for either the resi-
dent or the attending surgeon. Such operations per-
formed by residents have immense educational value
and add to the attractiveness of training programs.
If it were ethically acceptable to defraud under some
circumstances, the categorical imperative would
imply that fraud is acceptable in other comparable sit-
uations. The duty to the insurer and to society is greater
than the duty to an individual patient. It is seductive
to shade indications when one is new in practice and
has large debts and a family to support and the party
being deceived is a large, impersonal, and presumably
rich third-party carrier. Deceptive coding in this
circumstance is even more unacceptable because it
involves pure economic gain without any educational
value.
Ends and Not Means
This aspect of deontology states that persons should
be treated as ends in themselves and not merely
as a means to some other goal. Each person is an
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6 • ETHICS IN PLASTIC SURGERY 99
individual who possesses individual human dignity and
worth. Plastic surgeons have traditionally valued and
treated the disfigured and deformed with dignity,
and procedures to improve appearance recognize and
respect dignity. Each person who undergoes surgery
is the end to which training and skills are to be directed,
not the means to better training or riches.
Resident training programs present a special chal-
lenge. Many patients under the care of residents are
socioeconomically disadvantaged and thus vulnera-
ble. Exploitation takes many forms: residents operat-
ing with less supervision than would be provided to
private patients, or one or more patients serving as
subjects for experimental techniques, perhaps even
without protocol or institutional review. Although the
operation would be an acceptable goal in the scenario
presented, the means to achieve it are unethical and
do not justify defrauding others.
Kant's ethical theories are complex and controver-
sial. There is doubt whether absolute rules determined
by the categorical imperative can always provide a solu-
tion to moral difficulties. There are many examples of
several "duties" being in seeming conflict: a duty to
keep a promise to attend a conference and the duty
to help a patient in need. There is inherent difficulty
in ranking maxims, such as "always telling the truth"
and "lying when telling the truth would hurt a patient."
Despite these limitations, the theory captures many
intuitive beliefs and provides a test, the categorical
imperative, for determining specific duties.
AUTHORITARIANISM
For most of history, morality was determined by the
ruling authority, often religious. What the king said
or the Pope said was right because he said so. There
was little in the way of philosophical reflection or delib-
eration. Although a desire for human freedom may
be universal, its realization is relatively recent and
limited to relatively few countries in the world. The
founders of the United States established a unique and
wonderful experiment in government of and for the
people. Citizens of the United States have agreed on
certain inalienable rights: to life, liberty, and the pursuit
of happiness. Into the Constitution we have incorpo-
rated religious ethics, human rationality, and princi-
ples of duty and utilitarianism, attempting to recognize
freedom for all and freedom from any particular reli-
gion. In recent decades, technology and society have
moved away from religious authority and toward
increasing secular individualism. Neuhaus 17 has suc-
cinctiy stated that in effect, we have made our public
square "naked" of religion. He believes this to be unfor-
tunate in that modern secular decisions are sometimes
devoid of the counsel that religion can provide.
Although patients and surgeons may have different
religious beliefs and different cultural and ethnic
100 I • GENERAL PRINCIPLES
backgrounds, we have attempted to find our common
ethical ground in the rule of Law.
Utilitarianism attempts to measure actions on the
basis of their outcome, whereas deontology empha-
sizes intent and good will and looks intently at the
process involved. In the United States, the general pop-
ulation has arrived at a new way of applying author-
ity, by the governed, recognizing individual rights
and freedoms. However, professionalism is a more
pertinent concept, and a better approach is that of
virtue.
Professionalism and Virtue-Based
Ethics
Ethics moved from the original virtue approach of Aris-
totle to philosophical approaches of utilitarianism and
deontology or duty. The issues were less focused on
how a good person should act; instead, they were
focused on the process for resolving moral conflicts.
Principles and rules-based ethics became the prima
facie approach. Much of medical ethics became ethics
addressed to situations, or situational ethics.
In the last several decades, there has been a return
18
to virtue ethics. Pellegrino has analyzed how ethical
applications have changed through the ages and
brought us back to virtues. The best qualities of human
behavior, those that are most admired among profes-
sionals and nonprofessionals alike, are "virtues." The
more we can identify, recruit, and educate virtuous
persons in the healing arts, the less the need for rules
and discipline. Beginning with Aristotle, the central
virtue was practical wisdom, the intellectual virtue
without which one cannot, it is said, possess the other
virtues: "Practical wisdom, then, must be a reasoned
and true state of capacity to act with regard to human
goods . . . plainly, practical wisdom is a virtue, not
an art."8
Some virtues are intellectual; prudence and prac-
tical wisdom are realized through teaching and learn-
ing and are not mere cleverness and cunning. Some of
the virtues are in one's character, such as courage,
justice, and temperance, and are realized through
habitual exercise. To 1^ lacln tyre, virtue is "an acquired standing of human behavior and relationships.
M
human quality, the possession and exercise of
which tends to enable us to achieve those goods
which are internal to the practices and the lack
of which effectively prevent us from achieving any
such goals."
To Maclntyre, virtue is the quality that helps one
achieve the very essence of what it means to be a pro-
fessional. To be a good and moral plastic surgeon, one
must adopt the "goods" that signify being a profes-
sional—to have a practice. These are not the practices
that go into organizing an efficient office and a good
business plan but rather a form of social practice that
exemplifies the demonstration of virtues. A "practice"
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is "any coherent and complex form of socially estab-
lished co-operative human activity through which
goods internal to that form of activity are realized in
the course of trying to achieve those standards of excel-
lence which are appropriate to, and partially definitive
of, that form of activity, with the result that human
powers to achieve excellence, and human conceptions
of the ends and goods involved are systematically
extended."*4
INTERNAL GOODS
19
Ballard examined Maclntyre's definition of practices
and identified a set of specific characteristics: "A coher-
ent, complex form of socially established cooperative
activity... that produces internal goods of the activ-
ity by participants striving to excel by the standards of
the activity... that systematically extends the partic-
ipants' skills and their concepts of goods and purposes
of the activity."
On examination, these characteristics apply to the
profession of plastic surgery. The practice of medi-
cine and specifically of plastic surgery is a social activ-
ity. It involves cooperative activity in dealing not only
with patients but also with many others in the health
care endeavor. The body of knowledge is broad yet
specific and presents a coherent, albeit complex,
approach to the care of patients.
Maclntyre defined internal goods as those that lead
to virtue. Virtue includes the qualities that allow one
to achieve and possess the goals or goods of the activ-
ity. These internal or intrinsic goods are the virtues
of the profession: honesty, integrity, prudence, tem-
perance, and practical wisdom that would include
surgical judgment and skill. These characteristics or
internal goods are the fundamental basis for profes-
sionalism and moral behavior. The development of
professionalism or a practice to Aristotle and to Mac-
lntyre requires that as "novices," that is, students and
residents, advance in their efforts, they should acquire
the goods of the profession. The specialty of plastic
surgery involves the acquisition of knowledge of
science and the arts, technical expertise, and an under-
The standards of plastic surgery require intellec-
tually and technically challenging activities. As a
specialty, through various organizations, boards, and
review committees, surgeons have endeavored to
establish and maintain standards. Those seeking to
become plastic surgeons should internalize these
objective standards and model themselves after exem-
plary teachers. The ongoing practice of the specialty
cannot be monitored by outside agencies at all times,
in all situations, particularly in the relative privacy
of one's own consultation room or surgical suite.
Whether it is in sport or the practice of surgery, prac-
tices cannot exist on rules alone; rules cannot replace
TfcWttf'SeldW image...
the internal goods and character that a virtuous
practice demands.
The goal of a residency program is to develop and
extend the skills of plastic surgeons necessary for the
safe conduct of the specialty. The pursuit of excellence
in learning and the maintenance of excellence as a
plastic surgeon may be compared with the demands
placed on an athlete. Some talents, such as intelligence,
intuition, tactile skills, communication skills, and an
artistic view of the world, are great natural advantages.
A unique approach to problems of disfigurement and
deformity is what ultimately differentiates the plastic
surgeon from other practitioners.
EXTERNAL GOODS
External goods are the temptations that challenge and
interfere with excellence in professions and practices.
Examples of these external goods are prestige, power,
and wealth. Practices are not techniques for pursuing
extrinsic goods. Most persons enter the profession of
medicine motivated, at least in part, by altruism. Altru-
ism is difficult to sustain, and cynics observe that even
altruism has conflicting motives, such as achieving the
admiration and praise of others. However, prestige can
become seductive. It can be motivating to experience
pleasure from prestige and recognition from a com-
munity of peers. With prestigious positions, there exists
an element of power—the power to bestow favor and
perhaps to influence society. Whereas recognition is
pleasurable, it remains an external good and does not
make the recipient a better or more virtuous surgeon.
Wealth is the third and most obvious external good.
For centuries, physicians were compensated, but few
became rich. Much has changed, and the relationship
of physicians with patients and third parties has pre-
sented a whole new set of ethical issues. Some sur-
geons can and do become rich. The costs of becoming
a plastic surgeon are immense, not only in the direct
cost of medical school but also in the cost of oppor-
tunities that were missed during the years of school-
ing and residency. The need to retire substantial debt
is often a major determinant in choosing the type and
location of a practice. However, it is also true that the
business of the specialty has often transcended the
necessity to provide substantial wealth. The plastic
surgeon has, in aesthetic surgery, an almost unique
opportunity to practice largely outside the organized
health care delivery system and is constrained only by
the marketplace. To expand the business of plastic
surgery by sales and marketing techniques is tempt-
ing. All business schools devote considerable time in
the curriculum to advertising, marketing, and
diversification of product-line. These are all factors
that do not make one a better surgeon and may, in
fact, cause ethical conflict because they are inconsis-
tent with the internal goods of the profession.
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6 • ETHICS IN PLASTIC SURGERY 101
APPLICATION OF
ETHICAL THEORIES
Religious and philosophical concepts serve as the basis
for ethical theory. It is not surprising that the appli-
cation of theory also presents complex problems.
Fundamental to the approach of ethics has been the
exploration of ideas of utilitarianism^ deontology, and
the role of authority in applying morality. The limi-
tation of these approaches has been described as emo-
tivism, an approach to ethics reduced to individual or
group preference. The exploration of virtue and the
application to the internal goods of professionalism
are even more integral to self-regulation and moral
behavior. The practice of medicine has often been a
solitary pursuit, and even now many practice alone,
often outside the scrutiny of the health care system.
Principlism and Rules-Based Ethics
The four main principles of modern medical ethics
are beneficence, nonmaleficence, autonomy, and justice
(Table 6-3). These principles represent an efficient cat-
egorization of many historical and disparately applied
religious and philosophical approaches. Most courses,
even comprehensive ones, begin with these solid prin-
ciples of applied medical ethics. Even though these prin-
ciples are often referred to as rules, they are not series
of statutes or regulations. These principles are not a
formula for simple answers to complex questions.
BENEFICENCE
Although not necessarily the most fundamental of all
ethical principles, beneficence is the cardinal, almost
paradigmatic, ethical principle for medicine. Many
would say it is the greatest, and if this principle were
regularly applied, no other ethical principles would
be needed. A variation of the Hippocratic Oath is
recited at graduation by almost every medical school.
Most prominently in the Oath is the charge, "I will
apply, for the benefit of the sick, all measures which
are required . . . " 6
TABLE 6-3 • FOUR MAIN PRINCIPLES OF
MODERN MEDICAL ETHICS
Beneficence The moral obligation to act in the
best interest of others (patients)
Nonmaleficence The moral obligation to protect
patients from harm and
negligence
Autonomy The recognition that ail persons
have an unconditional right to
determine their own destiny
Justice The recognition that goods and
services should be fairly
distributed among all citizens
102 I • GENERAL PRINCIPLES
The importance of beneficence to Beauchamp and
Walters20 renders it one of the prima facie principles
of biomedical ethics. The broadest concept of bene-
ficence is the moral obligation to act in the best inter-
ests of others and includes mercy, love, altruism, and
charity. It underlies the theory of utilitarianism.
The greatest happiness for the greatest number is a
broad application of beneficence> as is to do good for
ones neighbor. The Christian narrative of the Good
Samaritan exemplifies the application:
A man was on his way from Jerusalem down to Jericho when
he was set upon by robbers, who stripped and beat him and
went off and left him half dead. It so happened that a priest
was going by and when he saw him passed by on the other
side. So too a Levite came by and passed on the other side.
But a Samaritan, when he saw him was moved to pity, went
up and bandaged his wounds, bathing him with oil and wine.
He brought him to an inn and paid for his further care.
(Luke 10:30-37.)21
This is beneficence; the care bestowed was kind and
delivered by a stranger. The stranger, historically, would
have been considered an enemy of the injured trav-
eler. In armed conflicts, the medical care rendered by
both sides to captured combatants is expected to be
skillful and beneficent. Both the motives and the acts
themselves are beneficent, devoted to good. Beneficence
is applied by asking one not only to treat another as
you would wish to be treated but also to exercise a
degree of selflessness that approaches an ideal and is
not merely a fulfillment of obligation. Mother Teresa
is widely regarded as a modern Good Samaritan. The
donation of a kidney to another, even a stranger, is an
example of extreme beneficence. The role of a physi-
cian and surgeon, although it does not regularly
demand such a degree of self-sacrifice as a condition
for professionalism, does imply that one act for the
benefit of another. From the beginning of medicine,
patients and society have assumed that one's individ-
ual physician and surgeon would always act in the
patient's best interest. The nature of the principle
of beneficence is perhaps more clearly understood
in relation to the second prima facie principle,
nonmaleficence.
NONMALEFICENCE
The Hippocratic Oath continues with the following:
"I will keep them from harm and injustice."5 Non-
maleficence, as described in the Oath, directs that
patients be protected from harm and injustice and, by
implication, that the physician and surgeon should
not injure a patient. The idea of protecting the patient
from harm is a broader responsibility than merely being
cautioned against doing harm. The widely quoted
maxim primum non nocere (first, do no harm) is not
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actually in the Hippocratic Oath, and its origins are
not totally clear. It is difficult conceptually to separate
beneficence and nonmaleficence because the definition
and exposition of one demand attention to the other.
One should do good; one should not do evil. These
concepts are so central to what constitutes due care
that they are, when breached, the basis for professional
malpractice.
Sadly, the duties imposed by these principles are
sometimes more clearly expressed when they are
violated. Beauchamp and Childress22 express this as a
failure of care or negligence when "the professional
has a duty to the affected party, the professional
breaches that duty, the affected party experiences a
harm, and finally, the harm is caused by the breach of
duty." Although this description maybe of a legal stan-
dard, negligence, it also represents a moral and ethical
standard of behavior. What is a good and what might
constitute harm is subjective. The middle of the 20th
century ushered in dramatic changes in care. One
example of a technological change is the respirator.
Respiratory failure, unless it is almost immediately
reversed, leads to death. However, respirators repre-
sent a common fear of many people who are opposed
to the idea of having their lives sustained in this manner.
In the face of complex decisions, the traditional power
of the physician to decide what is the good for an indi-
vidual patient is no longer acceptable. The concept of
beneficence in practice risks inadvertent paternalism
on the part of the physician. Many older physicians
grew up in an era in which informed consent often
involved no more than the patient's affirming that
the physician should do whatever was thought to
be best. The recognition of the patient's right to self-
determination has limited the historical responsibil-
ity of the surgeon to "do the right thing."
AUTONOMY
The concept of autonomy or self-determination has
acquired many meanings. These definitions include
liberty, rights of privacy, individual choice, freedom
of will, and the right to decide what is done to one's
body. Kant, in his theory of deontology, argued that
autonomy flowed from the recognition that all persons
have unconditional worth and that each has a right
to determine one's own destiny. To violate another's
autonomy would be to treat the person as a means
and not as an end. Moral philosophers and the legal
system in the United States grant wide latitude in allow-
ing individuals to determine their own life's course
and actions, including the right to refuse all medical
care even when such a refusal will result in death. The
doctrine of informed consent evolved from the prin-
ciple of autonomy. For a person to act autonomously
in making decisions about a proposed surgical pro-
cedure, the individual must have sufficient informa-
l ^ t t f ' a e l c r K f image...
tion and the capacity or comprehension to make a
decision.
Informed Consent
SUFFICIENT INFORMATION. A person making a
decision about his or her health and well-being must
have adequate information about the nature of the
intervention as well as risks, possible benefits, and alter-
natives. The standards for what is appropriate infor-
mation vary. In some countries, the standard is still
that which most "prudent" surgeons would provide
their patients. In the United States, the standard is what
the "prudent patient" would want to know to make
an informed decision. In some states, there is a more
difficult requirement that insists the information be
tailored to the need of individual patients, to their
ability to process information and develop under-
standing. The level of disclosure and opportunity for
reflection vary with the circumstances, complexities,
and dangers of the intervention. In emergencies, con-
sent may be assumed for lifesaving procedures. When
there is more opportunity for communication and dis-
cussion, more information is, of course, required.
When the patient is being considered for new, inno-
vative, or experimental procedures, the discussion
must be detailed and formal. When residents are to be
involved in any procedures, the nature of their respon-
sibility must be made entirely clear to patients.
The provision of sufficient information is a moral
and ethical imperative; how it is documented is a
medicolegal consideration. In the early developmen-
tal days of gender transformation surgery, the com-
plexities of the condition and the nature of the
procedures made it necessary for many persons to be
involved. Confirmation of the process made video-
taping of the entire consent process appropriate.
Many legal experts continue to point out that even
though documentation may seem adequate, the
patient's understanding and expectations are often a
pivotal issue in malpractice litigation. Perhaps the most
common tendency of patients is to underestimate the
amount of discomfort encountered after surgery and
minimize the severity of potential complications.
DECISIONAL CAPACITY. The process of informed
consent implies a two-part phenomenon. No amount
of information is sufficient if the patient or those
responsible for making the decision do not compre-
hend what is presented. The patient may not be capable
of understanding the information because of age, edu-
cational background, language, or cultural impedi-
ments. A diverse population in this country or in
another where a surgeon may be participating in a
humanitarian mission presents a particular challenge
in attempting to provide sufficient information to
patients. Although the legal issues might be less
oppressive, the ethical responsibilities are in no way
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6 • ETHICS IN PLASTIC SURGERY 103
reduced. In a pluralistic society, many will bring reli-
gious or cultural traditions that are in conflict with
the information presented. For example, the family's
belief that a cleft lip and palate deformity is the result
of invasion by some evil spirit may be so strongly
held that acceptance of a scientific explanation is
incomprehensible.
Patients may not be able to understand informa-
tion because of temporary mental incapacity as the
result of chemical intoxication, fever, concussion, or
other passing conditions. Their ability to understand
may be permanently compromised by mental illness.
In such instances, surrogates are necessary. For some
patients, information may evoke such a degree of
anxiety that further information cannot be assimilated
and incorporated. The diagnosis of cancer may cause
this type of anxiety, and it is known that discussions
about treatments might best be deferred until a later
visit. Similarly, the discussion of breast reconstruction
with a patient who has just been informed that cancer
is present may be delayed. Reconstruction may seem
unimportant when a patient is faced with the choices
of treatment to be considered and evaluated, even if
it will have a major influence on the decision regard-
ing primary treatment.
The surgeon must do more than merely relay infor-
mation. Failure of the patient to comprehend may be
related to the technical information presented, even
though the surgeon may think it is being presented in
simplistic language. Because some patients may wish
to please the surgeon, they may appear to understand
when they are actually confused. The process of pre-
senting information and ensuring that the patients and
families understand is sometimes better handled by
other members of the surgeon's team who can take
more time with the patient and have a less authorita-
tive presence.
• S C E N A R I O : B A D L Y
B U R N E D P A T I E N T
An 18-year-old is brought to the burn unit by the emer-
gency services. He sustained a 60% total body surface
area burn, all of which appears to be full-thickness
injury. Possible upper respiratory injury required
the insertion of an endotracheal tube. The patient
requires emergency decompressing escharotomies
and possible fasciotomies to the extremities.
During the initial period in the care of this patient,
emergency medical technicians are granted consider-
able latitude in performing lifesaving maneuvers,
such as establishing an airway and gaining vascular
access. A physician who happens by the scene is encour-
aged to participate and is legally protected, except for
104 I • GENERAL PRINCIPLES
the most egregious acts of negligence or abandonment,
under Good Samaritan legislation. From the moment
the patient arrives at the hospital, however, issues of
autonomy and informed consent must be considered.
Because the patient is in no position either to receive
or to process information in the early period of his
injury, every effort to gain consent from surrogates
must be made, and the surgeons should minimize the
degree to which they act independently. When imme-
diate family or other surrogates are not initially
available, the legal surrogate is the hospital and its
designated administrator. Thereafter, the surrogate
must be identified, and when there is a question, the
law usually provides a surrogate or the way for the
court to appoint one. This circumstance presents a
challenging situation for identifying when, during the
course of the recovery process, the patient gradually
becomes individually responsible for decision-making.
Mr. Dax Cowart was severely burned in 1973, and
his care and struggles with the issues of his autonomy
were filmed.23 The surgical care rendered was exem-
plary, and the patient's mother and attorney were both
supportive of the health care team. Mr. Cowart became
very discouraged and determined, a year into his care,
that he should be allowed to die. Mr. Cowart's case
has since served as a paradigm in medical ethical dis-
cussions.24 The patient presented in the scenario had
an injury similar in severity to Dax Cowart's, and
although surrogates must be immediately identified,
it should not be forgotten that this patient will also
regain consciousness and with it the desire and ability
to aid in decision-making. The tension between Mr.
Cowart's autonomy and the effort to act beneficently
is powerful and poignant.
Confidentiality
What a patient tells the physician or surgeon is private
and should not be divulged to others without the
patient's permission. The Hippocratic Oath specifies,
"What I may see or hear in the course of the treatment
or even outside of the treatment in regard to the life
of men, which on no account one must spread abroad,
I will keep to myself, holding such things shameful to
be spoken about." 5
The responsibility for confidentiality is shared by
other professionals, such as attorneys and clergy. The
surgeon has an ethical responsibility to the patient and
to society to maintain an accurate record of the patient's
condition and care. To share information with others
not held to such standards of confidentiality violates
the patient's privacy and right to confidentiality.
When third-party payers, particularly the government,
became involved in the physician-patient relationship,
the requirements for information became intrusive but
are considered legitimate for purposes of authorizing
compensation. Surveys have shown that in the hos-
pital setting, as many as 100 persons may have a right
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Dr.Mustafa D.
to review a patient's medical record. Modern infor-
mation technology and computerized medical records
may expand access to a patient's record to many more.
This may be appropriate for those whose medical con-
ditions (e.g., diabetes or heart disease) require com-
plicated therapies and medications. Such medical
information is difficult to verbally convey to succeeding
caregivers. Those patients whose care is related to
mental illness, sexually transmitted diseases, AIDS,
or aesthetic surgery might be reluctant to have their
medical records accessible by computer. New privacy
rules have now been established by federal statutes
designed to protect the patient's confidentiality.
However, these may tend to make information too
inaccessible to health care providers. Good medical
care requires that an accurate record be maintained
and the patient's confidence in handling sensitive
personal information be protected.
In summary, autonomy recognizes individual rights.
It is an empowering concept that puts individual
patients in charge of their own health care. The rela-
tionship between surgeon and patient has changed into
one that is often more impersonal than in previous
eras. Such arrangements are uncomfortable for sur-
geons. A health care delivery system in which every
person has the freedom to choose the best available
type of treatment under all circumstances runs the risk
of failure of expectations and resentment.
JUSTICE
The imagined surgical ideal of doing "good" for all
patients and refraining from causing or allowing
harm is not possible. The goal of providing perfect
information to all patients who are, in turn, able to
comprehend and act wisely on such information is
also not possible. The best treatment or operation for
any given situation cannot always be known. The
concept of providing the best care to every patient as
an ideal is also seductive, but the reality of finite and
limited resources cannot be ignored. This recognition
that autonomy is limited by the rights of others
describes the principle of justice. John Rawls25 argues
that rational people would agree that all individuals
should have equal rights including basic liberty.
Although autonomy is critical, it is limited by the rights
of others. Justice can take several forms.
The concept of "distributive justice'* is based on the
belief that as nearly as possible, necessary goods
should be provided to all citizens. The basic freedoms
of individuals in the United States are life, liberty, and
the pursuit of happiness. There is an expectation that
all will be treated equally under the law, be free from
unreasonable search and seizure, and have fundamental
needs of shelter and food provided. Added to this are
the basic necessities of a free society, such as police
and fire protection, as well as public education and
TfeW*tf(9eld,!# image...
health care. When there is a sufficient supply of goods
available, even the most destitute in American society
can gain access to food and at least temporary shelter.
Most of society desires that necessary health services
also be available. Some argue that such services con-
stitute a right When some service or good becomes a
right, this promotes an obligation to provide that good
or service. The obligation may become a mandate to
a provider who cannot, thereafter, legitimately with-
hold the goods or services from those who have a right
to access them. Firemen and policemen must be avail-
able to fight fires or crime even if it is inconvenient
or dangerous. Society also expects at least emergency
health care to be available at all times.
It is a matter of justice to determine how to dis-
tribute scarce medical resources.26 Human organs are
a good example of a scarce resource. Distribution based
arbitrarily on race, gender, ethnic background, or some
other class distinction is a violation of ethical reasoning
and against public policy. Distribution of lifesaving
resources based entirely on queue unfortunately leads
to the death of some patients before they reach the
top of the list. Distribution based on severity of illness
is not purely objective and results in organ distribu-
tion to only the sickest who have the least chance for
success; others who might profit are deferred until they
are sick enough or possibly too sick. Distribution based
on ability to pay is not acceptable, although an inabil-
ity to cover costs one way or another often does exclude
some patients. Distribution based on a market model
of buying and selling organs, for example, is currently
against public policy. Distribution based on age may
not be attractive to senior citizens. However, if senior
citizens were considered part of an entire class, this
distribution would seem to be morally acceptable. Dis-
tribution that excludes persons because of undesir-
able behavior, such as criminals or alcoholics, is more
problematic since choosing persons on the basis of
their past or future value to society is subjective. Dis-
tribution based on a lottery may seem frivolous but,
in fact, maybe the most just approach. In this system,
as the pool of persons deemed eligible for transplan-
tation is identified, each person in that group is
randomly assigned a number. When a donor organ
becomes available, a patient's number is randomly
chosen. Such an approach would randomly choose
favorable as well as unfavorable candidates.
The discussion of organ transplantation is an
example of problems in the current health care system
with limited resources. Although it is true that public
services are not provided equally, all citizens should
be provided with police and fire protection. All persons
should receive public health benefits such as clean
water, vaccination against communicable diseases, and
oversight of safety in the workplace. Unfortunately,
not all persons can receive a liver transplant, no matter
how ill or deserving they may seem.
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6 • ETHICS IN PLASTIC SURGERY 105
The issue of justice in the health care system is
a very real ethical concern for plastic surgeons. As
decisions are made about resources, such vague and
ill-defined terms as necessary, medically indicated, and
elective are often used as criteria for inclusion. Much
of the work in plastic surgery falls outside the common
perception of what these terms mean. There is the risk
that plastic surgeons will not be included in major
policy decisions because such terms as necessary are
not thought to apply to their services.
Rules-based ethics have become the "gold standard"
for medical ethicists when the prima facie principles,
including justice, are discussed. The advantage of rules
is that they can objectify some situations The Con-
stitution is the standard for identifying how Ameri-
can society should be established and what rights and
privileges should be accorded to individuals. In general,
if all citizens agreed on what is right and what is wrong,
and if they behaved morally, law would be unneces-
sary. If individual practitioners agreed on what is ethical
and chose to behave ethically, much of rules-based
ethics would be unnecessary. Conversely, when prac-
titioners violate ethical norms, no amount of law or
regulation can identify and discipline them all.
Casuistry
An additional systematized model and approach to
ethics is casuistry. Casuistry means simply "case based"
and involves a search for clinical examples with which
individual ethical problems can be compared. 27 Virtue
ethics describes professionalism in rather broad strokes
that relate primarily to individuals; virtue is difficult
to apply to specific circumstances. Most ethicists are
also not completely comfortable with basing decisions
solely on principles such as beneficence or autonomy,
particularly since almost all difficult ethical issues
involve competing principles.
- • • S C E N A R I O : THE
B I R T H D A Y OF
I N F O R M E D C O N S E N T
Martin Salgo was a 55-year-old man who went to Stan-
ford University Hospital in 1954 with symptoms of
intermittent claudication. A relatively new procedure
at the time, aortography, was performed, and Salgo was
subsequently paralyzed from the waist down. Justice
Bray, in adjudicating a negligence suit brought against
the institution, observed that "a physician violates his
duty to his patient and subjects himself to liability if
he withholds any facts which are necessary to form the
basis of an intelligent consent by the patient to the
proposed treatment." {Salgo v Leland Stanford, Jr.,
University Board of Trustees, 317 P2d 170 [Cal Dist Ct
App 1957].)
106 I • GENERAL PRINCIPLES
This landmark legal case, decided on October 22,
1957, is considered the "Birthday of Informed
Consent." Some of the strongest Iundamentals of ethics
are contained in narrative such as that of Mr. Salgo.9
He argued that he was not told ofthe dangers of aor-
tography, such as the possibility of paralysis, and that
he had no opportunity to refuse the test on the basis
of unacceptable risk. The power of the sacred story or
myth to influence people has been a major part ofthe
foundation of religion. The Bible describes ethical
behavior in the form of stories, parables, or prophe-
sies. The example of the Good Samaritan instructs
behavior toward those in need, even if the person is
a stranger or an enemy. Martin Luther nailed his
protests to the door of the cathedral at Wittenberg,
and the Reformation was under way. Centuries later,
Martin Luther King, Jr. led a civil rights revolution
through nonviolent protest. In our system of govern-
ment, the Constitution has served as the foundation
for Law, but the application of that law is often in the
form of landmark cases. Brown v Board of Education
eliminated "separate but equal>y public education, and
Roe v Wade established the right to abortion. These
cases are examples of casuistry. They are landmarks
that set precedents to which future cases and patterns
of facts will be compared and then followed or
distinguished.
Precedent-setting situations, such as Salgo, have
been the cornerstone of modern bioethics.28 In the
Karen Ann Quinlan case, an unconscious patient in a
persistent vegetative state was maintained on artificial
life support. Her story and the legal processes that fol-
lowed established criteria for whom and under what
circumstances such life support can be withdrawn. The
case of Nancy Cruzan, in similar circumstances,
explored issues related to maintaining or withdraw-
ing artificial nutrition. The description ofthe lost and
now found sponge at the beginning of this chapter
exemplifies such issues, including the difficulties and
consequences of truth telling. A case could theoreti-
cally be compared with the facts or narrative of
previous cases to predict whether a plaintiff could
successfully pursue a cause of action.
One of the criticisms of casuistry dates back cen-
turies: there are few universal truths. The idea of and
search for moral absolutes is difficult, and although
genocide, slavery, and rape seem to be without any
moral justification, other ethical questions are complex
with mitigating circumstances that might change the
application of any rule. There is, in practice, no true
ethical algorithm that can be followed in all instances.
Ethics committees sitting in hospitals or regional and
national organizations have broad representation of
physicians, nurses, and interested parties from the com-
munity, some of whom may have no exposure to formal
ethical reasoning. The study and discussion of cases
involving similar facts have served as the basis for
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Dr.Mustafa D.
recommendations made by these committees. The
use of narrative and the study of similar cases have,
as in the legal system, made casuistry one of the best
approaches in determining how to manage some
difficult questions. There are few absolute ethical
truths. Similarly, there are always new situations and
new ethical dilemmas.
Ethics of Care (Feminist Ethics)
Virtue ethics emphasized the importance ofthe indi-
vidual "character" qualities of those involved in prac-
tices and the professions. The ethics of care, also called
feminist ethics, similarly looks to character traits as
the foundation of ethics. It looks through a more
personal lens at the importance of relationships and
emphasizes compassion, sympathy, fidelity, and love.29
It recognizes that the caring labors include minister-
ing to the needs of the young and old, the sick and
dying, and the frail and dependent, "securing and
reproducing through paid and unpaid labor many basic
conditions of life for legions of fully able persons."
Such care falls disproportionately to women. Carol
Gilligan30 challenged descriptions of moral develop-
ment, particularly subjects of justice and care. She
described a "different moral voice" in women's inter-
pretation of the structure of moral reasoning and
commitment to certain moral values such as caring.
In addition to caring, it is an ethic of accepting respon-
sibility for others.
The situation most often described is that of the
mother gazing at her infant; it recognizes the
unqualified positive nature of the relationship. A
mother rarely needs to be told to be beneficent toward
her infant, nor does she need to be admonished to do
no harm. It is a major and shocking news item when
a mother purposely injures her child. Much of health
care has traditionally been given by religious persons
who offered their services because of a religious
calling. Care ofthe disfigured, the disabled, the severely
crippled, and the aged is also, fundamentally, a labor
of love. It is most satisfactorily based on love of the
patient by a family member or by one devoted to God.
The willingness to devote oneself to the "underpaid"
service of others, whether it is in the care of the chil-
dren in one's home or serving in the armed forces to
defend a nation at war, represents the convenient social
virtues. Others who exemplify these services or social
virtues are elementary school teachers, firemen, police-
men, and those who deliver social services. These
persons are never compensated monetarily propor-
tionate to their contribution to society. Those in reli-
gious life, the priests, ministers, rabbis, and imams,
are expected to be available to the suffering at the most
critical of life's moments and with essentially no
financial remuneration. For much of history, nurses
were trained in religious orders and worked at little
VtJWR^SeldW image...
societal cost. But times have radically changed. Third-
party insurance, a product of the last 50 years, has
established an expectation among physicians, partic-
ularly surgeons, of due compensation for work per-
formed. A segment of society continues to expect that
physicians should be available like firemen, policemen,
and clergy. Physicians should be available, particularly
in emergencies, even if they are not paid. There is a
continuing tension between the fundamental criteria
of professionalism and the harsh demands of a
marketplace.
The concept of an ethical standard based on a
mother-child dyad might not seem applicable to less
intimate relationships such as health care. Some might
also argue that there are major gender differences in
ethical approaches. Men are thought to be more
dependent on and respectful of such concepts as
courage, honor, and the rules of law. An ethic of caring
might seem to apply more to feminine emphasis on
attunement, empathy, and relationship. Contrary to
these more stereotypical expectations, an ethic of
mutual caring serves as a model used by the United
States Marine Corps and other branches of the mili-
tary. The respect and care for a person on whom one
might depend for survival is a powerful incentive for
mutual care. A tradition in the military is that no fallen
comrade will be abandoned on the field of batde, and
laying down of one's life for another is also part of
honorable warrior tradition. Much of the basis for pro-
fessionalism in physicians and surgeons, nurses, and
ministry, as in the Marine Corps, could be considered
an ethic of caring.
ETHICAL PROCESSES
Ethical decision-making is most often an informal,
almost instinctive process (Table 6-4). It primarily
involves the surgeon's individual ethical values and the
needs and rights of individual patients. The day-to-
day practice of plastic surgery requires multiple small
ethical decisions that are handled individually and
TABLE 6-4 • ETHICAL PROCESSES/
DECISION-MAKING
Impartiality The interests of every person
should be understood, and the
decision-maker should consider
the consequences for each
person as if he or she were in
that person's position
Consistency An understanding and application of
standards of actions and results
Precedent setting The recognition that ethical
decision-making often sets
precedents because of the
subjective nature of ethical issues
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6 • ETHICS IN PLASTIC SURCERY 107
instinctively. The larger and more complicated ethical
questions usually involve others and fortunately yield
time for reflection and deliberation. Although ethics
may lack some of the precision of science, decisions
should be subjected to intellectual rigor. Related to
the advice to spread the problem among others is the
recognition that ethical problems might involve a sense
or at least a fear of having done something wrong.
This is when sharing the dilemma with trusted
colleagues can help one gain perspective and support
as well as a clearer view of options.
• S C E N A R I O :
A Q U E S T I O N OF
C H A R A C T E R
A junior resident from a nearby training program is
rotating with you and your partners to gain experi-
ence in a broad, rounded group practice situation. Your
administrator confides to you that the resident has
become sexually involved with one of your young nurse
assistants in the office and that they may be sharing
"recreational" drugs.
This situation is presented not so much to eluci-
date the specific issues of possible sexual misconduct
or the use of illegal drugs but to examine the processes
for handling a complex problem. An informal dis-
cussion with the resident is unlikely to rectify under-
lying issues. Simply dismissing him with instructions
to return to his program director is also insufficient.
Although most problems may be less complicated than
this scenario, the approach to ethical problems should
be reflective, impartial, and consistent. Decisions
involving residents and colleagues may also be used
as precedents in subsequent situations.
Impartiality
One would likely become angry at a resident taking
advantage of generosity and trust in a clinical setting.
It threatens the reputation of the group and may endan-
ger care of patients. It is not to be taken lightly, but it
is also, as with most ethical problems, not to be handled
impulsively or on the basis of emotion. There are many
stakeholders in this situation: the program director,
colleagues, the resident, and the office staff. All of these
persons should be involved in the process to make it
impartial as well as fair and transparent. If the disci-
plinary process is reviewed by outsiders, it can then
be demonstrated that it was appropriately conducted.
John Rawls25 established an approach to ethical issues
in which participants would stand behind a figurative
veil of ignorance. This concept does not refer to opacity
that would hide the facts. In this scenario, the process
108 I • GENERAL PRINCIPLES
of handling the resident would be so fair that were
one assigned to stand in the shoes of any of the par-
ticipants, after the veil was lifted, the process would
appear to be and actually would be fair. The interests
of every person should be understood, and the deci-
sion-maker should consider the consequences for each
person as if he or she were in that persons position.
In dealing with individual patients, it is similarly
difficult to be impartial. It is inherent to the situation
that the relationship with patients always involves a
conflict of interest. Surgeons are rewarded more for
operating than for not operating. Surgeons cannot be
totally impartial observers; they are participants. The
decision to operate in aesthetic surgery may not be as
clear as in other circumstances. It is subject to the
surgeon's expertise, comfort level with the procedure,
and interpretation of the patient's suitability. One of
the ethical principles described before was deontol-
ogy, the observation that one should act so as to be
able to universalize your action without contradiction.
In other words, an operation should not be performed
unless the surgeon would be willing to perform the
same procedure on all persons with the same condi-
tion or even, perhaps, to have it performed on himself
or herself.
Consistency
Impartiality is a broad and fundamental issue focus-
ing beyond the specific individuals involved. Since the
decisions extend beyond the principals, the decisions
must also be consistent. Although one should not have
to anticipate a series of misbehaving residents, one
should also not treat the situation in such a way as to
assume it is unprecedented. All of science, biology, and
even the highly individualized nature of plastic surgery
assume there is some standard to actions and results.
Incisions can be expected to heal in a predictable
fashion; infections can be minimized by employing
sterile techniques, and excellent results are reproducible
with careful planning and well-conducted surgical care.
Surgical knowledge is cumulative and built on the
surgeon's own experience as well as that of others.
Ethics, as a discipline, also has its own accumulated
body of knowledge derived from religion, philosophy,
and the experience and wisdom of our predecessors.
Precedent Setting
In addition to impartiality and consistency, there is
the recognition that ethical decision-making sets
precedents. As in the judicial system, there is some
latitude in deciding ethical issues. The concept of an
eye for an eye was not a literal charge to effect cruel
punishment. Rather, it directed that the punishment
should be proportionate to the situation. One of the
concerns with the current system of compensation for
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medical malpractice is that despite its legality, it does
not always follow appropriate ethical processes. The
adjudicators are not always impartial, nor do they stand
behind Rawls' veil of ignorance. The decisions are not
consistent from case to case and sometimes seem
frivolously inconsistent, arbitrary, and capricious.
This makes the use of precedent almost impossible.
Finally, tort litigation for medical negligence does not
rely as heavily on precedent as other civil or criminal
proceedings do, and the settlements are unpredictable.
ETHICS FOR PLASTIC SURGERY
Much of the discussion of ethical principles, theories,
applications, and processes may seem to apply more
to universal ethical situations than to individual plastic
surgeons. Plastic surgery shares some basic charac-
teristics with all surgery, but it is also an artistic
specialty that demands a high level of technical per-
formance. As with all of medicine, the primary respon-
sibility must always be toward the individual patient
who comes under a surgeon's care. This responsibil-
ity contains all the elements of professionalism and
the principles contained within the Hippocratic Oath,
and yet the responsibility is perhaps greater because
plastic surgeons, especially cosmetic surgeons, often
see a different type of patient—one who is often normal
and well.
Aesthetic Surgery for
the Healthy Patient
• SCENARIO:
NASAL CONTOUR
IMPROVEMENT
A healthy 15-year-old girl comes to a plastic surgeon
for aesthetic improvement of her nose. There has been
no injury, and her airway is perfect. The dominant
physical characteristic is a prominent nasal hump.
Plastic surgeons have entered, almost uniquely, into
the complex world of operating on healthy patients
for purposes of improving or enhancing specific char-
acteristics. As a specialty, aesthetic surgery is defined
as that which is conducted on essentially normal tissue
for purposes of improving or enhancing appearance.
This definition excludes tissue injured by burns or lac-
eration. Although damaged tissue may be healed and
surgery performed for enhanced appearance, it is not
considered aesthetic surgery by definition. Correction
of tissue laxity resulting from normal aging processes
is paradigmatic of aesthetic surgery. In between these
examples are a number of gray areas of normalcy and
aesthetics; enlarging breasts that are too small is con-
mage
sidered aesthetic surgery, and reducing those that are
too large is not aesthetic. The scenario of the 15-year-
old patient is an example of purely aesthetic surgery.
Enhancement surgery has profound ethical implica-
tions beyond the rather narrow applications in aes-
thetic surgery. Eric Parens, 3 ' in reviewing the issue of
enhancement, began with the ethical dilemma of a
young boy who is doomed to grow up too short because
of a growth hormone deficiency. He is compared with
a normal boy who has very short parents and is pre-
dicted to grow to exactly the same height as the other
boy. What is the distinction in determining that the
former is deserving of treatment with growth hor-
mones whereas the latter is not? Will the ultimate
suffering from being too short not be the same?
Would a young girl with a nose that was injured in an
accident, but without breathing problems, be more
deserving of a rhinoplasty?
The very fundamental definition of health and the
goals of medicine are brought into question. Some
would argue that disease and disability are departures
from normal and that the goal of medicine should be
only to maintain, restore, or compensate for loss of
function caused by disease or disability. Consistent with
this argument, burn scars should be revised, but only
to functionality. If the scar is not distorting and pre-
venting closure of the eyelid or lips, for instance, cor-
rection of burn scars for the sake of appearance alone
would not be warranted. The goal of medicine would
be to restore but not to enhance.
There are others who would argue, more expan-
sively, that health is a state of complete physical, mental,
and social well-being and would justify any effort to
achieve this ideal. One problem with these definitions
and their distinctions is how to apply them to broad
health care decisions and the distribution of limited
resources. The goal of complete well-being may be
beyond any society's ability to define, much less
deliver. The ethical issue of fairness cannot be ignored;
are the new advances available only to the rich and
privileged few? Additional questions in this line of rea-
soning would include not only enhancement surgery
but also the use of developing biotechnology. Should
genetic technology, for instance, be used only to
reduce suffering from severely deforming or debili-
tating conditions, or should it be used to enhance some
characteristics for those so inclined? There is no ques-
tion that the issues of "normalcy" are based in culture
and society.
The situation of the healthy person requesting
enhancement surgery places additional ethical respon-
sibilities on plastic surgeons. The first of these addi-
tional responsibilities is as teacher. The word doctor
means teacher and implies a primary responsibility.
The subject of enhancement surgery to improve on
what society deems normal requires additional efforts
on the part of plastic surgeons to be teachers of patients.
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6 • ETHICS IN PLASTIC SURGERY 109
The level of success demanded in such surgery is daunt-
ing. Complications must be reduced to levels lower
than what might be acceptable in more traditional
surgery. The surgeon must provide the patient with a
degree of information and ensure a degree of under-
standing beyond what would be acceptable for other
types of surgery. Finally, as an ethical imperative, a
surgeon must, at all times, refrain from soliciting or
coercing patients into undergoing such surgery.
A second special role is that of plastic surgeon as
technician. During much of a plastic surgeon's form-
ative years in preliminary surgical residencies, there
is usually a subtle disparagement of the plastic surgeon.
There is an implication that this course is less than
that of the scholar or the true physician. However, there
are no more than a few thousand people in the world
capable of the conceptual and technical abilities of the
plastic surgeon. Although surgeons must, of course,
be empathetic and caring, the primary accomplish-
ment of the plastic surgeon is an excellent technical
result. A kind, caring, understanding manner assists
in caring for a patient with suboptimal results; however,
superb results are acceptable even from the nonem-
pathic surgeon. To be a highly skilled technician is an
ethical imperative for the plastic surgeon.
Professionalism
Almost from the beginning, physicians and surgeons
have cherished their collegiality. True professionals are
intrinsically dependent on developing the internal
goods exemplified by the virtues of practices. These
virtues will also dispose an individual toward fair,
honest, and equitable treatment of colleagues. The dis-
tinction between ethics and manners or merely good
etiquette is not always clear. Professional courtesy was
an example of etiquette; economics have made it
difficult for almost all care providers, especially plastic
surgeons. With respect to colleagues and to society,
plastic surgeons have a responsibility to determine the
competence and safety of their colleagues. Privileges
and responsibilities of professionalism require that the
profession be self-regulating. Plastic surgery is one of
the primary specialties of medicine with its own body
of knowledge, both conceptual and technical. It is a
unique specialty, but it carries with it the implication
that only a plastic surgeon can determine whether
another plastic surgeon is competent.
COMPETENCE
Although competence is broadly understood by all, it
is difficult to define. Competence in plastic surgery
requires intellectual or cognitive knowledge, problem-
solving ability, an artistic view of the world, and tech-
nical skill. Competence also demands character traits
such as honesty, integrity, dedication, courage, and
110 I • GENERAL PRINCIPLES
empathy. It is difficult to measure competence in the
training period; it is even more difficult to evaluate
among practitioners.
Residency Training and Board Certification
The value of outside oversight on the structure, cur-
riculum, and educational processes for residency
programs in plastic surgery is widely accepted. The
officially designated function of the Residency Review
Committee is to protect the interests and well-being
of residents, to prevent overwork and exploitation, and
to ensure that a fair standard of evaluation is employed.
This committee is not able to determine the compe-
tence of individual residents; that is the responsibil-
ity of the program and its director. Competence of
residents is based on cumulative experience and obser-
vation during 2 to 3 years, depending on the program
and the daily interplay of attending surgeon and res-
ident. In general, there are no specific criteria or exact
standards that must be met by residents. Cognitive
accomplishments can be measured by in-service and
other examinations. Problem solving and technical
ability are assessed by experienced clinicians. Charles
Bosk32 wrote insightfully about the general surgery res-
ident evaluation process and described how errors and
failings were identified and decisions made about pro-
motions in general surgery residencies. Resident and
faculty errors could be categorized into judgmental,
technical, normative, and quasi-normative categories.
Judgmental and technical errors are intuitively obvious.
Normative errors refer to criteria of behavior such as
honesty, dependability, and other similar standards—
in general, a resident's character. These traits are what
have been previously described as the virtues of a pro-
fessional. Quasi-normative behavior, decision-making,
and errors were vague and ill-defined. Evaluation of
normative errors is based on perceptions of how well
a resident is able to identify and fulfill an attending
surgeon's needs. The resident's performance may be
judged by such subjective criteria as willingness to be
early and stay late and, in particular, for not making
waves. Even though the residency evaluation process
is highly controlled, intensely interactive, and sustained
over considerable time, the ultimate criterion for eval-
uation is often more subjective than objective. If the
evaluation of a resident is indeed a subjective process,
it is no surprise that measuring the competence of prac-
ticing surgeons, particularly those outside of hospital
systems, is a difficult task.
The primary function of the American Board of
Plastic Surgery is the review of individual candidates,
all of whom have finished an accredited residency
program. After a period of practice and presentation
of data from a year of surgical experience, successful
applicants are accepted for a two-step, written and oral,
examination process. When the examination is suc-
cessfully completed, the candidate is certified as having
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met the standards for competence. A major weakness
of the system of training and examination is that
some persons fail to meet the minimum standards
to become certified. Although they have been fully
trained and licensed, they can practice without
certification. There are few or no sanctions or limita-
tions that apply to those without certification in plastic
surgery. Because certification is required for mem-
bership in all of the major plastic surgery societies,
these persons continue to practice outside any possi-
ble peer review. Public education to seek surgery from
board-certified plastic surgeons has been partially suc-
cessful, but some patients are not so sophisticated.
Peer Review
The immense effort expended in residency training
and by review and examination is designed to assure
the public that a surgeon designated board certified
meets the standards of competence established by our
specialty. This designation, until recently, lasted a life-
time. The assumption that any initial finding of com-
petence had lifetime endurance was no more plausible
or acceptable than to expect an airline pilot, once
certified to fly, to continue in competency indefinitely
and to be capable of handling all the new planes. It is
only in recent years that our specialty has accepted the
concept of re-certification, and even now, much of the
evaluative process will be limited to the cognitive mate-
rial that can be tested in a written examination. How
does one really measure the competence of a plastic
surgeon?
• S C E N A R I O : I N J U R E D
PLASTIC S U R G E O N
A 35-year-old board-certified plastic surgeon sustained
a serious head injury that rendered him unconscious
for days and left him with residual physical limita-
tions. When he requested that his privileges be rein-
stated, the Dean of the Medical School and the
Hospital Medical Staff Committee demanded that his
"competence" to practice be evaluated.
The challenges of identifying whether a surgeon
recovering from an accident or any other disability
requires evaluation of competence demand a unique
set of criteria. The surgeon in the scenario passed all
examinations with exemplary scores before and after
the accident described. However, evaluation of his
ability to relate to patients, to teach, and to operate
was more of a problem. His injury caused speech
difficulties that made him difficult to understand. This
was later often misinterpreted as speech impairment
due to drugs or alcohol. He devised a script to use on
introducing himself to patients that explained his con-
dition and encouraged patients to ask questions. His
T^Wttf<aelcrw image...
technical ability to suture wounds and to perform vas-
cular anastomoses was demonstrated first in an animal
laboratory. A psychiatrist who specialized in evaluat-
ing patients with head injury assessed his psycholog-
ical status. To determine his ability to plan, participate
in, and actually effect the judgment necessary to
perform plastic surgery procedures was a different
matter. To ask him to repeat a formal residency was
not fair or feasible. Suggestions that he seek an alter-
native specialty were demeaning to him and the other
specialty. A complex evaluative process was under-
taken. Fellow plastic surgeons agreed to involve him
in their procedures, explaining the situation to patients,
obtaining their consent to his involvement, and mon-
itoring him as he participated in their operative care.
At the conclusion of each patient encounter and oper-
ative procedure, a detailed evaluation form was com-
pleted. A special monitoring process was approved by
the hospital legal department because he was on dis-
ability and without privileges. Of course, he was also
without malpractice coverage. The entire process was
evaluated and approved by the human investigation
committee of the institution. Only two of a number
of fellow surgeons agreed to this time-consuming
process. However, after almost 9 months, the surgeon
regained his privileges. Discussion with the many
national and local organizations as well as the boards
and review committees indicated that this process was
without precedent. This scenario revealed the lack of
established criteria and standard processes for evalu-
ating practicing surgeons who may become compro-
mised by a disability. Few surgeons practice in large
university or group situations where these types of
resources are available. The circumstances of the
scenario described were unique. Such programs
are simply not feasible for a continuing evaluation of
practicing surgeons.
Despite the daunting challenges described, plastic
surgeons do have an ethical responsibility to be
involved in ensuring competence of those within the
specialty. Evaluative procedures are difficult to estab-
lish and validate and are often labor-intensive. The
process of observing and measuring residents in train-
ing involves many persons, almost day to day, over many
years. The challenge of participating in the evaluation
of residents as well as of other surgeons who have been
ill or injured is daunting.
DISCIPLINE
The situation of the injured surgeon and his compli-
cated re-entry process ended well. Many other sce-
narios involving questions of competence are not
resolved so well. In practice, surgeons are not evalu-
ated for their "hands-on skills" until some untoward
event comes to the attention of colleagues, hospital
legal staff, or others. Interventions are often informal
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6 • ETHICS IN PLASTIC SURGERY 111
and may result in resignation or reduced privileges.
There are several difficulties in assessing practice pat-
terns and outcomes to determine if a surgeon is prac-
ticing below an acceptable level. There are even more
complicated issues when effecting change is involved.
• SCENARIO:
PROFESSIONAL
STANDARDS
A plastic surgeon in a major university-affiliated hos-
pital had practiced for many years as part of a faculty
practice plan. Since she practiced in a specialized area,
no one else on the faculty or in the community had
the expertise to evaluate her performance. When a new
chief of service and several new faculty members joined
the institution, it became clear to them that her per-
formance was suboptimal. Informal but successful
efforts were made to reduce her privileges. When the
involved senior surgeons left the institution, her
privileges were restored.
The scenario described involved a form of peer
review that is common in many hospitals. It involved
"whistle-blowing" on a surgeon who had a long
history at the institution and many deep and long-
standing friendships based on shared training, prac-
tices, and institutional history. There are many other
situations in which practitioners may share ethnic and
cultural backgrounds that establish a special collegiality
and a sense of mutual protection. Since her practice
was specialized, she functioned below the radar, and
the other faculty members were not in a position to
judge competency because of their limited contact and
understanding of the current standards. Other plastic
surgeons were also not sufficiently familiar with
expected levels of performance and were not willing
to be involved. Residents may serve as an ongoing peer
review and alert system. Residents are in a precarious
position when they challenge faculty members,
however, since removing or failing to remove such
faculty puts the residents at risk of retaliation.
In the scenario of the injured surgeon, his colleagues
were put in a position of monitoring him with an
unparalleled degree of intrusiveness and intimacy. In
some groups, partners and associates may operate
together. In residency programs, some of the faculty
are regularly subject to informal evaluation by others,
and review of their patients in conferences subjects
them to a high degree of outside scrutiny. Such sur-
geons should be applauded for their openness, self-
confidence, and acceptance of these processes. For many
plastic surgeons, however, practice is an individual and
often solitary experience; their self-evaluation places
immense and sometimes impossible ethical demands
112 I • GENERAL PRINCIPLES
on them. Even when substandard practice and poor
outcomes surface, often by malpractice claims or
reports of patients to licensing committees, any eval-
uative process is difficult and unwelcome. A medical
license is a property right enabling one to practice, de
jure, a right in the law. A board certificate also enables
one to practice in a specialty as determined by hospi-
tal privileges; it may become a license de facto. There
are definitive legal protections afforded the holder of
a license or board certificate. Limitation or removal
of either can be devastating and is rarely accomplished
without the protection of due process in a formal legal
action.
CHEMICAL IMPAIRMENT
The first scenario demonstrated the problem of dealing
with surgeons who have been injured, the second with
a surgeon who was not performing at a satisfactory
level. The next scenario examines a different problem.
-•-SCENARIO: C H E M I C A L
I M P A I R M E N T
A plastic surgeon in his mid-40s was noted by his col-
leagues to be drinking a bit more than in the past.
Recently divorced, the surgeon had seemed depressed
and less engaged with his colleagues. Although he had
never been seen intoxicated in the hospital, he seemed
to make rounds at odd hours during the night and
was often absent for several days at a time. Residents
reported that the surgeon was irritable and, on several
occasions, forgetful of the planned surgical procedure.
Not surprisingly, the incidence of mental illness,
chemical dependency, and suicide is as high among
plastic surgeons as in the rest of the population. For
the injured surgeon, the recognition of his diagnosis
was immediate and distinct; it was the process and
extent of his recovery that were difficult to measure.
In alcoholism and other forms of chemical depend-
ency, it is the diagnosis that is difficult. There never
seems to be enough evidence. It has been said that
the absence of evidence is not evidence of absence (of
impairment). Once the diagnosis of chemical depend-
ency is established and the addicting agents are
removed, unless there has been severe degeneration,
the competence of recovering surgeons usually returns.
It would be helpful if the selection process for those
entering plastic surgery could identify and eliminate
those disposed to chemical addiction. Entry into res-
idency programs follows a period of intense sorting.
College life, medical school, and surgical residencies
are opportunities for winnowing those who are unfit.
Residency programs and early years in practice are
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emotionally challenging. Training requires long hours,
the acquisition of a large volume of knowledge, and
mastery of difficult techniques. Mistakes are inevitably
made because of errors in j udgment or execution. Fur-
thermore, dealing with patients who are ill, unhappy,
or dying often drains reserves of emotional resources.
Little emotional and psychological energy is left for
personal or intimate life. Finally, residents are often
practicing without major social support and often feel
isolated. Klamen33 has reported that most individuals
have 12 to 15 persons in their "support system" on
whom they can call. This number diminishes to 6 to
8 in medical school. During the first year of residency,
when one is often practicing in a new city with intense
work requirements, the support system is often no
more than one.
The identification of a surgeon who is impaired by
alcohol or other addicting substances is a challenge
but also an ethical responsibility of colleagues. The
ethics of caring imposes a certain moral responsibil-
ity on others to help identify and support recovery of
those afflicted. Surgeons who are impaired by injury,
illness, age, or chemical addiction should not be allowed
to endanger patients.
EXPERT WITNESS TESTIMONY
There is an additional issue that deserves considera-
tion, and that is the role of the plastic surgeon as expert
witness. Plastic surgeons have a responsibility to
society at large to ensure and to maintain the highest
standards of care for patients. One of these responsi-
bilities, as citizens and professionals, is to aid the judi-
cial system in seeking redress for patients injured by
negligence. The tort system is designed to compen-
sate patients injured through the fault of the surgeon.
It is not a perfect system, and the process is often expen-
sive, inexact, punitive, and grindingly slow. However,
an expert witness serves a critical and useful role in
helping to define violations in standards of care. In
addition to efforts at examination, certification, re-
certification, peer review, and quality control, there
are times when a surgeon must serve as a consultant
and expert to the court. For proper ethical standards
to be maintained, minimum guidelines must be
observed.
Expert Consultant to the Court
Expert witnesses are enlisted by either the plaintiff's
or defendant's counsel. The most sound ethical stance,
irrespective of which side is represented, is to look on
oneself as a consultant to the court and jury. The goal
of involvement in the process should be to inform.
This is accomplished by delivering a fair, honest,
informed, balanced expert opinion about the case ren-
dered. Although one may have strong personal opin-
ions, it is inappropriate to be an advocate for one side,
M M M M W image...
to shade opinions, or to withhold information. One
key consideration is whether one can honestly be con-
sidered an expert in the specific surgical care being
adjudicated. Although plastic surgery is a broad spe-
cialty and broad understanding is demanded at the
time of initial certification, specialized interests and
expertise evolve, and the practices of most surgeons
concentrate in limited areas. To be an expert, one
should be aware of the standard of care at the time of
the alleged occurrence. This strongly implies that the
witness should be in active practice or only recently
retired and has practiced in the specialized area under
consideration. An expert must be broadly and deeply
conversant with the area being discussed and have an
awareness and understanding of current literature
and practices. The expert must thoroughly review
the medical facts of the case to treat them fairly and
honestly. The expert must recognize that legitimate
differences of approach may well be acceptable and
prevent bias toward a particular form of treatment.
There have been examples of retired surgeons serving
extensively as expert witnesses to complement their
retirement incomes. For a short time after retirement,
their opinions and expertise are valuable and timely.
Compensation should be commensurate with the
expert's level of expertise and with the time and effort
involved. It is ethically inappropriate to link compen-
sation to outcome, and plastic surgery experts must
not function on a contingency basis. Contingency
establishes a conflict of interest in that it gives the
surgeon a stake in the outcome. The expert witness
must be impartial and recognize that the primary role
is to the court, the jury, and society.
CODES OF BEHAVIOR
In some of the earliest written documents, human
beings attempted to define specific principles to
conduct their lives. They have been variously codified
in many different ways. Exodus (20:1) yielded the Ten
Commandments and the New Testament the golden
rule to "treat others as you would like them to treat
you."21 The story of the Good Samaritan helps iden-
tify the duty an individual has to a neighbor, which
may include our enemies as well as our friends. Perti-
nent to our discussion of dependency, Reinhold
Niebuhr offered the Serenity Prayer, the officially
adopted prayer of Alcoholics Anonymous, in one of
his sermons: "God, give us grace to accept with seren-
ity the things that cannot be changed, courage to change
things that should be changed, and the wisdom to
distinguish the one from the other."34
The government of the United States is of and for
the people and includes personal rights encoded in
the first 10 amendments to the Constitution, the Bill
of Rights. The codes of behavior for surgeons and
physicians have largely evolved from the Hippocratic
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6 • ETHICS IN PLASTIC SURGERY 116
Oath. On close inspection, this oath has only nine
major categories. These codes and principles are
written with practical reference to individuals, physi-
cian-surgeons, and patients and do not deal in ethical
or philosophical abstractions. The Code of Ethics of
the American Medical Association also has nine major
principles (Table 6-5). 3S Although the American
College of Surgeons has no specific code, the princi-
ples are incorporated in the Fellowship Pledge and are
easily reduced to five categories: qualifications of
surgeons, relation to patients, relation to colleagues,
relation to society in general, and education. 36 The
American Board of Plastic Surgery code is reduced to
six major principles, 37 and the American Society of
Plastic Surgeons has identified 11 principles (Table 6-
S).38 The following section examines the Code of Ethics
of the American Society of Plastic Surgeons in detail.
Code of Ethics of the American
Society of Plastic Surgeons38
On the basis of the fundamental principles, theories,
and applications that have been discussed, the Code
of Ethics of the American Society of Plastic Surgeons
is the most thoroughly acceptable articulated set of
standards on which plastic surgeons, as a specialty,
have agreed.
The preamble establishes the purpose of the Amer-
ican Society of Plastic Surgeons and broadly reflects
the roles and responsibilities of plastic surgeons:
To benefit humanity by advancing the art and science of
plastic and reconstructive surgery; to promote the highest
standard of professional skill and competence among plastic
surgeons; to promote the exchange of information among
plastic surgeons; to promote the highest standard of per-
sonal conduct among plastic surgeons and physicians; to
provide the public with information about the scientific
progress in plastic and reconstructive surgery; to promote
the purpose and effectiveness of plastic surgeons as is con-
sistent with the public interest.
The preamble promotes high standards for plastic
surgeons as skillful professionals, colleagues, and
members of society in general. These are the elements
of professionalism and are more clearly outlined in
the 11 general principles.
The principal objective of the medical profession is to render
services to humanity with full respect for human dignity.
Physicians should merit the confidence of patients entrusted
to their care, rendering to each a full measure of service and
devotion.
The first principle of the code incorporates many
of the major ethical theories that have been previously
discussed. Respect for human dignity incorporates all
image...
! 14 I • GENERAL PRINCIPLES
TABLE 6-5 • THE AMERICAN MEDICAL
ASSOCIATION PRINCIPLES
OF MEDICAL ETHICS
Preamble
The medical profession has long subscribed to a body
of ethical statements developed primarily for the
benefit of the patient. As a member of this profession,
a physician must recognize responsibility to patients
first and foremost, as well as to society, to other health
professionals, and to self. The following Principles
adopted by the American Medical Association are not
laws, but standards of conduct which define the
essentials of honorable behavior for the physician.
Principles of Medical Ethics
I. A physician shall be dedicated to providing
competent medical care, with compassion and
respect for human dignity and rights.
II. A physician shall uphold the standards of
professionalism, be honest in all professional
interactions, and strive to report physicians
deficient in character or competence, or engaging
in fraud or deception, to appropriate entities.
III. A physician shall respect the law and also
recognize a responsibility to seek changes in those
requirements which are contrary to the best
interests of the patient.
IV. A physician shall respect the rights of patients,
colleagues, and other health professionals, and
shall safeguard patient confidences and privacy
within the constraints of the law.
V. A physician shall continue to study, apply, and
advance scientific knowledge, maintain a
commitment to medical education, make relevant
information available to patients, colleagues, and
the public, obtain consultation, and use the talents
of other health professionals when indicated.
VI. A physician shall, in the provision of appropriate
patient care, except in emergencies, be free to
choose whom to serve, with whom to associate,
and the environment in which to provide medical
care.
VII. A physician shall recognize a responsibility to
participate in activities contributing to the
improvement of the community and the
betterment of public health.
VIM. A physician shall, while caring for a patient, regard
responsibility to the patient as paramount.
IX. A physician shall support access to medical care
for all people.
Copyright 1995-2004, American Medical Association.
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of the rules-based principles of beneficence, non-
maleficence, autonomy, and justice. It particularly
recognizes that all persons possess human dignity,
including the deformed, disfigured, elderly, and men-
tally challenged. A failure to recognize human dignity
may lead to a conclusion that one is unworthy, unwor-
thy of care, or even unworthy to live. The full measure
of service and devotion is specifically unlimited in quan-
tity or quality and, although difficult to fit within rules-
based ethics, fulfills what would be expected under
virtue ethics and the ethics of caring. The statement
that physicians should merit the confidence of patients
is also a dominant feature of the Hippocratic Oath: "If
I do not violate this oath, may I enjoy life and art,
respected while I live and remembered with affection
thereafter.**6
These words may seem a bit stilted in today's lan-
guage, but the message is clear and remarkably time-
less. More than a mere promise made by those who
enter the profession, it is a sacred covenant to be broken
or compromised at the risk of disgrace. It is also the
good name of the entire profession that is under
question in the face of unscrupulous, fraudulent, and
incompetent practitioners.
Physicians should strive continually to improve medical
knowledge and skill, and must make available to their patients
and colleagues the benefits of their professional attainments.
Physicians have an affirmative duty to disclose new medical
advances to patients and colleagues.
This principle makes it the responsibility of the
plastic surgeons to maintain their individual knowl-
edge and skill. The surgeon is charged with the respon-
sibility of making available to the patient information
about and access to the best available care, even if the
individual surgeon's armamentarium may not have
that surgical or medical skill. It charges one to incor-
porate new procedures if they are better for the con-
ditions being treated. A patient with a wound best
treated with a free microvascular flap transplantation
should have this treatment made available, if possi-
ble. If the surgeon does not choose to learn or to
perform such procedures, the surgeon must still
inform the patient of the best alternative and refer the
patient to a colleague who is knowledgeable and
capable. It also means that new observations, inno-
vations, and discoveries must be shared in open forum
by presentations, publications, and open demonstra-
tions, even if it means sharing such observations with
non-plastic surgeons. The history of medicine has been
marred by examples of failure to share new informa-
tion. There is the tale of the Chamberlains, obstetri-
cians to royalty in England, who kept secret and within
the family the discovery of obstetric forceps, perhaps
depriving thousands of the safety in delivery provided
by this discovery. There is, in plastic surgery, a belief
TtSWK^aeleW image...

6 • ETHICS IN PLASTIC SURGERY 115

TABLE 6-6 • AMERICAN SOCIETY OF PUXSTIC SURGEONS CODE OF ETHICS: GENERAL PRINCIPLES

I. The principal objective of the medical profession is to render services to humanity with full respect for human
dignity. Physicians should merit the confidence of patients entrusted to their care, rendering to each a full
measure of service and devotion.

II. Physicians should strive continually to improve medical knowledge and skill, and must make available to their
patients and colleagues the benefits of their professional attainments. Physicians have an affirmative duty to
disclose new medical advances to patients and colleagues.

III. Physicians should practice a method of healing founded on a scientific basis, and should not voluntarily
associate professionally with anyone who violates this principle.

IV. The medical profession should safeguard the public and itself against physicians deficient in moral character or
professional competence. Physicians should observe all laws, uphold the dignity and honor of the profession,
and accept its self-imposed disciplines. They should expose, without hesitation, illegal or unethical conduct of
fellow members of the profession.

V. Physicians may choose whom to serve. In emergency situations, however, physicians should render service to
the best of their ability. Having undertaken the care of a patient, a physician may not neglect the patient; and
until the patient has been discharged, a physician may discontinue services only after giving adequate notice.

VI. Physicians should provide services under the terms and conditions which permit the free and complete
exercise of sound medical judgment and skill. Nothing contained in this provision shall be construed to limit
price competition among physicians.

VII. In the practice of medicine, a physician should receive professional income only for:
A. Medical services actually rendered or supervised by the physician;
B. Sale of medically-related products approved by the physician;
C. Services provided by ancillary personnel known to and associated with the physician.
No physician shall pay nor receive a commission for referral of patients. (10/99)

VIII. A physician should seek consultation upon request, in doubtful or difficult cases or whenever it appears that
the quality of medical service may be enhanced thereby.

IX. A physician may not reveal a patient's confidence, any observed characteristics of the patient, or any
information obtained from the patient in a professional capacity, unless required to do so by law or unless it
becomes necessary in order to protect the welfare of the individual or of the community. (10/99)

X. The honored ideals of the medical profession imply that the responsibilities of the physician extend not only to
the individual, but also to society. Activities, which have the purpose of improving both the health and well
being of the individual and the community, deserve the interest and participation of the physician.

XI. To assist the public in obtaining medical services, physicians are permitted to make known their services
through advertising. Advertising, however, entails the risk that the physician may employ practices that are
false, fraudulent, deceptive, or misleading. Regulation is, therefore, necessary and in the public interest.
Subsection II of the Specific Principles permits public dissemination of truthful information about medical
services, while prohibiting false, fraudulent, deceptive or misleading communications, and restricting direct
solicitation. (10/99)

Copyright 1995-2004, American Medical Association.

among some historians that the Brancas in Sicily had
the secret to nasal reconstruction that was not snared
with others to preserve their own practices. It has been
speculated that Gaspar Tagliacozzi learned of these
techniques and that his presentations and publications
shared this advance with the world. 8 Jealousies and
interspecialty rancor, particularly among some surgi-
cal specialties, have been partially attributed to failure
to share information and failure to participate in the
education of residents in other specialties. This general
principle of sharing with colleagues does not seem to
limit sharing to those who are in the same institution
or even the same specialty.
Several decades ago, a clever academician from
Boston, Tom Lehrer, released a series of ditties he
recorded from his singing-piano renditions at frater-
nity houses. One of these relayed the secret to academic
success:
Plagiarize,... let no one else's work escape your eyes,
Remember why the good Lord made your eyes,
So don't shade your eyes,
But, plagiarize, plagiarize, plagiarize . . . !
Only be sure to always call it please, research.39
It has been observed that if you steal from another's
writing, it is plagiarism; however, if you steal from two

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Dr.Mustafa D.
116 I • GENERAL PRINCIPLES
or more, it is research. The history of medicine is replete
with examples of misplaced credit for scientific
advances. The use of others' material, published or
unpublished, without clear and convincing credit is
misuse of another's intellectual property and is ethi-
cally considered stealing. There is in academics a desire
to have many publications, for promotion and for
election to prestigious societies. This can lead to the
publication of fragmented data or less than complete
publishable units to gain two or three publications
rather than combining them into a single paper. It also
leads to inclusion of names on papers of some whose
contribution was slight or even nonexistent but polit-
ically desirable. It is ethically appropriate to parse the
authorship to make sure that contributions were real;
it is no more acceptable to include a name of a non-
contributor than it would be to give a share of a sur-
gical fee to one who had not participated.
These concerns should not dissuade surgeons from
sharing experiences. It matters not how often one has
performed an innovative procedure in the privacy of
an office surgical suite. Individual patients may have
benefited. However, unless the findings have been pre-
sented to others, particularly in writing, they remain
untested by objective evaluation and will be of no value
to other patients. The world can only credit and derive
real benefit from those who share their knowledge.
The converse of this is a caution to publish only that
believed to be scientifically valid. Sorting of patients
for presentation has a very human bias toward choos-
ing those with the best result even if it is not the norm.
Presentation of aesthetic surgical techniques and
innovations places a particular ethical charge on the
authors and presenters since bias in selection may be
personally satisfying but misleading for those con-
sidering the adoption of the presented approach.
Statistical analysis of scientific papers is now routine
for most journals of record but is still a difficult issue
for aesthetic surgeons.
Physicians should practice a method of healing founded on
scientific basis, and should not voluntarily associate pro-
fessionally with anyone who violates this principle.
This principle has two major components: the
scientific practice of the specialty and those with whom
one may associate. The need to practice on a scientific
basis is a surprisingly difficult charge to plastic sur-
geons. Plastic surgery must meet the standards of safety
that apply to all aspects of surgery. Hospitals struggle
with objective criteria, such as mortality rates, infec-
tion, blood use, readmission, and other semiquanti-
tative measurements, some of which are not really
applicable to plastic surgeons. Plastic surgeons often
operate outside the hospital in semiautonomous facil-
ities where ongoing data collection is difficult. Com-
munication among such facilities is problematic, and
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Dr.Mustafa D.
difficulties experienced in one facility may be unknow-
ingly repeated in another. In one state, the licensing
board recognized that there had been eight deaths in
outpatient facilities in a little over a year and that half
of them were related to combining abdominoplasty
and liposuction procedures. 40 Surgeons working in
such facilities, without the oversight afforded by hos-
pitals, assume a special moral and ethical responsi-
bility to ensure quality. When this type of data is
reported, the ability of autonomous surgical facilities
to be self-regulating is legitimately questioned.
Beyond the fundamental concerns with safety,
there is a real difficulty in defining objective outcome
standards for procedures and conditions for most of
medicine and surgery. For plastic surgery procedures,
particularly those dealing with appearance, the crite-
ria are largely subjective in nature. Plastic surgeons
argue further that normalcy, or certainly beauty,
cannot be measured in such a way as to achieve
scientific validity. These difficulties do not relieve the
specialty of the responsibility for seeking objective
outcomes. A particularly pertinent situation is that
regarding outcomes from the use of silicone gel pros-
theses in breast implant surgery. When serious ques-
tions about safety were raised and discussed with
industry and regulatory agencies, plastic surgeons indi-
vidually and as a specialty were presented with an
ethical challenge. It became ethically improper to con-
tinue use of such implants until such time that safety,
on behalf of the patients, could be unequivocally estab-
lished. More than a decade later, the safety of such
implants still cannot be established to the uniform sat-
isfaction of impartial scientists. In emotionally con-
tentious situations, with litigation depending on the
proof of safety, the challenge of gathering data may
be daunting. However, this does not ethically relieve
those involved from either confirming safety or dis-
continuing the use of such products.
To suggest that objective data cannot be obtained
becomes ethically unacceptable and implies that
methods of healing cannot be scientifically evaluated.
Plastic surgeons, as a group and as individuals, measure
the outcome of procedures on an ongoing basis. It
becomes an ethical imperative to maintain good
records and regularly assess the results of practice.
The mandate to ground the specialty in the scientific
method goes beyond the individual and recognizes that
"a series of anecdotes does not constitute data." Pre-
sentations of individual series, illustrated by selected
examples, usually of exemplary results, are not equiv-
alent to critical analysis. The best available standard
of scientific inquiry is the prospective, randomized,
double-blind study. Procedures should be chosen
randomly among eligible patients, and evaluation of
the outcome should be conducted by impartial
observers. There are those who would raise the imme-
diate ethical objection that under beneficence and duty,
*&Wttf«ad(Wimage...
each surgeon must do for each individual patient only
that which is believed to be of the greatest benefit for
that patient, not for the surgeon's series and not for
science in general. This leads to a form of circular rea-
soning and would be a persuasive argument if one were
quite sure exactly what was best for any patient. For
several generations, surgeons knew for sure that only
the Halsted mastectomy offered the best chance for
cure of breast cancer. However, when several options
are available, what is not known leads to open inquiry.
What is not known is less dangerous than what is
known for sure that turns out to be wrong.
A scientific approach, particularly when bilaterally
symmetric procedures are being conducted, would be
to perform different procedures on each side. This
can be ethically accomplished if the procedures being
evaluated are both considered safe and effective
and the only real variable is which might be better.
For instance, a study of bilateral augmentation
mammaplasties might well have been conducted with
use of differently designed implants on the two sides.
In another circumstance, the efficacy of various
approaches to face lifts might be compared by
superficial musculoaponeurotic system deep-plane and
skin-only procedures, with one procedure done on one
side, another on the other side, and an impartial
observer evaluating the outcome. Recently conducted
studies have surprisingly demonstrated that sham
operations on internal derangements of the knee were
as effective as arthroscopic procedures designed to
correct the disruption. 41 These creative studies were
all within the bounds of ethics, despite the belief that
they could not be ethically accomplished. 42
Ethical concerns are appropriate in experimenta-
tion on human subjects. This is particularly true when
the experiment involves sham procedures or place-
bos. The Codes of Behavior developed at Nuremberg
and Helsinki directly addressed how such surgical
experimentation is to be conducted. 20 These codes do
not say that experimentation is immoral or unethi-
cal. Studies must always be based on the best scientific
information available and be conducted on patients
only when all other forms of evaluation have been
exhausted. For aesthetic surgery, the final experimen-
tal situation has to be performed on humans. The
conduct of experimental surgery, or any other form
of investigation, is ethically and legally appropriate only
in circumstances in which review and approval of the
protocol by appropriate institutional committees have
been obtained. A critical ethical consideration in con-
ducting such experimental surgery is the unfailing
honoring of the patient's autonomy. This places an
enormous and special responsibility on the surgeons
and evaluative team to provide and ensure full under-
standing by the patient. Potential subjects must have
the ability to consent or to refuse without coercion.
It is not ethically appropriate, for instance, to perform
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6 • ETHICS IN PLASTIC SURGERY 117
such experiments only on clinic patients or on pris-
oners. The patient's actual or perceived ability to obtain
surgery may be dependent on the patient's agreeing
to such experimental procedures. The refusal of sur-
geons to participate in such studies on the grounds
that they are in private practice is misguided. The argu-
ment that participating in studies may subject them
to litigation is also unsubstantiated, particularly when
protocols have met criteria of institutional review. To
always perform the "standard" procedure, whatever
it may be, while seeming to be ethically defensible,
is ultimately self-defeating and eventually violates
the ethical charge to base procedures on scientific
principles.
A second component of this principle is the charge
to not voluntarily associate professionally with anyone
who violates this principle (to practice on a scientific
basis). Some of these concerns date to the time when
the American Medical Association and the American
College of Surgeons had formal proscriptions against
associating with chiropractors. Prolonged and con-
tentious litigation determined that such a prohibition
was illegal.43 In recent years, there has been a renewed
interest in what are termed natural healing methods,
much of which is based on Eastern religions and holis-
tic approaches to life, death, health, and disease. Reli-
gion, faith, and medicine remain inseparable. Instant
communication and worldwide travels have intro-
duced acupuncture, contrapunction, and moxibustion
into the Western world. Homeopathy, naturopathy,
and any term that implies "natural" are perceived
by patients as attractive alternatives. Many of those
natural products are now recognized as dangerous and
may, in combination with other medicines, cause severe
health problems, including many associated with
blood pressure and coagulation. Spirituality and faith
are important components of healthy living and
provide a positive approach to people undergoing
surgery. However, there are practitioners who offer
patients alternatives outside scientific medicine. This
portion of the code prohibits voluntary association
with, support of, or referral to practitioners who may
harm patients. This principle does not, of course, pre-
clude association with the skilled persons who assist
in preoperative evaluation, during surgical procedures,
and postoperatively in facilitating recovery through
therapy and aesthetic support. Such associations and
the appropriate delegation of some aspects of care are
ethically appropriate.
The medical profession should safeguard the public and itself
against physicians deficient in moral character or profes-
sional competence. Physicians should observe all laws,
uphold the dignity and honor of the profession, and accept
its self-imposed disciplines. They should expose, without
hesitation, illegal or unethical conduct of fellow members
of the profession.
Tew R^eicr «f image...
118 I • GENERAL PRINCIPLES
This principle embodies many of the issues dis-
cussed previously. The profession should safeguard the
public and itself against physicians deficient in moral
character and professional competence recognizes that
the principles of beneficence, nonmaleficence, auton-
omy, and, particularly, justice relate not just to the indi-
vidual patient and surgeon but to the profession and
society at large. The issues of professional competence
were previously addressed, but the issues of moral char-
acter are of particular concern. The Hippocratic Oath
charged that the physician should enter no house for
sexual purposes: "Whatever houses I may visit, I will
come for the benefit of the sick, remaining free of all
intentional injustice, of all mischief and in particular
of sexual relations with both female and male persons,
be they free or slaves."5 Much of the Hippocratic Oath
may be considered out of touch with current times.
However, the concern for moral character of surgeons
is as true today as it was in the time of Hippocrates.
The patients of plastic surgeons are some of the most
vulnerable. The conditions treated, often the most inti-
mate issues of identity and sexuality, establish an intrin-
sic vulnerability. It is a matter of good legal sense and
protection but, more important, right behavior that
the surgeon always deal with the patients in a way that
recognizes and avoids even the appearance of impro-
priety. From the beginning of medical school during
the dissection of another human being's body, one will
continue to encounter and enter into an intimacy that
few are privileged to experience. One can never retreat
from the respect and reverence taught in the earliest
days of medical school. It is a heavy responsibility, and
the inherent temptations are real.
The use of a third person as chaperone in all cir-
cumstances where a male surgeon deals with the female
patient is one way of ensuring propriety in the physi-
cian-patient relationship. There is, however, a ques-
tion as to the duration of the plastic surgeon-patient
relationship. One surgeon, arguing before a discipli-
nary committee, insisted that since he had removed
the sutures from the patient's breast augmentation
wounds, the physician-patient relationship had ended
and sexual intercourse on the way home from the
office was not inappropriate. Psychologically, some
would argue that such a relationship never ends. There
is no arbitrary time frame that can be applied to every
condition. The removal of a small mole or closure of
a minor laceration establishes a less intense relation-
ship than does body contouring or breast augmenta-
tion. Unfortunately, exact time frames cannot be
established. At a minimum, the prior surgeon-patient
relationship must have been clearly dissolved before
any social contact is initiated. If the surgeon in any
way uses or exploits prior trust, knowledge, emotions
or any influence derived from the prior professional
relationship [AMA, E8.14], the conduct is clearly
unethical. 44 It is most difficult to not exploit prior
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Dr.Mustafa D.
trust in establishing any intimate relationship with a
patient.
Sexual misconduct is not limited to patients. The
broad subject of sexual harassment may also occur in
the plastic surgeon's workplace. Harassment can occur
any time it interferes with work or academic environ-
ment if it results in intimidating, hostile, or offensive
work or academic environment [AMA, E3.08].44 Sexual
relationships between a plastic surgery supervisor and
a resident are a matter of grave concern because of
the inherent inequality in status and power. Such
conduct may have an adverse relationship to patient
care and the training program in general and is
unacceptable even if it is presented as consensual.
Morally inappropriate behavior may be related to
or exacerbated by mental illness or the use of alcohol
and other mind-altering drugs. Disciplinary com-
mittees struggle with whether inappropriate behav-
ior is the result of such conditions. An ethical rule of
thumb is that surgeons behaving in an inappropriate
or unsafe fashion mustbe removed from contact with
patients until the situation is corrected. Alcoholism
and other chemical dependencies identified outside
the surgical practice, when no patients have been
injured, may be treated but not necessarily punished.
When patients have been injured, the dependency does
not excuse culpability and disciplinary action as well
as treatment.
Ethical impropriety can be shown for failure of the
next charge that physicians should observe all laws. The
most common reasons that physicians and surgeons
are brought before disciplinary committees are sexual
misconduct, chemical dependency, and professional
incompetence. Limitations on licenses also occur
because of convictions for criminal behavior. Most
criminal offenses are related to drugs or fraud and
deceit in billing. Although most criminal offenses are
necessarily immoral or unethical, some actions may
be unethical even if they are not illegal. Inflated charges
or misidentification of diagnoses or procedures is
unethical even if not illegal. There are those who justify
coding all repairs as complicated, even if the repairs
should rightfully be considered simple. Excessive
billing is always inappropriate; however, in emergency
circumstances in which patients are extremely
vulnerable, it is particularly offensive.
They should expose, without hesitation, illegal or unethi-
cal conduct of fellow members of the profession.
The issues of whistle-blowing are complicated. The
ethical imperative must be tempered by the very real
life consequences of calling another's practice pattern
or conduct into question. It is exceedingly difficult to
document misbehavior even among residents and
faculty in the relative transparency of an academic
department. Even in the standardized and protected
VtJWR^aelcrMfimage...
environment of the board examination process, exam-
iners have been threatened with litigation because they
failed candidates. Those who have called others to task
on such issues as alleged inappropriate surgery, inexact
or sloppy science, or plagiarism have found themselves
isolated. They are often without the anticipated and
warranted support of colleagues. It has been said that
no good deed goes unpunished. The assurance of com-
petence and moral rectitude among plastic surgeons
is one of the most widely desired and appropriately
anticipated responsibilities toward society. The legal
protections afforded the accused make these respon-
sibilities most challenging.
Physicians may choose whom to serve. In emergency situ-
ations, however, physicians should render service to the best
of their ability. Having undertaken the care of a patient, a
physician may not neglect the patient; and until the patient
has been discharged, a physician may discontinue services
only after giving adequate notice.
The implications of this principle are profound.
Plastic surgeons are, in general, under no responsi-
bility to accept all patients who request care. A surgeon
is under no obligation to accept a patient for purposes
of providing a service that is not scientifically valid.
A surgeon is under no obligation to accept a patient
for purposes of providing a service that is contrary to
the religious beliefs of the surgeon, except under the
rarest of circumstances. The Roman Catholic surgeon
may refuse, for example, to perform an abortion. Refus-
ing to care for a patient because of ethnic background,
minority status, sexual orientation, or ability to pay,
particularly in an emergency situation, is morally
tenuous. Although refusal to be involved in any emer-
gency care may be acceptable for individual surgeons,
it has developed into a serious image problem for the
specialty as a whole. In the eyes of colleagues in other
disciplines, plastic surgeons have become isolated from
mainstream medicine and appear unwilling to render
any but predictably lucrative care.
It is unequivocal that once a patient is accepted,
service will be rendered to the best of one's ability. It is
a further disincentive, however, for surgeons to provide
emergency care since such care must be continued until
the patient has been discharged and care may be dis-
continued only after giving adequate notice. Beyond
this mandate, surgeons recognize that patients are not
discharged until they have received the maximum
benefit to be expected from their care. When a patient
develops a wound healing problem or infection or a
surgical result is not satisfactory for almost any reason,
one cannot simply discharge that patient. It is also
difficult to give adequate notice, which involves more
than a phone call or a refusal to make an appointment
for the patient. It requires written documentation, ade-
quate time during which the patient can safely make
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6 • ETHICS IN PLASTIC SURGERY 119
alternative arrangements, and a positive effort on the
part of the physician to ensure that alternative care is
appropriate. Furthermore, there is an obligation to
ensure that the physician to whom the patient is
referred will actually accept the patient. Moral and
ethical responsibilities to patients, once accepted, no
matter what the circumstances, are all but sacred and
discontinued with utmost care for the patient.
Physicians should provide services under the terms and con-
ditions which permit the free and complete exercise of sound
medical judgment and skill. Nothing contained in this pro-
vision shall be construed to limit price competition among
physicians.
This principle would never have been written into
a code of ethics 50 years ago. Physicians and surgeons
at that time negotiated with patients in an open fashion,
and arrangements often were altered on the basis of
a patients ability to pay. It was never ethically appro-
priate to offer one level of care for the poor but better
care at a higher price if they were wealthy. Through
insurance coverage and Medicare, third parties have
been invited into the physician-patient relationship
and have profoundly changed much of the relation-
ship. Insurance initially offered compensation on the
basis of what the surgeon charged, later on the basis
of what it cost the surgeon to provide the service.
Managed care attempted to limit both care and the
associated costs. Quality of service is difficult for
anyone to establish, and differential payment for
more highly trained specialists was not fiscally sound.
There is an ethical tension between the desire to provide
optimum care and the need to conserve society's
resources. Although individual surgeons may strive to
provide optimum care for all patients, at a societal level,
not all patients can be provided optimum care when
simply adequate care will suffice. The best care for
patients with liver failure may be a liver transplant,
but the constraints of limited organs for transplanta-
tion and the expensive nature of the surgery make it
impossible to provide such care for all patients. A kind
of rationing is accomplished at least partly on the ability
of the patient or insurance coverage to pay. The use
of specialized and expensive skin substitutes in the life-
saving care of burned patients in burn centers might
exhaust funds necessary for the care of other patients.
Surgeons are facing tragic choices on a daily basis. Some
plastic surgeons are told that they can repair cleft
palates on infants only if it is done on an outpatient
basis under local anesthesia. Hospitalization is con-
sidered inappropriate and would not be authorized.
Plastic surgeons have been told by third-party payers
that they cannot revise disfiguring scars after a burn
injury unless the scars are causing ill-defined func-
tional limitation. Such situations may cause ethical
dilemmas in which the rather obvious good of the
120 I • GENERAL PRINCIPLES
patient is in conflict with the fiscal good of the insti-
tution or society in general. These issues are particu-
larly poignant in plastic surgery procedures that
initially provide little or no compensation and are later
denied compensation altogether. Hot only the surgi-
cal fee but also all associated hospital and other costs
are denied.
Nothing contained in this provision shall be construed
to limit price competition among physicians. The
wording of this statement is more typical of a regu-
lation of the Federal Trade Commission than a code
of ethical behavior. The provision implies that should
surgeons be willing to offer their services at a fee less
than that of a colleague, they must be allowed to do
so. The alternative would constitute fixing of fees
among surgeons, which would be unethical. A special
situation falling under this principle is that of the
resident-training aesthetic clinics, which must be
conducted by training programs. Such programs offer
aesthetic procedures to patients who could otherwise
not afford them. The exchange is allowing a resident,
under supervision, to actually perform the procedure.
In such circumstances, the attending surgeon has the
ethical responsibility to ensure a level of care compa-
rable to that which would be obtained through the
services of the attending surgeon. That said, it is rec-
ognized that a skillful and experienced plastic surgeon,
operating in one's own facility with trained staff, is
presumably going to produce a superior result. Curi-
ously, the actual difference in the outcome in the two
circumstances is difficult to establish. Such programs
have been criticized for charging fees that are less than
the common fee in the community. The needs of the
program usually override these objections.
A corollary to this situation is the practice of
surgeons* sharing their operative experience with
residents. For much of traditional reconstructive
procedures, particularly in burn care, reconstructive
microsurgery, and complex reconstructive flap pro-
cedures, a team approach is most appropriate, and the
planned execution of the procedure is easily explained
to patients and families. Less clear is the propriety
of sharing a portion of an aesthetic procedure that
involves a private patient with a resident surgeon. Most
patients expect, unless otherwise specifically counseled,
that the surgeon from whom they sought care would
actually perform the procedure. An even more ambigu-
ous situation is the one in which the patient is assigned
to an attending surgeon through the emergency
department. Delegation of the care to a resident
without immediate, physical supervision is appropri-
ate only if the resident's abilities and experience are
ensured and the attending surgeon is readily available.
The issue of payment is ethically clear. If the attend-
ing surgeon assumes the role of individual supervi-
sion and is physically present, a fee is legally and
ethically appropriate. As the degree of supervision
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becomes less immediate, and particularly when the
supervisor is not constantly and physically present,
the charging of a full surgical fee is not appropriate,
as is detailed in the next principle.
In the practice of medicine, a physician should receive pro-
fessional income only for:
A. Medical services actually rendered or supervised by the
physician;
B. Sale of medically-related products approved by the
physician;
C. Services provided by ancillary personnel known to and
associated with the physician.
No physician shall pay nor receive a commission for refer-
ral of patients.
Historically, one of the reasons that the American
College of Surgeons was established in 1913, in addi-
tion to a desire to promote excellence in surgical care,
was to address the perceived evil of fee-splitting. The
Fellowship Pledge of the College specifically states that
I will take no part of any arrangement, such as fee splitting
or itinerant surgery, that induces referral or treatment for
reason other than the patient's best welfare.36
The Plastic Surgical Code has almost the same pro-
scription: No physician shall pay or receive a commis-
sion/or referral of patients. The surgeon has an almost
sacred responsibility under any ethical theory—
beneficence and nonmaleficence, under duty, under
virtue—to ensure that the patient receives the best pos-
sible care. It includes more than the performance of
the most appropriate surgical procedure. It includes
choosing a facility that is the safest and, if possible,
the most economical. It includes the provision of assis-
tance in the operating room by skilled personnel. It
includes assurance of competent anesthesia coverage.
The responsibility extends to the assurance that the
cardiologist or psychiatrist, for example, is chosen on
the basis of skill and experience and not because he
or she is willing to offer a kickback to the referring
surgeon. Incentives for referral may be subtle, such as
consultation of patients for whom such referral is not
medically appropriate. There may be, for instance,
secondary gain in obtaining a cardiology consultation
for healthy young patients or routine consultation by
infectious disease consultants for all patients admit-
ted to a burn center. Such referral practices, when they
are not medically indicated, are inappropriate uses of
resources and are of particular ethical concern when
all consultants are members of the same faculty prac-
tice plan or group practice.
Changes in practice patterns have resulted in
changes in the scope of the surgeon's responsibilities.
Gone are the days when surgical interns personally
performed urinalyses and blood glucose determina-
T^Wttf'fcttHiW image...
tions or obtained and read the electrocardiogram. Sur-
gical care has moved first from the hospital's main oper-
ating room to specially designed outpatient facilities
and now often to the surgeon's own facility. The
surgeon may delegate care that is not directly related
to the diagnosis or surgical procedure. Some surgeons
appropriately use internists to perform all general
preoperative evaluations, anesthesiologists to conduct
supervision in the perioperative phase, and trained
assistants to perform much of the technical care post-
operatively. Some who specialize in extremity surgery
might have the full-time assistance of physical and
occupational therapists. Many whose practice is largely
aesthetic find it useful to employ people with ex-
pertise in makeup and counseling for skin care. Such
involvement of others as part of ongoing surgical man-
agement provides a level of comprehensive care that
is highly efficient and valuable to patients. If, however,
these services are mandated for all patients, even when
such care is not medically indicated, it is not appro-
priate. The patient is being used'as a means of revenue
generation, rather than having his or her well-being
considered.
A common characteristic of professionals is that
their primary contribution is service. An increasingly
common practice among plastic surgeons, in addition
to providing the services, is the provision of goods.
When the goods, such as medications, creams, emol-
lients, and other products, are provided for the best
interest of the patient and at a fair price, there is no
ethical problem. If, however, patients are encouraged
or required to purchase products as a condition for
surgical care, particularly when the indications are not
clear, this represents exploitation and is not ethical.
As one example, a plastic surgeon, in exchange for a
commission from the manufacturer, required that all
patients take a specially compounded and expensive
vitamin preparation and nutritional supplement as
part of preoperative and postoperative care. This was
a precondition for the patients'acceptance for aesthetic
surgery. The patients had no way of knowing that there
were no data to support such "treatment."
A physician should seek consultation upon request, in doubt-
ful or difficult cases or whenever it appears that the quality
of medical service may be enhanced thereby.
This principle is almost the converse of the previ-
ous situation in which unnecessary use of consulta-
tion or provision of goods or services is imposed on
patients. That physicians should seek consultations
would seem obvious; and yet, many plastic surgeons
were trained in general surgery at a time when trainees
were commonly encouraged to believe, contrary to
considerable objective evidence, that they were capable
of handling all medical conditions, irrespective of
whether they were directly related to the surgical
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6 • ETHICS IN PLASTIC SURGERY 121
problem. Calling on residents or attending physicians
in other specialties for help in managing patients
was sometimes considered a sign of weakness and
discouraged. Mature plastic surgeons recognize the
wisdom of involving their colleagues from other fields
in the management of their patients. This responsi-
bility may be difficult to fulfill at times when it is nec-
essary to request consultations from other specialties
in direct competition with the plastic surgeon (e.g.,
dermatologists or otolaryngologists). Ethical standards
make it not only prudent but also imperative to request
additional consultation when the best interests of a
patient are involved.
A physician may not reveal a patient's confidence, any
observed characteristics of the patient, or any information
obtained from the patient in a professional capacity, unless
required to do so by law or unless it becomes necessary
in order to protect the welfare of the individual or of the
community.
The issue of confidentiality has been discussed
under the patient's autonomy. This principle, so fun-
damental to the physician-patient relationship, has sur-
vived as part of the Hippocratic Oath. The legitimate
needs of third-party payers, quality of care reviewers,
and others to have access to intimate data often conflict
with the physician's responsibility to withhold mate-
rial shared in confidence. Patients need to be advised
of the responsibilities that surgeons have to disclose
that which is pertinent to those who have a legitimate
need for the information. The need to divulge a
patient's contagious condition or, in psychiatry, a
patient's threat of bodily harm to another is mandated
by law, and these are ethically sound reasons for a
limited violation of confidentiality. Inadvertent reve-
lation of information is also an issue. Talk in the sur-
geons' lounge or in the hallways and elevators may be
overheard by persons not entitled to such informa-
tion. The desire to share private observations about
patients who are public figures may be almost irre-
sistible. At all times, surgeons must be careful not to
divulge anything of the identity of a patient whose
image is shown at a scientific meeting or in publica-
tion. Organized surgical meetings are most particu-
lar about such presentations, but less well monitored
are seminars presented by surgeons as marketing
opportunities. A particular concern is the presenta-
tion of patients in a local hospital or university
seminar or grand rounds where attendance is relatively
open. Many people with an interest in aesthetic
surgery may avail themselves of the opportunity to
attend such programs. Finally, a particular concern
from a legal as well as an ethical standpoint is the pres-
entation of complications at morbidity and mortal-
ity conferences. A particularly memorable example was
a grand rounds in which a surgeon showed a video-
image...
122 I • GENERAL PRINCIPLES
tape of a technical error he had made during the course
of a major procedure, an error that led to serious com-
plications and death. The surviving relatives of the
patient had not been informed of this error but were
in attendance at the presentation.
The honored ideals of the medical profession imply that the
responsibilities of the physician extend not only to the indi-
vidual, but also to society. Activities, which have the purpose
of improving both the health and well-being of the
individual and the community, deserve the interest and
participation of the physician.
The opportunity given to become physicians and
subsequently plastic surgeons is one that can never
truly be deserved or earned. The dedication, hard work,
and sacrifice required for practitioners in the specialty
of plastic surgery should not be minimized. In the best
of circumstances, all individuals should have access
to plastic surgical care. The plastic surgical commu-
nity has been at the forefront in organizing and con-
ducting international projects to offer free care to the
disfigured and deformed around the world. Many have
donated untold hours, days, and longer to such proj-
ects, but we must not forget that many citizens within
the United States may not be able to afford plastic
surgical care.
The ethical principle involved is justice; plastic
surgeons have a responsibility as citizens to con-
tribute to societal well-being. As the keepers of a
valuable and scarce resource, plastic surgeons have a
special societal responsibility to carefully place these
resources.
There are complex ethical concerns for humani-
tarian missions to foreign countries. Many people in
underdeveloped countries are malnourished and suffer
from infectious diseases or other problems that would
disqualify them from surgery within the United States.
Visiting teams rarely have the opportunity to perform
appropriate assessment of risks, and with major cul-
tural and language barriers, provision of adequate
information to families is difficult if not impossible.
The patients may be so desperate that informed
refusal is all but impossible. Too often, presentations
at meetings include series of patients who underwent
experimental procedures done abroad. These include
procedures that would not have been acceptable in
American hospitals or practices without protocols and
institutional review and meticulous consent proce-
dures. The visiting team is not always made up of
surgeons whose skills in the area are current; not all
surgeons regularly perform cleft lip and palate surgery.
Residents accompanying such visiting groups are
given responsibilities that would not be appropriate
within the United States, where they are based on level
of training and expertise. Follow-up care is often
entrusted to persons who would not be qualified
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
according to standards of care within the United States.
Although these missions serve an apparent goal of
helping a select group of patients, this goal can never
justify an inferior level of care.
To assist the public in obtaining medical services, physicians
are permitted to make known their services through adver-
tising. Advertising, however, entails the risk that the physi-
cian may employ practices that are false, fraudulent,
deceptive, or misleading. Regulation is, therefore, necessary
and in the public interest. Subsection II of the Specific Prin-
ciples permits public dissemination of truthful information
about medical services, while prohibiting false, fraudulent,
deceptive or misleading communications, and restricting
direct solicitation.
Plastic surgeons have been involved in the process
of increasing public awareness of the specialty and of
individual surgeons. It has brought the specialty
immense attention. There are virtuous characteristics
or internal goods that make a professional better,
including courage, honesty, temperance, and practi-
cal wisdom. There are also external goods, such as pres-
tige, power, and money, that may divert one from
virtue. No amount of prestige, power, or money makes
a plastic surgeon a better surgeon. There has been no
more challenging ethical issue in plastic surgery
morality than advertising. The fundamental relation-
ship of surgeon to patient is one of unequal power.
The discrepancy in knowledge and information and
the opportunity to gain access to some service make
the surgeon more powerful. The misuse of such power
to gain, for instance, sexual favor is morally and eth-
ically repugnant. Advertising is most often directed
toward conditions that are not life-threatening and
can involve the most intimate personal insecurities
of body image. The subject of advertising is one of
the most thoroughly addressed issues in the Code of
Ethics. Some of the concerns and proscriptions relate
to style, etiquette, good taste, and legal considerations.
The fundamental issue, however, is the potential for
the misuse of power as well as fraud and deceit.
• S C E N A R I O : S U R G I C A L
M E M O R A B I L I A
A board-certified plastic surgeon has agreed to be
involved in a fund-raising project for the largest center
for abiised persons in his community. To further this
worthy goal, he has offered to donate an augmenta-
tion mammaplasty, including implants, to the highest
bidder, with bidding to begin at $10,000. Such an
intriguing offer has generated immense interest, and
as the bidding begins, he signs programs and is
handing out signed surgical caps.
I t J W t ^ a d e W image...
There are those who view all advertising as a per-
version of the professions. For years, advertising was
considered unethical, but any current efforts to prevent
advertising by plastic surgeons are not only futile but
also illegal. Perhaps the single most important ethical
principle in medicine is beneficence, the charge to
always do good or that which is in the best interest of
the patient. A corollary is nonmaleficence, to keep the
patient from harm. Both ensure that the patient is in
a position to make an informed decision either to
accept or to refuse surgery. Surgeons always have a
conflict of interest; operations are how they make a
living. It is morally imperative to recognize and assid-
uously avoid anything that puts one's interests before
those of the patient. The most obvious issue, there-
fore, is the use of power in the form of persuasion or
apparent medical opinion to solicit patients to undergo
procedures that are not in their best interest. The use
of false, fraudulent, misleading, or deceptive infor-
mation is manifestly unethical as well as illegal and in
violation of all codes of conduct of professionals. A
surgeon's offering operations as a prize or reward at
an auction or lottery, as in the scenario, is unethical.
There is no way of knowing in advance whether the
winner is a suitable candidate and whether, under such
circumstances, an objective professional judgment
could even be made. The signing of autographs and
surgical caps, as prominent athletes might do for a
fee, only adds to the unprofessional nature of this
situation. It is also a matter of ethical concern when
surgical procedures are bartered in exchange for
recognition by the media or as compensation for some
other favor.
A most controversial application of this portion of
the code related to organized participation in and
approval by American Society of Plastic Surgeons and
other plastic surgery organizations for the television
program Extreme Makeover.*5 Patients are solicited by
the network for the program and are not charged for
their surgery in exchange for having their surgery
televised. Patients are reported to be meticulously
screened, and the final decision regarding suitability
for the procedures is made by the operating surgeon.
Recognizing that ethical problems require delibera-
tion, the ethical discussions involved the leadership of
several organizations. There were serious efforts made
to be impartial and consistent. It was recognized that
any decision might set a precedent. Those involved in
the discussion recused themselves from any possible
benefit from the program; they would not be eligible
to be the surgeon. There was concern about the appear-
ance that the patients were competing in a contest in
which an operation was the prize. There was concern
about the inevitable degree of self-promotion such an
appearance by the surgeon would represent. It was
decided that untoward results or complications would
simply not be shown on television. The seduction of
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Dr.Mustafa D.
6 • ETHICS IN PLASTIC SURGERY 123
the potential patients of receiving a "free" makeover
is immense. A subsequent program involved actual
competition among patients to reward those with the
best result. Advertising by its very nature is designed
to attract patients and thereby enhance the prestige
or power of the surgeon, as well as the plastic surgery
organization, and lead to increased revenue. These are
the types of external goods that may threaten the very
integrity of the professions.
The ethical theories and process find their appli-
cation in the Code of Ethics of the American Society
of Plastic Surgeons, which represents the specialty of
plastic surgery. The principles outline, in rather broad
strokes, the responsibilities of a professional to patients
and to society. When individual professionals embrace
the concepts enhancing the internal goods of practice
in the form of virtue ethics and the ethics of care,
patients will be served well and ethical dilemmas
resolved. The principles also offer some specificity in
areas where plastic surgeons, like other professions,
have been tempted by external goods of power, pres-
tige, and money. To the degree that internal goods are
maximized, the effects of the external goods will be
minimized and discipline will be unnecessary.
TRUTH TELLING
In a capsule summary of truth telling, Jonsen46 out-
lines the reasons that truth is critical to medicine.
There is a strong moral duty to tell the truth.
Fundamental to any approach to ethics, science,
and most professional relationships is fidelity and
expectation that truth will be shared. Physicians occa-
sionally encounter patients who choose to deceive the
caregiver. This may be done for purposes of com-
pensation to further interests in litigation or because
the patient is mentally disturbed, such as in Mun-
chausen syndrome. Whatever the underlying motiva-
tion, a solid and effective therapeutic environment
cannot exist if a patient does not tell the truth. The
responsibilities also accrue to the physician, who has
a duty to tell the truth to the patient.
Patients need and expect the truth about their medical
conditions to plan, consent to, or refuse care.
The principle of self-determination cannot be served
and autonomy cannot exist in the absence of truthful
information. Informed consent requires not only
sufficient information about the patient's unique con-
dition but also full disclosure of the procedure to be
performed, including the risks and benefits. Although
there may be a motivation to withhold information,
the patient cannot possibly make any determination
about further care without having the truth.
Concealment of the truth is likely to undermine the
physician-patient relationship.
124 I • GENERAL PRINCIPLES
The physician-patient relationship is a true fiduciary
relationship and cannot effect its purpose if infor-
mation is concealed that is relevant to an informed
decision. Rawls invoked a veil of ignorance as a prin-
ciple; it means to put yourself in the position of the
patient, and you can come to no conclusion but to
tell the truth. It is not difficult to imagine one's own
reaction if relevant information were concealed.
Tolerance of concealment by the profession may
undermine the trust of the public.
Failure to tell the truth destroys the physician-patient
dyad. However, it can also undermine the entire pro-
fession. Diminishing expectations threaten the very
existence of any profession.
Physicians suspect that the truth will be harmful to
patients.
So much of the history of the physician-patient rela-
tionship has been paternalistic; a tacit expectation exists
that the physician will always do what is best for the
patient. There are still the occasional patients for whom
the whole process of informed consent and truth telling
seems superfluous. Such a position is risky for the
patient and risky for the surgeon. The idea that the
truth would be emotionally harmful and patients can
rarely accept bad news has long been discontinued.
Whereas it may cause tension, there are almost no data
to support the idea that truth, even unpleasant truth,
is harmful. The discovery that one has been deceived
is far more destructive than unpleasant truth.
Most patients, particularly those with serious illness,
wish to know the truth of their conditions.
Modern technology, particularly the use of respi-
rators, has raised the specter that patients will not be
in control of their own care, particularly end-of-life
decisions. Advance directives, designation of surro-
gates, estate planning, and honorable dealing with
loved ones and friends mandate that patients be told
the truth.
The Law protects physicians who withhold the truth in
only the most unusual of circumstances.
The tradition of medicine has been one in which
truth telling was often subJLigated to other consider-
ations. In many ways, the law has become the common
secular yardstick for ethical behavior. The law pro-
tects physicians who withhold important information
in only the most unusual of circumstances, and should
such consideration arise, it would be prudent to obtain
that protection from the court in advance. One is not
at risk in being honest with the patient.
The patient must be told about complications for
all the reasons presented. There is a strong moral duty
to tell the truth, and patients expect that the truth
will be told. Concealment of the truth, when it is
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Dr.Mustafa D.
discovered, totally undermines the physician-patient
relationship and, more broadly, undermines the trust
of the public. The mitigating circumstances of degree
of harm and potential long-term effects may influence
the timing and style of the presentation of the truth;
the discussion need not be harsh or frightening, but
it must be truthful.
In the broadest sense, the profession of medicine
owes society an explanation of the limitations as well
as benefits of modern medicine. Society needs the truth
about the failures as well as the successes. Medical and
surgical error and complications are not uncommon.
Much of the malpractice crisis is attributed to the dis-
proportionate level of expectations of patients and
juries compared with the reality of less than perfect
results. Surgery on healthy patients for purposes of
aesthetic enhancement has been presented in a seduc-
tive fashion by many, and unpleasant results are
disproportionately devastating to those affected.
Complications can result in appearance that may be
worse than the preoperative condition.
Jay Katz9 wrote that masks have been used histor-
ically by actors on the stage to hide true appearances,
and physicians and surgeons do much of their work
behind masks, hiding uncertainty, fear, and the pos-
sibility of human error. The underlying concern about
advertising and marketing among plastic surgeons is
less about the fact of advertising than it is about the
mask of deception that entices and seduces. One can
only hope that the specialty of plastic surgery will con-
tinue to evolve and enable as many patients as possi-
ble to benefit while reducing the number of those who
do not.
REFERENCES
1. CamusA:Thewagerofourgencration.In CamusA: Resistance,
Rebellion, and Death. New York, Vintage International, 1960:242.
2. Simon R: Fair Play; Sports, Values and Society. Boulder, Colo,
Westview Press, 1991.
3. Dcverette RJ: Practical Decision Making in Health Care Ethics:
Cases and Concepts. Washington, DC, Georgetown University
Press, 1995.
4. Abelson R, Friqeugnon M-L: Ethics for Modern Life, 4th ed.
New York, St. Martin's Press, 1991:2.
5. The Hippocratic Oath: Text, Translation, and Interpretation.
Ludwig Edelstein, trans. Baltimore, Johns Hopkins Press, 1943.
6. The Hippocratic Oath, modern version; Louis Lasagna, Acad-
emic Dean of the School of Medicine, Tufts University, 1964.
7. Fasching DJ, Dechant D: Comparative Religious Ethics: A Nar-
rative Approach. Maiden, Mass, Blackwell, 2001.
8. Maclnty re A: A Short History of Ethics. New York, Touchstone
Press, 1966.
9. Katz J: The Silent World of Doctor and Patient. London, The
Free Press, 1984.
10. Tagliacozxi G: De Curtorum Chirurgia per Insitioncm. Venice,
Gaspare Bindoni, 1597.
11. KrizekTJ: Infanticide. Marquette Med Rev 1957;22:143-147.
12. Krizek TJ: Who shall live? In Serafin D, Georgiade N, eds:
Pediatric Plastic Surgery. St. Louis, CV Mosby, 1984:3-7.
13. Fuchs VR: Who Shall Live? Health, Economics, and Social Choice.
New York, Basic Books, 1974.
*8*ftf<adtfW image...
14. Maclntyre A: After Virtue. Notre Dame, Ind, Notre Dame Press,
1984.
15. Munson R: intervention and Reflection: Basic Issues in Medical
Ethics, 6th ed. Belmont, Calif, Wadsworth Thompson Learn-
ing, 2000.
16. Furrow BR, Greaney TL, Johnson SH, et al: Bioethics: Health
Care Law and Ethics, 3rd ed. St. Paul, Minn, West Publishing,
1997.
17. Neuhaus RJ: The Naked Public Square: Religion and
Democracy in America. Grand Rapids, Mich, WB Ecrdmans,
1984.
18. Pellegrino ED, Thomasma DC: The Christian Virtues in
Medical Practice. Washington, DC, Georgetown University
Press, 1996.
19. Ballard BW: Understanding Maclntyre. Lanham, Md, Univer-
sity Press of America, 2000:11.
20- Beauchamp TL, Walters L: Contemporary Issues in Bioethics,
5th ed. Belmont, Calif, Wadsworth, 1999.
21. Suggs MJ, Sakenfeld KD, Mueller JR, eds: Oxford Study Bible,
revised English ed. New York, Oxford University Press, 1992.
22. Beauchamp TL, Childress JF: Principles of Biomedical Ethics,
4th ed. New York, Oxford University Press, 1994.
23. Please Let Me Die! [videotape]. Psychiatric Disorders Film No.
29. University of Texas Medical Branch, Galveston Texas, May
1974.
24. Kliever LD.ed: Dax'sCase: Essays in Medical Ethicsand Human
Meaning. Dallas, Texas, Southern Methodist University Press,
1989.
25. Rawls J: A Theory of Justice. Cambridge, Mass, Harvard Uni-
versity Press, 1971.
26. Loewy EH: Textbook of Healthcare Ethics. New York, Plenum
Press, 1996.
27. Jonsen AR, Toulmin S: The Abuse of Casuistry: A History of
Moral Reasoning, Berkeley, Calif, University of California
Press, 1988.
28- Jonsen AR, Veatch RM, Walters L: Source Book in Bioethics: A
Documentary History. Washington, DC, Georgetown Univer-
sity Press, 1998.
29. Walker MU: Moral Understanding: A Feminist .Study in Ethics.
New York, Routledge, 1998.
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Dr.Mustafa D.
6 • ETHICS IN PLASTIC SURGERY 125
30. Gilligan C: In a Different Voice. Cambridge, Mass, Harvard
University Press, 1982.
31. Parens E: Is Better Always Good? The Enhancement Project,
Special Supplement to the Hastings Center Report. Garrison,
NY, The Hasting Center, Jan-Feb 1998.
32. Bosk C: Forgive and Remember. Chicago, 111, The University of
Chicago Press, 1979.
33. Klamen D: Psychiatrist on Illinois State Medical Society
Committee on Physician Health. Personal communication,
1990.
34. Brown RM: The Essential Reinhold Niebuhr: Selected Essays
and Addresses. New Haven, Conn, Yale University Press,
1986:251.
35- AMA Code of Medical Ethics: Current Opinions and
Annotations. Chicago, 111, American Medical Association,
2002-2003.
36. American College of Surgeons: Deliberations on the Statements
on Principles. Chicago, 111, American College of Surgeons,
1997.
37. American Board of Plastic Surgery: Code of Ethics. Philadel-
phia, Pa, American Board of Plastic Surgery, 2003.
38. American Society of Plastic Surgeons: Code of Ethics, revised
10/99. Arlington Heights, 111, Roster Publication, 2003.
39. Tom Lehrer Revisited 1959. Lobachevsky, Rhino Records,
Burbank, Calif, Reprise Records.
40. St. Petersburg Times, Florida, February 9,2004.
41. Moseley JB, O'Malley K, Peterson NJ, et al: A controlled trial of
arthroscopic surgery for osteoarthritis of the knee. N Engl J
Med 2002;347:81-88.
42. Horng S, Miller FG: Is placebo surgery unethical? N Engl J Med
2002;347:137-139.
43. Pursuant to a settlement agreement in Wilk et al v AMA et al,
September 1987.
44. American Medical Association, Code of Ethics. Available at:
www. a ma -assn.org. Accessed 2004.
45. Leonardo J: Leaderships issues OK for Extreme Makeover TV.
Arlington Heights, III, Plastic Surgery News, March 2003:1,17,
35-37.
46. JonsenAR.SieglerM.WinsladeWJ:ClinicalEthics,4thcd. New
York, McGraw-Hill, 1998:66.
 image...
CHAPTER
7
•
Liability Issues in Plastic
Surgery: A Legal Perspective
ERLE E. PEACOCK, Jr., MD, JD
MEDICAL MALPRACTICE
Overview
Being an Effective Witness
Informed Consent
Risk Management
MEDICAL MALPRACTICE
Overview
It is almost certain that the minute a physician pur-
chases insurance covering medical malpractice, he or
she will be sued for malpractice; it is only a matter of
time. Actually, on the average, one of every five physi-
cians will be sued every year.' On the average, there-
fore, a practicing plastic surgeon can expect to be sued
for medical malpractice about every 5 years. In many
respects, therefore, being a health care provider in these
times is like being president of a diving board company;
liability comes with the territory and is almost inevitable
in the business environment of medicine. Practicing
medicine in modern times requires accepting that
patients view physicians as providing a service that is
bought and sold on an open market and comes under
warranty. If that product does not meet the self-
generated expectations of the purchaser, exercise of the
warranty seems a completely nonpersonal business
tactic that follows naturally and should be expected
by all involved. The enormous pain and expense that
litigation causes a defending physician is not a con-
sideration by most plaintiffs and their attorneys; liti-
gation is simply an opportunity to recover what they
perceive to be rightfully theirs.
The answer to this unfortunate and extremely
expensive attitude is not, as most physicians and physi-
cian organizations seem to believe, tort reform. The
concept that medical malpractice suits are the result
of greed, although sometimes correct, is not accurate.
They are actually the result of technologic advances
and changing social and economic conditions.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
PEER REVIEW
CONTRACTS
FRAUD AND ABUSE
Malpractice suits against physicians were relatively rare
before the "plaster revolution" when physicians began
to treat fractures rather than amputate limbs. 2 The
fetal monitor has been responsible for increasing the
number of suits against obstetricians, and laparoscopy
is now the leading cause of malpractice suits against
general surgeons. Because the public insists on more
technologic advances, malpractice suits can be expected
to increase, not decrease, because of feeble attempts at
tort reform. The plaintiff's bar is a powerful influence
in most state legislatures. Although some improvement
has been achieved, such as defining more accurately
the qualifications for expert witnesses and reducing
the time limits in various statutes of limitation, the
only meaningful tort reform involves significant lim-
itations on damage awards, particular awards for such
difficult to define entities as pain and suffering, con-
sortium, and future expenses. Placing a cap on damages
sufficient to discourage suits for medical malpractice
has been found unconstitutional by the supreme courts
of more than half of the states that have enacted such
legislation.3 The issue has not been presented to the
United States Supreme Court, but many analysts
believe economic caps will be found unconstitutional
at that level also. It is highly unlikely that appellate courts
will ever accept the notion that physicians deserve
special protection from civil liability. In fact, the very
opposite may be the case because of what is perceived
by many to be extremely favorable treatment of physi-
cians by the courts. 4 Thus, it appears that health care
providers simply have to recognize that insurance pro-
vides a "deep pocket" reserve for medical mishaps.
Dealing with legal redress, frivolous and justified, is
127
128 I • GENERAL PRINCIPLES
simply part of the cost to be balanced with the rewards
from medical practice.
More efficacious than trying to force tort reform
are attempts to understand the legal system and
become more accomplished at working with lawyers
and insurance company representatives. An important
first step is to understand the objectives of both. Many
physicians are under the mistaken impression that
insurance companies and their appointed legal repre-
sentatives have a duty to defend a physician accused
of medical malpractice. This is simply not true. Careful
examination of most malpractice insurance policies
reveals complete absence of the word defense. The duty
of medical malpractice insurance carriers is to indem-
nify their insured, not defend them. Common law states
that an insurance company actually has a duty only
"to investigate and settle expeditiously."5 Expressed
differently, the primary duty of a medical malpractice
carrier is to its stockholders, not to the physicians it
insures. The lawyers insurance companies hire to rep-
resent their insured are responsible to the insurance
company they work for, even though some, perhaps
many, are sympathetic to the dilemma malpractice alle-
gations force on physicians and will do what they can
to serve the needs of the physician until such needs
run counter to the duty of their employer.
Some insurance companies have voluntarily inserted
no settlement without agreement of the insured
clauses in their policies, and others have made such
clauses possible for an increased premium. This is a
two-edged sword. The holder of such a policy cannot
abuse it by refusing a reasonable settlement offer; if he
or she does so and the eventual judgment exceeds the
settlement offer, the insured physician may end up per-
sonally responsible not only for the difference between
the settlement offer and the ultimate judgment but
also for attorneys' fees and court costs incurred after
a reasonable settlement offer was tendered.
The major problem with settlement for the insured
physician, particularly in a frivolous lawsuit, is manda-
tory reporting to the National Physicians Data Bank.
Physicians were much more willing to settle lawsuits
before settlements had to be reported and before
managed care entities had access to Data Bank
statistics.
Experience with the present state of malpractice lit-
igation in a managed care setting points out the need
in some instances for personal counsel in addition to
insurance company representation.The greatest deter-
rent to having personal counsel is having to bear addi-
tional personal expense after years of paying what seem
to most physicians unreasonably high premiums. The
answer to this problem is careful evaluation of insur-
ance company-appointed counsel to determine
whether personal counsel is needed at all (often it is
not) and, if personal counsel is needed, to use it only
during carefully restricted times for specific purposes
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
to keep expenses minimal. Such times include the eval-
uation of expert testimony after depositions have been
taken, jury selection, and, most important, settlement
considerations. An insurance company-appointed
lawyer has a duty to help his employer settle as cheaply,
although not necessarily as quickly, as possible. The
physician is not usually interested in the amount of
the settlement but is very interested in getting the entire
business over with as soon as possible. Paramount for
the plastic surgeon, however, is staying out of the Data
Bank or, if that is impossible, having the most favor-
able report possible go to the Data Bank, including a
carefully written 2000 character alternative report the
physician is allowed to write that is attached perma-
nently to the Data Bank report and, therefore, presented
to any eligible inquirer in the future. There are lawyers
who specialize in knowing Data Bank regulations and
who can be extremely valuable in helping to formu-
late a settlement that is favorable for the defendant
physician's needs. Most insurance company represen-
tatives have little or no interest in a physician's Data
Bank concerns and, even more important, may have
little or no experience in dealing with Data Bank
regulations and options.
Being an Effective Witness
Plastic surgeons are called on to testify in one of three
categories. The first is as an expert witness called by
a plaintiff or defendant to assist the trior of fact (judge
or jury). Another is as a defendant, in which case the
physician should usually be tendered an expert witness.
A third is to be called as a treating physician, who may
or may not be classified an expert witness. A major
consequence of this classification is the type of ques-
tions that can be posed. An expert witness is called
because some issue at trial is outside of the experi-
ence and judgment of the judge or jury. The expecta-
tion is that the expert witness, because of education
and experience, can interpret complex issues for the
laity. Expert witnesses are allowed to express opinions
and to draw conclusions based on their qualifications
and experience. A fact or treating witness, however,
can testify only on matters of fact—usually what the
witness saw, heard, smelled, or experienced firsthand.
A few exceptions, such as observations about inebri-
ation or estimated speed, are allowed, but for the most
part, a fact witness can testify only as to what he or
she witnessed. If a witness is tendered an expert,
however, and is accepted by the court as an expert, he
or she can then state opinions and conclusions rela-
tive to the issues.
Plastic surgeons are usually approached by a plain-
tiff's or defendant's attorney. They are asked to review
a medical record in which malpractice has been alleged
against another plastic surgeon. It is important to
determine which side is seeking the plastic surgeon's
image...
7 • LIABILITY ISSUES IN PLASTIC SURCERY: A LEGAL PERSPECTIVE
help because if review of the medical record reveals
favorable information for the requesting attorney, the
reviewing surgeon will be expected to be willing to
testify at deposition and in court. There is, therefore,
no point in reviewing a record if the plastic surgeon
is not willing to testify under oath about the results of
the review. It is not wise to review a case at the request
of a plaintiff's lawyer unless a few conditions are
fulfilled.
It is important that good plastic surgeons be willing
to review a plaintiff's records; if good surgeons do not
perform this task, not-so-good surgeons can be found
and justice is less likely to be served as the quality of
expert testimony diminishes. There is real medical mal-
practice going on: patients who have been harmed
negligently are entitled to compensation, and an
expert witness is necessary for such compensation to
be awarded. Review of potential malpractice, however,
should be the responsibility of senior plastic surgeons
who are well established in a community and in their
profession. It is not fair to ask a young plastic surgeon
trying to establish a practice and gain admission to
professional societies to criticize another plastic
surgeon's care. It is also advisable to limit review of a
plaintiff's case to a geographic area at least 500 miles
distant from the reviewer's office. The consequences
of testifying against a colleague may be too great, even
for a senior practitioner, if both are in the same or close
geographic area.
In summary, our judicial system depends on expert
medical testimony. It is an important duty of all pro-
fessional people to provide that service—both for the
good of the system and as a duty to patients. As a prac-
tical matter, however, the duty to review and testify for
a plaintiff should fall primarily on senior plastic sur-
geons residing at a reasonable distance rather than on
young plastic surgeons establishing a practice and
trying to achieve favorable local recognition.
After a plastic surgeon has reviewed a record and
stated an opinion that the lawyer wishes to use as sworn
testimony, the potential expert witness will have to be
made available to opposing counsel so the opposition
can determine how the witness will testify at trial. Justice
abhors a surprise, and both sides of an adversary pro-
ceeding have a right to learn anything they can about
what the other side will attest to during trial. Discov-
ery is accomplished by written questions and answers,
admissions and denials, production of documents, and
deposition.
The most important principle for the expert witness
is to maintain neutrality. Showing bias or prejudice
seriously compromises the credibility of an expert
witness. A second principle is that the expert should
give as little information as possible at the deposition.
As much as possible, short answers (such as yes, no,
or I do not know) are preferable to expansive, detailed
responses. It is absolutely essential to be truthful; it is
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129
not required, however, to give more than a narrow
answer to exactly what was asked. For example, if it is
asked whether the sutures Dr. X used to close a patient's
wound fall below the standard of the profession, give
the best answer. If this is untrue, the answer is simply
no. To answer "no, but it is not the closure I use" is not
only redundant but deadly to the defendant the expert
witness may be trying to support. There is a great ten-
dency for expert witnesses, particularly surgeons, to
embellish testimony in the hope of overwhelming the
opposition with their superior knowledge. It never
works! All an expert accomplishes by laying out every-
thing he or she knows about a subject at deposition is
to give the opposing side 3 or 4 months to prepare for
such testimony and to enlist expert witnesses who will
offer contradictory testimony at trial. Everything a
potential expert witness gives the other side at depo-
sition can be used in some way to impeach that witness
during cross-examination at trial.
It is also important to allow a slight pause before
answering any question. Not to do so invariably gives
the other side a freebie—meaning getting the answer
to a question that should never have been asked if the
other attorney had an opportunity to object. It is
common practice for an experienced attorney to find
any subject he or she can get the expert witness to talk
aboutduringdeposition.lt does not really matter what
the subject is as long as the witness gets in the habit
and rhythm of answering questions quickly on sub-
jects he or she likes to talk about. Then, before the expert
witness realizes it, an important—even ultimate—
question is inserted, and the rhythm of answering
quickly is continued and a vitally important question
that the witness would not have been required by court
rules to answer has been answered, and the other side
has the information.
Plastic surgeons should never speculate during dep-
osition. If they know the answer to a proper question,
it must be given. If witnesses have an opinion, they
must admit it and give that opinion (as narrowly as
possible) if requested to do so. If the witness does not
know the answer to the question or does not have an
opinion, the proper response is to say "I do not know"
but never to speculate.
An expert witness should never become fatigued
during deposition. A simple request to recess or to
return on another day may be in order. The expert
witness should not argue and should never be sarcas-
tic or cute and must always resist the temptation to
belittle the lawyer conducting the deposition. That
lawyer has the right to learn anything he or she can
about where the expert witness stands, and justice
demands that the witness cooperate with him or her
even though such cooperation should be as restrictive
as it can be within the borders of truthfulness. The law
requires a truthful answer; the law does not require
volunteering anything.
130 I • GENERAL PRINCIPLES
At trial, demeanor is extremely important for wit-
nesses and most of all for a defendant witness. Every
member of the jury venire is a potential juror, and all
of them are present in the courtroom and judging the
defendant by appearance. It is best to appear profes-
sional and attentive. Compassion and some degree
of humility are appreciated by jurors. Arrogance, eva-
siveness, and vindictiveness are qualities that will be
noted and potentially hurt a defendant. The message
a defendant witness wishes to convey is one of com-
passion for the patient but utter wonderment about
why the patient is suing when the defendant did every-
thing possible to help the patient.
Impeachment is the bete noire for every expert
witness. Witnesses well prepared by good lawyers will
usually perform well on direct examination. Cross-
examination is where ignorance or ineptitude on the
part of the witness comes out, or to put it another way,
cross-examination is where a good expert witness earns
his or her fee.
The goal of cross-examination is to impeach an
expert witness. Impeachment is usually accomplished
by making light of the expert's credentials, bringing
out limitations in the expert's experience as applied to
the case at bar, pointing out bias and prejudice, and—
most to be feared of all—demonstrating untruth-
fulness. It is the dream of every trial lawyer to
cross-examine an expert witness who has just testified
effectively on direct examination and successfully prove
to the jury that the expert cannot be trusted.
Lack of trust in impeachment is often attempted
by making the witness own up to inconsistencies
between trial testimony and testimony presented at
deposition. The best insurance against such incon-
sistency is to read one's deposition at least three times
before trial. Next, it is important to remember that
particularly if the deposition and direct testimony are
long and complicated, some inconsistencies are
inevitable. When they occur, it is essential not to appear
to have been caught in a deliberate lie. An experienced
expert witness can admit to inconsistencies without
appearing to be dishonest or careless. Explanation
should be offered if the cross-examiner allows; if
not, the witness should remain calm and remember
that if real damage occurred, redirect examination
by the other attorney will give the witness ample
opportunity to correct any impression of dishonesty.
The worst mistake is to give credence to an unjust
impression by appearing embarrassed or defensive
rather than offering to be capable of easily explain-
ing why testimony is not inconsistent if all of the facts
are known.
A learned treatise is also used to impeach an expert
witness in a medical malpractice case. Again, pre-
vention is the best defense. An experienced expert
witness never testifies that any book or paper is com-
pletely accurate or that any authority is completely
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Dr.Mustafa D.
clairvoyant or infallible. Plastic surgery obviously is
not an exact science; therefore, there is usually plenty
of room for an expert witness to allow the facts of the
case at bar to be distinguished from what some
authority or authoritative treatise declares.
Being a defendant expert witness is different only
in that the defendant is expected to be prejudiced and
does not have to be concerned about giving an appear-
ance of neutrality. During deposition, defendant expert
witnesses have an almost uncontrollable urge to tell
everything they can think of to make allegations appear
frivolous. It is their first chance to defend themselves,
and it is doubly important, therefore, to do everything
possible to prepare defense witnesses so that they resist
the tendency to say more than they have to say. The
defendant expert witness must keep answers short and
narrowly framed so that just the question posed is
answered and nothing more. Compassion and humil-
ity are important; jurors inevitably take up for a plain-
tiff if they think a defendant physician is attacking his
or her own patient.
The treating physician expert witness has a major
problem—to recognize limitations and tell only the
truth without speculation. The ultimate or dispositive
question, of course, in personal injury cases is usually
one of causation. Most often, the answer is not certain,
but the plaintiff wants the physician to give definitive
or dispositive testimony about causation and wants
the resulting injury to appear as severe as possible. It
is tempting to acquiesce to a patient's expectations,
particularly in trying to build a practice specializing
in reconstructive surgery. However, the legal system
depends on fairness to both sides, and the truth is often
that causation is not completely certain even though
the resulting injury may be consistent with the claimed
cause. Testimony about cause should usually be
expressed as consistent, but not necessarily certain. For
example, a good expert witness can testify that finding
typical carpal tunnel signs and symptoms is consis-
tent with prolonged keyboard use even though it is
not absolutely certain. There are many causes of carpal
tunnel syndrome, and to state that it is certain that any
one condition caused it probably is going beyond
the data available. This is particularly true in con-
ditions of unknown etiology or existence (such as
fibromyalgia).
Witnesses should never appear embarrassed about
answering questions for which they are being paid, if
their fee is reasonable. It is good advice to pick out
some juror who appears to have leadership potential
and look directly into that juror's eyes while testify-
ing. A soft, properly timed smile and direct eye contact
can instill trust even during a relatively short expo-
sure. Of course, the witness should face the attorney
when a question is being asked but may then turn to
the jury box and make appropriate eye contact and
use any other appropriate body language that gives
image...
7 • LIABILITY ISSUES IN PLASTIC SURGERY: A LEGAL PERSPECTIVE
some sense or feeling of bonding in a common search
for truth.
Informed Consent
Informed consent cause of action appears in approx-
imately 16% of medical malpractice cases. It is prob-
ably higher in plastic surgery, in which the procedures
are not as easily defined. Cosmetic surgery can be the
most dangerous type of consent issue for a plastic
surgeon.
The law of informed consent is state law; there is
no national standard. In some states, the law is statu-
tory (made by legislature); in others, common law
(court-made law) controls. Finally, in both statutory
and common law states, the standard can be either a
local community standard or a reasonable person stan-
dard. It is important for plastic surgeons to know the
standard and adhere strictly to it.
A reasonable person standard is attractive to plain-
tiffs because there is no need for an expert witness for
consent issues to be raised. All the jury has to do is
decide whether the patient was told all a reasonable,
prudent person would need to know to make an
informed decision. In local community standard
states, a plaintiff must find either a local physician or
some outside physician who can testify convincingly
to being familiar with that community standard and
then testify that the standard of consent in that com-
munity was not achieved.
The historical basis for consent law is that a person
has the right to determine what is done to her or his
body; anything involving unwanted touching without
consent is battery.6 The basis for informed consent is
that a patient must be sufficiently informed to choose
between alternative procedures, including no treatment
at all. In most states, Tennessee and Pennsylvania for
many years being the only exceptions, failure to obtain
informed consent is not battery but negligence.7 Neg-
ligence is not an intentional tort and is, therefore,
covered by typical malpractice insurance. Battery, in
contrast, is an intentional tort, and most policies do
not cover intentional torts. Hence, it is essential to know
consent law in the state in which practice is conducted.
Consent can be written or implied. The reason
written consent is superior is that the burden of proof
(a critical issue in litigation) is on the plaintiff to prove
that informed consent was not obtained. If written
consent was not obtained, the burden of proof switches
to the defending plastic surgeon to prove that informed
consent was obtained. In the case of a tie, the actor
with the burden of proof loses.
Consent should never be obtained in the form of a
contract for a final result. It is acceptable to give the
general results of a procedure (e.g., 90% of patients
are pleased with the results of cosmetic rhinoplasty);
there is nothing contractual in giving that sort of
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31
information as part of informed consent. It is dan-
gerously contractual to say, for instance, "Your nose
will look like Ronald Coleman's nose," and that sort
of information should not be offered. In this regard,
the use of computer images and photographs entails
a degree of risk. It should be made clear to patients
that no contract is being formed to make the nose
appear like any photograph, computer image, or
plaster mold that was used in work-up of the patient.
Informed consent should be obtained by the
surgeon who will operate on the patient. Prepared forms
can be used but should be personalized by writing in
any items that are needed to meet local or community
standards for that operation on that particular patient.
It is not legally acceptable for a practicing plastic
surgeon to obtain informed consent and then to have
a resident or fellow perform surgery on an anesthetized
patient. Such practice needlessly exposes the resident
to a charge of battery. The major problem is what to
include to make consent become informed consent.
The often repeated rule of thumb is that untoward
events that happen relatively frequently (such as hem-
orrhage or infection), even though usually not serious,
and the infrequent serious complication should be
disclosed. The common law legal standard is that
anything that a reasonable person under similar cir-
cumstances would need to know to make a wise deci-
sion about a proposed procedure or treatment should
be disclosed. Physicians have lost informed consent
malpractice cases most often because of failure to accu-
rately and clearly inform the patients of their diagno-
sis, risks and predicted outcome, and prognosis with
and without treatment.
Personal information that may require disclosure
includes conflicts of interest,such as acquired immun-
odeficiency disease and hepatitis—particularly for sur-
geons. Conflicts of interest should clearly be stated,
although it is probably not necessary to disclose minor
financial ties to large equipment makers or implant
and drug manufacturers. Lack of experience was
held to be a necessary revelation in the case of a neu-
rosurgeon who was proposing to perform his first
operative correction of a cerebral aneurysm. 8 A key
factor in the case was that another neurosurgeon in
the same local area was more experienced in this type
of surgery. The court ruled that the patient was enti-
tled to know the contrasting experience of the two neu-
rosurgeons who were available. The courts are split over
whether a surgeon should disclose that he or she is
human immunodeficiency virus (HIV) positive or has
had hepatitis. Unfortunately, both the American
Medical Association and the American Dental Asso-
ciation have published ethical position statements
requiring disclosure of HIV infections.9 These ethical
position statements were quoted in cases in which the
court found surgeons to have a duty to inform patients
of HIV infections. l0 Drug or alcohol dependence is not
132 I • GENERAL PRINCIPLES
a part of informed consent. Substance abuse has been
considered the domain of hospital privileges com-
mittees and licensure.
Implied consent may be a defense to negligence alle-
gations involving written informed consent, but it is
dangerous to rely on implied consent because the
burden of proof lies on the defendant to prove consent
was clearly implied and that it was also informed.
Several reliable witnesses are essential in the defense
of such a case. Waiver of informed consent is not a
good defense." A patient who refuses to listen to a
surgeon trying to inform him or her about a proce-
dure, even if the patient volunteers to waive legal
requirements, should not be allowed to do so. A plastic
surgeon should insist on written informed consent and
should not agree to operate without obtaining it. Hos-
pital blanket authorization should not be relied on
entirely by plastic surgeons. Cosmetic and recon-
structive surgery is too personal and too variable to be
covered adequately by a blanket institutional author-
ization. Clinical trials also produce a problem, and
plastic surgeons involved in them should be certain
that informed consent has been outlined specifically
by a knowledgeable attorney for patients engaged in
that exact trial. No deviation should be permitted. The
old defense of therapeutic privilege, often used for
hyperthyroid patients before it was possible to render
them euthyroid preoperatively, should never be relied
on. Family members may insist that a patient not be
told the diagnosis or exactly what is planned because
of perceived ill effects that such truthfulness would
convey. Patients with capacity to give consent should
always be treated as deserving the full spectrum of infor-
mation needed to make an informed decision.
It isnot,ofcourse,necessarybylawto obtain consent
in emergencies. Good Samaritan service outside of a
hospital does not require obtaining informed consent,
but the Good Samaritan defense does not apply to treat-
ment by strange physicians who happen to be in the
vicinity of a patient in a hospital setting.
In summary, informed consent under statutory and
common law standards is an important consideration
for plastic surgeons. The highly personal and almost
always elective nature of cosmetic and reconstructive
surgery requires special attention to details that only
the surgeon who will perform the procedure can
explain. Printed brochures, videotapes, and even expe-
rienced physician assistants can help educate patients,
but in the last analysis, the law has established a legal
obligation for the surgeon who is to perform the pro-
cedure to inform patients about every aspect of a con-
templated operation that any reasonable person would
need to know to make a wise decision. The law does
not require that patients be told every conceivable mis-
adventure but only what is reasonable under existing
circumstances. For instance, tellinga patient that injury
to the facial nerve could occur in a face lift does not
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Dr.Mustafa D.
protect the plastic surgeon from malpractice allega-
tions if a facial paralysis is caused by negligence. The
danger of facial paralysis is really not a factor that rea-
sonable patients need to know about in considering
whether to have a face lift by a competent plastic
surgeon. Not to include the danger of facial paralysis
in obtaining consent to remove a parotid tumor,
however, particularly when there is a possibility the
tumor may be malignant, would be found by most
courts to be gross negligence. Judgment is required by
all parties. In many respects, the skill in obtaining
informed consent appears under the law to really be a
highly technical application of the golden rule.
Risk Management
The general principles of risk management arc known
to most plastic surgeons because of repeated exposure
and required education by insurance carriers. As far
as special risks encountered by plastic surgeons are con-
cerned, it is worthy of note that of all the major risk
factors that have been studied, specialty and type A
personality are the only factors that equate significantiy
with the risk of being sued. Thus, plastic surgeons are
in a high-risk category—almost as high as the top level
of neurosurgeons, anesthesiologists, and orthope-
dists. Major factors in office practice have been part-
nership rather than corporation status, consent being
less than reasonably informed or so explicit as to be
logically interpreted as contracts or guarantees, defi-
cient records, and ill-advised waivers. Interestingly, age,
gender, board certification,patient volume, type of hos-
pital, quality of residency, and past litigation do not
correlate with the risk of future malpractice litigation.
Well above half of malpractice suits are filed because
of perceived physician deception, including attempts
to collect an unpaid bill.12 It probably does not pay to
take aggressive steps to collect a bill under any cir-
cumstances other than the occasional patient who
pockets an insurance payment owed to a physician.
Experienced plastic surgeons have recommended,
in addition to the major factors listed before, the fol-
lowing specific considerations. Always speak first to
patients and always speak on the same structural level
(not with a patient lying down). Try to use a patient's
exact words, such as terrific, cool, or maxed out Keep
notes on individual preferences, such as examination
room preferences, and review these notes and find a
way to use the information. Be very clear about the
next step and use written information when possible.
Always make a presurgical telephone call and be known
as the only physician in town who always returns tele-
phone calls to patients on the same day. Never hang
up a telephone first. Find a way to say "You are right"
as often as possible; everyone likes to be right! Take
precautions such as handwashing in front of patients.
Always have a chaperon for female patients and make
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7 • LIABILITY ISSUES IN PLASTIC SURGERY: A LECAL PERSPECTIVE
confidentiality an obsession. Dictate office notes
immediately and operative notes at least on the same
day of the procedure. See and talk with patients before
any tests or examinations are performed. And find some
way to preserve the enthusiasm of the first day of prac-
tice and let it show in as many ways as possible: people
love others who love their work.
Finally, there is the moral and ethical dilemma that
malpractice threats cast over the practice of medicine.
Defensive medicine is expensive and can be risky to
patients as well. Plastic surgeons are not faced with
the serious defensive dilemmas of some specialists,
such as pediatricians, who have to decide whether to
perform a spinal tap in every child with a high fever
and the possibility of meningitis. In making defensive
medicine decisions, about all a good plastic surgeon
can do is to make the best medical science decision
first, then balance the risk of a medical malpractice
consequence (which actually is pretty low; only one of
eight patients who have legitimate malpractice allega-
tions ever sue) 13 and try to balance the risk to physi-
cian and patient as fairly as possible. Good record
keeping and good communication about such deci-
sions are the best protection against unjust litigation,
even though there is no absolute immunity and
undoubtedly never will be.
PEER REVIEW
The courts, as a general rule, prefer not to become
involved in peer review disputes. State law in every state
authorizes the Board of Trustees of a hospital to
appoint, to not appoint, or to revoke privileges of any
health care provider they wish for any reason they deem
appropriate. Hospital privileges are just that, and the
decision to award or to revoke privileges is considered
a professional judgment that the courts, in their own
words, have no business second guessing. The only time
peer review disputes become matters for the courts to
decide in most states is when privileges are revoked or
denied maliciously or arbitrarily and capriciously. It
is extremely difficult for even a deserving plaintiff to
prove malice; arbitrary and capricious decisions are,
therefore, most often alleged in civil courts.
An arbitrary decision is one that does not appear
to be based on the evidence before the governing body.
A decision to revoke a surgeon's hospital privileges
based on poor record keeping when the evidence cited
reveals excellent records would be a viable basis for a
claim of arbitrary action. Capricious behavior relates
to decisions that appear to have been made suddenly
and without the due process called for by the institu-
tion's regulations and bylaws. The courts will not, as
a rule, ever order a hospital to be found guilty of arbi-
trary and capricious action to give a physician hospi-
tal privileges. What they will do, however, is order
the hospital to follow its own procedures and redo
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133
the action to provide procedural and substantive due
process. Of course, if the plaintiff can show damages
caused by malicious, arbitrary, or capricious actions,
the courts may award monetary relief. Damages are
usually sought for antitrust violations, defamation, and
tortuous interference with economic relations.
The usual scenario for flawed peer review results
when managed care organizations, such as a physician-
hospital organization, become too exclusive or develop
an illegal monopoly. For example, a town with six car-
diologists may see five cardiologists selling their prac-
tices to the hospital and becoming hospital employees.
The sixth, who elects to maintain solitary practice on
a fee for service or some other basis, then becomes an
economic competitor of the physician-hospital organ-
ization. The five cardiology employees of the hospital
usually have or ultimately achieve critical power by
becoming members of the credentials committee, by
appointment to the executive committee, or by being
seated on the board or even becoming president of the
medical staff or executive committee. Such power gives
the physician-hospital organization enormous advan-
tage that can be used to discourage economic compe-
tition and, if that power becomes corrupt, to deny or
rescind hospital privileges for outsiders. This is flawed
peer review at its worst!
The first corrupt peer review action to reach the
appellate court level involved all of the vascular sur-
geons in Astoria, Oregon, except one, who ultimately
sued the remaining vascular surgeons under Sherman
I Antitrust Protection." 1 The result was a devastating
loss for the group and a huge monetary award for the
surgeon who had been mistreated. Antitrust action pro-
vides for triple damages and attorney fees; the result
was so economically ruinous to the defendants that it
appeared unlikely that any reasonable physician would
ever serve on peer review again. Because of this, Con-
gress got into the act by passing the Health Care Quality
Improvement Act of 1986, Public Law 99-660. This
federal law provides, among other things, limited
immunity to individuals serving peer review functions
provided any action is taken (1) in the reasonable belief
that the action was in the furtherance of quality health
care, (2) after reasonable effort to obtain facts, (3) after
adequate notice and hearing procedures, and (4) in
reasonable belief that the actions were warranted by
the facts known. 15 Conditions 1,2, and 4 are not very
meaningful to an abused plastic surgeon; it is too easy
for the institution to claim immunity under these pro-
visions even after the fact. Number 3—adequate
hearing and notice—can be another matter, however.
Administrators, because of impatience or judgment
clouded by vindictiveness or economic necessities or
just plain ignorance of the institution's rules and reg-
ulations, frequently will take shortcuts that leave peer
review action vulnerable to attack and exposure by an
injured party. Contrary to common belief, peer review
154 I • GENERAL PRINCIPLES
action is not protected absolutely, and courts can order
peer review documents to be produced during dis-
covery. Nevertheless, peer review minutes and actions
should never be released except in response to a court
order. Malpractice attorneys are not entitled to view
peer review activities under most circumstances.
One of the most egregious flaws is the careless or
intemperate use of summary suspension. According
to most hospital bylaws or medical staff rules and reg-
ulations, summary suspension should be used only
in extreme situations in which immediate danger is
present to the life or safety of patients. This is advis-
able; summary suspension denies defendants any due
process or ability to defend their privileges until they
have been lost. It is sort of like hanging a suspect and
then bringing the corpse into the courtroom for a trial.
Even though it is rarely necessary, summary suspen-
sion is frequendy used by by administrators and physi-
cians as a way of quickly getting rid of a staff member.
Summary suspension may injure patients and always
hurts the reputation of the institution and loyalty of
the medical staff. When summary suspension is used,
the indication should be crystal clear. Professional
medical and legal advice should be sought and followed.
Investigations should be carried out as quickly as pos-
sible—certainly in less than 30 days so the consequences
of Data Bank involvement can be avoided should a
mistake have been made.
Peer review is an extremely important quality assur-
ance measure that patients, providers, and the public
have a right to expect; physicians should serve on peer
review committees when their turn arises. It is critical
that the profession police itself if external policing is
to be avoided. On the other hand, it is just as impor-
tant to note that the immunity granted by Public Law
99-660 is not absolute. The law is riddled with holes
that an enterprising plaintiff's attorney can exploit
when peer review is flawed. Before serving on peer
review, a plastic surgeon should obtain legal assurance
of indemnification against liability and may need per-
sonal insurance coverage as well. Malpractice policies
do not provide peer review protection.
Prevention is the best answer to flawed peer review.
When a potential victim sees the first sign (usually
unwarranted review of records) that something may
be amiss, he or she should go direcdy to his or her
superiors and request an informal hearing to expose
the motives and to clarify any concern about profes-
sional competence. Failure to expose the problem and
to solve it early makes it necessary to obtain personal
legal counsel, preferably from an attorney experienced
in health care law and hospital procedures. It usually
is not profitable to wait until damaging action has been
taken before going to an attorney to "seek revenge." It
is difficult to defend against charges of professional
inadequacy; the burden of proof is on the defendant,
and unfair as it may seem, the facts are that if a
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Dr.Mustafa D.
hospital really wants to revoke or deny the privileges
of a member of the medical staff, for any reason, it
usually can do so if it goes about the process in con-
formity with its own rules and regulations and is patient
in achieving the results. There have been some exam-
ples of huge punitive damages awarded to physicians
who were treated unfairly on credentialing matters,
but they are relatively rare. Rather than plan revenge
(a court can never be expected to order a hospital to
grant or to restore privilege) by seeking monetary
damages, it is usually best to anticipate what is hap-
pening and to correct the problem if possible or, if not,
to resign voluntarily if it can be done early enough to
avoid Data Bank regulations requiring that changes in
privileges be reported or that resignation be reported
during a formal investigation of privileges. Unfair as
this course may seem, it is usually better than resort-
ing to the courts, which usually takes years for an issue
to be resolved, costs tens of thousands of dollars of
personal expense, and in the end can only result in
awarding of damages to a deserving victim—which
usually is not what the victim wants in the final analy-
sis. It is a far better course to withdraw if conditions
cannot be changed, provided withdrawal can be done
before positions are memorialized, so that a damag-
ing record is avoided. A good attorney can help to
accomplish this if given the opportunity early enough.
There is not much that attorneys can do except add
expense when they get into the game too late unless
there is such outrageous activity that a jury trial will
result in award of massive damages.
CONTRACTS
A contract is a promise that the courts will enforce.
Obviously, the courts will not enforce all promises, and
so legal assistance is essential for physicians entering
into various business relations with each other and with
health care entities. Many physicians have adopted a
cavalier approach, saying "I can't understand all that
legalese; I'll just start to work and if I'm not treated
right I'll sue 'em " Disgruntled physicians challenging
contracts in this manner almost always lose because
the other side has usually constructed a contract that
protects from breach by a careless or inattentive party.
It is well worth the rather nominal expense of having
a lawyer spend an hour going over a contract before
it is signed compared with the relatively bottomless
legal pit of trying to get out of a contract when the
other side is represented by expert legal counsel, ensur-
ing maximum protection of the client.
The key to successful health care contracting is to
realize that you get what you are able to negotiate. Con-
tracts offered only on a "take it or leave it" basis are
usually one-sided and should probably be avoided if
possible. Only a lawyer can fully appreciate the legal
strength for enforcement of a contract or a disputed
VeWH^aeldW image...
7 • LIABILITY ISSUES IN PLASTIC SURGERY: A LEGAL PERSPECTIVE
clause in a contract. It is essential for a physician to
know exactly what the price will be if breach is neces-
sary to get out of an untenable situation. The goal of
working with a lawyer in a preliminary stage is to be
represented by someone during negotiations who can
aid in eliminating or changing unfavorable aspects and
subsequently provide clear definition of the cost of
breach. One definition of a good contract is one in
which both sides walk away dissatisfied. No contract
is perfect for both sides. The goal is to end up with the
most good features for both sides with cost of breach
still being reasonable for both sides if the bad factors
become intolerable.
The single most important issue in most managed
care or other physician employment contracts is how
to get out of the contract if need be. Common boiler-
plate contract language says either that employment
is at will or that employment can be terminated only
for cause. It is tempting to have a contract for a desir-
able job stating that the physician can be terminated
only for cause. Such contracts are really two-edged
swords because cause is almost always a litany of
real or trumped up allegations of inadequate care of
patients. If such allegations can be made to stick suc-
cessfully and the employer is a qualifying health care
entity under Data Bank regulations, termination will
result in a Data Bank report that will be available to
any other qualifying health care agency. Because it is
relatively easy to come forth with a litany of health care
standards and perceived deviations and because it is
relatively difficult for a physician to defend against such
allegations, the best alternative in most instances is to
eliminate termination clauses that read "only for
cause." If termination can be at will, Data Bank report-
ing is not required. After all, if an entity wishes to get
rid of a physician, it really does not matter in the long
run what the reason is, some way will be found to do
it. Why not just make it at will to begin with and save
countless hours and the expense of endless wrangling?
It is probably better in the present managed care envi-
ronment to be fired at will from half a dozen health
maintenance organizations rather than to be fired for
cause from a single qualifying entity. In summary, loose
at it may seem, the best contracts for plastic surgeons
arc usually contracts stating that termination can be
by either side for any reason or for no reason at all at
any time (with reasonable notice).
Of similar and equal importance are noncompete
clauses. Noncompete clauses are being discussed and
disputed in every jurisdiction. Until recently, most
courts would not enforce a noncompete clause that
1
extended more than 5 miles from the place of busi-
ness or for more than 3 years after breach of the con-
tract. Greater distances and longer periods simply were
ruled to be against public policy—the needs of patients
specifically. Even the 5-mile 3-year limits are under
attack now in a number of jurisdictions. Bills are being
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Dr.Mustafa D.
135
introduced in state legislatures to make any noncom-
pete clause in a physician's contract unlawful. It is not
clear what the final result will be, but the tendency
appears to be one of not enforcing noncompetition
clauses as such but instead recognizing that local com-
petition is destructive to the party that suffered breach
and that liquidation damages are fair and should be
levied against the breaching party. As a result, many
employment contracts now contain only liquidation
damage provisions in case of breach and do not have
noncompete clauses as such. The amount of liquida-
tion damages is negotiable; a good lawyer can ensure
that such damages are reasonable and by doing so can
keep noncompetition penalties from destroying an oth-
erwise satisfactory contract. The uniformly despised
"hold harmless" clause ubiquitously present in early
health maintenance organization contracts is begin-
ning to disappear. It can almost always be negotiated
out of a physician's contract if an attempt is made to
do so. If a hold harmless clause cannot be eliminated
from a contract, the plastic surgeon should notify his
or her malpractice carrier before signing. Many mal-
practice carriers will cancel coverage if the insured signs
a contract containing a hold harmless clause. The best
rule now is never to sign an employment contract that
requires the physician to indemnify or hold harmless
any other party.
To cover all of the fine points of successful health
care contracting is obviously beyond the scope of this
treatise. A few warnings that have emerged from the
author's experience, however, can be covered. They
include specifying the date of payment for services and,
if possible, inclusion of incentives for prompt com-
pliance. Mistakes in determining the coverage of
patients treated should not be the responsibility of the
treating physician unless the physician makes the
mistake. A rigid standard of medical care and record
keeping should not be imposed, particularly in a vague
or ambiguous way, over that expected by a reasonable
prudent person or rendered by physicians providing
similar care under similar circumstances in that com-
munity. Malpractice insurance coverage should include
"tail coverage." The cost of tail coverage after 1 or 2
years of practice can exceed the annual premium for
a typical "claims made" malpractice policy. Adding tail
coverage to liquidation damages can make breach of
contract financially impossible.
Quality assurance and peer review functions should
be spelled out clearly in managed care contracts. Some
form of physician representation is desirable. Many
managed care contracts place these important func-
tions entirely in the hands of senior partners or direc-
tors. This issue focuses on the need in any contractual
arrangement to identify who can be trusted if war
breaks out. After all, no contract is any stronger than
the actors who formed it. An unsatisfactory contract
may be entered into when there is identifiable strength
136 I • GENERAL PRINCIPLES
of leadership and quality of character that can be trusted
to be right or fair when disputes arise.
All good contracts have a clear expiration date and
clearly state any obligations, or lack thereof, to renew.
All contracts should prohibit the employer from
disclosing any information about the plastic surgeon
unless such disclosure is required under law. The written
contract must incorporate any verbal representations
made to the surgeon. Although the parole evidence
rule, which covers this important aspect of contract-
ing, is full of legal loopholes, a lawyer will know the
loopholes and be able to protect the client before the
contract is signed.
Some contracts require that disputes be settled by
arbitration or that arbitration must be attempted before
legal redress. Arbitration clauses are illegal in some
states, and they probably should be negotiated out of
most employment contracts if the contract calls for
binding arbitration. The right to go to court is a fun-
damental one; it is not a good idea to bargain away
any fundamental right of American citizenship just for
the sake of a few patient referrals. A good lawyer will
not advise a physician client either to accept or to reject
an employment contract; that really is not the lawyer's
job unless he or she is asked specifically to do so. The
goal of a lawyer in preparing a client to accept or to
reject a contract is to negotiate the best possible terms
and then to make crystal clear the cost of breach if
unfavorable terms persist and later become unbear-
able. This may be as complicated as researching the
present status of noncompete clauses in a particular
locale or as simple as making a list of how many times
the words shall, will, and must appear in clauses out-
lining duties of the physician versus how many times
the words may, could, and might appear in the clauses
outlining responsibilities of the employer.
FRAUD AND ABUSE
Fraud is defined legally as intentional perversion of
truth for the purpose of inducing another in reliance
on it to part with something of value or to surrender
a legal right. Abuse is anything contrary to good order
or business practice established by usage. Writing a
progress note covering a patient's visit that was not
made and using the note to document a bill to a third-
party payer is a clear example of fraud. Leaving a
signature stamp in a pocket of a coat hanging in the
physician's coat room is an example of abuse.
Fraud and abuse by health care providers resulted
in more than $20 billion (11% of total outlays) being
paid for improper claims in 1997. This was an improve-
ment over 14% in 1996.16 These convictions were
covered by criminal, civil, and administrative law agen-
cies. Criminal investigations numbered more than 2000
in 1995 and have increased 200% every year thereafter.
Civil investigations increase approximately 100% a year.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
Why this should be is not entirely clear, although when
one recognizes that health care in America is greater
than a trillion dollar a year industry, it is not unex-
pected that some criminals inevitably are attracted.
Sadly, some physicians seem to be tempted by a feeling
that their legitimate pay is inadequate and that cheat-
ing the federal government is a victimless crime.
Crimes are the result of breaking a statutory law.
The laws most often broken by health care providers
are the anti-kickback statutes, the false claims statute,
and the self-referral statutes (Stark I and Stark II). Mail
fraud, RICO, and conspiracy allegations are often
tacked on in a major crime prosecution. The most dan-
gerous statutes for unsuspecting or naive physicians
are anti-kickback and self-referral statutes; the most
dangerous statute for careless or negligent physicians
is the false claims act. Improper coding, of course, is
the major offense. The Kassebaum-Kennedy or Insur-
ance Portability Act made huge increases in the budget
to fight fraud and abuse and to punish offenders,
including sending physicians to federal prison to
protect health plans from overpaying.17 The bill also
calls for a $10,000 fine for each instance of incorrect
coding, allowing little consideration for an honest
mistake. The message sent by the Kassebaum-Kennedy
bill is loud and clear. If a health care provider fails to
comply with a statutory obligation to provide only
"medically necessary" services, absolutely correctly
coded, the provider can be reduced to poverty and
possibly sent to prison. In addition, rewards to inform-
ants (called relators) and prosecutors also were
increased, as were the number of investigators to seek
out fraud and abuse violations by physicians. Inves-
tigators include employees and the public at large (qui
tarn provision), state organizations called MFCU
(Medicaid Fraud Control Units, which are 90% fed-
erally funded), intermediate managed care organiza-
tions, the Office of the Inspector General, and the
Department of Justice and the FBI. Qui tarn is short
for "qui tarn pro domino rege quam pro se imposo
sequitur," which translated means "who brings the
action as well for the king as for himself." It means
that anyone wishing to file charges of fraud against a
health care provider can do so in federal court, fol-
lowing which the government has 60 days to investi-
gate and decide whether to take over prosecution of
the case. If the United States does not assume prose-
cutorial function, the private citizen can prosecute,
and if the physician is found guilty and penalized, the
qui tarn prosecutor (relator) receives at least 25% and
not more than 30% of the proceeds. If the United States
intervenes, the qui tarn informer can continue to par-
ticipate in prosecution and will receive at least 15%
and not more than 25% of the proceeds. Some rela-
tors have received millions of dollars in fraud and abuse
allegations against health care providers. Fraud and
abuse cases are usually heard in criminal court, where
image...
7 • LIABILITY ISSUES IN PLASTIC SURGERY: A LEGAL PERSPECTIVE
the standard has to be guilty beyond a reasonable
doubt. They are also heard in civil court, where the
standard of guilt is preponderance (51%) of the evi-
dence, and by administrative law judges, where the
standard is whatever it takes to convince a judge of
innocence or guilt. Cases heard before administrative
law judges are appealable to various appeal boards and
the courts.
During the past decade, when fraud and abuse
appeared to Congress and the Justice Department to
be an extremely serious problem of expanding pro-
portions, the standard for criminal conviction was
"knew or should have known."This standard gave little
opportunity for an honest mistake defense. Such a stan-
dard, coupled with the right to inspect health care
records without necessarily showing probable cause,
was oppressive to the point of probably being uncon-
stitutional. There was a time when a physician sus-
pected or even accused of fraud against the government
received less due process than if he or she had been
accused of murder or other high crime. The situation
was so far out of balance that relief was necessary and,
mercifully, came in several ways.
One important measure of relief came in the form
of changing the criminal standard from "knew or
should have known" to "reckless disregard or inten-
tional ignorance." This change provided some leeway
for an honest mistake when there was never any intent
to be reckless or to intentionally disregard the law.
However, there are those who still believe the present
standard is too lenient and that physicians should once
more be held to the "know or should have known"
criminal standard.
In spite of encouragement through public
announcements and circulated documents, a re-
decision by the Fifth Circuit Court of Appeals has
declared qui tarn prosecution unconstitutional. 18 The
decision, meaning that a citizen does not have stand-
ing to sue in the name of the United States, is now
being reviewed by the entire court of appeals. If allowed
to stand, this decision could make a huge difference
in the number of frivolous prosecutions of physicians,
particularly by disgruntled employees, divorced
spouses, and disappointed patients.
Last, statements from the Justice Department in
Health and Human Services suggest that federal inves-
tigators are concentrating their efforts now in trying
to expose and to obtain conviction for criminal activ-
ity; they do not seem to be as interested in prosecut-
ing honest mistakes as in the past.19 The investigation
and prosecution of intentional crime is, of course, in
everyone's best interest.
Experience in fraud and abuse defense makes
several recommendations possible. First, a plastic
surgeon who is being investigated for fraud and abuse
should obtain legal counsel immediately. If law enforce-
ment officers arrive with a court-ordered subpoena,
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Dr.Mustafa D.
137
the physician and the physician's employees must
submit to immediate search and seizure of whatever
the investigating officers deem relevant and material.
Resistance to a court-ordered subpoena is unlawful.
If an investigation is requested by an investigator who
does not have a search warrant, nothing should be
turned over until an attorney determines the neces-
sity to do so. Investigators without a search warrant
are not entitled to any record or information in a physi-
cian's office for 24 hours, and only an attorney should
determine what they are entitled to and what should
be given to them after that. Anyone claiming to be a
health care investigator should be required to produce
identification and to request in writing exactly what
is wanted for inspection. A written receipt should be
obtained for anything an investigator removes. Large
offices should have a special, fairly senior person des-
ignated and trained to deal with investigations. Small
offices should instruct all personnel to be polite but
not to cooperate with individuals claiming a right to
inspect records. In short, nothing should be revealed
and no records shown except through an attorney
unless, of course, law enforcement officers arrive with
a properly executed search warrant.
The final consideration is voluntary reporting of
mistakes. In the case of incorrect payments, simple
return of the money through the intermediate payer
is all that is required. In more complicated or long-
standing situations in which an error in coding or billing
is discovered, voluntary reporting should be done only
through and by an attorney. Laws and regulations
change frequently in this area; plastic surgeons simply
cannotstay abreast of the changes, particularly regard-
ing what kind of mistakes need to be reported and what
the best avenue for reporting them is to prevent unnec-
essary suspicion and investigations.
In summary, in the not too distant past, the alarm-
ing, almost exponential rise in fraud against Medicare
and Medicaid payers was responsible for severe penal-
ties and surveillance. It seems clear now that the justice
system may have overreacted and, in some cases, been
too zealous in prosecuting physicians who had merely
been unaware or made only unintentional mistakes.
During this period, there was a serious risk of false
accusations and overbearing penalties. It appears now,
however, that although fraud and abuse are still major
problems for third-party payers and that major efforts
to expose and to punish criminals are needed, some
balance is being restored to the justice system, and there
is less reason for honest plastic surgeons to fear unjust
investigation and punishment. The correct response
now is to know the general theme of the major laws,
such as false claims acts against the government, anti-
kickback statutes, and self-referral statutes. False claims
accusations can be avoided by scrupulous attention
to coding and billing procedures. Anti-kickback and
self-referral issues should be cleared by a health care
image...

138 I • GENERAL PRINCIPLES

attorney or even by obtaining a ruling from the appro-
priate government agency before participation in any
8.
scheme that might be illegal in these areas. By so doing, 9.
honest plastic surgeons can practice without fear of
fraud and abuse allegations.
10.
REFERENCES 11.
1. Daniels S: Tracing the shadow of the law: jury verdicts in medical 12.
malpractice cases. Justice System J 1990;14:4-39.
2. DeVille K: Medical malpractice in twentieth century United
States; the interaction of technology, law and culture. Int J 13
Technol Assess Health Care 1998;14:197-211.
3. Kridelbaugh WW, Palmisano OJ: Compensation caps for
medical malpractice. ACS Bull 1993;78:27-30.
4. Furrow BR, Grcaney TL, Johnson SH, et al: Reforming tort system 14
for medical injuries. In Furrow BR, Greaney TL, Johnson SH, 15
et al, eds: Health Law, vol 1. St. Paul, Minn, West Publishing, 16.
1995:518-519.
5. Thomas SS: An insurer's right to settle versus its duty to defend 17.
non-meritorious medical malpractice claims. J Legal Med
1995;16:545-583. 18
6. Schloendorffv Society of New York Hospital 105NE92(NY 1914),
overruled by Bing v Thunig, 163 NYS2d 3 (NY 1957). 19
7. Furrow BR, Greaney TL, Johnson SH, et al: Physician obliga-
tions to obtain a patient's informed consent. In Furrow BR,
Greaney TL, Johnson SH, et al, eds: Health Law, vol 1. St. Paul,
Minn, West Publishing, 1995:409-431.
Johnson v Kohemoor, 525 NW2d 71 (Wise App 1994).
Olson SM, Howard-Martin J: Controversy brews over guide-
lines for AIDS-infected health care workers. Healthspan
1991;8:13-15.
Faya vAlmaraz, 329 Md 435,449,450.
King N: Patient waiver of informed consent. N C Med J
1993;54:399-401.
KelletAJ: Healing angry wounds.Therolesof apology and medi-
ation disputes between physicians and patients 1. Missouri J
Dispute Resolution 1987:111-131.
Wciler PC, Hiatt HH, Newhouse JP, et al: A Measure of Mal-
practice: Medical Injury, Malpractice Litigation and Patient
Compensation. Cambridge, Mass, Harvard University Press,
1993:43-62.
Patrick vBurget, 486 US 94,108 SCt 1658,100 LEd2d 83 (1988).
42 USCA §11101-11152.
Contone L: Corporate compliance: critical to organizational
success. Nursing Economics 1999;17:15.
Health Insurance Portability and Accountability Act of 1996
(Public Law 104-191). Kasseba urn -Kennedy bill.
Riley vSt Luke's Episcopal Hospital, No. 97-20948 (5th Cir Nov
15 1999).
Klein SA: Doctors "not being targeted." Fraud enforcers say
they're not going to jump on simple errors. AMA News, March
16,1998:3-30.

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
image...
CHAPTER
8•
Liability Issues in Plastic
Surgery: An Insurance
Perspective
MARK GORNEY, MD
PATIENT SELECTION CRITERIA
LEGAL PRINCIPLES APPLIED TO PLASTIC SURGERY
Standard of Care
Warranty
Disclosure
PSYCHOLOGICAL AND PSYCHIATRIC ASPECTS OF
MODIFYING ANATOMY
Effective Communication as a Claims Prevention
Anger: A Root Cause of Malpractice Claims
Characteristics of Trouble-Prone Patients
THE WHEEL OF MISFORTUNE
Breast Augmentation
Breast Reduction
Scarring
Face Lift and Blepharoplasty
PATIENT SELECTION CRITERIA
A plastic and reconstructive surgeon practicing in the
United States in the last 3 decades of the 20th century
will find it virtually impossible to end his or her career
unblemished by a claim of malpractice. However, well
above half of the malpractice claims are preventable.
Most are based on either the failure of communica-
tion or faulty patient selection criteria, not on techni-
cal faults.
Selection of patients is the ultimate inexact science.
It is a mixture of surgical judgment, gut feelings, per-
sonality interactions, and the strength of the surgeon's
ego. Regrettably, late in the 20th and early 21 st century,
economic considerations have played a significant role.
Regardless of technical ability, someone who appears
cold, arrogant, or insensitive is far more likely to be
sued than is one who relates at a "human" level. Obvi-
ously, a personality that is warm, sensitive, and natu-
rally caring coupled to a well-developed sense of humor
and cordial attitude is much less likely to be the target
of a malpractice claim. The ability to communicate
clearly and well is probably the most outstandingchar-
acteristic of the claims-free surgeon. Communication
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Dr.Mustafa D.
Rhinoplasty and Septoplasty
Abdominoplasty
Skin Resurfacing
Suction-Assisted Lipectomy
Miscellaneous
INFORMING YOUR PATIENTS BEFORE THEY CONSENT
"Prudent Patient" Test
Refusals
Consent-in-Fact and Implied Consent
Minors
Religious and Other Objections
How Much Is Enough?
The Six Elements of Informed Consent
Documentation
The Therapeutic Alliance
is the sine qua non of building a physician-patient
relationship. Unfortunately, the ability to communi-
cate well is a personality trait that cannot readily be
learned in adulthood. It is an integral part of the
surgeon's personality. This, however, is another chapter
by itself.
LEGAL PRINCIPLES APPLIED TO
PLASTIC SURGERY
Standard of Care
Malpractice is defined as "treatment that is contrary
to accepted medical standards and which produces inju-
rious results in the patient." Because most medical mal-
practice actions are based on laws governing negligence,
the law recognizes that medicine is an inexact art and
that there can be no absolute liability. Thus, the cause
of action is usually the "failure of defendant/physician
to exercise that reasonable degree of skill, learning, care,
and treatment ordinarily possessed by others of the
same profession in the community." Whereas the term
communitywas accepted geographically in the past, it
is now based on the supposition that all physicians keep
139
140 I • GENERAL PRINCIPLES
up with the latest developments in their field. Com-
munity, then, is generally interpreted as a "specialty
community." The standards are now those of the
specialty as a whole without regard to geographic
location. This is what is commonly referred to as
"standard of care."
Warranty
The law holds that by merely engaging to render treat-
ment, a physician warrants that he or she has the learn-
ing and skill of the average member of that specialty
and that he or she will apply that learning and skill
with ordinary and reasonable care. This warranty is
one of due care. It is legally implied; it need not be
mentioned by the physician or the patient. However,
the warranty is one for service, not cure. Thus, the physi-
cian does not imply that the operation will be a success,
that results will be favorable, or that he or she will not
commit any medical errors not caused by lack of skill
or care.
Disclosure
In attempting to define the yardstick of disclosure, the
courts divide medical and surgical procedures into two
categories:
1. common procedures that incur minor or very
remote serious risk, including death or serious
bodily harm (e.g., the administration of peni-
cillin); and
2. procedures involving serious risks for which the
physician has an "affirmative duty to disclose the
potential of death or serious harm and is bound
to explain in detail, the complications that
might possibly occur."
Affirmative duty means that the physician is obliged
to disclose risks on his or her own, without waiting for
the patient to ask. The Supreme Court of the United
States long ago established that it is the patient, not
the physician, who has the prerogative of determining
what is in his or her best interests. Thus, the physician
is legally obligated to discuss with the patient thera-
peutic alternatives and their particular hazards to
give that patient sufficient basis of information with
which to decide in which direction his or her best
interests lie.
How much explanation and in what detail are dic-
tated by a balance between the surgeon's feelings about
his or her patients and the legal requirements appli-
cable. It is simply not possible to tell patients every-
thing without scaring them out of their surgery.
Rather, the law states that patients must be told the
most probable of known dangers and the percentage
of that probability. The rest maybe disclosed in general
terms while reminding the patient that he or she also
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Dr.Mustafa D.
has a statistical possibility of falling down and getting
hurt that same day.
Obviously, the most common complications should
be volunteered frankly and openly, and their proba-
bility, based on the surgeon's personal experience,
should also be discussed. Finally, any or all of this infor-
mation is wasted unless it is documented in the patient's
record. For legal purposes, if it is not in the record, it
never happened!
PSYCHOLOGICAL AND
PSYCHIATRIC ASPECTS OF
MODIFYING ANATOMY
The growing popularity of elective aesthetic surgery
makes it imperative to establish clear criteria of patient
selection. Absent this discrimination, there will be an
inevitable and steady increase in patients' dissatisfac-
tion and litigation.
Who, then, is the "ideal" candidate for aesthetic
surgery? There is no such thing, but the surgeon should
note any personality factors that will enhance or detract
from the physical improvements sought.
There are basically two categories that make the
patient an unlikely candidate for elective aesthetic
surgery. The first is anatomic unsuitability. The second
is psychological inadequacy. Because psychological
inadequacy is by far the more important, the surgeon
must differentiate between healthy and unhealthy
reasons for seeking aesthetic improvement.
Strength of motivation is critical. It has a close
relationship with the patient's satisfaction postopera-
tively. Furthermore, a strongly motivated patient will
have less pain, a better postoperative course, and a
significantly higher index of satisfaction regardless of
result. Although these characteristics are virtually
impossible to predict with absolute accuracy, it is pos-
sible to establish some reasonably objective criteria of
a patient's liability potential (Fig. 8-1).
Effective Communication as a
Claims Prevention
All litigation in plastic surgery has the common
denominator of poor communication. Underlying all
dissatisfaction is a breakdown in the rapport between
patient and surgeon. This vital relationship is often
shattered by the surgeon's arrogance, hostility, and cold-
ness (real or imagined) and mostly by the fact that "he
or she didn't care." There are only two ways to avoid
such a debacle: (1) make sure that the patient has no
reason to feel that way and (2) avoid a patient who is
going to feel that way no matter what is done.
Although the physician's skill, reputation, and
other intangible factors contribute to a patient's sense
of confidence, rapport between patient and physician
image...

8 • LIABILITY ISSUES IN PLASTIC SURGERY: AN INSURANCE PERSPECTIVE 141

between anxiety and anger is tenuous, and the con-

5 version factor is uncertainty—fear of the unknown. A
patient frightened by a postoperative complication or
/
uncertain about the future may surmise that "if it is
the doctor's fault, then the responsibility for correc-
4
tion falls on the doctor."
£
The patient's perceptions may clash with the physi-
<D cian's anxieties, insecurities, and wounded pride. The
£ 3 patient blames the physician, who in turn becomes
o defensive. At this critically delicate juncture, the physi-
o cian's reaction can set in motion or prevent a natural
2 chain reaction. The physician must put aside feelings
of disappointment, anxiety, defensiveness, and hostil-
ity to understand that he or she is probably dealing
1 with a frightened patient who is using anger to gain
"control" of the situation. Subsequent developments
can be changed by whatever understanding, support,
1 2 3 4 5 and encouragement seem appropriate to the situation.
Deformity
The patient's perception that the physician understands
FIGURE 8 - 1 . Depiction of a patient's objective defor- that uncertainty and will join with him or her to help
mity along the horizontal axis (as judged by the surgeon) overcome it may be the deciding factor in whether the
versus the patient's degree of concern about that defor- patient will seek legal counsel (Fig. 8-2).
mity (vertical axis) as perceived by the patient. Two oppo-
site extremes then emerge: One of the worst errors in dealing with angry or
1. The patient with major deformity but minimal concern dissatisfied patients is to try to avoid them. It is nec-
(lower right-hand corner). This is a patient with essary to actively participate in the process rather than
an obvious major deformity in whom it is clear that avoid the issue.
any degree of improvement will be regarded with
satisfaction.
2. The patient with minor deformity but extreme concern
(upper left-hand corner). This, in contrast, is the patient
Characteristics of
with a deformity that the surgeon perceives to be so Trouble-Prone Patients
minor as to be negligible but who demonstrates an
inordinate degree of concern and emotional turmoil. GREAT EXPECTATIONS. There are certain patients
These are the patients who are most likely to be who have an extremely unrealistic and idealized but
dissatisfied with whatever the outcome. In addition, vague conception of what elective aesthetic surgery is
the surgical outcome has little relationship with the going to do for them. They anticipate a major change
emotional distress. The anxiety expressed about the
"deformity" is merely a manifestation of inner turmoil, in lifestyle with immediate recognition of their newly
which is better served by a psychiatrist's couch than acquired attractiveness that will lead to boundless admi-
a surgeon's operating table. ration and limitless improvement in the quality of life.
Most who seek aesthetic surgery fit somewhere on a diag- These patients obviously have an unrealistic concept
onal between the two contralateral corners. The closer of where their surgical journey is taking them and have
the patient comes to the upper left-hand corner, the more great difficulty in accepting the fact that any major
likely is an unfavorably perceived outcome as well as a surgical procedure carries inherent risk.
visit to an attorney.

is based on forthright and accurate communication. Improper performance 60%

It is faulty communication that most often leads to the
\
inevitable vicious circle that follows: disappointment, Dissatisfaction
anger, and frustration on the part of the patient; reac- (failed expectations)
tive hostility, defensiveness, and arrogance from the 22.6%
physician, deepening the patient's anger; and finally a
visit to the attorney.
\
Anger: A Root Cause of Miscellaneous
17.4%
Malpractice Claims
FIGURE 8 - 2 . Principal reasons a patient will visit
Patients feel a sense of bewilderment and anxiety when an attorney's office after a plastic or reconstructive
elective surgery does not go smoothly. The borderline procedure.

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
TeWR^aacTKf image...
142 I • GENERAL PRINCIPLES
EXCESSIVELY DEMANDING PATIENTS. In general, the
patient who brings photographs, drawings, and exact
architectural specifications should be managed with
great caution. Such a patient has little comprehension
that the surgeon is dealing with human flesh and blood,
not wood or clay. This patient must be made to under-
stand the realities of what surgery is about, the vagaries
of the healing process that is controlled by the patient's
genetic characteristics, and the margin of error that is
a natural part of any elective procedure. Such patients
show little flexibility in accepting any degree of failure
on the part of the surgeon to deliver exactly what they
anticipated.
INDECISIVE PATIENTS. TO the question "Doctor, do
you think I ought to have this done?" the prudent
surgeon should respond, "This is a decision that I
cannot make for you. It is one you have to make your-
self. I can tell you what I think we can achieve, but if
you have any doubt whatsoever, I recommend strongly
that you think about it carefully before deciding
whether or not to accept the risks I have discussed with
you." The more the decision to undergo surgery is
motivated from within and not "sold," the less likely
are recriminations to follow an unfavorable result.
IMMATURE PATIENTS. The experienced surgeon
should assess not only the physical but also the emo-
tional degree of maturity that the patient exhibits.
Youthful or immature patients (age has no relation-
ship to maturity) usually have excessively romantic
expectations and a highly unrealistic concept of what
the surgery will achieve. Often, when confronted with
the mirror postoperatively, they are likely to react in
disconcerting or even violent fashion if the degree of
change achieved does not coincide with their precon-
ceived notions.
SECRETIVE PATIENTS. Certain patients wish to
convert their surgery into a"secret" and request all kinds
of elaborate precautions against anyone's knowing what
they are doing. Aside from the fact that such arrange-
ments for secrecy are difficult to achieve, this tendency
is a strong indication that the patient has a suspicious
degree of guilt about the procedure being undertaken.
Thus, there is a higher likelihood for subsequent
dissatisfaction to be expressed.
FAMILIAL DISAPPROVAL. It is far more comfortable,
although not essential, if the immediate family approves
of the surgery being sought, particularly in the case of
a minor. If there is disapproval, not uncommonly, errors
in communication or less than optimal results imme-
diately produce an automatic"See, I told you so!" reac-
tion, which deepens not only the guilt of the patient
but also the dissatisfaction and increases the likelihood
of a claim.
PATIENTS YOU DO N O T LIKE (OR W H O DO NOT LIKE
YOU). Regardless of the surgeon's personality,
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
inevitably in life there are people whom you simply
do not like or who do not like you. Most experienced
surgeons know within minutes of entering the exam-
ining room whether they will or will not be operating
on that patient. Accepting a patient whom you basi-
cally dislike is a serious mistake. A clash of personali-
ties for whatever reason is bound to affect the outcome
of the case regardless of quality of the postoperative
result. No matter how "challenging" such a case may
appear, it is far better to decline.
THE "SURGIHOLIC." A patient who has had a
variety of plastic surgery procedures performed, and
who is a "surgiholic," has a poor self-image for which
he or she is trying to compensate by repeated aesthetic
procedures, whether they are needed or not. In addi-
tion to the obvious implications of such a personality
pattern, the surgeon is always confronted with a much
more difficult anatomic situation because of the pre-
vious surgeries. He or she also risks unfavorable com-
parison with previous surgeons. The percentage of
degree of improvement often simply is not worth the
risk.
Generally speaking, there is a clear risk-to-benefit
ratio to every surgical procedure. Circumstances differ
with each patient, but there is a rule of thumb appli-
cable to all candidates for elective aesthetic surgery.
If the risk-to-benefit ratio is favorable, the surgery
should probably be encouraged and has a high degree •
of probability of success. If, on the other hand, the risk-
to-benefit ratio is unfavorable, not only does the reverse
apply, but the unintended side effects of the unfavor-
able outcome may turn out to be completely dispro- <
portionate to the surgical result. The only way to avoid
this debacle is to learn how to distinguish those patients
whose body image and personality characteristics make
them simply unsuitable for the surgery they seek.
THE WHEEL OF MISFORTUNE
A plastic surgeon has a dual responsibility, completely
different from that of any other kind of practitioner.
Most physicians care for sick people and try to make
them well; the plastic surgeon takes someone who is
well and makes that person temporarily unwell to make
him or her better. Unfortunately, the perception of
whether the physician succeeded is very much in the
eye of the patient. Thus, the plastic surgeon is the only
kind of specialist who may finish his or her treatment
completely successfully by any objective criteria and
still have a dissatisfied patient. This consideration makes
any insurance carrier leery of offering coverage to those
who perform aesthetic surgery.
A substantial number of the existing carriers will
not cover plastic and reconstructive surgeons who
perform aesthetic surgery. Most insurance companies
offering coverage to aesthetic surgeons find that the
overwhelming majority of their claims come from
image...
8 • LIABILITY ISSUES IN PLASTIC SURGERY: AN INSURANCE PERSPECTIVE
Lipoplasty 3% Facial resurface 2%
Low frequency Chemical peel
High severity Laser
Abdomen 5%
Misc 7%
FIGURE 8-3. Statistically, the cause of action seems to
stem from specific types of elective aesthetic surgery.
approximately 8 to 10 operations (Fig. 8-3). However,
they account for a substantial percentage of their overall
loss (Fig. 8-4).
Some carriers have different premium structures
for those surgeons who perform only aesthetic surgery
compared with those who perform mostly recon-
structive surgery. The exposure is obviously a great deal
less. The medical-legal exposure also varies greatly by
geography. It stands to reason that premiums have to
be significantly higher in an urban area than in a rural
one and that they also vary greatly according to geog-
raphy. There is hardly any comparison, for example,
between exposures in Indianapolis and those in Los
Angeles, Miami, or New York.
It is well recognized that the loss experience in plastic
surgery is notable for its frequency rather than sever-
ity (Fig. 8-5). Currently, anyone in private practice can
anticipate some contact with the legal system (not nec-
essarily leading to a full-bore lawsuit) every 2.4 years.
Although severity has never characterized plastic
FIGURE 8 - 4 . Percentage of claims lost by plastic
surgeons (cosmetic versus reconstructive).
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
143
Allocated claims:
claims against which money was reserved
3,823
FIGURE 8-5. The number of allegations against plastic
surgeons affiliated with The Doctor's Company (TDC)
between its inception (1975) and the end of 1999 is a
staggering 76,646. Of these, only 3,823 are "allocated"
claims. This means the case has sufficient validity to cause
the TDC claims department to put up reserves propor-
tionate to their estimation of the potential cost of final
adjudication. It also gives credence to the fact that the
vast majority of claims against TDC plastic surgeons are
frivolous.
surgery's loss experience in the past, the trend is clearly
toward larger settlements and awards, particularly for
those patients in whom an elective procedure has
resulted in a fatal outcome.
Breast Augmentation
Unquestionably, the leader in any medical liability
carrier's plastic surgery loss experience is breast surgery,
both augmentation and reduction. Of these two cat-
egories, augmentation is by far the greatest. Approxi-
mately 44% of all elective aesthetic surgery claims
involve augmentation. Setting aside for the moment
the hotly debated issue of whether gel-filled devices
cause autoimmune disease, the genesis of dissatis-
faction and the main complaints have been the
following:
• Encapsulation with distortion and firmness
• Wrong size (too little or too much)
• Infection
• Repetitive surgeries and attendant costs
• Nerve damage with sensory loss
Breast Reduction
In the breast reduction category, the genesis of
dissatisfaction includes the following:
• Unsatisfactory scar
• Loss of nipple or breast skin cover requiring
revision and grafting
• Asymmetry "disfigurement"
144 I • GENERAL PRINCIPLES
Scarring
Most surgeons assume the patient understands that
healing entails formation of scar. Unfortunately it is
seldom discussed in the preoperative consultation. In
plastic and reconstructive surgery, the ultimate appear-
ance of the resulting scar can be the major genesis of
dissatisfaction. It is imperative that the plastic surgeon
obtain from the patient clear evidence of his or her
comprehension that without scar, there is no healing.
Patients must be made to understand that their healing
qualities are as individual to them as the texture
of their hair or the color of their eyes; it is built into
their genetic program. Documentation of such con-
versation in the preoperative chart should go a long
way toward making any resulting claim far more
defensible.
Face Lift and Blepharoplasty
Face lift and blepharoplasty account for approximately
11% of claims. The most common allegations are
• Excessive skin removal resulting in a "stary" look
• Dry eyes or inability to close
• Nerve damage resulting in distorted expression
• Skin slough resulting in excessive scarring and
revisional surgery
• Cost of additional revisional surgeries
The trend toward performance of most of these pro-
cedures on an outpatient basis deserves some comment.
In a survey of blepharoplasty lawsuits done someyears
ago, it was discovered that the only trait all patients
had in common was that they were discharged very
shortly after the termination of the outpatient surgery
(Fig. 8-6). On arrival home, all did something to gen-
erate a sudden rise in blood pressure at the time of
maximal reactive hyperemia as the epinephrine in
the local anesthetic wore off (e.g., constipated bowel
FIGURE 8-6. The distribution of location where most
incidents arise.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
movement, sudden coughing fit, bending over and
reaching down to tie shoes). It is imperative that all
patients undergoing outpatient surgery that involves
undermining of heavily vascularized tissues be strictly
warned not to undertake any maneuvers that will gen-
erate such sudden elevations in blood pressure. In addi-
tion, it is strongly recommended that no patient be
discharged from an outpatient surgical facility until at
least 3 hours have elapsed and there is evidence that
all the local anesthetic effects have worn off.
Rhinoplasty and Septoplasty
This category constitutes approximately 8% of
the claims. The most common allegations are the
following:
• Unsatisfactory result: improper performance
• Continued breathing difficulties
• Asymmetry
• Cost of revisional surgery
The most common is rhinoplasty. Of all the oper-
ations performed by plastic and reconstructive sur-
geons, regrettably this is the one with the highest
degree of unpredictability. The problem is greatly
aggravated by inappropriate patient selection crite-
ria. In these claims, there is almost universally a great
gap between the patient's expectations and the results
obtained even under the best of circumstances. The
inappropriate use of imaging devices often causes
the patients to have totally unrealistic expectations,
as does the showing of "brag books" with only excel-
lent results. The clear implication is "this is the kind
of work that I do, and this is what you can expect."
Unfortunately, for many patients, the actual result falls
short of the promise, and the usual cycle is put into
motion: surprise, disappointment, anger, perceived
arrogance, increased avoidance, rising hostility, visit
to the lawyer.
Abdominoplasty
Abdominoplasty with or without suction-assisted
lipectomy represents approximately 3% of claims with
the following allegations:
• Skin loss with poor scars
• Nerve damage
• Inappropriate operation
• Infection with postoperative mismanagement
There is little question that suction-assisted
lipoplasty before the actual abdominoplasty has
significantly increased the morbidity in this operation
and therefore doubled the number of claims in this
category. There is clearly a much higher percentage of
skin sloughs in those procedures preceded by suction-
assisted lipectomy.
ItJWR^aacrw image...
8 • LIABILITY ISSUES IN PLASTIC SURGERY: AN INSURANCE PERSPECTIVE
Skin Resurfacing
Chemical peels and laser resurfacing constitute the next
category of claims, again in the range of roughly 3%.
The principal allegations here are the following:
• Blistering or burns with significant scarring
• Infection with postoperative mismanagement
• Permanent discoloration postoperatively
Because of the unpredictability of individual healing
characteristics, it is probably a good idea to do a "test
patch" in an area that can be hidden (e.g., the back of
the neck). Certainly, the documentation preceding this
operation should contain clear warnings that quality
of healing is linked to the individual's genetic charac-
teristics and cannot be predicted. The operator must
make it clear to the patient that final color and texture
determination is not always in the hands of the
surgeon and that heavy makeup may be needed for an
indeterminate time.
Suction-Assisted Lipectomy
Suction-assisted lipectomy, whether conventional or
ultrasonic, has now clearly become the single most
requested elective aesthetic procedure in the United
States. Approximately 145,000 of these procedures were
performed in the year 1997, according to statistics of
the American Society of Plastic and Reconstructive Sur-
geons. However, the rising popularity of this proce-
dure has brought with it a host of problems. To begin
with, because this is not a surgical procedure in the
"traditional" sense, it is being performed by a wide
variety of practitioners, some of them with no surgi-
cal background or clear understanding of the surgical
anatomy involved. Second, it is a procedure that is most
commonly performed on an outpatient basis outside
of the control of any regulatory authorities. In addi-
tion, with the advent of "tumescent" techniques, an
unseemly race has developed to see who can suction
out the most fat. The net result has been a dramatic
rise in severe morbidity and fatal outcomes from so-
called high-volume liposuction. What is high volume?
It is generally agreed that anything above 5000 mL of
extracted fat constitutes high volume. More impor-
tant, the extraction of this amount of fat causes pro-
found physiologic changes, which in turn can lead to
severe complications or fatal outcomes. The infusion
of large amounts of fluid with even a weak solution of
lidocaine has also resulted in a number of fatal out-
comes due to anesthetic overdose. To make matters
even worse, these procedures are often combined
with other prolonged operations. Experience clearly
indicates that when a patient has been on the table
under anesthesia for more than 6 hours, undergoing
multiple procedures, the percentage of complications
or fatal outcome rises dramatically.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
145
There are two categories of liability from conven-
tional assisted lipectomy procedures:
M I N O R ALLEGATIONS
• Disfigurement and contour irregularities
• Numbness
• Disappointment or dissatisfaction
MAJOR ALLEGATIONS
• Unrecognized abdominal perforations requiring
lifesaving or disabling secondary surgery or
resulting in death
• Lidocaine overdose with fatal outcome
• Pulmonary edema from overhydration
• Pulmonary embolism and death
It should be obvious that the cavalier way in which
this operation is increasingly being performed requires
rethinking, particularly when the amount of fat
extracted is major. In a number of venues in the United
States, the state medical regulatory authorities are
beginning to take notice, and unless there is a significant
downturn in the morbidity of this procedure, there
will undoubtedly be some regulatory intervention to
control the rising tide of misfortune.
Miscellaneous
Approximately 5% of all complaints against plastic and
reconstructive surgeons have to do with miscellaneous
allegations:
• Untoward reaction to medications or anesthesia
• Improper use of preoperative or postoperative
photographs
• Sexual misconduct (male physician or employee)
There are certain common threads among all
procedures performed by plastic and reconstructive
surgeons that are commonly not brought to the atten-
tion of the patient in the preoperative consultations
or often represent the triggering mechanism for the
claim. They are
• Unexpected scarring
• Lack of adequate disclosure (tailored to the
patient's level of understanding)
• General dissatisfaction: the patient's expectations
were not met or were unrealistic to begin with
At a time of convulsive change in the history of health
care delivery in the United States, certain socio-
economic factors also come into play. With the rising
number of practitioners, competitive pressures have
begun to affect patient selection criteria. There is a clear
trend toward substitution of surgical judgment (and
even common sense) for economic considerations.
Because of the economic constrictions placed on
medical incomes, many practitioners see elective
146 I • GENERAL PRINCIPLES
aesthetic surgery as the last area of practice unencum-
bered by either insurance or governmental restrictions.
This has attracted many individuals with inadequate
qualifications. Even within the ranks of board-certified
plastic surgeons, the rising trend toward "marketing"
and the need to "sell" surgery (which should always be
motivated by the patient's self-perception) have further
blurred patient selection criteria. Although it is virtu-
ally impossible for a plastic and reconstructive surgeon
to go through a 30- to 40-year career without a medical
liability claim, it is certainly still possible to reduce the
eventuality of this unpleasant experience by the appli-
cation of simple principles: maintain good commu-
nication and rapport with the patient through good
times and bad; restrict your practice to those proce-
dures with which you feel thoroughly comfortable; pay
close and careful attention to documentation of your
activities; and above all, realize that a normal temper-
ature and a valid credit card by themselves are poor
criteria for elective aesthetic surgery.
INFORMING YOUR PATIENTS
BEFORE THEY CONSENT
In the language of medical liability, no concept has
received as much misinterpretation as "informed
consent." In the last 5 years, most medical liability car-
riers have experienced a significant increase in claims
that allege failure to obtain a proper informed consent
before treatment. This trend is particularly noticeable
in claims against surgical specialties, in which a sub-
stantial portion of treatment is elective.
Simply stated, informed consent means that adult
patients who are capable of rational communication
have to be provided with sufficient information about
risks, benefits, and alternatives to make a decision
and expressly give permission for a proposed course
of treatment. (The same is true for "emancipated" or
"self-sufficient" minor patients.) In most states, physi-
cians have an affirmative duty to disclose such infor-
mation. This means that you must not wait for
questions from your patients; you must volunteer the
information.
Without informed consent, either expressed or
implied, you risk legal liability for a complication or
untoward result—even if it was not caused negligently.
The central thesis of this widely accepted legal doc-
trine is this: The patient must be given all information
about risks that are relevant to a meaningful decision-
making process. It is the perogative of the patient, not
the physician, to determine the direction in which it
is believed his or her best interests lie. Thus, reason-
able familiarity with therapeutic (and diagnostic) alter-
natives and their hazards is essential.
Do patients have the legal right to make bad
judgments because they fear a possible complication?
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
Increasingly, the courts answer affirmatively. Once the
information has been fully disclosed, that aspect of the
physician's obligation has been fulfilled. The weighing
of risks is usually not a medical judgment but is instead
reserved for the patient alone.
"Prudent Patient" Test
In many states, the most important element in claims
involving disputes over informed consent is the
prudent patient test. The judge will inform the jury
that there is no liability on the physician's part if a
prudent person in the patient's position would have
accepted the treatment had he or she been adequately
informed of all significant perils. Although this concept
is subject to re-evaluation in hindsight, the prudent
patient test becomes most meaningful when treat-
ment is lifesaving, urgent, or at least prophylactic.
The concept may also apply to simple procedures
for which the danger is commonly appreciated to
be remote. In such cases, disclosure need not be
extensive, and the prudent patient test will usually
prevail.
On occasion, however, "simple" procedures like
administering an injection of penicillin may incur
serious medical risks of bodily harm or death. For these
procedures, it is wise to fully discuss risks and to follow
informed consent procedures, even though the risks
are remote.
Refusals
As part of medical counseling, many state laws mandate
that physicians warn patients of the consequences
involved with failing to heed medical advice by refus-
ing treatment or diagnostic tests. Obviously, patients
have a right to refuse. In such circumstances, it is essen-
tial that you carefully document such refusals and their
consequences and that you verify and note that the
patient understood the consequences.
Documentation is particularly important in cases
involving malignant disease, when rejection of tests
may impair diagnosis and refusal of treatment may
lead to a fatal outcome. Remember to date all such
entries in the patient's record.
If the information you present includes percent-
ages or other specific figures that allow the patient to
compare risks, be certain that your figures conform
with the latest reliable data.
Consent-in-Fact and
Implied Consent
What is the distinction between ordinary consent to
treatment (consent-in-fact) and informed consent?
VtSWt^aeleMtf image...
8 • LIABILITY ISSUES IN PLASTIC SURCERY; AN INSURANCE PERSPECTIVE
Simply stated, informed consent verifies that the
patient is aware of anticipated benefits as well as risks
and alternatives to a given procedure, treatment, or
test. On the other hand, proceeding with treatment of
any kind without actual consent is "unlawful touch-
ing" and may therefore be considered battery.
When the patient is unable to communicate ration-
ally, as is the case for many patients seen on an emer-
gency basis, there may be a legally implied consent to
treat. The implied consent in an emergency is assumed
only for the duration of that emergency.
If the patient is an unemancipated minor or
is incompetent, the authority to consent is usually
transferred to the patient's legal guardian or closest
available relative. When certain procedures such as
operations on minors are contemplated, the physician
assumes a special risk and should be absolutely certain
to obtain full permission from the parents, guardian,
conservator, or state official who has jurisdiction.
In some instances, completing certain forms may be
prescribed by law.
In an emergency, however, you must not delay in
treating a minor or an incompetent person when such
a delay might adversely affect the outcome of the case.
In such circumstances, anything less than prompt atten-
tion and treatment will increase your exposure to
liability.
Minors
Except in urgent situations, treating minors without
consent from a parent, legal guardian, appropriate gov-
ernment agency, or court carries a high risk of legal or
even criminal charges. There are statutory exceptions,
such as for an emancipated adolescent or a married
minor. If you regularly treat young people, you should
familiarize yourself with the existing statutory provi-
sions in your state and keep up to date.
Religious and Other Objections
On occasion, you may be placed in the difficult posi-
tion of being refused permission to treat or to conduct
diagnostic tests on the basis of a patient's religious or
other beliefs. Although grave consequences may ensue,
there is little that you can do in most states beyond
making an intense effort to convince the patient.
In some states, court intervention may be obtained.
Here, too, knowing the law of the state in which you
practice is advisable.
If a patient is either a minor or incompetent (and
the parent or guardian refuses treatment) and you know
serious consequences will ensue if appropriate tests
and treatment are not undertaken, your legal and moral
obligations change. You must then resort to a court
order or another appropriate governmental process in
an attempt to secure surrogate consent.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
147
In an emergency, if there is not sufficient time to
file a formal petition, you may request intervention by
a judge or other person with authority to act on the
patient's behalf. If such permission is given by tele-
phone, witnesses should be listening in. The partici-
pation of personal or hospital legal counsel is advisable
to ensure that the legal requirements applicable in your
locale are met.
Documentation that includes accurate dates and
times is absolutely mandatory to protect you from pos-
sible later actions by disaffected parents, guardians, or
heirs.
How Much Is Enough?
The extent to which disclosure must be offered obvi-
ously varies with the urgency of the test or treatment.
A patient who presents with a condition requiring
emergency care is held to imply consent for you to
provide such care. In addition, in instances in which
a life or limb is at stake, some Good Samaritan statutes
may provide shelter from subsequent litigation.
However, whereas consent may be implied, you
should still make an effort to obtain consent from a
patient who is capable of rational communication or
from any family member immediately available.
In all cases, the following guidelines apply:
• Do disclose the identity of the treating physician
or operating surgeon if he or she differs from the
attending physician.
• Do discuss the risk of death or serious harm, if
applicable.
• Do not inform the patient that the procedure is
simple and that no complications will occur.
• Do not perform procedures in addition to the
principal procedure without specific consent
unless an emergency situation develops.
• Do not expect to obtain informed consent by
merely answering questions that the patient asks;
volunteer the appropriate information.
• Do provide the patient with an opportunity to
ask questions.
The Six Elements of Informed
Consent
When treatment is urgent (e.g., in a case of severe
trauma), it may be needless and cruel to engage in exten-
sive disclosure that could augment existing anxieties.
However, you should inform the patient fully and com-
pletely of the treatment's risks and consequences and
record such discussions. Table 8-1 includes the six
elements of valid informed consent.
In situations in which the nature of the tests or treat-
ment is purely elective, as with cosmetic surgery, the
disclosure of risks and consequences may need to be
148 I • GENERAL PRINCIPLES
TABLE 8-1 • SIX ELEMENTS OF VALID
INFORMED CONSENT
Discuss the following six elements of a valid informed
consent with your patients and their families:
The diagnosis or suspected diagnosis
The nature and purpose of the proposed treatment or
procedure and its anticipated benefits
The risks, complications, or side effects
The probability of success, based on the patient's
condition
Reasonable available alternatives
Possible consequences if advice is not followed
expanded. Office literature can provide additional
details about the procedure. In addition, an expanded
discussion should take place regarding the foreseeable
risks, possible untoward consequences, or unpleasant
side effects associated with the procedure. This expan-
sion is particularly necessary if the procedure is new,
experimental, especially hazardous, purely for cosmetic
purposes, or capable of altering sexual capacity or
fertility.
Documentation
Written verification of consent to diagnostic or ther-
apeutic procedures is crucial as a claims prevention
technique. Remember, a physician's handwritten nota-
tion that includes the entry's date and time can make
the difference between a totally defensible case and one
that is lost. A simple entry of several lines might suffice,
such as,"Have discussed in detail objectives, technique,
and potential complications of procedure. Have also
discussed location and possible appearance of scars
and sources of dissatisfaction. All questions answered.
Patient understands and accepts."
Also remember, however, that in an increasing
number of circumstances, laws now require the com-
pletion of specifically designed consent forms. Studies
indicate that physicians sometimes underestimate
the patient's ability to understand. If your records
disclose no discussion or consent, the burden will be
on you to demonstrate legally sufficient reasons for
such absence. It is a test of your good judgment of
what to say to your patient and of how to say it to
obtain meaningful consent without frightening the
patient.
No permit or form will absolve you from respon-
sibility if there is negligence; nor can a form guaran-
tee that you will not be sued. Permits may vary from
absurdly simple to incomprehensibly detailed. Most
medical-legal authorities agree that a middle ground
exists. All agree that lay terms should be used.
A well-drafted informed consent document is
proof that you tried to give the patient sufficient
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
information on which to base an intelligent decision.
Such a document, supported by a handwritten note
and entered in the patient's medical record, is often
the key to a successful malpractice defense when the
issue of consent to treatment arises.
The Therapeutic Alliance
Obtaining informed consent need not be an imper-
sonal legal requirement. When properly conducted,
the process of obtaining informed consent can help
establish a "therapeutic alliance" and launch or rein-
force a positive physician-patient relationship. If an
unfavorable outcome occurs, that relationship can be
crucial to maintaining the patient's trust.
A patient's usual psychological defense mechanism
against uncertainty is to endow his or her physician
with omniscience in the science of medicine, an aura
of omnipotence. By weighing how you say something
more heavily than what you say, you can turn an
anxiety-ridden ritual into an effective claims preven-
tion mechanism. Psychiatric literature refers to this as
the "sharing of uncertainty." Rather than shattering a
patient's inherent trust in you by presenting an insen-
sitive approach, your dialogue should be sympathetic
to the patient's particular concerns or tensions and
should project believable reactions to an anxious and
difficult situation.
Consider, for example, the different effects that the
following two statements would have:
1. "Here is a list of complications that could occur
during your treatment [operation]. Please read
the list and sign it."
2. "I wish I could guarantee you that there will be
no problems duringyour treatment [operation],
but that wouldn't be realistic. Sometimes there
are problems that cannot be foreseen, and I want
you to know about them. Please read about the
possible problems, and let's talk about them."
By using the second statement, you can reduce the
patient's omnipotent image of you to that of a more
realistic and imperfect human being who is facing,
and thus sharing, the same uncertainty. The implica-
tion is clear: we—you and I—are going to cooperate
in doing something to your body that we hope will
make you better, but you must assume some of the
responsibility.
To allay anxiety, you may seek to reassure your
patients. However, in so doing, be wary of creating
unwarranted expectations or implying a guarantee.
Consider the different implications of these two
statements:
1. "Don't worry about a thing. I've taken care
of hundreds of patients like you. You'll do just
fine."
 image...

8 • LIABILITY ISSUES IN PLASTIC SURGERY: AN INSURANCE PERSPECTIVE 149

2. "Barring any unforeseen problems, I see no
reason why you shouldn't do very well. I'll cer-
tainly do everything I can to help you."
If you use the first statement and the patient does
not do "fine," he or she is likely to be very angry with
you (it may also be interpreted as implied warranty).
The second statement gently deflates the patient's fan-
tasies to realistic proportions. This statement simul-
taneously reassures the patient and helps him or her
to accept reality.
The therapeutic objective of informed consent
should be to replace some of the patient's anxiety with
a sense of his or her participation with you in the pro-
cedure. Such a sense of participation strengthens the
therapeutic alliance between you and your patients.
Instead of seeing each other as potential adversaries if
an unfavorable or less than perfect outcome results,
you and your patients are drawn closer by sharing
acceptance and understanding of the uncertainty of
clinical practice.

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Dr.Mustafa D.
CHAPTER
9
Photography in
Plastic Surgery
WILLIAM Y. HOFFMAN, MD
HISTORY
CAMERAS AND LENSES
FLASH
FILM
DIGITAL IMAGING
Digital Cameras
Photography is inextricably intertwined with plastic
surgery, both historically and in modern practice. The
advent of popular photography in the second half of
the 19th century and subsequent development of pho-
tographic magazines revolutionized people's percep-
tion of themselves and of the world. This no doubt
contributed to an increased sense of self-image in the
general public that paralleled the development of
aesthetic surgery.
The use of photography to record congenital and
acquired anomalies began almost as soon as photog-
raphy itself. Today, photographs are used routinely to
record patients' appearance before and after procedures
as well as to record those procedures themselves.
Because much of plastic surgery is visible externally,
photographs constitute both a medical and a legal
record of a patient's progress. It is therefore impera-
tive that plastic surgeons understand the basics of pho-
tographic technique and that a standardized method
for recording patients' photographs be developed and
followed routinely.
Until recently, photography was completely reliant
on film, which in modern times has been a silver-based,
light-sensitive chemical reaction. In the past few years,
the advent of digital photography has made it possi-
ble to record photographs in digital form, which can
represent an enormous savings in terms of both
expense and convenience. However, unlike film, digital
images can much more easily be manipulated, and par-
ticular attention must be paid to methods of storage.
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Dr.Mustafa D.
Resolution
Storage and Backup
STANDARDIZATION OF PHOTOGRAPHS
MEDICOLEGAL ASPECTS OF PHOTOGRAPHY
HISTORY
The introduction of the daguerreotype in 1839 repre-
sented the first widely available photographic process.
Photographs of clinical conditions appeared at almost
the same time as the new medium was used to docu-
ment social and other conditions. Gurdon Buck
(known for Buck fascia and Buck traction) was a New
York surgeon in the mid-1800s who was particularly
interested in orthopedic and plastic surgical problems.
He is credited with the first clinical photograph, a
daguerreotype of a leg fracture, in 1845. Later, the wet-
plate technique made photographic prints possible, and
Buck took extensive preoperative and postoperative
photographs of his patients, including Civil War
injuries and cleft lip repairs.1,2
George Eastman invented the dry-plate technique
in 1879. His company, which became Eastman Kodak
in 1892, introduced the first negative on flexible film in
1885 and the first roll film camera in 1888, ushering
in the age of snapshot photography with the slogan
"You push the button—we do the rest." The early
cameras used film 2'/ 4 inches wide; 35 mm film was
introduced in 1914, Kodachrome, the first commer-
cial transparency film, was introduced in 1935.
CAMERAS AND LENSES
The process of taking a photograph involves allowing
an appropriate amount of light to strike the film,
151
152 I • GENERAL PRINCIPLES
regardless of whether the film is the traditional silver
halide emulsion on acetate or a digital recording device.
The camera usually contains the shutter, which mod-
ulates the time that the light strikes the film; the lens
contains a diaphragm, which adjusts the amount of
light passing through to the film for the time that the
shutter is open. The lens also focuses the image on the
film; this is actually upside-down and reversed, but
the image is usually corrected in the viewfinder for
the photographer.
The most common camera used for clinical pho-
tography is the single-lens reflex (SLR) camera. A
mirror in front of the film projects the image from the
lens upward into a prism, which uprights the image
and allows the viewer to see exactly what the lens is
"seeing." Most SLR cameras use interchangeable lenses.
Rangefinder cameras have a viewfinder that is not seeing
through the lens and uses two small images that are
brought together for focus. Smaller cameras, also
termed point-and-shoot cameras, have a separate
viewer but usually use autofocus lenses. Both of the
latter types of cameras have the disadvantage of not
seeing the exact image seen by the lens; this is partic-
ularly a problem in close-up photographs, where
parallax may show an image in the viewfinder distinctly
different from what is actually being recorded on film.
Digital point-and-shoot cameras overcome this
problem with an LCD screen that shows the actual
image being recorded.
The focal length of a lens refers to the distance from
the posterior element of the lens to the film plane when
an object at "infinity" is in focus. A standard or
"normal" lens is one that produces minimal distor-
tion, again at infinity; this is generally defined in film-
based photography as a distance that is the diagonal
of the negative size. For 35 mm film, which produces
a negative 24 x 36 mm in size, this is actually around
43 m m ; 50 mm lenses have long been considered the
standard lens for 35 mm photography. Today, many
cameras come with a zoom lens with 50 mm focal
length being somewhere near the middle of the zoom
range. Most digital cameras have an effective "nega-
tive" (the CCD), which is smaller than a 35 mm neg-
ative, and the focal length of the lenses is often put in
35 mm "equivalent" numbers for reference. This may
also affect lens choices in digital cameras with inter-
changeable lenses because the smaller portion of the
image that is being sampled lengthens the effective
focal length of the lens.
Lenses with a focal length shorter than a standard
lens are considered wide angle; those with a longer
focal length arc considered telephoto. These are impor-
tant for a number of reasons. The most significant in
plastic surgery is the distortion that occurs as one
moves closer to the subject; the other is the change in
depth of field that occurs with lenses of varying focal
length.
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Dr.Mustafa D.
If a normal lens is used to photograph a face that
fills the frame (see later, standardized views), the camera
has to be moved close to the patient, and some dis-
tortion will occur (Fig. 9-1). In general, a medium
telephoto lens, with a focal length from 90 to 110 mm,
will avoid this distortion and give a more realistic view
of the face. These lenses are often referred to as medium
telephoto or portrait lenses- The additional distance
is useful from a consideration of the patient's space
and comfort with the photographic process; in the oper-
ating room, that distance makes it much easier to take
close photographs without risk of contaminating a
sterile field. When the full torso or lower extremity is
photographed, it is often easier to use a normal lens
because the distance to the patient is then reduced; at
the greater distance needed to capture a wider field,
the normal lens will not distort significantly.
It is important to reiterate that the focal length of
a lens is stated in terms of 35 mm film. The newer
digital SLR cameras have sensor arrays smaller than
the size of 35 mm film, and these cameras in general
increase the focal length of a lens by about 50%. Thus,
a 60 mm lens used on the digital camera becomes the
equivalent of a 90 mm lens used on a 35 mm camera.
At the time of this writing, there is one camera (by
Canon) that has a sensor the same size as 35 mm film,
and by publication, there will certainly be others.
Zoom lenses are commonly found on point-and-
shoot cameras and are readily available for SLR
cameras as well. These have the obvious appeal of
reducing the number of lenses needed (often to one;
in less expensive cameras, the lenses are not remov-
able). However, in attempting to standardize photo-
graphs for plastic surgery, the zoom lens is difficult to
use because there is usually no indication of the focal
length that is selected. One solution is to maximize
the zoom for any photographs of faces; some cameras
have preset focal length for portraits, and this would
be a reasonable alternative. In the SLR camera with
interchangeable lenses, setting the zoom to the same
focal length for specific photographs will help in stan-
dardization. The best solution, however, is to use a
fixed focal length lens, usually a medium telephoto
macro lens, for facial photographs. Most manufacturers
produce lenses with focal lengths of 90 to 110 mm.
These lenses have magnification ratios on the barrel
of the camera so that distances can be preset and com-
plete standardization obtained. These magnification
ratios, also known as reproduction ratios, refer to the
ratio between the size of the image on the film and
the size of the actual subject. The reproduction ratios
are based on 35 mm film; because the sensors on most
SLR digital cameras are smaller, this means the actual
reproduction ratio will be somewhat higher. Never-
theless, the same setting will translate into the same
distance to be used at all times for the same photo-
graphs, and this will give consistent results.
TfcWWaatfW image..

9 • PHOTOCRAPHY IN PLASTIC SURGERY 153

FIGURE 9 - 1 . Lens focal length. A, Frontal photograph of face taken with 90 mm lens equivalent (60 mm on digital
SLR camera). At a comfortable distance of approximately 1 meter, the single flash on the camera lights the face more
evenly, and there is no significant distortion. B, Same magnification taken with normal lens, 50 mm equivalent; note
that the subject is much closer to the camera, producing distortion of facial features. The flash is on the left side of
the camera, and the angle of the flash is also exaggerated by the proximity of camera to subject.

Cameras have two main settings: shutter speed and
aperture. The shutter speed is an actual measurement
of the time that the shutter is open, usually a fraction
of a second. Without a flash, hand movement is usually
detectable at speeds slower than 1 /30 second. Electronic
flash needs to be synchronized with the shutter
opening, usually requiring a speed slower than 1/250.
Most modern SLR cameras will automatically set the
shutter speed to 1/125 or 1/250 when the flash is
activated.
The lens has a diaphragm that can be adjusted
to vary the amount of light hitting the film or the
digital sensor. This is referred to as the aperture;
the widest possible aperture is often used to refer
to the "speed" of the lens and reflects the relative
ability of the lens to be used in low light without flash.
The aperture is referred to by a number called the
f/stop; the unusual use of the slash mark in the term
refers to the fact that the number is a ratio between
the actual size of the aperture and the focal length of
the lens. The standard f/stop numbers—2, 2.8, 4,
5.6, 8, 11, 16, 22—actually represent a geometric
progression; each increase is a halving of the amount
of light admitted by the lens and is thus reciprocal
with shutter speeds, which are also expressed in a
progression (1/15, 1/30, 1/60, 1/125, 1/250). This
reciprocal relationship means that there are multiple
combinations of shutter speed and f/stop that can
result in the same amount of light getting through
the lens.
Depth of field, an important concept in clinical pho-
tography, refers to the distance in front of and behind
the focal plane of the film that appears to be in focus.
Depth of field increases with smaller apertures (f/stop),
represented by larger numbers on the lens; it also
increases with shorter focal lengths (Fig. 9-2). As
a longer lens is used, even the medium telephoto
recommended for facial photography, depth of field
will be decreased. In clinical photography, maximiz-
ing depth of field will improve the detail in the final
photograph. It is therefore important to decrease the
aperture used, which often requires overriding the auto-
matic features of the camera and using either manual
or aperture priority metering.

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Dr.Mustafa D.
 image..

154 • GENERAL PRINCIPLES

B
FIGURE 9-2. Depth of field. A, Photograph taken at f/4 shows foreground object in
sharp focus while the jar that is behind the focal plane of the photograph is out of focus.
B, When the same photograph is taken at f/11 (note: the flash has compensated with
greater output for the smaller aperture, so that the exposure is identical), both objects
are in focus even though the focal plane of the photograph has not changed.

FLASH its own batteries; because the built-in flash in many

The flash is almost as important as the camera and
lens in plastic surgery photography. The brightness of
the flash determines the f/stop that can be used, and
as noted before, the smaller the f/stop, the greater the
depth of field. Ultimately, a stronger flash will give the
best possible depth of field. A separate flash also has
cameras is a significant factor in battery life, the
proprietary batteries in the camera will last longer.
In addition, the position of the flash in relation-
ship to the camera position is important because of
the shadows formed (Fig. 9-3). Ideally, in any side or
quarter view, the flash should be on the same side of
the camera as the anterior part of the patient (unless

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Dr.Mustafa D.
 9 • PHOTOGRAPHY IN PLASTIC SURGERY 1 55

A B

C D
FIGURE 9 - 3 . Flash position. A, Frontal view of face with flash mounted on top of camera. With a
digital SLR camera, this is taken as a horizontal photograph and then cropped to the vertical. B, The
flash is mounted on the left side of the camera when the camera is turned for a vertical photograph.
Note the greater contour definition on the subject's left side, particularly in the medial canthal area and
the cheek. The camera could be turned the opposite way for emphasis of other contours on the right.
C, Lateral view, with lens on the left side of the camera; the shadows are behind the subject, and the
single flash provides even illumination. D, In this lateral view, the flash is positioned on the right side of
the camera; there is still a vertical view, but it is in the opposite direction. The shadow in front of the
subject is distracting and makes appreciation of the profile more difficult.

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Dr.Mustafa D.
156 I • GENERAL PRINCIPLES
the back is being photographed), placing the shadow
behind the patient. This means that the camera must
be turned over for views of the opposite sides. Even
better, multiple flashes can be used to eliminate
shadows; this requires a dedicated photography area
where the flashes can be placed on a permanent basis.
Ring flashes have been used to reduce shadows as
well, but these are really designed for macro photog-
raphy. Unfortunately, ring flashes tend to eliminate
shadows to the point of making contour difficult to
distinguish and are not recommended for photogra-
phy of patients.
FILM
Although there has been a major shift away from film
to digital photography, it is important to understand
some of the advantages of film. First, film represents
a stable record, whereas digital photographs can be
modified. Film is also stable when it is stored appro-
priately; digital images can be lost if they are not prop-
erly backed up. Film also has a higher "resolution" (to
use a digital term) than any but the most expensive
digital cameras; however, this gap in resolution is
rapidly closing and is not really significant for the
purposes of clinical photographs.
The disadvantages of film are obvious compared
with digital photographs. Foremost is the expense of
buying and processing the film. Second, scanning slides
for digital records or presentation, although possible,
is not really practical on a large scale for plastic sur-
geons. Third, the storage of slides or negatives can take
up a great deal of physical space. Last, slides will lose
color over time, especially if they are used for pres-
entation with bright projectors.
Specific film types have different characteristics.
Negative films have much greater latitude (producing
an acceptable image even with errors in exposure) and
are often used for snapshots and prints; slide or trans-
parency film is used for projection. Kodachrome is
unique in modern transparency films in that the three
colors that make up the spectrum (yellow, cyan,
magenta) are actually incorporated into separate
layers of the film and are developed separately in a
proprietary process by Kodak. This gives a result that
has greater storage stability than other films, in which
the three colors are developed simultaneously in what
is termed E-6 (again, from Kodak) processing. E-6
developing has the advantage of being readily avail-
able from many laboratories, often with fast results.
Films may also vary in color characteristics. Spe-
cific emulsions have been developed for portraiture,
for flash photography, and for landscapes. In general,
the more saturated color results in an abnormal
appearance in clinical photography, and the plastic
surgeon should use Kodachrome or Ektachrome or Fuji
Sensia transparency film for these reasons. Even with
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Dr.Mustafa D.
these films, the emulsion may vary with temperature
and time; most film companies produce "professional"
films, which are designed for greater stability and more
reproducible results—at a higher cost.
DIGITAL IMAGING
At the time of this writing, most plastic surgeons are
converting to the use of digital photography for their
record keeping. Digital photography has a number of
clear advantages. First is cost; although a digital
camera generally costs more than a comparable film
camera, there is no cost for film and processing. Errors
in photography are erased, rather than discarding
already developed (and paid for) slides. Errors are also
discovered at the time, so that photographic oppor-
tunities are not lost. Even an expensive digital camera
will generally pay for itself in a year, and subsequently
savings accrue to the practice. The computer needed
to access and view the digital photographs is already
part of most offices' equipment. 3
Presentation technology has shifted dramatically
toward digital projectors in the new millennium; digital
photographs are readily incorporated into presenta-
tion software on the computer, and presentations
can easily be transported on laptop computers or on
CD-ROM. Similarly, digital photographs can be
compressed and transmitted over the Internet for
consultation or discussion. The ability to duplicate
digital photographs allows them to be stored in dif-
ferent "files" for different purposes; the image of a par-
ticular patient does not have to be taken out of the
record to be used in a presentation. Dedicated systems
are available that will combine written and digital
records so that a patient's entire record, including pho-
tographs, is readily available on a personal computer.
Digital images maybe generated from three primary
sources. A digital camera records photographs in digital
formats and is the most common source of digital
images used in a plastic surgery practice. Trans-
parencies and negatives can be digitized in a film
scanner; a dedicated film scanner will generally give
better results than an adapter on a flatbed scanner.
This offers the alternative of having an original film
record as well as a digital image; but at the same time,
it obviates some of the advantages of digital photog-
raphy, doubles the storage issues, and requires signif-
icant additional time by personnel. A flatbed scanner
will produce a digital image from printed material.
Last, two- or three-dimensional digital images can be
made directly on the computer by use of dedicated
software programs; this is used more for artwork but
will obviously not be a major part of the plastic
surgeon's work.
Digital photography affords the surgeon the pos-
sibility of image processing, that is, altering the pho-
tograph. This allows the surgeon to show patients
W*ttf<4M(fW image...
possible outcomes of surgery on their own photo-
graphs. Of course, this is computer generated rather
than a true outcome, and the surgeon must take great
care to show results that he or she thinks are reason-
ably attainable for the patient. The commercially avail-
able programs generally print a disclaimer with any
hard copy to ward off claims of implied guarantees.
If digital photographs are kept as the only record,
it is important that only copies be altered, as the com-
puter will keep a record of the date of the photograph
as well as of the most recent modification. Digital
watermarks are another method of ensuring the
date and original photograph are preserved without
alteration.
Digital Cameras
Most of the digital cameras being used clinically today
arc point-and-shoot cameras; that is, they use fixed
zoom lenses as opposed to interchangeable lenses, auto-
focus as opposed to manual focus. The problem of
parallax correction is addressed by viewing the image
on a small LCD screen in the back of the camera. In
some models, this screen swivels and tilts, allowing
the photographer to see the image from a different
angle than the camera. An intermediate solution is the
camera with an electronic viewfinder that simulates
the SLR type of viewfinder.
Digital SLR cameras were extremely expensive and
were purely in the realm of the professional photog-
rapher until the past 2 years, when several of the major
camera manufacturers released SLR digital cameras
for around $2000. The first digital SLR camera under
$1000 was introduced in late 2003, and additional
cameras will certainly be introduced; indeed, it is likely
that film cameras will become more rare and expen-
sive as the price of digital cameras drops, as the supply
and demand begins to shift toward digital. Because
SLR cameras use interchangeable lenses, an appropriate
lens adds additional cost; if the same manufacturer as
the surgeon's previous film SLR camera makes the
digital camera, the same lenses may be used, recog-
nizing that the same lens will have a different effec-
tive focal length on the digital camera.
The advantages of a digital SLR camera are the same
as those of a film-based SLR camera; by use of single
focal length lenses and manual controls on these
cameras, standardization of photographic technique
can be obtained. This is critical to obtaining compa-
rable preoperative and postoperative photographs. In
addition, the lenses are of higher quality, giving the
photographs greater sharpness that is independent of
the resolution chosen (see following section).
Rather than using film, the digital camera records
the image from the sensing chip to a storage card in
the camera. There are a variety of proprietary memory
cards available, all of which have been rapidly drop-
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Dr.Mustafa D.
9 • PHOTOGRAPHY IN PU\STIC SURCERY 157
ping in cost. For a medium resolution setting, a large
number of photographs can be recorded on a card of
64 or 128 MB, although "microdrives" up to 1 GB are
available. Downloading the photographs from the
camera to a computer can be done directly, but most
cameras use a USB connection, which is fairly slow
for this purpose. If possible, a faster connection
(Firewire, or IEEE 1294; USB 2.0) is desirable. Inex-
pensive card readers are available that use such con-
nections even if the camera does not have one, and
for laptops, a PCMCIA card reader is the fastest method
available for digital transfer.
As with film, the chips in digital cameras often have
specific color balance. Of course, it is not possible to
change film if one is unhappy with the balance, and
this is something to examine before camera purchase.
Most cameras have an acceptable balance for skin color.
The color can be controlled in some cameras by chang-
ing the setting for white balance; this requires some
experimentation on the user's part. Alternatively, the
color balance can be controlled later in an image
processing program. 4
Resolution
It is essential to understand what is meant by resolu-
tion of digital cameras, printers, and scanners. On film,
individual silver ion particles change with exposure
to light; in the digital camera's chip, the sensors convert
the light to digital pixels (short for picture elements)
that record information such as light intensity and
color. The more pixels recorded, the greater the reso-
lution. Digital cameras are generally advertised with
reference to their maximum resolution, generally 3 to
6 megapixels (MP); this is obtained by multiplying
the horizontal and vertical dimension of the sensor
in pixels. For example, 1600 by 1200 pixels gives a little
more than 1.9 million pixels in the total array and may
be referred to as a 2 MP resolution.
In most digital cameras, there is a choice of reso-
lutions, which can be as low as 640 x 480 pixels and
as high as 3024 x 2016 for a 6 MP camera. The higher
the resolution, the better the output quality; at the
same time, higher resolution will produce larger files
for storage. Enlargements up to 8 x 10 inches can be
made with 4 MP output, around 1600 x 2400 pixels.
Even a smaller file, around 3 MP, can give good results;
the difference is primarily noted with enlargement or
extreme cropping (Fig. 9-4). Just as with film cameras,
the final quality of the image depends not only on the
resolution of the sensor but also on the quality of the
lens as well as accurate exposure and focus.
Compression is the last element in the output of a
digital camera. In addition to choices of resolution,
digital cameras also offer a choice of saving the data
for each pixel—referred to as RAW or TIFF files—or
in compressed format. JPEG (an acronym for the Joint
158 I • GENERAL PRINCIPLES

FIGURE 9-4. Resolution. A, Full-frame photograph; at this size, the difference between 3 and 6 megapixels is
not visible. The black rectangle outlines the area to be enlarged. B, Enlargement of 3 MP image; the pixels are
visible at this magnification. C, Enlargement of 6 MP image; the image is noticeably smoother when it is enlarged
significantly.

Photographic Experts Group, a subsidiary of the
International Standards Organization) is the most
common method of compression and can be done at
different levels; more compression gives smaller files
but is more likely to produce artifacts. This may be
confusing in some cameras because a "high" setting
may refer to either higher compression (lower quality)
or higher quality (less compression). An important
aspect of JPEG compression is that if any alteration
of an image (as in Photoshop) is performed, re-saving
the image will result in additional artifact from the
compression; for this reason, it is better always to save
an original and then work on copies.
From a practical standpoint, the choice of resolu-
tion in digital photography must balance storage space
on a server against output. The highest resolution
digital photograph on a 6 MP digital SLR camera pro-
duces a file of more than 17 megabytes. With a high-
volume hard drive of 200 gigabytes, this means that
about 11,750 photographs could be stored. However,
backup and retrieval times will be long, and the size
of the files will be cumbersome in a PowerPoint pres-
entation. Since a 6 MP photograph can be enlarged
to at least 11 x 14 inches, and probably larger, this
level of resolution is really unnecessary for printing
at 4 x 6 inches, projection, or display on a computer
monitor. My preference is to use a 4 MP setting, where
the complete RAW file is 4 MB and a high-quality com-
pressed file is between 500K and 1 MB. This produces
files that are more than adequate for display or print-
ing but of reasonable size for storage and transfer to
other media, such as CDR.
Printer and scanner resolutions are expressed as
dpi or dots per inch. This does not correspond directly
to pixel resolution in the camera. The printer trans-
forms the digital information for each pixel from the
photograph into tiny dots that are placed on the paper,
but each color must be changed to dots of three

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Dr.Mustafa D.
image...
primary colors (red, yellow, green) as well as black;
thus, a printer with a stated resolution of 1440 dpi
really corresponds to one quarter of that, that is, 360
dpi. In general, scanning or printing at 200 to 300 dpi
will give satisfactory results up to 8 x 10 inches with
inkjet or dye sublimation printers.
Storage and Backup
Digital photographs offer a considerable advantage
over film in terms of storage because many photo-
graphs can be kept in a relatively small space. Copies
can be made with a keystroke, permitting use in Power-
Point presentations or other modalities without loss
of the original. With any digital information, backup
copies are crucial. Hard drives and even optical media
such as CD or DVD are vulnerable to the elements.
Ideally, photographs are stored on a server with a dupli-
cate system for daily backups on site, and some sort
of backup should be done off site weekly or at least
monthly so that the photographs can be recovered even
if some physical catastrophe such as fire were to strike.
All storage and retrieval systems must be password
protected to ensure confidentiality of patients and
HIPAA compliance.
Retrieval of photographs is of equal importance.
Hard copies of digital photographs can be printed and
kept in the patient's chart, but computer-based storage
offers the additional advantage of immediate access
and of maintaining photographs in a searchable data-
base. There are a number of programs available for
both Macintosh and Windows formats; some have been
developed specifically for plastic surgery and can be
integrated with other office management software;
others are stand-alone graphics management software
that the user can customize to his or her preferences.
As with any database, it is important to consider long-
term expansion and retrieval needs at the outset.
STANDARDIZATION OF
PHOTOGRAPHS
Whether photographs are being taken with film or
digital cameras, it is critical that standardized tech-
nique be used for each area of the body that is pho-
tographed. This allows useful comparison of
preoperative, postoperative, and later photographs.
Ideally, all aspects of the clinical photograph should
be standardized, including the camera, focal length
and aspect ratio of the lens used, position, background,
lighting, and exposure. The Committee on Clinical
Photography of the Plastic Surgery Educational Foun-
dation has established photographic standards for
plastic surgery that have been published in book form
and journals. Although these were published for 35
mm photography, the same recommendations apply
to digital photography. 5 A laminated chart of stan-
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Dr.Mustafa D.
9 • PHOTOGRAPHY IN PLASTIC SURGERY 159
dardized views is available from the American Society
of Plastic Surgeons and is recommended for reference
(Fig. 9-5).
As noted previously, the SLR camera offers the best
quality and can easily be standardized in terms of lens
and exposure settings. Grid lines in the viewfinder are
an invaluable aid for orientation of the subject in pho-
tographs. Only the most expensive digital SLR cameras
have chips that are the same size as 35 mm film, and
for this reason, the focal lengths of the lenses and the
magnification ratios are still based on the 35 mm
cameras and need to be adjusted for digital cameras.
A 50 mm lens is recommended for chest, torso, and
lower extremity; a 90 to 105 mm macro lens is used
for face, hand, and close-up photography. Fixed focal
length lenses are preferred over zoom lenses, especially
because they can be preset to specific distances and
magnifications so that photographic techniques can
be reproducible.
The optimum lighting arrangement requires a ded-
icated photography room in the office; two primary
lights and one or two lights on the background will
display contour without severe shadows. If a flash on
camera is used, one must be attentive to the shadows
that are formed; if the flash is turned to one side
or another, the shadows are markedly altered. In
general, a single flash on the camera should be on
the same side as the nose (or the anterior surface of
the torso or limbs) to keep the shadow behind the
patient.
The background should be clear of any distractions;
a solid painted wall or a roll of photographic back-
ground paper can be used. Similarly, the patient
should be free of accessories; glasses and earrings should
be removed, and hair clips are used to show the fore-
head and ears. Clothing and jewelry are removed for
torso photographs; photographic garments are used
when needed.
Intraoperative photographs should be taken after
the field is cleared of equipment and distracting ele-
ments. It is important to include anatomic landmarks
to orient the viewer. A wide view may help with ori-
entation before a close-up. Photographs should be
taken orthogonally, either along the longitudinal axis
of the patient or at right angles; oblique angles are
more difficult for the viewer to interpret. A series of
photographs should be taken from the same viewpoint
for consistency.
Facial photographs should include the ears and the
neck. On macro lenses, a reproduction ratio of 1:9 or
1:10 is ideal; 1:4 is used for sections of the face, gen-
erally upper or lower halves. Full-face, oblique, lateral,
and worm's-eye views should be obtained routinely;
posterior views with the hair pinned up are impor-
tant for ears (Fig. 9-6).
The angle of the head in relationship to the camera
is critical; a minor degree of angulation will change
image..

160 • GENERAL PRINCIPLES

v - v _ uv
iF*
m V, 111 • *J HPN
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PLASTY SNtx-Os'S oxr5l TON

The standardphotographic views illustrated in this card were established by the

Educational Technologies Committee of the Plastic Surgery Educational
Foundation. We feel these poses best document the pertinent anatomy of the
patient without distortion or distraction.

Standardized photography ensures that comparisons of pre op andpostop

images will yield meaningful observations. All clinical photographs should be
taken using the same equipment and procedures. Camera, film, lighting,
magnification, framing, patient positioning and patient preparation all need to
be consistent.

Referencing the images and information in this card during patient photography
should help any plastic surgery practice to capture consistent pre- and post-op FIGURE 9-5. The reference card,
images. V/hen capturing post operative photos, it is a qood idea to have the entitled Photographic Standards
patient's pre op images on hand as well. in Plastic Surgery, published by
the American Society of Plastic
Surgeons, can be used for photo-
graphing patients with standardized
views.

the appearance dramatically in some instances. The
Frankfort horizontal plane, which is a plane through
the inferior orbital rim and the upper tragus of the
ear, should be parallel to the floor, and the camera lens
should be in that plane (Fig. 9-7). Grid lines in the
viewfinder are an aid in obtaining consistency in the
angle of the camera and the subject.
Intraoral photographs are useful in showing
occlusion as well as oral disease and surgical repairs.
Occlusal views are mandatory in the treatment of any
jaw or dentoalveolar fractures as well as in orthog-
nathic surgery. Retractors for the cheeks are used for
occlusal views, which should be anteroposterior and
oblique; special mirrors arc available for intraoral
photographs (Fig. 9-8).
Photographs of the body are taken with repro-
duction ratios of 1:12 for the breasts or abdomen
alone; 1:18 is recommended for larger areas (breast
and abdomen for TRAM flaps, abdomen and thighs
for liposuction). For body contouring, posterior and
posterior oblique views should be obtained in addi-
tion to the anterior, oblique, and lateral views (Figs.
9-9 and 9-10).
Arms and legs should be photographed to include
elbows or knees, with a reproduction ratio of 1:12
(1:5 for hands alone). Functional views—dorsiflex-
ion and plantar flexion of the foot, full flexion and
full extension of the fingers—are important in docu-
menting preoperative and postoperative outcomes.
MEDICOLEGAL ASPECTS OF
PHOTOGRAPHY
The patient's confidentiality was espoused as early as
Hippocrates: "Whatever, in connection with my pro-
fessional practice or not, in connection with it, I see

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Dr.Mustafa D.
image...

9 • PHOTOCRAPHY IN PLASTIC SURGERY 161

FIGURE 9 - 6 . Standardized views of the face. A to C, Frontal, oblique, and lateral views (the opposite
lateral and oblique would be taken but are not included here). Note that the camera is on the plane of the
Frankfort horizontal (1:10 magnification). Note that the entire neck is included in these photographs. It is
important for lateral photographs to have the patient turn the entire body rather than just the head alone.
D, Worm's-eye view. The ears can be used to keep the head level in this view. E and F, Close-up views of
upper and lower facial halves (1:4 magnification). Oblique and lateral views at this magnification should also
be obtained, particularly of the upper half for eyes and nose.

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Dr.Mustafa D.
162 • GENERAL PRINCIPLES

FIGURE 9-7. Effect of head position. A, The Frankfort horizontal is shown on this lateral photo-
graph; it is a plane that extends through orbitale (the inferior orbital rim) and the upper border of
the tragus. B, Anteroposterior photograph taken in the proper plane. C, The camera is below the
Frankfort horizontal. D, The camera is above the Frankfort horizontal. Note the difference in the
appearance of the overall height of the face, the amount of scleral show, and the prominence of
the nose and chin, among other features. Note that in C and D, the angle of the face off the hori-
zontal is less than 10 degrees, despite the obvious differences.

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 image...

9 • PHOTOGRAPHY IN PLASTIC SURGERY 163

FIGURE 9-8. Intraoral photographs. A, View taken with bilateral cheek retractors (1:4 magnification). B and C,
The use of a warm mirror will give the best view of the entire maxillary or mandibular arch. D, Typical view in the
mirror of the maxillary dental arch and anterior palate.

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Dr.Mustafa D.
164 I • GENERAL PRINCIPLES

FIGURE 9-9. A and B, Standardized views of the breasts. Placement of the hands on the hips for the lateral view is
useful to show any postoperative scars, the inframammary fold, and other features. Again, the shoulders are aligned
with the top of the photograph (1:12 magnification).

or hear, in the life of men, which ought not to be spoken
of abroad, I will not divulge, as reckoning that all such
should be kept secret" Clinical photographs, although
constituting a medical record, also represent a unique
incursion into a patient's privacy. It is important
for plastic surgeons to recognize that patients have
specific legal rights that apply to both the taking of
photographs and their use.
In instances in which photographs have been taken
of unconscious patients without consent, the taking
and keeping of those photographs has been found to
be an intrusion on the patient's privacy. Similarly,
publication or broadcast of a patient's photographs
without consent has been considered "unreasonable
publicity." Consent should be obtained from every
patient before photographs are taken and kept in the

MM*

B
FIGURE 9 - 1 0 . AandB, Standardized view of chest and abdomen. As with the other examples, this simply shows
two views; laterals and other obliques would also be obtained. Note that the shoulders are lined up with the top of
the photograph (1:18 magnification).

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Dr.Mustafa D.
 image...
medical record; in general, the safest course of action
is to have specific consent for publication or display
of photographs. This would include the use of pho-
tographs to show other patients as examples of sur-
gical outcomes and the display of photographs at
medical meetings as well as more public uses.
Legally, the person who takes a photograph owns
the rights to the photograph, unless the photographer
is in the employ of the plastic surgeon or if a profes-
sional photographer agrees that the photography is
"work for hire." It is also possible for the physician to
have the right to a photograph transferred in a con-
tractual agreement. However, the subject's likeness is
his or hers unless a release or consent form has been
signed.
The use of computer imaging software has in-
troduced new legal issues, specifically whether the
altered image that the patient sees represents an
implied contract. At the time of this writing, there have
been no successful lawsuits for the "implied guaran-
tee" of an altered digital image that is shown or given
to the patient, but there is certainly a risk that this
could occur, particularly if the alteration went well
beyond the bounds of what is practical to achieve.
If imaging is used with a patient, it is important that
the possible outcome shown to the patient is possi-
ble, and the patient must understand that the actual
result may differ from what can be generated on the
computer. 6
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Dr.Mustafa D.
9 • PHOTOGRAPHY IN PLASTIC SURGERY 165
SUMMARY
Photographs are an indispensable clement of the prac-
tice of plastic surgery. As such, it is important that the
surgeon apply the same principles to his or her pho-
tography that are used for surgery—study of basic prin-
ciples, standardization of technique, critical evaluation
of results, and care for the patient's privacy and rights.
REFERENCES
1. Burns SB: Early medical photography in America (1839-1883).
IV. Early wet-plate era. N Y State J Med 1979;79:1931-1938.
2. Rogers BO: The first pre- and post-operative photographs of
plastic and reconstructive surgery: contributions of Gurdon Buck
(1807-1877). Aesthetic PlastSurg 1991;15:19-33.
3. Galdino GM, Swier P, Manson PN,Vander Kolk CA: Converting
to digital photography: a model for a large group or academic
practice. Plast Reconstr Surg 2000;106:119-124.
4. Galdino GM, Vogel JE, Vander Kolk CA: Standardizing digital
photography: it's not all in the eye of the beholder. Plast Recon-
str Surg 2001;108:1334-1344.
5. DiBernardo BE, Adams RL, Krausc J, et al: Photographic stan-
dards in plastic surgery. Plast Reconstr Surg 1998;102:559-568.
6. Chavez AE. Dagum P, Koch RJ, Newman JP: Legal issues of com-
puter imaging in plastic surgery: a primer. Plast Reconstr Surg
1997;100:1601-1608.
Additional Reading
Milburn K: Digital Photography Bible. Foster City, Calif, IDG Books
Worldwide, 2000.
Nelson G, Krause JL: Clinical Photography in Plastic Surgery. Boston,
Little, Brown, 1988.
 image...

CHAPTER

10
•
Anesthesia for Plastic Surgery
PAUL F. WHITE, PhD, MD • JEAN P. WADDLE, MD

PREOPERATIVE PREPARATION AND EVALUATION OF Positioning of the Patient

THE PATIENT Special Anesthetic Considerations
Airway and Dental System REGIONAL ANESTHESIA
Cardiovascular System Local Anesthetics
Respiratory System Facial Nerve Blocks
Gastrointestinal System Extremity Nerve Blocks
Central Nervous System Central Neuraxis Blocks
Endocrine System
CONSCIOUS SEDATION AND MONITORED
Reproductive System ANESTHESIA CARE
Past Surgical History
Medication History OFFICE-BASED ANESTHESIA
American Society of Anesthesiologists' Physical RECOVERY FACILITIES
Status Classification Postanesthesia Care Unit
Preoperative Medications Step-Down (Phase II) Unit
GENERAL ANESTHESIA Fast-Tracking Concept
Definition and Goals Postoperative Complications
Induction Agents
Airway Devices UNIQUE CONSIDERATIONS FOR PLASTIC SURGERY
Maintenance Anesthetics PROCEDURES
Intravenous Adjuvants Laser Abrasion
Opioid Analgesics Liposuction
Opioid Agonist-Antagonists Burns and Debridement Procedures
Nonopioid Analgesics Face Lift Procedures
Prevention of Postoperative Nausea and Vomiting Nasal Procedures
Fluid Management Facial Fractures
Temperature Regulation Breast Surgery

Plastic surgery procedures are performed on both an
ambulatory (outpatient) basis and an inpatient basis,
depending on the complexity of the patient's opera-
tive course. With the recent growth in office-based
surgery, the percentage of outpatient plastic surgery
procedures continues to increase.1 Surgery performed
outside the conventional hospital environment offers
advantages for patients, health care providers, and
third-party payers. Patients benefit from ambulatory
surgery because it decreases separation from home
and family, lessens the likelihood of contracting
hospital-acquired infections, and reduces postopera-
tive complications. Anesthetic management of the plastic
surgery patient must provide a calm preoperative
course, a well-managed intraoperative period, and the
appropriate preparation for the patient's final desti-
nation. New anesthetic drugs and devices allow quicker
recovery times while minimizing postoperative com-
plications. Regardless of the location of plastic surgery,
for an "optimal" outcome to be achieved, careful atten-
tion must be given to preoperative preparation, intra-
operative anesthetic management, and postoperative
care.
PREOPERATIVE PREPARATION
AND EVALUATION OF
THE PATIENT
The primary goals of anesthetic care for plastic surgery
patients are to minimize surgical morbidity, to provide
appropriate hemodynamic control and comfort for the
patient during the operation, and to ensure a prompt
recovery without side effects. The first step of the anes-
thetic management is a thorough preoperative evalu-
ation. Preoperative preparation and evaluation of the
patient reduce apprehension about surgery, improve
the patient's compliance, reduce surgical morbidity,
improve health care efficiency, and may decrease

167

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Dr.Mustafa D.
168 I • GENERAL PRINCIPLES
TABLE 10-1 • MALLAMPATI AIRWAY
CLASSIFICATION
Class I Faucial pillars, soft palate, and uvula can be
visualized
Class II Faucial pillars and soft palate can be
visualized, but uvula is masked by the
base of the tongue
Class III Only soft palate is visualized
perioperative cost.2"5 The preoperative anesthetic eval-
uation begins with a thorough history, which then
guides preoperative laboratory evaluation.
Airway and Dental System
Preoperative airway evaluation is essential because
adequate preoperative preparation can help avoid an
airway emergency. A thorough airway examination
evaluates anatomic features, dentition, cervical spine
mobility, and temporomandibular joint mobility.
Visualization of the glottic opening is limited when
alignment of the oral, pharyngeal, and laryngeal axes
is impaired. Anatomic characteristics that limit align-
ment include short neck, limited cervical mobility, pro-
truding maxillary incisors, receding mandible, and poor
mandibular mobility.6 Dental examination should
identify any loose or missing teeth and removable dental
prosthesis.
Examination of the oral cavity helps identify
difficult intubations. Mallampati et al7 observed
patients sitting with the tongue maximally protruded
and found a correlation between the structures visu-
alized and the ease of intubation (Table 10-1). In a
class I airway, the tonsillar pillars, soft palate, and uvula
are visualized. In a class II airway, the faucial pillars
and soft palate are visualized, but not the uvula. In a
class III airway, only the soft palate is seen (Fig. 10-1).
A significant correlation exists between the ability to
visualize pharyngeal structures and the ease of laryn-
goscopy and intubation.
CLASS I CLASS II CLASS 111
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Dr.Mustafa D.
Cardiovascular System
Cardiac disease affects perioperative management. The
presence of hypertension, valvular disease, coronary
artery disease, or congestive heart failure should be
carefully assessed, especially in the elderly cosmetic
surgery population. Hypertension is the most common
cardiac disease in the surgical patient. Before surgery,
the systolic pressure should be below 180 mm Hg, and
the diastolic pressure below 110 mm Hg. Data suggest
that patients with a diastolic blood pressure above
l i O m m H g have an increased incidence of myocar-
dial ischemia, congestive heart failure, and cardiac
death. 8 With the possible exception of diuretics,
patients should be instructed to continue antihyper-
tensive medication on the day of surgery. Valvular heart
disease requires antibiotic prophylaxis (Table 10-2).9
Patients with coronary artery disease should have a
history of stable angina before elective plastic surgery.
Patients with unstable angina or poorly compensated
congestive heart failure are not good candidates for
elective plastic surgery.
Numerous reports indicate the lack of benefit of
unnecessary laboratory tests and perhaps even harm
associated with them. 10 Preoperative electrocardiog-
raphy is needed only for the elderly, for patients with
a history of cardiac or pulmonary disease, and with a
history of irradiation. Furthermore, only patients with
a history of congestive heart failure, malnutrition, and
diuretic or digoxin intake need preoperative determi-
nation of serum electrolyte values and creatinine
testing. Routine chest radiography is not beneficial,
and erroneous diagnoses lead patients to unnecessary
and potentially detrimental clinical interventions. 10,n
Respiratory System
Respiratory diseases increase the risk of perioperative
complications, and it is important to ascertain a history
of smoking, chronic obstructive pulmonary disease,
emphysema, asthma, recent upper respiratory illness,
or sleep apnea. Smoking increases perioperative
complications, and patients should be encouraged to
FIGURE 1 0 - 1 . The airway classifica-
tion system used to assess the risk of
airway obstruction and difficulty in per-
forming tracheal intubation (due to rel-
ative tongue size to mouth opening) in
the Samsoon and Young modification of
the Mallampati airway classification.
(From Mallampati SR: Recognition of the
difficult airway. In Benumof JL ed:
Airway Management: Principles and
CLASS IV Practice. St. Louis, Mosby, 1996:126.)
 image...
TABLE 10-2 • RECOMMENDATIONS FOR ADULT SUBACUTE BACTERIAL ENDOCARDITIS
PROPHYLAXIS
Situation
Dental, Respiratory, and Esophageal Procedures
Standard prophylaxis
Unable to take oral medications
Allergic to penicillin
Allergic to penicillin, unable to take oral medications
Genitourinary and Gastrointestinal Procedures
High-risk patients
High-risk patients allergic to ampicillin and amoxicillin
Moderate-risk patients
Moderate-risk patients allergic to ampicillin and amoxicillin
* Gentamicin dose not to exceed 120 mg.
stop at least 1 week before undergoing anesthesia.
Carboxyhemoglobin levels decrease within hours of
smoking cessation, increasing oxygen tissue availabil-
ity. Cessation of smoking for 4 to 6 weeks decreases
postoperative pulmonary complications, and not
smoking for 2 to 3 months before surgery improves
ciliary function, improves pulmonary mechanics, and
reduces sputum production. 12 Although providing
anesthesia for an elective procedure in a patient with
an upper respiratory infection remains controversial,
it is usually reasonable to proceed with surgery in
healthy, afebrile individuals having clear rhinorrhea
and normal findings on lung examination.
Obtaining a detailed history from an asthmatic
patient determines the severity of the disease and the
effectiveness of current medical management. A recent
history of steroid use may require intraoperative
steroid administration. Patients having an asthma exac-
erbation should have elective surgery delayed until
symptoms improve. Routine inhaled bronchodilators
should be continued through the day of surgery.
Gastrointestinal System
The gastrointestinal system review should determine
whether there is a history of gastric esophageal reflux,
peptic ulcer disease, hiatal hernia, morbid obesity, or
diabetic gastroparesis. These diseases increase stomach
acidity or contents, increasing the risk of aspiration
pneumonitis. Aspiration pneumonitis occurs in 1.4 to
6 cases per 10,000 anesthetics and has a 5% mortality
rate. 13 Pneumonitis is more severe if the gastric pH is
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Dr.Mustafa D.
0 • ANESTHESIA FOR PLASTIC SURGERY 169
Drug and Dosage Regimen
2.0g amoxicillin orally 1 hr before procedure
2.Og ampicillin IV within 30min of procedure
600mg clindamycin, 2.0g cephalexin, 2.0g cefadroxil,
500 mg azithromycin, or 500 mg clarithromycin
orally 1 hr before procedure
600 mg clindamycin IV or 1.0g cefazolin IV
2.Og ampicillin IV and 1.5mg/kg gentamicin* within
30min of procedure; ampicillin 1.0g6hr after
I.Og vancomycin over 1-2 hr and 1.5mg/kg
gentamicin* within 30min of procedure
2.0g amoxicillin orally 1 hr before procedure or 2.0g
ampicillin IV within 30min of procedure
1.0g vancomycin IV over 1 -2 hr within 30 min of
procedure
less than 2.5, the gastric volume is greater than 25 mL,
or the aspirate is particulate. Patients at high risk for
aspiration pneumonitis may benefit from prophylaxis
with a histamine 2 receptor blocking agent. To mini-
mize stomach contents, all patients are instructed not
to eat solid food before surgery. Current data suggest
that clear liquid intake up until 2 hours before elec-
tive surgery does not adversely affect gastric contents
in healthy patients.M The half-life of clear stomach fluids
is 10 to 20 minutes, and residual volume after 2 hours
is less in patients ingesting small amounts of clear fluids
than in fasted patients. 15 Therefore, the fasting guide-
lines are generally 2 to 3 hours for clear liquids and 6
to 8 hours for solid food.
The gastrointestinal system review should also
include a history of preexisting liver disease and ethanol
consumption. Chronic liver disease can interfere with
the metabolism of some anesthetic agents. Chronic
alcohol abuse also increases anesthetic requirements. 16
Only patients with moderate to severe liver disease may
benefit from preoperative liver function studies.
Central Nervous System
If cerebrovascular insufficiency is present, special
care should be taken to maintain intraoperative blood
pressure close to baseline values. The patient's head
should be kept in a neutral position to maximize blood
flow. If a patient has a seizure disorder, the adequacy
of current medical management should be ascertained.
A recent increase in the frequency of seizures war-
rants further evaluation with possible adjustments
170 1 • GENERAL PRINCIPLES
to the anticonvulsant medications before elective
surgery.
Endocrine System
Diabetes is the most common endocrine disease
managed in the surgery setting. Oral hypoglycemics
and insulin doses are managed in a variety of ways,
depending on dosage and time of surgery. Most
important, blood glucose monitoring is needed
throughout the surgical day to prevent hypoglycemia
or hyperglycemia. Outpatients with diabetes should
be scheduled as first cases, and an intravenous line is
started on arrival for surgery. In hyperthyroid or
hypothyroid patients, elective surgery should be
deferred until patients are euthyroid and asymptomatic.
Reproductive System
Female patients of reproductive age should be asked
about the likelihood of pregnancy. A urine pregnancy
test can be performed if needed. Only nonelective pro-
cedures are performed during pregnancy, and if pos-
sible, these are scheduled during the second or third
trimester. A history of heavy menstrual bleeding can
cause anemia. If significant surgical blood loss is pos-
sible, the hemoglobin level should also be determined
preoperatively.
Past Surgical History
Obtaining a history of prior anesthetic complications
is important because it may help guide medical man-
agement. A history of significant postoperative nausea
and emesis warrants antiemetic prophylaxis. Patients
who report "tube" placement while awake or dental
damage from intubation may require awake intuba-
tion. A history of an unexpected or prolonged intu-
bation may indicate a neuromuscular disease. A history
of a high fever or prolonged intubation in a patient or
a family member of a patient may suggest malignant
hyperthermia and require avoidance of certain anes-
thetic agents.
Medication History
A medication history, for prescription and nonpre-
scription agents, is obtained from all patients. Oral
medications should be continued through the day of
surgery. However, diuretics, oral hypoglycemics, and
usual doses of insulin may be held. Antihypertensives
are usually continued through the day of surgery
because well-controlled hypertensive patients have less
intraoperative blood pressure lability. Patients with
glaucoma should continue all parasympathetic and p-
adrenergic antagonist therapy through the perioper-
ative period to minimize the risk of an attack of acute
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Dr.Mustafa D.
angle glaucoma. Because systemic absorption occurs
with topical (J-adrenergic antagonist medications
(e.g., timolol), intraoperative bradycardia, hypoten-
sion, and bronchospasm can occur in patients using
topical timolol.
Patients should be questioned about herbal or diet
medication intake. The use of herbal medications is
increasing in our society, and some produce adverse
perioperative effects. Ginkgo biloba inhibits platelet
aggregation, and case reports of spontaneous bleed-
ing exist, particularly when it is combined with aspirin
or warfarin (Coumadin). St. John's wort is promoted
as a natural antidepressant. St. John's wort extract
inhibits serotonin, dopamine, and norepinephrine
reuptake and may prolong the effects of certain anes-
thetic agents. Fen-phen, a combination drug contain-
ing a serotonin agonist and a sympathomimetic, has
been taken off the market because of its relationship
to valvular cardiac defects and a case report of an anes-
thetic death that occurred in a patient taking fen-phen
for weight loss. Ma huang (herbal fen-phen) contains
ephedra, which may cause hypertension, insomnia,
arrhythmias, nervousness, and headaches. As a result
of chronic catecholamine depletion, patients taking ma
huang may be resistant to the effects of ephedrine in
treatment of hypotension. If possible, patients should
discontinue all diet and herbal medications 2 weeks
before surgery.
American Society of
Anesthesiologists' Physical
Status Classification
On the basis of the patient's physical status, anesthe-
siologists assign an American Society of Anesthesiol-
ogists (ASA) class (Table 10-3). The classification
system communicates the patient's disease status but
does not necessarily estimate anesthetic risk. A patient
assigned to ASA class I has no systemic disease. A patient
assigned to ASA class II has mild to moderate systemic
disease (e.g., hypertension, asthma, mild obesity). A
patient assigned to ASA class III has a severe systemic
disturbance (e.g., diabetes, coronary artery disease). A
patient assigned to ASA class IV has a severe systemic
disease that is life-threatening (e.g., congestive heart
failure, unstable angina). Patients assigned to ASA class
V are moribund patients who have little chance of sur-
vival but are submitted to surgery as a last resort. An
E is added after the ASA class if the surgery is an emer-
gency, regardless of ASA status.
Preoperative Medications
Preoperative medication reduces the patient's anxiety
and facilitates a smooth perioperative course. Common
classes of preoperative medications include sedatives,
sympatholytics, analgesics, and antisialagogues.
ItSWS^afltfW image...

10 • ANESTHESIA FOR PLASTIC SURGERY 171

TABLE 10-3 • AMERICAN SOCIETY OF ANESTHESIOLOGISTS* PHYSICAL STATUS CLASSIFICATION

SYSTEM

Classification Description Example

Healthy
Mild systemic disease with no functional limitation Controlled asthma
Severe systemic disease with functional limitation Coronary artery disease
IV Severe systemic disease that is a constant threat to life Unstable angina
V Moribund patient with death expected within 24 hours Ruptured aortic aneurysm
E Emergency surgery Appendectomy

Sedatives, or anxiolytics, are commonly given before
transport of the patient to the operating room. Ben-
zodiazepines (e.g., midazolam, lorazepam, diazepam)
produce antianxiety effects and amnesia with minimal
cardiopulmonary depression. Midazolam is the most
popular perioperatively because it is short acting and
two to four times as potent as diazepam (Fig. 10-2).
Lorazepam is 5 to 10 times more potent than diazepam
but less useful intraoperatively because the sedative-
amnestic effects of a single dose of oral lorazepam can
persist for 24 to 48 hours.
Preoperative sympatholytics attenuate the sympa-
thetic nervous system response to intubation and sur-
gical stimulation. Clonidine, a central-acting a 2 agonist,
6 -
Midazolam
5 -
8 and vomiting. Commonly used antiemetics include
I 4-
Diazepam
is used as an antihypertensive agent and to reduce anes-
thetic requirements.
Opioid analgesics are occasionally given as a pre-
medication if the patient is experiencing acute or
chronic pain during the transition to the operating
room. In analgesic doses, opioids cause drowsiness but
do not produce hypnosis or amnesia. During opera-
tions, opioids are frequently used to suppress the
acute cardiovascular responses to painful stimuli and
to reduce the anesthetic requirement. Common side
effects of opioids are sedation, dizziness, nausea and
vomiting, respiratory depression, ileus, and urinary
retention.
Patients at risk for aspiration or nausea are often
administered prophylactic medication preopera-
tively. Patients with morbid obesity, gastrointestinal
reflux, hiatal hernia, and diabetes mellitus have an
increased risk for aspiration, and metoclopramide
and a histamine 2 receptor antagonist (e.g., cimetidine,
ranitidine, famotidine) are often given. However, there
is no evidence that prophylaxis decreases the incidence
of aspiration or improves outcome after ambulatory
surgery.17 Prophylaxis is often given, particularly in the
outpatient setting, to minimize postoperative nausea
droperidol, hydroxyzine, and serotonin antagonists
(e.g., ondansetron and dolasetron).

3-
""i
0.1 0.2 0.3
Benzodiazepine dose
(mg/kg)
FIGURE 1 0 - 2 . Dose-response curves for the level of
sedation as a function of dose of midazolam (Versed) or
diazepam (Valium). A score of 2 indicates minimal seda-
tion, and a score of 6 equals unconscious (hypnotic) state.
Midazolam has a steeper dose-response than diazepam.
(From White PF, Vasconez LO, Mathes SA, et al: Com-
parison of midazolam and diazepam for sedation during
plastic surgery. J Plast Reconstr Surg 1988;81:703.)
GENERAL ANESTHESIA
Definition and Goals
General anesthesia is a. drug-induced loss of con-
sciousness during which patients are not arousable,
even by painful stimulation. Patients often need assis-
tance to maintain a patent airway, and positive-
pressure ventilation may be required because of
depressed spontaneous ventilation or drug-induced
depression of neuromuscular function (ASA Standards,
1999). The goal of general anesthesia is to provide
unconsciousness, appropriate hemodynamic control,
and perhaps skeletal muscle relaxation. The ideal
general anesthetic should have rapid onset, stable
hemodynamics, and rapid recovery of protective

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172 I • GENERAL PRINCIPLES

TABLE 10-4 • INDUCTION CHARACTERISTICS OF INTRAVENOUS ANESTHETICS

Characteristic Thiopental Methohexital Ketamine Etomidate Propofol

Pain of injection 0 ** * ** « *»*

Slow onset 0 0 * 0 0
Myoclonic activity 0 * ** * * *** *
Respiratory upset ** ** * 0 0
Cardiovascular depression • • * 0 0 »**
Ventilatory depression «* * 0 * • *

Scale: 0 = best; "* = worst

Adapted from White PF, ed: Anesthesia for Ambulatory Surgery. International Anesthesia Clinics. Boston, Little, Brown, 1994:1-16.

airway reflexes and cognitive and psychomotor func-
tions. A wide variety of pharmacologic agents are avail-
able for induction and maintenance of general
anesthesia. The most common induction agents for
general anesthesia are barbiturates (e.g., thiopental and
methohexital), propofol, ketamine, and etomidate.
Induction agents vary in induction and recovery char-
acteristics (Tables 10-4 and 10-5).
Induction Agents
METHOHEXITAL AND THIOPENTAL
Thiopental and methohexital are the barbiturates most
commonly used in clinical anesthesia. Although propo-
fol is considered the drug of choice for ambulatory
procedures, barbiturates are the most cost-effective for
inpatient plastic surgery. After intravenous barbitu-
rate administration, there is mixing with the central
blood pool, and barbiturates are then distributed to
body tissues. Distribution depends on the tissue per-
fusion rate, tissue affinity for the drug, and relative con-
centrations of the barbiturate in the tissue versus the
blood. At the site of barbiturate action, the brain, equi-
libration occurs rapidly because of the high solubility
of the drug and the high perfusion of the brain. Brain
barbiturate concentrations decrease rapidly as the drug
redistributes to less well perfused tissue (e.g., muscle
and fat), and rapid awakening occurs. Elimination
of barbiturates occurs through liver metabolism. If
repeated doses of barbiturates are given, saturation of
inactive sites may occur, resulting in a prolonged drug
effect.
Barbiturates cause direct peripheral vasodilation
and depress myocardial contractility.18 In healthy
patients, barbiturate administration activates the
barostatic reflex, which increases heart rate, produc-
ing minimal change in blood pressure. 19 In contrast,
patients relying on high sympathetic tone to maintain
blood pressure (heart failure, severe hypovolemia) have
an exaggerated decrease in blood pressure with usual
barbiturate induction doses.
Barbiturate administration produces a dose-
dependent decrease in respiratory rate and tidal
volume. Induction doses of barbiturates nearly always
produce apnea. Both methohexital and thiopental blunt
the ventilatory response to hypoxemia and hypercap-
nia.20 However, lower (sedative) doses of barbiturates
are compatible with adequate spontaneous ventilation.
Barbiturates are potent cerebral vasoconstrictors.
Methohexital and thiopental decrease cerebral blood
flow, cerebral blood volume, intracranial pressure, and
cerebral metabolic oxygen requirements. 21 Because
methohexital and thiopental reduce metabolic oxygen
requirements and intracranial pressure, these agents
are commonly used for patients with intracranial
lesions.

TABLE 10-5 • RECOVERY CHARACTERISTICS OF INTRAVENOUS ANESTHETICS

Characteristic Thiopental Methohexital Ketamine Etomidate Propofol

Emergence time *• * ** • 0
Orientation time * * *** * 0
Residual sedation *** * ** * 0
Nausea and vomiting « * * *** 0
Home readiness ** • * * ** *• 0

Scale: 0 = best; "* = worst.

Adapted from White PI:,cd: Anesthesia for Ambulatory Surgery. International Anesthesia Clinics. Boston, Little, Brown, 1994:1-16.

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 image...

10 • ANESTHESIA FOR PLASTIC SURCERY 173

*p<0.05

Baseline PACU 120 Baseline PACU

A B

80

| 60
£o

c 40
O

8 2°

0
Baseline PACU 30 60 90 120 Baseline PACU 30 60 90 120
Time interval (min) Time interval (min)
D
FIGURE 1 0-3. Comparative residual postoperative sedation (A), drowsiness (B), confusion (C), and clumsiness (D)
scores for patients receiving either midazolam (D) or propofol (•) for sedation during local anesthesia. Mean values
(+SEM) are reported, with *P < .05 considered significantly different. PACU, postanesthesia care unit. (From White PF,
Negus JB: Sedative infusions during local and regional anesthesia: a comparison of midazolam and propofol. J Clin
Anesth 1991;3:32.)

PROPOFOL After an initial bolus of propofol, plasma levels decline

Since the introduction of propofol into clinical prac-
tice, it has been widely used as an intravenous anes-
thetic because of its predictable recovery and favorable
postoperative side effect profile.22 Recovery of cogni-
tive function is rapid when a single dose, repeated doses,
or a continuous infusion of propofol is administered
(Fig. 10-3).23 Propofol is the only available induction
agent that does not produce a significant amount of
postoperative nausea and vomiting. The rapid re-
covery and minimal nausea and vomiting with pro-
pofol are important clinical features for outpatient
procedures.
The unique pharmacokinetic properties of propo-
fol contribute to its favorable clinical characteristics.
rapidlybecause of redistribution of propofol from the
brain to less well perfused sites like muscle and fat. The
distribution clearance of propofol is similar to that of
thiopental, and plasma levels of thiopental and propo-
fol initially decline at similar rates. The capacity of the
peripheral sites of distribution is large, and the rate of
equilibrium with the central compartment is slow.
When an infusion of propofol is terminated, the con-
centration is much higher in the central compartment
than in the peripheral compartments, and hence
redistribution continues to occur.24 The concentration
in the central compartment declines both from metab-
olism (elimination) and from continuing redistribu-
tion. Subsequently, the rate of decline of propofol is

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Dr.Mustafa D.
174 I • GENERAL PRINCIPLES
much more rapid than that of thiopental because of
its high metabolic clearance rate. The metabolic
clearance of propofol exceeds hepatic blood flow,
suggesting that propofol also has extrahepatic sites
of metabolism. The net result is a rapid decline in
propofol concentration to levels below those associ-
ated with hypnosis, permitting rapid awakening.
The complete elimination of propofol may take many
hours, or even days, but it has little effect on clinical
recovery.25
Clinically, propofol compares favorably with other
anesthetic techniques. Propofol offers advantages in
terms of a more rapid recovery and reduced postop-
erative nausea and vomiting. However, some of
the benefit from propofol appears to result from the
substitution of propofol for barbiturates during the
induction period. The maintenance anesthetic appears
to have less impact on the recovery time after short
(less than 30-minute) procedures than with longer
procedures.
Investigators have evaluated the use of propofol-
based maintenance anesthetic techniques in both
healthy patients and those with reduced left ventric-
ular function.26 Compared with thiopental or etomi-
date, propofol appears to have greater direct negative
inotropic effects on heart papillary muscle.27 The
decrease in systemic arterial blood pressure during
propofol infusions is a result of its direct negative
inotropic actions and arterial and venous dilation. 28
Propofol should be used cautiously if patients have
impaired left ventricular function or are inadequately
hyd rated.
Patients with chronic obstructive pulmonary disease
who are mechanically ventilated and receive propofol
have a reduction in peak inspiratory pressure and
airway resistance.29 The bronchodilatory effect of
propofol may be related to a direct relaxant effect on
bronchial smooth muscle. Compared with barbiturates,
there is less wheezing in both asthmatic and non-
asthmatic patients after tracheal intubation with
propofol. 30
In clinical practice, propofol is associated with cere-
bral vasoconstriction, decreased cerebral blood flow,
and reduced cerebral metabolic requirement for
oxygen.31 Propofol appears to have a cerebral protec-
tive action similar to that of barbiturates. Because
changes in blood pressure after propofol induction
doses are frequently reflected by changes in cerebral
perfusion pressure, propofol should be carefully
administered to patients with reduced intracranial
compliance. Administration of propofol to patients
with a seizure disorder remains controversial. However,
increasing evidence suggests that propofol possesses
profound anticonvulsant activity.32
Pain after injection of propofol occurs in 28%
to 90% of patients. Although the mechanism res-
ponsible for the pain is unknown, it may be due to
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Dr.Mustafa D.
activation of the kinin cascade.33 The pain is a func-
tion of the drug itself rather than of the formulation. 34
The use of small veins on the dorsum of the hand is
associated with a greater incidence of pain compared
with large veins in the antecubital fossa. Decreasing
the speed of injection or injecting propofol in a fast-
flowing intravenous line in the dorsum of the hand is
of little benefit in reducing the incidence of pain. 33 The
use of local anesthetics ( 1 % to 2% lidocaine) reduces
the pain resulting from propofol injection.35
KETAMINE
Ketamine is a phencyclidine derivative described as a
dissociative anesthetic. Patients receiving ketamine are
in a trance-like state (often with eyes open), discon-
nected from surroundings, and profoundly analgesic.
Ketamine differs from other intravenous induction
agents that depress all of the central nervous system.
In contrast, ketamine depresses some regions of the
neocortex and subcortical structures (e.g., thalamus)
while activating other parts of the limbic system (e.g.,
hippocampus). Ketamine is highly lipid soluble with
low protein binding and is therefore extensively dis-
tributed in the body. Redistribution of ketamine from
the brain to more poorly perfused tissue is the main
factor in terminating its action.
Ketamine administration increases heart rate, mean
arterial blood pressure, and plasma norepinephrine and
epinephrine levels.36,37 The circulatory effects of
ketamine are likely caused by central sympathetic
stimulation. 38 A direct myocardial depressant effect of
ketamine occurs after large bolus doses or rapid injec-
tion. Clinical experience suggests that ketamine aug-
ments epinephrine-induced arrhythmias. 39 Ketamine
directly dilates vascular smooth muscle and produces
sympathetically mediated vasoconstriction, the net
effect being a minimal change in systemic vascular
resistance. Although ketamine increases coronary
blood flow, it may not be sufficient to meet the oxygen
demands of the heart in the presence of ketamine-
induced tachycardia and hypertension; therefore,
circulatory stimulation should be minimized by
benzodiazepine premedication.
Compared with the other intravenous induction
agents, ketamine has unique effects on the pulmonary
system. Ketamine maintains minute ventilation and
tidal volume and increases intercostal muscle activity.
When given slowly, ketamine is not associated with
any change in arterial oxygen or carbon dioxide
content. 40 Ketamine produces bronchodilation in
asthmatic patients. 41 Ketamine bronchodilation occurs
even after P-blockade and appears to be mediated by
a direct smooth muscle relaxant effect of ketamine. 42
Salivary and tracheobronchial secretions are increased
by ketamine. Both laryngeal and pharyngeal reflexes
are well maintained, and patients often maintain an
tt3*ftf<a«!tfW image...
airway and swallow during ketamine anesthesia. There-
fore, pulmonary aspiration is less likely to occur with
ketamine than with other general anesthetics. Nonethe-
less, normal safety precautions should be used during
ketamine administration to patients with an increased
risk for pulmonary aspiration.
Patients with intracranial lesions can have transient
increases in intracranial pressure after ketamine admin-
istration. However, spontaneously breathing animals
with normal intracranial pressure values showed no
increase in intracranial pressure compared with a group
of animals with preexisting increased intracranial pres-
sure.39 Ketamine increases cerebral blood flow and
should be avoided if abnormal cerebral perfusion exists.
The nonpurposeful tonic-clonic and athetoid-like
movements seen during and after ketamine adminis-
tration can be disturbing to medical personnel. These
purposeless movements, unusual eye signs (nystagmus
and pupil dilation), and circulatory stimulation asso-
ciated with ketamine make it difficult to evaluate the
"anesthetic depth" of the patient. Therefore, the prac-
titioner may have to rely on empirical infusion rates
for ketamine.
Pleasant and unpleasant dreams, visual distur-
bances, hallucinations, floating sensations, alterations
in mood and body image, and delirium can occur
during the recovery phase of ketamine anesthesia.
Although flashbacks several weeks after ketamine
anesthesia have been reported, a multi-institutional
study could not detect any long-lasting psychomimetic
sequelae.39 Factors associated with a higher incidence
of emergence reactions include age above 14 years,
female gender, habitual dreaming, history of psycho-
logical problems, and excessive doses of ketamine. 39
With a reduction in ketamine dose and the addition
of benzodiazepines, psychomimetic reactions occur less
frequently.
ETOMIDATE
Etomidate is a carboxylated imidazole derivative that
produces rapid induction of anesthesia. Etomidate is
metabolized primarily by liver esterases and, to a lesser
extent, plasma esterases. Although etomidate has a rapid
clearance, redistribution is the main factor contribut-
ing to rapid awakening after a single bolus.
The cardiovascular effects of etomidate are differ-
ent from those of other induction agents. Etomidate
has minimal effects on heart rate, mean arterial pres-
sure, cardiac output, contractility, and systemic vas-
cular resistance.43 The lack of negative inotropic effects
with etomidate administration is beneficial to patients
with cardiovascular disease. Etomidate produces
minimal respiratory depression. Less respiratory
depression occurs with etomidate than with metho-
hexital, thiopental, or propofol, and minute ventila-
tion can actually increase with etomidate. 44 Etomidate
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10 • ANESTHESIA FOR PUSTIC SURGERY 175
markedly reduces cerebral oxygen consumption, cere-
bral blood flow, and intracranial pressure without
producing significant changes in mean arterial blood
pressure. Therefore, etomidate can be safely given to
patients with intracranial disease.
Disadvantages of etomidate include pain on injec-
tion, myoclonic activity, high incidence of postoper-
ative nausea and vomiting, and adrenal corticoid
suppression. The pain with injection of etomidate
is from its solvent, propylene glycol. However, etomi-
date dissolved in an alternative solvent, Lipofundin,
produces no pain on injection.45 Myoclonic activity
occurs with etomidate administration, although the
incidence is reduced if prior opioids are given, a priming
dose of etomidate is given before induction, and eto-
midate is dissolved in Lipofundin rather than in pro-
pylene glycol. Prolonged infusions of etomidate
produce transient adrenal insufficiency.46 The inhibi-
tion of steroid synthesis is measurable in outpatients
receiving a single dose or brief infusion of etomidate,
although the clinical significance of this is unclear.
After a single dose of etomidate, Cortisol function
returns to normal within 6 to 8 hours. 46 Because of
the high incidence of postoperative nausea and vom-
iting (30% to 50% after ambulatory anesthesia),
myoclonic activity, and adrenocorticoid suppression,
etomidate is usually reserved for patients with cardiac
compromise.
Airway Devices
NASAL CANNULAS
The administration of supplemental oxygen with
nasal cannulas can improve tissue oxygen saturation
in sedated patients. Commercially available products
arc designed to sample respiratory gases as well as to
provide supplemental oxygen. The Salter type of nasal
cannula monitors end-expiratory carbon dioxide to
quantify respiratory'rate, allowing titration of adjunc-
tive sedative and analgesic drugs during local anesthesia.
FACE MASK
Face masks are used for ventilation and administra-
tion of oxygen and anesthetic gases. Effective mask ven-
tilation requires a skilled practitioner using specific
hand placement to obtain a tight fit. Mask ventilation
can be difficult in obese patients and in patients with
head and neck tumors or infections. Because mask ven-
tilation does not protect against regurgitation, it is con-
traindicated in situations in which there is an increased
risk for aspiration (e.g., hiatal hernia, pregnancy, recent
oral intake, intestinal ileus). When the airway cannot
be maintained with manipulation of the mask,
mandible, or neck, insertion of a nasal or oral airway
is often beneficial. Nasal and oral airways keep the
tongue off the posterior pharynx. Oral airways can
176 I • GENERAL PRINCIPLES
produce laryngospasm or bronchospasm and should
be inserted only in an adequately anesthetized patient.
The advantage of the face mask is that it provides general
anesthesia without requiring intubation of the trachea,
decreasing the incidence of dental trauma and sore
throat. The face mask, compared with the tracheal tube,
often hastens emergence from anesthesia.
CUFFED OROPHARYNGEAL AIRWAY
The cuffed oropharyngeal airway (COPA) is a Guedel
airway with a specially designed cuff that creates a seal
at its distal end between the patient's airway and the
anesthesia delivery system. The cuffed oropharyngeal
airway was recently introduced for clinical use as an
alternative to the laryngeal mask airway and face mask
during general anesthesia. When the cuff is inflated, it
displaces the base of the tongue anteriorly and pas-
sively elevates the epiglottis away from the pharyngeal
wall. The cuffed oropharyngeal airway requires less
anesthetic drugs than does the laryngeal mask airway
for insertion. The cuffed oropharyngeal airway is
inserted successfully by inexperienced users more than
90% of the time on the first attempt. 47 However, manip-
ulations of the device are often required to maintain
airway patency. Studies comparing the laryngeal mask
airway and the cuffed oropharyngeal airway have found
both devices to be safe and effective for use in spon-
taneously breathing anesthetized patients as well as
during positive-pressure ventilation. 48 However, the
laryngeal mask airway allows positive-pressure venti-
lation at slightly greater peak inspiratory pressures.
LARYNGEAL MASK AIRWAY
The laryngeal mask airway (LMA) was developed in
1981 and offers many advantages compared with a face
mask or tracheal tube. 49 The LMA is inserted blindly
into the pharynx, forming a low-pressure seal around
the laryngeal inlet, with the distal part of the mask con-
forming to the hypopharynx (Fig. 10-4). LMA place-
ment is easy to learn and quickly mastered by medical
personnel. 50 The LMA can usually be placed more
quickly than a tracheal tube. Unlike a tracheal tube,
the LMA cannot be misplaced into the esophagus or
main stem bronchus. The LMA has a 4% to 12% inci-
dence of a sore throat, compared with at least 28%
with a tracheal tube 49 and no higher than with a face
mask and oropharyngeal airway. There are less hemo-
dynamic changes with LMA placement compared with
a tracheal tube. 51 The LMA is placed without a laryn-
goscope, and there are no reports of dental damage
with LMA insertion. 52 Airway management is often
easier with the LMA compared with a face mask.
Episodes of hemoglobin desaturation and intraoper-
ative airway manipulations occur more frequently with
a face mask compared with the LMA.50 Compression
of the eye or facial nerves is more common with a face
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Dr.Mustafa D.
mask than with the LMA. In addition, the LMA scav-
enges waste gases more effectively than a face mask
does. There are no significant differences in emergence
and recovery times between the LMA and face mask,
and the LMA can provide superior surgical operating
conditions compared with the face mask.53
The primary disadvantage of the LMA is that aspi-
ration of gastric contents can occur because, unlike
with a tracheal tube, there is no cuff below the vocal
cords that prevents regurgitation from entering the
lungs. The incidence of regurgitation with the LMA is
uncertain. One study showed that the LMA produced
a sustained fall in lower esophageal sphincter pressure
to 3.6 cm H 2 0 (normal, 51 cm H 2 0). 5 4 If there is in-
adequate anesthetic depth, air swallowing during
spontaneous ventilation with the LMA can occur. Air
swallowing, leading to gastric distention, and lower
esophageal sphincter pressure may increase the risk of
regurgitation. The frequency of coughing and laryn-
gospasm with the LMA is similar to that with a face
mask. Unlike a tracheal tube, the LMA is large and semi-
rigid and cannot be easily moved from one side of the
mouth to the other during an operative procedure.
During cosmetic plastic surgery, the LMA tube may
be found too cumbersome (or disruptive) to the facial
symmetry.
The LMA is difficult to insert if patients cannot
extend the neck or open the mouth more than 1.5 cm.
Use of the LMA should be avoided if pharyngeal disease
exists, such as an abscess or hematoma. The LMA is
contraindicated if there is airway obstruction below
the larynx. The LMA should not be used if patients
have low pulmonary compliance or high airway resist-
ance (e.g., morbid obesity, bronchospasm, pulmonary
edema or fibrosis, thoracic trauma). Because the inci-
dence of regurgitation and laryngospasm increases with
the LMA and inadequate anesthetic depth, this should
be avoided. A new airway device, the intubating LMA,
is designed to facilitate blind tracheal intubation. 55
TRACHEAL INTUBATION
Tracheal intubation allows easy access to the surgical
field when operations occur on the head and neck. A
tracheal tube also provides a more secure airway when
an existing anatomic problem or operative procedure
may compromise the airway. The tracheal tube pro-
vides the best protection against aspiration and is rec-
ommended if there is an increased aspiration risk.
Finally, the tracheal tube, when it is used with a neu-
romuscular blocking agent, facilitates muscle relaxation
during the operation.
The most frequent complication of tracheal tube
placement is damage caused by the laryngoscope. When
used improperly, the laryngoscope can cause damage
to teeth and soft tissues, including the lips and gums.
Laryngospasm can occur if laryngoscopy is performed
T^gypR^aelcrKfimage..

10 • ANESTHESIA FOR PLASTIC SURGERY 177

FIGURE 1 0 - 4 . The sequence of steps for proper placement of a laryngeal mask airway. A, With the left hand stabi-
lizing the occiput, the posterior surface of the lubricated, deflated cuff is firmly applied against the hard palate as it is
advanced into the pharynx. B, The cuff is advanced into the posterior pharynx. The right index finger still firmly presses
the posterior surface of the cuff against the palate. C, The cuff is pushed into the hypopharynx. Further gentle down-
ward pressure on the shaft or proximal connector should ensure complete insertion. D, Without holding the device,
the cuff is inflated with the appropriate volume of air. The mask will often rise about 1.5 cm as it settles into its final
position. (From Pennant JH, White PF: The laryngeal mask airway: its uses in anesthesiology. Anesthesiology 1993;79:144.)

without an adequate depth of anesthesia. There is
also the risk of an unrecognized endobronchial or
esophageal intubation, leading to hypoxia and, if unrec-
ognized, cardiovascular collapse.
Maintenance Anesthetics
VOLATILE ANESTHETICS
Inhalation anesthetics remain the most popular drugs
for maintenance of general anesthesia. An ideal volatile
anesthetic would have a low blood-to-gas solubility to
allow rapid onset and elimination without postoper-
ative side effects (e.g., nausea and vomiting, dizziness,
drowsiness). Ideally, inhalation anesthetics would be
minimally metabolized; avoiding toxic degradation
products minimizes organ damage. Inhalation agents
need to be potent, so they can be mixed with a viable
amount of oxygen. Inhalation agents must be
nonflammable in the presence of oxygen, nitrous oxide,
and air. The ideal inhalation agent should have minimal
cardiovascular effect. To date, not all of these criteria
exist with any of the currently used inhalation anes-
thetic agents: halothane, enflurane, isoflurane,
sevoflurane, and desflurane (Table 10-6).
Halothane
Halothane is the oldest inhalation anesthetic agent cur-
rently used but is now commonly replaced by newer
anesthetic agents. The blood-gas partition coefficient
of halothane is 2.5, making it the most soluble

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178 I • GENERAL PRINCIPLES
TABLE 10-6 • COMPARATIVE EFFECTS OF VOLATILE ANESTHETICS
Property Halothane Enflurane
* *
Induction characteristics 0 0
Hemodynamic stability • • • *
Respiratory stability 0 »*
Ability to titrate • »«
Emergence characteristics * ** * *
Postoperative side effects **» * *
Potential toxicity and metabolism • • • * *
Cost (at low flow) 0 * *
Scale: 0 a best; *" = worst.
Adapted from White PF, ed: Ambulatory Anesthesia and Surgery. Philadelphia, WB Saunders, 1997:379.
inhalation agent used, causing slower induction and
emergence times. The respiratory effects of halothane
are a decreased minute ventilation and a depressed
ventilatory response to hypoxia and hypercapnia.56
Halothane relaxes bronchial smooth muscle and has
a nonirritating odor, making it suitable for inhalational
inductions and asthmatic patients. Halothane produces
a dose-dependent decrease in arterial blood pressure
secondary to a decrease in myocardial contractility and
cardiac output. Halothane inhibits the baroreceptor
reflex, and therefore the heart rate usually remains
unchanged despite a decrease in blood pressure.
Halothane has no significant effect on systemic vas-
cular resistance. Halothane sensitizes the myocardium
to endogenous and exogenous catecholamines, increas-
ing the risk for cardiac dysrhythmias. Last, there is
a rare association between halothane and hepatic
necrosis. Because of concerns about hepatotoxicity,
ventricular arrhythmias, and slow emergence times,
halothane is not recommended as a maintenance anes-
thetic in adults.
Enflurane
Enflurane has a blood-gas partition coefficient of 1.68
and therefore slower induction and emergence times
than those of isoflurane, desflurane, and sevoflurane.
As with all the inhalation agents, a dose-dependent
decrease in minute ventilation occurs with enflurane
as well as a reduced response to arterial hypoxia and
hypercapnia. Enflurane relaxes bronchial smooth
muscle. Enflurane produces a dose-dependent reduc-
tion in arterial blood pressure, primarily by decreas-
ing cardiac output and myocardial contractility.
Enflurane, to a small extent, reduces systemic
vascular resistance. Enflurane sensitizes the cardiac
myocardium to circulating levels of catecholamines,
but much less than halothane does.
Isoflurane
Isoflurane is a commonly used anesthetic with a blood-
gas partition coefficient of 1.4, providing a fairly rapid
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Dr.Mustafa D.
Isoflurane Desflurane Sevoflurane
* • * •
0 * 0
• * 0
** 0 0
0 »*
0 0
0 • •
*• • * » •
induction and emergence. Like all the inhalation
agents, isoflurane decreases minute ventilation and
blunts the normal ventilatory response to hypoxia
and hypercapnia. Isoflurane has a relaxant effect on
bronchial smooth muscle. Isoflurane smells pungent
and can induce airway irritation, coughing, breath
holding, and even laryngospasm. Therefore, isoflurane
is not well suited for inhalational induction of anes-
thesia. Isoflurane produces a dose-dependent reduc-
tion in arterial blood pressure, primarily through
peripheral vasodilation. Consequently, isoflurane can
increase the heart rate 20% above preoperative values.
Isoflurane decreases stroke volume and increases heart
rate, and therefore cardiac output is usually preserved.
In vitro, isoflurane depresses myocardial contractility.
However, in healthy patients, cardiac depression
is not seen because of functioning compensatory
mechanisms.
Desflurane
Desflurane was developed in the late 1980s and gained
rapid popularity for ambulatory surgery.57 Desflurane
is the least soluble of the inhaled anesthetic agents,
with a blood-gas partition coefficient of 0.42. The low
solubility of desflurane contributes to a more rapid
induction and emergence as well as better control of
anesthetic depth.58 Desflurane is highly resistant to
biodegradation, reducing the potential for organ tox-
icity. Desflurane depresses minute ventilation and
decreases the ventilatory response to hypercapnia and
hypoxia. Desflurane also relaxes bronchial smooth
muscle, but it is an airway irritant and can be as-
sociated with a high incidence of breath holding,
apnea, and coughing. Desflurane produces a dose-
dependent reduction in arterial blood pressure, pri-
marily by decreasing peripheral vascular resistance.59
Rapid induction of desflurane to high concentrations
can cause tachycardia and transient hypertension sec-
ondary to autonomic nervous system stimulation.60
Desflurane does not sensitize the myocardium to cat-
echolamines. Desflurane needs to be stored in a special
TtJWftf'aeltfWimage...
heated vaporizer because of its low boiling point and
high vapor pressure.
Sevoflurane
Sevoflurane is the most recent inhalation anesthetic
introduced into clinical practice.61 Sevoflurane has a
low blood-gas partition coefficient (0.7), providing
rapid induction and emergence from anesthesia as well
as easy titration to varying anesthetic depths.
Sevoflurane depresses ventilation and inhibits the ven-
tilatory drive to hypercapnia. However, unlike
desflurane, sevoflurane is not pungent and does not
cause airway irritation, making it highly suitable for
inhalational inductions.62 Sevoflurane reduces arterial
blood pressure by decreasing peripheral vascular
resistance. Cardiac output is maintained in healthy
individuals.63 Sevoflurane has minimal effect on heart
rate and is not arrhythmogenic.64 Sevoflurane does not
require a special vaporizer for its administration.
However, sevoflurane is not as stable as desflurane, and
degradation of sevoflurane in the presence of soda lime
forms a potentially toxic breakdown product (com-
pound A).65 Compound A produces nephrotoxicity in
rats, but its clinical significance in humans is unclear.
In addition, serum fluoride levels of patients are ele-
vated in proportion to the amount of sevoflurane expo-
sure.66 However, sevoflurane has been used in more
than 1 million patients in Japan, with no reports of
serious hepatic or renal toxicity.67
Nitrous Oxide
Nitrous oxide has been used for more than a century
to supplement anesthesia. Similar to sevoflurane and
desflurane, nitrous oxide has a very low blood-gas par-
tition coefficient of 0.47. The greatest disadvantage of
nitrous oxide is its low potency, which requires adjunc-
tive agents for a complete anesthetic. However, nitrous
oxide provides amnestic and analgesic qualities, and
in combination with other inhalation agents, it reduces
the amount of more expensive agents. Nitrous oxide
has benign cardiovascular and respiratory effects and
has no significant organ toxicity. The primary poten-
tial disadvantage of nitrous oxide is its alleged ability
to increase the risk of postoperative nausea and vom-
iting. However, numerous controlled studies have failed
to demonstrate an increase in postoperative nausea and
vomiting when nitrous oxide is used as an adjuvant
for maintenance anesthesia.68,69
Intravenous Adjuvants
MUSCLE RELAXANTS
Muscle relaxants are used as an adjuvant to anesthetic
management, facilitating tracheal intubation or opti-
mizing surgical conditions. Numerous muscle relax-
ants are available that vary in rapidity of onset and
block termination. Depolarizing and nondepolarizing
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10 • ANESTHESIA FOR PLASTIC SURGERY 179
TABLE 10-7 • POTENTIAL SIDE EFFECTS OF
SUCCINYLCHOLINE
Myalgias
Hyperkalemia
Malignant hyperthermia
Increased intracranial pressure
Increased intragastric pressure
Increased intraocular pressure
Cardiac arrhythmias
Prolonged block with abnormal plasma cholinesterase
muscle relaxants are two basic classes of muscle
relaxants.
Succinylcholine
Succinylcholine is the only ultrashort-acting depolar-
izing muscle relaxant used today (Table 10-7). Suc-
cinylcholine attaches to the cholinergic receptor, the
ion channel opens, and the cellular membrane depo-
larizes. The most prominent muscarinic side effect
is bradycardia, common in children or if doses arc
repeated within 5 minutes.70 The onset of succinyl-
choline is the fastest (45 to 60 seconds) of any neuro-
muscular blocking agent and resolves without reversal
in 5 to 7 minutes. Succinylcholine is rapidly metabo-
lized by plasma cholinesterases, accounting for its short
duration of action. However, succinylcholine has a
long duration of action if patients have an atypical
cholinesterase enzyme, and an intubating dose can last
longer than 2 hours.
Succinylcholine is used when muscle relaxation is
needed only for tracheal intubation, during brief oper-
ations, for treatment of laryngospasm, or when a
difficult intubation is suspected. Disadvantages of
succinylcholine include postoperative myalgias, which
can last up to 2 or 3 days. Succinylcholine can also
produce hyperkalemia and subsequent dysrhythmias.
The opening of the cholinergic ion channel causes an
efflux of potassium and, in normal patients, raises
the serum potassium 0.5 mEq/L.71 However, in some
disease states (e.g., recent burn, neurologic injury,
neuromuscular diseases), an exaggerated efflux of
potassium occurs, leading to cardiac arrhythmias.
Succinylcholine increases intraocular and intracranial
pressure and is avoided in open eye injuries or intracra-
nial disease. Succinylcholine can trigger malignant
hyperthermia and should not be used if there is a family
history of malignant hyperthermia. Therefore, prac-
titioners are increasingly using nondepolarizing muscle
relaxants, which can be classified as short, intermedi-
ate, and long acting (Table 10-8).
Mivacurium
The available short-acting muscle relaxants include
mivacurium and rapacuronium. Mivacurium has
an onset of approximately 2.5 minutes and a total
image...
180 I • GENERAL PRINCIPLES
TABLE 10-8 • CHARACTERISTICS OF NONDEPOLARIZING NEUROMUSCULAR BLOCKING DRUGS
Muscle Relaxant Onset (min)
Mivacurium 2-2.5
Rapacuronium 1.2-1
Atracurium 2-3
Vecuronium 2-3
Rocuronium 3-4
Cisatracurium 5 40-50
Pancuronium 3-3.5
Scale: 0 = no cardiovascular activity; *** = significant cardiovascular effects.
Numbers based on 2 x 95% effective dose.
Adapted from Doiiati F: Neuromuscular blocking drugs for the new millennium: current practice, future trends—-comparative pharmacology of neuro-
muscular blocking drugs. Ancsth Analg 200;90:S2-S6.
duration of action of 25 minutes.72 Mivacurium is
extensively metabolized by plasma cholinesterase,
accounting for its short duration of action.72 Miva-
curium can be associated with histamine release,
particularly when large doses are given rapidly. Miva-
curium undergoes a rapid spontaneous recovery, elim-
inating the need for routine antagonism of residual
neuromuscular blockade, wh ich may decrease the inci-
dence of postoperative nausea and vomiting.73 Similar
to succinylcholine, mivacurium provides good to
excellent intubating conditions in 2 to 3 minutes.
However, the clinically effective duration of action is
20 to 25 minutes, and mivacurium does not appear to
offer any clinical advantage over succinylcholine.74
Rapacuronium
Rapacuronium is a new short-acting nondepolariz-
ing muscle relaxant. It has a rapid onset and short
duration of action that is reversible even with a pro-
found block.75 Rapacuronium has onset in 60 to 90
seconds and is useful for rapid sequence intubations.75
The duration of action of rapacuronium after the intu-
bating dose is 14 ± 6 minutes,76 compared with 10 ±
2 minutes and 20 ± 6 minutes for succinylcholine
and mivacurium, respectively.77 Because of its rapid
spontaneous neuromuscular recovery rate, the dura-
tion of action of rapacuronium can be further reduced
by reversal with anticholinesterases. The reversal of
rapacuronium-induced block with edrophonium can
be readily antagonized during propofol anesthesia.
However, reversal of rapacuronium appears to be less
predictable during sevoflurane-based anesthesia.78
The neostigmine-induced recovery time of approxi-
mately 10 minutes is similar to the spontaneous
recovery time of succinylcholine.75,79 However,
recovery after a prolonged infusion or multiple doses
of rapacuronium is more prolonged, analogous to
the time course of an intermediate-acting drug.80
Cardiovascular side effects of rapacuronium include
tachycardia and hypotension, apparently unrelated to
histamine release.81 In addition, early rapacuronium
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Clinical Duration of Action (min) Cardiovascular Effects
15-25 * * *
10-20
35-45 **
35-45 0
30-40 •
0
90-120 ** »
studies reported cases of severe bronchospasm.
Although it is unclear whether this was a direct
result of rapacuronium or secondary to tracheal
intubation in a "lightly" anesthetized patient, ra-
pacuronium has been withdrawn from the market
by the manufacturer until further studies are
completed.
Atracurium
Atracurium is an intermediate-duration nondepolar-
izing muscle relaxant. Atracurium undergoes sponta-
neous degradation at physiologic temperature and pH
by the Hofmann elimination reaction, and it is also
metabolized by nonspecific plasma esterases.82 There-
fore, termination and elimination of atracurium are
independent of metabolic pathways and organs.83
Atracurium has an onset time of 3 minutes, a clinical
duration of 30 to 40 minutes, and a time to 95% recov-
ery of 45 to 60 minutes.82 Atracurium can be associ-
ated with histamine release, particularly when large
doses are given rapidly.
Vecuronium
Vecuronium is an intermediate-duration nondepo-
larizing muscle relaxant. Vecuronium is primarily
metabolized in the liver, and its elimination may be
prolonged in the presence of liver disease.84 Vecuro-
nium lacks any cardiovascular side effects.85 Vecuro-
nium has an approximate onset time of 3 minutes,
clinical block duration of about 20 to 30 minutes, and
complete recovery time of 45 minutes after an intu-
bating dose.
Rocuronium
Rocuronium is a newer intermediate-duration non-
depolarizing muscle relaxant. It has a more rapid onset
than atracurium or vecuronium, providing good
intubating conditions within 60 to 90 seconds when
two times the intubating dose is given.86 Although
rocuronium has a faster onset than vecuronium
and atracurium, duration of action and rate of
MMMMrMNmage...
elimination are similar. Rocuronium has minimal car-
diovascular side effects. Rocuronium appears to
be eliminated in the liver, and patients with liver disease
may be expected to have a prolonged blockade.87
Cisatracurium
Cisatracurium, an isomer of atracurium, is another
intermediate-duration nondepolarizing muscle relax-
ant. Similar to atracurium, it undergoes Hofmann elim-
ination, and its clearance is unchanged in the presence
of end-organ disease.88 Cisatracurium has a slower
onset time of approximately 5 minutes, has a clinical
duration of 45 minutes, and reaches 70% recovery at
about 67 minutes.88 Cisatracurium, unlike atracurium,
is not associated with any histamine release.
Opioid Analgesics
Opioid analgesics are used extensively throughout the
practice of anesthesia. Opioids arc used as premed-
icants, as intravenous adjuvants during surgery, and
in the postoperative management of surgical patients.
As premedicants, opioids serve to provide sedation and
relaxation before arrival to the operative suite. As adju-
vants to intravenous anesthetics, opioids are used to
suppress the acute hemodynamic response to intuba-
tion and other painful surgical stimuli. Residual opioid
effect can be used to make the transition to a smooth
awakening at the end of a procedure.
A variety of opioids are available today, all of which
have a similar side effect profile but differ primarily in
their onset timeand clinical duration (Table 10-9).Pure
opioid agonists include morphine, meperidine, fen-
tanyl, alfentanil, sufentanil, and remifentanil. The prin-
cipal effect of opioids is analgesia. The processing of
pain information is inhibited by a direct spinal effect
at the dorsal horn, and the rostral transmission of noci-
ceptive information is decreased by the activation of
descending inhibitory pathways in the brainstem. The
emotional response to pain is altered by opioid actions
on the limbic cortex.
TABLE 10-9 • OPIOID EFFECTS
Analgesia
Respiratory depression
Sedation
Euphoria
Vasodilation and bradycardia
Cough suppression
Miosis
Nausea and vomiting
Ileus
Skeletal muscle rigidity
Smooth muscle spasm
Bladder dysfunction and incontinence
Chronic tolerance and physical dependence
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Dr.Mustafa D.
10 • ANESTHESIA FOR PLASTIC SURGERY 181
The limiting side effect of opioids is respiratory
depression, especially when they are administered to
spontaneously breathing patients under general anes-
thesia or intravenous sedation (Fig. 10-5). Opioids act
on the respiratory centers in the medulla to depress
the ventilatory response to hypercapnia and hypoxia.
Initially, opioids decrease respiratory rate and increase
tidal volume, producing an overall decrease in minute
ventilation. As the opioid dose increases, tidal volume
subsequently decreases. Equianalgesic doses of all
opioids produce similar amounts of respiratory depres-
sion, and there is no convincing evidence that any
opioid is more or less dangerous than morphine. All
opioids can produce nausea and vomiting. Stimula-
tion of opioid receptors in the chemoreceptor trigger
zone in the area postrema activates the "vomiting center."
An occasional opioid side effect is skeletal muscle
rigidity. When large doses of opioids are rapidly given,
skeletal muscle rigidity is more likely to occur. All
opioids can produce skeletal muscle rigidity, but it is
most commonly seen with fentanyl, sufentanil, and
alfentanil. The rigidity occurs in the chest wall, abdom-
inal, neck, and extremity muscles and can be so severe
that ventilation is prevented.89 The inability to venti-
late is due to the lack of compliance in the chest wall
muscles as well as constriction of the laryngeal and
pharyngeal muscles. The administration of neuro-
muscular blocking agents is effective in terminating
the rigidity.
Opioids are considered to be cardiac stable drugs,
but certain cardiovascular effects do occur. All opioids,
except meperidine, cause a dose-dependent bradycar-
dia. Bradycardia is produced by a stimulant effect on
the central nuclei of the vagus nerve. Bradycardia is
often more pronounced with fentanyl, sufentanil, alfen-
tanil, and remifentanil. Meperidine, however, produces
tachycardia because its structural similarity to atropine
exerts atropine-like effects. Morphine and meperidine
can produce a nonimmunologic release of histamine
from tissue mast cells, causing itching, hives, and in
some cases hypotension. Hypotension can occur with
any opioid administration by direct vascular smooth
muscle relaxation effect or a reduction in sympathetic
tone.90 Meperidine is the only opioid that can produce
a negative inotropic effect.
All opioids cause contraction of smooth muscle and
decrease propulsive activity of the gastrointestinal tract,
producing ileus and constipation. Opioids produce
smooth muscle contraction of the biliary tree and
spasm of the sphincter of Oddi, leading to biliary colic
in susceptible individuals. An increase in bladder tone
through the detrusor and urinary sphincter can lead
to a sense of urinary urgency and inability to void.
The pharmacokinetics of opioids varies widely and
is often the primary consideration in choosing an
opioid. The peak respiratory and analgesic effects of
morphine occur more slowly than with other opioids
182 I • GENERAL PRINCIPLES

I 100 E I 100 E I 100 E 60 E I 4E

77
73
32

21
15
o.1 0.0 0| • 0.0 0.0
0 2 (%) N20 (%) N2 (%) C02 (t) ISO (%)
NORMAL OPERATION 20BPM

20MINS TREND C02 WAVE .5 CM/SEC

MODE VIEW SCALE ALARM

I 100 E I 100 E )E I 60 E 4E

77 74
| 35
FIGURE 10-5. A, Capnograph
tracking of expired carbon dioxide
20

02 (%)
14 0.1 0.0
N20 (%)
NORMAL OPERATION
N2 (%)
o
J
C02 (t)
0.0 0.0
ISO (%)
18BPM
levels at a nasal cannula during
monitored anesthesia care in a
patient receiving propofol infusion,
25 to 75 ug/kg/min intravenously,
for sedation during a urologic pro-
60 cedure. B, Immediately after sup-
plementation with an opioid
analgesic (fentanyl, 25 u.g intra-
venously), a marked slowing of the
respiratory rate and increase in
end-expiratory carbon dioxide
concentration were noted. (From
Stevens MB, White PF: Monitored
anesthesia care. In Miller RD, ed:
20MINS TREND C02 WAVE .5 CM/SEC Anesthesia, 4th ed. New York,
B MODE VIEW SCALE ALARM Churchill Livingstone, 1994:1474.)

and may not occur until 10 to 15 minutes after an intra-
venous bolus. Meperidine has a faster onset and
shorter duration of action compared with morphine.
Fentanyl, alfentanil, and sufentanil have similar
pharmacokinetics. The peak effects of fentanyl and
sufentanil occur in 3 to 5 minutes, whereas those of
alfentanil take 90 seconds. After a bolus, the analgesic
effect of alfentanil dissipates more rapidly than that
of fentanyl or sufentanil.
Remifentanil is a unique opioid agonist that is
degraded by nonspecific blood and tissue esterases,
independent of organ function.91,92 After a remifen-
tanil bolus, its analgesic effects dissipate within a
few minutes. When remifentanil is given as part of
a balanced anesthetic technique, recovery time is
independent of the opioid dose. Remifentanil is there-
fore useful in short cases requiring an intense opioid
effect with a rapid recovery. A potential disadvantage
of remifentanil is that other forms of analgesia will be
required if significant postoperative pain is present.
Opioid Agonist-Antagonists
Opioid agonist-antagonists, such as nalbuphine and
butorphanol, produce opioid-like effects with mod-
erately long durations of action as well as some degree
of competitive antagonism to morphine and other pure
antagonists. The agonist-antagonists all behave like
partial agonists. These drugs have shallower dose-
response curves and produce lower maximal effects as

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Dr.Mustafa D.
H&Wttf'aatfW image...
well as limiting toxic side effects. Nalbuphine and butor-
phanol are used primarily for moderate postsurgical
pain and in the obstetric patient.
Nonopioid Analgesics
The nonopioid analgesics, such as acetaminophen, non-
steroidal anti-inflammatory drugs (NSAIDs), and
ketamine, are becoming increasingly popular for the
preventive treatment of postoperative pain. Nonopi-
oid analgesics can be combined with opioids to
decrease the amount of opioid given, limiting unde-
sirable opioid side effects such as nausea and vomit-
ing, ileus, urinary retention, and respiratory depression.
ACETAMINOPHEN
Acetaminophen (7.5 to 15mg/kg) is used for treat-
ment of mild to moderate pain. Acetaminophen has
anticyclooxygenase activity that inhibits prostaglandin
production. Prostaglandin production is inhibited
principally in the hypothalamus, providing fairly
strong antipyretic and analgesic effects. However, the
anti-inflammatory effects of acetaminophen are weak,
perhaps from its limited peripheral effects. Given orally,
acetaminophen takes approximately 1 hour to reach
its peak effect, and when it is administered rectally,
absorption tends to be somewhat delayed and erratic.
A rectal dose of 35 mg/kg is equivalent to 1 mg/kg of
ketorolac in reducing postoperative pain without
increasing operative site bleeding. Rectal acetamino-
phen produces a dose-related morphine-sparing effect
after day case surgery in children.93 In addition, chil-
dren with adequate analgesia with acetaminophen
have less postoperative nausea and vomiting. Aceta-
minophen is metabolized in the liver. Acetaminophen
is a popular perioperative medication, particularly
because it lacks any gastrointestinal or platelet side
effects. However, acetaminophen can be associated with
hepatic toxicity, particularly in children when exces-
sive doses are given.
NONSTEROIDAL
ANTI-INFLAMMATORY DRUGS
Numerous NSAIDs exist, including ibuprofen, naprox-
en, diclofenac, and ketorolac. These drugs inhibit
cyclooxygenase, the enzyme that transforms arachi-
donic acid into prostaglandins, prostacyclins, and
thromboxanes. Prostaglandins mediate the release of
tachykinins (e.g., substance P), which leads to pain and
inflammation in injured tissue. Because of the avail-
ability of intravenous and intramuscular NSAIDs, these
pharmacologic agents can be administered during
anesthesia.94
The onset of the analgesic effects of NSAIDs is slower
than that of opioids, requiring 15 to 30 minutes after
intravenous dosing. Although NSAIDs are effective in
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10 • ANESTHESIA FOR PLASTIC SURGERY 183
relieving acute pain, none is as effective as opioids.
NSAIDs have weak analgesic properties during surgery
and are inadequate when used as the sole intraopera-
tive analgesic. Ketorolac does not decrease the volatile
anesthetic required, nor does it effectively block the
autonomic responses to surgery.95 Although the liter-
ature is inconclusive regarding the importance of pre-
emptive analgesia, most studies involving outpatients
undergoing ambulatory surgery suggest that preop-
erative administration of NSAIDs will decrease the
requirement for opioid analgesics in the early post-
operative period.94 One would expect ketorolac in com-
bination with opioid analgesia to be associated with a
reduced risk of postoperative nausea and vomiting and
respiratory depression compared with use of opioids
alone. However, although ketorolac decreases the
postoperative requirement for opioid medication after
laparoscopic cholecystectomy, its use does not always
reduce postoperative emesis or ventilatory impair-
ment.96 The perioperative use of ketorolac raises con-
cerns in plastic surgery because of the increased risk
of postoperative bleeding and renal impairment.
Side effects of the nonspecific cyclooxygenase
inhibitors are well documented and often limit their
usefulness. Inhibition of prostaglandin synthesis causes
renal arteriolar constriction, with chronic use impair-
ing renal function. The reversible inhibition of throm-
boxane production impairs platelet aggregation,
leading to bleeding and postoperative hematoma for-
mation. The NSAID ketorolac has been found to be
no more effective than high-dose acetaminophen in
providing analgesia for a tonsillectomy and causes more
problems with hemostasis.97 No difference in analgesic
efficacy has been found between oral ketorolac
and hydrocodone-acetaminophen after outpatient
arthroscopy.98 Prostaglandin inhibition also impairs
maintenance of the gastrointestinal mucosal barrier,
leading to ulceration. However, there is no evidence
of serious NSAID toxicity after brief perioperative
exposures in healthy outpatients.
The original NSAIDs are nonspecific cyclooxyge-
nase (COX) inhibitors, active at both COX-1 and COX-
2 receptor sites, producing a broad side effect profile.94
The COX-2-specific inhibitors have a much improved
side effect profile. Celecoxib and rofecoxib are new oral
NSAIDs that work specifically at the COX-2 receptor.
The COX-2 receptor inhibitors block the conversion
of arachidonic acid to the prostaglandins that mediate
pain and inflammation while having no effect on the
prostaglandins formed under the control of COX-1
that mediate normal homeostasis in the gastrointesti-
nal tract, kidneys, and platelets.99 Controlled trials
demonstrate that celecoxib is as effective as naproxen
in providing pain relief for osteoarthritis and rheuma-
toid arthritis and as effective as aspirin after dental
extractions. The incidence of gastrointestinal ulcers is
significantly lower with celecoxib than with naproxen
184 I • GENERAL PRINCIPLES
and similar to that of placebo.10n Of the available COX-
2 antagonists, rofecoxib appears to be the most effec-
tive in the management of acute postoperative pain.
An intravenous formulation of the new COX-2
inhibitor valdecoxib, known as parecoxib, is currently
undergoing clinical investigations in the United States.
KETAMINE
Ketamine is a phencyclidine derivative that is described
as providing dissociative anesthesia because it produces
a unique state of unconsciousness in which the patient
is in a cataleptic trance-like state disconnected from
the surroundings and profoundly analgesic. Ketamine
produces nystagmus, vocalization, and myoclonic
movements with induction. Even with unconscious-
ness, protective airway reflexes of coughing and swal-
lowing are often maintained. Ketamine causes minimal
respiratory depression and is an effective bron-
chodilator. The most significant drawback to ketamine
is the occurrence of emergence phenomena that vary
from delirium to hallucinations to vivid dreaming. Both
midazolam and propofol are highly effective in pre-
venting emergence delirium with ketamine.39 In addi-
tion, ketamine stimulates the cardiovascular system,
causing an increase in heart rate, blood pressure, cardiac
output, and pulmonary vascular resistance.39 Con-
sequently, ketamine has traditionally been used in
specific conditions when increasing cardiac output is
desirable, such as cardiac tamponade, hypovolemia,
and shock. It is not advisable for patients with poorly
controlled hypertension, arrhythmias, ischemic heart
disease, and psychological disease.
Prevention of Postoperative
Nausea and Vomiting
Postoperative nausea and vomiting (PONV) occurs
in approximately 20% to 30% of patients, and
intractable nausea occurs in 0.1% of patients.101
Emesis is controlled by the vomiting center in the
medullary reticular formation. Stimulation of the
dopamine, histamine, muscarinic, cholinergic, sero-
tonin, and opioid receptors can result in nausea and
emesis. Numerous agents are available for treatment
and prophylaxis of PONV (Table 10-10), yet the best
strategy for its prevention and therapy remains con-
troversial.'02 Clinicians still debate which patients
benefit from antiemetic prophylaxis against PONV,
along with the preferred drug, dose, and timing of
administration. A large, randomized, controlled clin-
ical trial evaluating the efficacy of antiemetics does
not exist. Rather, the issue has been addressed by meta-
analysis of small, single-site clinical studies. However,
meta-analyses of PONV studies have inherent weak-
nesses of publication bias, nonstandardization of
confounding factors, and variable outcome measures.17
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Dr.Mustafa D.
Currently available data from meta-analyses of PONV
studies simply address the PONV incidence, rather
than more pertinent issues of the patient's satisfac-
tion and return to work. A cautious attitude should
be taken to accepting clinical practice guidelines
based solely on meta-analytic techniques used to eval-
uate PONV.
Preoperative, intraoperative, and postoperative
factors can increase the risk of PONV (Table 10-11).
Patients who are obese, female patients, and patients
with a history of motion sickness, diabetic gastroparesis,
hiatal hernia, or increased anxiety are at increased
risk for PONV. Certain surgical procedures, such as
laparoscopy and strabismus surgery, are associated with
increased incidence of PONV. Postoperative factors,
such as hypovolemia, forcing oral intake, and severe
pain, can also contribute to PONV.69
Many patients are willing to accept some pain and
sedateness to control PONV.'03 However, the decision
to use prophylactic antiemetic therapy should be made
on a risk-to-benefit and cost analysis basis. The sero-
tonin antagonists have minimal side effects but are
expensive; therefore, routine prophylactic use is often
discouraged. In contrast, droperidol is inexpensive, but
doses above lmg (10|ig/kg) can cause adverse side
effects, including sedation, dysphoria, and extrapyra-
midal effects. Patients at increased risk for PONV
warrant prophylactic therapy, but with consideration
of the cost and side effect profile of the antiemetic drug
being used.
Fluid Management
Appropriate perioperative fluid management, in addi-
tion to effective perioperative pain management, helps
provide hemodynamic stability for the operative
patient. Many patients arrive at the operative suite with
some degree of fluid restriction. Adequate hydration
before induction of anesthesia will decrease postop-
erative side effects, including dizziness, drowsiness,
fatigue, and thirst as well as nausea and vomiting (Fig.
10-6).I04 Most surgical procedures cause blood loss and
shift body fluids to various compartments. If fluids are
not adequately replaced, hypovolemia can occur.
Intraoperative fluid management should account for
the patient's preexisting fluid deficit, provide mainte-
nance fluid, and replace fluid to compensate for blood
loss and fluid shifts.
Fluid management begins with a preoperative
assessment of the patient's fluid balance. Preoperative
determination and correction of hypovolemia are
important because circulatory changes that occur with
anesthesia induction and surgery are augmented in the
presence of hypovolemia. Initial fluid status evalua-
tion begins with a careful preoperative history to deter-
mine the last oral intake, any preoperative bowel disease
(bowel obstruction, emesis), or history of a bowel
T^Wttf'aelcrKf image...

0 • ANESTHESIA FOR PLASTIC SURGERY 185

TABLE 10-10 • RECEPTOR SITE AFFINITY OF ANTIEMETIC DRUGS

Dopamine Muscarinic Histamine Serotonin

Drug Group (D 2 ) (cholinergic) (H 2 ) (5-HT 5 )

Phenothiaztnes
Fluphenazine * ** # - »*
Chlorpromazine * ** * * * ****
Prochlorperazine **** *
Butyrophenones
Dropendol *•** *
Halopendol ****
Domperidone •* • •
Antihistamines
Diphenhydramine « ** • •**
Promethazine * * »* **+*
Anticholinergic
Scopolamine • * ***
Benzamides
Metoclopramide *** «*
Antiserotonin
Ondansetron • ***
Dolasetron *** *
G rani set ron • • ** •

Scale: * = minimal; **** • maximal.

From Watcha MF, White PF: Postoperative nausea and vomiting: do they matter? Eur I Anesth 1995;12:18-23.

preparation. Physical examination findings of tachy-

cardia, hypotension, or orthostatic hypotension may
TABLE 10-11 • RISK FACTORS FOR indicate hypovolemia. Poor skin turgor, dry mucous
POSTOPERATIVE NAUSEA membranes, and low urine output also indicate hypo-
AND VOMITING volemia. If severe hypovolemia is suspected, electrolytes
should be measured to help guide replacement therapy.
Predisposing factors Fluids should be replaced before anesthetic induction
Female gender (perimenstrual > preovulatory) and surgery if moderate to severe fluid imbalance is
Motion sickness
present. As a general guide, fluid replacement for exist-
Vestibular disturbances
Nonsmoker ing deficits should occur during approximately 3 hours,
Early pregnancy with the first half of the deficit being replaced in the
Increased gastric volumes first hour and the remaining two quarters in each sub-
Excessive anxiety sequent hour.
Ingestion of solid food
Delayed gastric emptying In addition to replacement of the deficit fluid,
Anesthetic agents normal fluid intake should be maintained during the
Inhalation: volatiles, nitrous oxide surgical period. There are several formulas that provide
Intravenous: ketamine, etomidate estimates for fluid maintenance, such as for the first
Opioid analgesics: agonists, agonist-antagonists 10 kg of weight, replace with 4 mL/kg/hr; for the weight
Sugical procedures
Laparoscopy between 10 and 20 kg, replace with 2 mL/kg/hr; and
Lithotripsy for the weight above 20 kg, replace with 1 mL/kg/hr.
Strabismus correction Therefore, a person weighing 70 kg should receive
Tonsillectomy 110 mL/hr (40 mL + 20 mL + 50 mL) of maintenance
Middle ear operations fluid. Accurate assessment and replacement of intra-
Orchiopexy operative blood loss are also important. Careful exam-
Postoperative factors ination of the surgical field, surgical gowns, floor,
Severe pain
sponges, and wall suction will help determine a rea-
Hypotension, dehydration
Premature ambulation sonable estimate. Blood loss is replaced with crystal-
Forcing of oral fluids loid in a 1:3 ratio. If a blood transfusion is required,
this is replaced in a 1:1 ratio. In addition to produc-
From Watcha MF, White PF: Postoperative nausea and vomiting: its etiol- ing blood loss, surgical injury to tissue results in shift-
ogy, treatment, and prevention. Anesthesiology 1992;77:162-184.
ing of fluids from the intravascular and intracellular
compartments to "third space" areas. The amount of

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Dr.Mustafa D.
186 I • GENERAL PRINCIPLES

3?
U
c
I
o

30 M 60 M DIS DAY1 30 M 60 M DIS DAY1

Drowsiness Dizziness
B

HIGH INFUSION 0 LOW INFUSION

30 M 60 M DIS DAY1 30 M 60 M DIS DAY1

Thirst Nausea

FIGURE 10-6. The effect of preoperative hydration status on the incidence of postoperative drowsiness (A), dizzi-
ness (B), thirst (C), and nausea (D). 30M.30 minutes postoperatively; 60M, 60 minutes postoperatively; DIS, at dis-
charge; DAY 1, first postoperative day. *P < .05 between the high- and low-infusion groups. (From Yogendran S,
Asokumar B. Cheng DC, et al: A prospective randomized double-blinded study of the effect of intravenous fluid therapy
on adverse outcomes on outpatient surgery. Anesth Analg 1995;80:682.)

fluid shift depends on the area ofsurgery and can vary
from 1 mL/kg/hr for minor surgeries to 15mL/kg/hr
for large abdominal surgeries. Special considerations
occur with regard to fluid replacement during tumes-
cent saline-assisted liposuction. Several liters of infusate
(i.e., normal saline with lidocaine and epinephrine)
are typically injected beneath the skin. After comple-
tion of liposuction, some of this fluid remains and
is subsequently absorbed systemically. To avoid fluid
overload, this "extra" fluid should be considered in
calculating the volume of fluid replacement.
In general, fluids are usually replaced with a crys-
talloid solution. Glucose solutions are avoided because
diffusion occurs more quickly out of the intravascu-
lar compartment than with crystalloid solutions.
Blood products (red blood cells, fresh frozen plasma,
cryoprecipitate) are given only when deemed medically
necessary. In general, colloid solutions are more costly
to administer, and clinical trials do not show that colloid
solutions offer any benefit over the administration of
crystalloid solutions.105
Temperature Regulation
The induction of anesthesia causes a significant change
in thermoregulation, often producing hypothermia.
The human thermoregulatory system usually main-
tains core temperature within approximately 0.2°C.
Thermoregulatory responses include behavior (adjust-
ing thermostat, clothing), shivering, vasoconstriction,
and sweating. Anesthetics widen the temperature
range that does not trigger thermoregulatory defenses
to approximately 20 times the normal range. Hypother-
mia has negative consequences for the patient, and the
patient's temperature must be accurately measured to
help prevent its occurrence. According to the 1999 ASA
standards and guidelines, "every patient receiving
anesthesia shall have temperature monitored when

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clinically significant changes in body temperature are
intended, anticipated, or suspected." Body tempera-
ture can be monitored effectively at a number of sites,
including the tympanic membrane, bladder, esopha-
gus, and rectum. 106
Inhalation agents inhibit thermoregulation by
inhibiting vasoconstriction and shivering as well as
sweating.107 Regional anesthesia impairs both central
and peripheral thermoregulation, and hypothermia is
also common during spinal or epidural anesthesia. 107
Body heat flows from the central core to the periph-
ery because the peripheral temperature is always 1°C
to 2°C cooler than the core temperature. In addition,
patients lose heat from receiving cold intravenous fluids
and dry inhalation anesthetics, by being washed with
cold solutions, and from the surgical incision site.
A decrease of 1°C to 3°C below normal provides
substantial protection against cerebral ischemia.107
However, even mild hypothermia may lead to
postoperative shivering, which increases oxygen
consumption. Increased oxygen consumption can
precipitate myocardial ischemia in susceptible patients.
Wound infections are three times more likely to occur
in hypothermic patients undergoing elective colon
resection than in nonhypothermic patients. 108
Hospital duration is increased by 20% in colon resec-
tion patients who are hypothermic. 108 Mild hypo-
thermia reduces the resistance to surgical wound
infection by directly impairing immune function and
decreasing cutaneous blood flow, which reduces the
delivery of oxygen to the tissues. Mild hypothermia
reduces platelet function and decreases the activation
of the coagulation cascade. Hypothermia prolongs drug
action by decreasing the metabolism of most drugs,
including propofol, vecuronium, and atracurium.
The most effective way to maintain normothermia
is to decrease the thermal difference between the patient
and the room. A warm room decreases the tempera-
ture gradient from the patient to the room, and less
heat is lost from the patient to the environment.
Warming intravenous and irrigation fluids also helps
prevent heat loss. The forced-air warming devices are
effective in maintaining normothermia and may
decrease postoperative shivering.109
Hyperthermia may also occur and is most often
caused by excessive warming, infection, hyperthy-
roidism, or (extremely rarely) malignant hyperther-
mia. The hallmark of malignant hyperthermia is a
hypermetabolic state that initially presents with
increased end-expiratory carbon dioxide production.
Malignant hyperthermia is an inherited myopathy
characterized by a hypermetabolic state when the
patient is exposed to an appropriate triggering agent.
A defect at the sarcoplasmic reticulum leads to
decreased calcium reuptake. The intracellular calcium
increases tremendously, leading to sustained muscle
contracture, glycolysis, and heat production. The
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10 • ANESTHESIA FOR PLASTIC SURGERY 187
triggering agents for malignant hyperthermia are
depolarizing muscle relaxants (namely, succinyl-
choline) and all of the volatile anesthetic agents. The
incidence of malignant hyperthermia is 1 in 15,000
pediatric patients and 1 in 50,000 adults. All patients
should be questioned preopera tively about any history
in themselves or direct family members of high fever,
prolonged intubation, muscle disease, or unexpected
death after general anesthesia. Patients with a family
history of malignant hyperthermia should receive a
nontriggering anesthetic that avoids any of these agents
and uses a machine flushed with 10-liter flow of 100%
oxygen for at least 20 minutes.
The initial presentation of malignant hyperthermia
is usually an unexplained tachycardia, followed by an
increase in end-tidal carbon dioxide content, a decrease
in oxygen saturation, dysrhythmias, and muscle rigid-
ity. Hyperthermia occurs but is a late finding. If malig-
nant hyperthermia is suspected, an arterial blood gas
analysis should confirm metabolic acidosis. Other pos-
sible metabolic derangements include hyperkalemia,
hypercalcemia, hyperphosphatemia, increased creatine
kinase levels, and myoglobinuria. If malignant hyper-
thermia progresses, renal failure, cerebral edema, and
disseminated intravascular coagulation can occur.
The onset of malignant hyperthermia after expo-
sure to triggering agents can be delayed and may not
become overt until the recovery room. As soon as malig-
nant hyperthermia is suspected, it needs to be aggres-
sively treated. The first step in treatment is to call for
assistance and stop all triggering agents. Hyperventi-
late the patient with 100% oxygen and terminate the
surgical procedure. Administer dantrolene, which
impairs calcium-dependent muscle contractures. Aci-
dosis should be closely monitored and treated, and
urine output is promoted with fluids, furosemide, and
mannitol. Hyperkalemia should be treated with insulin
and glucose. Before dantrolene, the mortality rate from
malignant hyperthermia was 28%; however, with
dantrolene, the mortality rate has decreased to 10%. n 0
To diagnose malignant hyperthermia or to test sus-
ceptible relatives, a caffeine and halothane contracture
test can be performed on a skeletal muscle biopsy spec-
imen from the patient.
Positioning of the Patient
Anesthetized patients are at risk for injury from
stretching or pressure on nerves, vessels, joints, and
skin. Positioning of the patient requires close, critical
attention, and considerations vary according to whether
the patient's position is supine, prone, lateral decubi-
tus, or sitting. The majority of surgical procedures are
performed with the patient in the supine position. Arms
can either be placed at the side or extended. In general,
patients are more comfortable if their hips, knees, and
elbows are slightly flexed. Arms placed at the side should
188 I • GENERAL PRINCIPLES

have the elbows externally rotated to protect the ulnar
nerve. If the arms are extended, the angle should be
less than 90 degrees, with slight elevation of the sup-
portingsurface and external rotation of the elbow. Sup-
port of the legs is important, as is minimizing pressure
on the heels. A head support should be used to mini-
mize pressure on the occiput. Injuries to nearly all
nerves have been reported, including ulnar, brachial
plexus, sciatic, femoral, common peroneal,saphenous,
anterior tibial, obturator, and lateral femoral cutaneous
nerves.
Positioning of the patient for breast reduction
mammaplasties and augmentations requires special
considerations because of the intermittent sitting
position. The arms are typically extended to less than
90 degrees and supinated on a padded arm board with
an additional elbow pad positioned under each arm.
In addition, blankets are added on top of the arms and
taped in position. A safety strap is secured over the
patient's hips. Therefore, the arms are fully padded and
secured to the arm boards, and minimal movement
occurs when the patient assumes the sitting position.
However, vigilant observation of the arm position is
required during the sitting position.
In the standard prone position, the patient lies on
his or her ventral surface with the head face down (Fig.
10-7A). Excessive abdominal pressure decreases pul-
monary compliance, increases intracranial pressure,
and increases venous pressure. Rolls can be placed
extending from each acromioclavicular joint to each
anterior superior iliac spine to avoid excessive abdom-
inal pressure. Alternatively, rolls can be placed
transversely, extending across the chest below the
suprasternal notch, and across the anterior superior
iliac spines. To prevent compression of blood vessels
in the neck, head rotation should be minimized. The

B
FIGURE 10-7. The importance of proper padding is illustrated for the standard prone position (A) and the lateral
decubitus position (B). In the prone position, the trunk is supported at the anterior superior iliac spines and the acromio-
clavicular joints. In the lateral position, an axillary roll supports the chest to free the axilla, and the arms and legs are
supported with pillows. (From Cucchiara RF, Faust RJ: Patient positioning. In Miller RD, ed: Anesthesia, 4th ed. New
York, Churchill Livingstone, 1994:1057.)

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arms can be secured along the trunk or on arm boards,
with the arms abducted not more than 100 degrees
when they are anteriorly flexed. Arms should be well
padded below the elbow. Breasts should be positioned
medially or below supports. Feet are padded and slightly
elevated to prevent pressure and stretchingof the ante-
rior tibial nerve. There should be no pressure on the
genitalia or the eyes.
In the lateral decubitus position, the patient lies on
his or her side (Fig. 10-7B). The lower leg should be
flexed at the hip and slightly at the knee. The upper
leg is either straight or slightly flexed. The lower arms
can be abducted to a maximum of 100 degrees if the
elbow is flexed. The head and neck should be main-
tained in a straight line from the vertebral column.
The eyes should be without pressure. To prevent exces-
sive pressure on the brachial plexus, a chest roll is placed
below the axilla. Padding should be placed between
the knees. Tape can be placed over the pelvis to stabi-
lize the hips.
Special Anesthetic Considerations
MONITORING NEUROMUSCULAR
BLOCKADE
Monitoring neuromuscular blockade and ensuring
adequate reversal are important elements to return the
patient to spontaneous ventilation. Neuromuscular
blockade is assessed by the muscle response (adduc-
tor pollicis of the thumb) to supramaximal stimula-
tion of its motor nerve with a nerve stimulator. In
addition, clinical criteria can indicate adequate neu-
romuscular reversal. Signs of adequate recovery by
peripheral nerve stimulations are absence of fade on
train-of-four stimulation, absence of fade to a post-
tetanic stimulation, and presence of sustained tetanus
at 100-Hz stimulation. The clinical criteria for ade-
quate recovery are a sustained head lift for 5 seconds
and an inspired negative pressure of at least 20 cm H 2 0.
Unless complete recovery from neuromuscular
block occurs spontaneously (train-of-four ratio > 0.8),
it is often necessary to reverse the effects of these
agents.73 Nondepolarizing muscle relaxants are reversed
with anticholinesterases (neostigmine or edropho-
nium). The anticholinesterase inhibits the activity of
acetylcholinesterase, leading to accumulation of acetyl-
choline at the neuromuscular junction and muscarinic
sites, providing more acetylcholine to compete with
the neuromuscular agent at the receptor site. The mus-
carinic effects from reversal cause bradycardia, and
therefore the reversal agents are always administered
with atropine or glycopyrrolate.
MONITORING OF CEREBRAL FUNCTION
The EEG bispectral (BIS) index, a derived value from
the electroencephalograph, has been shown to be a
quantifiable measure of the sedative and hypnotic
effects of anesthetic drugs on the central nervous
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Dr.Mustafa D.
10 • ANESTHESIA FOR PLASTIC SURGERY 189
system.111 The BIS index value ranges from 0 to 100,
and decreasing values indicate more sedation and hyp-
nosis. A BIS value of less than 60 has a high probabil-
ity of correctly predicting absence of consciousness and
a low probability of recall. The BIS monitor is simple
to use, and titrating anesthetic agents with use of the
BIS monitor significantly decreases the anesthetic
agent and significantly hastens recovery."2,113 Other
EEG-based monitoring systems (e.g., physical state
analyzer [PSA], auditory evoked potential [AEP]) will
be available in the near future.
REGIONAL ANESTHESIA
Regional nerve blocks offer some advantages over
general anesthesia for selected patients. Regional anes-
thetics reduce the incidence of postoperative nausea
and vomiting.1 M Regional techniques can provide post-
operative analgesia, reducing postoperative narcotic
requirements. A reduction in narcotic dose reduces
postoperative nausea and vomiting and sedation. Dis :
advantages of regional techniques include a longer
preparation time than general anesthesia, the risk asso-
ciated with a numb extremity, and the possibility of
urinary retention with spinal or epidural anesthesia.
Local Anesthetics
Local anesthetics block the conduction of nerve
impulses by preventing sodium passage through the
nerve sodium channels. Local anesthetic effects are ter-
minated by diffusion from the nerve membrane. The
duration of action of local anesthetics is dependent
on the concentration of local anesthetic and the blood
flow to the nerve fiber (Table 10-12). The higher the
lipid solubility of the local anesthetic, the longer the
duration of action and greater potency. Local anes-
thetics cause varying degrees of vasodilation, which also
affects their duration of action and side effect profile.
Systemic toxicity to local anesthetics occurs from
excessive plasma concentrations of the drugs. An acci-
dental intravascular injection of a local anesthetic
during a nerve block is the most common cause of sys-
temic toxicity. However, toxic blood levels also occur
from excessive tissue injection and subsequent intravas-
cular absorption. Toxic central nervous system effects
of local anesthetics are restlessness, vertigo, tinnitus,
slurred speech, sedation, and ultimately generalized
tonic-clonic seizures and apnea. Local anesthetic-
induced seizures can be treated with benzodiazepines
or thiopental. Supplemental oxygen and appropriate
airway management should be provided. Because of
the high blood flow to the brain, the level of local anes-
thetic in the central nervous system decreases rapidly,
and toxic effects are usually short-lived.
The cardiovascular system is more resistant than
the central nervous system to local anesthetic toxicity.
Therefore, signs of central nervous system toxicity will
precede cardiovascular complications. Cardiovascular
image...

190 • GENERAL PRINCIPLES

TABLE 10-12 • RECOMMENDED CONCENTRATIONS OF LOCAL ANESTHETICS AND MAXIMUM DOSES

Clinical Epineph rine

Plain Solution Solution i Infiltration

Drug (Trade Name) Concentrations mg mg/kg mg mg/kg Duration (mitt)

Cocaine 196-496 200 1.5

Procaine (Novocain) 1%-10% 500 1000 45-60
Benzocaine 1496-20%
Tetracaine (Pontocaine) 1% 100 200 60-180
2-Chloroprocaine (Nesacaine) 196*596 800 11 1000 14 30-45
Lidocaine (Xylocaine) 0.596-5% 300 4.5 500 7 60-120
Mepivacaine (Carbocaine) 196-2% 400 500 7 90-180
Prilocaine (Citanest) 4% 400 500 60-120
Bupivacaine (Marcaine) 0.25%-0.75°/o 175 250 3 240-480
Etidocaine (Duranest) 11.5% 300 4 400 6 240-480
Ropivacaine (Naropin) 0.2%-1% 4 ?200 240-480
Levobupivacaine 0.25%-1% ? 240-480

From White PF, ed: Ambulatory Anesthesia and Surgery. Philadelphia, WB Saunders, 1997:409.

toxicity is manifested by hypotension and impaired
cardiac conduction. Local anesthetics cause a dose-
dependent, direct, negative inotropic effect on myocar-
dial contractility. Local anesthetics decrease the cardiac
action potential by limiting inward flow of sodium
current, prolonging the PR interval and widening the
QRS complex on electrocardiography. Local anesthetics
vary in their ability to produce cardiac toxicity. Tetra-
caine, bupivacaine, and etidocaine exhibit the great-
est cardiovascular toxic effects. Lidocaine is a fast-in,
fast-out sodium channel blocker, in contrast to bupi-
vacaine, which enters the sodium channel quickly but
departs slowly. Bupivacaine is therefore more likely to
precipitate cardiac arrhythmias. Some local anesthet-
ics are racemic mixtures of R(+) and S(-) enantiomers.
The sodium channel is more susceptible to blockade
by the R(+) enantiomer of bupivacaine than to ropi-
vacaine, a pure S enantiomer."5
Allergic reactions to local anesthetics are extremely
rare. Most adverse reactions to local anesthetics are
due to systemic toxicity rather than to an allergic reac-
tion. Ester local anesthetics produce metabolites related
to p-aminobenzoic acid and are therefore more likely
than the amide local anesthetics to produce allergic
reactions. There is no cross-reactivity between the two
classes of drug. Therefore, patients allergic to ester local
anesthetics can receive amide local anesthetics.
However, one must be sure that the allergic reaction
did not occur from the preservative in the commer-
cial preparation of the local anesthetic.
LIDOCAINE
Lidocaine is the most commonly used local anesthetic
because of its rapid onset, potency, topical anesthetic
activity, and moderate duration of action. The addi-
tion of epinephrine to lidocaine can extend its
duration of action up to 120 minutes. Lidocaine is
used in concentrations of 0.5% to 5.0% for infiltra-
tion, peripheral nerve blocks, and epidural and spinal
anesthesia. Lidocaine is also available in ointment, jelly,
and viscous and aerosol preparations for a variety of
topical anesthetic procedures. Lidocaine is metabo-
lized in the liver, and its metabolites have systemic
pharmacologic activity, which may play a role in tox-
icity after additive doses. The potential for systemic
toxicity is intermediate, with lidocaine between
procaine and bupivacaine. The Food and Drug Ad-
ministration recommended maximum adult dose of
lidocaine with epinephrine administered for regional
anesthesia is 7 mg/kg. However, recent data report
lidocaine doses as high as 55 mg/kg during tumescent
infiltration anesthesia, with no untoward side effects.
The slow release of lidocaine from the fat may account
for the tolerance to the higher dose.
BUPIVACAINE
Bupivacaine is a popular local anesthetic because it
has an acceptable onset time, a long duration of action,
and a profound conduction block with separation of
sensory and motor anesthesia. Bupivacaine is used in
concentrations varying from 0.125% to 0.75% for
infiltration, peripheral nerve blocks, and epidural and
spinal anesthesia. The major advantage of bupivacaine
is its ability to achieve sensory blockade at low con-
centrations with much less effect on motor blockade.
Because of this feature, bupivacaine is popular in obstet-
ric anesthesia and for postoperative epidural analge-
sia when movement of the patient is desirable.
Compared with lidocaine, bupivacaine is more car-
diotoxic. Bupivacaine is associated with cardiovascu-
lar collapse after accidental rapid intravenous
administration. Cardiotoxicity occurs more frequendy

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*t&*>t#(9elcrt# image...
in obstetric patients receiving 0.75% bupivacaine, and
this dose is no longer recommended for obstetric
patients.
ROPIVACAINE
Bupivacaine is produced as a racemic mixture ofenan-
tiomers containing equal proportions of the S and R
forms, but ropivacaine is the single Senantiomer. Ropi-
vacaine is similar to bupivacaine in onset and the extent
of sensory and motor blocks. Ropivacaine is admin-
istered in concentrations of 0.25% to 1.0% for infiltra-
tion, peripheral nerve block, and epidural anesthesia.
The sensory block provided by ropivacaine is similar
to that produced by an equivalent dose of bupivacaine.
The motor block produced by ropivacaine is slower in
onset and less intense and shorter in duration than
with an equivalent dose of bupivacaine. Motor block
intensifies as the dose of ropivacaine increases. Ropi-
vacaine has less cardiotoxicity than bupivacaine but
more than lidocaine.115
LEVOBUPIVACAINE
Levobupivacaine is the isolated $(-) isomer of bupi-
vacaine and is promoted as a less toxic alternative
to bupivacaine. Levobupivacaine has an anesthetic
potency equal to that of bupivacaine. Studies in
animals allegedly demonstrated that levobupivacaine
has a greater margin of safety than the commonly used
racemic mixture of bupivacaine (based on intravenous
administration of equal doses to sheep). Levobupiva-
caine is also alleged to be less toxic to the central nervous
system than bupivacaine. Both bupivacaine and lev-
obupivacaine depress the myocardium; however, fatal
arrhythmias are alleged to be less likely to occur with
levobupivacaine. 116
COCAINE
Cocaine is used as a topical anesthetic for mucous
membranes of the nose and throat because of its
excellent ability to produce local anesthesia and vaso-
constriction. Cocaine blocks the reuptake of norepi-
nephrine and therefore has a sympathomimetic effect.
The maximum recommended dose of cocaine is
1.0 mg/kg, and a 4% solution is recommended. At doses
above 1.0 mg/kg, tachycardia, hypertension, tremu-
lousness, seizures, and hyperthermia may occur.
Cocaine-associated hemodynamic changes can be
treated with (i-blocking drugs.
Facial Nerve Blocks
Innervation of the head and neck is through the 12
cranial and upper 4 cervical nerves. Sensory innerva-
tion of the face is from the three divisions of the trigem-
inal nerve: ophthalmic, maxillary, and mandibular.
Cutaneous innervation of the posterior head and neck
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10 • ANESTHESIA FOR PLASTIC SURGERY 191
is from the cervical nerves (Fig. 10-8). The terminal
sensory branches of the ophthalmic nerve (supraor-
bital and supratrochlear), maxillary nerve (infraor-
bital), and mandibular nerve (mental J may be blocked
to provide surgical anesthesia for superficial procedures
and postoperative analgesia. The individual nerves can
be blocked by use of a 23- to 25-gauge short needle
and injection of 2 to 4 mL of local anesthetic. The addi-
tion of epinephrine (1:100,000) to the local anesthetic
will provide vasoconstriction and reduce blood loss
during facial surgical procedures. Care should be taken
not to inject into the foramen. When the patient is
supine with pupils in the midline, the supraorbital,
infraorbital, and mental nerves lie along a line drawn
through the corner of the mouth and the pupil. The
supraorbital foramen is often palpable, and the supra-
orbital, infraorbital, and mental foramina lie in a line
approximately 2.5 cm from the midline.
The supraorbital nerve is found in a vertical line at
the level of the supraorbital notch. With needle inser-
tion in a cephalomedial direction, the local anesthetic
is injected between the skin and frontal bone. Medial
direction of the needle at this site will block the supra-
trochlear nerve, which supplies the skin of the medial
forehead and upper eyelid. The infraorbital nerve exits
through the infraorbital foramen, about 1 cm below
the orbital rim and 1 cm from the lateral wall of the
nose along the vertical plane through the eye. Block-
ade of the infraorbital nerve will provide anesthesia to
the lower eyelid, the lateral portion of the nose, and
the upper lip. The mental nerve emerges from the
mental foramen to provide sensation to the lower lips,
central mucous membranes, and submental cutaneous
area. The foramen is approached anteriorly, and
infiltration is performed close to the bone.
Sensory innervation to the ear is supplied by cuta-
neous branches of spinal and cranial nerves. The great
auricular and the lesser occipital nerves supply the pos-
terior surface of the ear and a variable portion of the
anterior surface, and the auriculotemporal branch of
the mandibular nerve supplies the remainder of the
anterior surface. The posterior aspect of the ear may
be anesthetized by infiltration close to the posterior
aspect of the auricle over the mastoid process with 6
to 10 mL of local anesthetic. The auriculotemporal
nerve is blocked by infiltration of 6 to 10 mL of local
anesthetic anterior to the ear, beginning at the zygoma.
Sensory innervation of the nose is primarily from
the infratrochlear, infraorbital, nasal palatine, and
external nasal nerves. Innervation of the anterior and
internal portions of the nose is predominantly through
branches of the sphenopalatine ganglion and the ante-
rior ethmoidal nerves. Regional anesthesia of the exter-
nal nose can be accomplished by blocking its external
innervation. Intranasal blockade of the nose is often
accomplished by applying cotton-soaked cocaine
applicators into the nose. Caution is advised to avoid
image...

192 I • GENERAL PRINCIPLES

Supratrochlear n.

Supraorbital n.

Infraorbital n.

- Menial n.

A B
FIGURE 10-8. A, Needle positions for blockade of the terminal sensory branches of the trigeminal nerve. A vertical
line connects the supraorbital notch, infraorbital foramen, and mental foramen. B, The dermatomes of the head, neck,
and face. (From Wedel DJ: Nerve blocks. In Miller RD, ed: Anesthesia, 5th ed. New York, Churchill Livingstone, 2000:1520.)

toxic doses of cocaine, and great care is needed if
epinephrine and lidocaine are also given.
Extremity Nerve Blocks
Many different types of extremity blocks are available
for both the upper and lower extremities. The upper
extremities can be anesthetized by an intravenous
regional technique and by axillary, supraclavicular, or
interscalene block. The intravenous regional (Bier)
block is the simplest and most reliable upper extrem-
ity regional block (Fig. 10-9). After placement of an
intravenous catheter in the hand on the operative side,
the extremity is elevated and wrapped tightly in a
bandage. A tourniquet is then inflated over the prox-
imal portion of the upper extremity, at least 100 mm Hg
above the patient's systolic pressure. When adequate
inflation has occurred, 40 to 50 mL of 0.5% lidocaine
is given through the catheter. Failure of this block is
rare but can occur if the tourniquet is not adequate.
Risk of the block is seizures from local anesthetic tox-
icity when the tourniquet is inadequate or acciden-
tally deflated. A contraindication to this block is a long
surgical procedure because tourniquet pain occurs at
approximately 60 to 90 minutes. A double-tourniquet
technique lengthens the time a patient tolerates the
tourniquet. Two adjacent tourniquets are placed on
the upper extremity, and both are initially inflated to
ensure proper function. Before the local anesthetic (e.g.,
lidocaine 0.5%) is injected, the lower cuff is deflated.
When the patient complains of pain in the upper arm
during the procedure, the lower tourniquet is inflated
and the upper cuff is deflated. Once both tourniquets
are deflated, there is minimal residual local anesthetic
effect, and patients may require postoperative pain
medication.
When a regional approach is planned for upper
extremity procedures lasting longer than 60 to 90
minutes, a brachial plexus block may be performed.
The brachial plexus can be blocked by one of three
approaches: axillary, interscalene, or supraclavicular.
These blocks provide anesthesia for several hours and
minimize postoperative narcotic requirements. The
interscalene block (Fig. 10-10) is most appropriate for
surgery performed on the shoulder as well as on the
arm. Interscalene block of the brachial plexus is
achieved by injecting 10 to 40 mL of local anesthetic
in the interscalene groove opposite the transverse
process of the sixth cervical vertebra (C6). A line
extended laterally from the cricoid cartilage intersects

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 image...

10 • ANESTHESIA FOR PLASTIC SURGERY 193

Venous
exsanguination
gravity

Esmarch
Dilute local
bandage
anesthetic
Intravenous
catheter

Syringe and
IV tubing

FIGURE 1 0-9. The sequence of events to perform an intravenous local anesthetic block (Bier block) by a double-
tourniquet technique. A, An intravenous regional block, equipment. B, Intravenous regional block, placement of intra-
venous catheter at distal site and venous exsanguination by gravity. C, Intravenous regional block, venous exsanguination
augmented with Esmarch bandage. D, Intravenous regional block, injection of local anesthetic at distal intravenous
site. (From Brown DL: Atlas of Regional Anesthesia, 2nd ed. Philadelphia, WB Saunders, 1999:67.)

the interscalene groove at C6. Paresthesias must be
elicited before injection. The risk of pneumothorax
with this approach is remote, although spinal and
epidural injection is possible, as is direct injection into
the vertebral artery.
The supraclavicular block is the most effective block
to provide anesthesia to the forearm and hand. A skin
wheal is made over the midclavicle posterior to the
subclavian artery. A 22-gauge needle is directed cau-
dally until bone is encountered. The needle is then
walked over the first rib until a paresthesia is obtained.
After a negative aspiration, 40 mL of local anesthetic
is injected incrementally. A supraclavicular block has
a higher incidence of pneumothorax (2% to 6%) than
does an axillary or interscalene block. Therefore, the
axillary block is usually preferred when anesthesia to
the arm but not to the shoulder is required.
The axillary block (Fig. 10-11) avoids the risk of
pneumothorax or intra-arterial injection into the
cerebral circulation. However, the musculocutaneous
and medial antebrachial cutaneous nerves must be
blocked by separate injections with an axillary block.
To perform the axillary block, the arm is abducted to
90 degrees and externally rotated. The axillary artery
is palpated and traced as far as possible into the axilla.
The needle is then inserted through the artery (transar-
terial approach) or just anterior to it when a pares-
thesia is elicited (paresthesia technique), and the local
anesthetic (40 mL) is injected. Regardless of the
approach, frequent aspirations during injection should
be performed to minimize the risk of an intravascu-
lar injection. For procedures involving the distal part
of the upper extremity or the hand, it is possible to use
peripheral nerve blocks at the elbow (Fig. 10-12) or
the wrist (Fig. 10-13).
For lower extremity surgery, anesthesia of the lower
leg can be induced by peripheral nerve block of the
sciatic and femoral plexus (Fig. 10-14), but the results

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194 I • GENERAL PRINCIPLES
Cricoid
Cartilage
Sternomastoid Muscle
Anterior Scalene Muscle
Middle Scalene Muscle
A B
FIGURE 10-1 0. The anatomic landmarks (A) and approach to palpation of the interscalene groove (B) to perform
an interscalene block. (From Cousins MJ: Neural Blockade in Clinical Anesthesia and Management of Pain, 2nd ed.
Philadelphia, Lippincott, 1988:399.)
are less reliable than with spinal or epidural blocks. If
anesthesia is required only for the foot, an ankle block
can be performed (Fig. 10-15). An ankle block requires
five separate injections for the posterior tibial nerve,
the sural nerve> the saphenous nerve, the deep per-
oneal nerve, and the superficial peroneal nerve.
Central Neuraxis Blocks
Spinal block is produced by injection of local anes-
thetic solutions into the subarachnoid space, whereas
an epidural block is produced by injection of local anes-
thetics into the epidural space. Spinal and epidural
blocks can produce the same density of block at an
equal level but vary in the onset of block, duration of
block, and some of the potential side effects.
Spinal and epidural blocks are used for many
surgical procedures, including those on the lower
abdomen, groin, pelvis, perineum, and lower extrem-
ities. Spinal anesthetics have onset nearly immediately,
and the duration can be adjusted by appropriate
drug selection. The very small dose of local anesthetic
drug (1 to 2mL) required for subarachnoid block
eliminates the possibility of systemic toxicity. The
concentration of local anesthetic and the particular
agent used determine the density and duration of
the block. The distribution of the local anesthetic
accounts for the anesthetic level and is largely deter-
mined by the density of the local anesthetic versus the
density of the cerebrospinal fluid and the position of
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Cricoid Cartilagi
External Jugular
Interscalene Groove
the patient during the first few minutes after spinal
placement.
An epidural anesthetic is similar to a spinal anes-
thetic but takes longer to place. An epidural catheter
may be threaded into the space and remains until the
end of the procedure. This allows incremental dosing,
contributing to a slower onset block but also a more
controlled degree of hypotension and final block level.
The slower onset of sympathetic blockade allows precise
hydration as the level advances. Epidural spread
depends on the volume of anesthetic given, and the
density of the block depends on the concentration of
the local anesthetic.
After placement of local anesthetic in the sub-
arachnoid or epidural space, sympathetic fibers are
blocked, then sensory, and finally motor nerves. Sym-
pathetic block decreases venous return and produces
bradycardia, which may result in hypotension. High
levels of motor blockade can also cause paralysis
of abdominal and intercostal muscles, leading to a
decreased ability to cough and to clear secretions.
Postdural puncture headaches can occur with either
spinal or epidural blocks. Postdural puncture headaches
are more common with a 22-gauge needle (versus a
25-gauge needle) and in young, female patients.117
Treatment of postdural puncture headache includes
the conservative measures of fluid, bed rest, and caf-
feine or, if it is persistent, an epidural blood patch.
Urinary retention is a complication of spinal and
epidural blocks. Return to full detrusor tone may
 image...

0 • ANESTHESIA FOR PLASTIC SURGERY 195

FIGURE 1 0 - 1 1 . Techniques used to perform

an axillary block. A, Intravenous techniques. The B
median (M) and musculocutaneous nerves lie on
the superior side of the artery (A), although the
latter may have already departed the axillary
sheath at the level of injection. The ulnar (U)
lies inferior, and the radial (R) is inferior and
posterior. The vein (V) lies in a variable position
superior to the artery. The locations of these Pectoral m.
structures vary with individual patients, and greater
the two positions demonstrated are the most
Coracobrachial
common patterns. B, The most common tech-
nique of blockade involves paresthesias of at Biceps usculocutaneous n.
least two of the nerves, usually starting with the
branch innervating the proposed surgical site.
A total of 20 to 40 mL of solution is required to Axillary a.
reach all of the branches, and a separate injec- - Median n.
tion may be needed for the musculocutaneous Ulnar n.
nerve if anesthesia of this branch is required for Radial n.
surgery. (Adapted from Mulroy MF. In White
PF, ed: Ambulatory Anesthesia and Surgery.
Philadelphia, WB Saunders, 1997:419.)

require 1 to 2 hours longer than the duration of the
local anesthetic agent. Overdistention of the bladder
may contribute to urinary retention, but the correla-
tion to intraoperative fluid administration is not
clear.118 Backache is a rare complaint after epidural or
spinal anesthetic and may be related more to surgical
position and ligament strain.
A unique complication of spinal anesthesia is tran-
sient neurologic symptoms. Patients develop buttock
and lower extremity pain or dysesthesias. Symptoms
usually resolve spontaneously by the third postoper-
ative day. Transient neurologic symptoms were first
described in patients receiving 5% lidocaine, and the
high concentration of local anesthetic was implicated
in a local toxic effect. However, subsequent studies have
failed to show a reduction in incidence with decreas-
ing concentrations of lidocaine.119 Other possible causes
include positioning of the patient, early mobilization,
needle trauma, neural ischemia, pooling of local anes-
thetics, and muscle spasms. Lidocaine and tetracaine
seem to have a greater potential than bupivacaine for
neurotoxicity at clinically relevant concentrations.
Regional anesthetic techniques can also be used as
adjuvants to general anesthesia to provide more effec-
tive postoperative pain management. In addition to
continuous peripheral nerve blocks, epidural catheters
can be placed before initiation of general anesthesia
and dosed intraoperatively and postoperatively with
preservative-free morphine (Duramorph) or bupiva-
caine 0.25%. Postoperative pain management with use
of epidural catheters compared with intravenous pain
management (e.g., patient-controlled analgesia) has
been shown to decrease postoperative pain with mobi-
lization, pulmonary complications, length of hospital

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196 l • GENERAL PRINCIPLES
Left anterior elbow
FIGURE 1 0 - 1 2 . Peripheral blocks at the elbow are per-
formed with the arm placed in the palm-up position. The
median nerve can be blocked by injecting 3 to 5 mL of
local anesthetic at the intersection of the intercondylar
line (connecting the medial and lateral epicondyles) and
the brachial artery (medial to the biceps tendon). The radial
nerve can be blocked at the elbow as it passes over the
anterior aspect of the lateral epicondyle by injecting 3 to
5 mL of local anesthetic 2 cm lateral to the biceps tendon
at the intercondylar line and advancing until bone is
encountered. (From Mulroy MF: Local and regional anes-
thesia. In White PF, ed: Ambulatory Anesthesia and Sur-
gery. Philadelphia, WB Saunders, 1997:420.)
stay, and postoperative thrombotic events, and recov-
ery of bowel function is possibly earlier. However, side
effects of postoperative epidural analgesia include
orthostatic hypotension and pruritus.
CONSCIOUS SEDATION AND
MONITORED ANESTHESIA CARE
The American Dental Association introduced the
term conscious sedation to describe a technique of ren-
dering a patient to a minimally depressed level of con-
sciousness during dental procedures. 12° The consciously
sedated patient maintains an airway independently and
responds appropriately to physical stimulation and
verbal commands. The goals of conscious sedation are
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Dr.Mustafa D.
to alleviate the discomfort of local anesthetic injec-
tion, to alter a patient's sense of awareness, and to reduce
overall physical stress. Conscious sedation lies on a con-
tinuum from minimal sedation (i.e., an awake, relaxed
state) to profound, deep sedation (i.e., an unconscious
or hypnotic state) or general anesthesia (i.e., lack of
movement in response to painful stimuli). Because
patients can move rapidly from a minimally depressed
state of consciousness to general anesthesia, and indi-
vidual patient responses vary to the same dose of a
sedative or analgesic drug, careful monitoring of the
patient is essential to all conscious sedation techniques.
In contrast to the usual "light" level of sedation
administered by nonanesthesiologists, when an anes-
thesia practitioner monitors a patient receiving local
anesthesia or administers sedative-analgesic medica-
tions, the technique is known as monitored anesthe-
sia care (MAC).121 The combination of local and
intravenous anesthetic agents for sedation and anal-
gesia is particularly well suited for outpatients. Many
procedures can be performed on an outpatient basis
with use of local anesthetic techniques combined with
new, shorter acting agents to provide anxiolysis, seda-
tion, and supplemental analgesia.
The marked variation in responses of individual
patients to a given dose of an anesthetic drug has led
the ASA to avoid the term conscious sedation.122 The
term sedation-analgesia is preferred, and the ASA
recommends that all patients receiving sedation-
analgesia be monitored by a designated individual who
is primarily responsible for administration of sedative
and analgesic drugs and monitoring of the patient's
vital signs. The ASA policy states that MAC requires
the same standard of care as a general or regional anes-
thetic technique. Therefore, MAC should provide a pre-
operative evaluation, an anesthetic care plan, and the
continuous presence of a member of the anesthesia
care team with the immediate availability of an anes-
thesiologist. The standards of monitoring include the
usual cardiovascular and respiratory monitoring
required for general anesthesia. The anesthesia provider
should be ready to administer any necessary adjuvant
so that the desired level of sedation, amnesia, anxiol-
ysis, and analgesia can be achieved without compro-
mising cardiovascular or respiratory function.
A wide variety of centrally acting intravenous and
inhaled drugs have been used during MAC, including
barbiturates, benzodiazepines, ketamine, propofol,
opioid and nonopioid analgesics, a 2 agonists, and
nitrous oxide. The most popular sedation-analgesia
techniques use benzodiazepines in combination with
opioids or sedative-hypnotics. Midazolam, a short-
acting benzodiazepine, is often used for short, outpa-
tient procedures. Short-acting opioids are often used
in combination with benzodiazepines to provide pain
control during injection of local anesthetic as well as
in stimulating parts of the procedure. Opioids help
 image...

10 • ANESTHESIA FOR PLASTIC SURGERY 197

Flexor palmaris
longus
Radial artery Median nerve
Ulnar artery
Radial nerve
Ulnar nerve
Radius Ulna

Extensor pollicis longus tendon

Radial n.

Extensor pollicis brevis tendon

FIGURE 10-1 3. Blockade of the terminal nerves at the wrist. A, The median nerve lies just
to the radial side of the flexor palmaris longus. The ulnar and radial nerves lie just "outside"
their respective arteries. B, The radial nerve has already begun branching at this level and must
be blocked by a wide subcutaneous ridge of anesthetic. C, Digital nerve block. A 25-gauge
needle is inserted into the dorsal aspect of the web space at a 45-degree angle at the level of
the change in skin texture and advanced until the bone is gently contacted. The needle is with-
drawn 3 to 4 mm, and 2 mL of solution without epinephrine is injected in a volar direction and
a third milliliter along the dorsal aspect of the phalanx. (B from Wedel DJ: Nerve blocks.
In Miller RD, ed: Anesthesia, 5th ed. New York, Churchill Livingstone, 2000:1520. A and C
from Mulroy MR In White PF, ed: Ambulatory Anesthesia and Surgery. Philadelphia, WB Saun-
ders, 1997:421.)

provide hemodynamic control. However, opioids in
combination with benzodiazepines often produce
respiratory depression, and supplemental oxygen and
pulse oximetry should be used.123 Alternatively, keta-
mine can be used with benzodiazepines, and much of
the respiratory depression is avoided. As discussed
earlier, ketamine should be used with benzodiazepines
to decrease the incidence of emergence reactions, and
an antiemetic may be needed. Propofol is a sedative-
hypnotic that is also available for sedation techniques,
but it must be carefully titrated and monitored because
it can easily lead to deep sedation or apnea.
The effective use of a MAC technique requires coop-
eration of the patient, effective local anesthesia, and

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198 I • GENERAL PRINCIPLES
gentle surgical technique. Although local anesthetic-
based techniques are generally assumed to be safer than
general or regional anesthesia, supplementation with
potent sedative-hypnotic and analgesic drugs may
result in significant depression of the central respira-
tory drive or transient upper airway obstruction. The
decision to use MAC in place of general or regional
anesthesia should be made only after careful assess-
ment of the patient's and surgeon's preferences as well
as any coexisting medical conditions. Consideration
should be given to the length of the surgical proce-
dure, and although there are no absolute criteria, we
generally avoid a MAC anesthetic at our institution if
the procedure is longer than 2 hours. Vigilant moni-
toring, supplemental oxygen, and availability of resus-
citation equipment are essential elements for the safe
practice of MAC
OFFICE-BASED ANESTHESIA
Office-based anesthesia is provided for surgery per-
formed outside a hospital or ambulatory care center.
Office-based surgery is one of the fastest growing areas
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Dr.Mustafa D.
FIGURE 1 0 - 1 4 . Nerve blocks for lower extremity
procedures. A, Anatomic landmarks for the lateral
femoral cutaneous, femoral, and obturator nerve
blocks. B, Obturator nerve block. The needle is walked
off the inferior pubic ramus in a medial and cephalad
direction until it passes into the obturator canal. (From
Wedel DJ: Nerve blocks. In Miller RD, ed: Anesthe-
sia. 5th ed. New York, Churchill Livingstone, 2000:
1520.)
of ambulatory surgical care because of its cost-saving
potential. In the early 1990s, only 3% to 5% of all sur-
gical procedures were performed in the office-based
setting. However, the number of office-based proce-
dures currently exceeds 15% of all elective ambulatory
surgeryprocedures.,24Thelocationistypicallyaphysi-
cian's office where there is an established surgical suite.
Office-based anesthesia offers confidentiality and con-
venience for patients. Office-based surgery can reduce
overhead and improve the physician's efficiency by
eliminating driving between surgical and office
locations.
All anesthetic techniques and agents are used to
deliver office-based anesthesia, including conscious
sedation, deep sedation, general anesthesia, and
regional anesthesia. Office-based anesthesia must
produce a rapid and smooth clinical onset, provide
acceptable surgical conditions, and facilitate a rapid
recovery with minimal side effects. When used in com-
bination with local anesthesia, propofol has become
the anesthetic of choice in many office-based centers
because of its excellent recovery profile.68 The use of
propofol in combination with nitrous oxide for office-
TeWttf'SelcrMf image...
Peripheral Nerve Blocks
FIGURE 1 0 - 1 5 . Position of the needle insertion sites
for performance of an ankle block. (From Mulroy MR In
White PF, ed: Ambulatory Anesthesia and Surgery.
Philadelphia, WB Saunders, 1997:426.)
based anesthesia allows patients to be fast-tracked and
discharged home quickly, without increasing the inci-
dence of postoperative nausea and vomiting.68
Because office-based anesthesia occurs in an iso-
lated setting without the support of the hospital envi-
ronment, care must be taken to ensure the patient's
safety. Medications should be regularly stocked and
equipment well maintained. A crash cart, defibrilla-
tor, oxygen source, and suction device need to be imme-
diately available at all times. Required equipment for
office-based anesthesia includes a blood pressure
monitor with several sizes of cuffs, electrocardiogram
monitor, pulse oximeter, temperature monitor, and
stethoscope. Airway supplies should include a large
variety of tracheal tube sizes, laryngeal mask airways,
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10 • ANESTHESIA FOR PLASTIC SURGERY 199
nasal and oral airways, emergency airway equipment,
and an Ambu bag. Office staff should be certified in
basic and advanced cardiac life support. Nursing per-
sonnel must be available for the patient's postopera-
tive recovery.
Office-based surgery began without regulations or
a set of standards, in contrast to operating room reg-
ulations in a hospital setting. Reports of mortality
during office-based surgery have focused on healthy
patients who were inadequately monitored and resus-
citated.125 Individual states (e.g., California,Texas, New
Jersey, Florida) are now mandating legislation for office-
based surgery and anesthesia. The importance of having
appropriate monitoring, resuscitative equipment and
medications, and personnel adept at assessing clinical
sedation and comfortable with resuscitative measures
cannot be overemphasized.
RECOVERY FACILITIES
Postanesthesia Care Unit
Postanesthesia care units (PACUs) provide postsurgi-
cal patients with continuous evaluation and special-
ized nursing care in the transition from surgery to their
ultimate destination, the hospital ward or home.
Phase I PACU recovery begins immediately after
surgery and requires a patient-to-nurse ratio of 1:1 or,
at most, 2:1. Appropriate equipment for phase I PACU
includes a noninvasive automatic blood pressure cuff,
electrocardiogram monitor, pulse oximeter, and core
body temperature probe. In addition, an emergency
airway cart, crash cart, and defibrillator should be
immediately available.
The ASA established standards for postanesthesia
care monitoring in 1999. The first states that "all patients
who have received general anesthesia, regional
anesthesia or monitored anesthesia care shall receive
appropriate postanesthesia management."The second
states that "a patient transported to the PACU shall be
accompanied by a member of the anesthesia care team
who is knowledgeable about the patient's condition.
The patient shall be continually evaluated and treated
during transport with monitoring and support appro-
priate to the patient's condition." The third states that
"upon arrival in the PACU, the patient shall be re-
evaluated and a verbal report provided to the respon-
sible PACU nurse by the member of the anesthesia care
team who accompanies the patient." Fourth, "the
patient's condition shall be evaluated continually in
the PACU." Finally, "the physician is responsible for
the discharge of the patient from the postanesthesia
care unit." Criteria used to determine the appropri-
ateness of discharge from the phase I PACU include
being awake and alert, maintaining an airway inde-
pendendy with a good oxygen saturation, and having
no signs of respiratory distress. The patient should have
200 I • GENERAL PRINCIPLES
TABLE 10-13 • PROPOSED PACU PHASE I
DISCHARGE CRITERIA
Awake and alert
Maintains airway unassisted
Oxygen saturation >9A% on room air
No surgical complications
Normal respiration rate
Stable blood pressure and heart rate
Lack of dizziness
Adequate pain control
No excessive nausea and vomiting
stable hemodynamics, adequate pain control, and no
excessive nausea and vomiting (Table 10-13).
Step-Down (Phase II) Unit
Phase II PACU recovery serves as a step-down unit from
phase I recovery for patients being discharged home.
Phase II recovery has less intensive medical attention,
and the patient-to-nurse ratio can be 4:1. In the phase
II recovery, an arterial blood pressure monitor, pulse
oximeter, crash cart, and defibrillator are needed.
However, the patient does not need to be continually
evaluated. At the endpoint of phase II recovery, the
patient is able to walk unassisted, and any drowsiness,
dizziness, orthostatic hypotension, nausea, vomiting,
or unrelieved pain is resolved. Tolerating oral fluid
intake and voiding are no longer considered manda-
tory before discharge after ambulatory surgery. The
endpoint of this phase of recovery is called home readi-
ness. Discharging the patient from the ambulatory
surgery facility by declaring that the patient is "home
ready" is an important step based on the fulfillment
of discharge criteria approved by the medical staff of
the facility. The phase II discharge scoring system is
commonly used for determining readiness for home
discharge (Table 10-14).'26
Fast-Tracking Concept
Fast-tracking in the ambulatory setting occurs when
a patient goes directly from the operating room to the
less extensively monitored phase II step-down unit
rather than to the PACU. Criteria for assessing the
patient in the operating room help determine fast-track
eligibility of outpatients undergoing ambulatory
surgery.124 The new fast-track scoring system addi-
tionally assesses pain and emesis (Table 10-15). Fast-
tracking outpatients after general anesthesia assumes
greater importance because of the cost-saving poten-
tial associated with facilitating the recovery process and
reducing overtime nursing costs. Given the inherent
risks of complications associated with bypassing the
phase I PACU, effective and reliable fast-track criteria
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TABLE 1 0 - 1 4 • PHASE II DISCHARGE
SCORING SYSTEM
Vital Signs
2 = Within 20% of preoperative value
1 = 20%-40% of preoperative value
0 =>40% of preoperative value
Activity and Mental Status
2 = Oriented x 3 and has a steady gait
1 = Oriented x 3 or has a steady gait
0 = Neither
Pain, Nausea* or Vomiting
2 = Minimal
1 = Moderate, having required treatment
0 = Severe, requiring treatment
Surgical Bleeding
2 = Minimal
1 = Moderate
0 - Severe
Intake and Output
2 = Has had PO fluids and voided
1 = Has had PO fluids or voided
0 = Neither
Total score is 10; score 9 or above is fit for discharge.
From Chung F: Postanesthetic discharge scoring system. J Clin Anesth
1995;7:500-506.
are essential. Anesthesiologists need to rapidly assess
a patient's postoperative alertness, physiologic stabil-
ity, and comfort level immediately before the patient
is transferred from the operating room. In a fast-
tracking program, it is important to minimize post-
operative side effects and to avoid increasing the
workload for nurses in the phase II recovery area.124
Postoperative Complications
Effective management of postsurgical and anesthetic
complications is an important function of the recov-
ery areas. These units must address issues of pain,
nausea and vomiting, dizziness, cardiorespiratory
stability, and any surgical complications. Respiratory
complications, including aspiration, stridor, hypo-
ventilation, and hypoxia, can occur in the PACU.
Hypotension and hypertension are the most frequent
cardiovascular complications occurring in the PACU.
Hypotension may be secondary to volume depletion,
bleeding, or vagal stimulation. Hypertension in the
PACU may be due to poorly controlled preoperative
hypertension, pain, anxiety, or a full bladder. Because
 image...

0 • ANESTHESIA FOR PLASTIC SURGERY 20

TABLE 10-15 • CRITERIA FOR FAST-TRACKING (BYPASSING PACU) REQUIRE THAT THE PATIENT
ACHIEVE A FAST-TRACK SCORE ABOVE 1 2 BEFORE LEAVING THE OPERATING
ROOM

Level of Consciousness Scores

Awake and oriented 2
Arousable with minimal stimulation 1
Responsive only to tactile stimulation 0
Physical Activity

Able to move all extremities on command 2

Some weakness in movement of extremities 1
Unable to voluntarily move extremities 0
Hemodynamic Stability

Blood pressure <15% of baseline MAP value 2

Blood pressure between 15% and 30% of baseline MAP value 1
Blood pressure >30% below baseline MAP value 0
Respiratory Stability

Able to breathe deeply 2

Tachypnea with good cough 1
Dyspneic with weak cough 0
Oxygen Saturation Status

Maintains value >90% on room air 2

Requires supplemental oxygen (nasal prongs) 1
Saturation less than 90% with supplemental oxygen 0
Postoperative Pain Assessment

None or mild discomfort 2

Moderate to severe pain controlled with IV analgesics 1
Persistent severe pain 0
Postoperative Emetic Syndrome

None or mild nausea with no active vomiting 2

Transient vomiting or retching 1
Persistent moderate-severe nausea and vomiting 0

From While PF, Song D: New criteria for fast-tracking after outpatient anesthesia: a comparison with the modified Aldretc's scoring system. Ancsth Analg
1999;88:1069-1072.

postoperative hypertension is most common in patients
with preexisting hypertension, effective blood pressure
control before the surgical procedure is beneficial. Effec-
tive pain management techniques may also be of help
in preventing postoperative hypertension. For proce-
dures with large fluid shifts, placement of a Foley
catheter to avoid a distended bladder can also help
prevent hypertension. If hypertension persists despite
these interventions, it may be necessary to administer
an intravenous hypotensive drug (e.g., labetalol,
hydralazine). Arrhythmias in the PACU may be due
to electrolyte disturbances, hypoxia, hypercapnia,
metabolic acidosis or alkalosis, or preexisting heart
disease.
Adequate pain control is an important issue for all
surgical patients. Both opioid and nonopioid analgesics
are available for the treatment of pain in the recovery
units. Outpatients will require adequate pain control
with an oral formation. Inpatients have a greater variety
of pain management options. Nevertheless, pain
should be under adequate control before transfer of
the patient to the postsurgical ward.
Nausea is a frequent postoperative complication in
the PACU. Postoperative nausea and vomiting can
prolong the ambulatory facility stay and even cause an
unanticipated hospital admission. Postoperative nausea
and vomiting are distressing to the patient and if severe
can cause dehydration and esophageal tears. If an

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
202 I • GENERAL PRINCIPLES
antiemetic was given intraoperatively, a different class
of antiemetic can often be administered postopera-
tively. If the patient is returning home, minimal to mod-
erate nausea may be tolerated. For inpatients who can
continue to receive treatment for emesis, patients can
be discharged to the ward with some nausea. In patients
at high risk for postoperative nausea and vomiting, or
in cases in which it is important to avoid emesis (e.g.,
face lift), postoperative nausea and vomiting prophy-
laxis is recommended with a combination of antiemetic
drugs or devices (e.g., ReliefBand). Low-dose droperi-
dol (0.625 to 1.25 mg) and dexamethasone (4 to 8 mg)
can be given at the beginning of the procedure, ade-
quate intravenous hydration should be provided, and
an antiserotonin agent (e.g., ondansetron, 4mg, or
dolasetron, 12.5 mg) can be given within 30 minutes
of the end of the procedure. The transcutaneous elec-
trical stimulating device known as a ReliefBand can
be an effective alternative to the 5-hydroxytryptamine3
(5-HT3) antagonist in the treatment or prevention of
postoperative nausea and vomiting. If postoperative
nausea and vomiting occur in the PACU after pro-
phylaxis with a combination of antiemetic drugs or
devices, it is often treated with promethazine (6.25 to
25 mg).
Postoperative dizziness and drowsiness are com-
plaints that can be related to residual anesthetic agents,
orthostatic hypotension, vagal stimulation, or motion
sickness. New agents, like propofol and desflurane,
are popular because of their rapid return to a
"clear-headed" state. In addition, short-acting ben-
zodiazepines, like midazolam, limit the feeling of
postoperative drowsiness.
Headache is another common postoperative com-
plaint. Fasting-induced hypoglycemia and caffeine
withdrawal may increase the incidence of postopera-
tive headaches. Patients who regularly consume coffee
are at increased risk for a postoperative headache. Not
surprisingly, patients who ingest caffeine on the
morning of surgery have a lower incidence of post-
operative headache.127
UNIQUE CONSIDERATIONS FOR
PLASTIC SURGERY PROCEDURES
Laser Abrasion
Facial resurfacing uses a carbon dioxide laser and
requires intense analgesia with minimal distortion of
the skin by the anesthesiologist. The wavelength of the
carbon dioxide laser is in the far-infrared region and
is absorbed by the first surface it encounters. Reflected
beams can be aimed at unintended sites, causing eye
damage or igniting flammable material. Therefore, all
persons in the operating room are at risk for corneal
damage when the carbon dioxide laser is in use. To avoid
eye injury, all personnel must wear eye protection. The
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Dr.Mustafa D.
patient's eyes, when not part of the surgical field, should
be closed and covered with saline-soaked gauze.
Airway fires are the most common serious side effects
of carbon dioxide lasers, with a reported incidence of
0.5% to 1.5%. Airway fires are obviously more of a
concern with laser operations involving the upper
airway, and a laser-safe tracheal tube should be used
in these cases. In addition, the lowest inspired oxygen
concentration needed to provide adequate oxygen sat-
uration for the patient should be used. Nitrous oxide,
which supports combustion, should be avoided.
Total intravenous anesthesia has been used effec-
tively in spontaneously breathing patients for face laser
resurfacing.128 Ketamine is a popular agent because it
provides intense analgesia with minimal respiratory
depression, often avoiding the need for supplemental
oxygen. However, ketamine is associated with cardio-
vascular stimulation and psychomimetic emergence
reactions. Combining ketamine,benzodiazepines, and
only small amounts of fentanyl with propofol reduces
the severity of intraoperative ventilatory depression
while minimizing the incidence of emergence reactions
and postoperative nausea and vomiting. In addition,
this technique can provide an adequate depth of anes-
thesia without the need for supplemental oxygen.
Liposuction
Liposuction is the most common cosmetic procedure
performed in the United States.129 Tumescent lipo-
suction is a relatively new technique and involves inject-
ing a solution before the aspiration of fat through
microcannulas. This technique has replaced standard
liposuction because several liters of fat are aspirated
with minimal blood loss. The infusate is typically a
liter of normal saline with 500 to 1000 mg of lidocaine,
0.25 to 1.0 mg of epinephrine, and 12.5 mmol of sodium
bicarbonate.130 Large-volume liposuction, defined as
removal of more than 5000 mL of aspirate, may require
several liters of infusate solution. The lidocaine and
epinephrine in the infusate prolong local anesthesia
and minimize blood loss. Anesthesia for tumescent
liposuction can be provided with conscious sedation,
epidural anesthesia, or general anesthesia.
Tumescent liposuction was originally thought to
be safer than traditional liposuction because of the
reduction in blood loss associated with the technique.
However, four perioperative deaths from tumescent
liposuction were reported and evaluated by the Chief
Medical Examiner of New York City.129 Two deaths
occurred from precipitous intraoperative hypotension
and bradycardia. One death was attributed to fluid over-
load, and one was attributed to thromboembolism.
Although the report suggests that lidocaine toxicity
may have played a role in some of the liposuction
deaths,129 this has been questioned because lidocaine
toxicity typically manifests as depression of cardiac
T^ftf^eldWimage..
contractility and cardiac conduction abnormalities.
Tumescent liposuction involves administration of
high doses of lidocaine (35 to 55 mg/kg/ 3 0 ; the Food
and Drug Administration recommended a maximum
adult dose of only 7 mg/kg even when mixed with epi-
nephrine. Nevertheless, for tumescent infiltration
anesthesia, dosages of 55 mg/kg of diluted lidocaine
have been considered safe for patients.131"133 Studies
demonstrate that lidocaine, given as tumescent fluid,
peaks 12 to 14 hours after injection and then decreases
during the subsequent 6- to 14-hour period. The serum
lidocaine levels determined during this period never
rise above 3 ^ig/mL, the level commonly associated with
subjective lidocaine toxicity.130
Fluid overload is another potential contributor to
adverse outcomes after liposuction procedures. A sub-
stantial amount of fluid is injected beneath the skin,
and although significant amounts are removed during
liposuction, some fluid remains to be absorbed sys-
temically. Therefore, the formulas available to estimate
intraoperative fluid replacement do not hold. Fluid
status needs to be carefully monitored, and a Foley
catheter is a valuable tool to help estimate fluid balance.
Epinephrine may also play a role in liposuction
mortality. Epinephrine (1 mg) is often added to every
1 liter of infusate, and up to 3 to 5 mg of epinephrine
may be administered during the course of the lipo-
suction procedure. However, it is diluted and appears,
to date, to be well tolerated.134 Liposuction research
continues to investigate drug absorption and inter-
actions, fluid management, prothrombogenic factors,
and liposuctioned volumes to determine the con-
tributors to the reported morbidity and mortality
rates.
Burns and
Debridement Procedures
Care of the acute burn patient and care of the chronic
burn patient differ in several important aspects.
Acutely, a burn patient presents with high levels of cir-
culating catecholamines, acute hypovolemia, capillary
leak with release of vasoactive substances, and myocar-
dial depression. After the first 24 hours, the circula-
tory system enters a hyperdynamic state often
accompanied by hypertension. Pulmonary injuries may
present as hoarseness and tachypnea. Respiratory
problems (oxygen desaturation and carbon monox-
ide poisoning) can be due to inhalation of flames,
smoke, steam, or toxic gases. Injury to the respiratory
tract should be suspected when there are facial burns,
singed facial hairs, respiratory distress, or wheezing.
Steam or chemical inhalation injury can cause alveo-
lar damage. Pulmonary edema often occurs. Injury
to the airway often requires immediate intubation
and subsequent tracheostomy if a prolonged course is
suspected.
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Dr.Mustafa D.
10 • ANESTHESIA FOR PLASTIC SURCERY 203
Neuromuscular junctions proliferate 24 hours after
a burn and remain increased until the burn is com-
pletely healed. If succinylcholine is given to the patient
during this time, an exaggerated release of potassium
occurs with high serum levels of potassium, poten-
tially causing fatal arrhythmias. Because of the prolif-
eration of neuromuscular junctions, the burn patient
is resistant to nondepolarizing muscle relaxants,
requiring two to five times the normal dose.
Blood and fluid replacement is difficult to estimate
in the acute burn patient. Inadequate hydration can
contribute to underperfusion of organs, and overag-
gressive fluid replacement can lead to heart failure.
Several formulas exist to provide guidance in fluid man-
agement of the acutely burned patient. In both the acute
and chronic burn patient, intravenous access may be
difficult to obtain because of burn and tissue scarring.
Perioral scarring can limit mouth opening, making
intubation difficult.
Face Lift Procedures
Face lift procedures are a common plastic surgery
procedure and can be performed with either local
sedation (MAC) or a general anesthetic. Because the
operative time for a face lift procedure can be several
hours, a general anesthetic is often preferred to ensure
the patient's comfort. To reduce the incidence of post-
operative bleeding, anesthetic techniques should min-
imize coughing and postoperative emesis. Propofol and
antiemetic prophylaxis with a 5-HT 3 antagonist can
reduce the incidence of postoperative nausea and vom-
iting. During face lift procedures, there is much move-
ment of the head, and the tracheal tube cannot be
secured with tape. Therefore, the tracheal tube is often
secured by suturing it to a tooth or the tongue.
Nasal Procedures
Both general anesthesia and local anesthesia with
sedation (MAC) are used for nasoplasty procedures.
General anesthesia is often supplemented with local
anesthesia for perioperative analgesia and epinephrine
for vasoconstriction. Cocaine is sometimes used for
its intense analgesia and vasoconstricting effects.
Cocaine blocks the reuptake of norepinephrine and
therefore has a marked sympathomimetic effect. As
mentioned earlier, the maximum recommended dose
of cocaine is 1.0 mg/kg, and common side effects
include tachycardia, hypertension, tremulousness,
seizures, and hyperthermia. The hemodynamic side
effects can be treated with (J-blockade. Premedication
with oral clonidine can be useful adjunctively to min-
imize the acute hemodynamic changes associated with
cocaine.135 Nasal and throat packing minimize the
amount of swallowed blood, reducing the risk of post-
operative nausea and vomiting.
204 I • GENERAL PRINCIPLES
Facial Fractures
Repair of facial fractures is most often performed under
general endotracheal anesthesia. Consideration must
be given to placement of the tracheal tube in rela-
tionship to the surgical field. Although these patients
may have a history of a previous head trauma, there
are no special anesthetic considerations or monitor-
ing requirements. The anesthetic technique should
be chosen on the basis of the patient's history and
risk for development of postoperative nausea and
vomiting.
Breast Surgery
Breast augmentation and mastopexy are outpatient
procedures, and breast reductions and reconstructions
are in some instances performed in an outpatient
setting. Therefore, efforts should be made to minimize
postoperative nausea and vomiting. Positioning of the
patient for breast reduction mammaplasties and aug-
mentations requires special considerations with respect
to the arms and hips because of the requirement for
use of the intermittent sitting position as described
previously.
SUMMARY
Many recently introduced drugs have pharmacologic
profiles that are ideally suited for facilitating a smooth
and rapid recovery after plastic surgery. Newer anes-
thetic drugs (e.g., desflurane, sevoflurane, remifentanil,
rapacuronium, COX-2 antagonists, ropivacaine,
levobupivacaine) and monitoring devices (e.g., BIS
monitor) can facilitate the recovery process. Given the
changing pattern of health care reimbursement, it is
incumbent on all practitioners to carefully examine
the impact of new drugs and devices on the quality of
anesthesia care being provided to the plastic surgery
patient. Future studies of new drugs and techniques
for anesthesia need to focus not only on subjective
improvements for the patient during the immediate
perioperative period but also on the overall cost-
effectiveness of the care being provided.' These studies
must compare the increased cost of newer treatments
with the potential financial savings resulting from
earlier hospital discharge, reduced consumption of sup-
plemental drugs, improvements in satisfaction of the
patient, and earlier return to work. The future chal-
lenge that all practitioners caring for plastic surgery
patients must face is to provide high-quality anesthe-
sia care in a wider variety of venues while ensuring the
patient's safety.'36
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79- McCourt KC, Mirakhur RK, Lowry DW, et al: Spontaneous or
neostigmine-induccd recovery after maintenance of neuro-
muscular block with Org 9487 (rapacuronium) following an
initial dose of Org 9487. Br J Anaesth I999;82:755.
80- Schiere S, Proost JH, Schuringa M, et al: Pharmacokinetics
and pharmacokinetic-dynamic relationship between rapacuro-
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Anesth Analg 1999;88:640.
81. Sparr HJ, Mellinghoff H, Blobner M, et al: Comparison of
intubating conditions after rapacuronium (Org 9487) and
succinylcholine following rapid sequence induction in adult
patients. Br J Anaesth 1999;82:537.
82. Hughes R, Chappie DJ: The pharmacology of atracurium: a
new competitive neuromuscular blocking agent. Br J Anaesth
1981;53:31.
83. Steulake JB, Waigh RD, Urwin J: Atracurium conception and
inception. Br J Anaesth 1983;55(suppl 1):35.
84. Lcbrault C, Bcrgcr JL, D'HoIlander AA, et al: Pharmacokinet-
ics and pharmacodynamics of vecuronium (ORGNC45) in
patients with cirrhosis. Anesthesiology I985;62:601.
85. Morris RB, Calahan MK, Miller RD, et al: The cardiovascular
effects of vecuronium and pancuronium in patients under-
going coronary artery bypass grafting. Anesthesiology
1983;58:438.
86. Cooper RA, Mirakhur RK, Clarke RSJ, et al: Comparison of
intubating conditions after administration of ORG 9426
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87. Foldes FF, Nagashima H, Nguyen HD( et al: The neuromus-
cular effects of ORG 9426 in patients receiving balanced
anesthesia. Anesthesiology 1991;75:191.
88. Belmont MR, Lien C, Quessy S, et al: The clinical neuro-
muscular pharmacology of 51W89 in patients receiving
nitrous oxide/opioid/barbiturate anesthesia. Anesthesiology
1995;82:1139.
89. Benthuysen JL, Smith NT, Stanford TJ, et al: Physiology of alfen-
tanil-induced rigidity. Anesthesiology 1992;64:440.
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mediated effects of morphine on skeletal muscle vascular resist-
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91. Dershwitz M, Roscow CE, Michalowski P, et al: Pharmacoki-
netics and pharmacodynamics of remifentanil in volunteer
subjects with severe liver disease compared with normal
subjects. Anesthesiology 1994;81:A377.
92. Shlugman D, Dufore S, Dershwitz M, et al: Respiratory effects
of remifentanil in subjects with severe renal impairment com-
pared to matched controls. Anesthesiology 1994;81:A1417.
93. Korpela R, Korvenoja P, Meretoja, OA: Morphine-sparing effect
of acetaminophen in pediatric day-case surgery. Anesthesiol-
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94. Souter AJ, Fredman B, White PF: Controversies in the peri-
operative use of nonsteroidal antiinflammatory drugs. Anesth
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95. Murray AW, Brockway MS, Kenny GNC: Comparison of the
cardiorespiratory effects of keroiolac and alfentanil during
propofol anaesthesia. Br J Anaesth 1989:63:601.
96. Liu J, Ding Y, White PF, et al: Effects of ketorolac on postop-
erative analgesia and ventilatory function after laparoscopic
cholecystectomy Anesth Analg Il.'93;76:l061.
97. Rusy LM, Houck CS, Sullivan LJ, et al: A double-blind evalu-
ation of ketorolac tromethamine versus acetaminophen in
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1995;80:226.
98. White PF, Girish JP, Carpenter RL, et al: A comparison of oral
kctorolacand hydrocodone-acetaminophen for analgesia after
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99. Fort J: Celecoxib.a COX-2 specific inhibitor: the clinical data.
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100. Simon LS, Lanza FL, Lipsky PE, et al: Preliminary study of the
safety and efficacy of SC-58635, a novel cyclooxygenase 2
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101. Van Wijk MGF, Smalhout B: A postoperative analysis of the
patient's view of anaesthesia in a Netherlands' teaching hos-
pital. Anaesthesia 1990;45:679.
102. White PF, Watcha MF: Postoperative nausea and vomiting:
prophylaxis versus treatment [editorial]. Anesth Analg
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comes are important to avoid? The perspective of patients.
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104. Yogendran S, Asokumar B, Cheng DC, et al: A prospective ran-
domized double-blinded study of the effect of intravenous fluid
therapy on adverse outcomes on outpatient surgery. Anesth
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105. Traylor RJ, Pearl RG: Crystalloid versus colloid versus colloid:
all colloids are not created equal. Anesth Analg 1996;83:209.
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1983:62:211.
107. Sessler D: Mild perioperative hypothermia. N Engl J Med
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108. Kurz A, Sessler DI, Lenhardt R: Perioperative normothermia
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hospitalization. N Engl J Med 1996:334:1209.
109. Smith I, Ncwson C, White PF: Use of forced-air warming during
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fol, alfentanil, and nitrous oxide anesthesia. Anesthesiology
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using bispectral index facilitates recovery after ambulatory anes-
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thetic care costs. Anesthesiology 1995;82:94.
115. McClure J: Ropivacaine. Br J Anaesth 1996;76:300.
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dose intravenous levobupivacaine in sheep. Anesth Analg
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117. Buettner J, Wresch KP, Klose R: Postdural puncture headache:
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*&Wttf ( aa<rw image...
118. Ryan JA, Adye BA, Jolly PC, et al: Outpatient inguinal hernior-
rhaphy with both regional and local anesthesia. Am J Surg
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119. Hampl KF, Schneider MC, Pargger H, et al: A similar in-
cidence of transient neurologic symptoms after spinal
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83:1051.
120. McCarthy FM, Soloman AL, Jastak JT: Conscious sedation:
benefits and risks. I Am Dent Assoc 1984; 109:546.
121. SaRegoMM,WatchaMF,WhitePF:Thcchangingroleofmon-
itored anesthesia care in the ambulatory setting. Anesth Analg
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122. American Society of Anesthesiologists: Practice guidelines for
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1996;84:459.
123. Tucker MR, Ochs M, White RP: Arterial blood gas levels
after midazolam or diazepam administered with or without
fentanyl as an intravenous sedative for outpatient surgical
procedures. J Oral Maxillofac Surg 1986;44:688.
124. White PF, Song D: New criteria for fast-tracking after outpa-
tient anesthesia: a comparison with the modified Aldrete's
scoring system. Anesth Analg 1999;88:1069.
125. Krippaehne JA, Montgomery MT: Morbidity and mortality
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126. Chung F: Postanesthetic discharge scoring system. J Clin Anesth
1995;7:500.
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10 • ANESTHESIA FOR PLASTIC SURGERY 207
127. Weber JG, Ereth MG, Danielson DR: Perioperative ingestion
of caffeine and postoperative headache. Mayo Clin Proc
1993;68:842.
128. Blakeley KR, Klein KW, White PF, et al: A total intravenous
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Engl J Med 1999;340:147I.
130. Klein J: Tumescent technique chronicles: local anesthesia, lipo-
suction, and beyond. Dermatol Surg 1995;21:449.
131. Grazer FM, dc Jong RH: Fatal outcomes from liposuction:
census survey of cosmetic surgeons. Plast Reconstr Surg
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132. Ostad A, Kageyama N, Moy RL: Tumescent anesthesia with a
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CHAPTER
11
•
Wound Healing: Repair
Biology and Wound and
Scar Treatment
H. PETER LORENZ, MD • MICHAEL T. LONCAKER, MD
ADULT WOUND REPAIR BIOLOGY
Inflammatory Phase
Proliferation Phase
Remodeling Phase
Regulation
FETAL WOUND REPAIR BIOLOGY
Overview
Transition to Scar Formation
Differences Between Fetal and Adult Repair
Tissue injury initiates a cascade of wound repair
processes that restore tissue integrity. In postnatal
mammals, scar and fibrosis are the result of repair except
in bone and specialized conditions of liver injury.
However, fetal skin can heal without scar and with
regeneration of dermal and epidermal appendage
architecture. Investigators are beginning to unravel the
mechanisms behind scarless repair, and application to
postnatal healing is likely in the near future. Experi-
mental wounds can be modulated to heal faster than
normal. Reversal of the healing impairment that
occurs in several pathologic states, such as diabetes and
steroid immunosuppression, has also been demon-
strated experimentally. Surgeons are now beginning
to have an active role in modulating the healing
processes with pharmacologic treatment of open
wounds.
ADULT WOUND REPAIR BIOLOGY
The repair cascade consists of inflammatory, prolif-
erative, and remodeling phases (Fig. 11 -1). These over-
lapping phases act in highly coordinated relationships
to heal skin defects. During the inflammatory phase,
hemostasis occurs and an acute inflammatory infil-
trate ensues. The proliferative phase is characterized
by fibroplasia, granulation, contraction, and epithe-
lialization. The final phase is remodeling, which is
commonly described as scar maturation.
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ADULT WOUND PATHOLOGY
Nonhealing Wounds
Excessive Healing
CLINICAL WOUND MANAGEMENT
Closed Wounds
Open Wounds
Excessive Scar Treatment
IMPACT OF SCAR ON PLASTIC SURGERY
Inflammatory Phase
Inflammation is the first stage of wound healing
and includes hemostasis. At the injury site, lacerated
vessels immediately constrict. Thromboplastic tissue
products, predominantly from the subendothelium,
are exposed. Platelets aggregate and form the initial
hemostatic plug. The coagulation and complement
cascades are initiated. The intrinsic and extrinsic coag-
ulation pathways lead to activation of prothrombin
to thrombin, which converts fibrinogen to fibrin,
which is subsequently polymerized into a stable clot.
As thrombus is formed, hemostasis in the wound
is achieved (Fig. 11-2).Theaggregated platelets degran-
ulate, releasing potent chemoattractants for inflam-
matory cells, activation factors for local fibroblasts and
endothelial cells, and vasoconstrictors. Adhesiveness
of platelets is mediated by integrin receptors such as
GpIIb-IIIa (au b p 3 ) on their surface.1
Immediately, the repair processes are initiated.
After hemostasis, local vessels dilate secondary to the
effects of the coagulation and complement cascades.
Bradykinin is a potent vasodilator and vascular
permeability factor that is generated by activation of
Hageman factor in the coagulation cascade.2 The
complement cascade generates the C3a and C5a
anaphylatoxins, which directly increase blood vessel
permeability and attract neutrophils and monocytes
to the wound. These complement components also
209
210 I • GENERAL PRINCIPLES

Clot formation Growth factor Collagen deposition Collagen cross-linking

Major event
[ Hemostasis elaboration

Inflammatory
Repair phase Proliferation / £_
Remodeling/ /

Fibroblasts ~~/ f
Lymphocytes
Cellular influx
Macrophages
[Neutrophils
Vascular response [ Vasodilation 7L
Vasoconstriction

Injury 3d 7d
• / / •
3 weeks
if- 1 -2 years
Time
FIGURE 1 1 - 1 . The temporal patterns of repair phase, cellular influx, and vascular response during wound repair.
The time points are approximate, and overlap occurs during these repair events. (Modified from Lorenz HP,
Longaker MT: Wounds: biology, pathology, and management. In Norton JA, et al, eds: Surgery: Scientific Basis
and Current Practice, vol I. New York, Springer-Verlag, 2000:222.)

stimulate the release of histamine and leLikotrienes
C4 and D4 from mast cells. The local endothelial cells
then break cell-cell contact and increase permeabil-
ity, which enhances the margination of inflammatory
cells into the wound site.2
The initial influx of white blood cells in the wound
is composed of neutrophils (Fig. 11 -3). This early neu-
trophil infiltrate scavenges cellular debris, foreign
bodies, and bacteria. Activated complement frag-
ments aid in bacterial killing through opsonization.
The neutrophil infiltrate is decreased in clean surgical
wounds compared with contaminated or infected
wounds.
Within 2 to 3 days, the inflammatory cell popula-
tion begins to shift to one of monocyte predominance
(Fig. 11-4). Circulating monocytes are attracted and
infiltrate the wound site.3 These monocytes differen-
tiate into macrophages and, in conjunction with the
resident tissue macrophages, orchestrate the repair
process. Macrophages not only continue to phagocy-
tose tissue and bacterial debris but also secrete mul-
tiple peptide growth factors. These growth factors
activate and attract local endothelial cells, fibroblasts,
and keratinocytes to begin their respective repair func-
tions. More than 20 different cytokines and growth
factors are known to be secreted by macrophages (Table

Epidermis

Blood vessel

Exposure of thromboplastic
tissue elements FIGURE 11-2. Hemostasis is
Dermis stimulated by platelet degran-
Fibroblast ulation and exposure of tissue
thromboplastic agents immedi-
ately after tissue injury. (Mod-
Resident monocyte
ified from Lorenz HP, Longaker
MT: Wounds: biology, pathol-
Platelet ogy, and management. In
Norton JA, et al, eds: Surgery:
Red blood cell Scientific Basis and Current
SQFat Practice, vol I. New York,
Springer-Verlag, 2000:222.)

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 image.
11 • W O U N D HEALING: REPAIR BIOLOGY AND W O U N D AND SCAR TREATMENT
Keratinocytes
Neutrophil
Fibrin matrix
Fibroblast
FIGURE 1 1-3. A neutrophil influx into the wound occurs
within 24 hours. The neutrophils scavenge debris and bac-
teria and secrete cytokines for monocyte and lymphocyte
attraction and activation. Keratinocytes begin migration
when a provisional matrix is present. (Modified from Lorenz
HP, Longaker MT: Wounds: biology, pathology, and man-
agement. In Norton JA, et al, eds: Surgery: Scientific Basis
and Current Practice, vol I. New York, Springer-Verlag,
2000:223.1
Scab
Fibroblast
Neutrophi
Macrophage
F I G U R E 1 1 - 4 . At 2 to 3 days after injury, the
macrophage becomes the predominant inflammatory
cell type in clean, noninfected wounds. Macrophages
regulate the repair process by secretion of multiple
growth factors, including types that induce fibroblast and
endothelial cell migration and proliferation. (Modified from
Lorenz HP, Longaker MT: Wounds: biology, pathology, and
management. In Norton JA, et al. eds: Surgery: Scientific
Basis and Current Practice, vol I. New York, Springer-
Verlag, 2000:223.)
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Dr.Mustafa D.
21
l l - l ) . 4 , 5 Depletion of monocytes and macrophages
causes a severe alteration in wound healing with poor
debridement, delayed fibroblast proliferation, and
inadequate angiogenesis. 6 The macrophage is the only
inflammatory cell type that is required for normal
repair, indicating its primary role in the regulation of
repair.
Proliferation Phase
FIBROPLASIA
During fibroplasia, fibroblasts synthesize and deposit
the replacement extracellular matrix (ECM) at the
wound site. The proliferative phase begins with degra-
dation of the initial fibrin-platelet provisional matrix.
Macrophages and the adjacent ECM release growth
factors that stimulate fibroblast activation. Local
fibroblasts become activated and increase protein syn-
thesis in preparation for cell division. As fibroblasts
proliferate, they become the predominant cell type
by 3 to 5 days in clean, noninfected wounds (Pig. 11-
5). After cell division and proliferation, fibroblasts
begin synthesis and secretion of ECM products. The
initial fibrin matrix is replaced by a provisional matrix
of fibronectin and hyaluronan, which facilitates
fibroblast migration. The control of ECM deposition
by fibroblasts is complex and partially regulated by
Scab
Keratinocyte
migration
Fibroblast
Neutrophil
Macrophage
FIGURE 1 1-5. Fibroblasts are activated and present
at the wound by 3 to 5 days after injury. These cells secrete
matrix components and growth factors that continue to
stimulate healing. Keratinocyte migration (epiboly) begins
over the new matrix. Migration starts from the wound
edges as well as from epidermal cell nests at sweat glands
and hair follicles in the center of the wound. {Modified
from Lorenz HP, Longaker MT: Wounds: biology, pathol-
ogy, and management. In Norton JA, et al, eds: Surgery:
Scientific Basis and Current Practice, vol I. New York,
Springer-Verlag, 2000:224.)
212 I • GENERAL PRINCIPLES

TABLE 11-1 • A PARTIAL LIST OF GROWTH FACTORS PRESENT AT THE WOUND SITE*

Growth Factor Cellular Source Target Cells Biologic Activity

TGF-pl and Macrophages, platelets, Inflammatory cells, keratinocytes, Chemotaxis, proliferation,

TCF-p2 fibroblasts, keratinocytes fibroblasts matrix production (fibrosis)
TGF-p3 Macrophages Fibroblasts Anti-scarring?
TGF-a Macrophages, platelets, Keratinocytes, fibroblasts, Proliferation
keratinocytes endothelial cells
TNF-a Neutrophils Macrophages, keratinocytes, Activation of growth factor
fibroblasts expression
PDGF Macrophages, platelets, Neutrophils, macrophages, Chemotaxis, proliferation,
fibroblasts, endothelial fibroblasts, endothelial cells, matrix production
cells, vascular smooth vascular smooth muscle cells
muscle cells
FCF-1.FCF-2. Macrophages, fibroblasts, Keratinocytes, fibroblasts, Angiogenesis, proliferation,
FCF-4 endothelial cells endothelial cells, chondrocytes chemotaxis
FCF-7 (KGF-1). Fibroblasts Keratinocytes Proliferation, chemotaxis
FGF-10(KGF-2)
ECF Platelets, macrophages, Keratinocytes, fibroblasts, Proliferation, chemotaxis
keratinocytes endothelial cells
1CF-1/Sm-C Fibroblasts, macrophages, Fibroblasts, endothelial cells Proliferation, collagen
serum synthesis
IL-laand IL-1p Macrophages, neutrophils Macrophages, fibroblasts, Proliferation, collagenase
keratinocytes synthesis, chemotaxis
CTCF Fibroblasts, endothelial cells Fibroblasts Downstream of TGF-pl
VEGF Macrophages, keratinocytes, Endothelial cells Angiogenesis
fibroblasts

'Redundant biologic effects occur through both autocrine and paracrine mechanisms.
TGF-p, transforming growth factor-p; TGF-a, transforming growth factor-a; TNF-a, tumor necrosis factor-a; PDGF, platelet-derived growth factor;
FGF, fibroblast growth factor; KGF, keratinocytc growth factor; EGF, epidermal growth factor; IGF-1, insulin-like growth factor 1; Sm-C, somatostatin C; IL-1,
interleukin-1; CTGF, connective tissue growth factor; VEGF, vascular endothelial cell growth factor.
Modified from Lorenz HP, Longaker MT: Wounds: biology, pathology, and management. In Norton JA, et al, eds: Surgery: Scientific Basis and Current
Practice, vol I. New York, Springer-Verlag, 2000:224.

growth factors and interactions of fibroblast cell
membrane receptors with the ECM.
Integrins are regulators of cellular function during
repair. They are transmembrane receptors with extra-
cellular, membrane, and intracellular protein domains.
Integrins are heterodimeric and composed of a and
P subunits that interact to form the active protein
receptor. Ligands to integrins include growth factors
and ECM structural components such as collagen,
elastin, and other cells.7 After ligands bind, phos-
phorylation occurs in the cytoplasmic domain of the
integrin receptor, which starts a signal transduction
cascade that ultimately changes gene expression, and
new cellular function ensues.
Fibronectin and the glycosaminoglycan hyaluronic
acid compose the initial wound matrix. 8 Hyaluronic
acid provides a matrix that enhances cell migration
because of its large water of hydration. Adhesion
glycoproteins, including fibronectin, laminin, and
tenascin, are present throughout the early matrix
and facilitate cell attachment and migration. Integrin
receptors on cell surfaces bind to the matrix
glycosaminoglycans and glycoproteins. As fibro-
blasts enter and populate the wound, they secrete
hyaluronidasc to digest the provisional hyaluronic acid-
rich matrix, and larger, sulfated glycosaminoglycans
are subsequently deposited. Concomitantly, new col-
lagen is deposited by fibroblasts onto the fibronectin
and glycosaminoglycan scaffold in a disorganized
manner, resulting in scar formation.
The major fibrillar collagens composing the ECM
in skin and scar are collagen types I and III. The ratio
of collagen type I to type III is 4:1 in both skin and
wound scar. Although type III collagen is initially
deposited in relatively greater amounts in wounds, its
amount is always less than type I collagen in mature
scar.
At least 19 different types of collagen are currently
known. 10 Most collagen types are synthesized by
fibroblasts; however, some types are synthesized by
keratinocytes. 11 The collagens share common char-
acteristics: the basic structural unit is a right-handed
triple helix. Unique structural properties that distin-
guish the different collagen types include segments
that interrupt the triple helix and fold it into other
structures with unique properties.
The major structural component of wound scar is
collagen. Fibroblasts synthesize and secrete collagens

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image...
11 • WOUND HEALING: REPAIR BIOLOGY AND WOUND AND SCAR TREATMENT
through a complex intracellular and extracellular
process. Coordinated transcription of genes on dif-
ferent chromosomes (2,6,7,12,13,17, and 21) occurs.
In addition, several intracellular and extracellular
modifications are required to form the new collagen
fiber.9 Collagens contain a high fraction of proline
amino acid residues, which is the basis of its triple
helix structure. In the ECM, tropocollagen is formed.
Tropocollagen molecules laterally aggregate and are
covalently cross-linked by the enzyme lysyl oxidase
to form collagen fibrils.12 The fibrils interact with other
fibril types, which then aggregate into fibers. For
example, in skin, collagen type I and type VI fibrils
interact to form the collagen fibers that are imaged
with electron microscopy.13 Fibers then aggregate
into bundles and form collagen scar.
GRANULATION
Granulation tissue is a dense population of blood
vessels, macrophages, and fibroblasts embedded within
a loose provisional matrix of fibronectin, hyaluronic
acid, and collagen. Granulation tissue is clinically
characterized by its beefy-red appearance (i.e., "proud
flesh") and is present in open wounds. It is a conse-
quence of the rich bed of new capillary networks
(neoangiogenesis) that form by endothelial cell divi-
sion and migration. The directed growth of vascular
endothelial cells is stimulated by platelet and activated
macrophage and fibroblast products. One example is
vascular endothelial growth factor, which induces
migration and proliferation of endothelial cells.14
Granulation tissue is a clinical indicator that an
open wound is amenable to skin graft treatment.
Wounds that benefit from skin grafts are of sufficient
size such that the healing time would be decreased
after grafting. Because granulation tissue has a high
level of vascularity due to the abundance of new
capillary formation, it readily accepts and supports
skin grafts.
An open wound invariably becomes colonized by
bacteria because it has no protective barrier to prevent
bacterial adherence to the exposed tissue. Although
colonization does not preclude healing, if clinical bac-
terial infection occurs, healing not only can be delayed
Open wound
FIGURE 1 1 - 6 . Wound contraction is the process in which the surrounding tissue is pulled radially toward the wound.
The wound size is decreased, which shortens the healing time. (Modified from Lorenz HP, Longaker MT: Wounds:
biology, pathology, and management. In Norton JA, et al, eds: Surgery: Scientific Basis and Current Practice, vol I.
New York, Springer-Verlag, 2000:224.)
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213
but also can be stopped. Clinical infection implies
bacterial invasion into the deeper layers of the
surrounding tissue. It is treated by debridement
of necrotic tissue, which is a nutrient source for
bacteria, and by appropriate antibiotic therapy.
CONTRACTION
Contraction is the process in which the surrounding
skin is pulled circumferentially toward an open wound
(Fig. 11-6). This phenomenon does not occur with
closed surgical incisions. Open wounds after trauma,
burns, and previously closed wounds secondarily
opened by infection are associated with contraction.
Wound contraction decreases the size of the wound
dramatically without new tissue formation. This repair
process speeds wound closure compared with epithe-
lialization and scar formation alone. In addition, the
area of insensate scar is smaller.
Animals have much greater capacity for wound
contraction than humans do. Most mammalian
animals (e.g., rodents, cats, dogs, sheep, and rabbits)
have a pannicuius carnosus, which is a myofascial layer
between the subcutaneous fat and musculoskeletal
layers. This anatomy results in a plane of low resist-
ance between two fascial layers, which allows enhanced
skin mobility and therefore contraction. The amount
of contraction is related to both the size of the wound
and mobility of the skin. In humans, contraction
is greatest in the trunk and perineum, least on the
extremities, and intermediate on the head and neck.
Eighty percent to 90% of wound closure can be due
to contraction in the trunk and perineum.15 These
regional differences in contraction are probably due
to relative differences in skin laxity.
The cellular mechanisms causing wound contrac-
tion are not well understood. The contractile forces
are likely to be generated by myofibroblasts, which
are fibroblast-like cells that contain smooth muscle
ct-actin and microfilaments in their cytoplasm.16
These cells may pull the surrounding skin toward
the wound by their movement through the matrix
scaffold or by intrinsic cellular forces.
Wound contraction must be distinguished from
contracture. Clinically, contracture is defined as tissue
,-*A^a
Scar
214 I • GENERAL PRINCIPLES

shortening or distortion that causes decreased joint
mobility and function. Scar contracture commonly
refers to decreased function in the area, whereas scar
contraction refers to shortening of the scar length
compared with the original wound.
EPITHELIALIZATION
Morphologic changes in keratinocytes at the wound
margin are evident within hours after injury. The
epidermal cell layer thickens and marginal basal cells
migrate over the wound defect (see Fig. 11-5). Once
these keratinocytes begin migrating, they do not
divide until epidermal continuity is restored. New
epithelial cells for wound closure are provided by fixed
basal cells in a zone near the edge of the wound. I7 Their
daughter cells flatten and migrate over the wound
matrix as a sheet (epiboly). Migration of keratinocytes
over the wound matrix is guided by cell adhesion
glycoproteins, such as tenascin and fibronectin, which
are their "railroad tracks." After the re-establishment
of the epithelial layer, keratinocytes and fibroblasts
secrete laminin and type IV collagen to form the base-
ment membrane. 18 The keratinocytes become colum-
nar and divide to restore the layering of the epidermis
and re-form a barrier to further contamination and
moisture loss.
Keratinocytes can respond to foreign body stim-
ulation with migration as well. Sutures in skin wounds
provide tracks along which these cells can migrate.
Fibrotic reactions, cysts, and sterile abscesses centered
on the suture can occur. These are treated by removal
of the inciting suture and epithelial cell sinus track
or cyst.
of matrix metalloproteinase-tissue inhibitor of matrix
metailoproteinase balance during wound ECM remod-
eling.21 Matrix metalloproteinase-deficient knockout
mice have delayed wound contraction and healing,
demonstrating the importance of a proper balance
for normal healing.22
Scar formation is the ultimate outcome of wound
repair in children and adults (Fig. 11-7). Scar has no
epidermal appendages (hair follicles and sebaceous
glands), and it has a collagen pattern that is distinctly
different from unwounded skin. New collagen fibers
secreted by fibroblasts are present as early as 3 days
after wounding. As the collagen matrix forms,
densely packed fibers fill the wound site. The ultimate
pattern of collagen in scar is one of densely packed
fibers and not the reticular pattern found in
unwounded dermis.
Wound scar remodeling occurs during months to
years to form a "mature" scar. The early scar appear-
ance is red due to its dense capillary network induced
at the injury site. When closure is complete, capillar-
ies regress until relatively few remain. As the scar redness
dissipates during a period of months, the true scar
pigmentation becomes evident. Scars are usually
hypopigmented after full maturation* However, scars
can become hyperpigmented in darker-pigmented
patients and in those lighter-pigmcnted patients whose
scars receive excess sun exposure. For this reason, sun

Remodeling Phase
The scaffold that supports cells in both the unwounded
and wounded states is the ECM, which is the Dermal scar
structural component of skin that must be repaired (collagen) ... //• -•;;-v-'SJl
after injury. The ECM is dynamic and is constantly
undergoing remodeling during repair, which can be
conceptualized as the balance between synthesis, dep-
osition, and degradation. Lysyi oxidase is the major
intermolecular collagen cross-linking enzyme. 12 Col-
lagen cross-linking decreases its degradation and
improves wound tensile strength. Collagenases,
gelatinases, and stromelysins are matrix metallo-
proteinases that degrade ECM components. These FIGURE 11-7. Adult and late-gestation fetal skin
proteinases are also active in carcinoma invasion into wounds heal with scar formation. Scar is composed of
the ECM and therefore have gained attention in densely packed, disorganized collagen fiber bundles.
Remodeling occurs for 1 to 2 years after injury and con-
recent years.19,20 The balance of collagen deposition sists of further collagen cross-linking and regression of
and degradation is in part determined by the regula- capillaries, which account for the softening of scar and its
tion of matrix mctalloproteinase activity. Proteins color change from red to white. (Modified from Lorenz
called tissue inhibitors of matrix mctalloproteinase HP, Longaker MT: Wounds: biology, pathology, and man-
agement. In Norton JA, et al, eds: Surgery: Scientific Basis
specifically inactivate the matrix metalloproteinases. and Current Practice, vol I. New York, Springer-Verlag,
Investigators are currently examining the regulation 2000:227.)

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Dr.Mustafa D.
image...
1 • WOUND HEALING: REPAIR BIOLOGY AND WOUND AND SCAR TREATMENT
1000
x T
<\J700-
E
E 600-
S
500-
Ul
400-
(/>
a> 300-
w
FIGURE 1 1 - 8 . Wound tensile strength c 200-
as a function of time. Maximal wound .0)
h-
tensile strength is 75% to 80% that 100-
of unwounded skin. (Modified from
Levenson SM, Geever EF, Crowley LV, 0
et al: The healing of rat skin wounds.
0 7
Ann Surg 1965; 161:293-308; with
permission.)
protection measures are recommended for patients
with early scars on sun-exposed areas such as the scalp,
face, and neck.
During remodeling, wounds gradually become
stronger with time. Wound tensile strength increases
rapidly from 1 to 8 weeks after wounding and corre-
lates with collagen cross-linking by lysyl oxidase.
Thereafter, tensile strength increases at a slower pace
and has been documented to increase up to 1 year after
wounding in animal studies (Fig. 11-8). However, the
tensile strength of wounded skin at best reaches only
approximately 80% that of unwounded skin.23 In addi-
tion, scar is brittle and less elastic than normal skin. It
is readily visible because of color, contour, and texture
differences compared with unwounded skin. Although
scars can be hidden well with proper surgical planning
and uneventful healing, they may have aesthetically
unacceptable appearances in nonelective wounds
after trauma and burns and in wounds with healing
problems.
Regulation
GROWTH FACTORS
Growth factors are the focal regulatory points of the
repair process. They are polypeptides that are released
by a variety of activated cells at the wound site (see
Table 11-1). They act in either a paracrine or autocrine
fashion to stimulate or to inhibit gene expression
by their target cells in the wound. In general, they
stimulate cellular proliferation and chcmoattract new
cells to the wound. Myriad growth factors are present
in wounds and many have overlapping biologic
functions. Most growth factors exist in several iso-
forms with several receptor types present in wounds,
which increases the complexity of growth factor
function.
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215
1 1 1 1 1 1 1 1 1 1 1 r
14 21 28 35 42 49 56 63 70 77 84
Time (days post wounding)
In addition to growth factor ligands, their sig-
naling receptors are another locus for regulation of
repair. Growth factors do not have an effect on target
cells without a functional signaling receptor present
on the cell surface. The level of regulation is complex
in that the growth factors have multiple different
receptor types to which they can bind and induce
cell signaling. Scientists are now beginning to under-
stand the relationships between receptor binding
affinity, growth factor isoforms, and target cell effect.
In the future, treatment of deficient wound healing
conditions may be possible by stimulating or neu-
tralizing specific receptors through pharmacologic
ligands.
Platelet-Derived Growth Factor
Platelet-derived growth factor (PDGF) is released from
platelet alpha granules immediately after injury. PDGF
attracts neutrophils, macrophages, and fibroblasts
to the wound and serves as a powerful mitogen.
Macrophages, endothelial cells, and fibroblasts also
synthesize and secrete PDGF in the wound. PDGF
stimulates fibroblasts to synthesize new ECM,
predominantly the noncollagenous components
such as glycosaminoglycans and adhesion proteins.
PDGF also increases the amount of collagenase
secreted by fibroblasts, indicating a role for this
growth factor in tissue remodeling.24,23 PDGF strongly
induces granulation tissue production and is now
available for the treatment of diabetic nonhealing
wounds.
Transforming Growth Factor-^
Transforminggrowth factor-(J (TGF-0) is a profibrotic
growth factor that directly stimulates collagen synthesis
and decreases ECM degradation by fibroblasts.26 It is
released from all cells at the wound site, including
216 I • CENERAL PRINCIPLES
platelets, macrophages, fibroblasts, and keratinocytes.
TGF-(J acts in an autocrine fashion to further
stimulate its own synthesis and secretion. TGF-P
also chemoattracts fibroblasts and macrophages to
the wound.
TGF-p accelerates wound repair when it is applied
experimentally to wounds that have no deficiency in
repair. However, the increase in repair rate is at the
expense of increased fibrosis, which could be a
detriment during normal skin healing. In addition,
increased TGF-p activity is associated with pathologic
fibrosis in multiple different organ systems including
heart, lung, brain, liver, and kidney. TGF-p stimulates
ECM synthesis by increasing collagen, elastin, and gly-
cosaminoglycan synthesis. It increases integrin expres-
sion, which enhances cell-matrix interactions. TGF-p
increases ECM accumulation by decreasing matrix
metalloproteinase and increasing tissue inhibitor of
matrix metalloproteinase expression. Through these
mechanisms, exogenous TGF-p augments fibrosis at
the wound site.27,28 Interestingly, studies in mice with
a lack of endogenous TGF-P activity demonstrate
accelerated healing with an impaired inflammatory
response.29 This finding underscores the complex
effects of TGF-P and other growth factors during the
repair process.
Fibroblast Growth Factors
The fibroblast growth factors (FGFs) are a group of
heparin-binding growth factors that are secreted into
the ECM, where they remain dormant until activated
by tissue injury. They are bound by heparin and the
glycosaminoglycan heparan sulfate. The have a broad
range of biologic functions, specific to each isoform.
FGF-1 (acidic FGF) and FGF-2 (basic FGF) stimulate
angiogenesis. 30 Endothelial cells, fibroblasts, and
macrophages produce FGF-1 and FGF-2. Basement
membrane serves as a storage depot for FGF-2, which
is released on degradation of the heparin components
of the basement membrane at sites of injury. FGF-1
and FGF-2 stimulate endothelial cells to divide and
form new capillaries. They also chemoattract endothe-
lial cells and fibroblasts.
FGF-7 (keratinocyte growth factor 1 [KGF-1]),
FGF-10 (keratinocyte growth factor 2 [KGF-2]), and
epidermal growth factor stimulate epithelialization.
KGF-1 and KGF-2 are expressed in wound fibroblasts
and promote keratinocyte proliferation and migra-
tion in a paracrine fashion. Decreased expression
of KGF-1 occurs in diabetic mouse wounds. 31 In an
ischemic rabbit wound model, exogenous KGF-2
treatment accelerates epithelialization without an
increase in scar formation. 32 Exogenous KGF-2 also
increases wound tensile strength, collagen content, and
epidermal thickness in animal models of normal
healing.33 It shows great promise for the treatment of
impaired wounds.
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Vascular Endothelial Growth Factor
Vascular endothelial growth factor (VEGF) is also
a potent angiogenic stimulus. 34 It acts in a paracrine
manner to stimulate vascular permeability and pro-
liferation by endothelial cells after release from platelets,
macrophages, fibroblasts, and keratinocytes.35,3* Its
expression is also increased in hypoxic conditions, such
as those found at the wound site.37
Other Growth Factors
Multiple other growth factors affect wound repair.
Epithelialization is also directly stimulated by epider-
mal growth factor, which is released by keratinocytes
to act in an autocrine fashion and promote keratinocyte
proliferation. Insulin-like growth factor 1 (IGF-1) stim-
ulates collagen synthesis by fibroblasts and interacts
synergistically with PDGF and FGF-2 to facilitate
fibroblast proliferation.38 Interferon-y has been shown
to downregulate collagen synthesis. The various
interleukins mediate inflammatory cell functions
at the wound site.39
Growth factors in pharmacologic doses can have
beneficial effects on the repair processes. Investiga-
tors have accelerated healing rates in normal wounds
by adding exogenous TGF-p, PDGF, IGF-1, or FGF-
2 6.30,40,41 Addition of these same growth factors has
also augmented repair in animal models of impaired
wound healing conditions such as diabetes and chronic
steroid use.42"45 Although further studies are needed
to determine the precise growth factor combination
that is optimal for specific wound types, clinical
use of a growth factor is now approved for diabetic
wounds and is likely to be approved for other impaired
healing conditions in the near future.
THE EXTRACELLULAR MATRIX
In normal, unwounded conditions, the ECM is a depos-
itory of growth factors in latent forms. With injury
and matrix destruction, growth factors are released
from the ECM in active form and thereby assist in ini-
tiating and regulating the repair process. For example,
TGF-P is bound in the ECM to the proteoglycan
decorin and is inactive when bound. At sites of injury,
TGF-p forms complexes with its binding protein,
latency-associated protein (LAP), and is released.
Under acidic conditions, such as at sites of hypoxia
and tissue injury, LAP dissociates and active TGF-P is
formed. 46 LAP can also be proteolytically cleaved and
released by matrix metalloproteinases and other pro-
teases at the wound site. Active TGF-P immediately
binds to its two serine-threonine kinase receptors
(RI and RII), which are present on fibroblasts,
macrophages, and endothelial cells.47-48 The TGF-p RI
and RII receptors form heterodimeric complexes with
each other, and TGF-p biologic activity is initiated in
the target cell through the Smad pathway.49
 image...
11 • WOUND HEALING: REPAIR BIOLOGY AND WOUND AND SCAR TREATMENT
The FGFs are another example of growth factors
bound by the ECM. PDGF has also been shown
to bind to ECM proteins. Through sequestration of
growth factors with their subsequent release during
injury, the ECM plays a fundamental role in wound
repair by presentation of growth factors that regulate
the repair processes.
FETAL WOUND REPAIR BIOLOGY
Overview
The therapeutic solution for the reduction and pos-
sible elimination of scar formation may be found in
the mechanisms responsible for scariess wound healing
in the fetus. The early-gestation fetus can heal skin
wounds with regenerative-type repair and without scar
formation.50"52 In scariess fetal wounds, the epidermis
and dermis are restored to a normal architecture. The
collagen dermal matrix pattern is reticular and
unchanged from unwounded dermis. The wound hair
follicle and sweat gland patterns are normal as well
(Color Plate 11-1). The wound is not evident grossly
unless a wound edge contour change is present, which
will cast a light shadow under appropriate circum-
stances (Fig. 11-9).53 Scariess healing by the fetus does
not depend on the fetal environment. Fetal skin grafts
heal wounds without scar after transplantation to
a postnatal environment. Thus, amniotic fluid, the
FIGURE 1 1-9. Fetal monkey full-thickness wedge exci-
sion lip wound made at the beginning of the third trimester
and harvested 2 weeks later. The cutaneous wound is iden-
tified by the sutures. No scar was present histologically,
and the orbicularis oris muscle re-formed across the
defect. Interestingly, the naris was deformed compared
with the contralateral side.
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217
intrauterine environment, and fetal serum factors
are not required for scariess healing. Scariess repair
appears to be inherent to the fetal tissue and prob-
ably depends on factors associated with skin
development. 54,55
The fetal environment alone cannot induce scar-
less healing in adult skin. When adult skin is trans-
planted onto a fetus and later wounded at a point in
gestation when fetal skin heals scarlessly, the adult skin
grafts still heal with scar formation. 56 The transfor-
mation of adult healing to scariess repair cannot be
accomplished simply by perfusion of adult skin with
fetal serum or by immersion in amniotic fluid. Thus,
induction of scariess healing in adult skin will require
more than a recreation of the fetal environment. The
adult repair processes will likely have to be modified
to recapitulate skin development. An understanding
of the biology of scariess fetal wound repair will help
surgeons develop therapeutic strategies to minimize
scar and fibrosis.
Transition to Scar Formation
Both gestational age and wound size determine
whether the fetus will heal a wound without scar.57,58
As gestation progresses, a transition from scariess
healing to healing with scar formation occurs before
birth. In large animal models, such as the fetal lamb
and monkey, this transition occurs during the early
part of the third trimester for incisional, closed
wounds. In addition, wound size affects the tempo-
ral occurrence of this transition. Open, excisional
wounds must be made earlier in gestation than closed,
incisional wounds for scariess healing to occur. Also,
larger open wounds must be made earlier in gesta-
tion than smaller open wounds for scariess healing.57
The exact reasons underlying these observations
remain unknown but probably relate to whether the
wound has healed before a certain threshold in devel-
opment. The shift from scariess healing to scar for-
mation is not abrupt but instead occurs gradually with
an intermediate repair outcome that is neither regen-
eration nor scar: the transition wound. The transition
wound has a normal reticular collagen and connec-
tive tissue matrix pattern but without restoration of
epidermal appendages. 53 Thus, it has features of both
scar (no appendages) and scariess (normal ECM)
healing.
Differences Between Fetal and
Adult Repair
FIBROBLASTS
Because fetal fibroblasts deposit matrix in a scar-free
pattern, they are crucial for scariess repair. A number
of studies have begun to define the functional
218 I • GENERAL PRINCIPLES
differences between fetal and postnatal dermal fibro-
blasts. First, fetal fibroblasts synthesize greater total col-
lagen than their postnatal counterparts do in vitro.59
Fetal fibroblasts respond to TGF-P stimulation with a
greater increase in collagen synthesis than do postna-
tal fibroblasts in vitro.60,61 However, postnatal fibro-
blasts express more collagenase than fetal fibroblasts
do. 59 Fetal fibroblasts also migrate at a faster rate than
postnatal fibroblasts. 62 Increased migration velocity
during repair is likely to affect collagen deposition and
cross-linking.
REPAIR RATE
Several parameters of repair are different in fetal
wounds compared with postnatal wounds. The rate
of repair for wounds of equal size is faster in the fetus.
The collagen synthesis rate is greater in fetal wounds.
In addition, the rate of epithelialization is faster in
the fetal wound. 63 Fetal wound repair may be more
rapid because there is little or no period of activation
for the fetal fibroblast to synthesize ECM at the wound
site.
INFLAMMATION
A key difference between fetal and postnatal tissue
repair is a reduced inflammatory cellular infiltrate in
fetal wound repair.64 Inflammation plays a prominent
role in postnatal repair, but it is not present in sig-
nificant amounts during scarless fetal healing. Few
inflammatory cells enter the fetal wound site before
the transition. This may be due to the immature fetal
immune system. However, a marked inflammatory
cellular infiltrate occurs later in gestation after the
transition when fetal wounds form scar. The amount
of inflammation correlates strongly with the amount
of scar formation.
GROWTH FACTOR EXPRESSION
Few growth factors associated with adult repair have
increased expression in scarless fetal wounds. This
is likely due to inherent major differences in the
regulation between the two repair systems. Growth
factors that are upregulated in scarless wounds are
increased more rapidly than in postnatal wounds. One
example is VEGF, which is rapidly expressed after
injury in scarless wounds but is delayed in postnatal
wounds. 65
The expression of TGF-p isoforms, receptors, and
bioactivity modulators has been analyzed in fetal
wounds. Compared with scarring wounds, scarless
fetal wounds have moreTGF-p3, receptor type II, and
fibromodulin expression. 66 In contrast, increased
TGF-P 1, receptor type I, and decorin expression is
associated with the transition to scar formation. Thus,
the expression profile of isoforms, receptors, and
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modulators for a growth factor can be different in
scarless and scarring wounds. By understanding the
scarless repair expression profile for a growth factor,
information is obtained that can permit recapitula-
tion of this profile during postnatal repair to reduce
scar formation.
Exogenous addition of several cytokines to fetal
wounds has also been performed and in every case
has resulted in accelerated scarring. The cytokines
tested include TGF-pl, TGF-p2, PDGF, and bone mor-
phogenetic protein 2, each of which has increased
expression during scar formation in postnatal
wounds.67*70 Thus, growth factors with increased
expression in scarring wounds probably modulate
scarless wounds in a similar fashion, which results in
scar formation.
DEVELOPMENTAL GENE EXPRESSION
Because fetal skin is growing and differentiating,
genes associated with development are likely to have
an important role during scarless healing. Their
expression may not occur during adult healing because
of inactivation at the end of development. Homeobox
genes are transcription factors that govern gene expres-
sion during embryogenesis. PRX2 is a homeobox gene
that has increased expression during scarless fetal
wound healing and only weak expression during
adult skin healing.71 Although its role in fetal skin devel-
opment and repair remains unknown, it is a promis-
ing new area of investigation with potential to further
our understanding of the mechanisms regulating
scarless repair.
MATRIX DIFFERENCES
Fetal skin and wound matrix are composed of more
hyaluronic acid than are postnatal skin and scar.
Hyaluronic acid stimulates fibroblast migration and
probably affects the ECM deposition pattern. 62 The
fetal skin and wound ECM has a relatively greater
amount of collagen type III, but how this affects
scar formation is not known. The collagen fiber
thickness is increased in scarring fetal wounds com-
pared with unwounded fetal skin as measured by
confocal microscopy. This distance between collagen
fibers is also greater in scarring fetal wounds, but
the mechanisms causing these earliest changes in
healing associated with scar formation remain to be
elucidated.52
Scarless fetal skin repair is the blueprint for ideal
repair. Although numerous studies have determined
differences in fetal and postnatal repair mechanisms,
little success has been achieved in modulating post-
natal wounds to heal without scar formation. The
mechanisms responsible for scarless repair remain to
be fully determined and when delineated will likely
lead to innovative anti-scarring treatment strategies.
VtSWH^aeldW image...
1 1 • WOUND HEALING: REPAIR BIOLOGY AND WOUND AND SCAR TREATMENT
ADULT W O U N D PATHOLOGY
Nonhealing Wounds
Chronic or nonhealing wounds are open wounds that
fail to epithelialize and close in a reasonable amount
of time, usually defined as 30 days. These wounds
typically are clinically stagnant and unable to form
robust granulation tissue. Many factors contribute to
inhibit healing in these patients, but no unifying theory
can explain the etiopathogenesis of each individual
nonhealing wound. Medical conditions such as dia-
betes, arterial insufficiency, venous disease, lym-
phedema, steroid use, connective tissue disease, and
radiation injury inhibit wound healing. Nonhealing
wounds can also be due to pressure necrosis,
infection (especially osteomyelitis), skin cancer, mal-
nutrition, chronic dermatologic disease, and other
metabolic conditions. In each case, treatment begins
with debridement of any necrotic tissue present. 72
However, despite optimal treatment for each clinical
problem, these wounds frequently still do not heal
and surgical intervention is required.
PRESSURE SORES
Wounds that develop over a bone prominence, usually
in the immobile patient, are termed pressure sores. They
are also called decubitus ulcers or bed sores. The
sacrum, ischium, and greater trochanter are the most
common locations affected.73 However, the metatarsal
heads, ankles, heels, knees, and occiput are suscepti-
ble under certain conditions. Another problem is malle-
olar skin pressure necrosis due to constricting cast
placement.
The amount of tissue pressure necrosis is deter-
mined by both the degree and duration of the pres-
sure. When the tissue pressure is greater than 25 to
30 mm Hg and capillary perfusion pressure is blocked,
microcirculation is compromised. Necrosis can occur
with as little as 2 hours of sustained pressures at this
level.74 Skin is more resistant to pressure necrosis than
are the underlying fat and muscle, which explains the
common finding of a small area of skin ulceration
overlying a large cavitary volume of subcutaneous fat
and muscle necrosis.
Treatment begins with identification and control
of the factors that lead to the increased pressure and
subsequent wound formation. Paralyzed patients
require periodic rotation and an air mattress or
another type of low-pressure bed. Wheelchair seat cush-
ions commonly need to be changed in patients with
ischial pressure sore. Behaviors, such as prolonged
sitting in wheelchairs without equal weight distribu-
tion, must frequently be modified. Lower extremity
contractures that cause excessive hip, knee, and
ankle pressure may need release. Tight casts should
be removed and replaced. Improperly fitting lower
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219
extremity prostheses can lead to stump wounds and
need modification. Other contributing factors, such
as malnutrition, infection, and diabetes mellitus,
should be identified and treated.
Most pressure sores will heal with avoidance of pres-
sure over the involved area. However, they heal with
scar, which is less resistant to trauma than normal skin
is. Thus, a higher incidence of recurrence exists after
spontaneous closure of these wounds than if they are
closed surgically with flaps of normal skin and muscle
over the bone prominence. 75,76
LOWER EXTREMITY WOUNDS
Leg wounds generally arise from either one of two
different vascular diseases: arterial or venous insuffi-
ciency. Most (80% to 90%) result from venous valvu-
lar disease (venous insufficiency).73,77,78
Venous
Increased venous pressure in the dependent lower
extremity with valvular incompetence leads to local-
ized edema with plasma extravasation. Fibrinogen
leakage results in formation of a fibrin layer around
the capillaries that impairs oxygen and nutrient dif-
fusion.79 Leukocytes may be trapped and activated in
obstructed capillaries. Oxygen radicals and proteases
may then be released, which causes tissue necrosis.
Postcapillary obstruction leads to an increased per-
fusion pressure and hypoxia, with further necrosis.
Without treatment, the wound size can easily con-
tinue to grow.
Arterial
Wounds require adequate oxygen delivery to heal.
Ischemic wounds heal poorly and have a much greater
risk of infection.80,81 Minor trauma, resulting from
scratches and abrasions that would otherwise heal
quickly in a well-vascularized extremity, can progress
to large wounds in ischemic limbs. Necrotizing infec-
tion that is not only limb but also life threatening can
develop. A reliable clinical sign of adequate arterial
inflow for healing is the presence of an arterial pulse.
If a single palpable pulse is present in the foot,
most wounds will heal. Transcutaneous oxygen meas-
urements have been shown to have an 8 3 % accuracy
in predictability of wound closure in an ischemic
extremity.82 A transcutaneous oxygen measurement
of 30 mm Hg at the wound edge denotes a wound
that is more likely to heal than not. A nonhealing
wound in an ischemic extremity is an indication for
revascularization. 83
Diabetic
Wound healing is impaired in diabetic patients
by several mechanisms. Neuropathy is frequently
present, which leads to decreased sensation and
220 I • GENERAL PRINCIPLES
biomechanical joint instability. Arterial insufficiency
is present in 30% to 60% of cases. Studies have impli-
cated reduced expression of growth factors in diabetic
wounds. Decreased expression of VEGF,84 IGF-1, 85
FGF-1, 86 KGF,31 and PDGF 87 has been demonstrated.
Sustained inflammation is present in diabetic mouse
wounds and may be induced by the increased expres-
sion of chemokines, which are the growth factors that
control leukocyte migration. 88 Apoptosis is also
increased in diabetic wounds. 89 Diabetic fibroblasts
and keratinocytes have reduced proliferation rates and
collagen production. 89 Wound healing is enhanced if
glucose levels are well controlled,90,9' which suggests
that many of these impairment mechanisms are
reversible in diabetic wounds.
RADIATION INJURY
External beam radiation through skin to treat deeper
disease has both acute and chronic effects on skin.
Acutely, a self-limited erythema may develop that
spontaneously resolves. The late effect of radiation
is a more significant injury to fibroblasts, keratino-
cytes, and endothelial cells. DNA damage to these
cells propagates and impairs the ability of these cells
to divide successfully. Irradiated tissue usually has
some degree of residual endothelial cell injury and
progressive endarteritis, which results in atrophy,
fibrosis, and poor tissue repair.92 Ultimately, the
affected skin may spontaneously break down, but
usually after repeated mild trauma. 92 When a surgi-
cal incision is placed through irradiated skin on the
trunk or extremities, it is not likely to heal. Although
improvement in repair can be achieved with hyper-
baric oxygen therapy,93,94 surgical intervention with
resection of the wound to normal, nonirradiated tissue
and coverage with a vascularized flap are frequently
necessary.
INFECTION
Wound infection is an imbalance between host resist-
ance and bacterial growth.95 Bacterial infection impairs
healing through several mechanisms. 96 At the wound
site, acute and chronic inflammatory infiltrates slow
fibroblast proliferation and thus slow ECM synthesis
and deposition. Although the exact mechanisms are
not known, sepsis causes systemic effects that also
impede repair.
A threshold number of bacteria in the wound is
necessary to overcome host resistance and cause clin-
ical wound infection. Bacterial contamination results
in clinical infection and delays healing if more than
105 organisms per gram of tissue are present in the
wound. 96,97 Skin grafts on open wounds are likely to
fail if quantitative culture shows more than 105 organ-
isms per gram of tissue, which provides further evi-
dence that bacterial load has an impact on repair.98
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Similarly, well-vascularized muscle flaps heal open
wounds successfully if bacterial loads are not greater
than 105 organisms per gram of tissue.99 These studies
demonstrate that high levels of bacteria inhibit the
normal healing processes.
Treatment of the closed, infected wound depends
on whether fluid or necrotic tissue is present. If no
fluid is draining or loculated, the cellulitis can be
successfully treated with appropriate antibiotics. The
wound should be opened and sutures removed; the
wound is irrigated and ddbrided if pus or necrotic
tissue is present. Administration of appropriate antibi-
otics after wound culture treats surrounding celluli-
tis. Signs of wound infection include fever, tenderness,
erythema, edema, and drainage.
MALNUTRITION
Wound healing is an anabolic event that requires
additional calorie intake. 100 However, the precise
calorie requirements for optimal wound healing
have not been determined. Large injuries such as
burns greatly increase metabolic rate and nutritional
requirements. 101 Severely malnourished and catabolic
patients clinically appear to have diminished healing;
however, no studies have definitely proved this
finding. 102 Experimentally, chronic protein depletion
impairs wound healing.103 Wound dehiscence risk is
increased in protein-depleted rats, but this can be
reversed with protein repletion immediately after
wounding. 104
Vitamin C (ascorbic acid) deficiency results in
scurvy. In these patients, wound healing is arrested
during fibroplasia. Normal quantities of fibroblasts are
present in the wound, but they produce an inadequate
amount of collagen.10: Vitamin C is necessary for
hydroxylation of proline and lysine residues,106 and
without hydroxyproline, newly synthesized collagen
is not transported out of cells. Without hydroxylysine,
collagen fibrils are not cross-linked. Both mechanisms
decrease wound tensile strength.
Vitamin A (retinoic acid) is involved in multiple
facets of repair: fibroplasia, collagen synthesis and cross-
linking, and epithelialization.105 Because vitamin A
requirements increase after injury, severely injured
patients require supplemental vitamin A to maintain
normal serum levels. Animal studies show that vitamin
A also reverses the impaired healing that occurs with
chronic steroid treatment.107,108 Although it is not
proved conclusively in human studies, most surgeons
administer vitamin A postoperatively to their patients
receiving steroid therapy. Vitamin A is fat soluble and
can be taken in toxic doses, so careful administration
is essential. The oral dose is 25,000 IU/day.105
Vitamin B 6 (pyridoxine) deficiency impairs
collagen cross-linking.109 Vitamin B! (thiamine) and
vitamin B2 (riboflavin) deficiencies cause syndromes
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11 • WOUND HEALING: REPAIR BIOLOGY AND WOUND AND SCAR TREATMENT
associated with poor wound repair. Supplementation
with these vitamins does not improve healing unless
a preexisting deficiency is present.
Deficiencies of trace metals such as zinc and copper
have been implicated in poor wound repair because
these divalent cations are cofactors in many
important enzymatic reactions. 105 Zinc deficiency is
associated with poor epithelialization and chronic,
nonhealing wounds. Trace metal deficiency is now
extremely rare in both enterally and parenterally fed
patients.
Excess administration of vitamins and minerals can
be detrimental and cause toxic effects, especially by
the fat-soluble vitamins. Adequate amounts are present
in today's enteral feeding solutions and as supple-
mental additives to parenteral solutions. Supplemen-
tal administration is necessary only in deficiency states
and certain unique clinical situations as described
before.
OBESITY
Obesity interferes with repair independently of dia-
betes.110 Obese patients with diabetes have impaired
wound healing independent of glucose control and
insulin therapy. Poor wound perfusion and necrotic
adipose tissue probably contribute to impaired healing
in both diabetic and nondiabetic obese patients.
CORTICOSTEROIDS
Both topically applied steroids and pharmacologic
steroid use impair healing, especially during the first
3 days after wounding. 111,112 Steroids reduce wound
inflammation, collagen synthesis, and contraction. 105
The exact mechanisms by which steroids impair
healing are not fully understood. Glucocorticoids
decrease PDGF and KGF expression in experimental
wounds.87,113 Steroids stabilize lysosomal membranes
and thereby decrease the release of lysosomes at the
repair site, which may slow repair processes. Because
steroids decrease inflammation, they may decrease host
bacterial resistance and thus increase wound infection
complications. The entire repair process is slowed, and
risk of dehiscence and infection is increased. Vitamin
A administration can reverse this effect.107,108
CHEMOTHERAPY
Both radiation and chemotherapeutic agents have their
greatest effects on dividing cells. During the prolifer-
ative phase of repair, numerous cell types are dividing
at the wound site. Antiproliferative chemotherapeu-
tic agents act to slow this process and thus retard
healing." 4 After oncologic surgical procedures, in most
institutions, chemotherapeutic agents are not admin-
istered until at least 5 to 7 days postoperatively to
prevent impairment of the initial healing events.
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221
Excessive Healing
Normal wounds have "stop" signals that halt the
repair process when the dermal defect is closed and
epithelialization is complete. When these signals arc
absent or ineffective, the repair process may con-
tinue unabated and cause excessive scar. The under-
lying molecular mechanisms leading to excessive
repair are not yet known. Profibrotic cytokine
overexpression has been implicated." 5,116 A lack of
programmed cell death, apoptosis, at the conclusion
of repair with continued presence of activated fibro-
blasts secreting ECM components has also been
implicated.117
Notwithstanding the molecular regulation of exces-
sive scar formation, there are clinical factors that affect
scar formation. To minimize visible scar on skin, elec-
tive incisions are least noticeable when they are placed
parallel to the natural lines of skin tension (Langer's
lines). This placement has two advantages: the scar is
parallel or within a natural skin crease, which cam-
ouflages the scar, and this location places the least
amount of tension on the wound. Wound tension
widens the scar. Sharply defined and well-aligned
wound edges that are approximated without tension
heal with the least amount of scar. Infection or
separation of the wound edges with subsequent
secondary intention healing also results in more
scar formation. Hyperpigmentation and hypopig-
mentation of scar increase its contrast with the
surrounding skin, making the scar more visible. Sun
protection of all wounds is recommended to prevent
scar hyperpigmentation.
HYPERTROPHIC SCAR
Hypertrophic scars and keloids are unique to humans
and do not occur in animals for unknown reasons.
These pathologic scar types are distinguished on the
basis of their clinical characteristics. Hypertrophic
scars are defined as scars that have not overgrown the
original wound boundaries but are instead raised. They
usually form secondary to excessive tensile forces
across the wound and are most common in wounds
across joint surfaces on the extremities but also
commonly occur on the sternum and neck. Physical
therapy with range-of-motion exercises is helpful
in minimizing hypertrophic scar as well as joint
contracture in the extremities.
Hypertrophic scar is a self-limited type of over-
healing that can regress with time. These scars gener-
ally fade as well as flatten to the surrounding skin level.
No clear histologic difference between hypertrophic
scar and keloid has been demonstrated. Early studies
found that keloids contain bundles of collagen around
focal nodules of fibroblast proliferation." 8 However,
later studies refute this distinction." 9 Because of
similar histologic findings in both hypertrophic scar
222 I • GENERAL PRINCIPLES
and keloid, they are more easily differentiated by their
clinical characteristics.
Hypertrophic scars and keloids are both fibro-
proliferative disorders of wound repair with excess
healing.115 However, because there are no animal
models of either condition, there are few biochemi-
cal and molecular data that distinguish the two enti-
ties in direct comparison. In addition, most studies
analyze either one or the other, but not both. In
general, both keloid and hypertrophic scar fibroblasts
have an upregulation of collagen synthesis, deposi-
tion, and accumulation. 116 It may be that keloid
fibroblasts respond to a greater degree than do hyper-
trophic scar fibroblasts to the signals stimulating scar
formation. For example, keloid fibroblasts respond
to exogenous TGF-p with a much greater increase
in collagen production than do hypertrophic scar
fibroblasts.120
KELOID
Keloids are scars that overgrow the original wound
edges. This clinical characteristic distinguishes keloid
from hypertrophic scar. True keloid scar is not
common and occurs mainly in darkly pigmented indi-
viduals with an incidence of 6% to 16% in African
populations.121 It has a genetic predisposition with
autosomal dominant features. The keloid scar con-
tinues to enlarge past the original wound boundaries
and behaves like a benign skin tumor with continued
slow growth. However, complete excision with primary
closure of the defect results in recurrence in the major-
ity of cases.
Keloid patients may have excessive start signals or
lack the appropriate stop signals for healing. In the
latter instance, the lack of stop signals results in con-
tinued and unchecked repair. A possible mechanism
of keloid formation may be the presence of persist-
ent signals pushing fibroblasts to keep "healing" the
wound site despite complete coverage of the original
wound. Studies have looked at apoptosis in normal
scar, hypertrophic scar, and keloid. Similar numbers
of apoptotic cells at the advancing wound edge in
both normal scar and hypertrophic scar have been
found.122 However, apoptotic gene expression is
decreased in keloids, suggesting persistence of acti-
vated fibroblasts.123
Keloids consist mainly of collagen and are relatively
acellular in their central portions with fibroblasts
present along their enlarging borders. They do not
contain a significant excess number of fibroblasts.
Keloid fibroblasts respond differently than normal
wound fibroblasts to growth factors found at the repair
site>ii6,i24.i25 F o r e x a m p i e ) TGF-P treatment causes a
greater degree of collagen gene expression in keloid
compared with normal wound fibroblasts in in vitro
studies." 6 In addition, there is a greater degree of
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Dr.Mustafa D.
profibrotic growth factor expression in keloids than
in normal wounds.124,126 Other mechanisms also con-
tribute to keloid formation. Keloid keratinocytes stim-
ulate increased collagen synthesis in both normal and
keloid fibroblasts compared with normal keratinocytes,
suggesting a multifactorial biomolecular cause for
keloid formation.127
CLINICAL WOUND MANAGEMENT
Management is based on the classification of the wound
type. Surgically closed incisions obviously require treat-
ment different from that of nonhealing open wounds.
Hypertrophic scars and keloids with their excessive
scarring require still different therapeutic approaches.
The treatment options for various wound types are
described.
Closed Wounds
Incisional wounds closed in layers along tissue planes
heal with primary intention. Deep sutures are placed
in collagen-rich layers such as fascia and dermis. These
strength layers can hold sutures under a high degree
of tension. Fatty tissue layers, such as subcutaneous
fat, do not have significant collagen and cannot hold
sutures under tension. For this reason, most surgeons
do not close the subcutaneous fat layer, even in the
morbidly obese patient. Dead space here is better oblit-
erated with a short course of closed suction drainage
postoperatively, which can prevent seroma formation
and possible infection.
The amount of tissue injury and degree of con-
tamination influence the length and quality of healing.
Small, clean closed wounds heal quickly with less
scar formation, whereas large, open dirty wounds
heal slowly with significant scar. To decrease scar
formation and risk of infection, meticulous hemo-
stasis should be performed. This limits the amount
of hematoma to be cleared and thus decreases
the inflammatory phase and probably decreases
scar. Because hematoma is a culture medium for bac-
teria, less bleeding also decreases the risk of infection.
By limitation of inflammation with sterile technique
and tight hemostatic control, repair by activated
fibroblasts can begin earlier and shorten the healing
period.
Smaller surgical scars are achieved with no skin
edge trauma and less resultant inflammation. Forceps
crush injury of the epidermis and dermis should be
avoided by use of fine forceps and skin hooks to retract
and assist in dermal closure. This decreases the
amount of necrotic tissue at the wound edge and
thereby reduces inflammation. Because suture mate-
rial is a foreign body, it generates an immune response
and is susceptible to infection. Some surgeons there-
fore close the epidermis with Steri-Strips. There is no
image...
11 • WOUND HEALING: REPAIR BIOLOGY AND WOUND AND SCAR TREATMENT
suture to leave "railroad track" scar or serve as an infec-
tion locus in the skin. Fibrin and other biologic glues
and sealants are now being developed for use during
wound closure with the potential benefit of less scar
formation.128'129
Closed wounds require less care than open wounds.
Closed wounds should be kept sterile for 24 to 48 hours
until epithelialization is complete. At this point, water
barrier function has been restored and patients can
be allowed to shower or wash. This has a psycholog-
ical benefit during the postoperative recovery period.
In addition, gentle cleansing removes old serum and
blood, which reduces potential bacterial accumula-
tion and infection risk.
Tensile strength of a closed incisional wound is only
20% that of normal skin at 3 weeks when collagen cross-
linking is becoming significant. At 6 weeks, wounds
are at 70% of the tensile strength of normal skin, which
is nearly the maximal tensile strength achieved by scar
(75% to 80% of normal; see Fig. 11-8).23 Therefore,
if absorbable suture is used to close deep structures
that are under significant tension, such as abdomi-
nal fascia, the suture should retain significant tensile
strength for at least 6 weeks before absorption severely
weakens the suture. In addition, heavy activity should
be limited for a minimum of 6 weeks when healing of
abdominal fascial layers is necessary.
Open Wounds
Open wounds heal with the same basic processes
of inflammation, proliferation, and remodeling as
do closed wounds. The major difference is that each
sequence is much longer, especially the proliferative
phase. There is much more granulation tissue forma-
tion and contraction. This type of healing process is
referred to as secondary intention.
Open wound edges are not approximated but are
instead separated, which necessitates epithelial cell
migration across a longer distance. Before epiboly can
occur, a provisional matrix must be present. Granu-
lation tissue must form. There are variable amounts
of bacteria, tissue debris, and inflammation present,
depending on wound location and etiology. Infection,
with high protein exudative losses and acute and
chronic inflammation, can dysregulate repair and
transform the healing wound into a clinically non-
healing wound. The exact molecular mechanisms
causing this shift from healing to a nonhealing wound
with infection remain unknown.
During the proliferative phase of an uncomplicated
course of secondary intention healing, a bed of gran-
ulation tissue will be present. If no infection is present
and the area is of sufficient size that healing will not
be complete for at least 2 to 3 weeks, placement of a
partial- or full-thickness skin graft should be consid-
ered. Grafts readily adhere to granulation tissue and
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223
will quickly speed the repair process. Partial-
thickness skin graft donor sites can heal in as little as
2 weeks, depending on graft thickness.
When an open wound heals, which is generally
defined as complete epithelialization, the dermal
defect has been filled with collagen scar covered by
epithelium. This scar has less tensile strength and is
more susceptible to trauma than normal skin is. Thus,
these scars more easily break down from local trauma
such as pressure.
TOPICAL WOUND TREATMENT
Necrotic material should be removed from open
wounds on initial presentation and subsequently as
it accumulates. Necrotic tissue serves only as a culture
source for bacteria and does not aid healing. The only
exception to immediate debridement is a dry, chronic,
arterial insufficiency eschar without evidence of infec-
tion. These types of wounds may be best treated by
revascularization before debridement.
Open wounds heal optimally in a moist, sterile envi-
ronment. Numerous experimental and clinical studies
have demonstrated that a moist environment speeds
healing.130,131 This is thought to occur by prevention
of desiccation at the base of the wound. Desiccation
causes necrosis at the base of the wound until an eschar
forms, which may take several days. During this time,
the wound is enlarging and initiation of the healing
process is delayed. When the wound is kept covered
and moist without infection, desiccation necrosis and
healing delay are prevented. 132
Chronic Open Wounds
A team approach for treatment of chronic wounds
is employed in wound centers. Members include a
plastic surgeon, vascular surgeon, orthopedic sur-
geon, podiatrist, internist, endocrinologist, hyper-
barist, and infectious disease specialist. The team
leader, usually a plastic surgeon, diagnoses the cause
of the wound, coordinates appropriate referrals, and
directs the overall wound care. Prosthetists, physical
therapists, enterostomal therapists, and clinical nurse
specialists complete the team. Because the etio-
pathogenesis of chronic wounds is multifactorial,
coordinated care by multiple specialists is required
for optimal results.
Treatment begins with debridement of necrotic
tissue, which removes a potential source of bacte-
rial infection and converts the chronic wound to an
acute wound. 133 Active medical comorbidities are
aggressively treated. The wound characteristics (size,
depth, infection, necrotic tissue component, edema,
drainage) are documented, and local wound care is
initiated. Care is continued until the wound is clean
and ready for reconstruction or heals by secondary
intention.
224 I • GENERAL PRINCIPLES
WOUND DRESSINGS
A plethora of wound dressings are available for
all types of wounds. No type has conclusively been
shown to accelerate healing above the others. However,
substantial improvement in both convenience and
comfort has been gained compared with saline gauze
dressings. A new class of engineered skin replace-
ments that show great promise in chronic wound care
has been developed and is changing chronic wound
care.
The optimal open wound dressing maintains a
moist, clean environment that prevents pressure and
mechanical trauma, reduces edema, stimulates repair,
and is inexpensive. Less frequent dressing changes and
prevention of skin irritation are also beneficial. At this
time, no ideal dressing exists.
The simplest and least expensive dressing remains
plain gauze and saline with or without antibiotic oint-
ment. Its major disadvantages are frequent and painful
changes, wound desiccation, and adjacent skin tape
irritation. However, it remains unsurpassed for gentle
debridement of infected wounds. Types of dressings
listed by class are shown in Table 11-2. The films are
gas permeable, maintain a moist environment, and
are useful for partial-thickness dermal wounds such
as skin graft donor sites. For highly exudative wounds,
the absorptive dressings are useful to create a moist
environment without excess fluid and proteinaceous
material accumulation.
Hydrocolloid dressings are useful for locations
where adhesion is necessary, such as the extremities
and over bone prominences. They are relatively thick
and can stay in place for 2 to 3 days. As their absorp-
tive capacity is reached, they lose adhesiveness, and
gentle atraumatic removal is facilitated. Hydrogels are
similar to hydrocolloid dressings except that they have
little adhesiveness and are especially useful for facial
wound dressings.
Subotmospheric Pressure Dressing
A subatmospheric dressing device* is available for
vacuum-assisted closure. The apparatus consists of a
sponge to fill the wound cavity, a vacuum pump, and
a transparent film. It can be used in both inpatient
and outpatient settings. m Vacuum-assisted closure is
useful for decreasing the size of large wounds on the
extremities and trunk in preparation for reconstruc-
tion. The device can aid the healing of pressure sores,
skin graft donor sites, and venous stasis ulcers.134,135
Treatment by vacuum-assisted closure has induced
granulation tissue formation over exposed bone and
tendon.136,137 The vulnerary mechanism is hypothe-
sized to be due to its reduction of surrounding tissue
edema, decrease of bacterial wound colonization, and
•VAC, KCI, Houston, Texas.
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Dr.Mustafa D.
increase in local blood supply, granulation, and wound
cell proliferation.
Lower Extremity Compression
Edema in the lower extremity—whether it is due to
venous insufficiency, lymphedema, cardiovascular
disease, or metabolic derangement—must be aggres-
sively treated if a wound is present. Elevation and com-
pression therapy must be applied. Four-layer dressing
wraps of the lower extremity consisting of gauze, cast
padding, Coban, and elastic Ace wraps are commonly
used. After a venous stasis wound has healed, 30 to
40 mm Hg pressure stockings must be worn contin-
uously to prevent recurrence, which can be as low as
17% during the next 3 years.138
ENGINEERED SKIN REPLACEMENTS
With the biotechnology revolution, several dermal
and skin replacements are now available through
tissue engineering technology (see Table 11-2). These
products have the additional potential benefit of
accelerating or augmenting repair because of their
biocomponents. Growth factors are present in prod-
ucts with acellular dermal matrices. Some products
contain living fibroblast and keratinocyte layers
that secrete matrix components and active growth
factors. These products are typically placed on open
wounds similarly to autologous skin grafts under
sterile conditions with bolster support. 139 Their
major advantages are the lack of a donor site wound
and scar and placement in an office setting. Their
costs are high, especially if they are applied recur-
rently to the same wound, yet models predict that
they can be less expensive than nonsurgical therapy.140
The bilayered human keratinocyte-fibroblast con-
struct on a bovine collagen matrix, Apligraf, has
been shown to improve healing of venous stasis,139 dia-
betic,141 and arterial insufficiency83 wounds. However,
these studies compare its use against local wound
care. No comparison has been made against autoge-
nous skin graft treatment. Although the unique biology
of engineered skin replacement dressings can aid in
the treatment of impaired wounds, their efficacy
compared with autogenous skin grafts has not been
determined.
PHARMACOLOGIC TREATMENT
Antibiotic Ointments
Antibiotic ointments are commonly used in burn
wound care as well as in deep partial-thickness
injuries. They remain controversial in the nonburn
patient because the risk for development of an inva-
sive infection by resistant bacteria may be too
high to justify their use. Open wounds are colonized
by bacteria, and systemic antibiotics are indicated
only if invasive infection is present. Nonburn
 image...

11 • WOUND HEALING: REPAIR BIOLOGY AND WOUND AND SCAR TREATMENT 225

TABLE 11-2 • CLASSES OF WOUND DRESSINGS AND ENGINEERED SKIN REPLACEMENTS*

Characteristics and
Class Composition Function Commercial Examples

Gauze Woven cotton fibers Permeable with desiccation; Curity

debridement; painful removal
Calcium alginate Seaweed polymer that forms Absorbs exudate; nonadherent; Algisorb, Sorbsan
a gel when it absorbs fluid nonirritating; requires a cover
dressing (permeable)
Impregnated Fine mesh fabric (silicone, Nonadherent; semipermeable Biobrane II
gauze nylon) with dermal porcine
collagens
Film Plastic (polyurethane); Allows water vapor permeation; OpSite, Tegaderm
semipermeable adhesive
Foam Hydrophilic (wound side) and Necrotic and exudative wounds Lyofoam, Allevyn
hydrophobic (outer side);
semipermeable
Hydrogel Water (96%) and polymer Aqueous environment; requires Vigilon, Aquasorb
(polyethyleneoxide) secondary dressing; no
adherence; not recommended
if infection is present;
semipermeable
Hydrocolloid Hydrophilic colloidal Absorbs fluid; necrotic tissue DuoDERM, IntraSite
particles and adhesive autolysis; little adherence;
• occlusive
Absorptive Starch copolymers, Absorbs exudate; used as a Geliperm, DuoDERM granules
powder and hydrocolloid particles filler; good for deep wounds
paste
Silicone Silicone sheets Sheet induces a localized Sil-K
electromagnetic field and
increased skin temperature;
decreases scar formation?
Subatmospheric Vacuum pump, sponge, Sponge conforms to wound and VAC device
pressure plastic film vacuum removes edema fluid
and bacteria; stimulation of
granulation, vascularization,
and wound cell proliferation
Dermal matrix Acellular matrix Permeable; increased AlloDerm (human, dermis),
replacement stimulation of repair? SIS (porcine, small bowel
submucosa), Integra (bovine
collagen, glycosaminoglycan,
and silicone epidermal-type
layer)
Dermal living Absorbable matrix populated Permeable; increased Dermagraft
replacement with fibroblasts stimulation of repair?
Skin living Bovine collagen matrix Impermeable; increased Apligraf
replacement populated with neonatal stimulation of repair?
human fibroblasts with an
outer layer of human
keratinocytes

^Multiple brands within each class are available, and a partial list is given. Although expensive, engineered skin replacements have great potential clinical
usefulness. No particular brands are recommended.
Dala partially taken from Fecdar JA: Clinical management of chronic wounds. In McCulloch JM, Kloth LC, Feedar JA: Wound Healing Alternatives in
Management. Philadelphia, FA Davis, 1995:137-185.
Modi6ed from Lorcnz HP, Longaker MT: Wounds: biology, pathology, and management. In Norton JA, et al, eds: Surgery: Scientific Basis and Current
Practice, vol I. New York, Springer-Verlag, 2000:225.

wounds without infection are likely to heal without
topical antibiotic treatment as long as local care is
adequate.
In burn patients, silver sulfadiazine is commonly
used. It is inexpensive, has few side effects, and rarely
induces bacterial resistance. It can be useful in chronic
wound dressings as well. It is well tolerated by pedi-
atric and geriatric patients alike.
Collagenases
The collagenases are useful for treatment of wounds
requiring fine debridement of necrotic tissue that is

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Dr.Mustafa D.
226 I • GENERAL PRINCIPLES
not amenable to surgical debridement. This could
be a thin layer of adherent exudate or small amounts
of necrotic tissue remaining after a bedside wound
debridement. Theoretically, collagenase would be
detrimental to a clean wound in the proliferative phase
when ECM synthesis and deposition favor accumu-
lation rather than degradation.
Growth Factors
Exogenous application of several growth factors has
been shown experimentally to accelerate normal
healing as well as to improve healing rates in impaired
models of healing.50,142'145 The best studied growth
factors with the most promise to improve healing are
PDGF, TGF-p, and members of the FGF family (see
Table 11-1). However, before widespread use, several
obstacles must be overcome, including efficacious
application, vehicle development, and cost. For
example, nonhealing human wound fluid has increased
protease activity, which probably would rapidly
degrade exogenously applied peptide growth
factors.146,147 A masked, randomized clinical trial of
exogenous growth factor treatment of pressure sores
demonstrated improved healing and cost savings with
FGF-2 treatment.148 These studies are particularly
difficult to design and to perform because of the
great degree of variability between patients in terms
of wound types, local wound care, and concomitant
control of active medical diseases. However, they are
needed to evaluate the efficacy and costs of this new
therapy.
In 1998, the first growth factor for treatment of
wounds was approved by the Food and Drug
Administration. Recombinant human PDGF-BB was
shown to improve healing of lower extremity diabetic
neuropathic ulcers in a double-blind, placebo-con-
trolled, multicenter study. This 20-week trial included
only patients with ulcers free of necrotic tissue and
with adequate oxygenation documented by a trans-
cutaneous oxygen tension of 30 mm Hg or greater.149
Complete wound healing occurred in 48% of the
treated group compared with 25% of the control
group.149 On the basis of this and other studies,
rhPDGF-BB is approved for the treatment of diabetic
neuropathic wounds. Soon other growth factors will
be approved as a topically applied wound pharma-
ceutical agent.
GENE THERAPY. Gene therapy to enhance wound
repair through introduction of a growth factor gene,
or other therapeutic gene, into repair cells is actively
undergoing investigation. With this approach, the gene
must be delivered to the target cell and its expression
sustained at a therapeutic level; the level and timing
of its expression must be reversibly controlled so that
it can be stopped when it is no longer needed.150 Several
delivery vehicles are being developed, each with
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Dr.Mustafa D.
unique advantages and disadvantages. Replication-
deficient adenovirus, herpes simplex virus type 1, and
retrovirus vectors have been successfully used to
transfect dermal fibroblasts and keratinocytes.151 Other
delivery approaches eliminate the virus and its pos-
sible risk of untoward side effects due to antigenic-
ity, potential recombination with wild-type viruses,
and cellular damage from persistent viral exposure.
Nonviral methods are categorized into chemical and
physical methods of gene transfer. Liposome-medi-
ated gene transfer is a chemical method in which the
gene is bound to a synthetic liposome vesicle and
carried into the target cell by endocytosis. Both the
FGF-1 and VEGF genes have been successfully trans-
ferred into experimental wounds.152,153 Particle-medi-
ated gene transfer (gene gun) directly injects DNA
into the cells and has been used for both epidermal
growth factor and PDGF gene transfer in experimental
wounds.154,155 Gene therapy is likely to become an
increasingly important tool for the treatment of non-
healing wounds as its methods advance. A phase I clin-
ical trial to evaluate the safety of adenovirus-mediated
rhPDGF-BB gene therapy for nonhealing diabetic
lower extremity wounds at the University of
Pennsylvania is currently planned.
Extreme redundancy exists in the function of
growth factors at the wound site. In addition, multi-
ple simultaneous processes are occurring during
repair. Thus, it is likely that multiple growth factors
may need to be added on impaired and even other-
wise normal wounds to effect a clinically significant
improvement in repair quality and rate. Different
growth factor combinations may be needed to treat
impaired wounds due to different underlying diseases,
such as diabetes versus arterial insufficiency. To further
complicate matters, neutralization of certain growth
factors may be necessary as well as augmentation of
other factors in the same wound. Our understanding
of the biomolecular regulation of repair is rapidly
expanding, and with further knowledge, investigators
will develop methodology to enhance the repair
outcome in terms of both quality and rate.
Excessive Scar Treatment
SCAR CLASSIFICATION
Before anti-scarring therapy is instituted, an accurate
description and classification of the scar type are
useful. This assists with assessment of the outcome
after late follow-up. A clinically based scar classifica-
tion scheme has been proposed by the International
Advisory Panel on Scar Management, which is com-
posed of plastic surgeons, burn surgeons, and der-
matologists (Table 11-3).157 Consistent and accurate
diagnosis of scar types is essential for optimal man-
agement and useful literature interpretation.
 image...
1 1 • WOUND HEALING: REPAIR BIOLOGY AND WOUND AND SCAR TREATMENT
TABLE 11-3 • CLINICAL CLASSIFICATION OF
SCARS
Scar Type Characteristics
Mature scar Alight-colored, flat scar
Immature scar A red, sometimes itchy or painful,
and slightly elevated scar in the
process of remodeling
Many of these will mature
normally over time and become
flat and assume a pigmentation
that is similar to the
surrounding skin, although they
can be paler or slightly darker.
Linear hypertrophic A red, raised, sometimes itchy
(e.g., surgical or scar confined to the border of
traumatic) scar the original surgical incision
This usually occurs within weeks
after surgery. These scars may
increase in size rapidly for 3 to
6 months and then, after a
static phase, begin to regress.
They generally mature to have
an elevated, slightly rope-like
appearance with increased
width, which is variable. The full
maturation process may take
up to 2 years.
Widespread A widespread red, raised,
hypertrophic sometimes itchy scar confined
(e.g., burn) scar to the border of the burn injury
Minor keloid A focally raised, itchy scar
extending over normal tissue
This may develop up to 1 year
after injury and does not
regress on its own. Simple
surgical excision is often
followed by recurrence. There
may be a genetic abnormality
involved in keloid scarring.
Typical sites include earlobes.
Major keloid A large, raised (>0.5cm) scar,
possibly painful or pruritic and
extending over normal tissue
This often results after minor
trauma and can continue to
spread for years.
From Mustoe TA, Cootcr RD, Gold MH, et ah International clinical rec-
ommendations on scar management. Plast Reconstr Surg 2002; 110:560-571;
with permission.
THERAPIES
Many treatment modalities have been developed
for the prevention and management of hypertrophic
scarring and keloids. Many of the techniques have well-
documented and time-proven clinical use, but few have
been supported by randomized, prospective studies.
This inherent problem makes choosing the best treat-
ment modality difficult on the basis of objective sci-
entific evidence. Therefore, most modalities are applied
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Dr.Mustafa D.
227
on the basis of the treating physician s personal biases
and experiences. Scar treatment modalities, with their
respective advantages and disadvantages, are listed in
Table 11-4.
PREVENTION
The first step toward treatment of excessive scarring
is early recognition and institution of therapy after
surgery or trauma. Meticulous tissue handling, sutur-
ing, and wound management with efforts to prevent
infection are mandatory. 157 Sun protection to reduce
scar hyperpigmentation is essential. Patients who
are at increased risk for excessive scarring benefit
from preventive techniques, which include silicone gel
sheeting or ointments, hypoallergenic microporous
tape, and concurrent intralesional steroid injection.157
Silicone gel sheeting is widely used for hypertrophic
scar and keloid treatment. Silicone gel sheeting has a
20-plus year history with several randomized, con-
trolled trials that support its safe and effective use.I58,15S
It is painless and thus useful for children. Proposed
mechanisms of action for scar reduction include
improved hydration and occlusion,160 increased tem-
perature elevation of 1°C (or less) that can affect col-
lagenase kinetics, and change in the adhesion molecule
expression of the lymphocytic infiltrate.161 When
treatment with silicone gel sheeting is not feasible (e.g.,
scar location on the face, scalp, or neck), silicone
oil-based creams are an alternative.162 We routinely use
silicone-based creams on our cleft lip repair scars and
have not had an allergic or other untoward reaction
to date.
Microporous hypoallergenic tape can relieve tension
across wounds and minimize the excessive scar risk
from shearing. Although there are no prospective,
controlled studies to support its use, tape is routinely
used and recommended by many authors. 157 The tape
is applied for a few weeks after surgery.
In patients who are at extremely high risk, such
as after excision of keloid or hypertrophic scar, con-
current intralesional steroid injections can be given
prophylactically, followed by monthly injections as
necessary. Success rates, measured by no recurrence,
are reported up to 92% for keloids and 95% for hyper-
trophic scars at a mean follow-up of 30.5 months. 163
TREATMENT ALGORITHM
Immature Hypertrophic Scors (Red)
Once excessive scarring is identified, the Interna-
tional Advisory Panel on Scar Management consen-
sus initial management is silicone gel sheeting, steroid
injection, and localized pressure therapy (Fig. 11-10).157
It can be difficult to predict whether immature hyper-
trophic scars (red, slightly raised) will regress or
progress. When erythema persists for more than 1
228 I • CENERAL PRINCIPLES

TABLE 11-4 • SCAR PREVENTION AND REDUCTION THERAPIES

Therapy Advantages Disadvantages

Surgical excision Excess scar removed High recurrence without adjuvant

Surgical lengthening (Z-plasty,
W-plasty)
Steroid intralesional injection
Silicone gel sheeting
Pressure therapy
Radiation after surgery
Laser
Cryotherapy
Microporous tape
Popular treatments (vitamin
E, onion extracts, and other
plant creams)
Physical therapy treatments:
ultrasound, pulsed electrical
stimulation, hydrotherapy,
massage
AntHnflammatory/proliferative
medication injections
(interferons, 5-fluorouracil,
bleomycin)
Increased mobility and range of motion
Cost, ease
Cost, ease of use, noninvasive
Noninvasive, some proven efficacy
Some proven efficacy
Pulsed dye 585-nm laser best for
decreasing red color; carbon dioxide,
Nd:YAC, pulsed erb:YAC
lasers have some reported efficacy
Some proven efficacy in keloid reduction
Ease, low cost
Ease, low cost
Patient participation—increased joint
range of motion; can decrease scar
pain, pruritus
Early controlled studies report success
therapy, cost
Some excess scar persists, occasionally
worse cosmesis
Multiple treatments; telangiectasia,
hypopigmentation
Difficult application on head, neck,
across joints
Cumbersome garment, cost high if
custom-made, constant use for
months to years
Risk of carcinogenesis, cost
Costs, multiple treatments, emerging
technology
Hypopigmentation, pain, skin atrophy
No proven benefit, except uncontrolled
reports
No proven benefit
No quantitative proven efficacy, cost
Emerging therapy, indications still being
determined

Data compiled from Mustoe TA, Cootcr RD, Gold M H , et al: International clinical recommendations on scar management. Plast Reconstr Surg
2002;110:560-571.

month, the risk for progression to linear hypertrophic
scar increases, and appropriate therapy should be
started. Many authors recommend treatment with
pulsed dye lasers to decrease scar vascularity at this
point.a7MM
for pruritic or resistant scars. Pressure therapy can
be added when feasible. Pulsed dye laser (585 nm)
treatment of hypertrophic scars is another alterna-
tive,165'168-'69 but support for its use lacks controlled
studies.

Linear Hypertrophic Scars Widespread Burn Hypertrophic Scars

(Red, Slightly Raised)
Treatment options include the application of pres-
sure garments or topical silicone sheets, 585-nm
pulsed dye laser therapy, and re-excision.166,167 The last
option is most useful in cases of excess scar due to
wound infection or dehiscence. If the original wound
was closed following the basic tenets described
and healed otherwise uneventfully, re-excision with
primary closure is not likely to result in an improved
scar. Recurrence of hypertrophic scar is high in these
circumstances, and therefore most plastic surgeons do
not treat hypertrophic scar with excision and primary
closure unless they plan adjuvant therapy.
Silicone gel has proven benefit from randomized,
controlled trials and is a recommended first-line
therapy.157 Concurrent steroid injections are helpful
(Red, Raised)
Extensive surface area burn hypertrophic scars may
best be treated at burn centers when feasible. Multi-
modality therapies are generally used; these include
silicone gel sheeting, custom-fitted pressure garments,
and physical therapy alone or with massage, electri-
cal stimulation, or ultrasound. Steroid injection of
especially difficult areas is sometime necessary. Laser
treatment can be useful.170 Surgical treatment with Z-
plasty, excision and grafting, and flap reconstruction
may be required.157
Minor Keloids (Red, Raised)
No uniformly successful treatment for keloid scar
exists. Excision and primary closure invariably result
in recurrence. Therefore, additional therapy is

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Dr.Mustafa D.
 image...

11 • W O U N D HEALING: REPAIR BIOLOGY AND W O U N D AND SCAR TREATMENT 229

Scar

Classification

I I 1
Immature hypertrophic Linear hypertrophic Minor keloid Major keloid Widespread burn
(red, slightly raised) (red/raised, itchy) (red, raised) -high risk- hypertrophic scar
(dark/raised) (red, raised)

If patient concerned or Silicone gel sheeting (2 months)

high risk for excessive
scar: tape or silicone
Initial gel sheeting/ointment Steroid injections 2.5-20 mg/mL (face); 20-40 mg/mL (body); Burn
management repeat monthly as needed specialty
Progress to treatment as unit
for hypertrophic scar
if erythema persists Localized pressure therapy if possible
more than 1 month Duration 3-12 months

Pressure
therapy Specific wavelength laser therapy Pressure
garments and/or
silicone gel
Secondary Surgery with adjunctive silicone gel sheeting sheeting
management (duration 2 months) (6-12 months)

Unit specializing in scar therapy

Combination/monotherapy—
Primarily: Steroids, silicones, pressure therapy, surgery/grafting
Occasionally: Cryotherapy, radiotherapy, laser, other therapies

FIGURE 1 1 - 1 0 . Scar management algorithm. (From Mustoe TA, Cooter RD, Cold MH, et al: International clinical
recommendations on scar management. Plast Reconstr Surg 2002; 110:560-571; with permission.)

necessary, and its efficacy depends on the timing of
the patient's presentation. Steroid injection directly
into the keloid has the most benefit early in the keloid
course.171 Steroid has been shown to decrease colla-
gen gene expression. 121,172 Mixed with 2% plain
lidocaine in a 50:50 ratio, triamcinolone acetonide,
10 mg/mL, is commonly used initially; if no response
occurs, 40 mg/mL concentration is attempted. Sili-
cone gel sheeting should be used concurrently.
Patients presenting with mature keloid lesions of
months to years in duration that are slowly changing
respond poorly to steroid injection and silicone sheet-
ing. Surgical excision with adjuvant therapy includ-
ing intralesional steroids,173,174 silicone sheeting,167
and pressure therapy 175 is a reasonable treatment
alternative. Careful follow-up is necessary to prevent
recurrence. A short course of low-dose radiation
therapy to the keloid excision site immediately after
excision has been shown to reduce the rate of
recurrence. 176
Major Keloids (Dark, Raised]
Major keloids are difficult to treat effectively, and many
are resistant to any treatment. Surgical therapy with
all adjunctive therapies described before may still fail
and result in recurrence. Radiation therapy is gener-
ally used in this group, provided the patient is not
young and accepts the possible risk of late cancer for-
mation. Before surgery is performed with postopera-
tive adjuvant therapy, patients should be counseled
about the high rate of recurrence with the risk that
the next keloid will be larger and more difficult to
control.
Newer treatment modalities, such as intralesional
injection of interferons (alfa, beta, and gamma), 5-
fluorouracil, and bleomycin, may be useful in the

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Dr.Mustafa D.
230 I • GENERAL PRINCIPLES
future. These act by decreasing inflammation and col-
lagen synthesis; however, their mechanisms of action
remain under investigation. Other novel strategies
include interference with profibrotic cytokine func-
tion (e.g., TGF-P) and collagen synthesis at the wound
site. As recommended by the International Advisory
Panel on Scar Management, these patients may best
be treated by clinicians with special interest in keloid
treatment. 157
IMPACT OF SCAR ON PLASTIC
SURGERY
Besides hypertrophic scarring and keloid formation
in the skin, scar affects every aspect of plastic surgery.
Scar and fibrosis are the outcome after tissue repair
and, when excessive, lead to clinical disease. For
example, fibrosis of joint capsules leads to contrac-
ture, which can be debilitating. Anastomotic fibrosis
of free jejunal flaps to the esophagus or pharynx leads
to lumen obstruction. Breast implant capsules are the
normal fibrotic response to injury, which can be exces-
sive and develop into capsular contracture. Nerve repair
sites with excess fibrosis commonly develop neuro-
mas and functional repair failure. Scarring at tendon
repair sites restricts motion. Dupuytren disease is a
fibroproliferative disorder that involves the palmar
fascia and the deep dermis. Each of these excessive
scarring conditions leads to morbidity of the patient,
which can require further surgical treatment.
A great deal of research is focused on development
of treatment strategies to reduce or to prevent scar-
ring. Prompted by fetal wound healing observations,
investigators initially analyzed the anti-scarring effect
of anti-TGF-p strategies. Treatment with neutralizing
antibody to TGF-p decreased the inflammatory
response and reduced scar formation in experimen-
tal postnatal rodent wounds. 177 ' 179 In a rabbit flexor
tendon repair model, neutralization of T G F - p l
reduced adhesions and improved postoperative range
of motion. 180 However, not all experimental reports
are in agreement with respect to TGF-P. In a rodent
skin w o u n d model, addition of TGF-p3 reduced
scar 181 ; but TGF-p3 addition did not reduce scar when
other investigators tested it in a rabbit ear w o u n d
model. 182 More evidence that TGF-p-related strategies
may be successful is provided by a study showing that
exogenous addition to wounds of fibromodulin, a TGF-
p modulator, reduces scar.183 Clearly, more studies are
needed, and because of the redundancy of action
a m o n g growth factors, TGF-P is likely not to be the
only growth factor targeted to reduce h u m a n scar and
fibrosis.
Other approaches to reduce scarring involve reduc-
tion of inflammation and collagen synthesis. Because
one of the hallmarks of scarless fetal repair is the
lack of acute inflammation, cytokines that reduce
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Dr.Mustafa D.
inflammation have been exogenously added to adult
wounds to reduce scarring. The most promising
report to date added an adenoviral vector, which over-
expresses interleukin-10, to adult mouse wounds.
Interleukin-10 treatment decreased inflammation and
induced scarless healing. 184 This exciting finding holds
great promise to enhance the quality of repair. These
initial reports are likely to be the first of many that
describe scar reduction techniques, which may trans-
late into useful clinical treatments.
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76. Kierney PC, Engrav LH, Isik FF, et al: Results of 268 pressure
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78. Margolis DJ, Cohen JH: Management of chronic venous leg
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11 • WOUND HEALING: REP>
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136. Greer SE, Longakcr MT, Margiotta M, et al: The use of subat-
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137. Fabian TS, Kaufman HJ, Lett ED, et al: The evaluation of
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138. Falanga V: Care of venous leg ulcers. Ostomy Wound Manage
1999;45(suppl):33S-43S, quiz 44S-45S.
139. Falanga V, Sabolinski M: A bilayercd living skin construct
(APLIGRAF) accelerates complete closure of hard-to-heal
venous ulcers. Wound Repair Regen 1999;7:201-207.
140. Schonfeld WH, Villa KF, Fastenau JM, et al: An economic
assessment of Apligraf (Graftskin) for the treatment of hard-
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141. Veves A, Falanga V, Armstrong DG, Sabolinski ML: Graftskin,
a human skin equivalent, is effective in the management of
noninfected neuropathic diabetic foot ulcers: a prospective
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Foot Ulcer Study. Diabetes Care 2001;24:290-295.
142. Greenhalgh DG, Sprugel KH, Murray MJ, Ross R: PDGF and
FGFstimulate wound healing in the genetically diabetic mouse.
Am J Pathol 1990;136:1235-1246.
143. Slavin J, Nash JR, Kingsnorth AN: Effect of transforminggrowth
factor beta and basic fibroblast growth factor on steroid-
impaired healing intestinal wounds. Br J Surg 1992;79:69-72.
144. Richard JL, Parer RC, Daures JP, et al: Effect of topical basic
fibroblast growth factor on the healing of chronic diabetic
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145. Jones SC, Curtsinger LJ, Whalen JD,et al: Effect of topical recom-
binant TGF-beta on healing of partial thickness injuries. JSurg
Res 1991;51:344-352.
146. Bullen EC, Longaker MT, Updike DL, et al: Tissue inhibitor of
metalloproteinases-1 is decreased and activated gelatinases are
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240.
 image...

COLOR PLATE 1 1 - 1 . Fetal rat skin wound made at gestational age 16.5 days (term = 21 days), stained with hema-
toxylin and eosin. The hair follicle pattern is normal, and there is no dermal collagen scar formation . Black arrows indi-
cate India ink tattoo made at the time of wounding to locate the scarless wound. A and C, Healed wounds harvested
at 72 hours (xlOO). The epidermal appendage (developing hair follicles) pattern shows numerous appendages in the
healed wound. B and D, Magnified views of the same wounds show epidermal appendages (open arrows) within the
wound site (x200). No inflammatory infiltrate is present. (Modified from Beanes SR, Hu FY, Soo C, et al: Confocal micro-
scopic analysis of scarless repair in the fetal rat: defining the transition. Plast Reconstr Surg 2002 ; 109:160-170.)

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Dr.Mustafa D.
age...
234 I • GENERAL PRINCIPLES
147. Yager DR,Nwomeh BC: The proteolytic environment of chronic
wounds. Wound Repair Regcn 1999;7:433-441.
148. Robson MC, Hill DP, Smith PD, et al: Sequential cytokine
therapy for pressure ulcers: clinical and mechanistic response.
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149. Steed DL: Clinical evaluation of recombinant human platelet-
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150. Yao F, Eriksson E: Gene therapy in wound repair and regen-
eration. Wound Repair Regen 2000;8:443-451.
151. Davidson JM, KriegT, Eming SA: Particle-mediated gene trans-
fer in wound healing. Wound Repair Regcn 2000;8:452-459.
152. Taub PJ, Marmur JD, Zhang WX, et al: Locally administered
vascular endothelial growth factor cDNA increases survival
of ischemic experimental skin flaps. Plast Reconstr Surg
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153. Sun L, Xu L, Chang H, et al: Transaction with aFGF cDNA
improves wound healing. J Invest Dermatol 1997; 108:313-318.
154. Benn SI, Whitsitt JS, Broadley KN, et al: Particle-mediated
gene transfer with transforming growth factor-beta 1 cDNAs
enhanceswound repair in rat skin. J Clin Invest 1996;98:2894-
2902.
155. Eming SA, Whitsitt JS, He L, et al: Particle-mediated gene
transfer of PDGF isoforms promotes wound repair. I Invest
Dermatol 1999;112:297-302.
156. Margolis DJ, Crombleholmc T, Herlyn M: Clinical protocol:
phase I trial to evaluate the safety of H5.020CMV.PDGF-B for
the treatment of a diabetic insensate foot ulcer. Wound Repair
Regen 2000;8:480-493.
157. Mustoe TA, Cooter RD, Gold MH, et al: International clinical
recommendations on scar management. Plast Reconstr Surg
2002;110:560-571.
158. Poston ): The use of silicone gel sheeting in the management
of hypertrophic and keloid scars. J Wound Care 2000;9:10-16.
159. Wong TW, Chiu HC, Chang CH, et al: Silicone cream occlu-
sive dressing—a novel noninvasive regimen in the treatment
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160. Sawada Y, Sone K: Hydration and occlusion treatment for hyper-
trophic scars and keloids. Br J Plast Surg 1992;45:599-603.
161. BorgognoniL: Biological effects of siliconcgelsheeting. Wound
Repair Regen 2002;10:118-121.
162. Sawada Y, Sone K: Treatment of scars and keloids with a cream
containing silicone oil. Br] Plast Surg 1990;43:683-688.
163. Chowdri NA, Masarat M, Mattoo A, Darzi MA: Keloids and
hypertrophic scars: results with intraoperative and serial post-
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1999;69:655-659.
164. Lupton JR, Alstcr TS: Laser scar revision. Dermatol Clin
2002;20:55-65.
165. AlsterT: Laser scar revision: comparison study of 585-nm pulsed
dye laser with and without intralesional corticosteroids. Der-
matol Surg 2003;29:25-29.
166. Alster TS, West TB: Treatment of scars: a review. Ann Plast
Surg 1997;39:418-432.
167. Lee SM, Ngim CK, Chan YY, Ho Mj: A comparison of Sil-K
and Epiderm in scar management. Burns 1996;22:483-487.
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168. AlsterTS.NanniCA: Pulsed dye lascrtreatmentof hypertrophic
burn scars. Plast Reconstr Surg 1998;102:2190-2195.
169. Nouri K, Jimenez GP, Harrison-Balestra C, Elgart GW: 585-
nm pulsed dye laser in the treatment of surgical scars starting
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discussion 73.
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171. Maguire HC: Treatment of keloids with triamcinolone
acctonide injected intralesionally. JAMA 1965;192:325-327.
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589.
173. Griffith BH, Monroe CW, McKinney P: A follow-up study on
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Reconstr Surg 1970;46:145-150.
174. Minkowitz F: Regression of massive keloid following partial
excision and postoperative intralesional administration of tri-
amcinolone. Br J Plast Surg 1967;20:432-435.
175. Palmicri B, Gozzi G, Palmieri G: Vitamin E added silicone gel
sheets for treatment of hypertrophic scars and keloids. Int J
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176. Klumpar DI, Murray JC, Anscher M: Keloids treated with exci-
sion followed by radiation therapy. J Am Acad Dermatol
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spectral nature of fetal and adult wound repair. Plast Recon-
str Surg 1996;97:854-860.
178. Shah M, Foreman DM, Ferguson MW: Control of scarring in
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179. Shah M, Foreman DM, Ferguson MW: Neutralisingantibody
to TGF-beta 1,2 reduces cutaneous scarring in adult rodents.
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180. Chang J, Thunder R, Most D, et al: Studies in flexor tendon
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2000;105:148-155.
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TGF-beta 1 and TGF-beta 2 or exogenous addition of TGF-
beta 3 to cutaneous rat wounds reduces scarring. J Cell
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182. Wu L,XiaYP, Roth SI,etal: Transforminggrowth factor-betal
fails to stimulate wound healing and impairs its signal trans-
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ulator, promotes scarless fetal repair. Surg Forum 2001 ;52:578-
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184. Gordon AD, Karmacharya J, Herlyn M, Crombleholmc TM:
Scarless wound healing induced by adenoviral-mcdiatcd
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569.
image...
CHAPTER
12•
Scar Revision
Nicholas Parkhouse, DM, MCh, FRCS • Tania C. S. Cubison, FRCS
• M. Dalvi Humzah, MBBS, FRCS, MBA
DEFINITIONS
AESTHETIC DESCRIPTION OF SCARS
MEDICAL DESCRIPTION OF SCARS
SCAR ASSESSMENT
REASONS FOR SCAR REVISION
EVALUATION
Preconsultation Preparation
History
Examination
The general principles of plastic surgery, as described
by many authors including Gillies and Millard,1,2 are
absolutely fundamental to the practice of scar revi-
sion, and many of the concepts that are referred to
in this chapter are equally applicable to other areas of
the specialty. The complete care of a patient with a
complex scarring problem, however, requires such
attention to these principles that specific considera-
tion is warranted.
Gillies and Millard1 initially published 16 princi-
ples of plastic surgery (Table 12-1); these were later
extended to 33, 2 then condensed by Millard into the
plastic surgeon's creed: Know the ideal beautiful
normal. Diagnose what is present; what is diseased,
destroyed, displaced, or distorted; and what is in excess.
Then, guided by the normal in your mind's eye, use
what you have to make what you want—and when pos-
sible go for even better than what would have been. A
successful outcome of scar revision surgery reflects the
matching of the patient's hopes and expectations with
the reality of what is technically achievable.
Scar revision is a commonly requested procedure
that is performed frequently by the majority of plastic
surgeons. The holistic approach to the patient is para-
mount in scar revision. The preoperative parts of the
treatment pathway are so fundamental to its success
that these issues are covered in some detail. Each patient
is individual, and it is inappropriate simply to select a
standard operation. Scar revision can be a complex
process that requires careful assessment, technical
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
DISCUSSION AND ISSUES OF CONSENT
The Unsatisfactory Result from Surgical Scar
Revision
Consent
TREATMENT
Staging
Nonsurgical Methods
Surgical Methods
expertise, and recognition of the underlying psy-
chosocial issues if a satisfactory outcome is to be
achieved.
DEFINITIONS
A scar can be defined theoretically in terms such as
those in the Short Oxford English Dictionary:
The trace of a healed wound, sore or burn. A fault or blemish
remaining as a trace of some former condition or resulting
from some particular cause.
A patient might consider it more as a visible stigma
that acts as a continual reminder of its cause, attracts
attention, and generates self-consciousness. In
etiopathologic medical terminology, a scar is"nonre-
generative wound healing" (Table 12-2). A preferred
scar is one that has matured rapidly without con-
traction or increase in width or formation of more
collagen than is necessary for its strength. On histo-
logic examination, a scar has altered dermal architec-
ture including the presence of cells such as the
myofibroblast.3
Even experimental "scarless" healing can result in
a disfigurement. In fetal animal experiments, the
healed area may not demonstrate the fibroblastic activ-
ity associated with normal scar formation but may
leave a linear deformity devoid of normal skin adnexal
structures. 4,5
235
 •

236 I • GENERAL PRINCIPLES

TABLE 12-1 • THE PRINCIPLES OF PLASTIC with common use of nicknames such as scarface. This
SURGERY can be distressing and can be an indication for
revision in a young patient.
Plastic surgery is a constant battle between blood Branding has been used in many cultures and his-
supply and beauty. torical times to identify the individual, especially the
Observation is the basis of surgical diagnosis. captive or slave; however, it is interesting that this prac-
Diagnose before you treat. tice has now been introduced as a modern form of
Make a plan and a pattern for this plan.
Make a record—sketches and photographs.
body art akin to tattooing. The prevalence of keloid
The lifeboat—another flap or skin graft. tendency in some racial groups forms part of their
A good style will get you through—dexterity and tribal culture, for example, the decorative forehead
gentleness. keloids of the Shilluk king from southern Sudan and
Replace what is normal in normal position and retain it the chest scarring of the Nuba tribe. 6
there.
Treat the primary defect first—borrow from Peter to The process of visual perception is important in
pay Paul only when Peter can afford it. how a scar is perceived. When, for example, a face is
Losses must be replaced in kind. viewed, one's eyes move from specific points in large
Do something positive—start with a landmark or two erratic movements. These points tend to be around
pieces that definitely fit.
the angles and junctions of specific facial features, and
Never throw anything away—a preserved piece may be
used later. these movements give information about shape and
Never let routine methods be your master. spatial relationships. Any unexpected change from
Consult other specialists. what is perceived as a normal facial feature is readily
Speed in surgery consists of not doing the same thing picked up as a visual cue. Therefore, a good scar is one
twice.
The aftercare is as important as the planning. that is perceived as a normal facial fold or contour
Never do today what can honorably be put off till line.7 The aesthetics and acceptability of scars on the
tomorrow—when in doubt, don't. face are related to the anatomic zones. Scars above the
Time, although the plastic surgeon's most trenchant infratemporal line are generally less threatening than
critic, is also his greatest ally. those below this landmark. This is related to the
concept that a mole in the central facial triangle may
From Gillies H.Millard DR:Thc Principles and Art of Plasiic Surgery. Boston,
Little, Brown, 1957. be considered to be a beauty spot, whereas a similar
lesion elsewhere would be a blemish.
An awareness of this important distinction is vital
AESTHETIC DESCRIPTION in the practice of scar revision. An example is the case
OF SCARS of a young man with acne scarring; although a good
surgical result may be possible from a procedure to
A scar is often mentioned as part of the description excise the pits, the resulting facial scar, even in a sat-
of an individual, and the details of scars are requested isfactory cosmetic line, may be reviewed as a mark of
in a passport as identifying features. The presence of violence and as such may prejudice chances of future
a notable scar need not be a negative issue; battle scars employment.
are traditionally worn with pride, and cases in history
and literature are as diverse as Shakespeare, Lawrence
Sterne, and Harry Potter. The umbilicus is another MEDICAL DESCRIPTION
distinctive scar that can cause significant distress to OF SCARS
the patient if it is absent or unusual. The actual scar can be described in medical termi-
Many scars do, however, carry a menacing, violent, nology as mature or immature and the scarring
or sinister impact, implying involvement in a fight or processes as normal or abnormal. "Normal" scarring
violent behavior. This is especially true of young ado- is the final result of the wound healing process and is
lescent and adult men with linear scars in the face. formed by the remodeled collagen after inflammation
Conspicuous scars may generate unwanted labeling and proliferation have abated. A normal scar is flat,
relatively narrow, and slightly paler than the sur-
rounding skin. If this process is abnormal, due to either
TABLE 1 2-2 • ETIOLOGY OF SCARS local factors or genetic tendency, an unfavorable scar
can result.
Surgery All new scars are raised, erythematous, and itchy.
Lacerations A hypertrophic scar is a florid, raised erythematous
Burns
Chronic wounds
lesion that remains within the confines of the origi-
Acne nal scar. It is difficult to define how long a scar should
Steroids take to mature and therefore when a scar is hyper-
trophic rather than immature. 8 Keloid scars, like

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Dr.Mustafa D.
*&WRj < aatfW image...
TABLE 12-3 • PROBLEM SCARS
Restrictive
Anatomic location
Stretched
Hypertrophic
Keloid
Psychological
Social issues
hypertrophic scars, are erythematous and pruritic, but
they behave more like hyperplastic tumors of con-
nective tissue, spreading in the dermis and adjacent
subcutaneous tissues. Keloid fibroblasts manifest a loss
of the normal feedback in the regulation of extra-
cellular matrix production. Age also plays a role;
young adults and children are more commonly affec-
ted. Childhood keloids may undergo rapid develop-
ment at puberty, and children who form hypertrophic
scars and keloids may not form them in later life.8
Hypertrophic and keloid are terms used loosely even
by plastic surgeons, but there are important practical
distinctions. Hypertrophic scars, although red and
lumpy, are normally self-limited and tend to settle with
time and conservative measures. Hypertrophic, lumpy
nodular burn scars are often referred to as and con-
sidered to be keloid but can often be reliably treated
by excision with good results because they are not true
keloid and respond well to intensive management
(Table 12-3).
SCAR ASSESSMENT
There are a large number of subjective and objective
tools for scar assessment, and there is currently no
general agreement on the most appropriate tool or
tools for scar evaluation. The Vancouver Burn Scar
Assessment Scale was published in 1990 and was
designed to assess changes in a scar with maturity and
to evaluate response to treatment (Table 12-4).9 It is
a noninvasive clinical assessment that assigns scores
to pathologic changes on the basis of their deviation
from normal skin. Four components are considered:
pigmentation, vascularity, pliability, and height. There
was good interrater reliability in the initial study.9
Baryza and Baryza10 found that by using a transpar-
ent administration tool to blanch the scar (necessary
to assess pigmentation and vascularity) and to measure
the height while providing an aide-memoire of the
score system, they could improve overall interrater
reliability. It is generally accepted, however, that the
Vancouver scale requires at least three examiners or
"raters" for reliable results to be achieved.3
Other systems for objective description and scoring
of scars exist. Beausang et al11 have described a clini-
cal scar assessment scale that has been successfully
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12 • SCAR REVISION 237
validated compared with histologic findings. This has
the advantage of being applicable to a wide variety of
scars, including surgical scars and nonburn trauma
(Table 12-5 and Fig. 12-1).
A variety of internationally recognized coding
systems can be used to classify scars or lacerations. These
include the Current Procedural Terminology code of
the American Medical Association12; the International
Classification of Disease; and, in the United Kingdom,
OPCS (Office of Population Censuses and Surveys)
codes.13 The MCFONTZL classification is a more
complex system of classification of facial lacerations
that combines anatomic location with a variety of
assessments of severity (Table 12-6). M
A variety of subjective and objective methods of
scar assessment have been reviewed with respect to
reliability (reproducibility) and accuracy (validity). 3
Hypertrophy is quantified by measurement of scar
thickness or volume either clinically or by use of in-
vestigations such as ultrasound examination and
histologic evaluation of biopsy specimens.
TABLE 1 2-4 • THE VANCOUVER BURN SCAR
ASSESSMENT SCALE
Pigmentation
0 Normal: color that closely resembles
the color of the rest of the body
1 Hypopigmentation
2 Hyperpigmentation
Vascularity
0 Normal: color that closely resembles
the color of the rest of the body
1 Pink
2 Red
3 Purple
Pliability
0 Normal
1 Supple: flexible with minimal resistance
2 Yielding: giving way to pressure
3 Firm: inflexible, not easily moved,
resistant to manual pressure
4 Banding: rope-like tissue that
blanches with extension of the scar
5 Contracture: permanent shortening of
the scar producing deformity or
distortion
Height
0 Normal: flat
1 <2mm
2 <5mm
3 >5mm
From Sullivan T, Smith J, Kermode J, ct al: Rating the burn scar. J Burn
GireRehabil 1990;11:256-260.
238 • GENERAL PRINCIPLES

FIGURE 1 2 - 1 . Scar scoring. Two

identical hernia operations result in
different scars. The left scar is
acceptable with a Vancouver score
of 1 and a Beausang score of 7 com-
pared with the right hypertrophic
scar with poor ratings of Vancouver
8 and Beausang 17.

The current standard of histologic assessment Contours can be assessed with optical or mechanical
requires analysis of collagen orientation, which has profilometers, and surface area can be measured with
only recently been possible by use of a computerized three-dimensional computer reconstructions of
method. Objective assessment of color has been made scanned images. Ultrasonography can assess scar
with spectrophotometric methods, and laser Doppler thickness, and a new method, anisotropy, also using
flowmeters have been used to assess vascularity. noninvasive sound waves, can supply information
about tissue stiffness.
These objective methods are still under evaluation
for use in research fields. They remain impractical for
TABLE 12-5 • CLINICAL ASSESSMENT SCORE
routine use in clinical practice.3
Visual analogue scale
Excellent Poor REASONS FOR SCAR REVISION
A Color (compare with surrounding skin) The reasons for scar revision can be functional, aes-
Lighter or darker
Perfect 1 thetic, or psychological, although a complex combi-
Slight mismatch 2 nation of factors has to be addressed in most situations.
Obvious mismatch 3 Patients present with a wide range of scar etiology from
Gross mismatch 4
B
Matte 1
Shiny 2
C Contour TABLE 12-6 • MCFONTZL ASSESSMENT SYSTEM
Flush with surrounding skin 1
Slightly proud/indented 2 A Area MCFONTZL aesthetic unit
Hypertrophic 3 designation
Keloid 4 S Side
D Distortion T Thickness Depth of penetration
None 1 E Extension Branching
Mild 2 R RSTL conformality Directionality (relaxed skin
Moderate 3 tension lines)
Severe 4 I Index laceration Laceration with maximum
continuous skin
E Texture interruption
Normal 1 S Soft tissue defect
Just palpable 2 K Coding Current procedural
Firm 3 terminology code
Hard 4
From Lee RH, Gamble WB, Robertson B, Manson PN: The MCFONTZL
Prom Beausang E, Floyd H, Dunn KW, ct at: A new quantitive scale for classification system for soft-tissue injuries to the face Plast Rcconstr Surg
clinical scar assessment. Plast ReconstrSurg 1998;102:1954-1961. 1999;103:1150-1157.

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 image...
the unsatisfactory surgical scar to the complex burn
reconstruction (see Table 12-2). Scars may be stretched
in width, and the width of visible disfigurement may
be increased by crosshatching due to suture marks.
Scars may be indented or depressed below the level of
the surrounding tissue, creating a contour deformity.
This is especially evident when a scar crosses a con-
vexly curved surface (e.g., the prominence of the chin).
Contracture of a curved scar will result in heaping-
up or pincushioning of the soft tissue within the con-
cavity of the curve. This is also especially obvious on
convex surfaces, and the contour irregularity is most
apparent in oblique light, which casts a shadow in
the depression. The scar may be tethered to deep
fascia or muscle, in which case puckering occurs, with
muscle contraction deepening the visible deformity.
Scars may be discolored for a number of reasons.
Persistent erythema in an otherwise well-healed scar
can be a cause for concern and may be amenable to
nonsurgical treatment. Postinflammatory hyper-
pigmentation is a common accompaniment to skin
injury in large well-defined ethnic populations with
mild skin pigmentation. It is managed conservatively
but should be discussed in detail before any second-
ary surgery. Hypopigmentation may be associated with
dermal injury and is common in patchy mixed-depth
burn injury. Hyperpigmcntation is associated with skin
grafts, and blue-gray discoloration may be associated
with embedded foreign materials such as road dirt
contamination at the time of the injury.
Pain in a scar can be an indication for revision irre-
spective of the appearance of the scar. Itching, pain,
and hypersensitivity are frequently associated with a
persistent hypertrophic or keloid scar. It seems likely
that immature regenerating sprouts of the nonmyeli-
nated C fibers penetrate scar tissue to a variable degree
in the early stages of their maturation. These fibers
produce the neuropeptides substance P and calcitonin
gene-related peptide, which have been shown to be
present in large quantities in painful and hypertrophic
scar tissue.15,16
Focal pain within a scar may be due to a cutaneous
neuroma; this classically produces exquisite tender-
ness associated with reflex withdrawal. Scars over bone
prominences, such as the subcutaneous border of the
tibia, are commonly associated with a deep-seated dis-
comfort when they are pressed or knocked because of
the lack of the normal subcutaneous tissue padding.
A traumatic or unsatisfactory surgical scar often
has significant overlay of psychiatric issues that need
to be carefully taken into account. The injury may have
been related to violent crime, or the operation may
have been part of an unpleasant illness, perhaps with
complications and even poor management.
An unsatisfactory surgical scar, typically the verti-
cal abdominal scar, is a common example of a scar
that is at 90 degrees to the lines of relaxed skin tension.
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12 • SCAR REVISION 239
This scar is always stretched and usually depressed,
tethered, and irregular where it skirts the umbilicus
and may have segmental hypertrophy. The patient's
expectation is of a fine white line, although this can
never be achieved. However, it can be improved by
application of the basic principles of scar revision.
EVALUATION
Preconsultation Preparation
A patient is usually referred by another physician for
a specialist's opinion. Often, poor scars are referred to
by physicians as keloid, although many are only wide
scars with visible stitch marks and no lumpiness. A
formal referral may contain useful historical infor-
mation about the origins of the wound, its manage-
ment, and its effects on the patient. Although it is usual
to take a full history from the patient, there may be
situations when this is inappropriate. The injury may
be difficult for the patient to discuss, and if the details
of the history are not likely to alter the management •
of the resultant scar, there is no requirement to upset
the patient or relatives. This should be considered sen-
sitively before embarking on the initial consultation.
The referral may also provide an insight into the under-
standing of the realities of scar revision surgery by the
physician, whose discussions with the patient before
the referral may have elevated the patient's expecta-
tions. It is important to maintain a sympathetic and
professional attitude to both the patient and the refer-
ring physician. An unsatisfactory surgical scar may have
been unavoidable because of the exposure required
(e.g., a midline laparotomy scar) or because of com-
plications such as infection.
In the current age of information technology,
many patients have easy access to large volumes of
information, and scientific research is widely covered
in the media. The Internet allows wide-ranging
searches to be performed, and there are many specific
patient-oriented Web sites available. The patient may
present with questions about "scarless" healing and
sheets of printed text about fetal wound research. There
have certainly been great advances in the scientific basis
for wound healing in recent years, but the patient must
be helped to understand that these advances have yet
to be implemented clinically.
Immediately before the consultation, it is helpful
to review the notes and any available photographs.
This helps the surgeon recall the details of the patient's
prior medical care and relevant details of previous con-
sultations and procedures. A good awareness of details
also inspires confidence in the surgeon and develops
a good patient-physician relationship. Allow adequate
time for the consultation, and if this is insufficient or
has to be cut short, it is better to arrange another
meeting rather than to rush this vital process. There
image...

240 • GENERAL PRINCIPLES

TABLE 1 2-7 • FACTORS THAT IMPAIR Examination

WOUND HEALING
The appearance of the scar is carefully considered; this
Intrinsic Factors Extrinsic Factors may be erythematous, pigmented, tattooed, telang-
iectatic (after steroids), widespread, tethered, hyper-
Ischemia Nutritional deficiencies trophic, or keloid. An assessment of scar maturity is
Infection Diabetes mellitus made, considering features such as redness, contour,
Foreign bodies Chronic renal failure lumpiness, tenderness, and painful itching. The scar
Cigarette smoking Steroids may be functionally restrictive because of contracture;
Venous insufficiency Chemotherapeutic agents
Radiation fibrosis
this can limit the range of joint movement and con-
Distant malignancy
Repeated trauma Old age siderably interfere with normal activities. The assess-
Local toxins Liver disease ment of the scar must include palpation for bands of
Cancer Other drugs contracture with different joint positions to fully appre-
Hereditary ciate its functional significance. Contracture can also
distort other anatomic structures, such as the eyelids,
From RamasasIrySS: Chronic problem wounds.Clin Pla$tSurgl998;25:367- causing deformity such as ectropion or asymmetry of
396. the features. The scar should be analyzed in terms of
its anatomic location, especially in relation to cosmetic
units and skin lines and within the context of other
scars where appropriate.
is no place for indirect consultation in scar revision.
The attending surgeon must see the patient in person, Good-quality clinical photographs are an essential
both to develop the patient's trust and to be confident part of the surgery of scarring, and these should be
that the trade-off between the advantages and disad- repeated during the follow-up phase. It is often helpful
vantages of surgical scar revision have been thoroughly to personally take photographs during the consul-
discussed. Although not always essential, it is often tation; this allows the surgeon to see the patient's
helpful to see the patient on more than one occasion response to the camera and provides a different view
before any procedure is undertaken. This is especially of the scar when it is framed in a viewfinder. Contour
important in complex reconstruction cases. deformity and tethering are best shown with oblique
light rather than direct frontal light. It is often useful
to take a series of pictures, varying the light in such
History cases. The appearance of tethered scars alters with
Establish the cause of the scar and the circumstances, muscle contraction, and it is useful to record the appear-
noting any adverse events during the healing process, ance with muscles relaxed and contracted. The patient's
such as infection or wound breakdown (Table 12-7).l7 consent must be obtained for these photographs, and
The age of the scar is vitally important, as are both sur- this should be in the written form if publication or
gical and nonsurgical interventions. Consider the research is planned.
patient's genetic predisposition and reaction to pre-
vious injury. Take into account relevant medical
conditions and medications. DISCUSSION AND ISSUES
It is important to ascertain whose idea the referral OF CONSENT
was, what aspects of the scar are most troublesome, The preoperative consultation is vital to develop a good
and the presence of associated psychological issues understanding of the individual and to ascertain the
(Table 12-8). A scar may be a reminder of a traumatic impact of each aspect of the scarring. The predomi-
incident or an unpleasant illness, and it is important nant problem may be functional, aesthetic, or psy-
to be sympathetic, nonjudgmental, and professional chological. In many patients, all three are equally
throughout. In selected areas, there may need to be a significant. It is often assumed that the problem is the
special sensitivity (e.g., it may be helpful to refer to an appearance alone, but in many patients, the main
episode of self-harm as "the accident"). problem is discomfort and tightness. Take into account
the patient's perception, requirements, and priorities
regarding the scar. As part of the consent process, it
is now more necessary than ever to have a frank and
TABLE 12-8 • WHY WAS THE REFERRAL
open discussion with the patient about the manage-
INITIATED?
ment options. Both surgical and nonsurgical methods
should be considered as well as their respective
Who? Patient, partner, peer group limitations and risks. The patient's reaction to these
What? Scar appearance, function
Why? Underlying psychological issues options helps you to understand his or her inter-
pretation of what the surgery entails.

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Unlike in routine procedures, it is difficult to
prepare standard information sheets for surgical scar
revision. However, not only does a clear handwritten
clinic note act as a good reminder to the surgeon, but
it also is the authors' preference that this be photo-
copied and given to the patient at the end of the con-
sultation. This forms a valuable basis for subsequent
discussions and can be particularly helpful in the event
of an unfavorable result.
Counseling is a vital part of the preoperative
phase, for the patient with unrealistic expectations will
be disappointed even with the best achievable surgi-
cal results. If, after sensitive discussion and repeated
consultation, you believe that no understanding has
been achieved regarding the reality of surgery, the
opportunity should be taken to explain the potential
for the patient's dissatisfaction or disappointment. It
may be preferable, for both surgeon and patient, to
decline to undertake surgery and possibly refer the
patient to a colleague for another opinion (see Chapter
8,Fig.8-l). 18
There may be patients with a problem that would
be improved by surgery but with whom you have not
developed a comfortable relationship. It is inadvisable
to operate on these patients, and they should be referred
to a colleague.
Consider whether you can offer the most appro-
priate surgery for the patient's problem and do not
hesitate to recommend a second opinion or to make
a referral to other clinicians with the appropriate sub-
specialist skill. If you are aware of a technique that is
likely to produce a better result than anything that you
can currently offer, consider developing that particu-
lar skill and reflect on the ways in which this experi-
ence may best be obtained before embarking on the
treatment yourself. In certain circumstances, it may be
additionally reassuring to both patient and surgeon to
arrange a super-specialist referral to an alternative sur-
geon who is a recognized authority in scar revision and
reconstructive surgery to confirm an operative plan,
even when you intend to perform the surgery yourself.
During the course of a career in plastic surgery, there
is usually a significant change in operative case mix.
This maybe due to personal surgical preference or the
interests of other local clinicians. It is important to
recognize this change and acknowledge that certain
previously managed conditions or performed pro-
cedures are no longer commonly encountered and
perhaps refer these patients to a colleague.
The Unsatisfactory Result from
Surgical Scar Revision
If a patient has previously had a scar revision that has
not achieved the desired result, it is important not to
rush into further surgical intervention. Temporize and
allow time for the scar and the patient's emotions to
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12 • SCAR REVISION 241
settle down. It is seldom indicated to undertake early
secondary scar revision, and a second opinion may be
helpful before the surgical plan is finalized. A perceived
poor result is a common problem, and this is funda-
mentally avoidable with good preoperative counsel-
ing to ensure the patient has realistic expectations. In
the secondary revision, a detailed explanation with real-
istic possibilities of improvement must be outlined,
and ensure in planning that it is possible to identify
why the previous surgical revision achieved a subop-
timal result. In the absence of a history of wound infec-
tion followed by dehiscence, it is wise to be cautious
in advising revision by simple excision and suture for
a second time.19
Consent
The conclusion of the consultation and planning
process is obtaining the patient's formal consent to the
surgery. It is in one sense an anachronism that this
process is still referred to as consent because in all cases
of elective surgical scar revision, the procedure is being
requested rather than imposed. Standards are locally
agreed and have been published by the Department
of Health in the United Kingdom.20
Consent is a patient's agreement for a health pro-
fessional to provide care. For the consent to be valid,
the patient must be competent to make the particular
decision, have received sufficient information to make
it, and not be acting under duress.
For significant procedures, it is essential for health
professionals to document clearly both a patient's agree-
ment to the intervention and the discussions that led
up to that agreement. This may be done either through
the use of a consent form (with further detail in the
patient's notes if necessary) or through documenta-
tion in the patient's notes that oral consent has been
given.
The consent process will have at least two stages:
first, the provision of information, discussion of
options, and initial (oral) decision; and second,
confirmation that the patient still wishes to go ahead.
It is important that both stages of this process be doc-
umented either in the patient's notes or on a consent
form. The health professional carrying out the proce-
dure is ultimately responsible for ensuring that the
patient is genuinely consenting to what is being done.
It is the responsibility of health professionals to ensure
that when they require colleagues to seek consent on
their behalf, the colleague is competent to do so; to
work within their own competence; and not to agree
to perform tasks that exceed that competence.20
TREATMENT
Timing of surgery can be either early or late in terms
of scar maturity. It is traditional to wait for scars to be
242 I • GENERAL PRINCIPLES
mature before performing scar revision to avoid oper-
ating on an actively hypertrophic scar when possible.
This maturation period is typically 18 months, but it
can be shorter or longer and may be difficult to assess.21
Borges19 has emphasized the potential for early revi-
sion of small scars or those that are placed in an un-
satisfactory line and are predictably going to be
hypertrophic or contracted, for if it is planned to excise
the entire scar, it is less important that the scar be
mature. Borges19 suggests that 2 months after injury
is the best time for scar revision in adults and older
children, preferring to wait for at least 6 months in
children younger than 7 years.
The scar should be reviewed at intervals to assess
the way in which the inflammatory phase of healing
is settling. As the inflammation settles, the scar and
surrounding tissues become softer, more mobile,
and supple. Secondary surgery before this stage of
maturation is more likely to be complicated by
excessive bleeding from persistently inflamed skin and
subcutaneous tissue and hampered by stiffness
and lack of tissue mobility, restricting the use of local
flaps.
In general> patients should be advised to wait
for a minimum of 18 months. If there is any doubt
whatsoever about scar maturity, it is always better
to wait longer. If in doubt about scar maturity,
wait.
Patients are usually reasonably keen to have their
surgery as soon as possible, but undue pressure to
proceed with surgery may be a relative contraindica-
tion to early surgery or elective revision in our prac-
tice. With patients with complex problems, there
is rarely any requirement for urgency, and a well-
formulated plan without undue pressure to proceed
is desirable. Although treatment must be tailored to
individual situations, disasters lurk in special arrange-
ments; undue pressure by the patient to proceed with
surgery may be due to an unrealistic expectation of
outcome.
Planning of the operating list is important, and
external factors must be taken into account. It is
necessary to remember that the surgeon is a human
being and requires adequate rest breaks if high-quality
surgery is to be performed throughout a long day. Extra
time should be allowed if a case is likely to be difficult,
if visitors are present, or if a teaching case is planned;
this information may not be available to the booking
clerk, so the planned list should be double-checked
by the surgeon. A rushed operation is likely to achieve
suboptimal results and should be avoided; therefore,
the patient must be rescheduled. If the surgeon and
team are not in optimal health or the environment is
unsuitable, perhaps because of noise or temperature,
this will also result in unnecessary surgical stress,
and the cancellation of the procedure should be
considered.
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Staging
Multiple stages may be used to achieve a desired end-
point with maximal predictability and minimal
associated morbidity and risk of complications. It is
frequently preferable to accept a series of worthwhile
partial improvements in a large scar or area of scar-
ring by a series of safe operations. Serial excision of a
scar may achieve in two or three lesser surgical proce-
dures what might otherwise require a single more major
and hazardous procedure with a less predictable final
result. In the more complex patient who has had mul-
tiple previous operations and has high expectations
of what may be achieved, it is frequently useful to
perform a minor procedure before a more complex
reconstruction, such as cervicofacial expansion or
resurfacing. It is then possible to see how the patient
responds to a partial improvement, and it allows the
surgeon to get a feel for the individual's tissues. This
may well dictate further recommendations for the sur-
gical plan. Begin with an area of the patient's maximal
concern, ideally where a favorable result is expected.
In certain circumstances, a radical procedure is nec-
essary and desirable. This will normally be performed
in our practice after one or more minor procedures
have been performed. At the planning stage, the likely
need for further operations should be emphasized to
any patient undergoing a radical operation. Major cer-
vicofacial resurfacing with release of scarring distor-
tion is performed before the reconstruction of anatomic
features, such as eyebrows or philtrum. In the major-
ity of cases, it is desirable to separate the resurfacing
of the nose from the resurfacing of the remainder of
the face.
A significant history of keloid scarring or an ethnic
predisposition will influence the choice of revision
procedure. In these cases, it is recommended that a
small operation be performed initially so that the
behavior of both the tissues and the patient can be
established.
Nonsurgical Methods
In general, there will have been a period of conser-
vative treatment before scar revision surgery. Where
postoperative scar control measures are likely to be
important (massage, compression devices, and topical
silicone gel sheet), it is well worth considering a period
of preoperative conservative treatment to establish the
patient's familiarity and compliance with the planned
aftercare measure (Table 12-9).22 This is particularly
valuable in children. This also allows time for the devel-
opment of a therapeutic rapport and establishment
of realistic surgical expectations before committing
to a more complex intervention. The scar may be
improved by these measures, and surgical interven-
tion can occasionally be avoided.
 image...

2 • SCAR REVISION 243

TABLE 12-9 • NONSURGICAL MEASURES TABLE 12-10 • FINE INSTRUMENTS

Massage Mapping pen

Silicone gel or sheeting Sommerlad pen
Vitamin E or A (retinoic acid) Barron knife handle
Pressure garments Fine skin hooks
Herbal extracts [Allium cepa, madecassol) Adson tissue forceps
Steroid injection (triamcinolone) Parkhouse needle holder
Antimitotics (bleomycin, 5-fluorouracil)
Laser (585-nm flashlamp-pumped pulsed dye, carbon
dioxide)
Soft tissue augmentation (bovine or autologous
collagen, fat or fibroblast transfer)
Radiotherapy (keloids)*
Interferon (keloids) Many scars need revision because the edges have
Cryotherapy not been apposed correctly. Accurate skin apposition
Makeup camouflage and eversion should be achieved, with use of fine mat-
tress sutures if necessary. Depending on the size of
'The risks of radiotherapy must be remembered, particularly in proxim- the wound excision, it is commonly necessary to close
ity to the thyroid and breast.
Modified from Su CW, Ali/adeh K, Hoddie A, I.ee RC: The problem scar.
with buried absorbable subdermal sutures and then
Clin Plast Surg 1998;25:451-465; and Chang CW, Ries WR: Nonoperative to appose the skin carefully. Skin apposition can
techniques for scar management and revision. Facial Plast Surg 2001; 17:283- also be achieved with a skin glue such as Dermabond.
288.
Interrupted sutures are recommended because they
can be used to feed in irregular margins of the wound
There is little doubt that the integrated molecular and also allow correct apposition of the wound
approach will have a part to play in the modification edges (Fig. 12-3). If a hematoma develops, it is
of wound healing. However, it seems that for the fore- possible to take out individual sutures as required.
seeable future, the scar will remain a challenge for Dehiscence of wound closed under tension is less likely
surgical revision techniques. with individual sutures, and the Gillies near-far pulley
stitch is recommended. 23 The placement of a tension
suture in the middle of the wound and then of others
Surgical Methods at each end allows redundancy to be worked into the
middle.
There is no substitute for meticulous attention to
detail, atraumatic technique, and use of fine instru- Sutures must be removed at an appropriate time
ments. The authors have found that a fine needle to reduce the risk of permanent suture marks. The
holder with integral scissors and a ratchet has been precise timing is invariably a compromise between
invaluable when many interrupted sutures are needed the site of the wound and the tension with which it
(Table 12-10 and Fig. 12-2). is closed.

~ !

. f

r I .

W£

\J % •M
t -1
>
1 W
FIGURE 1 2 - 2 . Fine instruments. .~ ±~\ ...

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Dr.Mustafa D.
244 I • GENERAL PRINCIPLES

" . - ' : • - ' . ' • ' ; • ' ' • ' . ' ' . ' . • • : ' : : '

j ; : =

Warn

-:

FIGURE 12-3. A Simple

interrupted suture. 6, Inter-
rupted inverted intradermal
suture. C, Near-far pulley
suture.

W O U N D PLATE relocation of these structures to their normal position

It is advisable to use an adjunct to wound support, is more important than the simple revision of the scar,
such as tape (Micropore or Steri-Strips), or an appli- even if this will result in new scarring or the use of
cation such as Dermabond. Local support of the wound flaps or grafts, which might result in a poorer color
produces a stable wound margin (wound plate); this match.1,19
prevents lateral shearing movement between the The landmark may be directly disrupted by the scar,
sutured margins, which may be the cause of micro- such as a step deformity in the vermilion border of the
trauma and impaired wound healing. The use of tape lip or the eyebrow or malposition of the alar base. A
closure also decreases the rate of infection and allows distant scar may also cause a more indirect effect as
an increased rate of wound healing to occur in a semi- a result of contraction, producing distortion such as
permeable moist wound environment.24
Borges19 cites the three scar revision techniques: TABLE 12-11 • IMPROVEMENTS IN AN
fusiform scar revision, Z-plasty scar revision, and W- UNSATISFACTORY SCAR
plasty scar revision (Fig. 12-4). These and similar pro-
cedures are described by Achauer25 as alphabet surgery Improvement of the direction of the scar
(Table 12-11). These techniques improve the direction Division of the scar into smaller components
in relation to the relaxed skin tension lines and reduce Leveling effect
the uninterrupted straight length into smaller seg- Improvements in the local condition of the wound
men ts, which have less contractile effect and thus relieve (compared with the original)
Halving in depth
the bowstring effect of the longer scar. Halving in surface
Camouflaging by alternating small scars with normal
RESTORATION OF unscarred tissue
Creation of accordion-like elasticity
ANATOMIC LANDMARKS
If an eyebrow, vermilion border, or other anatomic From Borges AF: Timing of scar revision techniques. Clin Plast Surg
landmark has been displaced by the initial injury, the 1990;17:71-76.

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Dr.Mustafa D.
 image...
RSTL
dHrtt-i
RSTL
/
1
I sion can also be used to provide more tissue for advance-
I ment or local flap coverage; however, it has a higher
I complication rate. There are certain sites where tissue
I expansion is the method of choice. The prime example
I &
B and serial excision make use of similar biomechanical
jsryKy'^
r RSTL
FIGURE 12-4. A, Fusiform excision in resting skin
tension line (RSTL). B, Z-plasty for scars at an acute angle
to the RSTL. C, Standard W-plasty for scars more than
60 degrees to the RSTL.
ectropion of the lower eyelid or eversion of the lower
lip. The restoration of these landmarks is achieved by
carefully tailored application of a range of techniques
often used in combination.
DIRECT EXCISION
When possible, completely remove the scar tissue and
close the wound primarily by advancement of the adja-
cent normal tissue. This may require undermining,
and it is frequently appropriate to undermine asym-
metrically to advance one side of the wound more than
the other. The final scar should be aligned with the
resting skin tension lines.
Fusiform scar revision is indicated where the orig-
inal scar follows the resting skin tension line, whether
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Dr.Mustafa D.
2 • SCAR REVISION 245
this is for an unsatisfactory surgical scar (including
marginal scars) or lacerations.lv,2li
In the management of keloid scarring, the tech-
niques of intralesional and extralesional incision are
used, and these are discussed elsewhere.27 Presuturing
may be used to pre-expand adjacent skin before the
excision of large areas of scarring. Presuturing may be
performed the night before surgery, perioperatively,
or on a delayed basis 2 weeks before the main proce-
dure is planned.28,29 Although presuturing or intra-
operative tissue expansion is effective, there has been
experimental evidence to suggest that undermining is
just as effective a method and produces similar
advancement.30"32
SERIAL EXCISION AND
TISSUE EXPANSION
Serial excision is recommended when a scar is too large
for a single fusiform excision without excessive tension
on the skin closure (Fig. 12-5). Staged tissue expan-
is burn alopecia of the scalp where a minimum of 30%
of the scalp is intact (Fig. 12-6). Both tissue expansion
properties of the skin (stress relaxation and creep33)
to make greater quantities of normal tissue (Table
12-12). Serial excision requires multiple procedures;
at each procedure, part of the scar is removed, and the
wound is closed primarily after local undermining or
advancement if appropriate. The number of stages is
determined by the local tissue elasticity, and it is impor-
tant not to excise too much tissue at each procedure.
The low complication rate of serial excision makes
it a reliable method of scar revision with minimal
morbidity between stages.34 Immediate intraopera-
tive tissue expansion has been suggested as a way of
TABLE 12-12 • COMPARISON OF SERIAL
EXCISION AND TISSUE
EXPANSION
Serial Excision Tissue Expansion
2 or more stages 2 stages
Low risk High risk
Longer interval Weeks between operations
Minimal care between Significant care, clinic visits
stages
Aggravated discomfort during
expansion
Pain with repeated injections,
weight, and stretching
Risk of infection
Mechanical failure of implant
Bone resorption
246 I • GENERAL PRINCIPLES

FIGURE 1 2-5. A and B, Serial excision of an area of previous split skin graft. C to F, First-stage serial excision of
hypertrophic scar as part of a serial excision plan. Note minimal undermining of the lower edge. The initial distortion
of the nipple settles with time.

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image...

12 • SCAR REVISION 247

FIGURE 12-6. A to C, Tissue expansion of the scalp showing

the considerable deformity that the patient must tolerate
during the expansion phase.

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Dr.Mustafa D.
248 I • GENERAL PRINCIPLES
increasing the area of potential excision and avoiding
the complications of staged tissue expansion. In the
a uthors' experience, this has proved disappointing, and
the main effect may be to increase the extent of under-
mining of the adjacent skin and subcutaneous tissues.
REORIENTATION
Optimal scar placement follows skin tension lines- On
the face, the margins of the cosmetic units in general
follow the lines of relaxed skin tension (Fig. 12-7 and
Table 12-13). 3547 Where the orientation of the scar is
unfavorable, the principle should be to reorient rather
than simply to excise and resuture. Examples include
a bridle scar crossing the alar-facial groove, the verti-
cal scar crossing the transverse line on the forehead,
and a vertical scar on the neck. Reorientation is
achieved by a Z-plasty in the alar-facial groove or neck
and by a W-plasty on the forehead.
There are certain areas on the face where it is difficult
to assess the optimal angle for scar placement, and
these include the labial-mental fold. The changes in
local stress with facial muscle movements result in dif-
ferent creases, and authors vary in their recommen-
dations. In practical terms, it is important to discuss
this with the patient preoperatively and to obtain
consent for a variety of options. In a concept similar
to that of circular excision of a lesion (Fig. 12-8), the
scar should simply be excised and the resulting defect
assessed. It will often become apparent where the
tension lies and if further release or reorientation is
required to achieve the optimal result.
Z-plasty is a simple fundamental technique in
plastic surgery and has a long history with major
modifications and some confusion regarding the first
descriptions of a true Z-plasty (Table 12-14).38 The
TABLE 12-13 • FACIAL LINES
Lines
Relaxed skin Follow the furrows formed
tension when skin is relaxed
lines
Langer Cleavage by puncture wounds 1861
and later circular excision
Cox Cleavage lines with marlinespike 1941
Rubin Lines from facial
"fingerprinting"
Kraissl Normal wrinkles of old age
Straith after contraction of muscles
Bulacio Skin punches
Thacker Circular excision and fusiform
closure
Information modified from Borges AF: Relaxed skin tension lines (RSTL)
versus other skin lines. Plast Reconstr Surg 1984;73:144-150.
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TABLE 1 2 - 1 4 • THE FOUR FUNDAMENTAL
FUNCTIONS OF Z-PLASTY
To lengthen a scar
To break up a straight line
To move tissues from one area to another
To obliterate or create a web or cleft
From Furnas DW; The four fundamental functions of the Z-plasty. Arch
Surg 1968;96:458-463.
Z-piasty is based on geometric principles that, although
clearly elucidated, do not apply in their strict sense in
the relatively elastic tissues of normal skin and less
elastic scar tissue.39'41
The Z-plasty has been developed further and can
now be considered in terms of stereometric, plani-
metric, skew, and multiple flap Z-plasty.42"45 The classic
stereometric Z-plasty is a 60-degree transposed trian-
gular flap.46 The 60-degree Z-plasty has a theoretical
increase in length of 7 3 % (mathematically equivalent
to root 3). 47 In practical use, the Z-plasty angles may
vary according to the placement of the proposed scar.48
The technique of a basic Z-plasty involves limbs of the
contractural diagonal and the transverse diagonal. After
transposition of the flaps, there are two effects: the
contractural diagonal lengthens, and the transverse
diagonal shortens.
In a well-designed Z-plasty, when the scar is excised
and the flaps are incised, the scar release will naturally
result in the flaps transposing themselves into a nearly
predicted position, interdigitating in the areas where
the scar has lengthened. If in any case a Z-plasty has
been poorly planned and the flaps do not sit com-
fortably, it is justified to resuture the flaps in their
original positions and to reconsider one's position.
In general plastic surgery using normal tissue,
the recommended level for undermining varies with
anatomic region and is related to blood supply. In the
Year face, the appropriate level is just deep to the dermis
including the subdermal plexus; in the limbs and trunk,
1962, the plane between the superficial and deep fascia
1973 is recommended. 49 In scarred tissues, the normal
anatomy of the skin is disrupted and the subdermal
plexus maybe unreliable; it is therefore recommended
to raise thick flaps to ensure adequate blood supply.
There are multiple variations in Z-plasty techniques
1947
(Fig. 12-9).50 The planimetric Z is a useful technique
1951 for correcting scars on plane surfaces. It avoids eleva-
1961 tions or depressions with a pure elongation of skin
1961, in the direction of the scar. A smooth scar line is pro-
1974 duced with the possibility of elimination of scarred
1976 skin areas due to scar excision. The angles of a plani-
metric Z tend to be at 75 degrees to the scar line;
the planimetric Z-plasty is 28% more efficacious in
producing lengthening of the scar.43
image...

12 • SCAR REVISION 249

C D
FIGURE 1 2 - 7 . A, Relaxed skin tension lines. 6, Schematic representation of those segments of Langer's cleavage
lines on an adult that flagrantly depart from the direction of resting skin tension lines. C, Bulacio's skin tension lines
and areas with tension uniformly distributed are depicted with small circles. 0, Cox's anti-RSTL cleavage lines, which
he determined by making skin punctures with a marlinespike. Continued

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Dr.Mustafa D.
250 I • GENERAL PRINCIPLES

• «

\ V
N
\
\
\
\
\ \ \N

\
N \ \

o
\ I
I-"" V

FIGURE 12-7, cont'd. E, Segments of Rubin's composite

'V s diagram of facial lines, which he attributed to the contraction
S s of facial muscles. F, Straith's lines closely follow the relaxed skin
tension lines, except at the glabella, columella, and mentolabial
fold. G, Anti-RSTL segments of Kraissl's lines, which he drew
falling on the wrinkle lines already present on the face and on
those that appeared after contraction of the muscles of facial
expression. (From Borges AF: Relaxed skin tension lines (RSTL]
G versus other skin lines. Plast Reconstr Surg 1984;73:144-150.)

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image...

12 • SCAR REVISION 251

-/ r \
OOQ
FIGURE 12-8. Circular excision results in an oval defect,
the direction of which is determined by local skin tension.

The skew Z-plasty is a technique in which the tip

angles of the two triangular flaps are unequal. This
technique is useful when local tissues prevent a sym-
metric Z-plasty. This allows topographic features of
unequal size to be shifted into relatively normal
anatomic position. This transposition flap causes dis-
tortion of the narrow flap with a tendency to form
a standing cone (dog-ear) with less disruption of the
surrounding areas.40
Multiple Z-plasties may be considered as a number
of Z-plasties in series or multiple flap Z-plasties (Figs.
12-10 and 12-11). The extension of a simple Z-plasty
in series has the advantage of producing a length
increase similar to a single Z-plasty but with less short-
ening of the transverse diagonals. One problem with
this technique is that the flaps do not always interdig-
itate easily. The multiple flap Z-plasties are numerous,
ranging from double opposing Z-plasties to between
four and six Z-plasties (Figs. 12-12 and 12-13). Vari-
ations of these can be used in different situations (Table
12-15).44 An elegant example of combinations of Z-
plasty and V-Y advancement is that of the jumping
man procedure described by Mustards to deal with
epicanthal folds.51

TABLE 12-15 • INDICATIONS FOR THE

Z-PLASTY IN LINEAR FACIAL
SCARS

Antitension line scars on eyelids, lips, and nasolabial

folds
Antitension line scars on forehead, temples, cheeks,
nose, and chin that run at an angle of less than 35
degrees to the relaxed skin tension lines
Very depressed antitension line scars anywhere and of
any length
Small antitension line scars FIGURE 1 2 - 9 . A to D, Classic stereometric 60-degree
Areas with multiple scarring Z-plasty. Continued

From Borgcs AF: Timing of scar revision techniques. Clin Plast Surg
1990;17:71-76.

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TeWttf<S0CM# image...

252 • GENERAL PRINCIPLES

A
/i
/ !
I
I

4.—,«1

••&HHH?-*.

! /
I/

FIGURE 1 2 - 9 , cont'd. £ to C, Planimetric Z-plasty.

W-
FIGURE 1 2 - 1 0 . Four-flap Z-plasty to release the first
web space.

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Dr.Mustafa D.
image...

12 • SCAR REVISION 253

arf*F**
^*<L» c

5<
'
B
I
I
c
^ '
rf«**
'<& D

•&HH&
A B
FIGURE 1 2 - 1 1 . A to C. Illustration of four-flap Z-plasty technique.

1
*>\ v 'T
_ •

FIGURE 1 2-1 2. >4 to E, Fusiform scar excision and double Z-

plasty to release the palm. Note the considerable elongation pro-
vided by simply removing the scar tissue before the Z-plasty is
cut.

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254 • GENERAL PRINCIPLES

D E
FIGURE 1 2-1 3. A to E, Multiple Z-plasties to release a neck web.

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image...
RELEASE
The three-dimensional nature of a scar is such that
both surface contracture and contracture between deep
and superficial layers can occur. This results in bands
of tight tissue on the surface and tethering of the skin
to underlying structures. Release of the superficial
surface scar results in a defect that can be filled with
either local flaps or grafts. Release of deep tethering
will often require the interposition of other tissue
to augment the volume of subcutaneous tissue or to
prevent retethering.
A disadvantage with the Z-plasty and in particular
the multiple Z-plasty is that both flaps require under-
mining to allow transposition. This may compromise
the blood supply to these flaps, particularly in those
areas that have been previously scarred. Where there
is a linear scar contracture, this may well be released
by a Y to V principle (Figs. 12-14and 12-15). When it
is carried out as a running YV-plasty, this allows a linear
scar to be lengthened without any flap transposition
FIGURE 1 2 - 1 4 . A and B, Y to V advancement
to release a presternal scar contracture forming a
webbed cleavage. B
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12 • SCAR REVISION 255
and compromise of blood supply. This technique
requires meticulous preoperative planning to ensure
that the YV-plasty is carried out properly. To lengthen
the scar tissue, the triangular flap of the Y is pushed
into the stem of the Y, forming a V. The incision is
carried through the full thickness of the scar into the
soft tissue beneath the scar. No undermining of the
flap tips is carried out, but these are simply pushed
into the defect (Fig. 12-16).
Scars in general may need releasing because of dis-
torting tension within the skin or tethering to deep
tissues. Where deep tethering is the problem, the solu -
tion is to release the scar and reposition or augment
the soft tissue. A classic example is the tethered tra-
cheostomy scar revised by use of platysmal turnover
flaps (Figs. 12-17 and 12-18). Areas of soft tissue loss
from deep burns, infection, or ischemic necrosis may
also result in severely tethered wounds. In blunt
trauma, there may be a fat fracture without a skin lac-
eration; this results in hematoma formation, and with
resolution the scar forms, pulling the dermis down
256 I • GENERAL PRINCIPLES

FIGURE 1 2 - 1 5 . A to D, Combination of the basic techniques—fusiform excision and Z-plasty in the axilla and Y-V
advancement in the cubital fossa.

FIGURE 1 2-16. A to C, Illustration of Y to V advance-

ment technique.

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image...

12 • SCAR REVISION 257

. '
A B
FIGURE 1 2 - 1 7 . A and B, Tracheostomy scar revision by use of a transposition flap of platysma with a Z-plasty ol
overlying skin.

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258 I • GENERAL PRINCIPLES
FIGURE 1 2 - 1 8 . A to D, Illustration of tracheostomy scar revision technique by use of a transposition flap of platysma
with a Z-plasty of overlying skin.
and resulting in a cosmetic defect although no actual
tissue loss has occurred. A layered closure by the vest-
over-pants technique will bring in tissue and help
prevent retethering.
Acne is a special problem with considerable psy-
chological overlay, but the general principles of partial
improvements and repeated treatments apply. Acne
presents a problem of multiple punched out "ice pick"
scars and general irregularity of the surface. In the mild
to moderate surface irregularity, either carbon dioxide
laser resurfacing or chemical peeling may be of benefit;
however, formal excision is usually required. Direct
excision of facial pits is extremely effective, and one
or two pits are excised initially to assess the result. Focal
excision is carried out with vertically incised edges,
releasing deep tethering, and very fine sutures to close
the wounds. Where there is a cluster of deep scars, it
may be worth excising a group together. A cluster of
focal scars can be treated as a single scar; however, the
implication of placing a new linear scar on the face
of a young man must be remembered. This is very
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Dr.Mustafa D.
different in women, in whom scars are looked on with
sympathy rather than suspicion.
CAMOUFLAGE
There are many techniques available for scar
camouflage; surgically, a basic principle is irregular-
ization of the scar. W-plasty52 has shorter limbs com-
pared with Z-plasty and produces no overall change
in length. Its use is recommended in specific areas
where scars are oriented perpendicular to resting skin
tension lines. It produces a regularly irregular scar with
removal of some normal tissue (Fig. 12-19A).
Scars that are separated from the resting skin tension
lines by between 35 and 60 degrees are improved by
the stairs W-plasty. Scars inclined more than 60
degrees are best corrected by regular W-plasty.26 The
standard W-plasty is an effective technique for revi-
sion of an unsatisfactory midline abdominal scar.19
Geometric broken-line closure is a more refined
technique of scar irregularization, producing an
 image...
^V
^r^^^f^r^H
B phase (Fig. 12-20). Once matured, the area is repre-
FIGURE 1 2 - 1 9 . A, Illustration of W-plasty technique.
B, Geometric broken-line closure technique.
irregularly irregular scar with a random design in the
final scar (Fig. 12-196). This procedure requires
meticulous planning and execution; it is technically
difficult and may require the mapping of a design on
paper before surgery. The concept of geometric
broken-line closure is also important for insetting full-
thickness grafts for skin resurfacing.
RESURFACING
Resurfacing of sheet scarring should be considered
when it is necessary to produce smooth textural form
to replace the unattractive, tight, and uneven hyper-
trophic scarring in certain anatomic regions (e.g., the
dorsum of the hand and face). In general, resurfacing
*\
H^^^^^
FIGURE 1 2 - 2 0 . Lizard skin effect of meshed
split skin graft on the hands.
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Dr.Mustafa D.
12 • SCAR REVISION 259
should be planned in aesthetic units, although it may
not be ideal in facial areas to resurface a whole unit if
this would involve removing undamaged tissue, for
example, scarring involving part of a cheek around
the jaw line. It is better to use the principle of
geometric broken-line closure and to limit the area of
excision to the damaged area only.
Resurfacing may use autologous tissue or synthetic
alternatives. The autologous tissues may take the form
of a thick split skin graft or full-thickness skin graft.**.
Synthetic materials represent a new technology that
is currently developing. At present, Integra is the only-
applicable commercially available product.
Reconstruction of certain areas with use of thin
split skin grafts or mesh grafts may result in a sheet
of scar tissue that is hypertrophic or contracted or,
worse still, has the appearance of lizard skin because
of the previous meshing to enable healing in the acute
sented by a sheet of hypertrophy and uneven scar-
ring. This can be quite distressing to the patients.
Priority areas where meshed skin grafts are con-
traindicated are the face and the dorsum of the hand,
particularly in female patients. Therefore, it is advis-
able not to mesh skin grafts in these areas, although
it may be necessary owing to shortage of skin and
difficulties in wound healing in the acute phase.
Resurfacing with thick split skin grafts that are not
meshed can be carried out by excision of the scarred
area just below the scar, leaving thin areas of dermis.
This preserves the underlying areolar fascia, particu-
larly overlying tendons and bones, together with the
veins, lymphatics, and sensory nerves in the area. A
thick split skin graft is harvested as a sheet with an
electric or gas-driven dermatome such as the Zimmer
dermatome, which can produce a maximum width
of 4 inches, or by a more traditional Padgett drum
dermatome (Fig. 12-21). In planning the resurfacing,
• ,
^
jf*
•"•i3 BL.*- w^
* H^^K
*-3S*^^ -~*£i..*4v
^B|
BWM *' .~>ra^-'>,_. 3
^^^H
260 I • GENERAL PRINCIPLES
the previously mentioned principles must be consid-
ered, particularly in areas where relaxation and stretch-
ing are critical. Linear scars and scars in the web spaces
are broken up by use of the principles of broken-line
closure or Z-plasty type scars (Fig. 12-22). Immobi-
lization and gentle pressure are required to allow the
skin graft to take, followed by gentle, limited move-
ment after approximately 10 days. During a period of
4 months, the grafts tend to regain a venous pattern
with anatomic creases over corresponding joints. 53
Full-thickness skin graft resurfacing uses similar
principles. A full-thickness skin graft represents an ideal
resurfacing material because it has the characteristics
and quality of normal skin. When it is carefully chosen,
there is a possibility of obtaining a texture and color
match close to uninjured skin. This technique is par-
ticularly useful in facial resurfacing and in recon-
struction around the neck; these two areas lend
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Dr.Mustafa D.
FIGURE 1 2 - 2 1 . Harvest of split
skin graft with a power Zimmer der-
matome.
themselves to full-thickness graft resurfacing with better
definition of certain anatomic areas (e.g., the cervico-
mental region) compared with coverage by flaps.
A potential disadvantage with this technique is that
there is significant donor site morbidity, although this
has uniformly been described by patients in our prac-
tice as "an acceptable price to pay." Pre-expansion
of the donor site has been suggested, but this adds
significantly to the risk of complications, and in
general we have thought it to be undesirable.
Excision of the scar is performed by sharp dissec-
tion, with particular attention paid to excision and
release of subcutaneous fibrosis (Fig. 12-23). Hemo-
stasis is achieved by tumescent infiltration of saline,
bupivacaine 0.25%, and epinephrine 1:100,000 and
by bipolar diathermy. After the pre-planned area of
scar has been excised, the resultant defect is invariably
substantially larger than the scar tissue removed,
FIGURE 12-22. The use of W-
plasty, broken-line technique, to
inset a sheet of Integra.
 image...

12 • SCAR REVISION 261

...

.--.- " "

FIGURE 1 2 - 2 3 . Full-thickness skin graft to resurface the neck. A, Preoperative photograph showing considerable
limitation of upward gaze due to neck contracture. B, Harvesting of full-thickness skin from the flank; note the fenes-
trations have been cut before harvesting. C, Placement of quilting sutures by use of fenestrations. D, The graft in posi-
tion; note the use of zigzag inset. Continued

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262 I • GENERAL PRINCIPLES

FIGURE 1 2 - 2 3 , cont'd. E, Postoperative dressing incorporating a splint. F to /, Postoperative result. The

neck collar is important to maintain the extension in the immediate postoperative phase.

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Ve^ftf<afl(S»W image...
making preoperative templating unhelpful. When the
excision and release are complete, the size of the defect
is measured. The skin graft donor site is marked out
10% larger than the measured dimensions, with atten-
tion paid to the orientation of the graft in relation to
the recipient site but without trying to accurately tem-
plate anatomic landmarks (Fig. 12-24). The final
tailoring of the graft is done in situ, and it is rare in
our experience for a graft to be made too large.
Areas to be resurfaced need to be carefully analyzed
to produce a single aesthetic area, with margins placed
as far as possible at aesthetic unit boundaries. The prin-
ciples of geometric broken-line closure may need to
be applied if partial aesthetic units are to be resurfaced
and when marginal scars run perpendicular to the
resting skin tension line (e.g., on the neck). The graft
is further stabilized with quilting sutures and then
immobilized with a bulky dressing. The stability of the
graft may be enhanced by the use of intermaxillary
fixation, close-fitting splints, and a period of sedation,
but this is not always necessary (Fig. 12-25).
The full-thickness donor site can sometimes be
closed primarily, but the defect usually requires a split
skin graft or repair with Integra. It is absolutely essen-
tial that the patient and the family understand the com-
plexity and the care that is required for this procedure
to be successful.54
Synthetic resurfacing involves use of a dermal sub-
stitute. The material currently available is Integra,
which is a bilaminar synthetic sheet composed of a
dermal template of bovine and shark collagen com-
bined with a thin silicone layer. The Integra is applied
after excision of the scarred area, and after a period
of 2 to 3 weeks, fibroblast ingrowth generates a "neo-
dermis," using the collagen template as a regenerative
framework. When the neodermis is stable, the silicone
layer is peeled off, and an ultrathin split skin graft
is harvested and applied on top of the neodermis.
As with full-thickness skin grafts, success requires
meticulous surgical technique and the avoidance of
hematoma and infection.
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12 • SCAR REVISION 263
In all these cases, it is desirable to avoid linear
scarring between the new sheets and unscarred areas;
the principles of Z-plasty and broken-line closure
are helpful to prevent contraction at these points.
Splinting may be necessary to overcome any ten-
dency for contractures to form in the reconstructed
areas.
POSTOPERATIVE CARE AND FOLLOW-UP
The postoperative options for scar care, such as
massage, pressure garments, and silicone gel, have an
established role, although few are of proven benefit.55
The choice and combination of choices in the indi-
vidual patient reflect the specific circumstances;
the character of patient and scar and issues such as
support, activity, and compliance need to be consid-
ered. A regimen of restricted activity or immobiliza-
tion may be imposed to assist in reducing the shearing.
This could simply be tape or glue to support the wound
plate, or a more complex tailored splint or brace could
be required. Other modalities are designed to help the
scar mature or to prevent hypertrophy.
Many straightforward scars can be effectively treated
and a satisfied patient discharged from further care.
Other patients will benefit from multiple corrections
over time and open access to long-term review.
Patients with complex problems become accept-
ing of the reality that they cannot be cured or their
scarring completely eradicated. It may be necessary to
tell such patients that "no more surgery should be done
for the time being." However, it is unhelpful and demor-
alizing to tell a patient with a substantial burden of
disfigurement that "no more can be done" in a final
way. Techniques and treatment modalities evolve over
time and scarring changes with growth and aging, and
many patients find discussion of options at intervals
over the years beneficial. With a wide range of tech-
niques available, it is important to select the appro-
priate technique for the particular problem and the
individual patient.
image...

264 I • GENERAL PRINCIPLES

FIGURE 1 2 - 2 4 . Neck resurfacing with full-thickness graft.

A, Preoperative photograph. B and C, Postoperative photographs.

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Dr.Mustafa D.
 image...

12 • SCAR REVISION 265

FIGURE 1 2 - 2 5 . Full face resurfacing. A, Preoperative photograph showing the contracted split skin graft restrict-
ing the mouth opening. B, Excision of split skin graft scar. C, Application of the sheet of full-thickness skin.
Continued

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
image..

266 I • GENERAL PRINCIPLES

FIGURE 1 2 - 2 5 , cont'd. Otof, Postoperative views showing

improved mouth opening and facial texture.

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
 image...
REFERENCES
1. Gillies H, Millard DR: The Principlesand Art of Plastic Surgery-
Boston, Little, Brown, 1957.
2. Millard DR: The Principilization of Plastic Surgery. Boston, Little,
Brown, 1986.
3. van Zuijlen PP, Angeles AP, Kreis RW, et al: Scar assessment
tools: implications for current research. Plast Reconstr Surg
2002;109:1108-1122.
4. Beancs SR, Hu FY, Soo C, et al: Confocal microscopic analysis
of scarless repair in the fetal rat: defining the transition. Plast
Reconstr Surg 2002;109:160-170.
5. Mackool RJ, Gittes GK, Longaker MT: Scarless healing. The fetal
wound. Clin Plast Surg 1998;25:357-365.
6. Brissett AE, Sherris DA: Scar contractures, hypertrophic scars,
and keloids. Facial Plast Surg 2001;17:263-272.
7. Burget GC, Menick FJ: Aesthetic Reconstruction of the Nose.
St. Louis, Mosby, 1994.
8. Su CW, Alizadeh K, Boddie A, Lee RC: The problem scar. Clin
Plast Surg 1998;25:451-465.
9. Sullivan T, Smith J, Kermode J, et al: Rating the burn scar. J Burn
Care Rchabil 1990;11:256-260.
10. Baryza MJ, Baryza GA: The Vancouver Scar Scale: an adminis-
tration tool and its intcrratcr reliability. J Burn Care Rehabil
1995;16:535-538.
U. Beausang E, Floyd H, Dunn KW, et al: A new quantitivc scale
for clinical scar assessment. Plast Reconstr Surg 1998; 102:1954-
1961.
12. Physicians* Current Procedural Terminology. Chicago, 111,
American Medical Association, 1998.
13. Office of Population Censuses and Surveys: Tabular List of the
Classification of Surgical Operations and Procedures, 4th revi-
sion. London, HMSO, 1990.
14. Lee RH, Gamble WB, Robertson B, Manson PN: The
MCFONTZL classification system for soft-tissue injuries to the
face. Plast Reconstr Surg 1999;103:1150-1157.
15. Parkhouse N, Crowe R, McGrouther AD, Burnstock G: Painful
hypertrophic scarring and neuropeptides. Lancet 1992;340:
1410.
16. Crowe R, Parkhouse N, McGrouther AD, Burnstock G:
Neuropcptide-containing nerves in painful hypertrophic
human scar tissue. Br J Dermatol 1994;130:444-452.
17. Ramasastry SS: Chronic problem wounds. Clin Plast Surg
1998;25:367-396.
18. Gorney M: Medical malpractice and plastic surgery: the
carrier's point of view. In Goldwyn RM, Cohen MN: The
Unfavorable Result in PlasticSurgery.AvoidanceandTreatmcnt,
3rd ed. Philadelphia, Lippincott Williams 8c Wilkins, 2001:38-
43.
19. Borges AF: Timing of scar revision techniques. Clin Plast Surg
1990;17:71-76.
20. Good Practice in Consent Implementation Guide: Consent to
Examination or Treatment. London, Department of Health,
2001.
21. Leung KS, Shcr A, Clark JA, et al: Microcirculation in hyper-
trophicscars after burn injury. J Bum Care Rehabil 1989; 10:436-
444.
22. Chang CW, Rics WR: Nonoperative techniques for scar man-
agement and revision. Facial Plast Surg 2001;17:283-288.
23. Gillies H: Plastic Surgery of the Face. London, Hodder &
Stoughton, 1920.
24. Edlich RF, Becker DG, Thacker JG, Rodeheaver GT: Scientific
basis for selecting staple and tape skin closures. Clin Plast Surg
1990;17:571-578.
25. Achauer BM: Reconstructing the burned face. Clin Plast Surg
1992;19:623-636.
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12 • SCAR REVISION 267
26. Borges AF: Scar analysis and objectives of revision procedures.
Clin Plast Surg 1977;4:223-237.
27. EngravLH, Gottlieb JR, Millard SP.etal: A comparison of intra-
marginal and extramarginal excision of hypertrophic burn scars.
Plast Reconstr Surg 1988;81:40-45.
28. Liang MD, Briggs P, Heckler FR, Futrcll JW: Presuturing—a new
technique forclosinglargcskin defects: clinical and experimental
studies. Plast Reconstr Surg 1988;81:694-702.
29. Istvan S: The delayed presuturing method. Plast Reconstr Surg
1995;96:240-241.
30. Neves RI, Saggers GC, Mackay DR, Manders EK: Assessing the
role of presuturing on wound closure. Plast Reconstr Surg
1996;97:807-811.
31. Wilhelmi BJ, Blackwell SJ, Mancoll IS, Phillips LG: Creep vs.
stretch: a review of the viscoelastic properties of skin. Ann Plast
Surg 1998;41:215-219.
32. Mackay DR, Saggers GC, Kotwal N, Manders EK: Stretching
skin: undermining is more important than intraoperative expan-
sion. Plast Reconstr Surg 1990;86:772-730.
33. Gibson T, Kenedi RM: Biomechanical properties of the skin.
Surg Clin North Am 1967;47:279-294.
34. Mostafapour SP, Murakami CS: Tissue expansion and serial
excision in scar revision. Facial Plast Surg 2001;17:245-252.
35. Borges AF: Relaxed skin tension lines (RSTL) versus other skin
lines. Plast Reconstr Surg 1984;73:144-150.
36. BorgesAF: Relaxed skin tension lines. Dermatol Clin 1989;7:169-
177.
37. Gibson T: Karl Langer (1819-1887) and his lines. Br J Plast Surg
1978;31:1-2.
38. Borges AF, Gibson T: The original Z-plasty. Br J Plast Surg
1973;26:237-246.
39. McGregor IA: The theoretical basis of Z-plasty. Br J Plast Surg
1957;9:256-259.
40. Furnas DW, Fischer GW: The Z-plasty: biomechanics and
mathematics. Br J Plast Surg 1971;24:144-160.
41. Furnas DW: The four fundamental functions of the Z-plasty.
Arch Surg 1968;96:458-463.
42. Roggendorf E: Planimetric elongation of skin by Z-plasty. Plast
Reconstr Surg 1982;69:306-316.
43. Roggendorf E: The planimetric Z-plasty. Plast Reconstr Surg
1983;71:834-842.
44. Hudson DA: Some thoughts on choosing a Z-plasty: the Z made
simple. Plast Reconstr Surg 2000;106:665-671.
45. Furnas DW: Z-plasties and related procedures for the hand and
upper limb. Hand Clin 1985;1:649-665.
46. Limberg AA: Planimetrie und Stereometric der Hauptplastik.
Jena, G.Fischer, 1967.
47. Humzah MD, Gilbert PM: Personal Communication.
48. McGregor IA: The Z-plasty. Br J Plast Surg 1966;19:82-87.
49. McGregor IA, McGregor AD: Wound Management. Funda-
mental Techniques of Plastic Surgery, 9th ed. New York, Churchill
Livingstone, 1995:10-
50. Hove CR, Williams EF III, Rodgers BJ: Z-plasty: a concise review.
Facial Plast Surg 2001;17:289-294.
51 - Mustarde JC: Repair and Reconstruction in the Orbital Region,
2nd ed. Edinburgh, Churchill Livingstone, 1980.
52. BorgesAF: The W-plastic versus the Z-plastic scar revision. Plast
Reconstr Surg 1969;44:58-62.
53. Chase RA: Resurfacing the hand with free skin grafts. In Brent
B: The Artistry of Reconstructive Surgery. St. Louis, Mosby,
1987:847-854.
54. FeldmanJJ: Facial resurfacing: the single-sheet concept. In Brent
B: The Artistry of Reconstructive Surgery. St. Louis, Mosby,
1987:327-342.
55. LyleWG:Siliconegelsheeting.PlastReconstrSurg2001;107:272-
275.
CHAPTER
13•
Transplantation in
Plastic Surgery
W. P. ANDREW LEE, MD • PETER E. M. BUTLER, MD, FRCS (Engl), FRCSI,
FRCS (Plast) • DAVID W. MATHES, MD
HISTORY
NOMENCLATURE
TRANSPLANTATION IMMUNOLOGY
Major Histocompatibility Complex
Other Transplant Antigens
Immunologic Rejection Cascade
Immunologic Screening
Current Immunosuppression
Immunologic Tolerance
The fields of transplantation and plastic surgery have
been closely linked. The need for plastic surgeons to
reconstruct tissue defects often dictates transplanta-
tion of tissues from other regions. Skin grafts, bone
grafts, and axial and random flaps from autogenous
sources are commonly transplanted tissues in every-
day practice. Skin substitutes prepared from allogeneic
or xenogeneic sources and frozen bone allografts are
also employed in selected clinical situations. Indeed,
the age of organ allotransplantation began when
Joseph E. Murray, a plastic surgeon, transplanted a
kidney between identical twin brothers in 1955.1 Such
"reconstructive surgery" using organ allografts was one
of the great achievements in 20th century medicine.
Despite the advances in plastic and reconstructive
surgery in recent decades, including refinement of
microvascular techniques and delineation of flap vas-
cular anatomy, many tissue defects still remain outside
the realm of capability for reconstructive surgeons.
These difficult problems occur when the principle of
replacing like with like tissues cannot be followed
because of lack of appropriate autogenous tissues.
Thus, the function of a severely injured extremity
cannot be adequately restored, the appearance of a
severely disfigured face cannot be satisfactorily
improved, and both the function and appearance of
an amputated extremity cannot be reconstructed.
Understandably, the inclination toward tissue
transplantation has led plastic surgery researchers to
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Dr.Mustafa D.
TRANSPLANTATION IN PLASTIC SURGERY
Skin
Bone
Cartilage
Nerve
Limb and Composite Tissues
FUTURE TRANSPLANTATION IN PLASTIC SURGERY
look to nonautogenous sources for reconstructive
material.2"5 The recently performed allotransplan-
tation of hand, larynx, and knee joints, although
hampered by the indefinite need for host immuno-
suppression, offered promise for a breakthrough.6*14
A widespread use of such composite tissue allografts
would greatly broaden the horizon of reconstructive
surgery.
HISTORY
The historical fabric of plastic surgery is heavily inter-
woven with that of transplantation and abounds with
myth and legend. Saints Cosmas and Damian were twin
brothers and converts to Christianity. Legend has
it that they removed the gangrenous limb of an aged
sacristan while the patient was asleep and successfully
transplanted in its place the leg of a deceased Ethiopian
Moor.15,16 The modern era in transplantation, however,
started with the Bologna surgeon Tagliacozzi, who in
his treatise of 1597, De Curtorum Chirurgia per
Insitionem [The Surgery of Mutilation by Grafting],
described a forearm flap to reconstruct the nose by
severing its original connections some weeks later.17
These methods had followed the ancient Indian plastic
surgical methods recorded in the Sushruta Samhita
manuscripts.18 British colonial expansion into India
led to the rediscovery of the ancient plastic surgical
methods as described in the Sushruta Samhita, with
269
270 I • GENERAL PRINCIPLES
the result that forehead flaps were reintroduced into
the West by Carpue in the early 19th century.19
Success with full-thickness autografts was reported
in Milan by Baronio, who described a series of famous
autologous skin grafting experiments in sheep.20 It was
not until 1869 that the problem of graft loss was over-
come by making grafts thinner. Reverdin21 derived his
method of using thin pinch grafts referred to as lam-
beaux cutanes. In parallel work, Bert demonstrated
that for a graft to survive, it required ingrowth of new
host vessels from the recipient bed, which explained
better survival of split-thickness grafts in compari-
son to full-thickness grafts. The development of a
consistent method for harvesting split-thickness skin
grafts by Thiersch in 1886 revolutionized the ability
to transplant skin graft. The question of survival of
allogeneic and xenogeneic skin after grafting onto
human recipients was answered in 1912 by Schone
and in 1914 by Lexer,22 who demonstrated that allo-
grafts did not survive more than 3 weeks after trans-
plantation. Further evidence was provided by Padgett23
in 1932 when he described 40 patients receiving skin
allografts; all grafts were rejected in 35 days. However,
he did demonstrate that skin grafts exchanged between
identical twins could survive indefinitely.
World War II accelerated progress in transplanta-
tion. It produced new clinical problems, such as
massive burns and new forms of renal failure. Gibson,24
a plastic surgeon at the Glasgow Royal Infirmary,
reported second-set rejection of skin allografts in the
treatment of pilots with burn injuries. (Second-set
rejection is defined today as accelerated rejection of
allogeneic tissue due to presence of humoral antibodies
caused by prior exposure to the same allogeneic
tissue.) Medawar then joined Gibson to investigate this
phenomenon and in combination with Billingham and
Brent laid the foundation of modern immunology.25
In 1955, Murray1 reported the first successful kidney
transplantation between identical twins. Subsequent
development of tissue typing and more sophisticated
methods of immunosuppression transformed allograft
transplantation into a routine clinical occurrence.
Kidney, liver, heart, and lung allografts today achieve
prolonged survival with lifelong immunosuppression.
Modern immunologic researchers are working toward
induction of tolerance to allogeneic and xenogeneic
tissue without long-term immunosuppression. Only
with this advance can the prospect of transplanting
skeletal or composite tissues be realized and the next
revolution in reconstructive surgery be achieved.
NOMENCLATURE
A graft is tissue separated from its donor bed tissues.
It may be transferred as a nonvascularized graft and
relies on ingrowth of new vessels from the recipient
bed for blood supply. A vascularized graft (or flap)
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Dr.Mustafa D.
remains attached to donor blood supply or becomes
revascularized through microvascular anastomoses to
recipient vessels. An autograft is tissue transplanted
from one location to another in the same individual.
An isograft is transplanted from a genetically iden-
tical donor to the recipient, such as transplants
between syngeneic mice and human monozygotic
twins. An allograft (homograft in older terminology)
is transplantation of tissues between unrelated indi-
viduals of the same species. A xenograft (heterograft
in older terminology) is transplantation between dif-
ferent species.
Transplantation may also be described in terms of
the site into which the tissue is transplanted. Ortho-
topic refers to transplantation into an anatomically
similar site; heterotopic refers to transplantation into
an anatomic site different from the site of origin.
TRANSPLANTATION
IMMUNOLOGY
Major Histocompatibility Complex
The most important antigens contributing to allograft
rejection are the major histocompatibility complex
(MHC) antigens. The MHC proteins are encoded in
a gene complex on the short arm of chromosome 6
and have different nomenclature between species: HLA
in humans, SLA in swine, H-2 in mice, and RT1 in rat.
MHC genes are expressed in a codominant fashion,
with one haplotype, or set of alleles, inherited from
each parent.
There are two major classes of MHC genes.Class I
MHC genes encode a transmembrane glycoprotein
complex with a polymorphic 44-kd heavy chain con-
sisting of three extracellular domains (al,a2,oc3). The
al domain is highly variable and contains sites for
antigen binding. The heavy chain is stabilized by non-
covalent binding to a lighter chain referred to as P2-
microglobulin. There are three distinct genetic loci for
the class I antigens in the human, HLA-A, HLA-B,
and HLA-C. Class I antigens are expressed on nearly
all nucleated cells and serve as the primary target for
cytotoxic (CD8+) T lymphocytes. Class II MHC genes
encode two noncovalently bound transmembrane pro-
teins, a 34-kd a chain and a 29-kd p chain. There are
three class II loci in humans: HLA-DR, HLA-DP, and
HLA-DQ.26 Class II antigens are expressed primarily
on vascular endothelium and cells of hematopoietic
stem cell origin such as lymphocytes and macrophages.
Both class I and class II molecules have a specific
site at which foreign peptide antigens can be presented
after they have been processed by the cell.27"31' Tissue
distribution is not the same in all species; humans, pigs,
and monkeys express class II antigens on endothelial
cells, whereas rodents and many other large species do
not.31 Matching of HLA-A, HLA-B, and HLA-DR has
^Wt^<aeicrw image...
13 • TRANSPLANTATION IN PLASTIC SURGERY
been found to be the most important factor in deter-
mining long-term renal allograft survival.32
Other Transplant Antigens
In addition to the MHC antigens, there are three other
classes of surface proteins: ABO blood group proteins,
minor histocompatibility antigens, and skin-specific
antigens.
The blood group antigens are important in clini-
cal transplantation because they are expressed on vas-
cular endothelial cells. Patients with type A or type B
blood develop natural antibodies to the other protein,
whereas patients with type O blood develop natural
antibodies to both type A and type B proteins.
Although ABO antigens will not stimulate cell-
mediated rejection, a brisk antibody-mediated attack
can rapidly lead to graft failure.33
Minor histocompatibility antigens are peptides of
self origin that are not presented by the MHC com-
plexes. Siblings (other than identical twins) with a com-
pletely matched MHC profile will still differ with
respect to minor antigens because of allelic variation
of the genes encoding those proteins. Although minor
antigens will stimulate a cell-mediated response, they
will not do so in a primary in vitro test. Rejection of
a graft due to minor antigens alone, therefore, often
proceeds at a slower rate.34
Skin-specific antigens (Sk antigen) are tissue-
specific proteins that can cause graft rejection by a
cell-mediated response. Consequently, skin is one of
the most difficult tissues to which transplantation
tolerance can be induced. 35
Immunologic Rejection Cascade
CELLS OF IMMUNE RESPONSE
A number of cells with varied but interconnected func-
tions participate in the process of graft rejection. They
work together to maintain the two main arms of the
immune reaction, the humoral response (B cells and
antibodies) and the cell-mediated response (T cells).
Macrophages
The macrophage performs the most ancient cellular
defense function: phagocytosis. It is of mesenchymal
origin and thought to arise from a bone marrow stem
cell. It can freely circulate throughout the body,
migrate through lymph nodes, or remain stationary
within tissues. Kupffer cells are specialized macrophages
that reside in the liver. The Langerhans cell is a
specialized macrophage that is specific to the skin.
The macrophage expresses class I antigens on its cell
surface, and as a highly specialized immune cell, the
macrophage also expresses class II MHC molecules.
Beyond simple destruction of cells, the main
purpose of the macrophage is to reprocess the
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271
breakdown products of ingested cells. These fragments
of foreign protein may then be bundled with a new
class II antigen molecule, and during the bundling
process, fragments of the foreign protein come to reside
in the peptide-binding groove of the class II molecule.
When the fragment is exteriorized, it faces outward
and is easily recognized by the immune system as
foreign. This process is known as antigen presentation.
Macrophages also secrete important cytokines,36,37 such
as interleukin-1 (IL-1). This polypeptide can, in a
hormonal fashion, stimulate the immunologic func-
tion of responding cells. These cells are critical to the
presentation of foreign antigen.
Natural Killer Cells
Another primitive cell derived from the bone marrow
stem cell is the lymphocyte (non-T, non-B) called
the natural killer (NK) cell. NK cells are thought to be
active in the antitumor response. 38 They are able to
demonstrate spontaneous tumoricidal properties on
exposure to tumor cells. This cell does not require
recognition of MHC molecules or antigen processing
(as do T cells and B cells).39 However, the exact method
this cell uses to recognize foreign cells remains unclear.
They are able to kill cells by incorporating a lipophilic
protein into the target cell membrane, which leads to
increased permeability and cell lysis. NK cells also
secrete several cytokines, including i n t e r f e r o n ^
interferon-a, and B-cell growth factor. They may also
serve to eliminate cells that fail to express normal self
MHC proteins and thereby be self-reactive.
Granulocyte
The granulocyte plays an important role in immune
homeostasis. Named for their histologic staining
properties, the three main cell lines are polymor-
phonuclear cells, eosinophils, and basophils. All of the
cell lines are derived from the same bone marrow pre-
cursor. As nucleated cells, they all express class I MHC
molecules; however, they do not express class II MHC
antigens. In addition, these cells express a number of
molecules important for their function (including
adhesion and interaction with other immune cells)
on their cell surface. These white blood cells carry
granules of toxic substances (peroxidases) and sub-
stances that attract other white blood cells and cellular
elements of the coagulation cascade. When stimulated,
the granulocyte secretes these granules, initiating local
inflammation in a relatively indiscriminate fashion.
B Lymphocyte
Named for their site of origin in the chicken, the bursa
of Fabricius, these cells play a central role in immune
defense. In humans, the bursa equivalent is thought
to be the fetal liver or bone marrow. Once these cells
are produced, they migrate to the lymph node and
spleen and appear to remain in these organs. These
272 I • GENERAL PRINCIPLES
cells express class I and class II MHC antigens. They
also display a variety of B cell-specific markers, known
as Bl to B8 (through which the lines of B cells can be
identified). Finally, they display immunoglobulin on
their surface. When stimulated, the B lymphocyte dif-
ferentiates into plasma cells. These smaller cells serve
as factories to produce specific antibodies. These soluble
antibodies support the humoral arm of the immune
response. Through rearrangement of a highly variable
genetic region during immune development, anti-
bodies are produced that can bind countless millions
of different epitopes.
IMMUNOGLOBULIN. Antibodies produced by B
lymphocytes and plasma cells take the form of
immunoglobulins. Immunoglobulins are proteins of
unique structure, composed of heavy and light peptide
chains. The "root" of the heavy chain complex is called
the constant fragment. The portion of an immuno-
globulin molecule where light chains form complexes
with heavy chains, at the site at which the antibody
will bind to its target, is designated the antibody-
binding fragment (Fab). Myriad possibilities exist
for antigen to a specific antibody to be made because
the Fab moiety is highly variable in its discrete struc-
ture. More than 100 genes code for specific segments
of the variable portions of the heavy and light chains,
leading to millions of potential immunoglobulin
specificities.
There are five general immunoglobulin classes: IgM,
IgG, IgE, IgA, and IgD. IgM is the first antibody formed
after exposure to common microbial antigens, followed
by the more durable IgG. IgE is involved in the hyper-
sensitivity reaction by binding to and activating spe-
cialized eosinophils (mast cells). IgA is secreted in saliva,
tears, and breast milk and thus augments resistance to
infection in these fluids. IgD is found on the surface
of immature B lymphocytes; its function remains
unclear. Immunoglobulins may be soluble or bound
to a cell's surface.
The main function of immunoglobulins is to
provide opsonization and to activate complement.
Opsonization occurs when the Fab fragment of an
immunoglobulin binds to its associated antigen, such
as an invading organism. Subsequent macrophage and
monocyte phagocytosis of the antibody-coated
microorganism is then markedly enhanced. Comple-
ment fixation occurs when the antibody-antigen
complex triggers the complement cascade.
Complement
An antigen-antibody complex may initiate the
complement cascade through a classical pathway.
Substances such as endotoxin may, without im-
munoglobulins, initiate the cascade through the
alternative pathway. Both pathways converge with the
activation of C3. The sequential activation of proteases,
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Dr.Mustafa D.
which define the complement cascade, results in a tight
cluster of proteins known as the membrane attack
complex. This complex is able to rupture the mem-
branes of foreign cells. In the normal host, this
cascade is kept in check by the regulatory protein Cl
inhibitor.
Dendritic Cells
These cells are derived from bone marrow stem cell
progenitors and are highly specialized antigen-
presenting cells. They appear to have no effector func-
tion. They reside in the intracellular and interstitial
space but migrate through the lymphatics and to the
spleen when activated. There they present their
antigens to T cell-rich areas.
T Lymphocytes
T lymphocytes have a central role in coordinating the
immune response, forming the cell-mediated arm of
the immune response. The T lymphocyte is named
for its site of origin, the thymus, and is one of the most
important elements of the immune system. T cells
derive from fetal stem cells in the thymus and undergo
an extensive process of elaboration and deletion
before being released into the body. The maturing T
cells are selected to recognize self MHC antigens and
become tolerant to them. Those cells that demonstrate
too high of an affinity to self are eliminated by
clonal deletion. Failure of this process may lead to
autoimmunity.
These cells express both class I and class II anti-
gens. In addition to HLA surface markers, lympho-
cytes also possess cell surface markers that serve to
distinguish one subpopulation from another within
the same individual. These are all glycoproteins and
are described by the common determinant (CD)
nomenclature (e.g., CD3).
Three broad classes of T cells are helper T (T„) cells,
cytotoxic T cells, and suppressor T cells. All T cells
express CD3 on the cell surface. Cytotoxic T cells (cells
that effect target cell killing) express CD8. Suppressor
T cells that can buffer and down-regulate the immune
response also express CD8.40,41 The helper T cell,
however, expresses CD4 and serves to amplify the
immune response through its interaction with other
cells and secretion of critical cytokines. Each T cell
expresses a T-cell receptor (TCR) capable of binding
antigen. The TCR, a 90-kd heterodimer composed of
an oc chain encoded on chromosome 14 and a P chain
encoded on chromosome 7, is located close to the CD3
antigen and the CD28 antigen. The TCR is relatively
flat and possesses an outward-facing surface. This
"antigen recognition platform" is the critical interface
for foreign peptide in the binding groove. As with B-
cell development, T cells undergo rearrangement of
genes coding for a hypervariable region on the recep-
tor proteins. This allows a body's population of T cells
T^i^WS'aeltfWimage...
13 • TRANSPLANTATION IN PLASTIC SURGERY
to respond to a nearly limitless array of foreign anti-
gens, with each individual T cell capable of binding
one specific antigen.
T-CELL BINDING AND ACTIVATION. Although the
TCR is capable of binding antigen, it will not recog-
nize the target molecule by itself.42 The TCR can bind
antigen only if it has been processed and presented by
an antigen-presenting cell together with an MHC
molecule; thus, it recognizes the MHC together with
the target antigen. This limitation of binding is referred
to as MHC restriction. CD4 (helper) T cells can only
bind antigen presented with M H C class II molecules;
CD8 (cytotoxic) T cells recognize antigen along with
MHC class I proteins. The helper T cell is most criti-
cal to the immune response because its activation results
in the production of cytokines that are necessary for
the function of many other immune cells. Binding of
a CD4 cell to an antigen-presenting cell that expresses
target antigen together with MHC class II molecules
initiates a predictable cycle of intercellular communi-
cation. The antigen-presenting cell is stimulated to
produce the cytokine IL-1, a powerful chemoattrac-
tant, a primary mediator in the acute-phase reaction,
and a potent activator of lymphoid cells. The T cell, in
turn, secretes IL-2, which is a required stimulant for
differentiation and proliferation of T cells. The IL-2
produced by the bound T cell has autocrine function
by binding to newly expressed self IL-2 receptors.
Secreted IL-2 also has paracrine function that affects
other T cells in the region, such as CD8 cells, which
require IL-2 for activation but do not produce it them-
selves. As CD4 cells become further activated, they
secrete IL-4 and IL-5, which stimulate the maturation
and proliferation of B lymphocytes. Furthermore, there
is evidence that two subsets of CD4 cells, T„l and T„2,
function to enhance alloreactivity and stimulate anti-
body production by B cells, respectively. With such a
central role by CD4 cells in cell signaling, it is easy to
understand the severely compromised immune
response from the loss of host CD4 cell function
secondary to human immunodeficiency virus
infection.43'46
ANTIGEN RECOGNITION AND GRAFF REJECTION. In
the case of allograft tissue, foreign antigens would be
recognized by host T cells after being processed by host
antigen-presenting cells and presented in the context
of self MHC. This is termed indirect presentation. In
addition, host T cells can direcdy recognize donor MHC
on donor antigen-presenting cells, termed direct pres-
entation. This mechanism helps explain the more
vigorous response to allograft tissue than to foreign
peptides alone.47
Clinically, rejection of allograft tissue can proceed
at different levels of intensity for different tissues. The
common component for rejection of any graft is inflam-
mation. This may be manifested as a loss of graft
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Dr.Mustafa D.
273
function with local or systemic signs of inflammation.
Several distinct clinical syndromes of graft rejection
with different time courses have been noted. These syn-
dromes differ with regard to the underlying primary
immunologic process.
Hyperacute rejection occurs almost immediately
after perfusion of the allograft with host blood. It is
the result of preformed antibodies to either ABO blood
group proteins or donor MHC molecules enacting a
rapid attack on the donor tissue. Complement acti-
vation results in destruction of vascular endothelial
cells and induces rapid thrombosis of vessels as well
as an amplification of the inflammatory signal. Stan-
dard screening before transplantation should detect
preformed antibodies, making hyperacute rejection a
rare clinical entity. Many mammals possess preformed
antibodies to other species that stand as a major
obstacle to xenotransplantation. 48
Acute rejection takes place days to weeks after
transplantation and occurs with rapid onset. This T
cell-mediated response is characterized by fever, graft
tenderness and edema, and loss of function. Intersti-
tial lymphocytic infiltration is seen on microscopic
examination. In addition, severe forms of acute
rejection may include a humoral attack on the graft,
resulting in a vasculitis.49
Chronic rejection is an indolent process occurring
months to years after transplantation. It is character-
ized by a progressive loss of tissue architecture with
fibrosis and mononuclear cell infiltration. The etiol-
ogy of chronic rejection is not well understood and
may be multifactorial. The process may be slowed
because of immunosuppression. It also may result from
the cumulative effect of damage to the graft from
ischemia during transplantation, graft infection, or
drug toxicity.
Immunologic Screening
Methods are available to predict the compatibility of
donor tissue to a particular recipient. The greatest value
of these clinical tests is to exclude recipients who would
be expected to manifest a hyperacute rejection to a
specific donor organ.
Blood group typing is an important first step in
determining transplant compatibility. An ABO mis-
match will result in certain failure because of preformed
antibodies. 50 Although it is possible to transplant type
O donor tissue into type A or type B recipients, the
limited sunply of donor organs in the United States
makes this practice uncommon.
HLA typing is used to match organs with potential
recipients. Serologic methods are employed to type
HLA-A, HLA-B, and HLA-DR. A heterozygous
individual with a complete match at all these loci is
referred to as a six-antigen match. For renal allografts,
HLA matching has been shown to affect graft survival.
274 I • GENERAL PRINCIPLES

Kidneys transplanted from HLA-identical siblings
have a 3-year success rate that well exceeds 90%, whereas
parent to child grafts have an 82% survival. Cadaveric
kidney grafts have a 70% 3-year survival rate.51 MHC
class II matching has been found to be more impor-
tant than class I matching for renal transplantation;
the reverse appears to be true for liver transplantation.
This would suggest differences in mechanisms of graft
rejection for different tissues.52 Serologic tissue typing
has certain limitations. An HLA antigen can be iden-
tified only if it is being searched for with a specific anti-
body. For example, if only a single HLA-DR phenotype
is identified in donor tissue, the individual could be
either homozygous for that allele or heterozygous with
an unrecognized HLA-DR antigen. This method of
testing fails to type the other class II antigens, HLA-
DP and HLA-DQ.
Crossmatching is a test that detects the presence of
preformed donor-specific antibodies in the serum of
a particular recipient. It represents the final definitive
screening measure before transplantation. In this
lymphocytotoxicity assay, donor lymphocytes are
incubated with recipient serum and complement. Cell
viability is then assessed by a dye exclusion technique.
A positive crossmatch, indicated by lysis of the donor
lymphocytes, suggests that a hyperacute reaction is
likely to occur. One pitfall of this test, however, is
that organ-specific antibodies may be missed if those
antigens are not expressed on the lymphocytes being
evaluated.
Antibody screening is another modality used in clini-
cal transplantation. Serum from prospective transplant
recipients is routinely tested in a lymphocytotoxicity
assay against a panel of cells from different donors with
known HLA antigens. The percentage of panel cells
lysed reflects the degree of panel-reactive antibody
(PRA)> demonstrating HLA antibodies in an indi-
vidual's serum. A high PRA suggests that a patient is
unlikely to have a negative crossmatch. This informa-
tion is used in determining organ allocation when the
tissue must be transplanted quickly. Individuals are
likely to have a high PRA if they have been sensitized
by previous transplantation, pregnancy, or blood
transfusions.
Current Immunosuppression
The multiple pathways and mechanisms employed by
the immune system to defend the body against both
extracellular and intracellular pathogens have presented
a significant barrier to the survival of transplanted
allografts. Immunosuppressive medications must
inhibit the body's ability to reject a transplanted organ,
but not at the expense of the defense network against
pathogens. The use of several immunosuppressive
agents has allowed the inhibition of the immune system
that maximizes the protection of the allograft with the
least cost to the body's overall ability to fight infection
and tumors (Table 13-1).
In all of the transplanted organs including the hand
transplants, it appears that it is central to prevent
allograft recognition during the peritransplantation
period. This is currently achieved through so-called
induction protocols. Several agents are currently used
to protect the transplant during that period of cytokine
excess observed after surgery (Table 13-2). After the
induction agents are used,"maintenance" medications
are used to maintain the transplant. Finally, when

TABLE 13-1 4- ANTIBODY-MEDIATED DRUGS

Agent Mechanism Action Side Effects

Antilymphocyte

Antilymphocyte Antibodies directed against Promotes T-cell clearance Thrombocytopenia, leukopenia,

globulin antigens on lymphocytes
Antithymocyte Antibodies directed against
globulin antigens on thymocytes
OKT3 Murine monoclonal antibody
directed against the CD3
subunit on human T cells
Anti-IL-2
through complement-
mediated lysis
Promotes T-cell clearance
through complement-
mediated lysis
Eliminates T cells by the
reticuloendothelial system;
blocks cytotoxic activity
of activated T cells
increased risk of viral reactivation,
serum reaction
Thrombocytopenia, leukopenia,
increased risk of viral reactivation,
serum reaction
Significant cytokine syndrome,
reactivation of viruses,
post-transplantation
lymphoproliferative disease

Daclizumab, Blocks binding to CD25 Limits T-cell expansion; acts None

basiliximab (high-affinity chain of IL-2 only on activated cells
receptor)

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Dr.Mustafa D.
 image...

13 • TRANSPLANTATION IN PLASTIC SURGERY 275

TABLE 13-2 • IMMUNOSUPPRESSIVE DRUGS

Agent Mechanism Action Side Effects

Calcineurin Inhibitors

Cyclosporine Binds to cyclophilin, blocks the Prevents cytokine Nephrotoxicity, hypertension

NF-AT transcription factor, inhibits transcription and neurotoxicity
production of IL-2, and promotes arrests T-cell activation
production of TCF-p
Tacrolimus Binds to FK-binding protein, blocks Prevents cytokine Nephrotoxicity, neurotoxicity,
(FK506) the NF-AT transcription factor, transcription and arrests diabetogenicity
inhibits production of IL-2, and T-cell activation
promotes production of TCF-p

Antiproliferative Agents

Azathioprine Inhibits DNA synthesis, interferes
(Imuran) with DNA repair mechanisms, and
inhibits conversion of IMP to AMP
and CMP
Mycophenolate Noncompetitive, reversible inhibitor
mofetil (MMF) of IMP dehydrogenase; interrupts
production of CTP and dCTP,
prevents critical step in RNA and
DNA synthesis
Blocks the proliferative Bone marrow suppression,
response (T and B cells) hepatotoxicity
Blocks the proliferative Gastrointestinal toxicity,
response (T and B cells), bone marrow suppression
inhibits antibody
formation, and prevents
clonal expansion of
cytotoxic T cells

Corticosteroids

Corticosteroids Binds to intracellular receptor, Blocks IL-1 andTNF-a Osteonecrosis, osteoporosis,

increases transcription of gene
for IKBCX, and prevents the
transcription of NF-KB (a key
activator of proinflammatory
cytokines)
production by antigen- growth suppression,
presenting cells, blocks glucose intolerance,
up-regulation of the hypertension, central
MHC, inhibits production nervous system effects
of interferon-? by T cells
and lysosomal enzymes
and migration by
polymorphonuclear cells

Macrolide Inhibitors

Sirolimus Binds to FK-binding protein, impairs Interrupts T-cell activation Hypertriglyceridemia, bone
(rapamycin) signal transduction by the IL-2 pathway marrow suppression
receptor, and arrests the cell cycle
of lymphocytes

ongoing rejection occurs, it is often necessary to use Glucocorticosteroids bind to an intracellular

"rescue" agents to stop ongoing rejection and salvage
a transplant that would otherwise be lost.
CORTICOSTEROIDS
These agents remain a central tool for both the pre-
vention and treatment of allograft rejection. Whereas
steroids are not effective as solitary agents to prevent
rejection, they have been shown to improve graft
survival in combination with other agents. When
used at high doses, they can also treat ongoing acute
cellular rejection. Despite these uses, steroids also
contribute to the morbidity associated with modern
immunosuppression.
receptor after nonspecific uptake in the cytoplasm. The
receptor-ligand complex then enters the nucleus,
where it acts as a DNA-binding protein and increases
the transcription of several genes.53 The most impor-
tant gene is thought to be IKBOC, which binds to and
prevents the function of N F - K B (a key proinflamma-
tory cytokine that is an important transcription factor
for T-cell activation). Steroids block the production
of IL-1 and tumor necrosis factor-a by antigen-
presenting cells. They also block interferon-y produc-
tion by T cells and migration and lysosomal enzyme
release by neutrophils. Steroids also mute the up-
regulation of the MHC and through their diminution
of the inflammatory responses decrease the degree of

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Dr.Mustafa D.
276 I • GENERAL PRINCIPLES
costimulation in the environment. Steroids do not have
an impact on the production of antibody.
ANTIPROLIFERATIVE AGENTS
Azothioprine
This was the first immunosuppressive agent employed
in transplantation. Azathioprine undergoes conver-
sion in the liver to 6-mercaptopurine and then to 6-
thioinosine monophosphate. These derivatives inhibit
DNA synthesis by alkylating DNA precursors and
inducing chromosome breaks through interference
with DNA repair mechanisms. In addition, they inhibit
the conversion of inosine monophosphate to adeno-
sine monophosphate and guanosine monophosphate,
which depletes the cell of adenosine. The effects of
azathioprine are nonspecific, and it acts not only on
dividing T cells but on all rapidly dividing cells. The
primary toxic effect is on the bone marrow, gut, and
liver cells. Azathioprine is ineffective as a single agent
and cannot be used as a rescue agent. It can be used
for maintenance when it is given in combination with
steroids and a calcineurin inhibitor.
Mycophenolate Mofetil
Mycophenolate mofetil (MMF), a more recent agent
approved for use in humans in 1995, acts through
noncompetitive, reversible inhibition of inosine mono-
phosphate (IMP) dehydrogenase.54 This modification
improves the bioavailability of mycophenolic acid.
Physiologic purine metabolism requires that guano-
sine monophosphate (GMP) be synthesized for the sub-
sequent production of guanosine triphosphate (GTP)
and deoxyguanosine triphosphate (dGTP). GTP is
required for RNA synthesis and dGTP for DNA syn-
thesis. GMP is formed from IMP by IMP dehydroge-
nase. MMF prevents a critical step in both RNA and
DNA synthesis. However, MMF does not affect the
"salvage pathway" for GMP production that is present
in most cells. This pathway is not present in lympho-
cytes, and MMF exploits this difference and spares most
other cells in the body, including neutrophils. MMF
blocks the proliferative response in both T and B cells,
inhibits antibody formation, and prevents clonal
expansion of cytotoxic T cells.
MMF decreases biopsy-proven rejection and the
need for antilymphocyte agents in rescue therapy
compared with azathioprine.55,56 MMF has replaced
azathioprine in patients with high risk for rejection.
However, MMF cannot be used as a sole immuno-
suppressive agent and must be paired with either
steroids or calcineurin inhibitors.
CALCINEURIN INHIBITORS
Cyclosporine
Cyclosporine is a cyclic endecapeptide that was iso-
lated from the fungus Tolypodadium inflatum Gams
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Dr.Mustafa D.
in 1972.57,58 This drug acts as a T cell-specific immuno-
suppressant, and its mechanism of action is pri-
marily through its ability to bind to the cytoplasmic
protein cyclophilin.57 The cyclosporine-cyclophilin
complex forms a high-affinity bond with calcineurin-
calmodulin complex and blocks the calcium-
dependent phosphorylation and activation of NF-AT.
The interference with NF-AT prevents the subsequent
transcription of the gene encoding IL-2. This process
also interrupts other genes critical for T-cell activa-
tion. In addition, cyclosporine increases transform-
ing growth factor-P transcription, which appears to
further down-regulate T-cell activation, decrease
blood flow to the area, and activate pathways critical
to wound healing.59,60
The effect of cyclosporine is reversible because it
blocks TCR signal transduction but does not inhibit
costimulatory signals.61 If the drug is withdrawn, the
T cell is not anergic but is again capable of mount-
ing an attack on its target. The effects of cyclosporine
can be overcome with the exogenous administration
of IL-2. This can explain why cyclosporine is not
effective once rejection is ongoing; it is useful only
as a maintenance agent and is ineffective as a rescue
agent.
Cyclosporine also has significant toxicity associated
with its administration. It has significant vasocon-
strictor effect (mediated by transforming growth
factor-P) on the proximal renal arterioles that decreases
renal blood flow by 30%. Its effects on the kidney can
promote fibrosis and hyperkalemia and may interfere
with the resolution of acute tubular necrosis. The
drug also has neurologic side effects, such as tremors,
paresthesias, headache, depression, confusion, and
seizures. It may also cause hypertrichosis and gingival
hyperplasia.
Tacrolimus
Tacrolimus (FK506), a macrolide produced by
Streptomyces tsukubaensis, was discovered in 1986.
Tacrolimus, like cyclosporine, blocks the effects of NF-
AT, prevents cytokine transcription, and arrests T-cell
activation. The intracellular target is an immunophilin
protein distinct from cyclophilin known as FK-binding
protein.62,63 The effect is additive to that of cyclosporine,
and these drugs cannot be given together because of
the prohibitive toxicity. Tacrolimus also increases the
transcription of transforming growth factor-P and thus
shares both the beneficial and toxic effects seen in the
administration of cyclosporine. It is, however, 100 times
more potent in its inhibition of the production of
IL-2 and interferon-y. The renal side effects are similar
to those with cyclosporine. It has more pronounced
neurologic side effects and a diabetogenic effect. The
cosmetic side effects are less that those with
cyclosporine. This drug has been proved to be effec-
tive as a maintenance drug for both liver and kidney
VtM>ttf i aelcW image...
13 • TRANSPLANTATION IN PLASTIC SURGERY
transplantation. It has only minimal use as a rescue
agent.64
Rapomycin
Rapamycin is a macrolide antibiotic derived from
Streptomyces hygroscopicus and is structurally similar
to tacrolimus.65,66 However, they antagonize each other's
biologic activity. Both of the drugs bind to the same
FK-binding protein, but rapamycin does not affect
the calcineurin activity.67,68 Instead, the interaction of
rapamycin and FK-binding protein complex impairs
signal transduction by the IL-2 receptor through its
interaction with a cytoplasmic protein (RAFT-1). In
doing so, the p70 S6 kinase cascade is interrupted and
T cells are prevented from entering into the S phase of
cell division.69 Thus, rapamycin is able to interrupt T-
cell activation and proliferation even in the presence
of IL-2.70 Other receptors that are affected are IL-4, IL-
6, and platelet-derived growth factor.
Rapamycin has been shown to prolong allograft
survival in multiple animal models and is being used
in several drug regimens. It has even been applied
to the experimental human hand transplantation
protocols. This drug has no nephrotoxicity. It does,
however, demonstrate some bone marrow toxicity and
has been observed to cause hypertriglyceridemia.
ANTILYMPHOCYTE PREPARATIONS
Antilymphocyte/Antithymocyte Globulin
Antilymphocyte globulin is produced by inoculation
of heterologous species with human lymphocytes, col-
lection of the plasma, and then purification of the IgG
fraction. The result is a polyclonal antibody prepara-
tion that contains antibodies against many of the
antigens on human lymphocytes. When thymocytes
are used as the inoculum instead of lymphocytes, the
product is known as antithymocyte globulin. The most
common ones employed in transplantation are made
in the horse* and in the rabbit. 1
The mechanism behind the effectiveness of these
drugs is through the coating of the T cells by the anti-
bodies.71,72 These coated T cells are then eliminated
by complement-mediated lysis and opsonin-induced
phagocytosis. The mere presence of the antibodies on
the surface of the T cell reduces its ability to express
an effective TCR signal. The overall impact of the anti-
bodies is to functionally remove the primary effector
cells required for acute rejection after transplantation.
These drugs have been employed as induction agents
at the time of transplantation to reduce the possibil-
ity that T cell-mediated antigen recognition will occur
when the graft is in its most vulnerable state. These
'ATGAM, Pharmacia & Upjohn, Kalamazoo, Mich.
'ATG (Thymoglobulin), SangStat Medical Corporation, Fremont, Calif.
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Dr.Mustafa D.
277
drugs are also used as rescue agents, and their effec-
tiveness is based solely on the ability to destroy cyto-
toxic T cells. Most of the side effects are due to the
drug's heterologous origin and the fact that it can also
bind to other cells. Therefore, one can observe throm-
bocytopenia, anemia, and leukopenia. The most
common reaction is a cytokine release syndrome. Chills
and fevers occur in up to 20% of the patients. A rash
consisting of raised erythematous wheals on the trunk
and neck is seen in 15% of patients. The use of
antilymphocyte drugs has been associated with the
reactivation of viral disease.
OKT3
This is a murine monoclonal antibody that is directed
against the signal transduction subunit on human T
cells (CD3). OKT3 is thought to bind to the CD3
subunit found on all mature T cells and result in
the internalization of the receptor, thus preventing
antigen recognition and TCR signal transduction. 73,74
In addition, T-cell opsonization and clearance by the
reticuloendothelial system occur. After the adminis-
tration of OKT3, there is a rapid decrease in the cir-
culating CD3* T cells. There is little or no effect on
those cells in the spleen and lymph nodes or thymus.
After several days, there is a return to T cells that
are CD4 + and CD8 + but that do not express CD3.
These "blind" T cells remain incapable of binding to
antigen and interfere with the process of antigen recog-
nition and generation of cytotoxic T cells. Finally, OKT3
blocks the cytotoxic activity of already activated T cells
by an inappropriate degranulation when the CD3 is
bound by OKT3. This mechanism is central to its effec-
tiveness but also to one of its most significant side
effects.
The administration of OKT3 can lead to a profound,
systemic cytokine response that can result in hypoten-
sion, pulmonary edema, and a fatal cardiac myode-
pression. In about 2% of patients, this syndrome is
manifested as an aseptic meningeal inflammation.
Methylprednisolone must be administered before the
delivery of OKT3 to blunt this adverse reaction. This
syndrome abates with subsequent doses. OKT3 is used
as a rescue agent to treat acute renal allograft rejec-
tion. OKT3 has also been employed as an induction
agent. The drug is superior to steroids in halting
ongoing rejection. However, it has also been shown to
cause a high viral reactivation rate for cytomegalovirus,
Epstein-Barr virus, and other viruses. It has been
associated with high rates of post-transplantation
lymphoproliferative disease.
Anti-IL-2
Two new monoclonal antibodies have become avail-
able for use in renal transplantation and have also been
employed in some hand transplantations. Both of these
agents (daclizumab and basiliximab) are directed
TeWftf^eldWimage...
278 I • GENERAL PRINCIPLES
against CD25, the high-affinity chain of IL-2 recep-
tor.75,76 These agents were designed to have the same
indications for treatment as antithymocyte globulin
and OKT3 without the significant side effects of those
agents.
The high-affinity chain on the IL-2 receptor is
required for T-cell expansion and targeting. This
receptor offers the advantage that the CD25 receptor
is present only on those active T cells. Theoretically,
this agent should affect only those cells that have been
activated against a new allograft. This agent is also useful
in that it does not lead to the activation of the T cell
and therefore potential cytokine release as is seen with
OKT3. These agents have also had several of the murine
portions of the molecule replaced with human IgG,
thus eliminating much of the nonspecific reactions
observed in the heterogeneous antibodies. These
agents can be used in the induction phase, but because
IL-2 is needed only in the initial activation of T cells,
it does not appear to be useful to stop ongoing rejec-
tion. Early studies of use as induction agents demon-
strated a lower incidence of acute rejection but no
long-term graft prolongation in both cardiac and renal
allografts.77
Immunologic Tolerance
The ultimate goal of transplantation science is to make
genetically disparate organs or tissues be accepted and
regarded as self. This would make chronic immuno-
suppression unnecessary and allow the recipient to
maintain an intact immune system to protect against
infections and malignant neoplasms. The tolerance
would also be "functionally complete," so that the life
expectancy of the organ would not be limited by
chronic rejection. This section provides an overview
of the various mechanisms of T- and B-cell tolerance
and what is known about their role in models of
transplant tolerance.
In the transplantation setting, it appears that T
cell-dependent immune responses are regarded as
being the primary cause of graft rejection. Thus, T-
cell tolerance is important to the generation of
tolerance to organ allografts. Mechanisms of T- and
B-cell tolerance can be divided into three broad cat-
egories: clonal deletion, suppression, and anergy.
Clonal deletion is the process whereby T cells with
particular antigen specificity are eliminated from
the repertoire. Anergy is a state in which T cells can
recognize a foreign antigen but are functionally inac-
tive and do not generate an immune response. Sup-
pression implies the presence of cells that are capable
of actively preventing other T cells from generating
a response. These mechanisms are not mutually exclu-
sive, and the establishment of tolerance may depend
on more than one of these pathways. The application
of these mechanisms for the induction of tolerance
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
offers the future plastic and reconstructive surgeon
the transplantation of foreign tissues without pro-
longed immunosuppression.
CLONAL DELETION
Clonal deletion is the process by which T cells that
express a TCR specific for a certain antigen are
eliminated. The deletion of these cells can occur in the
thymus (central deletion) or extrathymically in the
peripheral tissues (peripheral deletion). The thymus
is the major site for the generation of immunocom-
petent T lymphocytes. T-cell progenitors migrate from
the bone marrow to the thymus, where they undergo
a well-defined pathway of maturation. Once the T cells
express their respective TCRs, they then undergo a
process of selection. During this process, cells with
low-affinity TCRs are not stimulated to progress; this
is called positive selection. T cells in the thymus with
a high affinity for self antigen are eliminated by a
process called negative selection. When this process is
complete, the remaining T cells should be able to
recognize self and mount a response only when they
encounter foreign antigen. Extrathymic clonal dele-
tion has been described in several experimental models
using exogenous antigens78'80 as well as self antigens,81'83
demonstrating that elimination of self-reactive
antigens can occur after maturation in the thymus.This
mechanism may ensure tolerance to self antigens not
expressed in the thymus. Several strategies attempt to
influence this process.
The acceptance or tolerance of one's own tissues
first develops in utero along with an immunologic
ability to recognize foreign tissue. This phenomenon
was successfully exploited by Medawar in his original
experiments in which neonatal rodents were injected
with donor cells and went on to accept skin allografts.
The production of the tolerant state in an adult can
be achieved experimentally by various methods. A
combination of total body irradiation to remove
mature recipient T cells followed by donor bone
marrow infusion before transplantation induces a state
of chimerism. (The term chimera is derived from the
Greek mythological figure composed of the parts of
different animals.) The chimeric host then develops
an immune system that is tolerant of both donor and
self antigens. A further refinement is the use of total
lymphoid irradiation; the marrow cavities of long
bones are protected during irradiation, thus produc-
ing a state of mixed chimerism.84,85 These animals have
gone on to accept donor hearts and kidney allografts.
Another method of achieving transplant tolerance
involves intrathymic injection of donor cells. These
cells survive in the immunologically "privileged"
thymus and cause production of maturing T cells that
are tolerant of the donor alloantigen.86'88 All of these
methods are referred to as central mechanisms of
l'SWt'^aeldW image...
13 • TRANSPLANTATION IN PLASTIC SURGERY
tolerance induction and rely on the phenomenon of
clonal deletion.
ANERCY
For a T cell to become optimally activated, it requires
a second, independent costimulatory signal in addi-
tion to the primary signal that is generated through
the contact between the TCR and the MHC. When T
cells are stimulated in the absence of these signals, they
can become functionally nonresponsive to repeated
stimulation with antigen and are termed anergic.89 Two
major costimulatory interactions that take place
between a T cell and antigen-presenting cell involve
CD28/B7 and CD40L/CD40 pathways. 9092 There has
been considerable interest recently in trying to block
these pathways. Anergy is not automatically maintained
once it is induced, and the continual presence of
antigen has been shown to be required to maintain
tolerance.93,94 Tolerance relying on anergy may also be
a precarious state. It can be broken by infection and
inflammation. 95,96
The blockade of these second signals uses antibodies
(CD40, CTLA4) to specific receptors (CD40R, B27)
to induce a peripheral form of tolerance. The concept
that the presentation of antigen in certain situations
could down-regulate the immune system is not new.
Before the discovery of these receptors, previous
investigators had noted that donor-specific blood
transfusions appeared to increase graft survival,
supposedly by presenting MHC antigens in a limited
fashion and inducing a state of T-cell anergy rather
than activation.97 The interruption of the CD40 and
CD28 pathways (costimulatory blockade) at the time
of transplantation has been demonstrated to induce
a state of tolerance in several rodent models without
any significant infectious or malignant complications.
However, the application to the primate model has
not replicated these results and has demonstrated
only prolongation of allograft survival rather than
tolerance. Several modifications of this technique are
under study and may lead to a longer lasting state
of donor-specific T-cell anergy. Other methods of
peripheral tolerance induction include donor antigen-
presenting cell depletion or modification and anti-
CD4 antibody to block helper T-cell function.98 These
peripheral methods of tolerance induction have not
been as effective as the central mechanisms.
SUPPRESSION
A role for active suppression in inducing and main-
taining tolerance has been suggested by a number of
studies. However, the inability to propagate these cells
in vitro or to identify these cells in vivo has made it
difficult to identify the mechanism involved. Thus, the
mechanism of suppression has remained controver-
sial, although a number of transplantation models
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279
provide functional evidence for the existence of such
cells.99"101 Numerous models suggest that suppression
is mediated through the secretion of cytokines. One
possible explanation is that these cells secrete certain
protolerance cytokines (called T„2 response). This
suppression may also depend on cell-cell contact.
One such mechanism is the so-called veto cell. Veto
activity has been suggested to contribute to graft-
versus-host disease,102,103 bone marrow engraftment,104
and the transfusion effect.105 Currently, there is renewed
interest in the production and role of suppressor cells
in the induction and maintenance of tolerance in
animal models. A technique to produce suppressor cells
could increase the durability of tolerance and perhaps
be employed along with other techniques such as mixed
chimerism.
TRANSPLANTATION IN
PLASTIC SURGERY
Skin
SKIN AUTOGRAFT
Autologous skin grafts can be of either full or partial
thickness. The full-thickness skin graft gives an excel-
lent cosmetic result with limited graft contraction but
has the disadvantage of unreliable graft "take." The
amount of full-thickness skin graft is also limited by
donor site availability. In cases in which large areas are
to be covered, split-thickness skin grafting is used and
is the most commonly practiced form of tissue trans-
plantation in plastic surgery. It has the advantage of
large available donor areas and better graft take but
the disadvantage of increased graft contraction. Expan-
sion of the split-thickness skin graft by meshing with
expansion ratios from 1:1.5 to 1:9is both useful and
sometimes essential in large burns.
Donor sites for split-thickness skin graft harvest may
be limited in patients with extensive burns. This lack
of available tissue has spurred the development of
alternatives to conventional skin graft. Keratinocytes
can be grown in culture with the ability to expand the
available tissue 10,000-fold.106 This technique has
been applied in the treatment of large thermal injuries
as well as leg ulcers and other benign conditions. 107
The reported disadvantages with cultured keratinocytes
are that they are more sensitive to bacterial contami-
nation than a re split-thickness grafts, and take has been
reported as poorer in comparison to meshed graft.I08,109
They also blister spontaneously, are more susceptible
to minor trauma, and contract more than split-
thickness skin grafts do. 110 These effects are related to
a poorly developed dermis-epidermis junction. ' " T h e
lack of a dermal component in these autologous grafts
was overcome by a combination of cultured autolo-
gous keratinocytes and allogeneic dermis.' , 2 The tech-
nique has had favorable reports in patients with large
280 I • GENERAL PRINCIPLES
burns, but the problem of an allogeneic dermis
remains. Development ofanacellular or "artificial^skin
(Integra) consisting of dermal components, collagen,
and a glycosaminoglycan overlaid with a sheet of
Silastic addressed this antigenic problem. 113 A disad-
vantage of this approach is the need to skin graft the
"dermis" after removal of the outer Silastic dressing.
This has been superseded by seeding the graft with
keratinocytes at the time of initial application." 4
A skin substitute containing allogeneic or xeno-
geneic structural proteins and ground substance
seeded with autologous cells has also been described;
it is composed of cultured autologous fibroblasts
populating the dermis and cultured autologous
keratinocytes covering the dermis. 115 These collagen
gel dressings share the disadvantage of autologous cell
culture in that cells require time in culture for expan-
sion to usable numbers. An acellular dermal allograft
available commercially is AlloDerm.* A tissue-engi-
neered living allogeneic dermal construct, DermagrafV
consists of human neonatal dermal fibroblasts seeded
onto a synthetic mesh." 6 It has compared favorably
with skin allograft as a temporary cover for severe burn
wounds." 7,118 Another substitute is Graftskin,* which
is composed of a type I bovine collagen matrix seeded
with allogeneic human fibroblasts and overlaid with
allogeneic human keratinocytes." 9
SKIN ALLOGRAFT
Skin allografts have been/ound to be beneficial in large
burns either in combination with autograft or in iso-
lation.120*124 Techniques such as use of widely meshed
autologous split-thickness skin grafts with a meshed
allograft overlay have been shown to have improved
healing in comparison to autologous mesh alone. The
availability of skin allografts has increased with the
formation of regional tissue banks. Allogeneic skin may
be frozen and banked in a manner that allows it to
remain viable for a protracted period. Preservation with
glycerol reduces the antigenicity of skin allografts and
prolongs their survival.125 Glycerol-treated grafts have
been used in burn centers as coverage for burn wounds
before autografting126 or as composite grafts overlying
widely meshed autografts.122
Factors that limit widespread use are that harvest-
ing and banking services are not uniformly available,
demand outstrips supply, and there is a small but sig-
nificant risk of disease transmission. Cytomegalovirus
infection, hepatitis, and human immunodeficiency
virus infection have been reported in burn patients
after cadaveric skin use. 127 Cultured allogeneic
keratinocytes have also been used as a temporary
•LifeCell Corporation, Branchburg, New Jersey.
'Advanced Tissue Sciences, La Jolia, Calif.
'Organogenesis) Canton, Mass.
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Dr.Mustafa D.
covering and will survive with immunosuppressive
drugs. l28 Growth in culture is possible preemptively in
burn treatment, but skin allografts are susceptible to
rejection in addition to the problems associated with
cultured autografts.
SKIN XENOGRAFT
Porcine xenograft has been used as a temporary dress-
ing in large burns with seeding of autologous grafts
beneath it.'29 The application of xenogeneic dermis has
also been found valuable in preparing a wound for sub-
sequent grafting by stimulation of granulation tissue
formation. The acellular artificial skin described by
Burke" 3 uses a bovine collagen dermis that recipient
fibroblasts repopulate. Xenogeneic tissue has limited
uses in skin grafting because its cellular components
are susceptible to hyperacute rejection.130
Bone
BONE AUTOGRAFT
A series of basic histologic events follows transplan-
tation of a bone autograft.131 After transplantation,
the graft is surrounded by hematoma; the inflamma-
tory cascade follows in which infiltration of inflam-
matory cells is followed by ingrowth of new vessels
with removal and replacement of any dead or necrotic
tissue. Nonvascularized grafts undergo necrosis, most
of the osteocytes in the graft die, and only those on
the surface that re-establish blood supply survive.
The remainder of the graft is infiltrated by blood
vessels from the recipient site and is repopulated by
recipient osteocyte mesenchymal stem cells. Vascular
ingrowth in cortical bone occurs through preexisting
haversian canals. There is an initial increase in osteo-
clast resorption activity, which increases the porosity
and decreases the strength of the graft. Cancellous
grafts are more rapidly revascularized by virtue of their
open structure within 2 to 3 days. By comparison,
revascularization of cortical grafts may take up to 2
months. The process in which vascular tissue invades
the graft, bringing with it osteoblasts that deposit new
bone, has been termed creeping substitution. 132 Cor-
tical bone shows incomplete resorption of necrotic
bone, and the final graft mixture of living and dead
bone does not approach the strength of a cancellous
graft.131 Vascularized bone graft obviates the repara-
tive phase of a nonvascularized graft and does not
require a well-vascularized recipient bed. Biome-
chanically, vascularized bone grafts are also superior
to nonvascularized grafts.133
Reconstruction of larger bone defects is limited by
available autologous donor sites. An alternative being
investigated experimentally is that of autologous
osteocytes expanded in culture and grown in the
recipient on polymer scaffolds.134,135
l%W)W(aa<i1W image...
BONE ALLOGRAFT
The advent of well-organized tissue banks and
improved methods of bone graft sterilization and
preservation have allowed the clinical use of large bone
allografts.136"139 The use of frozen bone allograft has
become a common practice for the reconstruction of
long bone defects, with an estimated annual volume
of more than 200,000 procedures in the United
States.140 MacKewen is credited with the first clinical
use of allograft bone in 1881, followed by Lexer, Parrish,
and others.22,141"144 Few if any of the donor cells in
the nonvascularized bone graft survive. The bone
remaining acts as scaffold for ingrowth of recipient
mesenchymal stem cells (osteocyte precursors) that
repopulate the donor scaffold by creeping substitu-
tion.132 The larger graft acts as a mechanical spacer;
because of slow union, long-term fixation is required,
and as a result, the graft is susceptible to stress frac-
ture and loosening of metal fixation devices. Large joint
replacement has been in clinical practice for some time
with mixed results.22 Parrish 143 reported 50% collapse
with use of frozen whole bone ends in 21 cases. Mixed
results with use of large or smaller shell grafts for joint
resurfacing or replacement after surgical excision have
been reported.145'147 In craniofacial surgery, freeze-dried
bone allografts have been used in midface advance-
ments.' 48 The infection rate was high at 22%, but
osteotomies healed in all patients. Bone allograft with
autogenous bone chips has been reported in mandibu-
lar reconstruction. I49,15° In hand surgery, bone allograft
has been used to reconstruct defects after benign tumor
removal and for traumatic or congenital defects.151,152
No major complications were reported, such as infec-
tions, fractures, or nonunion.
Vascularized allogeneic bone is susceptible to
immunologic rejection.153"156 The humoral and cellu-
lar response generated has a time sequence similar to
that generated by any other allogeneic tissue.2 Although
individual bone cells express antigens, the predomi-
nant immunogenic cell in a bone allograft is thought
to be bone marrow derived.141 Removal of marrow as
in irradiation or by replacement with recipient marrow
has been shown experimentally to prolong allograft
survival.157"159 As with any other allogeneic tissue, this
rejection process can be ameliorated with immuno-
suppression.4,154-160,161
Cartilage
AUTOLOGOUS CARTILAGE
Cartilage is composed of chondrocytes within lacunae
dispersed throughout a water-laden matrix. There are
histologically three types: hyaline cartilage, elastic
cartilage, and fibrocartilage. The matrix is composed
predominantly of proteoglycans and type II collagen.
Cartilage has no blood supply and relies on diffusion
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3 • TRANSPLANTATION IN PLASTIC SURGERY 281
of nutrients and oxygen through the matrix. Chon-
drocytes, in contrast to osteocytes, have little repara-
tive ability and heal by forming fibrous scar tissue.162
The viscoelastic properties of the matrix provide car-
tilage with a "memory" in that it returns to its origi-
nal shape after deformation; the variable water content
in matrix causes a balanced tension within it and thus
maintains its three-dimensional shape.
Cartilage autograft is used regularly for nasal,
auricular, craniofacial, and joint surface reconstruc-
tion. ' 6 There are limited potential donor sites. Devel-
opment of experimental tissue engineering techniques
has allowed the expansion of chondrocytes in culture
to increase their numbers. These cells are seeded onto
biodegradable polymers to form new autologous
cartilage.134,135,170,171 Injectable polymer systems allow
delivery of autologous cartilage by needle, transcuta-
neously, or arthroscopically.172"174
CARTILAGE ALLOGRAFT
Chondrocytes express HLA antigens on their surface
and are immunogenic. 145 The matrix is only weakly
antigenic.175 Surgical scoring or dicing with resultant
exposure of allogeneic cells has been shown to hasten
resorption of allogeneic cartilage. 176,177 Cartilage
allografts have been used for applications similar to
those of autologous cartilage.178 Allogeneic cartilage
can be either preserved or fresh. Preserved cartilage
has the advantage of a more abundant supply without
the risk of infection that is associated with the use of
fresh cartilage.179"181 Cartilage allograft, usually with
irradiation pretreatment, has been used for volume
augmentation in the facial skeleton. Despite initial good
results in a large number of patients, 181 long-term data
suggest a high rate of resorption. 182 Whether this is
immunologically based or because preserved grafts tend
to contain no viable cells is a matter for debate. 183 It
has also been noted that smaller grafts are less sus-
ceptible than larger ones to graft volume loss.
CARTILAGE XENOGRAFT
Bovine-derived cartilage xenografts are susceptible to
xenogeneic mechanisms of rejection, which results in
a generally poorer outcome in comparison to either
allogeneic or autogenous cartilage grafts. Attempts to
modify these xenogeneic responses by altering the
graft's immunologic stereotactic structure have been
reported as being beneficial.184
Nerve
NERVE AUTOGRAFT
The best clinical outcome after nerve transection is
achieved with primary repair. Extensive injuries with
a nerve gap require a nerve graft to achieve nerve repair
without tension. The nerve graft undergoes the same
282 I • GENERAL PRINCIPLES
degenerative process as in the distal recipient nerve
after division.185 What remains of the nerve graft is
a myelin sheath with Schwann cells that act as a
biologic conduit for the regenerating axons. The most
common type of nerve graft is the interfascicular nerve
graft, which joins fascicular groups to their distal
matching group with an interposition nerve graft.186
Other types in modern practice are fascicular nerve
grafts (limited by matching proximal to distal fasci-
cle) and vascularized nerve grafts, thought theoreti-
cally to be of advantage although not of proven benefit
clinically.187,188 Other "conduits" have been used as
nerve grafts, such as silicone tubes seeded with
Schwann cells, autologous vein, freeze-fractured autol-
ogous muscle, and pH tubes.189 Artificial conduits have
demonstrated improved outcome when they have been
seeded with autologous Schwann cells. None of the
conduits to date has been found to be superior to nerve
autograft.
NERVE ALLOGRAFT
Nerve autograft has a limited number of donor sites.
In large nerve defects, nerve allograft has been used in
a small number of patients. Immunologic rejection of
nerve allograft can be prevented experimentally with
immunosuppressive drugs,190,191 and immunosup-
pressed axons will traverse the allogeneic graft in
rodents192"194 and nonhuman primates.195 Immuno-
suppression needs to be administered only while the
recipient axons traverse the allograft and can then be
terminated.196"198 Mackinnon199,200 reported a series of
seven patients who underwent nerve allografting in
the upper and lower extremities. Immunosuppression
was stopped 6 months after nerve regeneration across
the allografts. All but one patient demonstrated return
of motor and sensory functions.
Limb and Composite Tissues
Microvascular autogenous tissue transfer is a well-
established reconstructive modality.201,202 Such trans-
fers are limited by available donor sites, which may be
associated with potentially significant morbidity. The
ability to use allogeneicYimb or composite tissues such
as skin, subcutaneous tissues, muscle, bone, blood
vessel, and nerve would greatly broaden the realm of
reconstructive surgery. Extensive skeletal and soft tissue
defects or even whole limbs could then be replaced.
However, nonautogenous tissue is susceptible to
immunologically mediated rejection with subsequent
graft loss, and prolonged immunosuppression is the
only way at present to attain long-term allograft or
xenograft survival. To make composite tissue trans-
plantation clinically feasible, consideration should be
given to its technical, functional, and immunologic
aspects.
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TECHNICAL CONSIDERATIONS
Transplantation of vascularized limb or composite
tissues was made possible by the microsurgical
techniques first developed by Carrel and Guthrie in
1906.203,204 Microvascular anastomoses and revascu-
larization have become routine practice in large centers
with success rates in excess of 90%.20S,2°6 In contrast to
acute traumatic cases, such as replantation, allogeneic
transplantation may be performed in elective settings
after appropriate preparation, such as preoperative
angiography and donor selection. Advances in bone,
tendon, and nerve repairs may further enhance
eventual outcome. Finally, fetal composite tissue
transplantation may be technically feasible for certain
congenital conditions diagnosed prenatally. Although
such endeavor would involve a complex microvascu-
lar procedure with possible risks for the fetus, trans-
plantation in utero would offer potential immunologic
advantages in recipients with immature immune
systems.
FUNCTIONAL CONSIDERATIONS
Normal wound healing and bone growth occur in
transplanted composite tissue allografts after experi-
mental transplantation in various animal models.4'207,208
Return of neuromuscular function has been observed
in limb allografts of animals treated with immuno-
suppression,209,210 including those in the primates.211"213
Early motor and sensory recovery has also been
reported in a few cases of human hand transplanta-
tion.8,9 Thus, functional recovery after allogeneic
transplantation appears to follow the same principles
as in nontransplant situations and is influenced by the
recipient's age, systemic factors, and associated local
injuries.
IMMUNOLOGIC CONSIDERATIONS
A limb or composite tissue allograft consists of mul-
tiple discrete tissue components, such as skin, subcu-
taneous tissue, muscle, and bone, and each tissue has
been shown to be strongly antigenic.2 Both animal data
and early human experience have confirmed the need
for significant host immunosuppression to prevent
allograft rejection. The potential adverse effects of
indefinite, multiple-agent immunosuppression are
difficult to justify in the opinions of many for a sur-
gical procedure aimed at improving the quality of
life.214,215 The debate over the risk-benefit balance has
intensified since the first successful human hand
transplantation.216,217 However, both the proponents
and critics of the current transplants agree that sig-
nificant reduction of host immunosuppression, and
particularly tolerance induction to the allografts,
would help achieve widespread clinical application of
- composite tissue allografts.
image...

13 • TRANSPLANTATION IN PLASTIC SURGERY 283

EXPERIMENTAL LIMB TRANSPLANTATION significant mortality and morbidity, including

Limb allograft transplantation is possible experimen-
tally with different immunosuppressive regimens
(Table i3_3).207.209.2i2.2i3.2i8-228 I m m u n e m o d u l a t i o n
techniques that decrease the antigenicity of specific
components of a limb allograft were shown to prolong
survival.157*159 Although sporadic incidents of tolerance
have been reported after cessation of immuno-
suppressants, 219 long-term immunosuppression was
generally necessary to prevent allograft rejection.4
Combination therapy with cyclosporine and MMF was
more effective than monotherapy. 229 Although the rat
models provide important information on limb allo-
graft transplantation, the rodent immune system is fun-
damentally different from that of the human. A large
animal model such as pig or primate offers a much
closer analogy to the human immune system.
Ustuner et al228 reported transplantation of a
radial forelimb osteomyocutaneous flap between size-
matched outbred swine with use of a daily cyclosporine,
MMF, and prednisone oral regimen. Of the eight swine,
two sustained severe rejection, three demonstrated mild
to moderate rejection, and three were free of rejection
at the termination of the experiment at 90 days. No
drug toxicity was evident in serum hematologic and
chemical parameters of immunosuppressed animals.
The Louisville group 230 also examined the use of FK506,
MMF, and prednisone in the same swine model. Five
of nine animals that survived to the study end at 90
days were noted to be free of rejection. However, this
combination of immunosuppressants resulted in
abscesses, diarrhea, weight loss, and pneumonia.
Lee et al231,232 sought to achieve host tolerance to
musculoskeletal allografts through matching of the
MHC antigens between donor and host swine with
only a 12-day course of cyclosporine. Allografts from
MHC-mismatched donors treated with cyclosporine
and allografts from MHC-matched (minor antigen
mismatched) donors not treated with cyclosporine
were rejected. However, allografts from MHC-matched
donors treated with 12 days of cyclosporine showed
no evidence of rejection until sacrifice up to 47 weeks
after transplantation. Thus, genetic matching may
alleviate the need for immunosuppression after limb
transplantation. MHC matching can be extended
beyond family members, for example, as the National
Bone Marrow Registry exists to match M H C of
unrelated individuals.
The primate model offers the closest imitation to
human limb transplantation in anatomy and immune
system. In the 1980s, four studies of limb allograft
transplantation were performed on nonhuman pri-
mates.212,227,233,234 All of the studies involved the trans-
plantation of a hand or neurovascularized portion of
a hand with use of high-dose cyclosporine and steroids.
Many of the animals suffered multiple infectious com-
plications, with some succumbing to fatal malignant
neoplasms resulting from high levels of immunosup-
pression. Nonetheless, few primates demonstrated
prolonged survival of their allografts. These studies
confirmed the existing rodent and canine data that
monotherapy is ineffective in preventing limb allograft

TABLE 13-3 • EXPERIMENTAL LIMB ALLOGRAFT TRANSPLANTATION

Immunosuppressive Animal Survival

Agent Model (days) Author Year

6-Mercaptopurine, azathioprine Dog 18 Coldwyn 224 1966

Azathioprine, hydrocortisone, antilymphocyte globulin Dog 112 Lance226 1971
6-Mercaptopurine, azathioprine, prednisolone Rat — Doi 220 1979
Cyclosporine (25 mg/kg/day) Rat 100 Black 2 ' 9 1985
Cyclosporine (8 mg/kg/day) Rat >400 Furnas225 1983
Cyclosporine (15 mg/kg/day) Rabbit 90 Siliski 264 1984
15-Deoxyspirgualin Rat 18 Walter 265 1989
FK506 Rat 50 Kuroki 266 1989
FK506 Rat 102 Arai 2 ' 8 1989
Cyclosporine (10 mg/kg/day) Rat 14 Lee2 1991
Cyclosporine (5-10 mg/kg/day) Rat 365 Lee'1 1995
FK506 or cyclosporine Rat 300 Buttemeyer 267 1996
Rat 231-257 Benhaim 229 1996
Cyclosporine, MMF
Swine 90 Ustuner228 1998
Cyclosporine, MMF, steroid
Swine 90 Jones 250 1999
FK506, MMF, steroid Swine 175-329 Lee252 2001
Cyclosporine + MHC match Primate 304 Daniel 2 ' 2 1986
Cyclosporine, steroid Primate 296 Stark 227 1987
Cyclosporine (20 mg/kg/day) Primate 179 Hovius254 1992
Cyclosporine (25 mg/kg/day)

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Dr.Mustafa D.
284 I • GENERAL PRINCIPLES
rejection, even at toxic doses. Few allografts survived
long enough for functional recovery to be ascertained.
No study has been performed in the primates with com-
bination immunosuppressant therapy. The application
of such a regimen could provide insight into nerve
regeneration, bone healing, and ultimate recovery of
function.
HAND REPLANTATION AND
TRANSPLANTATION
Eighteen hand transplantations were performed world-
wide from 1998 to 2003, including six bilateral hand
transplantations. However, in early 2001, the world's
first transplanted hand was removed because of poor
function and graft rejection attributed to the recipi-
ent's noncompliance with his immunosuppressive
regimen. At the time of the first hand transplantation,
the procedure was hailed by some as a major advance
in reconstructive surgery.6 This case demonstrated the
importance of selection of patients and clear indica-
tions for hand transplantation.
Hand transplantation per se is not a major surgi-
cal or immunologic advance. Surgeons have had the
technical ability to reattach amputated parts of the
upper limb for more than 30 years. Replantation of
the upper extremity was first performed by Malt235 at
the Massachusetts General Hospital in 1962 and was
followed by the first microsurgical reattachment of an
amputated hand by Chen 236 in China. Whereas emer-
gency hand and digital replantation has been performed
routinely in microsurgical centers around the world,
transplantation of a hand is in many respects techni-
cally easier than the reattachment of an acutely
amputated one. Similarly, hand transplantations do
not herald a breakthrough in transplantation immunol-
ogy. New and more potent immunosuppressant drugs
can prevent rejection of even highly antigenic tissues,
as long as sufficiently high doses of different agents are
used. The critical issue is how much immunosup-
pression, and significant lifelong morbidity, can be
justified for a non-lifesaving procedure.
It is likely that the best functional result from limb
transplantation would at best be comparable to the
reported experience with limb replantation. Wang237
reported a 77% success rate in 91 cases of replanted
limbs. In that series, results were graded excellent in
18 patients and good in 38 patients; only 7 patients
had a viable but nonfunctional limb. In a multi-
institutional retrospective study, 56% of patients had
functional recovery in the excellent to good range after
replantation. 236 Other reviews of functional outcome
after replantation were less favorable.238 Ipsen et al239
reviewed their experience with limb replantation from
1978 to 1987. Of the eight patients who had a com-
plete amputation in Ipsen's series, there were no excel-
lent results; three patients had good recovery, four had
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Dr.Mustafa D.
fair recovery and partial functional return, and one
patient had a poor result. Others reported patients with
varying degrees of cold intolerance and poor sensi-
bility after replantation. 240
The other major consideration relates to the po-
tential for functional recovery after replantation. It
has generally been found that the more proximal the
level of amputation, the worse the functional outcome;
and the younger the patient, the better the neuro-
muscular recovery after nerve repair. Compared with
replantation after acute injuries, transplantation of
a hand allograft can be planned and executed elec-
tively with selection of appropriate donors and
recipients. The allograft may be harvested surgically
according to specific requirements, as opposed to the
frequent crush or avulsion injuries encountered in
amputation, and warm ischemia time may be mini-
mized. However, a chronically scarred recipient bed
may offset these advantages. Recipient muscle may
have become shortened or atrophied from disuse, and
nerve regeneration after prolonged inactivity may be
unpredictable. Finally, even with a patient compliant
with medication and hand therapy, there are concerns
that chronic rejection might compromise long-term
function.
Early Outcome of Hand Transplantation
The functional recovery of the first four human hand
transplants was evaluated by the Carroll test, which
assesses the global functional capabilities of the upper
limb in its everyday use.24' In general, a prosthesis scores
"poor" and the best replantation outcome scores
"good." The functional capacity of the transplanted
hands was considered poor in the first patient (whose
allograft underwent rejection), fair in two patients, and
good in one patient. 8,9 After 10 months, the patients
from Lyon and Louisville were able to perform simple
tasks of daily life, such as opening doors, holding and
paging through a newspaper, and filling up a glass of
water. Despite rapid progression of Tincl signs, nerve
regeneration did not result in reinnervation of the
intrinsic muscles or satisfactory distal sensitivity
indicated by the Semmes-Weinstein test.242 The psy-
chological and social benefits of hand transplantation
could not be quantified, however, because many recip-
ients expressed satisfaction with their transplants.
The functional results achieved in the first hand
transplantations also help place in perspective the
consequence of long-term immunosuppressive treat-
ment. During the first 8 to 20 months postoperatively
of the first four hand transplant recipients, the following
complications were observed: insulin-dependent dia-
betes mellitus, Cushing syndrome, cytomegaloviral
colitis, herpetic cutaneous infection, and recurrent
cutaneous mycoses.8,9,243 All the complications were
treated successfully with decreased immunosuppres-
sion. Episodes of graft rejection, noted grossly and
 image...
13 • TRANSPLANTATION IN PLASTIC SURGERY
histologically in the skin, were reversed with a tran-
sient increase in the i m m u n o s u p p r e s s a n t regimen.
FUTURE TRANSPLANTATION IN
PLASTIC SURGERY
Many regard the use of chronic high-dose i m m u n o -
suppression to achieve transplantation of limb allo-
graft difficult to justify clinically.214'217,244 Development
of effective regimens to induce host tolerance without
long-term immunosuppression, therefore, is essential
to alter the risk-benefit balance. Such regimens may
involve site-specific immunosuppression directed at
the graft, appropriate matching of M H C antigens
between d o n o r and recipient, 232 monoclonal antibod-
ies that block a particular step in the rejection cascade,
or exposure to donor antigen before transplantation
to create a chimera. 2 4 5
The use of new monoclonal antibodies such as CD40
ligand may allow the reduction of i m m u n o s u p p r e s -
sion. It has been observed that full activation of T cells
requires both cell-cell interaction and simultaneous
delivery of costimulatory signals. A T cell that encoun-
ters foreign antigen in t h e absence of necessary
cytokines fails to activate, which may lead to a state
of tolerance. 246 This mechanism is based on the
blockade of CD2B/CTLA4-CD80 and the CD40-CD40
ligand (CD 154) pathways. 247,248 Several n o n h u m a n
primate tolerance models to evaluate the effect of
interrupting these critical pathways have d e m o n -
strated prolonged survival of renal allografts. 249,250 It
remains to be seen whether such strategies could allow
limb transplantations to be performed with a low level
of immunosuppression.
An alternative strategy involves the use of bone
marrow or stem cells to induce a state of mixed
chimerism. Owen a n d Medawar observed m o r e than
a half-century ago that it is possible to induce toler-
ance by exposing the donor's bone m a r r o w to the
recipient's i m m u n e system before its maturity. 251 Such
fetal or neonatal induction of tolerance for m u s c u -
loskeletal allografts has been achieved in experi-
mental swine a n d rodent models, respectively.252"254
Successful adaptation of this approach would have
therapeutic potential for congenital conditions. Similar
application of mixed chimerism protocols could also
lead to tolerance induction in adults. 255,256 Foster et al257
demonstrated that rodent mixed chimeras would
accept syngeneic donor limb allografts. Huang et al258,259
have used a minimally toxic protocol to generate mixed
chimeras in the miniature swine with in vitro donor-
specific tolerance while preserving i m m u n o c o m p e -
tence to third-party antigens. Preliminary findings with
the same model d e m o n s t r a t e d tolerance to limb
allografts across major M H C barriers. 2 6 0
Composite tissue transplantation offers potential
solutions for many reconstructive problems, includ-
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
285
ing but not limited to limb amputation. Whereas the
current h a n d transplant recipients have demonstrated
survival of allografts while receiving h i g h - d o s e
immunosuppression, the risk-benefit balance remains
precarious for transplantations aimed toward improv-
ing the quality of the recipient's life. Successful adap-
tation of tolerance induction modalities reducing or
eliminating the need for chronic immunosuppression
may launch another transplantation frontier in recon-
structive surgery. 261 " 263
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155. Gornct MF, Randolph MA, Schofield BH, et al: Immunologic
and ultrastructural changes during early rejection of vascu-
larized bone allografts. Plast Reconstr Surg 1991;88:860-
868.
156. Innis PC, Randolph MA, Paskert JP, et al: Vascularized bone
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157. LeeWPA,RandolphMA,WeilandAJ,YarcmchukMJ:Prolonged
survival of vascularized limb tissue allografts after donor
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158. Lee WPA, Yaremchuk MJ, Manfrini M, et al: Prolonged sur-
vival of vascularized limb allografts from chimera donors. Plast
Surg Forum 1988;! 1:51.
T-e^H^aeldW image...
13 • TRANSPLANTATION IN PLASTIC SURCERY
159. Lee WPA, Butler PEM, Randolph MA, Yaremchuk MJ: Donor
modification leads to prolonged survival of limb allografts.
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160. Paskert JP, Yaremchuk MJ, Randolph MA, Weiland AJ:
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161. Paskert JP, Yaremchuk MJ, Randolph MA, Weiland AJ: The
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165. Gabrielli ME, Okamoto T, Marcantonio E, Barbosa CE:
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Nihon Univ School Dent 1986;28:87-99.
166. Grande DA, Pitman MI, Peterson L, et al: The repair of
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170. Langer R, Vacanti JP: Tissue engineering. Science 1993;260:920.
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186. Millesi H, Meissl G, Berger A: The interfascicular nerve graft-
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187. Best TJ, Mackinnon SE, Bain JR, et al: Verification of a free
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188. Gilbert A: Vascularized sural nerve graft. Clin Plast Surg
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189. Hazari A, Johansson-Ruden G, Junemo-Bostrom K, et al: A
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190. Anssclin AD, Pollard JD, Davcy DF: Immunosuppression in
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191. Bain JR, Mackinnon SE, Hudson AR.et al:Thc peripheral nerve
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193. Mackinnon SE, Midha R, Bain J, et al: An assessment of regen-
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194. Midha R, Mackinnon SE, Evans PJ.et al: Comparison of regen-
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195. Bain JR, Mackinnon SE, Hudson AR, ct al:The peripheral nerve
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196. Zalewski AA, Gulati AK: Rejection of nerve allografts after
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197. Zalewski AA, Azzam NA, Azzam RN: The loss of regenerated
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198. Mackinnon SE, Hudson AR, Bain JR, et al: The peripheral nerve
allograft: an assessment of regeneration in the immunosup-
pressed host. Plast Reconstr Surg 1987;79:436-446.
199. Mackinnon SE, Doolabh VB, Novak CB,Trulock EP: Clinical
outcome following nerve allograft transplantation. Plast
Reconstr Surg 2001;107:1419.
200. Hctt!aratchyS,MathesDW,PetitF,LeeWPA:Nerveallografting
representsa unique situation. Plast Reconstr Surg2002;109:825-
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201. O'Brien BM: Microvascular Reconstructive Surgery. Edinburgh,
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202. Weiland AJ, Kleinert HE, Kutz JE, Daniel RK: Free vascular-
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203. Carrel A, Guthrie CC: Anastomosis of blood vessels by the
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1906;72:1648.
290 I • GENERAL PRINCIPLES
204. Carrel A, Guthrie CC: Complete amputation of the thigh with
replantation. Am J Med Sci 1906; 131:297.
205. Weiland Aj, Villarreal-Rios A, Kleinert HE, et al: Replantation
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206. TamaiS:Twentyyears'experienccof limb replantation—review
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207. Hotokebuchi T, Arai K, Takagishi K, et al: Limb allografts in
rats immunosuppressed with cyclosporine: as a whole-joint
allograft. Plast ReconstrSurg 1989;83:1027.
208. Hotokebuchi T, Arai K, Miyahara H, et al: Limb allografts in
skeletally immature rats with cyclosporin: behavior of the
growth plate. Transplant Proc 1989;21:3183.
209. Press BH, Sibley RK, Shons AR: Limb allotransplantation in
the rat: extended survival and return of neurofunction with
continuous cyclosporin and prednisolone immunosuppres-
sion. Ann Plast Surg 1986; 16:313.
210. Guzman-Stein G, Shons AR: Functional recovery in the rat
limb transplant model: a preliminary study. Transplant Proc
1987;19:1115.
211. Egerszegi PE, Samulack DD, Daniel RK: Experimental models
in primates for reconstructive surgery utilizing tissue trans-
plants. Ann Plast Surg 1984; 13:423.
212. Daniel RK, Egerszegi EP, Samulack DD, et al: Tissue trans-
plants in primates for upper extremity reconstruction: a pre-
liminary report. J Hand Surg Am 1986; 11:1.
213. Hovius SER, Stevens HP, Van Nierop PW, et al: Replantation
of the radial side of the hand in the rhesus monkey, anatomi-
cal and functional aspects: a preliminary study of composite
tissue allografting.. Br J Hand Surg 1992;17:651.
214. Mathes DW,Lce WPA: Composite tissue transplantation: more
science and patience needed. Plast Rcconstr Surg 2001;107:
1066-1070.
215. Strickland JW: Hand transplant—technology over good sense.
Indiana Hand Center Newslett 1999;3:2-4.
216. Lee WPA, Mathes DW: Hand transplantation: pertinent data
and future outlook. J Hand Surg Am 1999;24:906-913.
217. Cooney WP, Hentz VR: Hand transplantation—primum non
nocere. Position statement: Council of the American Society
for Surgery of the Hand. J Hand Surg Am 2002;27:165.
218. Arai K, Hotokebuchi T, Miyahara H, et al: Limb allografts in
rats immunosuppressed with FK506. I. Reversal of rejection
and indefinite survival. Transplantation 1989;48:782-786.
219. Black KS, Hewitt CW, Fraser LA, et al: Composite tissue (limb)
allografts in rats. II. Indefinite survival using low-dose
cyclosporine. Transplantation 1985;39:365.
220. Doi K: Homotransplantation of limbs in rats: a preliminary
report on an experimental study with nonspecific immuno-
suppressive drugs. Plast Reconstr Surg 1979;64:613.
221. Fealy M J, Umansky WS, Bickel KD, et al: Efficacy of rapamycin
and FK 506 in prolonging rat hind limb allograft survival. Ann
Surg 1994;219:88-93.
222. Fritz WD, Swartz WM, Rose S, et al: Limb allografts in rats
immunosuppressed with cyclosporin A. Ann Surg 1984;199:
211-215.
223. Furnas DW, Black KS, Hewitt CW, et al: Cyclosporine and long
term survival of composite tissue allografts (limb transplants)
in rats. Transplant Proc 1983;15(suppl):3063-3068.
224. Goldwyn RM, Beach PM, Feldman D, et al: Canine limb homo-
transplantation. Plast Reconstr Surg 1966;37:184.
225. Hewitt CW, Black KS, Fraser LA, et al: Composite tissue (limb)
allografts in rats. I. Dose-dependent increase in survival with
cyclosporine. Transplantation 1985;39:360-364.
226. Lance EM, Inglis AE, Figarola F, Veith FJ: Transplantation of
the canine hind limb. Surgical technique and methods of
immunosuppression for allotransplantation. J Bone Joint Surg
Am 1971;53:1137.
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227. Stark GB, Swartz WM, Narayanan K, Moller AR: Hand trans-
plantation in baboons. Transplant Proc 1987;19:3968-3971.
228. Ustuncr ET, Zdichavsky M, Ren X, et al: Long-term composite
tissue allograft survival in a porcine model with cyclosporine/
mycophenolate mofetil therapy. Transplantation 1998;66:1581-
1587.
229. Benhaim P. Anthony JP, Ferreira L, et al: Use of combination
of low-dose cyclosporineandRS-61443inar3thindlimb model
of composite tissue allotransplantation. Transplantation
1996;61:527-532.
230. Jones JW Jr, Ustuner ET, Zdichavsky M, et al: Long-term sur-
vival of an extremity composite tissue allograft with FK506-
mycophenolate mofetil therapy. Surgery 1999;126:384-388.
231. Lee WPA, Rubin JP, Cober S, et al: Use of swine model in trans-
plantation of vascularized skeletal tissue allografts. Transplant
Proc 1998;30:2743-2945.
232. Lee WPA, Rubin JP, Bourget JL, et al: Tolerance to limb tissue
allografts between swine matched for major histocompati-
bility complex antigens. Plast Reconstr Surg 2001;107:1482-
1490.
233. Samulack DD, Dykes RW, Munger BL: Neurophysiologic aspects
of allogeneic skin and upper extremity composite tissue trans-
plantation in primates.Transplant Proc 1988;20(suppl 2):279-
290.
234. Hovius SE, Stevens HP, van Nierop PW, et at: Allogeneic
transplantation of the radial side of the hand in the rhesus
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709.
235. Malt RA, McKhann CF: Replantation of severed arms. JAMA
1964;189:716-722.
236. Chen ZW, Meyer VE, Kleinert HE, Bcasley RW: Present indi-
cations and contraindications for replantation as reflected by
long-term functional results. Orthop Clin North Am
1981;12:849-870.
237. Wang SH, Young KF, Wei JN: Replantation of severed l i m b s -
clinical analysis of 91 cases. J Hand Surg Am 1981;6:311-318.
238. Tamai S: Twenty years'experienceof limb replantation—review
of 293 upper extremity replants. J Hand Surg Am 1982;7:549-
556.
239. Ipsen T, Lundkvist L, Barfrcd T, Plcss J: Principles of evalua-
tion and results in microsurgical treatment of major limb
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1987. Scand J Plast Reconstr Surg Hand Surg 1990;24:75-80.
240. Vanstraelen P, Papini RPG, Sykes PJ, Milling MAP: The func-
tional results of hand replantation: the Chepstow experience.
J Hand Surg Br 1993;18:556-564.
241. Carroll D: A quantitative test of upper extremity function. J
Chronic Dis 1965;18:479-491.
242. Owen ER, Dubernard JM, Lanzetta M, et al: Peripheral nerve
regeneration in human hand transplantation. Transplant Proc
2001;33:1720-1721.
243. Lee WP, Breidenbach WC, Hodges A, et al: Lessons from hand
transplantation. Panel discussion, "Around the hand table."
Chicago, 111, American Association for Hand Surgery, Summer
2001:12. Hand Surgery Quarterly.
244. Hettiaratchy S, Butler PE, Lee WP: Lessons from hand trans-
plantations. Lancet 2001;357:494-495.
245. Mathes DW, Randolph MA, Lee WP: Strategies for tolerance
induction to composite tissue allografts. Microsurgery
200020:448-452.
246. Viola A, Schroeder S, Sakakibara Y, Lanzavecchia A: T lym-
phocyte costimulation mediated by reorganization of mem-
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247. Schoenberger SP, Toes RE, van der Voort EI, et al: T-cell help
for cytotoxic T lymphocytes is mediated by CD40-CD40L
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248. Grewal IS, Flavell RA: CD40 and CD154 in cell-mediated
immunity. Annu Rev Immunol 1998;16:111-135.
TfcxPttf'SelCiW image...
13 • TRANSPLANTATION IN PLASTIC SURGERY
249. Kirk AD, Burkly LC, Batty DS, et al: Treatment with human-
ized monoclonal antibody against CD 154 prevents acute renal
allograft rejection in nonhuman primates [seecomments]. Nat
Med 1999;5:686-693.
250. Kirk AD, Harlan DM, Armstrong NN, et al: CTLA4-Ig and
anti-CD40 ligand prevent renal allograft rejection in primates.
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251. Owen RD: Immunogenetic consequences of vascular anasto-
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252. Rubin JP, Cober SR, Butler PEM, et al: Injection of allogeneic
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253. Mathcs DW, Randolph MA, Butler PEM, et al: Intravascular
in utero injection of adult bone marrow leads to acceptance
of fully mismatched composite tissue allografts. Surg Forum
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254. Butler PEM,LeeWPA,Vande Water AP, Randolph MA: Neona-
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256. Sharabi Y, Sachs DH: Mixed chimerism and permanent
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264. Siliski JM, Simpkin S, Green CJ: Vascularized whole knee joint
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Transplant Proc 1989;21:3186.
266. Kuroki H, Ikuta Y, Akiyama M: Experimental studies of
vascularized allogenic limb transplantation in the rat using
a new immunosuppressive agent, FK-506: morphological
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3187.
267. Buttemeyer R, Jones NF, Min Z, Rao U: Rejection of the com-
ponent tissues of limb allografts in rats immunosuppressed
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97:139-148, discussion 149-151.
image...
CHAPTER
14
•
Skin Grafts
CHRISTIAN E. PALETTA, MD • JEFFREY J. POKORNY, MD
• PETER RUMBOLO, MD
HISTORY
SKIN ANATOMY AND PHYSIOLOGY
Epidermis
Dermis
Dermal-Epidermal Junction
Blood Supply
Hair Follicles
Sebaceous Glands
Apocrine Glands
Eccrine Glands
WOUND PREPARATION
HISTORY
Baronio' performed the first successful skin graft in
1804 on a lamb. However, it was not until Jacques
Rcverdin, a Swedish medical student studying in
Paris, placed 2- to 3-mm epidermal grafts onto a gran-
ulating wound in 1869 that skin autotransplantation
was born. Reverdin's experiment demonstrated that
skin transfer from one individual onto an open sore
of the same individual not only survived but actually
hastened wound healing.2 Consequently, a great deal
of interest in skin grafting developed throughout
Europe. Surgeons attempted grafts on all wounds and
used multiple donor sites, including skin from animals,
and predictably the results were disappointing. Sub-
sequently, the initial enthusiasm over skin grafting
began to waiver.
A few pioneers discovered some secrets to success-
ful grafting. George Lawson3 reported the first suc-
cessful full-thickness graft in 1871. Louis Oilier,4 a
French surgeon, described the first intermediate-
thickness skin graft and was using grafts as large as 8
cm 2 in 1872. Whereas Carl Thiersch, a prominent
German surgeon, erroneously thought that thin epi-
dermal grafts were required for successful donor site
healing, he was the first surgeon to recognize the im-
portance of preparing the recipient bed. In 1874,
Thiersch 5 described removing granulation tissue from
the wound before applying his graft, which dramati-
cally improved graft "take."
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
SKIN CRAFTS
Split Versus Full Thickness
Donor Sites
Harvesting
Preparing the Graft
Postoperative Care
Storage
Craft Survival
Graft Failure
SKIN SUBSTITUTES
THE FUTURE OF SKIN GRAFTING
Even with these historic developments, the use of
skin grafts was not widely accepted by surgeons at the
turn of the century. Results were unreliable, harvest-
ing was difficult, and some thought that skin grafting
resulted in two wounds instead of one. It was for this
reason that Otto Lanz, a Swedish surgeon, described
a method of meshing the harvested skin to obtain
additional length so that both the wound and the
donor site could be grafted.6 Some surgeons abandoned
Thiersch's epidermal grafts altogether and applied
Reverdin's technique in what is now known as pinch
grafts.
It was not until 1929 when Vilray Papin Blair and
James Barrett Brown, from Saint Louis, described their
technique and success with split-thickness skin graft-
ing that reliable results with skin grafts could be
expected. Blair and Brown differentiated between
full-thickness, intermediate-thickness, and epidermal
(Thiersch) grafts. They identified the advantages and
disadvantages of each. They described wound pre-
paration, graft harvest, graft application, contrain-
dications, and postoperative care. They dispelled the
misconception that donor sites would not heal if part
of the dermis were removed with the graft. These fun-
damental principles of skin grafting described by Blair
and Brown still hold true today.7,8
Once surgeons discovered the principles of suc-
cessful skin graft procedure, the challenge of skin graft-
ing was the harvest. Grafts were generally cut from the
donor site with a razor or long freehand blade, which
293
294 I • GENERAL PRINCIPLES

was both imprecise and technically difficult. This led
to the development of instruments to aid in the harvest
of skin grafts. The first device built specifically for har-
vesting of skin grafts was a simple instrument devel-
oped by Humby in 1936. The Humby knife was a razor
with a guard, which prevented the surgeon from cutting
too deep during the harvest.6 Although this dermatome
allowed faster and safer harvests, surgeons still did not
have precise control over the thickness of the grafts.
With the beginning of World War II in 1941 > there devel-
oped an urgent need in the Army for a consistent and
quick method to harvest skin. Earl Padgett,9 an Amer-
ican surgeon, in coordination with an engineer named
Hood, designed a dermatome that could be set at a
specific thickness in 1939. Just 6 years later, James
Barrett Brown introduced the first power-driven der-
matome. All three dermatomes are still used today, but
the power-driven dermatome is by far the most
popular. Because of the work of Reverdin, Thiersch,
Lanz, Blair, and Brown, surgeons today approach skin
grafting confidently, expecting success with each graft.
SKIN ANATOMY AND
PHYSIOLOGY
The skin covers the entire surface of the body and
is continuous with the epithelium of the digestive,
respiratory, and urogenital systems. It plays an impor-
tant role as a sensory organ and is important in vitamin
D metabolism.10 This epithelial layer performs two
essential functions. It provides a physical barrier to the
mechanical, chemical, and microbiologic insults of the
environment. The skin also plays an important role in
thermoregulation.
The skin consists of two distinct layers, an epider-
mis and dermis (Fig. 14-1). The epidermis, the outer-
most layer, is essentially avascular. The principal
function of the epidermis is a process called cornifi-
cation, which develops a tough layer of "dead" cells
that are capable of withstanding the rigors of the envi-
ronment. The dermis is the vascular bed to the epi-
dermis, and the capillaries present are able to regulate
temperature by either vasodilation (heat loss) or vaso-
constriction (heat preservation).
Epidermis
The epidermis varies in thickness from 0.04 mm on
the eyelid to 1.6 mm on the palms. It is made up of
four distinct cells: the keratinocyte, the melanocyte,
the Langerhans cell, and the Merkel cell. The epider-
mis first appears embryologically at 3 weeks as a single
layer of epithelial cells and is derived from ectoderm.
By 4 weeks, the epithelium splits into a basal

FIGURE 1 4 - 1 . A cross section of human skin demonstrating the relationship be-

tween the epidermis and dermis and skin appendages. Line A represents a thin split-
thickness (Thiersch) graft. Lines B and C represent levels of thick split-thickness skin
grafts. Line D represents a full-thickness graft. (From Rudolph R, Ballantyne DL Jr:
Skin grafts. In McCarthy JC, ed: Plastic Surgery. Philadelphia, WB Saunders, 1990:221.)

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
TekVttf'fcttltfW image...
germinal layer and an outer layer of flatter glycogen-
rich cells called the periderm. Throughout develop-
ment, an intermediate zone contains tonofilaments and
is connected by desmosomes. This layer eventually
develops keratohyalin granules at about 5 months. By
the sixth month, the skin is completely cornified and
five distinct layers exist. They are the basal layer or
stratum germinativum, the prickle cell layer or the
stratum spinosum, the stratum granulosum, the
stratum lucidum, and finally the stratum corneum. All
of these layers can be seen in the skin of the palms and
the soles, but only the stratum corneum and the stratum
germinativum are found in all parts of the body.
The melanocytes are derived from the neural crest
cells and arrive in the epidermis at the eighth week. By
the fifth month, the melanocytes begin producing
mclanosomes and then transfer the melanin to the ke-
ratinocyte. Langerhans cells are thought to be derived
from the hematopoietic stem cells and can first be seen
in the epidermis at the sixth week. Merkel cells appear
around week 16 of development. Although their cell
of origin is still debated, Merkel cells are thought
to be a derivative either of the neural crest or of the
ectoderm.
The primary purpose of the epidermis is to provide
a protective layer between an organism and its envi-
ronment. Through the process of cornification, a layer
of dead cells envelops the organism and acts as a barrier.
Cornification begins in the basal layer, where the cells
are columnar or cuboidal. These cells in the basal layer
contain large oval nuclei and basophilic cytoplasm.
Within this layer, the cells synthesize tonofilaments.
The tonofilaments aggregate throughout the cells1
ascent through the epidermis and become the kerati-
nous protein that fills the mature cornified kerat-
inocyte or corneocyte. In the next layer, the cells take
on a polygonal shape because of cell to cell connec-
tions called desmosomes. The cell to cell connections
resemble spines under light microscopy, hence the
name stratum spinosum. Near the top of the spinous
layer, the keratinocyte begins producing keratohyalin
granules, which become more prominent as the cell
ascends into the stratum granulosum. These granules
contain a histidine-rich cationic protein called profil-
aggrin. As the cell matures, the profilaggrin is degraded
into filaggrin, which acts as a glue that holds the keratin
filaments together in the cornified layer." A second
type of granule forms near the top of the spinous layer.
The lamellar granule contains free sterols, polar lipids,
and several hydrolytic enzymes. This granule fuses with
the keratinocyte cell membrane, discharging its
contents into the intercellular space. These granules
establish a hydrophobic crystalline sheet within the
intercellular space of the cornified layer, which is
thought to give the skin its impermeable quality.' 2
While the keratohyalin and lamellar granules are
forming, lysosomes are released into the cell. It is
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14 • SKIN GRAFTS 295
thought that the enzymes effectively digest the intra-
cellular organelles and nuclei. Tonofilaments and ker-
atohyalin granules are thought to be resistant to the
lysosomal digestive enzymes and subsequently fill the
mature corneocyte.
Near the top of the granular layer, a thickening
develops along the upper portion of the keratinocyte's
plasma membrane. This thickening, called the mar-
ginal band or the cornified cellular envelope, is formed
from numerous disulfide bonds and other resistant
chemical bonds between keratolinin and involucrin
and multiple neutral lipids.13 This marginal band pro-
vides the epidermis with a certain integrity that allows
it to withstand the chemical and physical insults of
the environment.
The process of cornification is an orderly sequence
of events. It starts at the basal layer where a cell begins
producing tonofilaments. These tonofilaments are the
precursors to a-keratin. As the cell ascends, it flat-
tens out and loses the intracellular organelles and
nuclei, which are replaced by keratohyalin granules.
Hydrophobic lipids are released and form crystalline
sheets in the stratum corneum that provide the epi-
dermis with its impermeable nature. The outermost
layer of the keratinocyte's plasma membrane thick-
ens through a series of chemical bonds to construct
an impermeable and resistant barrier to the insults of
the environment. The entire process takes about 19
days. The characteristics of cornification vary with loca-
tion. The cornified layer is pliable and soft on normal
skin; on the nail bed, the cornified layer is hard and
thick and forms the nail.14
Melanocytes reside in the basal layer of the epider-
mis, in a ratio of 1 melanocyte to every 10 keratino-
cytes.15 The primary function of the melanocyte is to
produce vesicles full of melanin called melanosomes.
These vesicles migrate to the tips of the dendrites of
the melanocyte where they are phagocytosed by the
surrounding keratinocyte. There are two types of
melanin: eumelanin, which has a characteristic brown
or black color; and pheomelanin, which accounts for
lighter colors like blond or reddish brown. The amount
of melanin is greater on the face compared with the
trunk. The primary function of melanin is to protect
the skin from the harmful effects of sunlight. 16 There
is also some evidence that melanin acts as a biochem-
ical neutralizer of oxygen free radicals.
The Langerhans cell is a specialized cell that resides
in the middle layers of the epidermis. The Langerhans
cell provides the immune characteristics of the skin
and plays a large role in contact dermatitis, allograft
rejection, and neoplasia surveillance.17
Also within the epidermis are specialized neu-
rosensory cells called Merkel cells. Most of these cells
are found in the epidermis of the palms and soles, nail
beds, and oral and genital epithelium. Merkel cells are
found close to neurites. They act as mechanorecep-
296 I • GENERAL PRINCIPLES
tors, and they are able to transmit mechanical forces
into action potentials along an associated nerve.18
Merkel cells have been found in the dermis away from
any neural elements, and the entire function of Merkel
cells is still unclear.
Dermis
The dermis is composed primarily of collagen, elastic
fibers, and ground substance. It is relatively noncel-
lular compared with the epidermis. The dermis con-
tains all of the nerves, vessels, and lymphatics of the
skin and also most of the glandular elements of the
skin. The dermis is 15 to 40 times thicker than the epi-
dermis, but because of its decreased cellularity, it con-
sumes much less energy than the epidermis. The "free
cells" found in the dermis are, in descending order of
frequency, fibrocytes, mast cells, histiocytes, Langer-
hans cells, lymphocytes, and rarely eosinophils.14
The mature dermis can be divided into two layers,
a superficial papillary layer and a deeper reticular layer.
The papillary layer contains disorganized collagen
bundles, elastic fibers, fibrocytes, and ground substance
and has a highly developed microcirculation. The
microcirculation in the papillary dermis provides the
blood supply for the metabolically active epidermis
(the epidermis has no inherent blood supply), and the
epidermis and papillary dermis are intimately related.
The reticular dermis is composed of thick bundles of
coarse collagen arranged in orthogonal patterns. Coarse
elastic fibers are interspersed between the collagen
fibers. The reticular dermis is less cellular than the pap-
illary dermis and contains less ground substance.
The dermis immediately adjacent to hair follicles,
apocrine glands, and eccrine glands resembles papil-
lary dermis despite the deep nature of some of these
glandular elements. This dermis is called periadnexal
dermis and along with the papillary dermis can be
referred to as adventitial dermis.
The ground substance found in the papillary dermis
and to a lesser degree in the reticular dermis is
composed primarily of the mucopolysaccharides
hyaluronic acid and chondroitin sulfate.19 Ground sub-
stance tends to have a gel-like consistency. Through
the process of aging, ground substance decreases and
is replaced by fibrous tissue.
Dermal-Epidermal Junction
The dermal-epidermal junction is the specialized site
of attachment between the epidermis and the papil-
lary dermis. Whereas it can be seen with light
microscopy and is best visualized with periodic acid-
Schiff staining, it is best seen with electron microscopy.
The most abundant cells at the dermal-epidermal junc-
tion are the basal keratinocytes. Other cells present
include melanocytes and Merkel cells.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
Electron microscopy has identified four layers in
the dermal-epidermal junction.20 The first layer is made
up of hemidesmosomes. The hemidesmosomes are
electron-dense structures located just above the plasma
membrane of basal keratinocytes. Tonofilaments from
basal keratinocytes are attached to the hemidesmo-
some and run perpendicular into the cell. The lamina
lucida is the second layer of the dermal-epidermal junc-
tion. It lies beneath the hemidesmosomes and consti-
tutes a 30-nm electron-lucent layer. Within the lamina
lucida reside sub-basal dense plaques, which rest
directly beneath each hemidesmosome. Anchoring
filaments run through the lamina lucida to connect
hemidesmosomes with the underlying basement mem-
brane or lamina densa. The lamina densa makes up
the third layer. It is an electron-dense 40-nm layer made
predominantly from type IV collagen. Direcdy beneath
the lamina densa is the fourth layer, a fibrous zone com-
posed of anchoring fibrils, type III collagen, and dermal
microfibril bundles. Anchoring fibers, which are not
synonymous with anchoring filaments, are composed
largely of collagen type VII.21 This interacts with the
collagen type IV of the lamina densa and helps keep
the lamina densa attached to the underlying dermis.
The dermal-epidermal junction provides three
major functions for the skin. First, it is a layer of attach-
ment between the epidermis and the dermis. Second,
it is thought that the basement membrane provides
all the support for the overlying epidermis. Third,
anionic proteoglycans such as heparan sulfate rest on
both the dermal and epidermal sides of the lamina
densa. These proteoglycans provide a chemical barrier
to the penetration of anionic macromolecules.22 The
principal barrier to chemical penetration is the corni-
fied layer of the epidermis, and the dermal-epidermal
junction plays only a minor role as a barrier. Some
researchers have suggested that the dermal-epidermal
junction may play a role in epidermal differentiation
during embryonal development, but this process has
not been fully defined.
Blood Supply
The cutaneous blood supply refers to the vascular
arrangement superficial to the deep fascia. After per-
forating the deep fascia, arteries may run for a vari-
able distance in the superficial fascia before sending
branches toward the dermis to join the subdermal arte-
rial plexus. The subdermal arterial plexus is the major
blood supply to the skin. Branches from the subder-
mal plexus supply the skin appendages and end in a
plexus located in the superficial layer of the papillary
dermis. Capillary loops in the dermal papillae provide
blood supply to the epidermis. Because of the inter-
connecting nature of the subdermal plexus, no portion
of skin is directly dependent on the proximal cuta-
neous perforator.23
VtSWttf'Selcrw image...
The venous drainage of the skin mirrors the arte-
rial network. Efferent loops of capillaries in the pap-
illary dermis empty into a subdermal plexus. The
venous subdermal plexus then drains into segmental
veins, which carry the venous return into the larger
subcutaneous veins.
The blood supply to the subdermal arterial plexus
comes from two types of cutaneous perforators. First,
the musculocutaneous perforators arise from vessels
deep to the underlying muscle and pierce the fascia to
terminate in the subdermal arterial plexus. Second, the
direct cutaneous arteries run parallel to the surface of
the skin superficial to the muscle fascia.24 These arter-
ies receive blood supply from segmental perforators
that penetrate the muscle at varying intervals. The direct
cutaneous arteries terminate into the subdermal
plexus.
Hair Follicles
Hair differentiation is first noted at 9 weeks of gesta-
tion as aggregates of mesenchyme form beneath
plaques of elongated epithelial cells. The process starts
on the head and moves in a cranial-caudal direction.
The mesenchyme begins to grow downward into
the dermis as the epithelial cells proliferate upward
through the epidermis, creating a canal called the
acrotrichia. On reaching the base of the developing
hair follicle, the epithelial plaque forms into a bulbous
structure that encompasses the underlying mes-
enchyme, which has differentiated into a nubbin of
vascular tissue. Once fully developed, the hair follicle
will consist of a follicular matrix, derived from ecto-
derm, and an underlying follicular papilla, derived
from mesoderm. 25
As the hair follicle is developing, three bulges form
on the sidewalls of the hair follicle. The deepest bulge
is the site of attachment for the hair erector muscle.
The middle bulge forms into a sebaceous gland. The
most superficial bulge develops into an apocrine unit.
This unit consists of the apocrine gland in the subcu-
taneous fat and the apocrine duct, which connects the
gland to the hair follicle. As these structures are devel-
oping, the follicular matrix forms an inner and outer
sheath, eventually creating embryonal hair.
The hair follicle can be straight, spiral, helical,
or wavy. The morphologic character of the hair
follicle varies with race; blacks have spiral hair folli-
cles, whereas Asians frequently have straight hair
follicles.
The hair follicle can be divided histologically into
four layers or zones. The infundibulum is that portion
of the hair follicle from the skin to the entrance of the
apocrine gland. The isthmus resides between the apo-
crine ostia and the sebaceous gland ostia. The stem of
the hair follicle is between the sebaceous gland entrance
site and the attachment of the erector muscle. The
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14 • SKIN GRAFTS 297
portion of the follicle deep to the erector muscle inser-
tion is the bulb. The bulb contains the follicular matrix
and the follicular papilla and is principally responsi-
ble for hair development (Fig. 14-2).26
Hair development goes through three distinct
phases in the adult. Active hair growth takes place
during the anagen phase. Involution of hair follicles
occurs during the catagen phase. The resting cycle of
hair growth is the telogen phase. During anagen, the
hair follicle consists of all four of the layers because
growth is active. During catagen, the bulb begins to
atrophy as keratinocy tes die and melanocytes stop pro-
ducing pigment. The hair follicle begins to shrink.
During telogen, the follicle contains only the infundibu-
lum and the isthmus, and the remaining histologic
zones have atrophied. It is at this time that the hair
itself is actually sloughed before anagen begins anew.
The length of time each hair follicle spends in each
phase varies by location. In the scalp, anagen can last
up to 10 years. Catagen lasts only 2 to 3 weeks, whereas
telogen lasts 3 to 4 months. Approximately 85% of the
hair follicles on the scalp are in anagen. For hair folli-
cles in the brow, trunk, and extremity, anagen does not
last longer than 6 months. 27
The characteristics of hair growth in the skin graft
resemble those of the donor site. This must be con-
sidered in choosing a donor site. Hair follicles often
grow in a slanted direction through the dermis. Inci-
sions in hair-bearing regions should be beveled in the
direction of hair growth to prevent undue destruction
of hair follicles.
-
Sebaceous Glands
Most sebaceous glands develop in the fourth week of
gestation and arise from a maturing hair follicle. They
are found in the greatest concentration on the scalp
and face and are largest on the forehead, back, and nose.
They are almost always associated with a hair follicle.
However, in certain regions, such as oral mucosa
(Fordyce spots), lip vermilion (Montgomery tubercles),
internal fold of the prepuce (Tyson glands), labia
minora, and eyelids (meibomian glands), the associ-
ated hair follicle consists only of an infundibulum. No
follicular stem or bulb is present.
Sebogenesis begins at the base of a sebaceous gland
lobule. A germ layer exists at the periphery of the seba-
ceous lobule. As the cells mature, they fill with lipid
and eventually lyse, releasing their contents into the
sebaceous duct. As the cell and its contents are released
in toto, a sebaceous gland is also known as a holocrine
gland. The content of sebaceous ducts is called sebum.
It is made of multiple lipid components, including
triglycerides, wax esters, squalene, cholesterol esters,
and cholesterol. 28 Bacteria (Propionibacterium) in
the infundibulum of the associated hair follicle break
down some of the lipids to free fatty acids. It has been
298 I • GENERAL PRINCIPLES
suggested that these free fatty acids lead to the inflam-
mation associated with acne vulgaris.
Sebum production is a continuous process that does
not rely on the nervous system. Sebaceous glands are
active during infancy but quickly involute. At age 8 to
10 years, the glands become active again, coinciding
with the onset of puberty. It appears that androgenic
steroids produced by the gonads and adrenal gland
control sebum production.29 The exact function of the
sebaceous gland is still unknown.
Apocrine Glands
Apocrine glands are found in the axillae, areola, scalp,
periumbilical region, perineal and circumanal areas,
prepuce, mons pubis, labia minora, external auditory
canal, and eyelids. The gland itself typically rests in
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
Upper
segment
Lower
segment FIGURE 1 4 - 2 . A typical hair follicle
illustrating the four histologic divisions.
The histology of a hair follicle varies
according to whether the hair follicle is
in anagen, telogen, orcatagen. Typically,
the upper segment is present during all
phases of hair growth. However, the
lower segment is present only during
anagen. (Revised from Moschella SL,
Hurley HJ: Dermatology. Philadelphia,
WB Saunders, 1992.)
the dermis or subcutaneous tissue and is attached to
an associated hair follicle, where it inserts just above
the entrance of the sebaceous gland. The apocrine
gland is a coiled gland whose cells continuously
secrete its contents into the apocrine duct through a
"decapitation" or "pinching-off" process. Apocrine
secretion is controlled by the autonomic nervous
system. Both unmyelinated adrenergic and choliner-
gic nerves innervate myoepithelial cells surrounding
the secretory cells.30 Catecholamines can also stimu-
late apocrine secretion. Bacteria in the follicular
infundibula and on the skin surface act on the apo-
crine secretion to produce short-chain fatty acids,
ammonia, and other malodorous products.
The exact content of apocrine secretion is currently
unknown. Apocrine secretion in some primates acts
as a sexual attractant or pheromone. Some believe it
tiSWRtettldW image...
serves this function in humans; however, there is no
proven function for apocrine glands in humans at this
time. Inflammation and obstruction of apocrine gland
secretion lead to the clinical condition known as
hidradenitis suppurativa. 31
Eccrine Glands
The eccrine gland is the only true sweat gland in
humans. Eccrine glands are present over the entire
surface of the skin except the lips, clitoris, labia
minora, and external auditory canal. The glands are
typically tubular and located at the base of the dermis
and empty into the skin. They develop independently
of the folliculosebaceous-apocrine unit and are of epi-
dermal origin. An infant is born with approximately
3 million eccrine sweat glands. No additional eccrine
glands form after birth.
The eccrine gland consists of a coiled secretory
gland, a coiled dermal duct, a straight duct that passes
through the dermis, and a spiraled epidermal duct
called the acrosyringium. The secretory gland releases
an isotonic solution that is a precursor to sweat. The
duct absorbs sodium in a partial exchange for potas-
sium, resulting in a hypotonic sweat consisting of
sodium, chloride, potassium, urea, lactate, bicarbon-
ate, ammonia, calcium, phosphorus, magnesium,
iodide, sulfate, iron, zinc, amino acids, proteins, and
immunoglobulins. The pH of sweat is between 4.5 and
5.5 and generally increases as the amount of sweat
increases.32 Eccrine glands are innervated by both
adrenergic and cholinergic fibers from the sympathetic
nervous system. However, eccrine glands are most sen-
sitive to acetylcholine.
The principal function of the eccrine gland is to
control body temperature through the process of evap-
oration. An increase in body temperature of 0.01°C
will activate the hypothalamic system. This will acti-
vate the sympathetic nervous system, causing the
number of eccrine glands actively secreting to increase.
In extreme temperature exposures, 2 to 3 liters of sweat
can be produced in an hour.33 During prolonged expo-
sure to high temperatures, eccrine glands become
"acclimatized" and are able to secrete larger amounts
of sweat at a greater rate in response to a relatively
smaller elevation in body temperature.
Eccrine glands on the palms, soles, axillae, and fore-
head tend to respond predominantly to emotional
stimuli as opposed to heat. This explains the familiar
"cold clammy hands" that develop during particularly
stressful situations.
WOUND PREPARATION
Before the skin graft is applied, it is essential that the
recipient wound be prepared for skin grafting. Many
skin graft failures can be attributed to inadequate
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14 • SKIN GRAFTS 299
recipient site preparation. It is important to ensure that
the wound being grafted has a vascularized bed free
of infection or malignant disease and that hemostasis
has been achieved.34 If these conditions have not been
met, it may be prudent to delay skin grafting until the
wound is better prepared.
Wounds can be divided into acute and chronic
wounds. Acute wounds are less than a week old. Most
acute wounds are the result of traumatic injuries, burns,
or oncologic resections. These wounds may contain
an eschar but are generally devoid of granulation tissue.
The nature of the injury,such as a crushing-type injury
or a heavily contaminated injury, may not be suitable
for immediate skin grafting.10
In approaching an acute wound, the first step is to
d^bride all devitalized tissue from the wound. Ail eschar
is removed, and the wound bed should be d£brided
to a point of active bleeding. The wound bed is then
examined. Fat, peritenon, and periosteum are poorly
vascularized, but they will generally support a split-
thickness graft. If the bed has a series of irregularities,
a meshed graft may be used because it will adhere better
than an unmeshed graft. If hemostasis cannot be
achieved, a pressure dressing can be applied, and the
grafting can be delayed.
Chronic wounds offer the surgeon a greater chal-
lenge to skin grafting. A chronic wound is any wound
that has been open for more than a week. Chronic
wounds may contain eschar, and they frequently
contain granulation tissue. Any traumatic wound that
has been treated open, venous stasis ulcers, vasculitis
ulcers, radiation ulcers, and pressure ulcers represent
chronic wounds.
Chronic wounds have been exposed to the envi-
ronment for a prolonged time; consequently, the infec-
tion rate is higher than in an acute wound. The wound
should be examined for signs of infection, which
include drainage, surrounding erythema, and gray or
tan granulation tissue. Should infection be suspected,
a tissue biopsy specimen can be sent for quantitative
wound cultures. If there are more than 105 organisms
per gram of tissue, the wound is infected, and skin graft-
ing should be delayed.35'37 Infected wounds can be
treated with either systemic or topical antibiotics until
the infection clears. One report indicates that fibrin
glue may allow successful grafting onto an infected
wound. 38
Ideally, the chronic wound should have healthy pink
or red granulation tissue and signs of epithelial migra-
tion at the wound margins. Some wounds never develop
such an ideal bed. Assuming the underlying cause is
not infectious, a trial of becaplermin (Regranex) may
stimulate granulation tissue and improve the chances
of skin graft success.39 Becaplermin is a recombinant
human platelet-derived growth factor that has been
reported to stimulate wound healing. Becaplermin has
been used to stimulate and expedite granulation tissue
image...
300 I • GENERAL PRINCIPLES
before skin grafting. Vacuum dressings have also
demonstrated an ability to stimulate granulation
tissue.40
The underlying medical condition of the patient
should be optimized before definitive skin grafting.8
In general, all active infections should be treated before
graft application. Wounds due to vasculitis frequently
require aggressive medical management of the vas-
culitis before skin grafting will be successful. Wounds
caused by arterial insufficiency may require angioplasty
or a vascular bypass procedure before skin grafting
will be successful. Good long-term results are notori-
ously difficult to obtain with skin grafting of pressure
ulcers and radiation ulcers; these wounds are best
treated with a flap whenever possible.
In the operating room, a chronic wound should be
deT>rided of any eschar and debris. Because granula-
tion tissue harbors bacteria, some surgeons advocate
tangential debridement of the granulation tissue. If the
granulation is not sharply ddbrided, it can be mechan-
ically d£brided with saline gauze. There is often sig-
nificant bleeding after debridement, and hemostasis
can be achieved with electrocautery, ligation, or pres-
sure. In burns, topical epinephrine-impregnated gauze
is used in combination with a pressure dressing to
obtain hemostasis of an extremity. Topical thrombin
and fibrin glue can also be useful in achieving hemo-
stasis. Fibrin glue is completely absorbable and has the
additional benefit of improving graft take.41 Oxycel and
Gelfoam are to be avoided because they provide a
barrier to graft adherence.10
SKIN GRAFTS
Skin grafts are used in a variety of clinical situations.
The essential indication for the application of a skin
graft is wound closure (Table 14-1). In general, full-
thickness skin grafts are applied to the regions of the
face, ears, and hands. Split-thickness skin grafts arc
usually placed on the trunk and genitalia. Skin grafts
are usually the initial treatment of choice for many
open wounds that cannot be closed primarily. Graft-
TABLE14-1 • INDICATIONS FOR SKIN
GRAFTING
Any traumatic wound that cannot be closed primarily
Defects after oncologic resection
Burn reconstruction
Scar contracture release
Congenital deficiencies of skin, such as syndactyly and
vaginal atresia
Hair restoration
Vitiligo
Nipple-areola reconstruction
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Dr.Mustafa D.
TABLE 14-2 • CONTRAINDICATIONS TO
SKIN GRAFTING
Absolute Relative
Wounds with avascular Pressure sores
beds WourTds due to irradiation
Infected wounds Wounds due to vasculitis
Wounds due to Wounds due to arterial
malignant neoplasia insufficiency
Wounds in cosmetically
sensitive areas
Malnutrition
ing offers the simplest method of wound closure in
the reconstructive ladder, assuming that primary
closure is not possible or would lead to undue tension.
Various forms of skin grafts are also useful in releas-
ing contractures, in certain forms of vitiligo, during
syndactyly release, and in treating hair loss.42"45 Skin
grafts are generally avoided in management of more
complex wounds. Conditions with deep spaces and
exposed bones, such as open sternal wounds, pressure
sores, and open fractures, normally require the use of
skin flaps or muscle flaps for stable wound coverage.
Skin grafts have limited success in wounds with a com-
promised blood supply, such as irradiated wounds and
ischemic ulcers (Table 14-2).
Split Versus Full Thickness
Skin grafts can include either a portion of the dermis
or the entire dermis. When a graft includes only
a portion of the dermis, it is referred to as a split-
thickness skin graft. When the graft contains the entire
dermis, it is called a full-thickness skin graft. The
amount of dermis included with the graft determines
both the likelihood of survival and the amount of
contracture. Split-thickness grafts can tolerate less
vascularity but have a greater amount of contracture.
Full-thickness grafts require a better vascular bed for
survival but undergo less contracture.46 Sensory recov-
ery of the full-thickness graft is superior to that of the
split-thickness graft.
A typical split-thickness skin graft is 0.30 to 0.45
mm (0.012 to 0.018 inch). Blood vessels typically
arborize as they ascend through the dermis; thus, the
cut vessels on the undersurface of the graft can easily
absorb nourishment for survival. Therefore, when a
skin graft is applied to close a wound with a tenuous
vascularized bed, such as over periosteum, peritenon,
or perineurium, split-thickness grafts are more likely
to survive. After a split-thickness graft is harvested,
the donor site generally heals spontaneously.
Epithelial cells deep in hair follicles and sweat glands
 image...

14 • SKIN GRAFTS 301

generally cover a typical split graft harvest site in 7 to
21 days, depending on the thickness of the graft. If
necessary, the donor site of a split-thickness graft can
be harvested again after the wound epithelializes. This
is often necessary in treatment of patients with large
surface area burns.
Full-thickness grafts contain both epidermis and
the entire thickness of the dermis. Unlike in split graft
donor sites, there are no residual epithelial cells capable
of resurfacing the donor site. Full-thickness graft donor
sites must be closed primarily. Thus, full-thickness
grafts are not normally used for large wounds. The
degree ofvascularity in the full-thickness skin graft is
greater than for a thinner split-thickness graft.
Donor Sites
Split-thickness skin grafts can be taken from any area
on the body, including the scalp. Despite the ability
to heal spontaneously, the split-thickness skin graft
donor site is frequently scarred or discolored. Donor
sites are frequently in areas hidden by modern-day
clothing. Popular areas for split-thickness graft harvest
include the thigh, trunk, and buttocks (Fig. 14-3).
Donor sites containing suspicious lesions are avoided
to prevent transfer of a malignant neoplasm with the
skin graft.47-48
Defects on the face are frequently closed with either
local flaps or full-thickness grafts. On occasion, a
split-thickness graft can be used. When placing a split-
thickness graft on the face, one should use a donor site
from the "blush zone." This gives a graft with the best
color match. The blush zone is above the shoulders
and consists of the scalp, neck, and supraclavicular
area.10,42,43 In taking a graft from a hair-bearing region,
it is important to take a thin graft because thicker split-
thickness grafts will contain undesired hair follicles and
eventually lead to hair in the graft.
In choosing a harvest site, it is important to keep
in mind the thickness of the donor site. Skin is typi-
cally thin in infants and the elderly. Men typically have
thicker skin than women do regardless of anatomic

Full-thickness
graft
Full-thickness
graft

FIGURE 1 4 - 3 . Available donor sites for skin grafts. (From Rudolph R, Ballantyne DL Jr:
Skin grafts. In McCarthy JG, ed: Plastic Surgery. Philadelphia, WB Saunders, 1990:221.)

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Dr.Mustafa D.
302 I • GENERAL PRINCIPLES
location. Skin is typically thicker on the trunk and
thighs and thinner on the eyelids and postauricular
areas.
A frequently overlooked source of skin grafts in
trauma situations is avulsed skin. This skin can be har-
vested in either a full- or split-thickness fashion and
applied to the resulting wound primarily or stored and
used later. In patients with combined Polydactyly and
syndactyly, the removed accessory digit may also be a
source of skin for the syndactyly release.49
The donor site of a split-thickness skin graft gen-
erally heals in 7 to 21 days. The most common treat-
ment of a split-thickness donor site is fine mesh gauze
impregnated with a lubricant and, possibly, an antibi-
otic. The gauze is applied immediately after harvest-
ing of the graft and is left on the donor site until it falls
off. The gauze provides a protective layer over the donor
site that helps with pain control during the healing
process. Re-epithelialization reliably occurs in 12 days
with this method of treatment. 50 Biobrane* is a bil-
aminate membrane composed of a knitted nylon fabric
bonded to an ultrathin layer of silicone rubber. Bio-
brane is transparent and transmits water vapor. Bio-
brane does adhere to the donor site, which improves
pain control. It also acts as a barrier toward bacteria,
but antibiotics are able to penetrate Biobrane. Because
Biobrane is synthetic, there is no risk of disease trans-
mission, and the risk of allergy is low. Healing time
with Biobrane is around 10 days.51,52 Bio-occlusive
dressings have been shown to have faster healing com-
pared with open treatment and offer superior pain
control. 53 OpSite 1 is a water-permeable, bio-occlusive,
plastic adhesive that has been advocated for donor
site treatment. Its advantages include less pain, short
healing time (10 days), and relatively less bulk.
However, OpSite frequently accumulates a serous
exudate, which requires drainage. OpSite has also been
associated with increased inflammation. 54,55 Many
split-thickness donor sites are too expansive to be easily
covered with OpSite.
The optimal treatment of a harvest site is auto-
grafting.56 When excess skin is available after grafting,
it can be placed onto the donor site rather than dis-
carded. It is possible to mesh a skin graft so there is
available skin for both the defect and the donor site.
Cultured kcratinocyte sheets have also been shown to
quicken donor site healing. Many burn units are using
skin allografts to treat donor sites,57 which has been
shown to quicken the healing process and improve pain.
This is an attractive treatment for extensive burns when
multiple harvests from the same donor sites are
required. 58 In addition, studies indicate that adminis-
tration of systemic growth hormones may decrease the
•Bcrtck Pharmaceuticals, Morgantown, West Virginia.
Smith & Nephew Inc., Largo, Florida.
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Dr.Mustafa D.
time for donor site healing by as much as 2 days.59 There
are a growing number of skin substitutes that can be
used for donor site wounds. These skin substitutes are
discussed extensively later in the chapter. Their use in
the treatment of donor sites is primarily limited by
their cost.
Harvest sites can deepen and become full-
thickness defects. This generally occurs in the elderly,
in infants, or in critically ill patients. It is thought to
be due to an infection of the harvest site. This com-
plication may require excision and grafting of the
original donor site.
Full-thickness grafts are most commonly used on
the face. In considering donor sites for facial defects,
it is important to consider the consistency, thickness,
color, and texture. Eyelid skin, which is thin and has
few glandular structures, is generally best replaced with
eyelid skin. Thick nasal skin has a relatively large
amount of glandular elements. It is better replaced
with the thicker skin from the nasolabial fold, supra-
clavicular area, or anterior auricular area. The ante-
rior auricular graft offers thicker skin than the
postauricular graft. When closed, the scar mimics that
of a face lift.60'61
Common sites for full-thickness skin grafts of the
head and neck include the postauricular region, ante-
rior auricular region, nasolabial crease, supraclavicu-
lar region, eyelids, and neck. Most wounds of the head
and neck can be closed with these donor sites. Exten-
sive defects may require skin grafts from the abdomen
or inguinal crease.
In children, full-thickness grafts will grow with the
developing child, reducing the risk of potential scar
contracture. 62 Full-thickness grafts are preferred on
most wounds in a young child. The inguinal crease
can frequently be used as a donor site for large full-
thickness grafts. It is important to harvest the graft
laterally and away from the potential hair-bearing skin
of the pubis. The donor site is well hidden in the
inguinal crease and is easily covered by clothing.
Full-thickness grafting is often used in special
circumstances. Nipple-areola reconstruction after
mastectomy can be accomplished with either a full-
thickness graft from the contralateral nipple-areola or
a skate flap in conjunction with a full-thickness graft
from the groin. Breast reduction in severe macromas-
tia uses full-thickness nipple grafting techniques.
Palatal and mucosal full-thickness grafts have been used
for nasal lining for traumatic nasal defects or after
cancer excisions. Hypothenar, wrist crease, and elbow
crease areas are established sites of full-thickness
grafts in hand surgery. Full-thickness scalp grafts have
been used to reconstruct eyebrows.
Situations may arise in which a large full-thickness
graft is desired and the donor site cannot be closed
primarily. A large full-thickness graft can be used to
cover extensive defects if the surgeon is willing to "trade"
image„.
wounds. In this instance, a large defect on the face can
be closed with a full-thickness graft, leaving a large
wound on the trunk or groin. A split-thickness graft
can be used to close the donor site of a full-thickness
harvest.
Donor sites from a full-thickness skin graft are rel-
atively easy to manage. They are treated like any closed
wound. Antibiotic ointment and open treatment or a
sterile dressing may be used. Typically, the wound will
epithelialize in 48 hours and go through the same mat-
uration phase as any closed wound. On occasion, a
full- thickness harvest site from the supraclavicular area
may develop into a hypertrophic scar. This can be
treated with compressive therapy and scar massage.
Harvesting
SPLIT-THICKNESS GRAFTS
The process of harvesting a split-thickness skin graft
entails cutting the skin at some point through the
dermis. This can be accomplished with two different
types of instruments, freehand and power-driven
dermatomes.
Freehand dermatomes include the Week blade, the
Humby knife, the Blair knife, and a simple scalpel. A
FIGURE 14-4. Available freehand dermatomes, from left to right: Week knife, Blair knife, Humby knife, Padgett-
Hood drum dermatome.
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14 • SKIN GRAFTS 303
freehand dermatome offers a quick method of har-
vesting a skin graft that does not depend on electric-
ity or pneumatic power. However, with freehand
dermatomes, one has difficulty controlling the exact
thickness and depth of the graft (Fig. 14-4).
Once the donor site has been identified, the area
can be anesthetized with local anesthetic with or
without epinephrine. Epinephrine can help control
the bleeding and lengthen the duration of the local
anesthetic. Donor sites can also be anesthetized with
regional nerve blocks, general anesthesia, or frost-
induced anesthesia.63 A template can be used to help
identify the amount of skin needed for the graft. If a
template is used, the graft should be cut to 5% larger
than the template to account for the skin contraction
that occurs after the graft is harvested. The Week blade,
the Humby knife, and the Blair knife are equipped with
a guard, which limits the depth of the skin graft.6,1 Typ-
ically, the guard is set at 0.30 to 0.45 mm (0.012 to 0.018
inch) for a split-thickness harvest. This should be ver-
ified by passing the beveled end of a No. 15 blade scalpel
between the guard and the knife. If the guard is set at
0.30 mm, the beveled end of the No. 15 blade will fit
snugly between the guard and the knife. An assistant
applies tension to the donor site, and the area is lubri-
cated with mineral oil or saline. The surgeon then passes
304 I • GENERAL PRINCIPLES
the knife parallel to the epidermis in a back-and-forth
direction, much like a musician playing a violin. The
assistant gently withdraws the resulting graft from the
dermatome as the surgeon continues the harvest.
In 1940, James Barrett Brown introduced the first
electrically driven dermatome. 8 Because of its simplicity
and reliability, the motorized dermatome has largely
replaced the freehand dermatome for large split-thick-
ness harvests. A power-driven dermatome uses a
rapidly vibrating blade and works much like a wood
planar. The air Zimmer dermatome, powered by com-
pressed water-pumped nitrogen, produces uniform
grafts of predetermined depth and width. It is the
most commonly used motorized dermatome today
(Fig. 14-5).
In using a motorized dermatome, the first step is
to assemble the dermatome. In general, a disposable
blade must be attached to the dermatome, followed
by a guard of a predetermined width. The depth of the
harvest is set and can be assessed by passing a No. 15
blade between the guard and the blade. The dermatome
is connected to a power source, unless the dermatome
is battery driven. The dermatome is then checked to
ensure that the instrument is receiving adequate power
before the actual harvest begins.
In general, when a power dermatome is being used
to harvest a split-thickness graft, the patient is under
FIGURE 14-5. Available motorized dermatomes, from left to right: electric Brown dermatome, air Zimmer der-
matome, Padgett dermatome.
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general anesthesia. However, regional blocks, local
anesthetic with or without epinephrine, or frost anes-
thesia can be used with power dermatomes. The donor
site is shaved and prepared with a standard operative
scrub. The area is then lubricated with saline or mineral
oil. An assistant may apply traction to provide a taught
donor site. The dermatome is then brought into contact
with the donor site at a 30- to 45-degree angle, and
the throttle is pressed, initiating the cut. Gentle down-
ward pressure is applied to the dermatome as the
machine is advanced flat to the skin. An assistant may
lift the graft from the pocket area of the dermatome
during the harvest so that the surgeon can assess the
depth of the cut. Once the harvest is complete, the
surgeon angles the dermatome upward and lifts off
the donor site while continuing to advance to cut the
graft. This technique provides reliable grafts of a pre-
determined depth and width, especially in harvesting
from a flat donor site like the thigh. Some modifica-
tions must be made in harvesting over a bone promi-
nence like the iliac crest or the scalp to ensure a uniform
graft.
Subcutaneous tissue infiltration with lactated Ringer
solution can facilitate skin graft harvest over a bone
prominence. One or 2 liters of fluid can be infiltrated
beneath the donor site. The infiltrate will stiffen the
skin and make for an easier and more predictable
VtJWftf'aeltfMf image...

14 • SKIN GRAFTS 305

harvest.65 Epinephrine (2 mL of 1:1000 epinephrine

per liter of lactated Ringer solution) can be added to
the tumescent fluid. This will significantly limit the
blood loss from the donor site after the harvest. This
technique is particularly useful in burn surgery.66
During the harvest, the surgeon should inspect the
graft to ensure appropriate depth. Graft thickness can
be determined by observing the graft and the donor
site. An ideal split-thickness graft should be slightly
translucent. An opaque graft indicates a deep split-
thickness graft or possibly a full-thickness harvest. The
donor site will also give clues to the depth of the graft.
Thinner harvests leave behind a multitude of small
bleeding points because the blood vessels arborize as
they travel through the dermis. Deeper harvests leave
relatively fewer and larger bleeding points in the
remaining dermis. If the donor site contains areas of
exposed fat, the harvest is full thickness in those areas.
There is no standard depth setting used in har-
vesting of a split-thickness skin graft. This is because
each patient's skin thickness varies. Infants and the
elderly typically have thin skin. The thickness of the
skin also varies according to the anatomic location on
the same individual. In certain patients, disease or med-
ication causes significant thinning of the dermis; for
example, patients taking corticosteroids generally have
very thin dermis. It is important to assess the donor
site during the harvest to prevent an unexpected full-
thickness defect.
Motorized and freehand dermatomes can also be
used for debridement of the eschar of full-thickness
burns. It has been shown that tangential excision of
burn eschar allows the surgeon to remove the eschar
to a level of normal bleeding tissue. Dermatomes also
have been used to remove hypertrophic scar to prepare
for overgrafting.
A third type of dermatome for harvesting split-
thickness skin grafts is the drum dermatome. The Reese
and Padgett-Hood dermatomes are the two best
known examples of drum dermatomes. Drum der-
matomes use a set of finely calibrated shims for har-
vesting split-thickness grafts. The drum dermatomes
are more difficult to use than motorized dermatomes
and do not allow the surgeon to modify the depth of
the cut during the skin graft harvest. Drum der-
matomes can be useful in harvesting of split-thick-
ness grafts from difficult areas, such as the back of the
neck or the buttocks (Fig. 14-6). Because the drum
dermatome is more difficult to use and to adjust, it
has largely been replaced by motorized dermatomes.
FULL-THICKNESS GRAFTS
The scalpel is generally the only instrument necessary
for harvesting full-thickness skin grafts. The template
can be made and placed on the selected donor site
and outlined. The skin graft is cut according to the
FIGURE 1 4 - 6 . Harvesting a split-thickness skin graft
with a drum dermatome. This photograph demonstrates
the proper use of the Padgett-Hood dermatome.
previously marked template in a full-thickness fashion.
All the dermis is included with the graft with as little
subcutaneous fat as possible. A useful technique is to
drape the graft over one's finger with a skin hook or
hemostat. This allows the surgeon to feel the thickness
of the harvest as the other hand cuts the graft.67 If any
fat remains attached to the graft, it can be removed
with curved sharp scissors. The donor site is then closed
primarily.
Full-thickness mucosal grafts are occasionally
desired for eyelid or nasal reconstruction. The inner
aspect of the cheek offers a large area of mucosa. Palatal
mucosa can also be used for nasal lining, and the result-
ing donor site heals spontaneously in 5 to 7 days. Septal
mucosa can be harvested for nasal or eyelid lining.
Septal cartilage can occasionally be included with the
graft to reconstruct the tarsal plate. Care must be taken
to preserve the contralateral mucosa and perichon-
drium to prevent a full-thickness defect in the nasal
septum. Full-thickness septal harvesting is aided by a
certain degree of hydrodissection, which occurs with
the administration of local anesthetic. Finally, con-
junctiva can be harvested as a full-thickness graft to
replace conjunctiva. In general, the harvest is aided by
the submucosal injection of anesthetic, and thin slices
of conjunctiva are harvested from the fornix. There is
a risk of eyelid contraction in harvesting of conjunc-
tiva, but this is minimized if the graft is narrow and
taken from the fornix.
Preparing the Graft
Once a full-thickness skin graft is harvested, little prepa-
ration is necessary before the graft is applied to the

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306 I • GENERAL PRINCIPLES
recipient site. Most full-thickness grafts need to be
defatted before being applied. It is important to keep
the graft moist during the deflating process and before
its application to prevent desiccation of the graft. Some
surgeons believe that small incisions in a full-thick-
ness graft may allow the graft to better contour to the
defect, and this is frequently referred to as "pie crust-
ing" the graft.
When the defect to be grafted is extensive or has a
multitude of convoluted surfaces, split-thickness skin
grafts can be meshed to expand the graft so that the
entire defect can be covered. Meshing a split-thickness
skin graft is an optional step that increases the surface
area that can be covered by the harvested graft.68 It can
also allow the graft to better adhere to a convoluted
wound. Meshing, however, is not without its disad-
vantages. A meshed graft heals in a checkerboard
fashion, leaving an aesthetically less attractive scar. Also,
the areas between the lattices heal by some degree of
secondary intention, causing contraction of the wound.
This is important if the wound is over a joint or on
the dorsum of the hand. Contracture in these areas
can lead to functional problems. Therefore, meshing
is indicated for large wounds or wounds with convo-
luted surfaces.
Meshing of split-thickness skin grafts is accom-
plished by passing the skin graft through a device that
cuts the graft into a lattice pattern (Fig. 14-7). The graft
can be expanded in a 1:1,1.5:1,2:1,3:1, or 9:1 pattern.
Expanding a skin graft beyond 3:1 is technically pos-
sible; however, this often leaves the graft friable and
difficult to inset. The greater the ratio, the greater
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amount of skin expansion is possible. Contracture is
also directly proportional to graft expansion.69 With
the exception of extensive burns, most split-thickness
grafts are meshed in a 1.5:1 fashion.
Meshing a skin graft does not prevent the forma-
tion of hematoma and seroma. It is important that
hemostasis be achieved before the application of the
skin graft to prevent graft loss from a hematoma. If a
hematoma or seroma is identified in the early post-
operative time frame, it can be expressed through the
meshed graft without disrupting the entire graft.
Once the bed is prepared, the skin graft is placed
on top of the bed. It is important to maintain the appro-
priate orientation of the graft, which is simple in heavily
pigmented individuals. It can be confusing in lightly
pigmented patients. The dermis has a typical shiny
appearance in comparison to the dull epidermis. The
graft is then positioned over the entire wound. This
can be accomplished by suturing the graft to one corner
of the wound while using the back of a forceps to gently
spread the graft out over the wound. The graft has a
tendency to fold over on itself, and this can be avoided
by paying close attention to the graft periphery. Any
excess graft is trimmed. The graft can then be held
in place with suture, surgical staples, or fibrin glue
(Fig. 14-8).
Before the dressing is applied, the graft should be
inspected for hematoma formation. Meshing a graft
does not eliminate the possibility of graft hematoma.
All hematomas should be drained, and it may be
necessary to remove the graft to obtain hemostasis
to prevent further hematoma formation. Flushing
FIGURE 14-7. The Zimmer skin
mesher. The cutting portion of this
device rests in the right lower corner
and comes in a variety of sizes includ-
ing 1.5:1, 2:1, 3:1, and 9:1.
•
image...

14 • SKIN CRAFTS 307

FIGURE 14-8. A, A large healthy wound that appears

ready to accept a skin graft. B, The appearance of the
split-thickness graft at 4 weeks. C, The final appearance
of the graft more than 1 year after grafting.

beneath the graft with saline removes blood clots and
provides for better adherence of the graft.
Postoperative Care
Good postoperative care begins with the dressing. The
first step is to apply a nonadherent dressing over the
graft. Adaptic, Telfa, Xeroform, or petrolatum gauze
is applied directly over the graft.The nonadherent prop-
erties of these types of dressings prevent the skin graft
from being debrided off the wound at the time of the
first dressing change. The remainder of the dressing
should apply gentle pressure on the graft to promote
graft adherence without causing pressure necrosis.
Cotton balls or fluffed gauze is then pressed onto the
wound to conform to the underlying bed. On an
extremity, a circumferential wrap can be applied
snugly across the wound to ensure contact between

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308 I • GENERAL PRINCIPLES
the graft and the host bed. The extremity may then be
immobilized with a splint, although early mobiliza-
tion has not been shown to delay wound healing.70
For grafts to the trunk or head and neck, a bolus or
tie-over dressing can be used (Fig. 14-9). To use a bolus
dressing, the graft must be fixated with a permanent
suture, which is intentionally cut long. This leaves
strands of suture that will be used to hold the dress-
ing on. Once the sutures are placed, petrolatum gauze
or Xeroform is applied on top of the graft. Fluffed gauze
or cotton balls are gently pressed onto the graft. The
suture strands are then tied together so that they hold
the dressing firmly onto the graft. The bolus dressing
FIGURE 14-9. A bolus dressing. A, Sutures used to
inset the graft are intentionally left long, and a nonad-
herent dressing is placed directly over the graft. B, Fluffed
gauze or cotton balls are placed over the nonadherent
dressing as the sutures are tied over the dressing. C, The
final appearance. (From Chase RA: Atlas of Hand Surgery.
Philadelphia, WB Saunders, 1974.)
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FIGURE 14-10. This patient underwent a Mohs exci-
sion of a basal cell carcinoma of the nasal dorsum. Recon-
struction was performed with a full-thickness skin graft.
A bolus dressing applied to the nasal dorsum is illustrated.
minimizes the risk of hematoma or seroma formation
and also prevents shearing forces from disrupting the
graft (Fig. 14-10).
A bolus dressing can be left in place for 7 to 14
days. If there is great concern about the graft, addi-
tional sutures can be placed at the time of surgery and
preserved for the next dressing change. This allows
the tie-over dressing to be changed and reapplied with
the extra or spare sutures. Alternatively, the original
bolster dressing can be applied by use of one of the
two strands of each suture. The second strand can be
saved to reapply the bolus dressing after the first dress-
ing change. When the bolster dressing is removed, the
gauze should be gently peeled from the wound to
prevent disruption of the graft from the host bed.
The first dressing change is important for graft sur-
vival. The timing of the first dressing change varies.
In heavily colonized wounds, early dressing changes
are preferred (1 to 3 days). For full-thickness grafts of
the hands or face, the initial dressing may not be
removed for 5 to 10 days. Once the dressing is care-
fully removed, the graft is examined. At 2 to 3 days,
the graft may still appear pale. However, vascular
ingrowth has already begun, and the grafts obtain a
image...
pink hue around the third or fourth postoperative day.71
Seromas and hematomas are expressed through nicks
in the skin graft. It is better to cut a small hole in the
graft over a hematoma than to dislodge surrounding
adherent graft to express the fluid through the graft
periphery. Eschar is d^brided because eschar offers an
excellent medium for bacteria. Once all seromas and
hematomas have been evacuated, a new dressing is
applied in a fashion similar to the original dressing.
If a bolus dressing is being removed at 10 to 14 days,
a second dressing may not be necessary and the graft
may be treated with moisturizing cream.
In Britain, "Stent" refers to a dental compound used
to apply compression to recently grafted oral wounds.
The skin graft is wrapped around the dental com-
pound with the dermal side out. The compound is
then placed into the buccal sulcus, holding the graft
firmly in place. The splint should be left in place for
6 weeks to 6 months to prevent graft contraction.
In the United States, Stent compound is difficult to
obtain. Many types of dental compounds can be used
to hold a skin graft in place. Plastic or rubber or methyl
methacrylate can be used to make a similar bolster
dressing. These can be attached to a temporary denture
or held in place with sutures.
In general, grafts should be covered and immobi-
lized for at least 5 to 7 days. Graft adherence occurs
rapidly during the first 8 hours after surgery and
continues until the fourth postoperative day. After a
minimum of 5 to 7 days, the extremity splints can be
removed, and the patient may be allowed to bathe,
assuming the patient is cooperative.
In infants or in sedated or immobile patients, grafts
can be treated open. This allows early and frequent
examination of the graft. Arm splints may be neces-
sary in small children to prevent them from manipu-
lating the graft. Fibrin glue can be used to fix the graft
to the underlying bed, preventing the need for suture
removal. This is an attractive alternative in young chil-
dren. This is a relatively simple manner of treating a
skin graft because there is no need for dressing
changes.
Storage
When excess graft is harvested, it may be prudent to
store the excess graft for a later operation. The easiest
method of preserving a graft is to replace the graft on
the donor site.10 This will preserve the graft for up to
5 days. The graft will ultimately take and will become
difficult to elevate after 5 days.
If the graft needs to be preserved for more than 5
days, it can be placed in a saline solution at 4°C. Antibi-
otics can be added to the solution, and this method of
storage will preserve a graft for around 21 days.72 Under
normal circumstances, freezing should be avoided.
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14 • SKIN CRAFTS 309
Various solutions are being studied to lengthen
graft preservation without refrigeration. A solution
containing a combination of growth factors, steroids,
insulin, and adenine called Ready Mix currently
achieves 60% keratinocyte viability at 30 days of
incubation.73
Long-term storage and allograft storage depend on
freezing techniques. Glycerol or dimethyl sulfoxide is
added to the solution to prevent tissue destruction by
the freezing process, and the grafts are rapidly frozen
with liquid nitrogen. When the grafts are needed, they
can be thawed and easily applied.74
Craft Survival
A skin graft is essentially a skin transplantation. The
graft is completely severed from its blood supply,
drainage system, and sensory innervation. The graft
is placed onto a vascular bed so that the graft will
become vascularized and sensate. The process of graft
survival has been well studied during the past century.
Immediately after grafting, the graft is dependent on
the serous exudate from the recipient site for survival
in a process called serum imbibition. Ultimately,
however, how the graft becomes vascularized is still
unclear.
SERUM IMBIBITION
Hubscher and Goldmann were the first physicians
to recognize the importance of serum nourishment
for graft survival.75,76 They termed this process "p^ as "
matic circulation" of a graft. Subsequently, numerous
studies have been performed that demonstrate how
a skin graft survives during its first 48 hours after
transplantation.
Immediately after a graft is placed onto the recip-
ient site, it begins to gain weight and appear edema-
tous.77*81 It is thought that plasma leaks from recipient
venules and, to a lesser extent, from capillaries and
arterioles.82 This plasma then fills the space between
the graft and the underlying host bed. The fibrino-
gen, within the plasma, settles out and forms a glue-
like substance anchoring the graft to the bed. The
remaining plasma is absorbed by the graft and
provides temporary nourishment for the graft. Studies
of this serum have revealed that it also contains
erythrocytes and polymorphonuclear leukocytes.83
Because the fluid taken up by the graft is free of fibrin,
it is technically termed serum. Thus, Converse,
Uhlschmid, and Ballantyne's proposed terminology
"phase of serum imbibition" has largely replaced
Hubscher and Goldmann's original plasmatic
circulation.84
Serum imbibition describes a well-understood
series of events. After a graft is harvested, the graft vessels
310 I • GENERAL PRINCIPLES
go into spasm, evacuating any old blood and serum.
Once laid onto the recipient site, the graft passively
absorbs the underlying serum through both the cut
endings of the vasculature and the porous dermis. The
graft becomes edematous and can increase in mass by
as much as 30%.85 Metabolism in the graft converts to
anaerobic metabolism and the pH in the graft falls to
6.8.86 The metabolic demands of the graft also fall;
adenosine triphosphate levels fall 70%, and glucose
levels fall 80%.87 Metabolic waste products from anaer-
obic metabolism may stimulate the revascularization
process. The graft remains edematous and in anaero-
bic metabolism for approximately 48 hours until revas-
cularization occurs and the graft is able to unload its
waste products. 88
Throughout the phase of serum imbibition,
endothelial ingrowth from the host into the graft is
occurring. Thus, vascular flow through the graft can
be established as quickly as possible. The phases of
revascularization and serum imbibition both begin
when the graft is inset onto the recipient bed. The phases
can be thought of as overlapping rather than as mutu-
ally exclusive.
GRAFT REVASCULARIZATION
How graft revascularization occurs has been a topic
of debate in plastic surgery for the last 140 years. Early
experiments by Bert89 noted microscopic anastomo-
sis between the recipient site and the graft, which he
termed abouchement. Thiersch 5 in 1874 confirmed
these findings in histologic sections of full-thickness
grafts and termed the process inosculation. The theory
of inosculation states that the cut vessels from the host
bed line up with the cut ends of the vessels of the
graft and form anastomoses. This provides inflow and
outflow for the graft. The process of inosculation has
been studied by a variety of techniques including
histologic studies and injection studies. Numerous
studies have documented the process of inoscula-
tion, especially in full-thickness grafts.90 The process
begins immediately, and vascular connections have
been demonstrated as early as 22 hours after graft-
ing.91 However, most studies indicate that a graft
becomes vascularized on postoperative day 4, and
flow becomes normal by postoperative day 29 in
autografts.92*95 In allografts, flow improves until day
6 and eventually halts on day 9 because of the rejec-
tion phenomenon. 96 ' 99
About 25 years after Bert described abouchement,
Garre, Hubscher, Goldmann, Jungengel, and Enderlen
discounted the inosculatory process and proposed
another theory to describe how grafts revascular-
i z e 75.76,100-102 T h e w o r k 0 f m e s e e a r iy researchers indi-
cated that the original vasculature in the skin graft
degenerates. Endothelial cells and capillary buds
from the host invade the graft, restoring blood flow.
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Dr.Mustafa D.
Histochemical studies, injection studies, and histologic
studies have also confirmed this method of graft revas-
cularization.103"107 Again, the process begins immedi-
ately, and as early as 9 hours after grafting, inflammatory
cells can be seen invading the graft.99 By the fourth
postoperative day, flow through the graft has been re-
established. The original graft vasculature degenerates,
and the vascular network throughout the graft evolves
from direct invasion from the host bed.
Through the numerous studies performed during
the last 140 years, a third theory has evolved to describe
skin graft revascularization. This theory states that the
original vasculature of the graft does indeed degener-
ate. However, the acellular basal lamina persists, pro-
viding a conduit for the ingrowth of the new vascular
tree from the host bed. This theory was first proposed
by Henry after his histologic studies identified acellu-
lar patent vascular channels in the skin graft 48 hours
after grafting, which later become endothelialized from
the invading host capillary buds.108,109
There is strong evidence supporting all three of the
proposed theories, and it is possible that graft revas-
cularization involves all three processes. Inosculation
may be responsible for early graft revascularization,
allowing the graft to unload the metabolic waste from
the phase of serum imbibition. Concomitantly, the cap-
illary buds and vascular endothelium developing in
the host bed invade the graft in both a random pattern
and through patent vascular channels. Grafts will
appear pink and blanch once they have revascularized.
Converse, Filler, and Ballantyne" 0 studied revas-
cularization of split-thickness grafts and compared
their findings with full-thickness grafts. They found
that the revascularization process in split-thickness
grafts is similar to that in full-thickness grafts. Revas-
cularization occurs by the ingrowth of capillary buds
from the underlying host bed and occurs around
postoperative day 4. It is widely believed that a split-
thickness graft can survive longer without revascu-
larization than a full-thickness graft can. Split-thickness
grafts contain fewer cellular elements than full-
thickness grafts do. Also, a thick dermis acts as a barrier
to diffusion of serum during the phase of serum
imbibition. A thin split-thickness graft can survive
longer during serum imbibition because there are
fewer cellular elements to nourish, and there is a
shorter distance of diffusion through the dermis. Thus,
in approaching a wound with a marginal vascular bed,
a thin graft is more likely to survive than a thick
graft.
In summary, early graft survival depends on a
process known as serum imbibition. Plasma leaked
from the venules of the host bed deposits its fibrin in
the interface between recipient site and graft, and the
remaining serum is absorbed by the graft, providing
nourishment. Some of the host and graft vessels form
anastomoses in a process called inosculation, which
T^gWftf'aeltfW image...
may provide early revascularization of the graft. Host
capillary buds invade the graft, and by the fourth post-
operative day, blood flow through the graft has been
restored. Flow through the graft continues to improve
until about 1 month after grafting, when the revas-
cularization phase is completed.
MATURATION
Once the graft becomes vascularized, the graft itself
continues to mature and contract over the course
of 6 to 12 months. A scar deformity from a split-
thickness skin graft should be observed clinically for
a minimum of 6 months before any attempt at scar
revision because the defect will shrink during that
time.
The most significant event that occurs during graft
maturation is wound and graft contraction. An
ungrafted wound will undergo contraction as part of
natural healing. This event is mediated by a cell known
as the myofibroblast and appears to be an active
process.'l Before a wound is grafted, many fibroblasts
have already differentiated into myofibroblasts. These
myofibroblasts will contract the wound despite the
application of a skin graft. In turn, the graft will also
contract to the dimensions of the underlying wound.
This process is called secondary contraction.
Primary contraction occurs immediately after a skin
graft is harvested and the fresh graft recoils from its
inherent elastic properties. Primary contraction is
greatest in full-thickness grafts and occurs less in
split-thickness grafts.'16 Primary contraction is easily
overcome clinically by stretching the graft during its
application.
Secondary contraction is of greater clinical sig-
nificance and is well understood. Dermis appears
to inhibit myofibroblast differentiation. Thus, full-
thickness grafts appear to contract less than split-
thickness grafts do.112 Thick split-thickness grafts
contract less than thin split-thickness grafts do. In an
interesting study by Corps,ll3atheory was proposed that
the relative thickness of the graft plays an important
role in secondary contraction as opposed to absolute
graft thickness. A 0.2-mm graft from the ventral surface
of the torso will undergo less secondary contraction
than a graft of the same thickness from the dorsum of
the torso. This is because ventral skin is relatively thin.
Secondary graft contraction is important to con-
sider in applying a skin graft over a joint, in the web
space of a hand, or in the eyelids and for scar con-
tracture surgery. In these patients, a full-thickness graft
should be used whenever possible. If the defect is too
large for a full-thickness graft, a split-thickness graft
may be used, but it should be cut as thick as possible
to prevent contracture formation.
Besides undergoing less secondary contraction, full-
thickness skin grafts appear to maintain the ability to
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Dr.Mustafa D.
14 • SKIN GRAFTS 31 1
grow.62,1'4 Consequently, full-thickness skin grafts are
used whenever possible in a pediatric setting. Split-
thickness skin grafts have less growth potential and in
some instances may continue to contract with time.
Thus, children with injuries requiring split-thickness
skin grafting are observed until growth has halted to
watch for contracture formation. This is especially true
in the pediatric burn patient.
During the maturation phase, the epidermis under-
goes a tremendous amount of hyperplasia. At 2 weeks,
the epidermis may be seven to eight times thicker tha n
the epidermis of the original graft.,15This is seen clin-
ically as crusting and scaling of the graft. This epider-
mal overgrowth will spread across a wound to help
heal any ungrafted portion of the wound.
One interesting and poorly understood process that
occurs in the graft of heavily pigmented individuals
is hyperpigmentation. This occurs most frequently
when grafts are applied to the palms and soles of the
foot. Grafts in these areas frequently hyperpigment
dramatically. All grafts in heavily pigmented indi-
viduals are susceptible to hyperpigmentation.116 This
problem is best prevented by carefully selecting a donor
site with skin that best resembles the pigmentation
of the recipient site.117 Some plastic surgeons think
that early sun exposure leads to permanent hyper-
pigmentation. Sun exposure should be minimized until
1 year after grafting. Once hyperpigmentation occurs,
it is difficult to treat. Dermabrasion and chemical peels
may reduce the hyperpigmentation."8
Nerves, Sweat Glands, and Hoir Follicles
It appears that nerve fibers degenerate within the graft
during the course of the first 30 days after transplan-
tation. New nerve fibers then invade the skin graft,both
from the periphery and from the graft base at around
40 days. A majority of these fibers then travel either
along the Schwann sheaths left from the original nerves
or along blood vessels. At 2 to 3 months, the fibrils
increase in number and begin to reach end organs near
hair follicles, sweat glands, and sensory end organs.119
The end result is a crude re-formation of the neural
network of the donor skin. Although sensation often
returns, it is usually not normal sensation. Pain gen-
erally returns first, and the graft may be hypersensi-
tive for up to a year after grafting.,0Touch, temperature,
and tactile discrimination return later. Although the
architecture of the neural network resembles the
donor site, tactile discrimination appears to better
resemble the recipient site.120
Sensation is better in full-thickness grafts than in
split-thickness grafts. Split-thickness grafts, however,
are often used on less vascular and larger wounds.
Recent data indicate that sensation depends not only
on the thickness of the graft but also on the condition
of the underlying host bed.121 Therefore, it is unclear
whether full-thickness grafts would acquire better
312 I • GENERAL PRINCIPLES
sensation than split-thickness grafts placed on the same
bed.
Sweat gland function often returns in both the split-
thickness and full-thickness skin grafts. Sweat gland
function appears to be superior in the full-thickness
graft. Sweat glands are dependent on neural innerva-
tion to function."'' Consequently, sweat does not occur
for 2 to 3 months after grafting. During this time, the
graft is susceptible to development of dry, scaly skin.
This can be prevented by the application of moistur-
izing cream. Once the sweat glands are reinnervated,
their behavior resembles that of the host bed rather
than of the donor site. Consequently, grafts to the palm
will often form sweat in response to emotional stimuli,
regardless of the donor site.
Many hair follicles are damaged or destroyed dur-
ing a split-thickness skin graft harvest. As a result,
hair growth in a split-thickness graft is unusual. In
full-thickness grafts, hair growth generally resumes
and maintains the property of the donor site. Full-
thickness skin grafts from the scalp are a popular
method of hair restoration in male pattern baldness
as well as in eyebrow reconstruction.122
Graft Failure
Any development that disrupts the process of serum
imbibition or revascularization will result in failure of
the skin graft (Table 14-3). The process of skin graft
take depends on a healthy and vascularized bed. One
of the more common causes of skin graft failure is an
inadequate bed. Exposed tendon, bone, and cartilage
will not support a skin graft and can be considered
a contraindication to skin graft application. Fat,
peritenon, perichondrium, and periosteum are poorly
vascularized, but they will support thin split-thickness
skin graft. However, conservative treatment with dress-
ing changes can allow granulation tissue to develop,
creating a vascularized bed, which improves the
chances of skin graft take.
Any barrier between the graft and the recipient bed
can prevent revascularization of the graft. The most
common barriers are blood, serum, and purulent mate-
rial. Hematoma, seroma, and infection can lead to either
partial or complete skin graft failure. If small fluid
TABLE 1 4 - 3 • FAILURE OF SKIN CRAFTING
Craft placed on avascular bed
Infection
Hematoma
Seroma
Shearing
Malnutrition
Poor underlying medical condition
Upside-down graft or other technical errors
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Dr.Mustafa D.
collections develop under a large skin graft, they can
be evacuated by making small cuts in the graft, often
saving a portion of the skin graft.
One of the most common causes of graft failure
is shearing of the graft. The small capillaries that
invade the graft are fragile and can be disrupted with
a minimum of force. Grafts can be devascularized
during a dressing change or during movement in the
early postoperative period. Consequently, grafts to the
extremity are usually immobilized, and all dressing
changes are performed with the utmost care for the
underlying graft.
Infection can cause destruction of the graft without
the formation of purulent drainage. Krizek and
Robson35 proved that a wound with more than 105
organisms per gram of tissue will not heal or accept
a skin graft. Some organisms, Pseudomonas being the
most common, can destroy a skin graft with little or
no purulence. The infection does not have to be limited
to the wound. In fact, James Barrett Brown and Vilray
Papin Blair recommended that a patient be completely
free of infection before skin grafting.7 This surgical
axiom holds true today. Systemic infection can lead
to poor wound healing and ultimately partial or total
graft failure.
Unfavorable systemic or local conditions can lead
to poor graft take. Malnutrition, vasculitis, malignant
disease, steroids, and chemotherapeutic medications
have all been shown to impair wound healing and to
impair graft take. Pressure and radiation injury impair
the recipient bed and can lead to total or partial skin
graft failure.
Technical errors during grafting are a relatively
uncommon cause of failure today. Grafts can be applied
upside-down or they can be handled roughly, leading
to total or partial loss. Dermatomes or meshers can be
too hot after sterilization and burn the graft during
the preparation phase.
SKIN SUBSTITUTES
Skin substitutes are generally categorized into three
separate groups: temporary, semipermanent, and
permanent. Temporary skin substitutes are placed on
either a partial- or full-thickness wound and remain
until the wound is healed. Semipermanent material
remains attached to an excised wound and is
eventually replaced with autologous skin grafts. Per-
manent skin substitutes encompass the incorporation
of an epidermal or dermal component and are designed
to replace autologous skin grafts.
Naturally occurring tissues include cadaver allo-
grafts, porcine xenografts, and amniotic membranes.
Skin substitutes can be categorized as synthetic bi-
laminates, collagen-based composites, and culture-
derived tissue. Examples of synthetic bilaminates are
Biobrane, TransCyte, and Integra. Collagen-based
TeWt^aeldW image...
dermal analogues include de-epithelialized allograft,
such as AlloDerm. Finally, culture-derived tissue
includes Apligraf.
The "gold standard" for temporary skin coverage
is cadaver skin or allograft. Allografts will take early,
but eventually the epidermal layer is sloughed. The graft
loses its barrier function once the epidermis is sloughed.
Therefore, the outer layer needs to be replaced for
definitive wound closure. The major problems with
cadaver skin are the cost and the possibility of disease
transmission.123 There are reports of hepatitis and
cytomegalovirus infection and one instance of human
immunodeficiency virus transmission attributed to the
use of allografts.124 Xenografts, usually from porcine
species, are more available than allografts. Xenografts,
because of their antigenic properties, will not revas-
cularize and will eventually slough. Consequently,
xenografts need to be replaced for wound closure.
Biobrane is a temporary biosynthetic skin sub-
stitute. The outer layer, which is analogous to the
epidermis, is constructed of a thin silicone film. The
silicone film has multiple small pores that allow
removal of exudate and penetration of antibiotics. This
layer acts as a mechanical layer protecting the wound
from the environment. The inner dermal layer is com-
posed of a three-dimensional nylon filament weave
impregnated with type I collagen. The inner layer helps
the Biobrane adhere to the wound.125
Integra* is a temporary bilaminate membrane
system. The dermal layer is made of a porous matrix
of cross-linked bovine tendon collagen and a gly-
cosaminoglycan (chondroitin 6-sulfate). This layer is
manufactured with a controlled porosity and defined
degradation rate. The pore size and other properties
are designed to serve as a template for ingrowth of
wound healing components. The epidermal layer
is made of a synthetic polysiloxane polymer. This
layer controls moisture loss from the wound. Once
the Integra is applied to the wound, fibroblasts,
macrophages, lymphocytes, and capillaries invade the
dermal layer. As the healing process proceeds, fibro-
blasts deposit a collagen matrix. The dermal layer of
the Integra is concurrently slowly degraded. Once the
collagen matrix is formed and the dermal layer is
completely degraded, a "neodermis" capable of sup-
porting a thin split-thickness skin graft has formed.
The epidermal synthetic layer is peeled offthe neo-
dermis, and a split-thickness autograft can be applied
for definitive wound closure.126
Integra offers many advantages in the treatment of
large partial- or full-thickness wounds. It is readily avail-
able and does not require a donor site. It immediately
converts an open wound into a closed wound. This
decreases the metabolic demand on the patient and
•Integra LifcSciences Corporation, Arlington, Texas.
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Dr.Mustafa D.
14 • SKIN GRAFTS 313
also reduces the risk of wound infections. The neo-
dermis developed by Integra resembles, histologically
and physiologically, normal dermis. Accordingly,
wound contraction is less of a problem compared with
a wound that is allowed to granulate. The aesthetic
results of wounds treated with Integra and split-
thickness skin grafts appear to be equivalent or
superior to those of wounds treated with immediate
autografting.127 Finally, grafting can be delayed until
a patient is stable and donor sites are plentiful.
AlloDerm* is an acellular de-epidermalized dermis
product that is a semipermanent skin substitute. This
product is processed cadaver skin that functions as
a dermal replacement. It is a cryopreserved and
lyophilized allodermis that acts strictly as a dermal sub-
stitute. It has no protective epidermal analogue. When
used on open wounds, it requires the application of
a thin split-thickness autograft or cultured ker-
atinocytes.I28 AlloDerm does become incorporated into
the host by tissue ingrowth. AlloDerm can be used to
resurface burn wounds and as a dermal replacement
in scar revisions or cosmetic surgery.129 Randomized
studies are under way to determine whether AlloDerm
improves cosmetic and functional outcomes of skin
grafting.
Dermagraft-TC* is a semipermanent biosynthetic
replacement for human skin. It consists of a matrix of
polyglycolic acid and polyglactin-910 fibers permeated
with human neonatal fibroblasts. The matrix is
absorbed in 60 to 90 days and is degraded primarily
by hydrolysis.130 Like AlloDerm, Dermagraft-TC
requires a split-thickness autograft or cultured ke-
ratinocytes for definitive wound closure.
Dermagraft-TC furnishes a continuous dermal
replacement layer beneath meshed skin grafts. Der-
magraft-TC routinely supports the take of an over-
lying skin graft. Dermagraft-TC has been studied in
the treatment of diabetic foot ulcers. The dermis of
patients with diabetes lacks collagen components,
matrix proteins, and growth factors found in normal
human dermis. Dermagraft-TC provides these dermal
components directly at the wound site in preparation
for split-thickness skin grafting.131
Apligraf5 is a bilaminate human epidermal and
dermal analogue that can act as a permanent skin sub-
stitute. The epidermal layer is formed by human ke-
ratinocytes with a well-differentiated stratum corneum.
The dermal layer is composed of bovine type I colla-
gen lattice impregnated with human fibroblasts from
neonatal foreskin. Whereas the matrix proteins and
cytokines found in human skin are found in Apligraf,
Apligraf does not contain Langerhans cells, melano-
cytes, macrophages, lymphocytes, neutrophils, blood
'LifeCell Corporation, Branchburg, New Jersey.
'Advanced Tissue Sciences, La Jolla, California.
^Organogenesis Inc., Canton, Massachusetts,
314 !• GENERAL PRINCIPLES
vessels, hair follicles, or sweat glands. Consequently,
Apligraf is not antigenic, and the dermal layer incor-
porates into the wound bed much like an autograft.
The epidermal analogue acts as a barrier and is even-
tually repopulated by host cells.' 32
Apligraf has been studied mainly in the treatment
of venous leg ulcers. The time to wound healing has
been shown to be significantly decreased with the use
of Apligraf compared with compression therapy
alone. 133 Unlike temporary skin substitutes, Apligraf
provides immediate coverage, new tissue formation,
and integration with host tissues. Apligraf is supplied
in a circular disk approximately 7 to 8 cm in diameter.
Therefore, large wounds require multiple plates of
Apligraf, which can be costly. Apligraf is contraindi-
cated in infected wounds and also in patients with a
bovine collagen allergy.
THE FUTURE OF SKIN CRAFTING
Skin grafting has been a useful tool for the recon-
structive surgeon for more than 100 years. Skin grafts
provide a simple method of wound closure when
primary closure is impossible. Grafting plays a crucial
role in b u r n surgery, in which the restoration of the
skin provides protection from infection a n d a barrier
to fluid loss. However, in areas of aesthetic concern,
m a n y surgeons choose to use flaps over grafts for their
improved cosmetic appearance. Consequently, skin
grafts are not always the first choice of the reconstructive
surgeon.
As the technology with skin substitutes a n d cul-
tured epithelium improves, skin grafts may again be-
come the cornerstone of reconstructive surgery. Dermal
analogues appear to improve the cosmetic results of
skin grafts, which may make flaps unnecessary for aes-
thetically sensitive areas. Eventually, skin substitutes
or a combination of dermal substitutes and cultured
epithelium may replace autografting altogether. Cur-
rently, skin substitutes and cultured keratinocytes
are expensive and flimsy, a n d they frequently heal
with a conspicuous and unfavorable scar. However, skin
substitutes and cultured epithelium do not require
a d o n o r site, which is a distinct advantage over
autografting.
Even though skin grafting has been well studied
during the past 100 years, the field is still rapidly chang-
ing and evolving. Skin substitution is still in its infancy.
As the technology improves, skin substitution may rev-
olutionize the field of skin grafting.
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46. Ragnell A: The secondary contracting tendency of free skin
grafts. Br J Plast Surg 1952;5:6.
47. Kavouni A, Shibu M, Carver N: Squamous cell carcinoma arising
in transplanted skin. Clin Exp Dermatol 2000;25:302.
48. Gamatsi IE, McCulloch TA, Bailie FB, Srinivasan JR: Malig-
nant melanoma in a skin graft: burn scar neoplasm or a trans-
ferred melanoma? Br J Plast Surg 2000;53:342.
49. Rudolph R, Earle AS, Fratiannd RB: Reduction mammoplasty
and other skin excisions as a source of homograft skin. Br J
Plast Surg 1975;29:121.
50. Gemberling RM, Miller TA, Carree H, Zawacki BE: Dressing
comparison in the healing of donor sites. J Trauma 1976; 16:812.
51. Zapata-Sirvent R, Hansbrough JF, Carroll W, et al: Compari-
son of Biobrane and Scarlet Red dressings for treatment of
donor site wounds. Arch Surg 1985;120:743.
52. Hansbrough JF: Use of Biobrane for extensive posterior donor
site wounds. J Burn Care Rehabil 1995;16:335.
53. Persson K.Salemark L: How to dress donor sites of split thick-
ness skin grafts: a prospective, randomized study of four dress-
ings. Scand J Plast Reconstr Surg Hand Surg 2000;34:55.
54. James JH, Watson ACH: The use of Opsite, a vapour permeable
dressing on skin graft donor sites. Br J Plast Surg 1975;28:107.
55. Iregbulem LM: Use of a semi-permeable membrane dressing
in donor sites in Nigerians. Ann Acad Med Singapore
1983;12(suppl):425.
56. Fatah MF, Ward M: The morbidity of split-skin graft donor
sites in the elderly: the case for mesh-grafting the donor site.
BrJPlastSurgl984;37:184.
57. Casin H, Ainaud P, Le Bever H, et al: Cultured epithelial auto-
grafts in extensive burn coverage of severely traumatized
patients: a five year single center experience with 30 patients.
Burns 2000;26:379.
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14 • SKIN CRAFTS 315
58. Duinslaeger L, Verbeken G, Vanhalle S, Vandetkelen A: Cul-
tured allogenic keratinocyte sheets accelerate healing compared
to Op-Site treatment of donor sites in burns. J Burn Care
Rehabil 1997;18:545.
59. Ghofrani A, Holler D, Schuhmann K, et ah The influence of
systemic growth hormone administration on the healing time
of skin graft donor sites in a pig model. Plast Reconstr Surg
1999;104:470.
60. Breach NM: Pre-auricular full-thickness skin grafts. Br J Plast
Surg 1978;1:124.
61. Corwin TR, Klein AW, Habal MB: The aesthetics of the preau-
ricular graft in facial reconstruction. Ann Plast Surg 1982;9:
312.
62. Baran NK, Horton CE: Growth of skin grafts, flaps and scars
in young minipigs. Plast Reconstr Surg 1972:50:487.
63. Furnas DW: Frost anesthesia for skin grafts. Plast Reconstr
Surg 1965;35:191.
64. Goulian DA: A new economical dermatome. Plast Reconstr
Surg 1968;42:85.
65. Silverstein P, McManus WF, Pruitt BA Jr: Subcutaneous tissue
infiltration as an adjunct to split-thickness skin grafting. Am
J Surg 1972:123:624.
66. CartottoR,MusgraveMA,BeveridgeM,etal:Minimizingblood
loss in burn surgery. J Trauma 2000;49:1034.
67. Palkar VM: Full-thickness skin grafting. J Surg Oncol
2000;73:31.
68. Tanner JC, Vandeput J, Olley JF: The mesh skin graft. Plast
Reconstr Surg 1964;34:287.
69. Fifer R, Pieper D, Hawtorf D: Contraction rates of meshed,
nonexpanded split-thicknessskin grafts versus split-thickness
sheet grafts. Ann Plast Surg 1993;31:162.
70. Wood S, Lees V: A prospective investigation of the healing of
grafted pretibial wounds with early and late mobilisation. Br
J Plast Surg 1994:47:127.
71. Smahal J, Clodius L: The blood vessel system of free human
skin grafts. Plast Reconstr Surg 1971;57:61.
72. Titley O, Cooper M, Thomas A, Hancock K: Stored s k i n -
stored trouble? Br J Plast Surg 1994:47:24.
73. Fahmy F, Navsaria H, Frame J, et al: Skin graft storage and
keratinocyte viability. Br J Plast Surg 1993;46:292.
74. Bravo D, Rislcy TH, Gibran N, et al: Effect of storage and preser-
vation method on viability in transplantable human skin allo-
graft. Burns 2000;26:367.
75. Goldmann EE: Die kunstliche Obcrhautung offener Krebse
durch Hauttransplantation nach Thiersch. Zentralbl Allg
Pathol 1890;1:505.
76. Hubscher C: Beitrage zur Hautverpflanzung nach Thiersch.
Beitr Klin Chir 1888:4:395.
77. Marckmann A: Biology of skin autografts. Dan Med Bull
1967:14:135.
78. Psillakis JM, de Jorge FB, Villardo R, et al: Water and elec-
trolyte changes in autogenous skin grafts. Discussion of the
so-called"plasmatic circulation "Plast Reconstr Surg 1969;43:
500.
79. Conway H, Joslin D, Rees TD, Stark RB: Observation on the
development of circulation in skin grafts. II. The physiologic
pattern of early circulation in autografts. Plast Reconstr Surg
1951:8:312.
80. Birch J, BrSnemark P-I: The vascularization of a free full thick-
ness skin graft. I. A vital microscopic study. Scand J Plast Recon-
str Surg 1969;3:1.
81. Birch J, Branemark P-I, Lundskog J: The vascularization of a
freefullthicknessskingraft.II.Amicroangiopathicstudy.Scand
J Plast Reconstr Surg 1969;3:11.
82. Kikuchi 1, Omori M: Demonstration of leaking vessels under
skin grafts. Plast Reconstr Surg 1970;45:66.
83. Hynes W: The early circulation in skin grafts with a consider-
ation of methods to encourage their survival. Br J Plast Surg
1954:6:257.
316 I • GENERAL PRINCIPLES
84. Converse JM, Uhlschmid GK, Ballantyne DL Jr: "Plasmatic
circulation"inskin grafts.The phaseof serum imbibition. Plast
ReconstrSurg 1969:43:495.
85. Converse |M, Ballantyne DL Jr, Rogers BO, Raisbeck AP:
"Plasmatic circulation" in skin grafts. Transplant Bull 1957;
4:154.
86. Rous P:The relative reaction within living mammalian tissues.
JExpMedl926;44:815.
87. Hira M, Tajima S: Biochemical study on the process of skin
graft take. Ann Plast Surg 1992;29:47.
88. Smahal J: The healing of skin grafts. Clin Plast Surg 1977;4:
409.
89. Bert P: De la greffe animale. Paris, JB Bailliere et Fils,
1863.
90. Converse JM, Smahal J, Ballantyne DL Jr, Harper AD: Inoscu-
lation of vessels of skin graft and host bed: a fortuitous
encounter. Br J Plast Surg 1975:28:274.
91. Davis IS.Traut HF: Origin and development of the blood supply
of whole-thickness skin grafts. An experimental study. Ann
Surg 1925:82:871.
92. Converse JM, Rapaport FT: The vascularization of skin auto-
grafts and homografts; an experimental study in man. Ann
Surgl956;143:306.
93. Haller JA Jr, Billingham RE: Studies of the origin of the vas-
culature in free skin grafts. Ann Surg 1967; 166:896.
94. Rollc GK. Taylor AC, Charipper HA: A study of vascular changes
in skin grafts in mice and their relationship to homograft break-
down. J Cell Comp Physiol 1959;53:215.
95. Ohmori S, Kurata K: Experimental studies on the blood supply
to various types of skin grafts in rabbits using isotope P32.
Plast ReconstrSurg 1960;25:547.
96. Edgcrton MT, Edgerton PJ: Vascularization of homografts.
Transplant Bull 1955;2:98.
97. Kamrin BB: Analysis of the union between host and graft in
the albino rat. Plast Reconstr Surg 1961;28:221.
98. Scothorne RJ, McGregor IA: The vascularization of autografts
and homografts of rabbit skin. J Anat 1953;83:379.
99. Egdahl RH, Good RA, Varco RL: Studies in homograft and
hcterograft survival. Surgery 1957;42:228.
100. Garre' C: Obcr die histologischen Vorgange bei der Anhcilung
der Thiersch-schen Transplantationen. Beitr Klin Chir
1889;4:625.
101. Jungengel M: Die Hauttransplantation nach Thiersch. Verh
PhysMedGesWurzb 1891;25:1.
102. Enderlen: Histologische Untersuchungcn liber die Einheilung
von Pfropfungen nach Thiersch and Krause. Dtsch Z Chir
1897;45:453.
103. Converse JM, Ballantyne DL Jr: Distribution of diphospho-
pyridine nucleotide diaphorase in rat skin autografts and
homografts. Plast Reconstr Surg 1962;30:415.
104. AntopolW.Glaubach S.Goldman L:The use of neotetrazolium
as a tool in the study of active cell processes. Trans N Y Acad
Sci 1950;12:156.
105. Smahal J: The revascularization of a free skin autograft. Acta
Chir Plast 1967;9:76.
106. Mir y Mir L: Biology of the skin graft. New aspects to consider
in its revascularization. Plast Reconstr Surg 1951;8:378.
107. Medawar PB: The behaviour and fate of skin autografts and
skin homografts in rabbits. J Anat 1944;78:176.
108. Henry L, Marshall DC, Friedman EA, et al: A histologic study
of the human skin autograft. Am J Pathol 1961 ;39:317.
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109. Zarem HA.Zweifach BW.McGehee JM: Development of micro-
circulation in full thickness autogenous skin grafts in mice.
Am J Physiol 1967;212:1081.
110. Converse JM, Filler M, Ballantyne DL Jr: Vascularization of
split-thickness skin autografts in the rat. Transplantation
1965:3:22.
111. Guber S, Rudolph R: Collective review—the myofibroblast.
Surg Gynecol Obstet 1978; 146:641.
112. Rudolph R:The effect of skin graft preparation on wound con-
traction. Surg Gynecol Obstet 1976; 142:49.
113. Corps BV: The effect of graft thickness, donor site and graft
bed on graft shrinkage in the hooded rat. Br J Plast Surg
1969;22:125.
114. Klein L, Rudolph R: 3H-Collagen turnover in skin grafts. Surg
Gynecol Obstet 1974;139:883.
115. Gillman T, Penn J, Bronks D, Roux M: Reaction of healing
wounds and granulation tissue in man to auto-Thtersch,
autodermal and homodcrmal grafts. Br J Plast Surg 1953;6:153.
116. TsukadaS:The melanocytes and melanin in human skin auto-
grafts. Plast ReconstrSurg 1974;53:200.
117. Rudolph R: Skin grafting. In Goldwyn RM, ed: The Unfavor-
able Result in Plastic Surgery: Avoidance and Treatment, 2nd
ed. Boston, Little, Brown, 1984:148.
118. Mir y Mir L: The problem of pigmentation in the cutaneous
graft. Br J Plast Surg 1961:14:303.
119. Ponte'n B: Graftedskin—observations on innervation and other
qualities. Acta Chir Scand Suppl 1960;257:1.
120. Fitzgerald MJT, Martin F, Paletta FX: Innervation of skin grafts.
Surg Gynecol Obstet 1967; 124:808.
121. Weiss-Becker C, Fruhstorfer H, Friederich H, Winter H: Rein-
nervation of split skin grafts in humans: comparison of two
different methods of operation. Scand J Plast Reconstr Hand
Surg 1998;32:157.
122. Orentreich N: Autografts in alopecias and other selected der-
matologic conditions. Ann N Y Acad Sci 1959:83:463.
123. Kcalcy GP: Disease transmission by means of allograft. J Burn
Care Rehabil 1997;18:10.
124. Pirnay J, Vandenvelde C, Duinslaeger L, et al: HIV transmis-
sion by transplantation of allograft skin: a review of the liter-
ature. Burns 1997;1:1.
125. Smith DJ Jr: Use of Biobrane in wound management. J Burn
Care Rehabil 1995:16:317.
126. Fitton AR, Drew P, Dickson WA: The use of bilaminate artifi-
cial skin substitute (Integra) in acute resurfacing of burns: an
early experience. Br J Plast Surg 2001 ;54:208.
127. Chan ES, Lam PK, Liew CT, et al: A new technique to resur-
face wounds with composite biocompatible epidermal graft
and artificial skin. J Trauma 2001 ;50:358.
128. Rennekampff H, Kiessig V, Griffey S, et al: Acellular human
dermis promotes cultured keratinocyte engraftment. J Burn
Care Rehabil 1997;18:535.
129. Terino EO: AlloDerm acellular dermal graft: applications in
aesthetic soft-tissueaugmentation. Clin Plast Surg 2001 ;28:83.
130. Spielvogel RL: A histologic study of Dermagraft-TC in patients'
burn wounds. J Burn Care Rehabil 1997;18:sl6.
131. Eaglstcin WH: Dermagraft treatment of diabetic ulcers. J Der-
matol 1998:25:803.
132. Kirsner RS: The use of Apligraf in acute wounds. J Dermatol
1998:25:805.
133. Falanga V: Apligraf treatment of venous ulcers and other chronic
wounds. J Dermatol 1998:25:812.
image...
CHAPTER
15•
Vascular Territories
G. IAN TAYLOR, MBBS, MD, FRACS, FRCS, FACS • ANDREW IVES
MBChB • SHYMALDHAR, MD
HISTORICAL BACKGROUND
BASIC RESEARCH
Arterial Territories
Venous Drainage
Neurovascular Territories
Comparative Anatomy
THE ANCIOSOME CONCEPT
Territories
ANATOMIC CONCEPTS
In 1977, Converse1 stated that "there is no simple and
all-encompassing system which is suitable for clas-
sifying skin flaps. It is now generally agreed that the
anatomical vascular basis of the flap provides the most
accurate approach for classification." The veracity of
this statement has been borne out with the passage of
time.
The vascular architecture of the body is arranged
anatomically as a continuous series of vascular loops,
like the tiers of a Roman aqueduct, that increase in
number while their size and caliber decrease as they
approach the capillary bed. The reverse situation occurs
on the venous side. This anatomic arrangement of the
vascular "skeleton" is shown beautifully in the cor-
rosion cast studies of newborn babies performed by
Tompsett2 that reside in the Hunterian Museum at The
Royal College of Surgeons in London (Fig. 15-1). Note
how the main arterial loops hug the bony framework
and the secondary arcades follow the intermuscular
and intramuscular connective tissue framework. The
"keystones" of these arcades are represented usually
by reduced-caliber ("choke") arteries and arterioles,
matched on the venous side by avalvular (oscillating)
veins that permit bidirectional flow.
This clever arrangement of the vascular anatomy
allows the equilibration of flow and pressure of the
blood as it arrives at the capillary bed and provides the
framework for a venous return, which departs at a
reduced yet constant pressure. It will be seen that choke
arteries and avalvular veins form an essential role in
controlling this pressure gradient across the capillary
bed (Fig. 15-2).
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
CLINICAL APPLICATIONS
The Doppler Probe and Mapping of Perforators
Axes of Skin Flaps
Skin Flap Dimensions
The Delay Phenomenon
Fasciocutaneous Flaps
Musculocutaneous Flaps
Composite Flaps
Tissue Expansion
Liposuction
HISTORICAL BACKGROUND
Plastic surgery evolved as a specialty in Europe and
North America to restore the mutilated victims of the
two World Wars. With artistic flair and geometric pre-
cision, tissues were advanced and rotated. They were
transposed locally and dispatched to distant sites on
limb carriers, only to be rebuffed on occasion by necro-
sis. Gillies often lamented that "plastic surgery is a
constant battle between blood supply and beauty."3
Gradually, rigid length-to-breadth flap ratios were cal-
culated for different regions of the body because most
of the flaps were designed without a precise knowl-
edge of the vessels on which they were based.
This anatomic information was available but hidden
in texts in foreign languages. In 1889, Manchot4 per-
formed the first examination of the cutaneous vas-
cular territories. His treatise, Die Hautarterien des
menschlkhen Korpers [The Cutaneous Arteries of the
Human Body], was published in German and has finally
been made available in English.5 Manchot identified
the cutaneous perforators, assigned them to their
underlying source vessels, and charted the cutaneous
vascular territories of the body (Fig. 15-3). He did not
have the advantage of radiography since Rontgen was
not to make his discovery until several years later;
nevertheless, the accuracy of Manchot's work has
mostly stood the test of time.
In 1893, Spalteholz6 published an important paper
on the origin, course, and distribution of the cutaneous
perforators, studied in different regions of adult and
neonatal cadavers. He injected into the arteries gelatin
317
318 I • GENERAL PRINCIPLES
FIGURE 1 5 - 1 . Tompsett arterial skeleton of the body.
(From Taylor Gl, Palmer JH: The vascular territories [angio-
somesl of the body: experimental study and clinical appli-
cations. Br J PlastSurg 1987;40:113.)
to which various pigments were added. The soft tissues
were fixed in alcohol and subtracted in xylol, and the
resulting vascular network was embedded in Canada
balsam. Spalteholz's main study concentrated on the
detailed circulation of the skin. He made an impor-
tant distinction between direct cutaneous vessels, whose
main purpose is to supply the skin, and indirect cuta-
neous vessels, which are terminal branches of vessels
supplying the deeper organs, especially the muscles.
A detailed account of this work was published by
Timmons 7 in a review of the landmarks in the anatomic
study of the skin's blood supply.
The next major study was performed by Salmon,8,9
a French anatomist and surgeon in the 1930s. Manchot
had defined approximately 40 cutaneous territories that
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Dr.Mustafa D.
excluded the head, neck, hands, and feet. Salmon knew
of Manchot's studies and set out to reappraise his work.
Aided by radiography, he was able to delineate the
smaller radicles of the cutaneous circulation and
charted more than 80 territories encompassing the
entire body (Fig. 15-4). Salmon noted the intercon-
nections that exist between perforators, and his obser-
vation of the density and size of the vessels in different
regions of the body led him to define what he called
the hypervascular and hypovascular zones. His work
has become available in English.10
In 1975, another important study, published in
German by Schafer,11 focused on the lower extremity.
The venous plexus was investigated as well as the
arterial network. Scribtol and an ink-serum mixture
were injected into the lower limbs of adults and into
the entire circulation of fetal and neonatal cadavers.
Schafer concluded that most cutaneous arteries emerge
in rows from the intermuscular septa or occasionally
from the intramuscular septa. In addition, he high-
lighted the two systems of perforating veins: the venae
communicantes, large veins that pierce the deep fascia
and connect the superficial venous plexus to the deep
venous system; and the venae comitantes, small,
usually paired veins that accompany the cutaneous
arterial perforators.
Early last century, advances on the clinical front gave
significance to the work of these great anatomists. In
1906, Tansini12 reported a latissimus dorsi flap sup-
plied by the thoracodorsal artery. In 1919, Davis13 pub-
lished Plastic Surgery and introduced many of the
chapters with illustrations from Manchot's book. In
1921, Blair14 described a forehead flap based on the
superficial temporal vessels, and in 1929, Esser pub-
lished Artery FlapsP In 1937, Webster16 again cited
the work of Manchot when he described a long, bi-
pedicled thoracoepigastric flap based on named ar-
teries that extended from the groin to the axilla. Shaw
and Payne17 used the clinical information available in
wartime to provide one-stage direct flaps for hand
reconstruction. In 1965, Bakamjian18 drew attention
to the long paramedian perforators of the internal
thoracic system.
The 1970s witnessed the beginning of the"anatomic
revolution." McGregor and Morgan19 differentiated
between large flaps based on a known axial blood supply
and those based on random vessels in the area. Daniel
and Williams 20 reappraised the work of Manchot and
others and classified the cutaneous arteries into direct
cutaneous and musculocutaneous vessels.
Studies on the free flap by Taylor and Daniel21 and
Daniel and Taylor22 were published in 1973, and a few
years later the musculocutaneous flap was revived by
M c C r a v / ^ a n d Mathes and Nahai.26 Both procedures
demanded a precise knowledge of the cutaneous vas-
culature. In the search for new donor sites for tissue
transfer, surgeons returned to the dissection room.
image...
Arterial
Capillary
FIGURE 15-2. Schematic representa-
tion of the arterial supply and venous Venous
drainage of the capillary bed. Note the
choke arteries (small arrows) and bidi-
rectional avalvular veins (small shaded
arrows) that allow equilibration of flow and
pressure to and from the capillary bed.
Many new and exciting techniques were developed.
However, there was a tendency for the techniques to
neglect the aesthetic side of plastic surgery. The results
could sometimes be what McDowell27 described as
"globs and blobs."
To escape from the hamburger of muscle and skin,
surgeons soon rediscovered that blood vessels follow
fascial planes. In the 1980s, a new model emerged—
the fasciocutaneous flap. 28 With this development
there has been an explosion of new terms and new
classifications of the cutaneous circulation. The the-
saurus of flaps now includes a bewildering array of
terms, such as axial, random, direct cutaneous, mus-
culocutaneous, fasciocutaneous, supercutaneous,
septocutaneous, and perforator. Indeed, there has
been an attempt to classify flaps into no less than 10
types and subtypes on the basis of the origin of the
cutaneous perforators. 29
In many ways, these terms are simply different
expressions of the basic cutaneous architecture that
Manchot and Salmon wrote about 100 and 50 years
ago, respectively. A reappraisal of their work is timely,
especially in view of the modern concepts of flap
surgery. The reawakened interest in cutaneous anatomy
has encouraged workers to explore new methods of
investigating the circulation both in vivo and in vitro.
The use of fluorescein by McGregor and Morgan 19 and
prostaglandin E by Nakajima, Maruyama, and Koda30
has increased understanding of the manner in which
individual vascular territories relate dynamically to the
neighboring territories when their anastomoses are
intact.
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Dr.Mustafa D.
5 • VASCULAR TERRITORIES 319
32mmHg
15mm Hg
It would be difficult to improve on the radiographs
produced by Salmon using lead oxide, but attempts at
simplifying his mixture have produced satisfactory
results.31,32 Improved radiographic film has assisted the
imaging of small blood vessels.
The relationship of vessel size to vascular territory
has been correlated by Cormack and Lamberty 33 with
use of digitizing tablets linked to a microcomputer.
These workers also discussed in detail the axiality of
vessels in the fasciocutaneous system. Cormack and
Lamberty34 published a book, The Arterial Anatomy of
Skin Flaps, that contains a concise appraisal of the
history, anatomy, and clinical aspects of skin flap
surgery.
In our department, the authors have performed
more than 3000 fresh cadaver studies, investigating
various regions, tissues, and combinations of tissues.
This has included an investigation of the entire integu-
ment and underlying deep structures in a series of total
body studies of the arteries, 35 which led to the angio-
some concept, discussed in detail in a later section.
This was followed by studies of the veins36 and the
neurovascular territories of the body37 and detailed
studies of the angiosomes of the forearm,38 the leg,39
and the head and neck40 as well as a comparative study
of a series of mammals. 41
As well as the explosion in flap surgery that has
occurred undoubtedly as a result of the extensive
anatomic investigations, areas of plastic and recon-
structive surgery have also often benefited from the
increase in knowledge gained by the reappraisal of the
body's vasculature. Tissue expansion, first described
320 • GENERAL PRINCIPLES

FIGURE 15-3. A Cutaneous vascular territories, ventral surface: 1, superficial supe-

rior epigastric artery; 2, superficial inferior epigastric artery; 3, superior and inferior
epigastric arteries; 4, external pudendal arteries; 5, dorsal penile arteries; 6, perfo-
rating branches from the intercostal arteries; 7, perforating branches from the lumbar
arteries; 8, superficial circumflex iliac artery; 9, profunda femoris artery (circumflex
femoral arteries); 10, femoral artery; 11, superficial genicular rete; 12, anterior tibial
artery; 13, posterior tibial artery; 14, popliteal artery (sural arteries); 15, thoracic
arteries; 15a, thoracoacromial artery; 16, perforating branches of the internal mammary
artery; 17, thyrocervical trunk; 18, superior thyroid artery; 19, subcutaneous ante-
rior deltoid artery; 20, brachial artery; 21, superior ulnar collateral artery; 22, radial
artery; 23, median artery; 24, ulnar artery. B, Cutaneous vascular territories, dorsal
surface: 1, dorsal branches from the intercostal arteries; 2, dorsal branches of the
lumbar arteries; 3, dorsal branches from the sacral arteries; 4, posterior perforat-
ing branches of the intercostal arteries; 5, posterior perforating branches of the lumbar
arteries; 6, thyrocervical trunk (a, of the superficial artery; b, of the transverse scapu-
lar artery; c, of the transverse cervical artery); 7, subcutaneous posterior deltoid
artery; 8, superficial circumflex scapular artery; 9, inferior radial collateral artery;
10, superior ulnar collateral artery; 11, cubital rete; 12, radial artery; 13, ulnar artery;
14, external and internal interosseous arteries; 15, superior gluteal artery; 16, infe-
rior gluteal artery; 17, internal pudendal artery; 18, obturator artery; 19, perforat-
ing branches of the profunda femoris arteries; 20, popliteal artery; 2 1 , anterior and
posterior tibial arteries.

by Neumann, 42 is a well recognized form of delay; its
success depends on the plasticity and adaptability of
the skin-underlying tissue to alter its vascularity
through anastomoses (true and choke) as a result of
sustained constant expansion pressure. Prefabrication
and prelamination are two growing areas of plastic sur-
gical research, and these again have the basis for their
success embedded within the vascularity of the skin
and its tissues and its ability to open existing channels
and networks or even to induce vascular neogenesis
within the field. The increasing trend in distraction
techniques, especially in craniomaxillofacial surgery,
has occurred from a deeper understanding of vascu-
lar territories in the body with the ability for bone to
be distracted between its accompanying soft tissues with
great success while not succumbing to necrosis.
The transverse rectus abdominis muscle (TRAM)
flap of Hartrampf, Scheflan, and Black43 is an example
of the angiosome concept with the ability to raise lower
abdominal skin-muscle flaps based on the superior
epigastric artery by further understanding and inves-
tigations of the blood supply to the rectus abdominis

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Dr.Mustafa D.
image...

15 • VASCULAR TERRITORIES 321

FIGURE 1 5 - 4 . The cutaneous territories as defined by

Salmon, 1936. Summary of the cutaneous arterial terri-
tories of the ventral surface of the body: 1, occipital artery;
2, superficial temporal artery; 3, ophthalmic artery; 4,
sternocleidomastoid artery; 5, facial artery; 6, thyroid
arteries; 7, transverse cervical and suprascapular arter-
ies; 8, deltoid branch of the acromiothoracic trunk; 9, cir-
cumflex humeral arteries; 10, small thoracic branches
of the acromiothoracic trunk; 11, profunda brachii
artery; 12, brachial artery (muscle branches); 13, brachial
artery (direct branches); 14, epicondylar arteries; 15,
epitrochlear arteries; 16, radial artery; 17, ulnar artery;
18, deep palmar arch; 19, superficial palmar arch; 20,
anterior interosseous artery; 2 1 , internal mammary
artery; 22, external mammary (lateral thoracic) and sub-
scapular arteries; 23, intercostal arteries; 24, superficial
superior epigastric artery; 25, lumbar arteries; 26, infe-
rior superficial epigastric artery; 27, deep epigastric artery;
28, external superior pudendal artery; 29, external infe-
rior pudendal artery; 30, superficial circumflex iliac artery;
3 1 , femoral artery; 32, artery to the vastus lateralis muscle;
33, superficial femoral artery; 34, artery to the adductor
muscles; 35, lateral articular branches; 36, medial artic-
ular branches; 37, genus descendens artery; 38, anterior
tibial artery; 39, posterior tibial artery; 40, peroneal artery;
4 1 , dorsalis pedis artery; 42, medial plantar artery.

muscle and the perforators to the overlying skin. Inves-
tigators have pushed the boundaries once again with
the rediscovery of the perforator flap, whereby a large
TRAM skin flap can be raised with preservation of most
of the underlying rectus muscle and hence a reduc-
tion in the potential problems of a hernia.44
Finally, in the area of liposuction, obvious success
depends not only on achieving the desired contour but
also on doing so with survival of the overlying integu-
ment! An improved knowledge of the vasculature to
both the deep and superficial layers of fat, noting that
the vessels follow the connective tissue framework
between the fat locules, has led to a greater under-
standing of this procedure and its limitations and
potential complications.
BASIC RESEARCH
A brief account of the authors* work is essential to
understand how the vascular territories of the body
were defined, how the angiosome concept evolved, and
where these studies overlap or vary from those of
previous workers. The angiosome (from the Greek
angeion, meaning vessel, and somite, meaning segment
or sector of the body derived from soma, body) is
defined as a composite block of tissue supplied by a
main source artery. The source arteries (segmental or
distributing arteries) that supply these blocks of tissue
are responsible for the supply of the skin and the under-
lying deep structures. When pieced together like a
jigsaw puzzle, they constitute the three-dimensional

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Dr.Mustafa D.
322 I • GENERAL PRINCIPLES
FIGURE 15-5. Cadaver with body landmarks and inci-
sion lines marked.(From Taylor Gl, Palmer JH: The vas-
cular territories [angiosomes] of the body: experimental
study and clinical applications. Br J Plast Surg 1987;
40:113.)
vascular territories of the body (see "The Angiosome
Concept").
The investigations were conducted in fresh cadav-
ers. They involved dissection, ink injection, and radio-
graphic studies with use of barium sulfate initially
but later a mixture containing lead oxide. In each case,
the anatomic studies were problem oriented in a desire
to provide a surgical solution to the patient's needs.
The investigations initially involved an analysis of
various regions of the body to define possible donor
sites for free skin flap transfer.45 The studies subse-
quently focused on other tissues and included the
anatomic basis for the transfer of bone, 46 nerve,47 and
certain muscles.21,48 Encouraged by the success of some
of the resulting clinical procedures, the authors
expanded the research to investigate composite units
of tissue, supplied by a single vascular system. Units
of skin and tendon,49 muscle with nerve,50 and skin,
muscle, and bone51'53 were analyzed. It was from this
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Dr.Mustafa D.
work that the angiosome concept germinated. Various
regions including the anterior abdominal wall,21,48,54,55
the anterior thorax,56,57 the lower limb, and the upper
limb were studied. The results added strength to the
angiosome concept of the blood supply and revealed
the interconnections that exist at all levels between adja-
cent vascular territories, a relationship that is evident
throughout the body.58
Since commencing the total body studies, we have
performed dissection and radiographic analysis of
numerous human and animal cadavers (Fig. 15-5). The
injected substance (modified from Salmon's original
mixture) contained lead oxide, gelatin, and a preser-
vative.32
The integument (skin and subcutaneous tissue)
was removed, and the sites of emergence of the dom-
inant cutaneous perforators (0.5 mm or more) were
identified on the surface of the deep fascia with
lead beads. An average of 256 such perforators were
identified per body. The integument was removed in
each subject to provide as wide an expanse of tissue
for study as available. The subjects were chosen and
the incisions were planned to provide a comparison
between sexes and to obtain anterior, posterior, lateral,
bird's-eye, and worm's-eye views of the cutaneous
vasculature. Previous workers, including Salmon, had
made topographic boundary incisions to remove areas
of skin, particularly in the lines of the groins, axillae,
neck, and limb joints. These junctional regions are
of great clinical importance, and for this reason the
incisions were designed to retain their continuity
wherever possible.
The integument was radiographed, and a montage
of the entire cutaneous circulation was constructed in
"plan view" (Figs. 15-6 and 15-7). Although Manchot
and Salmon described the origin and course of the cuta-
neous arteries, and Salmon9 made a separate study
of the individual muscles, neither worker illustrated
the course of the arteries between the deep tissues and
the skin. Therefore, the skin and subcutaneous tissues
were cut into parallel strips and placed on their side,
and radiographs were taken to provide "elevation
views" of the vessels in different regions of the body
(Fig. 15-8).
The deep tissues were also radiographed and the
cutaneous perforators were traced to their underlying
source arteries and color coded. The results were aver-
aged from each study and plotted on a diagram of the
body (Color Plate 15-1). Finally, in one subject, the
integument was not removed; instead, cross sections
of the limbs and the torso were made at 5-cm inter-
vals to retain in continuity the vessels between the deep
tissues and the skin.
Subsequently, the investigations were expanded to
map out the venous territories (venosomes) of the body
along with the neurovascular territories of the skin and
muscle. These results have led to an overall picture of
the vascular territories of the entire body.
image...

5 • VASCULAR TERRITORIES 323

FIGURE 1 5 - 6 . Lateral view of one female

subject (A) and anterior view of another (B).
The arm has been removed in A, Note the
network of large vessels that sweep laterally
from the ventral and dorsal midlines, ascend
from the groins, descend from the shoulder
girdle, and converge on the summits of the
scalp and the breasts. This demonstrates the
principle that vessels radiate from fixed
concave zones and radiate to mobile convex
areas. A lower midline scar interrupts the
vessels in B with compensatory opening of a
large choke vessel above the umbilicus
(arrow) to re-establish the flow across the
midline. (From Taylor CI, Palmer JH: The vas-
cular territories jangiosomes] of the body:
experimental study and clinical applications.
Br J PlastSurg 1987:40:113.)
A B

The remainder of this section gives a brief overview
of the arterial, venous, and nervous territories of the
body.
Arterial Territories
The arterial supply to the body is a continuation of
the basic concept that the entire vascular system is
designed to provide a constant pressure at the capil-
lary bed. All the arteries form a continuous network
of vessels throughout each tissue and throughout the
body, linked together as arcades by vessels often of
reduced caliber.
The course of the cutaneous perforators depends
on the proximity of the source artery to the under-
surface of the deep fascia. In each case, they follow the
intermuscular and intramuscular septa, supplying
branches to each tissue that they pass. They generally
fall into two groups, direct and indirect. The direct
vessels constitute thepr/marycutaneous supply regard-
less of whether they follow intermuscular septa or pierce
muscles en route, their main destination being the skin.
The indirect vessels can be considered the secondary
cutaneous supply.* They emerge from the deep fascia
* Authors* note: Recently, there has been a reclassification of some of the
cutaneous arteries, so that previously named "direct" cutaneous vessels that
pierce muscle via intramuscular septa to reach the skin have been renamed
"indirect" cutaneous perforators. Those that follow intermuscular septa are
still labeled as direct cutaneous arteries. Hence, the primary cutaneous supply
may be either by direct (septocutaneous) or by indirect (musculocutaneous)
perforators.
as terminal branches of arteries whose main purpose
is to supply the muscles and other deep tissues. They
reinforce and are interconnected with the primary
cutaneous supply. They tend to be sparse where the
muscle has a large excursion beneath the deep fascia
but are plentiful where the muscle is fixed.
The direct cutaneous vessels arise from
1. the source arteries just beneath the deep fascia
(e.g., the superficial inferior epigastric artery);
2. the direct continuation of the source artery (e.g.,
the cutaneous branches of the external carotid
artery);
3. a deeply situated source artery or one of its
branches to a muscle; they follow the intermus-
cular septa to the surface (e.g., the cutaneous
branches of the lateral circumflex femoral
artery); and
4. the source artery as it courses on the under-
surface of a muscle; a single large vessel or a
number of vessels is given off, and each pierces
the muscle vertically or obliquely to reach and
penetrate the deep fascia (e.g., the cutaneous
perforators of the internal thoracic and the deep
inferior epigastric arteries).
The direct cutaneous perforators pierce the deep
fascia near where it is anchored to bone or the
intermuscular and large intramuscular septa (see
Color Plate 15-1). These lines and zones of fixation
also correspond to the fixed skin areas of the body.
From these points, the vessels flow toward the con-

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Dr.Mustafa D.
324 I • GENERAL PRINCIPLES
FIGURE 15-7. Montage of the cutaneous arteries of
the body. The skin has been incised along the ulnar border
in the upper extremities, and the integument has been
removed with the deep fascia on the left side and without
it on the right. Note (1} the direction, size, and density of
the perforators, which are large on the torso and head
and get progressively smaller and more numerous toward
the periphery of the limbs, and (2) the reduced-caliber
(choke) anastomotic arteries, which link the perforators
into a continuous network. (From Taylor CI, Palmer JH;
The vascular territories [angiosomes] of the body: exper-
imental study and clinical applications. Br J Plast Surg
1987;40:113.)
vexities of the body surface, branching within the
integument. The wider the distance between the cav-
ities and the higher the summit, the longer the vessel
(see Fig. 15-8).
The size and density of the direct perforators also
vary in different regions. For example, in the head, neck,
torso, arm, and thigh, the vessels are larger, longer, and
less numerous. In the forearm, leg, and dorsum of the
hands and feet, the vessels tend to be smaller, shorter,
and more numerous. In the palms of the hands and
the soles of the feet, where the skin is securely fixed,
the density of perforators is at a maximum. Hence,
the primary supply of each cutaneous territory varies
between source arteries. Each of these territories is
reinforced by indirect perforators.
The course of the cutaneous perforators between
the deep fascia and the skin also varies in different
regions. Regardless of their site, however, they follow
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Dr.Mustafa D.
the connective tissue framework of the superficial
fascia, interconnecting at all levels. They ramify on the
undersurface of the subcutaneous fat adjacent to
the deep fascia and then branch and course toward
the subdermal plexus, working their way between the
fat locules. The smaller vessels tend to course verti-
cally toward the skin, whereas the larger vessels branch
in all directions in a stellate pattern or course in a par-
ticular axis, branching as they pass parallel to the skin
surface.
In the scalp and limbs, where the skin is relatively
fixed to the deep fascia, the larger vessels hug that
surface. They course on the deep fascia for a consid-
erable distance in the loose areolar layer that separates
them from the subcutaneous fat (see Fig. 15-8). This
is especially true when a perforator accompanies a
cutaneous nerve.
In the loose skin areas of the body, the direct cuta-
neous vessels course for a variable distance parallel to
the deep fascia. They are more intimately related to
the undersurface of the subcutaneous fat, however,
being plastered to it by a thin fascial sheet that sepa-
rates them on their deep surface from a plexus of smaller
vessels. This plexus lies in loose areolar tissue on the
surface of the deep fascia. It is formed by branches that
arise from the direct perforators as they pierce the deep
fascia and the connections these branches make with
smaller indirect perforators. The large direct perfora-
tors then pierce the subcutaneous layer. They ascend
within the superficial fascia (subcutaneous fat) to reach
the rich subdermal plexus, where they travel for con-
siderable distances (see Fig. 15-8).
Within the deep tissue, whether muscle, tendon,
nerve, or bone, a pattern similar to that in the integu-
ment exists, with a three-dimensional network of vessels
interlinking between vascular territories, the perime-
ters of which are linked by choke arteries. Within the
muscles, these choke vessels often exhibit a character-
istic corkscrew appearance.
As far back as 1-794, John Hunter59 noted the anas-
tomoses that occur between arteries, citing the vas-
cular arcades in the hand and feet as examples. He
stated also that the arcades occur more frequently as
the arteries become more distal. The arterial arcades
in the bowel mesentery are a classic example of this
(see Fig. 15-33). They are smaller and more numer-
ous as they approach the intestine. This basic pattern
exists in all tissues and is modified by the function of
that tissue. Even during tissue repair, the pattern of
vascular arcades is reproduced in granulation tissue.
Venous Drainage
As with the arterial supply to the skin, the cutaneous
veins also form a three-dimensional plexus of inter-
connecting channels with a dominant stratum in the
subdermis (Fig. 15-9). Whereas many of these veins
image...

15 • VASCULAR TERRITORIES 325

-*--**_

FIGURE 1 5-8. Sectional strip radiographic studies of the breast (A), thigh (B), sole of the foot (C), and buttock (D).
D includes the underlying gluteus maximus muscle. The schematic diagram illustrates the dominant horizontal axis of
vessels that provides the primary supply to the skin in each case and its relationship to the deep fascia (arrow). In A,
they predominate in the subdermal plexus. Note from left to right the internal thoracic perforator and lateral thoracic
artery converging on the nipple in the radiograph of the loose skin region of the torso. In B, they are seen coursing on
the surface of the deep fascia in this relatively fixed skin area. In C, the source artery itself is the dominant horizontal
vessel supplying the skin, coursing beneath the deep fascia in this rigidly fixed skin region. In D, small arrows define
the deep fascia, and the large arrow indicates the large fasciocutaneous branch of the gluteal artery, which descends
with the posterior cutaneous nerve of the thigh. (From Taylor Gl, Palmer JH: The vascular territories [angiosomesl of
the body: experimental study and clinical applications. Br J Plast Surg 1987;40:113.)

possess valves in a particular direction, they are often
connected by avalvular veins. These avalvular (oscil-
lating) veins allow bidirectional flow between adjacent
venous territories. They connect veins whose valves
may be oriented in opposite directions, thus provid-
ing for the equilibration of flow and pressure. Indeed,
there are many veins whose valves direct flow initially
in a distal direction, away from the heart, before joining
veins whose flow is proximal. An example of this is the
superficial inferior epigastric vein that drains the lower
abdominal wall integument toward the groin. In
some regions, valved channels direct flow radially
away from a plexus of avalvular veins, for example, in
the venous drainage of the nipple-areola complex. In
other areas, valved channels direct flow toward a central
focus, as seen in the stellate branches of the cutaneous
perforating veins of the limbs (see Figs. 15-35 to
15-41).
In general, the cutaneous veins partner the arteries.
From dermal and subdermal venous plexuses, the veins
collect either into horizontal large-caliber veins, where
they often relate to cutaneous nerves and a longitudi-
nal system of chain-linked arteries, or alternatively in
centrifugal or stellate fashion into a common channel
that passes vertically down in company with the cuta-
neous arteries to pierce the deep fascia. Thereafter, the
veins remain in company with the direct and indirect
cutaneous arteries, draining ultimately into the venae
comitantes of the source arteries in the deep tissue.
In general, the origin, course, and distribution
of the veins are a mirror image of the deep arteries,
but they are larger and more plentiful. Although the
anatomy of the veins is subject to considerable varia-
tion between sides in the same individual as well
as between other individuals, the pattern of venous
arcades is evident throughout. These arcades gener-
ally become smaller and more numerous as the periph-
ery of the region or the tissue is reached.
The site and density of the valves within the deep
venous network are variable. The deep veins follow
the bony skeleton of the body or the intermuscular
septa with their associated arteries. In some regions,
these veins are single; in others, they are duplicated as
venae comitantes. In the limbs, the veins commence
distally in the hands and feet as single channels linked
by venous arcades. These arcades become progressively

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Dr.Mustafa D.
image...
526 I • GENERAL PRINCIPLES
/ •
FIGURE 15-9. The venous network of the integument
of a female subject. (From Taylor Gl, Caddy CM, Watter-
son PA, Crock JG: The venous territories [venosomes] of
the human body: experimental study and clinical impli-
cations. Plast ReconstrSurg 1990:86:185.)
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Dr.Mustafa D.
larger as they approach the wrist and ankle. The veins
are duplicated in the forearm and the leg, and each
pair of veins is linked by a rich stepladder of venous
channels that are usually free of valves. These venae
comitantes then reunite to form single channels. In
the lower limb, this occurs in the popliteal fossa, but
in the upper limb, the union is most commonly in the
proximal arm or even as high as the axilla.
In the torso, the pattern of arcades is conspicuous;
the parent veins are oriented as longitudinal and trans-
verse arcades that match the pattern of the source artery.
Distinct territories are evident. Where choke arteries
define the arterial territories, they are matched by oscil-
lating veins in the venous network. The existence of
venae comitantes is variable (Fig. 15-10).
Within the muscle, the intramuscular venous
network mirrors that of the arterial side. Where arte-
rial territories are linked by choke arteries or true
anastomotic arteries without changing caliber, the
venous territories of the muscles, which drain in oppo-
site directions, are linked by avalvular oscillating
veins. Broadly, the muscles can be classified into three
types on the basis of their venous architecture. Type
I muscles have a single venous territory that drains
in one direction. Type II muscles have two territories
that drain from the oscillating vein in opposite direc-
tions. Type III muscles consist of three or more venous
territories that drain in multiple directions (Figs.
15-11 and 15-12).
The extramuscular veins are of two types. The
first group consists of the efferent veins. They contain
valves and drain the muscles to their parent veins.
The other group consists of the afferent veins. They
are derived from the overlying integument as mus-
FIGURE 15-10. Arterial (left) and
venous (right) studies of the ante-
rior torso. Note the "corkscrew"
choke arteries that link adjacent ter-
ritories in the arterial study and the
mixture that has extruded from the
deep inferior epigastric veins as a
result of the resistance of the valves.
Radiographic lead beads identify the
origin of the cutaneous perforators
from their source vessels in the arte-
rial study. (From Taylor Gl, Caddy
CM, Watterson PA, Crock JG: The
venous territories [venosomes] of
the human body: experimental
study and clinical implications. Plast
ReconstrSurg 1990;86:185.)
VtSWftf'SelcrKf image...

15 • VASCULAR TERRITORIES 327

r — > ^ \~
FIGURE 1 5 - 1 1 . Radiographs of B
venous injection studies of the
supraspinatus (A), gracilis (B), and
sartorius (C) muscles. (From Taylor
CI, Caddy CM, Watterson PA, Crock
JG: The venous territories |veno-
somes) of the human body: experi-
mental study and clinical implications.
Plast Reconstr Surg 1990;86:185.)

culocutaneous perforators or from adjacent muscles
(see Fig. 15-12).
Neurovascular Territories
Fresh human cadavers were injected with a radiopaque
lead oxide mixture, and the nerves were dissected
and labeled with fine computer wire. The nerves
and vessels were then segregated by subtraction
radiography.
The most obvious feature seen throughout the skin
(and repeated in the muscle) is the linear arrangement
of the nerves and their branches, compared with the
looping arcades of the interconnecting vessel network,

FIGURE 1 5 - 1 2 . Venous tracing of

muscles in Figure 15-11. Note the oscil-
lating veins that separate them into type
I, ll.and III muscles and the efferent veins \
entering the supraspinatus and gracilis
muscles (dashed arrows). (From Taylor
CI, Caddy CM, Watterson PA, Crock JC:
The venous territories [venosomes) of the
human body: experimental study and
clinical implications. Plast Reconstr Surg
1990;86:185.)

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Dr.Mustafa D.
328 I • GENERAL PRINCIPLES

of the thigh and the superficial circumflex iliac artery

below the inguinal ligament; see Fig. 15-29). Alterna-
tively, the nerve leaves one vascular system with which
it is traveling in parallel to cross the path of another
(e.g., the lateral intercostal nerve, which courses ini-
tially with its artery and then leaves it to meet the
superficial inferior epigastric vessel). In many of these
cases, secondary or tertiary branches of the artery often
peel off to accompany the nerve (see Fig. 15-29).
In general, for cutaneous nerves, the orientation
is longitudinal in the limbs, transverse or oblique
in the torso, and radiating from loci in the head
and neck. Of particular note is that the cutaneous
nerves, like the arteries, pierce the deep fascia at fixed
skin sites.
The vascular architecture of the intramuscular
veins and arteries, as has been discussed previously,
is almost identical for each muscle. Therefore, to
simplify the description of the nervous supply to the
muscles, only the arterial relations of the nerves are
discussed and illustrated. The intramuscular branches
of the nerves were dissected to, but not within, the in-
dividual muscle bundles. The following observations
were made.

1. The nerves follow the connective tissue framework.

FIGURE 15-13. The neurovascular patterns found in
the integument. A, A long artery connected to its neigh-
bor by a true anastomosis courses with the nerve. B, A
chain-linked system of arteries hitchhikes with the nerve.
C, The nerve and artery pierce the deep fascia at sepa-
rate sites. Branches of the vessel peel off to accompany
the nerve as it crosses the main arterial trunk. D, The
nerve at first courses parallel to an artery and then
approaches the neighboring artery from its periphery to
descend along its branches toward the main trunk. E, The
nerve crosses the primary and secondary arcades of the
artery before coursing parallel to the vascular network.
(From Taylor Gl, Gianoutsos MP, Morris SF: The neu-
rovascular territories of the skin and muscles: anatomic
study and clinical implications. Plast Reconstr Surg
199404:1.)
with the nerves taking the shortest route between two
points.
Each cutaneous nerve is accompanied by an
artery, but the relationship is variable. Some of the
arrangements seen in the integument are shown in
Figure 15-13. In each case, either a long artery or a
chain-linked system of arteries "hitchhikes" with the
nerve.
When the cutaneous nerve and artery appear at the
deep fascia together, their relationship is often estab-
lished early (e.g., the lateral intercostal neurovascular
perforators on the torso or the saphenous system in
the lower limb). However, the nerve sometimes pierces
the deep fascia at a point remote from the emergence
of its associated artery (e.g., the lateral cutaneous nerve
Dissection showed the motor nerves coursing
in the connective tissue sheath from its origin
at the nerve trunk to the neurovascular hilum
of the muscle. Thereafter, the nerve and its
branches follow the intramuscular connective
tissue to reach the muscle bundles.
2. The nerves are economical. As in the integument,
the linear course of the motor nerves is in stark
contrast to the sinuous or arching pattern of the
vessels. The nerves take the shortest extramus-
cular and intramuscular routes compatible with
the function of each muscle.
3. Neurovascular relationsvary with the muscle and
the extramuscular course and the intramuscu-
lar branching of the nerves and the vessels. Some
muscles have a single nerve supply; others
receive multiple branches. All receive multiple
arterial pedicles. However, despite the variables,
certain observations can be made.
• Each motor nerve is accompanied by a vas-
cular pedicle, but the reverse does not apply.
• The motor nerve is usually accompanied
by the dominant vascular pedicle. There are
exceptions to this, however. For example,
the nerve supply to sternomastoid is usually
accompanied by a minor vascular pedicle.
• The nerve may enter the muscle before
branching.
• Once within the muscle, the nerve divides
early, and its branches sweep rapidly into posi-
tion, parallel to the muscle fibers. The vessels,
however, branch and form primary and

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image...

15 • VASCULAR TERRITORIES 329

TYPE I TYPE II TYPE III TYPE IV

Single unbranched nerve Single branched nerve Multiple branches from Multiple branches from
entering the muscle entering the muscle same nerve trunk different nerve trunks
FIGURE 15-1 4. Classification of muscle on the basis of nerve supply. Compare with classification of Mathes and
Nahai based on arterial supply. (From Taylor Gl, Gianoutsos MP, Morris SF: The neurovascular territories of the skin
and muscles: anatomic study and clinical implications. Plast Reconstr Surg 1994;94:1.)

secondary arcades, often crossing the muscle CLASSIFICATION

bundles and nerves before tertiary and qua-
ternary branches are provided to the muscle
fibers.
Ultimately, the terminal branches of the vessels and
nerves come into close contact and course together in
the connective tissue framework parallel to the muscle
bundles.
Many ways have been used to classify muscles on the
basis of morphology, function, blood supply, or nerve
supply (Table 15-1). Following the neurovascular
studies, they can also be categorized according to their
most common mode of innervation (Fig. 15-14).
TYPE I. The muscle is supplied by a single motor
nerve that divides usually after entering the muscle

TABLE 15-1 • CLASSIFICATION OF SOME MUSCLES BASED ON THEIR NERVE SUPPLY

Type I Type II Type III Type IV

Latissimus dorsi Deltoid Gastrocnemius Rectus abdominis

Extensor indicis Gluteus maximus Sartorius Levator scapulae
Extensor pollicis longus Trapezius Tibialis anterior Internal oblique
Abductor pollicis longus Vastus lateralis Flexor digitorum superficialis Digastric
Palmaris longus Serratus anterior Subscapularis Erector spinae
Teres minor Flexor carpi ulnaris Teres major
Extensor hallucis longus Biceps brachii Triceps
Plantaris Brachialis Extensor carpi ulnaris
Popliteus Flexor pollicis longus Extensor digitorum longus
Flexor hallucis longus Gluteus medius
Pectineus Gluteus minimus
Adductor longus Vastus medialis
Adductor brevis Vastus intermedius
Peroneuslongus
Soleus
Tibialis posterior

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330 I • GENERAL PRINCIPLES
(Fig. 15-15). Multiple vascular pedicles supply each
muscle and form a continuous network throughout
the tissue. It is possible in each case to remove a vas-
cularized segment of muscle with its nerve supply and
yet leave viable muscle in situ.
TYPE II. A single motor nerve supplies each of the
muscles in this group, but this time the nerve divides
before entering the muscle. Muscles in this group
include the deltoid (Fig. 15-16), gluteus maximus,
trapezius, vastus lateralis, serratus anterior, and flexor
carpi ulnaris.
Although not necessarily desirable, it is possible
to subdivide each muscle into separate neurovascular
units because each has multiple vascular pedicles. Clin-
ically, serratus anterior is often used in this way, taking
the lower digitations with their common motor nerves
and their blood supply from the thoracodorsal system.
TYPE III. Multiple motor nerve branches derive
from the same nerve trunk (Fig. 15-17). Once again,
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Dr.Mustafa D.
FIGURE 15-15. Schematic diagram (left)
of type I muscle to match radiograph (right)
of latissimus dorsi. Nerves and vessels are
seen together in the radiograph. The nerves
are straight, whereas the vessels are spiral.
(From Taylor Gl, Gianoutsos MP, Morris SF:
The neurovascular territories of the
skin and muscles: anatomic study and
clinical implications. Plast Reconstr Surg
1994;94:1.)
it is possible to subdivide each muscle into separate
functional units because of the multiple vascular
pedicles as well as the several nerve branches. Gas-
trocnemius is often split in this way, taking one head
for reconstruction, leaving behind the other functional
unit with its neurovascular supply attached.
TYPE IV. Multiple motor nerves are derived from
different nerve trunks (Fig. 15-18). It is apparent that
each muscle can be subdivided anatomically into several
functional units because of the multiple, often seg-
mental neurovascular pedicles. Indeed, several of these
muscles are formed developmentally by the fusion of
adjacent somites (e.g., rectus abdominis and internal
oblique).
Comparative Anatomy
The purpose of this section is to provide a more com-
plete picture of the vascular territories. As we shall see,
FIGURE 15-16. Schematic diagram of
type II muscle to match radiograph of
deltoid. The nerves, labeled with computer
wire, appear black and the vessels pale
and "ghost like" in this subtraction study.
(From Taylor CI, Gianoutsos MP, Morris
SF: The neurovascular territories of the
skin and muscles: anatomic study and
clinical implications. Plast Reconstr Surg
1994;94:1.)
 image...
FIGURE 15-17. Schematic diagram (left) and
subtraction radiograph (right) of the type IN
gastrocnemius muscle. The nerves appear black
and the vessels white in the radiograph. (From
Taylor CI, Gianoutsos MP. Morris SF: The neu-
rovascular territories of the skin and muscles:
anatomic study and clinical implications, Plast
Reconstr Surg 1994;94:1.)
the angiosome concept can be applied equally to other
members of the animal kingdom as well as to humans. 41
In plastic surgery, selection of various animals for
the study of flap physiology is based on cost, conven-
ience, availability, or pressure from certain protective
societies rather than on a profound knowledge of their
vasculature. The pig, for example, is a fixed skin animal,
and because human integument is also fixed in many
areas, it has been assumed that this animal is therefore
most ideally suited for experiments on skin flaps; but
one wonders the value of such research if the vascu-
lar tree supplying the integument in this animal were
vastly different from that of the human.
Study of these animals also leads us to gain a further
insight into the development and arrangement of the
vascular system. It may aid in identification of the ideal
animal for other experiments, such as investigation of
the delay phenomenon, use of tissue expansion, pro-
gramming of vessels, and prefabrication of flaps—
whether they are skin, other tissues, or combinations
of tissues.
When the radiographs of four animals are reviewed
(Figs. 15-19 to 15-22), it is obvious there is a marked
dissimilarity in the vasculature of the integument
between them and that of the human (see Fig. 15-7).
Surprisingly, however, this is in marked contrast to the
dramatic similarity of the radiographs of deep tissue
of the mammalian torsos (Fig. 15-23).
The pattern of the cutaneous vasculature of the
integument ranges from the fixed skin of the pig (sup-
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Dr.Mustafa D.
15 • VASCULAR TERRITORIES 331
plied by a large number of small vessels over most of
the hemitorso) to the mobile skin of the rabbit, in which
four large vessels supply the majority of this area. The
duck, not surprisingly, shows considerable diversity in
its integument vasculature. Nevertheless, basic patterns
are evident, having been modified by the growth and
functional demands of the species.
The similarity in vasculature of the deep tissue is
not confined to merely the anterior torso. Certain
muscles between species have a remarkably similar
vascularity, as can be seen in Figure 15-24.
It appears that the vascular blueprint of the deep
tissues of the torso of mammals remains relatively
constant. It is simply enlarged from the fetus to the
adult and from small to large mammals. The reason
for this may be that the functional requirements of
the torso are the same in each mammal, that is, res-
piration, protection of the viscera, and aid in removal
of the contents. Beyond the deep tissues of the torso,
it appears that the vasculature of the overlying in-
tegument, the head and the neck, and the limbs
has been modified to meet the functional demands of
each species as Hunter 9 predicted more than 200 years
ago.
Similarities are also seen in comparing the torso
studies of mammals with those of other species, for
example, the bird. In each case, vascular arcades arise
from three basic sites: cranially from the subclavian
and axillary vessels (aortic arch), laterally from the aorta
(descending part), and caudally from the iliac and
TeWttf'adtfW image..
332 I • GENERAL PRINCIPLES
i Salmon, along with the results of our total body studies
*r
l/w
FIGURE 15-18. Schematic diagram (left) and subtrac-
tion radiograph (right) of the type IV rectus abdominis
muscle. The nerves appear black and the vessels "ghost
like" in the radiograph. {From Taylor CI, Gianoutsos MP,
Morris SF: The neurovascular territories of the skin and
muscles: anatomic study and clinical implications. Plast
Reconstr Surg 1994;94:1.)
femoral vessels (terminal aorta). These three arcades
form the basic vascular loops in the body that are
common throughout the animal kingdom, including
the human.
An underlying theme of the vascular architecture
is that of vascular loops and arcades. Comparison of
the vascular architecture in the human with that of
other animals and other species reveals a similar
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
arrangement. In loose skin animals, the arcades in
the integument are stretched over long distances (see
Fig. 15-21). In the wings of insects and in the leaves
of plants, the "veins" assume a pattern of inter-
connecting arcades similar to those of the intestinal
mesentery (see Figs. 15-33 and 15-34).
THE ANGIOSOME CONCEPT
Following a review of the works by Manchot and
of the blood supply to the skin and the underlying
deep tissues, it has been possible to segregate the body
anatomically into three-dimensional vascular terri-
tories named angiosomes. These three-dimensional
anatomic territories are supplied by a source (segmental
or distributing) artery and its accompanying vein or
veins that span between the skin and the bone (Fig.
15-25; Color Plates 15-2 and 15-3). Each angiosome
can be subdivided into matching arteriosomes (arte-
rial territories) and venosomes (venous territories).
Forty of these territories were initially described,35 but
subsequent investigation has led to many of these ter-
ritories being subdivided further into smaller com-
posite units and revealed some that do not reach the
skin surface. For example, recent work has illustrated
no fewer than 13 angiosomes of the head and neck,
originally mapped as 8 supplied by branches of the
external carotid, internal carotid, and subclavian
arteries.40
These composite blocks of skin, bone, muscle, and
other soft tissues fit together like the pieces of a jigsaw
puzzle. In some of the angiosomes, there is a large over-
lying cutaneous area and a relatively small deep tissue
region; in others, the reverse pattern exists. Each angio-
some is linked to its neighbor at every tissue level, either
by a true (simple) anastomotic arterial connection
without change in caliber of the vessel or by a reduced-
caliber choke anastomosis. A similar pattern with
avalvular (bidirectional or oscillating) veins on the
venous side defines the boundaries of the venosome
(see Color Plate 15-3).
As can be seen by comparing the illustration of
the angiosomes with that of the venosomes (see Color
FIGURE 15-19. Arteriogram of the
skin of the pig. Note numerous small
perforators on lateral torso, a superfi-
cial vein that has filled in the study
(arrow), the larger segmental vessels
near the ventral and dorsal midline, and
the large perforator of the deep cir-
cumflex iliac artery near the hip. (From
Taylor CI, Minabe T: The angiosomes
of the mammalsand other vertebrates.
Plast Reconstr Surg 1992:89:181.)
fl&WWadtfW image...
FIGURE 1 5 - 2 0 . Angiogram of the dog.
Note the large perforator of the deep cir-
cumflex iliac artery and the thoracodorsal
artery (arrows) near the hip and shoulder,
respectively. (From Taylor CI, Minabe
T: The angiosomes of the mammals and
other vertebrates. Plast Reconstr Surg
199209:181.)
^5-
•A v"
Plates 15-2 and 15-3), the oscillating veins match the
choke arteries. What confused the picture in the past
were the large longitudinal valved channels in the
integument that transgressed these territories in the
limbs. However, when an island skin flap is raised,-
whether it is based on the underlying muscle, the inter-
muscular septa, or the source vessels, the horizontal
venous channels are disconnected and the venous
drainage is thrust onto the venous perforators. Hence,
the clinical significance of these venous territories in
the skin becomes evident.
The angiosome concept has several important
clinical implications:
1. Each angiosome defines the safe anatomic
boundary of tissue in each layer that can be
FIGURE 15-22. Arteriogram of the duck.
Note the discrete territories bounded by
choke arteries and the long, stretched-out
perforator of the transverse cervical artery
in the mobile skin area of the neck (arrow).
(From Taylor Gl, Minabe T: The angiosomes
of the mammals and other vertebrates.
Plast Reconstr Surg 1992;89:181.)
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
15 • VASCULAR TERRITORIES 333
FIGURE 1 5 - 2 1 . Arteriogram of the
rabbit. Note the very large perforators
of the deep circumflex iliac artery and
thoracodorsal arteries dorsally and
the superficial inferior epigastric artery
and lateral thoracic arteries ventrally.
Note also the large vessels supplying
the ear. (From Taylor CI. Minabe T:
The angiosomes of the mammals and
other vertebrates. Plast Reconstr Surg
1992:89:181.)
transferred separately or combined on the
underlying source vessels as a composite
flap. Also, the anatomic territory of each tissue
in the adjacent angiosome can usually be cap-
tured with safety when it is combined in the flap
design.
Because the junctional zone between adjacent
angiosomes usually occurs within muscles of the
deep tissue, rather than between them, these
muscles provide an important anastomotic
detour (bypass shunt) if the main source artery
or vein is obstructed.
Because most muscles span two or more angio-
somes and are supplied from each territory, one
is able to capture the skin island from one angio-
some by muscle supplied in the adjacent terri-
•fcCV..
TSF\ %
TeWttf'fcelcriSfimage..
334 I • GENERAL PRINCIPLES
Human B Pig
Dog
tory. As we shall see later, this fact provides the
basis for the design of many musculocutaneous
flaps.
Territories
The angiosome concept has led to the segregation
of the body anatomically into three-dimensional
vascular territories. Further work has led to the
investigation and detailing of angiosomes in certain
parts of the body. Some of these regions are highlighted
to expand and to clarify the concept.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
FIGURE 15-23. Injection stud-
ies of the anterior torso with the
integument removed and umbili-
cus located (large dot). The studies
of the human and dog {A and C)
are almost identical, with the deep
inferior epigastric artery larger
than the deep superior epigastric
artery. In the rabbit and pig [B and
D), the reverse applies. (From
Taylor Gl, Minabe T: The angio-
somes of the mammals and other
Rabbit vertebrates. Plast Reconstr Surg
1992:89:181.)
THE FOREARM38
SKIN. The cutaneous perforators arise directly
from the source arteries or from their muscle branches.
They follow the intermuscular septa distally. Proximally,
they often pierce the muscle bellies near where the
muscles are fixed at their origins from bone or from
intermuscular septa. The perforators become more
numerous but smaller distally, with the maximum
number being seen in the palm, where the skin is most
rigidly fixed. The cutaneous perforators on both the
anterior and posterior surfaces of the forearm emerge
in rows (Color Plate 15-4).
image...

15 • VASCULAR TERRITORIES 535

u*«

.sit

FIGURE 15-24. Comparative study

of the rectus abdominis muscle from
the various mammals studied. There
is striking similarity between the
studies. However, in all animals except
the pig, the muscle extends onto the
thorax more cranially than in the
human, and this region of the rectus
receives additional branches from the
internal thoracic artery. The recipro-
cal size relationship of the deep supe-
rior epigastric artery and deep inferior
epigastric artery between species is a
good example of the law of equilib-
rium. (From Taylor Gl, Minabe T: The
angiosomes of the mammals and other
f \ 7
vertebrates. Plast Reconstr Surg
1992;89:181.) Human (x 1/4) Pig (x 1/4) Dog (x 1/3) Rabbit (x 1/3)

MUSCLES. In general, muscles are supplied by vas-
cular pedicles from each angiosome territory that they
span. These can be divided into the anterior group and
the posterior group.
The anterior group can be subdivided further
into the superficial muscles and the deep muscles. The
superficial muscles proximally receive branches from
the brachial artery, the ulnar artery, or the ulnar recur-
rent artery. Distally, they receive branches from the
radial artery or ulnar artery (Color Plate 15-5).
The deep anterior muscles are supplied by the radial
artery, the anterior interosseous artery, and the ulnar
artery. Note in Color Plate 15-5 that the junctional
zone between angiosomes occurs primarily within
the muscles and that most muscles span at least two
angiosomes.
The posterior group again can be divided into
superficial and deep muscles. The superficial muscles
receive blood from the radial recurrent artery, which
supplies the proximal and lateral halves of their muscle
bellies. The distal and medial halves of these muscles
receive blood from the posterior interosseous and the
interosseous recurrent arteries (Color Plate 15-6). The
deep muscles receive their blood supply from the radial
recurrent artery, interosseous recurrent artery, poste-
rior interosseous artery, and anterior interosseous
artery.
When cross-sectional studies of the forearm are
reviewed, it becomes clear that the angiosomes of each
source artery span between the skin and the bone (Color
Plate 15-7). It is noteworthy that the proportional
representation of each source artery varies between
levels in the forearm. Although the angiosome of the
anterior interosseous artery does not reach the skin in
Color Plate 15-7, it eventually surfaces in the distal
forearm posteriorly or where the anterior interosseous
artery provides a dominant median branch. In the latter
case, it supplies the skin on the volar surface.
BONES. The bones of the forearm also conform to
the angiosome concept.
The radius is supplied mainly by the radial artery
by means of several large proximal branches and by
very small distal septoperiosteal and musculoper-
iosteal branches. In the middle, it receives a nutrient
branch from the anterior interosseous artery. Distally,
it also receives one or two small septoperiosteal
branches from the anterior interosseous artery, and
there is another blood supply from the posterior
interosseous artery through the muscles that are
attached to the bone.
The ulna is supplied predominantly by the ulnar
artery again through several large proximal and several
small distal septoperiosteal branches. In the middle,

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Dr.Mustafa D.
336 I • GENERAL PRINCIPLES

•*•

A B
FIGURE 1 5 - 2 5 . The technique by which the angiosomes were defined. A, The cutaneous perforators with their choke
connections are depicted on the left. The origin of the perforators from their underlying source arteries and their muscle
branches is shown on the right. B, The vascular territories of each source artery are illustrated in the integument (left)
and deep tissues (right) by lines drawn through the choke connecting vessels. Note that the territories correspond in
these two layers and how they appear as sectors in the limbs. (From Taylor Gl, Palmer JH: The vascular territories
[angiosomes] of the body: experimental study and clinical applications. Br J Plast Surg 1987;40:113.)

it receives a nutrient branch from the posterior
interosseous artery. Again, as with the radius, another
blood supply enters through muscles attached to the
ulna, derived from branches of the anterior interosseous
artery.
Clinical Implications
DONOR SITE MORBIDITY. From these data, it is
evident that the radius and ulna, and nearly every
muscle in the forearm, receive a contribution from at
least two source arteries. Also, there are intramuscu-
lar and extramuscular anastomoses around the elbow
that are usually well developed, especially on the radial
side. In addition to the connections within the muscles
and skin, particularly well-developed anastomoses
occur between vessels that travel on and within the
deep and cutaneous nerves.
When the radial artery flap is harvested, the only
muscles that lie solely within this angiosome are the
brachioradialis, extensor carpi radialis longus, and
extensor carpi radialis brevis, supplied by its radial
recurrent branch. However, this branch has an excel-
lent anastomosis with the profunda brachii artery.
Experience confirms this observation and has shown
that dissection of the radial forearm flap can proceed
safely right up to the origin of the radial artery from
the brachial artery, with either division of its recur-
rent branch or inclusion of this vessel with one or more
of "the mobile mass" muscles.
A proximal dissection of the ulnar artery to its
origin from the brachial artery, however, especially
if the radial artery is smaller than usual, may lead to
problems.
The flexor digitorum profundus and flexor carpi
ulnaris are the only muscles supplied solely by the ulnar

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Dr.Mustafa D.
TtJWS^aeltJW image...
arterv and its anterior interosseous or recurrent
interosseous branches (see Color Plate 15-5). If these
branches (or the common interosseous artery itself)
are divided at their origin while a skin flap is harvested
on the ulnar artery, survival of part or all of the flexor
carpi ulnaris and flexor digitorum profundus will then
rely on (1) the anastomosis between the ulnar recur-
rent and the ulnar collateral vessels proximally, an anas-
tomosis that may not be so well developed in some;
(2) the anastomosis between branches of the radial
artery and the anterior interosseous artery in the
midforearm, especially within the flexor pollicis
longus; or (3) the connections between the anterior
interosseous and a reconstituted posterior interosseous
artery in the distal forearm.
In contrast to the flexor digitorum profundus, the
flexor digitorum superficialis is better protected
because it has an additional contribution from the
radial artery angiosome.
VOLKMANN ISCHEMIC CONTRACTURE. This con-
dition was first described by Richard von Volkmann
as a post-traumatic contracture more than a century
ago. In 1975, Tsuge60 classified the condition into three
clinical types based on a large series of 71 cases.
Mild Type. In this group, the condition involved
the deep muscles in the flexor compartment of the
forearm, affecting the flexor digitorum profundus
usually and the flexor pollicis longus rarely. In the case
of the flexor digitorum profundus, the lesion was
usually partial, and the middle and ring fingers were
the digits most commonly involved.
Moderate Type. In this group, the condition
extended to include not only the flexor digitorum
profundus and flexor pollicis longus but also the
intrinsic muscles of the hand and some of the super-
ficial forearm flexors, especially those of the wrist. In
addition, there was usually disturbance in the sensory
distribution of the median or ulnar nerve.
Severe Type. The condition extended in this group
to involve the extensor muscles and the remaining
flexor muscles of the forearm, together with necrosis
of either the median or ulnar nerve and sometimes
the overlying skin.
If one compares the three clinical pictures described
by Tsuge with the angiosome territories, it appears that
both the anatomy of the blood supply to the forearm
muscles and the period of ischemia may be prime
factors in the pathogenesis and severity of this
contracture.
The flexor digitorum profundus and the flexor carpi
ulnaris are potentially the muscles most vulnerable
to ischemia in the forearm. The flexor digitorum pro-
fundus lies deepest and most distant from the anas-
tomotic pathways potentially available to re-establish
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Dr.Mustafa D.
15 • VASCULAR TERRITORIES 337
its circulation, especially the center of the muscle, which
provides tendons to the middle and ring fingers. This
may explain why only part of this muscle may be the
sole expression and manifestation of ischemia in the
mild type of contracture.
In the moderate and severe types of contracture,
the period of ischemia would seem to play a domi-
nant role in the eventual outcome. Nevertheless, the
re-establishment of the circulation to the radial artery
and its angiosome territory, by means of anastomotic
pathways at the elbow, compared with the state of the
re-established circulation to its ulnar artery counter-
part may explain the variable clinical picture seen in
the two types. Anatomically, the lateral anastomotic
pathway at the level of the elbow is better established
than the medial one in most cases. This is due to the
size of the anastomotic vessels and the fact that
the brachioradialis and extensor carpi radialis longus
muscles arise much more proximally on the humerus
than their flexor muscle counterparts on the medial
side. These latter muscles have only tendon attachments
to the medial epicondyle of the humerus, whereas a
large bulk of muscle, with intrinsic vascular anasto-
mosis, crosses the elbow laterally. The presence of a
relatively robust anastomosis may also have some
bearing on the fact that extensor muscles are involved
only late in the severe type of ischemia.
FREE FLAP D O N O R SITES. From the angiosome
concept, and applying the anatomic knowledge in the
previous sections, various tissues can be combined or
raised separately on the forearm on the various source
arteries and their accompanying veins. It has been
shown clinically that the dimensions of a flap designed
in one angiosome can be extended to include the
anatomic territory of the adjacent angiosome in each
tissue layer.
In the proximal forearm, the cutaneous blood supply
from the radial and particularly the ulnar artery is often
musculocutaneous. This is seen especially where
muscles are fixed to bone or where they have a
common fascial attachment, often before the muscles
separate into their individual identities. In these cir-
cumstances (e.g., where the muscles arise from the
common flexor or common extensor origin), the cuta-
neous vessels are derived usually from muscle branches
and emerge from the muscles near these fixed attach-
ments to bone or fascia.
THE LOWER LEG39
In the lower leg, the source arteries and their respec-
tive venae comitantes travel adjacent to, but not
within, the rigid fascial envelopes of the leg. Here they
are invested in loose connective tissue.
SKIN. The cutaneous vessels in the lower leg, as in
the forearm, arise from the source arteries or their
338 I • GENERAL PRINCIPLES
muscle branches. They pierce the deep fascia in lon-
gitudinal rows in the vicinity of the intermuscular septa
or beside tendons. They supply branches to each tissue
they pass, whether bone, muscle, nerve, fat, tendon, or
fascia. On the anterior surface proximally, these per-
forators usually emerge between the tibialis anterior
and extensor digitorum longus, where they are derived
frum the anterior tibial artery, or between the flexor
digitorum longus and soleus muscles, where they arise
from the posterior tibial artery (Color Plate 15-8).
Branches are seen also emerging between the tibia and
tibialis anterior muscle and between the extensor dig-
itorum longus and the peroneal muscles, these being
derived from the anterior tibial artery. Distally, the
vessels appear between the muscle bellies or between
the tendons of the extensor digitorum longus, exten-
sor hallucis longus, or peronei, obtaining their supply
from the anterior tibial artery. Over the subcutaneous
surface of the tibia where the skin is fixed, the deep
fascia is continuous with the periosteum of the bone.
In this area, branches of the anterior tibial and poste-
rior tibial arteries anastomose freely over the surface
of the periosteum.
In the posterior aspect of the leg, vessels pierce the
deep fascia around the perimeter of muscles and
tendons or from intramuscular septa. On occasion, they
have a long intramuscular course and appear as ter-
minal branches of a muscle artery; this is seen espe-
cially in the proximal perforators of the peroneal artery.
MUSCLES. In the lower leg, a picture similar to that
in the forearm is seen, with muscles being supplied by
vascular pedicles from each angiosome territory they
span.
Anterior Muscles. The muscles in this compart-
ment are supplied exclusively by the anterior tibial
artery (Color Plate 15-9). A common vessel frequently
passes through one muscle belly to supply the next as
well as providing a cutaneous perforator.
This group of muscles is particularly vulnerable to
ischemia because they are housed in a compartment
with rigid walls across which vascular connections are
sparse. This is particularly so medially, where the tibia
is subcutaneous. Here the only connections between
the anterior tibial and posterior tibial arteries are by
means of the periosteum of the bone and from within
the cutaneous network. As can be seen from Table
15-2, all the muscles of this compartment lie in one
territory.
Lateral Muscles. The peroneus longus and per-
oneus brevis are supplied by the anterior tibial and
peroneal arteries, thus forming an important, albeit
tenuous, intramuscular connection between their two
source arteries (see Color Plate 15-9). These muscles
are housed within a tight compartment bordered by
the fibula, the anterior and posterior intermuscular
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TABLE 15-2 • LEG MUSCLE ANCIOSOMES
One territory
Tibialis anterior
Extensor digitorum longus
Extensor hallucis longus
Peroneus tertius
Two territories
Peroneus longus
Peroneus brevis
Flexor digitorum longus
Flexor hallucis longus
Three territories
Gastrocnemius
Soleus
Popliteus
Tibialis posterior
septa, and the deep fascia. As with the anterior group
muscles, the blood supply frequently passes through
one peroneal muscle to reach the next, often hugging
the fibula during its course.
Posterior Group. The muscles here can be divided
into a superficial group, comprising the gastrocnemius
and soleus, and the deep group, comprising the flexor
hallucis longus, flexor digitorum longus, tibialis
posterior, and popliteus.
The superficial group lies superficial to and is sup-
plied by branches of the popliteal, posterior tibial, and
peroneal arteries. Of particular note, blood supply to
the gastrocnemius arises proximally in the popliteal
fossa from the popliteal artery with separate vessels to
each head. Each vessel is long. However, they have a
poor anastomosis with each other and with the other
source vessels in the leg.
This is in marked contrast to the soleus, where the
blood supply is provided by a large number of short
vessels from the three source arteries mentioned, which
anastomose freely within the muscle, thus forming a .
vital anastomotic link in the leg.
The deep muscles are supplied by the popliteal
artery by means of its inferior genicular branches,
the posterior tibial artery, the peroneal artery, and
a contribution from the anterior tibial artery (Color
Plate 15-10).
The only muscle bellies of any significance to
cross the knee joint are the popliteus and gastrocne-
mius; the others are represented by tendons. Because
the blood supply of the gastrocnemius has poor con-
nections with neighboring vessels, especially distally
in the calf (see earlier), it is apparent that the intra-
muscular anastomotic link between the thigh and the
leg is tenuous. It relies heavily on the extramuscular
anastomosis between the geniculate vessels and the
intramuscular anastomosis within the popliteus
muscle.
Tt&VR^aelcrtSf image...
The junctions between angiosomes, and hence the
anastomoses between adjacent source arteries, occur
usually within tissues, especially the muscles, rather
than between them (Color Plate 15-11).
Clinical Implications
This anatomic knowledge has certain clinical impli-
cations with respect to the lower leg.
CUTANEOUS SUPPLY. Proximally in the leg, the
cutaneous vessels often arise as terminal branches of
the muscle arteries and travel to the surface nearby
or adjacent to (not within) the intramuscular or
intermuscular septa.
In the middle of the leg, the vessels tend to have a
more direct course to the skin but again travel close to
the septa, either adjacent to or within muscles. As they
travel, they usually supply sizable branches to the bones,
the muscles, and other tissues.
In the distal part of the leg, the cutaneous vessels
have an even more direct course to the skin. However,
they still provide branches to the tendons (especially
the Achilles tendon), the bones, and the deep fat
deposits during their course, a point to be remem-
bered in dissecting the skin paddle of a fibula osteo-
cutaneous flap.
The subcutaneous periosteal surface of the tibia
contains anastomoses between the posterior and
anterior tibial arteries. Most pretibial lacerations occur
superficial to the periosteum and "shear off" the cuta-
neous arteries that emerge from this plexus, thus
explaining the high incidence of traumatic skin flap
necrosis.
CONNECTIVE TISSUE FRAMEWORK. The source
arteries and their venae comitantes travel adjacent to,
but not within, the rigid fascial envelopes that make
up the respective compartments of the leg. They travel
in loose connective tissue, plastered usually to one side
of the fascial sheet. This is important surgically, for
example, to approach these vessels to dissect the pedi-
cles of free flaps, to use the vessels as recipient sites for
transplantation or replantation, or to avoid them in
decompressing the leg of a patient with a compart-
ment syndrome.
COMPARTMENT SYNDROMES. It seems more than a
coincidence that the compartment whose blood supply
is anatomically most vulnerable to ischemia, the ante-
rior tibial compartment, is the one most often affected
by exercise to give the painful condition of "shin
splints." The only vessel supplying the muscles of this
compartment is the anterior tibial artery with its venous
drainage paralleling the arterial supply.
FLAP D O N O R SITES. Following McGraw and
DibbelPs work on the musculocutaneous territories in
the leg and PonteVs work, which drew attention to the
vessels hugging the deep fascia and septa in this region,
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
15 • VASCULAR TERRITORIES 339
a large number of flaps have been described based prox-
imally and distally in the leg. In most cases, they have
been designed after a review of the anatomy of the leg
vessels. Wei et al61 have shown that a skin flap can be
included with the fibula as a free flap. On review of the
cutaneous perforators of the lateral aspect of the leg,
it can be seen that the skin paddle should be designed
distally in the leg to capture direct septocutaneous per-
forators from the peroneal artery. This is better than
running the risk proximally of requiring a tedious intra-
muscular dissection to incorporate the terminal twigs
of one of the muscle branches of the peroneal artery,
especially those supplying the soleus muscle.
ANASTOMOSES AROUND THE KNEE. In the previous
section on the forearm, emphasis was placed on the
anastomoses around the elbow joint. Here, the mass
of the brachioradialis, brachialis, and common flexor
and extensor muscles plays an important role in bypass-
ing potential obstruction of the brachial artery. The
rich intramuscular anastomoses within these mus-
cles between the radial and profunda brachii artery
branches laterally, and between the ulnar and ulnar
collateral vessels medially, supplement the extra-
muscular anastomoses.
Around the knee, the story is very different. Few
muscle bellies actually cross the knee joint; most are
represented by tendons. The largest of these, the
gastrocnemius, has a blood supply that arises in the
popliteal fossa, not above it, and has a relatively poor
connection with other vessels in the leg.The main anas-
tomoses between the thigh and leg are extramuscular
(except for popliteus), represented by the geniculate
vessels. This helps explain the observation by Hunter
and Salmon that ligation of the popliteal artery, prox-
imal to the sural arteries, has a major effect on the blood
supply to the distal leg.
In the popliteal fossa distally, the soleus muscle
receives large branches from the popliteal artery,
which link the branches of the posterior tibial and per-
oneal vessels within the muscle substance. This may
explain why ligation of the popliteal artery distal to
the takeoff of its branches to the soleus at the distal
end of the popliteal fossa had little effect on perfusion
of the leg, as observed by Salmon.
ANGIOSOMES OF THE HEAD
AND NECK40
The head and neck region is similar to the leg and
forearm region in that the angiosome territories are
connected usually within the tissues, such as muscle,
skin, specialized organs, or glands, rather than between
the tissues. The muscles usually have vessels of two or
more angiosomes supplying them and in general can
be classified into three major groups on the basis of
the similarity of their arterial supply. In some areas,
the midline anastomoses are rich, especially in the
image...
340 • GENERAL PRINCIPLES
integument of the scalp, forehead, and lips. In other
regions, such as the tongue and palate, the midline vas-
cular connections have been found to be poor. In the
head and neck, three angiosome territories—those of
the vertebral, lingual, and ascending pharyngeal—are
confined to the deep tissues without cutaneous
representation.
SKIN AND SMAS. The blood supply to the skin of
the face, scalp, and neck follows the connective tissue
framework. The main skin perforators pierce the deep
fascia from fixed skin sites, especially around the base
of the skull, around the orbits, around the nostrils,
over the parotid gland, along the skin crease lines of
the face, and beside the muscles in the neck. They then
radiate into mobile skin areas and are intimately asso-
ciated with the superficial musculoaponeurotic system
(SMAS) layer in the face, the platysma in the neck, and
the galea in the scalp (Fig. 15-26).
Vascular arcades occur in the scalp between the
occipital, posterior auricular, and superficial tempo-
• -
c D
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Dr.Mustafa D.
ral branches of the external carotid system and the
supraorbital, supratrochlear, and dorsal nasal branches
of the internal carotid system. The major veins and
arteries in the head and neck often run a different course
and may be at a distance from each other.
In the neck, the blood supply is more sparse, with
the main perforators emerging from their source
arteries where the skin is attached (over the trapezius
muscle at its anterior border; along the anterior and
posterior borders of the sternomastoid; along the
hyoid bone above and the clavicle and sternum below).
They form a rich plexus within the platysma muscle
anteriorly (the counterpart to the SMAS in the neck)
en route to the skin. The external ear is supplied by
two angiosome territories from the superficial tem-
poral and the posterior auricular (Fig. 15-27).
The external nose has an abundant blood supply
from the ophthalmic branch of the internal carotid
and the facial branch of the external carotid artery.
Classically, the external nasal branch of each ophthalmic
artery runs down the dorsum of the nose to anasto-
FIGURE 15-26. Fresh cadaver lead
oxide arterial study of the lateral (A)
and anterior (B) view of the compos-
ite skin and SMAS unit in the head and
neck. The occipital {a}, superficial tem-
poral (b), and ophthalmic (c) arteries
have been labeled. Note that the facial
vein (v) runs a more direct course and
at some distance to its arterial coun-
terpart, the facial artery (d). The skin
layer (C) alone reveals a vast arterial
"blush" zone of the skin and SMAS
shown in sagittal view. Note (1) the
rich arterial anastomotic "waves"
formed between the branches of the
occipital, superficial temporal, and
ophthalmic arteries in the scalp, (2)
the cluster of small vessels supplying,
the fixed skin area over the parotid
gland and masseter muscle compared
with the large branches of the facial
artery that supply the mobile anterior
face, and (3) the relative paucity of
large vessels in the neck except in the
anterior triangle. The SMAS layer is
seen only in D with the muscles of facial
expression outlined. They are frontalis
(1), procerus (2), corrugator (3), orbic-
ularis oculi (4), levator labii superioris
alaeque nasi (5), nasalis (6), levator
labii superioris (7), zygomaticus minor
(8), zygomaticus major (9), orbicularis
oris (10). depressor anguli oris (11),
depressor labii inferioris (12), mentalis
(13), and platysma (14). (From House-
man ND, Taylor CI, Pan WR: The angio-
somes of the head and neck: anatomic
study and clinical applications. Plast
Reconstr Surg 2000,105:2287.)
• •
 image...

15 • VASCULAR TERRITORIES 341

FIGURE 1 5 - 2 7 . Lead oxide arte-

rial study (A) of the blood supply of
the ear and adjacent tissues. Note
the arcades formed between the
superficial temporal and posterior
auricular arteries, highlighted with •
arrows. Schematic picture (B) shows B
the branches of the superficial tem-
poral (dark) and posterior auricular
(light) supply to the front and back
of the ear, respectively. Note also
the true and choke anastomoses
between these two arteries in the
scalp. C and D provide a close-up
examination of the arterial anatomy
of the external nose. Note the
arcades that occur around the alar
dome between the columella branch
of the superior labial artery and the
facial artery. The facial vein has also
been partially filled with lead oxide
and has been highlighted by the
arrows. (From Houseman ND, Taylor
CI, Pan WR: The angiosomes of the
head and neck: anatomic study and
clinical applications. Plast Reconstr
Surg 2000; 105:2287.)

mose freely with the lateral nasal branch of the facial
artery on each side as well as its superior labial branches.
In summary, therefore, the external nose, like the exter-
nal ear, has two angiosomes supplying it on each side
and provides a major connection between the inter-
nal and external carotid systems (Color Plate 15-12;
see also Fig. 15-27).
The majority of the veins in the head and neck region
are avalvular, and most of the valved veins have ostial
valves sited at the entry of these bidirectional or oscil-
lating veins into the large collecting directional veins.
MUSCLES. As can be seen from Table 15-3, the
muscles may be grouped according to the number of
angiosome territories they span and from which they
receive a vascular supply. These muscles are subgrouped
into regions. Together they form an important vascu-
lar connection through their intramuscular anasto-
moses, between branches of the internal carotid,
external carotid, and subclavian vessels.
Muscles of Facial Expression. These muscles lie
within the mobile panniculus of the scalp, face, and
neck and the aponeurosis of the SMAS. They are inti-
mately related to, are supplied by, and contain within
themselves the major branches and cutaneous divi-
sions of the occipital, superficial temporal, oph-
thalmic, facial, superior thyroid, and inferior thyroid
arteries (see Fig. 15-26D and Color Plate 15-12). This
whole muscle aponeurotic layer tethered at various
points around the skull thus forms a rich continuous
anastomotic layer extending from the occiput across
the top of the head and face to the root of the neck.
Because of the mobility, either the scalp or face, or a
combination, can be involved in degloving and scalp-
ing injuries. However, because of the rich anastomo-
sis between arteries both longitudinally and transversely
across the midline, combined with the poverty of
venous valves within their network, successful replan-
tation of the part without the need for large numbers
of vascular anastomoses has been performed.

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Dr.Mustafa D.
342 I • GENERAL PRINCIPLES

The platysma muscle forms a vascular link between TABLE 15-3 • ANGIOSOME SUPPLY OF THE
the external carotid and subclavian arteries through HEAD AND NECK
its branches of the superior thyroid or submental
branch of the facial artery above and the transverse Muscles of Mastication
cervical and inferior thyroid arteries below. As a result,
the muscle can be raised on either the superior or One territory
inferior pedicle. Lateral pterygoid
Medial pterygoid
The orbicularis oris muscle provides a vascular link Two territories
between the left and right sides of the face through the Buccinator
facial artery and its superior and inferior labial artery Temporalis
branches. The robustness of this blood supply has been Masseter
used clinically for more than 100 years in the Abbe Posterior Neck Muscles
flap 1,62 lip reconstruction.
One territory
Ocular Muscles. The six ocular muscles all lie
Obliquus capitis superior
within the territory of the ophthalmic artery angio- Two territories
some. They are therefore potentially vulnerable to Levator scapulae
ischemia. However, peripherally they are protected by Rectus capitis posterior major
rich anastomoses formed between branches of the oph- Rectus capitis posterior" minor
thalmic artery with (1) branches of the facial artery Three territories
on the face and (2) branches of the internal maxillary Splenius capitis
Splenius cervicis
artery in the temporal fossa and the nasal and cranial Semispinalis capitis
cavities. Semispinalis cervicis
Obliquus capitis inferior
Muscles of Mastication. As a group, these muscles Longissimus cervicis
cross three angiosome territories, forming a link Four territories
between the superficial temporal, internal maxillary, Trapezius
Five territories
and facial arteries through intramuscular connections Trapezius
(Color Plate 15-12). Because buccinator, temporalis, Longissimus capitis
and masseter are supplied by branches from two angio- Note: Variation in number of angiosomes of trapezius
somes, these muscles are the subject of many impor- is due to variability in dorsal scapular artery origin
tant flaps in the region with the muscle being raised Lateral Neck Muscles
on either vascular pedicle.
Two territories
Posterior Neck Muscles. As a group, these muscles Scalene anterior
span and are supplied by up to six angiosome territo- Scalene medius
ries. There is thus a staircase of intramuscular vascu- Scalene posterior
lar anastomoses, especially within the trapezius muscle; Four territories
between the intercostal branches of the aorta; the Sternocleidomastoid
suprascapular, transverse cervical, deep cervical, and Anterior Neck Muscles
vertebral branches of the subclavian artery; and the
occipital branch of the external carotid artery (Color One territory
Plate 15-13). Thyrohyoid
With respect to the trapezius, there is a significant Two territories
Sternohyoid
variation in its vascular anatomy, depending on the Longus cervicis
origin of the dorsal scapular artery. This may arise either Longus capitis
as a branch of the transverse cervical artery or as a Three territories
separate branch from the third part of the subclavian Digastric
artery. As a result, the trapezius has either four or five Omohyoid
territories (see Table 15-3).

Lateral Neck Muscles. This group comprises the

sternocleidomastoid muscle and the deep scalene
muscles. Each spans two or more angiosomes and
as a group through intramuscular links provides a
pathway between the transverse cervical and inferior
thyroid branches of the subclavian artery and the supe-
rior thyroid and the occipital branches of the external
carotid artery (see Color Plate 15-13A and B).
Of note, the sternomastoid has four angiosome ter-
ritories, the principal two being from the occipital and
the superior thyroid arteries. The lower two territo-
ries tend to be less dominant, coming from the infe-
rior thyroid and the transverse cervical arteries. In
head and neck reconstruction, the sternomastoid
muscle has been used for many years. It can be based

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Dr.Mustafa D.
TtSWRfaeldW image...

15 • VASCULAR TERRITORIES 343

TABLE 15-4 • ANGIOSOME SUPPLY OF THE Internal Nose. This area is supplied by three
AERODICESTIVE SYSTEM primary sources from the ophthalmic, maxillary, and
facial artery angiosomes. There are a large number of
Nose (bilateral) anastomoses with the blood supply to the external nose
(Color Plate 15-13B).
Two territories
External nose Tongue and Floor of Mouth. The tongue can be
Three territories divided into extrinsic and intrinsic musculature. The
Internal nose extrinsic muscles are either one-territory or two-
Tongue and Floor of Mouth (bilateral) territory muscles. Of note, the mylohyoid is supplied
on its superficial surface by the submental branch of
Extrinsic the facial artery on each side; anastomosis in the midline
One territory forms an arterial loop. On its deep surface, it is sup-
Geniohyoid plied by the lingual artery and the mylohyoid branch
Styloglossus of the internal maxillary artery. The bulk of the intrin-
Genioglossus sic muscles are supplied by terminal branches of the
Hyoglossus lingual artery as the vessel enters the posterolateral
Two territories
Mylohyoid
portion of the tongue on each side. It also receives a
Stylopharyngeus small supply from the facial artery. Of note, however,
Intrinsic the tongue has an obvious midline raphe, with a poor
Two territories vascular crossover between the right and left sides (Fig.
15-28). This is of importance in resection of tongue
Palate, Pharynx, Esophagus, and Trachea (bilateral) tumors, raising the possibility of tongue tip necrosis
on the ipsilateral side if the lingual artery is sacrificed.
Five territories exist from hard palate to upper
esophagus. There is a paucity of vessels in the midline
of the palate. Palate, Pharynx, Larynx, Esophagus, and Trachea.
The region from the hard palate to the upper portion

either superiorly or inferiorly. However, when it is

based superiorly, the skin flap located at the lower
pole of the muscle has had a high incidence of loss
of the skin paddle because of its poor blood supply.
This relates to the number of vascular territories that
blood from the superior pole must cross to reach the
skin paddle.

Anterior Neck Muscles. Apart from the small

thyrohyoid muscle, which occupies the angiosome
territory of the superior thyroid artery, the remainder
of these muscles occupy at least two territories (see
Table 15-3). These muscles form a link between
the occipital, lingual, and facial arteries (Color Plate
15-13Q.

AERODIGESTIVE SYSTEM. This system is supplied by

no less than seven angiosome territories (Tables 15-4
and 15-5; Color Plate 15-13B).

TABLE 15-5 • ANGIOSOME SUPPLY OF THE

SALIVARY GLANDS AND THYROID

One territory
Parotid
Submandibular FIGURE 1 5 - 2 8 . Radiograph of the tongue; note the
Sublingual almost avascular midline. (From Houseman ND, Taylor
Two territories (on each side) CI, Pan WR: The angiosomes of the head and neck:
Thyroid anatomic study and clinical applications. Plast Reconstr
Surg 2000:105:2287.)

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Dr.Mustafa D.
344 I • GENERAL PRINCIPLES
of the esophagus spans and is supplied by five angio-
somes. These comprise the internal maxillary, facial,
ascending pharyngeal, superior thyroid, and inferior
thyroid arteries. There is a paucity of vessel crossover
in the region of the hard palate, and this appears to
extend into the pharynx in a fashion similar to the
paucity in the midline of the tongue. Below this the
anastomosis is rich.
Glands. The salivary glands occupy one territory
each. The parotid gland receives its supply from the
transverse facial branch of the superficial temporal
artery as well as a number of smaller branches from
the superficial temporal artery itself.
The submandibular gland is supplied by the facial
artery as it runs in the groove between the gland and
the mandible. The sublingual gland receives its supply
by sublingual branches of the lingual artery.
The thyroid gland spans two angiosome territories
on each side, being supplied by the superior and in-
ferior thyroid vessels. These vessels have a rich anas-
tomotic network within each lobe of the thyroid and
form an important connection between the subcla-
vian and the external carotid systems on each side and
between each side.
A N A T O M I C CONCEPTS
The following concepts provide an overview of the
blood supply to the integument and to the deep tissues.
They are fundamental to the mapping of the vascular
territories and to the planning of incisions and flaps.
They help explain the anatomic variations that exist
between the vessels of different regions of the body
and allow better understanding of the various
classifications of the cutaneous blood supply that have
appeared in the literature. Finally, they provide the basis
for interpreting many physiologic and pathologic
processes, including the delay phenomenon and the
necrosis line of flaps.
VESSELS FOLLOW THE CONNECTIVE
TISSUE FRAMEWORK OF THE BODY
This concept is fundamental to the design of flaps in
general and to fasciocutaneous and septocutaneous
flaps in particular. The connective tissue framework
of the body is a continuous syncytium, like the walls
of a honeycomb, calcified in some areas to form the
bony skeleton, which houses, permeates, and supports
the specialized tissues. The vessels follow this frame-
work down to the microscopic level as if for support
and protection.
In general, if the connective tissue is rigid, such as
intermuscular septa, periosteum, or deep fascia, the
vessels travel beside or on it. If the connective tissue is
loose, they travel within it. The vessels occasionally
travel in a fibrous sheath or a bony canal, but this tunnel
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always contains loose areolar tissue. Gray's Anatomf*
stated the reason for this: to allow the veins to dilate
and the arteries to pulsate.
The pattern is well illustrated if the arterial network
is traced from the heart to the periphery. The major
arteries are closely related to the bones of the axial skele-
ton (see Fig. 15-1). Their branches at first follow the
intermuscular septa. In the deep tissues, they pene-
trate the muscles (usually on their deep surface),
tendons, bones, nerves, and deep fat deposits. As the
vessels divide and subdivide within the specialized
tissues, their branches again follow the connective tissue
framework to reflect the architecture of the tissue
in question. The arterial framework is beautifully
illustrated in the corrosion cast studies of Last and
Tompsett.2'64
The cutaneous perforators exhibit the same pattern.
They arise from their source artery (segmental or dis-
tributing artery) or one of its muscle branches and
follow the intermuscular or intramuscular septa toward
the surface (see Fig. 15-8). They pierce the deep fascia,
branch, and ramify on its surface and ascend in
the connective tissue framework of the superficial
fascia, traveling between the fat locules to reach the
subdermal plexus.
During their course, the cutaneous vessels provide
branches to the adjacent tissues, whether they are
muscle, nerve, bone, fascia, or fat.
The cutaneous perforating veins can be traced in a
retrograde fashion by means of the intermuscular and
intramuscular septa to the outer layer of the deep fascia,
where they usually form rich plexuses on either side
of its surface. From there, they can be followed along
the connective tissue framework of the superficial
fascia, worming their way between the fat locules until
they meet and become continuous with the horizon-
tal plexus of large superficial veins near the dermis.
The explanation for the coexistence of the blood
vessels and the connective tissue framework lies in
the developing human embryo. Many of the studies
of human development have been based on data
obtained from the developing chick embryo. Never-
theless, it is known that within the human embryo,
the vascular system is the first tissue to differentiate in
the mesoderm as a continuous network of vessels. The
connective tissue can be regarded as being what is left
of the mesoderm after the specialized tissues have devel-
oped from it.65 As growth and differentiation progress,
vessels become encased within the various tissues and
are continuous with vessels coursing between the tissues
by way of vascular pedicles at various sites. It is rea-
sonable to speculate that if the specialized tissues such
as muscle, nerve, and fat have developed within this
mesh of connective tissue and vessels, this could ex-
plain why vessels have become captured within and
compressed between the specialized tissues. It would
explain why they follow the intermuscular septa, the
TtJWttf^eltJMff image...
intramuscular septa, the deep fascia, and the connec-
tive tissue septa of the superficial fascia to reach the
skin. As mobility develops between tissue planes, pre-
sumably some of the interconnections between vessels
would have been lost by apoptosis, with a compensa-
tory enlargement of vessels arising from fixed tissue
sites. This concept can be applied to the raising of
fasciocutaneous flaps (see later section).
ARTERIES RADIATE FROM FIXED TO
MOBILE AREAS AND VEINS CONVERGE
FROM MOBILE TO FIXED AREAS
Few arteries cross mobile tissue planes. Instead, they
cross where tissues are anchored and radiate parallel
to the plane of mobility, often for long distances. This
pattern is seen typically where muscles piston beneath
the deep fascia, where the integument glides above it,
or where the deep fascia (e.g., the galea) is mobile over
bone.
The cutaneous vessels pierce and emerge from the
outer layer of the deep fascia near where it is anchored,
either to its deep septa or to bone. The overlying integu-
ment is fixed also to the deep fascia at these sites. The
fixed skin regions are seen easily in a well-muscled indi-
vidual as grooves and valleys. They can be seen around
the perimeter of muscles, especially where they inter-
digitate; over well-developed intermuscular septa;
over the flexor surface of joints; adjacent to the dorsal
and ventral midline of the body; around the base of
the skull; and in the region of some bone prominences
(Fig. 15-29; see also Fig. 15-28).
From the grooves and valleys in the deep fascia, the
arteries flow toward the convexities of the body
surface, branching within the integument. The wider
the distance between the concavities and the higher
the summit, the longer is the vessel. This pattern is well
demonstrated in the blood supply to the integument
of the scalp, nose, ears, breasts, and genitalia; the exten-
sor surface of the joints; and the bulging surface of
muscles (see Fig. 15-6).
Where the skin is relatively fixed to the deep fascia
over a wide area (e.g., in the scalp and many areas of
the limbs), the vessels remain close to the surface of
the deep fascia for a considerable distance. In the loose
skin areas of the body, especially over the pectoralis
major muscle, the iliac fossa, and the extensor surface
of joints, the vessels course for a short distance adja-
cent to the deep fascia. Soon they are plastered to the
undersurface of the subcutaneous layer by a thin
glistening sheet of fascia, and they then pierce the fat
obliquely to reach the subdermal plexus, where they
travel for long distances.
The veins course parallel to the plane of mobility,
often for long distances, and cross where the tissues
are anchored to fascia or bone. This is seen at the same
site as the arteries.
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15 • VASCULAR TERRITORIES 345
Within the subdermal plexus and in the subcuta-
neous fat, the veins and arteries often travel nearby
at a distance and only come together when they pierce
the outer layer of the deep fascia. Veins leave the sub-
cutaneous tissue and pierce the deep fascia where
the integument is anchored to it. This occurs around
the perimeter of muscles, in particular where they
interdigitate, over well-developed intermuscular
septa. This is especially true in the limbs, where
they are concentrated in longitudinal rows over
the flexor surfaces of joints (e.g., the cubital fossa,
axilla, popliteal fossa, and groin); adjacent to the dorsal
and ventral midlines of the body; around the base of
the skull and orbital margins where the galea is
anchored; and where the deep fascia is fixed to bone,
such as the subcutaneous border of the tibia (Color
Plate 15-1).
In the deep tissues, veins leave muscles usually near
their attachments to bone or fascia, most commonly
on their deep surfaces. If a group of muscles has a
common origin, for example, where the flexor and
extensor muscles arise from the epicondyles of the
humerus, the venous drainage of each is frequently
collected into a large venous arch that courses in the
muscle mass close to the bone.
It follows that where a tissue is mobile over a long
distance, whether muscle, skin, tendon, or nerve, large
flaps are available for transfer and should be based on
the fixed margin or end of that tissue. There are numer-
ous situations in which this observation is used in every-
day clinical practice. For example, the large axial skin
flaps based on the fixed area of the groin, the paraum-
bilical region, and the parasternal region use the mobile
skin areas over the anterior abdominal and chest walls.
The commonly used muscle and tendon transfers are
also based on this principle.
Conversely, if mobility exists between tissue planes,
this provides a relatively avascular plane. This fact was
well known to the Indians of North America in bygone
times, and currently surgeons take advantage of this
observation when they place a prosthesis beneath the
breast or the pectoralis major muscle. Significant bleed-
ing is encountered only around the perimeter of these
pockets where the tissues are fixed.
VESSELS HITCHHIKE WITH NERVES
Recent work has confirmed that the intimate rela-
tionship between nerves and blood vessels that is known
to exist in the deep tissues and in some areas of the
integument is in fact present in all regions of the skin
and subcutaneous tissues of the body, especially where
a cutaneous nerve courses on the surface of the deep
fascia. An artery may accompany the nerve for a con-
siderable distance, often connecting with its neighbor
in chain-link fashion to provide the basis for an axially
oriented neurovascular flap.
346 I • GENERAL PRINCIPLES

A t . ' - - ,7' ,

• i'r'i
/ •

& €-M-7k ft: •**-• /' n\ /' " ^ N J - 4

8&s
^
V k1*
B
FIGURE 1 5 - 2 9 . Arterial injection of the right upper limb and torso. A Note the chain-
linked systems of arteries (arrows) that course with the cutaneous nerves in the upper limb.
B, On the torso, the nerves are marked on the arterial study. They course with the cutaneous
arteries, cross them at angles and collect arterial branches, or approach the arteries from
opposite directions (arrows). (From Taylor CI, Palmer JH: The vascular territories langio-
somes] of the body: experimental study and clinical applications. Br J Plast Surg
1987;40:113; and Taylor CI, Gianoutsos MP, Morris SF: The neurovascular territories of the
skin and muscles: anatomic study and clinical implications. Plast Reconstr Surg 1994;94:1.)

The cutaneous vessels and the nerve are occasion-
ally in juxtaposition; in other situations, they course
parallel to each other but at a distance. When the cuta-
neous nerve crosses a fixed skin site, it frequently "picks
up" its next vascular companion (Fig. 15-29; see also
Fig. 15-13).
There are numerous instances throughout the body
where this pattern of distribution of nerves and vessels
exists to supply the integument. This includes the supra-
orbital, infraorbital, and occipital neurovascular
bundles in the head; the supraclavicular nerves col-
lecting branches of the suprascapular and supracla-
vicular vessels as they cross the clavicle onto the chest;
the intercostal neurovascular bundles on the torso; and
the cutaneous nerves of the arm, forearm, thigh, leg,
and digits, which are accompanied by long named or
unnamed vessels or a chain-linked system of vessels.
The cutaneous nerves are accompanied by a longi-
tudinal system of arteries and veins that are often the
dominant blood supply to the region. The veins in

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fl&Wttf'aatfW image...

15 • VASCULAR TERRITORIES 347

company with the nerves are frequently large venous

freeways, such as the cephalic, basilic, long saphenous,
and short saphenous systems. The arteries either are
long vessels (e.g., the supraorbital, lateral intercostal, or
saphenous arteries) or exist as a chain-linked system
of cutaneous perforators, often joined in series by true
anastomoses without change in caliber (see Fig. 15-29).
The nerves pierce the deep fascia together with the
vessels, they emerge separately and cross the vessels at
an angle, or they approach the vessels from opposite
directions. In each case, as if drawn by a magnet, the
main trunk of the vessel or some of its branches peel
off to course parallel (see Fig. 15-13) to the nerve. These
vessels either course in proximity to the nerve or travel
nearby (see Fig. 15-29B).
This neurovascular relationship presents another
basis for the design of long flaps with the added poten-
tial of providing sensation at the repair site. Many of
the current"axial" or "fasciocutaneous" flaps are in fact
neurovascular flaps. The original long and short
saphenous flaps described by Ponten are cases in point.

VESSEL SIZE A N D ORIENTATION ARE THE

PRODUCT OF TISSUE GROWTH A N D
DIFFERENTIATION
Two centuries ago, John Hunter 59 suggested that at some
stage of fetal development, and certainly at birth, there
are a fixed number of arteries in the body. This has
been the authors' impression in comparing the number
of cutaneous perforators encountered while raising the
same flap in a child and in an adult.
If this concept is correct, it provides a plausible ex-
planation for the density and morphology of the cuta-
neous arteries in different regions of the body. It
explains why vessels radiate from concavities and con-
verge on convexities and why the vessels in some areas
are small and close together, whereas in others they
are large and spaced well apart.
There are numerous examples to support this
hypothesis (Fig. 15-30). The sternomastoid and trape-
zius muscles split from the same somite. 66 The trape-
zius "drags" its supplying transverse cervical artery (and
nerve) across the root of the neck to the back, together
with a large band of skin that it nourishes. Manchot 4,5
suggested that the long course and the direction of the
superficial superior and inferior epigastric arteries
are brought about by the extension of the fetal torso.
If one remembers that the cutaneous perforators pierce
the deep fascia at fixed points and that they all inter-
connect, this would explain why, as the brain and skull
expand, the scalp vessels hypertrophy and are stretched
from the base of the calvaria toward its vertex. Simi-
larly, this could explain why large vessels converge on
the nipple from all directions as the breast develops.
This pattern is seen also in the limbs. Growth of the
long bones would stretch the vessels apart and there-
FIGURE 1 5 - 3 0 . Diagram showing how the size and
course of the direct cutaneous perforators x and y, which
emerge from fixed points in the deep fascia, could be
modified by growth either before or after birth. In A, the
perforators, which are fixed in number and position, form
a major connecting network on the surface of the deep
fascia in the "resting state." In B, they are stretched with
the deep fascia by the expansion of underlying tissues
(e.g., the scalp vessels as the brain and skull expand during
fetal development). In C, as the breast develops within
the integument, the vessels are displaced toward the
dermis and lengthened as they converge on the nipple.
In D, they are stretched apart in the limbs as the long
bones grow, but they still retain their original relationship
to the deep fascia. In E, the vessels are again stretched
apart by growth, but the mobile relationship between the
undersurface of the integument and the deep fascia is
responsible for their oblique course. This pattern is char-
acteristic of the loose skin areas of the torso. (From Taylor
Gli Palmer JH: The vascular territories [angiosomes] of
the body: experimental study and clinical applications. Br
J PlastSurg 1987;40:113.)
fore make clear why vessels radiate in all directions
from the flexor surface of the joints.
Where skin becomes mobile over the deep fascia,
certain vessel connections are lost in these areas. One
would expect compensatory hypertrophy of the
remaining vessels, and indeed this is so. In mobile skin
areas, large vessels are seen in the integument arising
from fixed points around the perimeter and running
parallel to the skin surface for long distances.
Perforators of the internal thoracic system and the

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348 I • GENERAL PRINCIPLES
cutaneous branches that radiate from the groin are
excellent examples.
The primitive cutaneous perforators in the fetus
branch in all directions after piercing the deep fascia
and have a stellate appearance. This pattern is retained
into adulthood in many regions of the body. When a
perforator departs from this pattern and becomes ori-
ented in one direction, it highlights the differential
increase in growth that has occurred along that axis
or the influence of a developing cutaneous nerve. Where
small perforators are clustered close together, this
pattern suggests that by comparison the growth and
hypertrophy in the area are less than at those sites where
the perforators are large and spaced well apart. This is
well demonstrated by comparing the perforators in
the proximal and distal regions of the limbs. This
concept has important implications in tissue expan-
sion (see section on clinical applications).
VESSELS INTERCONNECT TO FORM A
CONTINUOUS THREE-DIMENSIONAL
NETWORK OF VASCULAR ARCADES
Arteries
This is evidence in each tissue whether it is the integu-
ment, muscle, nerve, or bone. The arteries do not supply
discrete areas with occasional anastomoses. Instead,
their branches are linked with each other and with the
branches of neighboring vessels to form arches. The
keystones in these arcades are formed sometimes by
true anastomoses without change in caliber. More com-
monly, they are represented by reduced-caliber choke
arteries and arterioles. The perimeter of choke or anas-
tomotic vessels defines the anatomic territory of each
artery (Fig. 15-31). Thus, each tissue is supplied by a
FIGURE 1 5 - 3 1 . Dotted line through choke connecting
vessels of a large acromiothoracic perforator to define its
anatomic territory. Compare with Figure 15-29S, left side
of chest. (From Taylor CI. Palmer JH: The vascular terri-
tories [angiosomes] of the body: experimental study and
clinical applications. Br J Plast Surg 1987;40:113.)
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
series of linked arterial territories, some small and some
large.
The concept is three-dimensional and was docu-
mented by Hunter in 1794.39 He cited the vascular
arcades in the hands and the feet as examples and stated
that the arcades are smaller and occur more frequently
as the arteries become more distal (Fig. 15-32). Thus,
like a Roman aqueduct, the arterial framework con-
sists of tiers of vascular arcades that commence from
the aorta and become progressively smaller as the cap-
illary bed is approached. In general, the large arcades
are formed by the segmental or distributing source
arteries (e.g., the intercostal, radial, ulnar, and deep
epigastric arteries) that course between the tissues. Suc-
cessive tiers of arcades are formed by the arteries, arte-
rioles, and capillaries that supply those tissues.
The arterial arcades in the bowel mesentery are a
classic example (Fig. 15-33).They are smaller and more
numerous as they approach the intestine. The basic
pattern exists in all tissues and is modified by the mor-
phology and fu nction of that tissue. Even during tissue
repair, the pattern of vascular arcades is reproduced
in granulation tissue. Undoubtedly there are many
reasons for the interconnections that exist between
arteries, but almost certainly one of these is to allow
the equilibration of pressure across the arcades before
the capillary bed is perfused.
Comparison of the vascular architecture in humans
with that in other animals and other species reveals a
similar arrangement of arcades. In the wings of insects
and in the leaves of plants, the veins assume a pattern
of interconnecting arcades similar to those of the intes-
tinal mesentery (Fig. 15-34).
Veins
Commencing at the capillary bed, the venous arcades
have a design similar to that of the arteries but in reverse,
with the tiers becoming larger and less numerous until
the ultimate arcade is reached—the arcade represented
by the superior and inferior venae cavae, with the heart
situated at the keystone. These arcades link adjacent
venous territories in and between tissues.
Within this network, there is a basic venous module
that is repeated in the tiers of the venous network,
modified in size and shape by the structure and func-
tion of the tissue and the embryologic growth and dif-
ferentiation that have given rise to its adult form (Fig.
15-35A). It is stellate or medusoid in form and con-
sists of a number of collecting veins that converge on
a pedicle. A good example of this arrangement is
the cartwheel of superficial veins that converge on the
saphenous bulb in the groin. In some areas, the trib-
utaries are polarized from one direction, like a tree
that has been blown by the wind (Fig. 15-35B); this
is true in the scalp, in muscles, and in the leg where
the short saphenous vein approaches the popliteal
fossa.
 image...

5 • VASCULAR TERRITORIES 349

v* ^*

->*b

y, ••--

FIGURE 1 5 - 3 2 . Radiographs of
the integument of the upper limb and
hand. The skin has been incised along
the ulnar border in A. It has been
removed with the deep fascia in B
and without it in C. Note (1) the size
and density of perforators in differ- jc'
V
. •Kttv*
ent regions of the limb and especially
compare them in the volarand dorsal
aspects of the hand and (2) the con-
vergence of vessels over the dorsum
of the joints of the thumb and fingers.
(From Taylor CI, Palmer JH: The vas-
cular territories [angiosomes] of the tt^
»
body: experimental study and clini-
cal applications. Br J Plast Surg
1987;40:113.)

The branches within each "venous tree" are linked

FIGURE 1 5 - 3 3 . The interconnecting arcades of the
small intestine. (From Crosthwaite GL, Taylor Gl, Palmer
JH: A new radio-opaque injection technique for tissue
preservation. Br J Plast Surg 1987;40:497.)
by channels, often free of valves, that are oriented like
the rungs of a ladder or the circumferential loops of a
cobweb. These arcades are well demonstrated in the
hands, in the feet, in the cubital fossa, and between the
venae comitantes that accompany the arteries. Periph-
erally, the radiating branches of each venous tree are
linked to those of its neighbor, again by avalvular veins,
to complete the network (Fig. 15-35C). In the integu-
ment, large horizontal channels have developed within
this reticular framework to subserve the specialized
function of thermoregulation (Fig. 15-35D). Their
connections with the deep veins are retained as large
channels, the venae communicantes, or by means
of the smaller venae comitantes of the perforating
cutaneous arteries (Fig. 15-36).
The venae communicantes usually relate to the large
longitudinal channels in the limbs. They are accom-
panied frequently by small perforating arteries. On
occasion, an artery is not present. By comparison, the
venae comitantes of the perforating arteries are always
present, and they are smaller and approximate to the

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image...
350 • GENERAL PRINCIPLES
B 113.1
caliber of the arteries. Although these veins are some-
times paired as they approach their destinations in the
deep tissues, they are often single, as seen in our cross-
sectional studies (Figs. 15-37 to 15-40).
Thus, the blood supply of the body consists of a
three-dimensional mesh of vessels that spans the body
like a national road map of interconnecting roadways
and subways. The meshwork is composed of a series
of linked vascular territories, fed at fixed skin points
by arteries that pierce the deep fascia and drained by
veins at the same points. When a flap is elevated, a series
of arterial territories is captured in succession by the
vessels in the base of the flap.
VESSELS OBEY THE LAW OF
EQUILIBRIUM
This concept was described by Debreuil-Chambardel
and is mentioned in Salmon's description of the cuta-
neous arteries.8,10 Basically, this states that"the anatom-
ical territories of adjacent arteries bear an inverse
relationship to each other yet combine to supply the
same region." If one vessel is small, its partner is large
to compensate, and vice versa. This is well illustrated
in the variability in size between each of the paraster-
nal perforators of the internal mammary artery and
between the internal mammary perforators and the
cutaneous perforator of the adjacent angiosome, the
acromiothoracic (see Figs. 15-6 and 15-7).
VESSELS HAVE A RELATIVELY CONSTANT
DESTINATION BUT MAY HAVE A
VARIABLE ORIGIN
This is typical of the vessels that emanate from the groin
to supply the skin of the lower abdomen and upper
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FIGURE 1 5 - 3 4 . The wing of
a moth (A) and the leaf of tree
(B) showing their intercon-
necting arcades of "veins." (From
Taylor CI, Palmer JH: The vascular
territories [angiosomes] of the body:
experimental study and clinical appli-
cations. Br J Plast Surg 1987;40:
thigh. The superficial inferior epigastric and the
superficial circumflex iliac arteries, for example, may
arise either separately from the common femoral artery
or as a combined trunk from that vessel or from one
of its branches. Whatever the case, their destination
is constant to supply the integument of the lower
abdomen and the hip (see Figs. 15-7 and 15-29).
VENOUS NETWORKS CONSIST OF
LINKED VALVULAR AND AVALVULAR
CHANNELS THAT ALLOW EQUILIBRIUM
OF FLOW AND PRESSURE
When one visualizes the veins of the body, one gener-
ally conjures up a picture of numerous large venous
channels in the subcutaneous and deep tissues studded
liberally with valves that direct flow toward the heart.
Although this is true to some extent, there are numer-
ous venous channels, large and small, that are free of
valves and allow flow within their lumens in either
direction. Conversely, there are many small veins that
have valves at or near their ostia (sentinel valves) as
they enter large channels (Fig. 15-41).
Directional Veins
These valved veins typically exist either as longitudi-
nal channels, which are well developed in the subcu-
taneous and deep tissues of the limbs, or as a stellate
pattern of collecting veins, which converge on a
pedicle. The cutaneous perforators and the pedicle-
draining muscles are good examples of the latter
arrangement. Because many of their tributaries have
valves oriented distally as they converge on the pedicle,
they provide the anatomic basis for distally based flaps
(see Fig. 15-35).
T^WR^dtfW image...

15 • VASCULAR TERRITORIES 351

Oscillating Avalvular Veins

These avalvular vessels are numerous and may reach
large dimensions. They connect and allow free flow
between the valved channels of adjacent venous ter-
ritories, territories whose valves are oriented in the
opposite direction (see Figs. 15-35 and 15-36). Also
found between the valved channels of the same
system, they match and accompany the choke arter-
ies of the arterial framework. In the same way that
the choke arteries define the arterial territories, these
oscillating veins define the perimeter of the venous
territories (see Fig. 15-36). This is well illustrated in
the study of the muscles (see Figs. 15-11 and 15-12)
and in some areas of the integument, especially the
torso, the head, and the neck. In the skin of the limbs,
this pattern is overshadowed by the large superficial
channels in the subdermal plexus but is apparent in
cross-sectional studies. If one mentally subtracts the
long, large venous channels from the picture in the
limbs, the remaining stellate pattern of the perforat-
ing veins matches that of the perforating arteries. It
is noteworthy that there is a rich network of large
oscillating veins in the anterior thigh. This may
provide an explanation for arterialized venous free
flaps.

If one traces the venous pathway of the cutaneous

FIGURE 1 5 - 3 5 . Schematic diagrams of the basic
venous module (A), its modified arrangement in different
areas (B), and how these modules interconnect to form
a continuous network (C). In the integument, this network
of venous perforators is reorganized in the subdermal
plexus to form longitudinal channels (D). The valved
segments are solid, and the avalvular oscillating veins
are open. (From Taylor CI, Caddy CM, Watterson PA, Crock
JC: The venous territories (venosomes) of the human
body: experimental study and clinical implications. Plast
ReconstrSurg 1990;86:185.)
perforators, or the pedicles draining the muscles, in
retrograde fashion from their entry into the parent
veins (venae comitantes) to their origin at the capil-
lary level, there exists an interesting sequence of
valved and avalved segments in the venous tree
(see Fig. 15-41). This is an important consideration
because it highlights our difficulties in trying to
perfuse the venous system and the potential ob-
struction to flow if one attempts to arterialize a venous
free flap.
An ostial valve typically guards the entry of the
pedicle into the parent vein. As one ascends the venous
tree, valves are met in the trunk, at the confluence of
the collecting veins, and for a variable distance along
these branches. Thereafter, the channels are devoid of
valves, and these oscillating segments may span long
distances, branching and interconnecting as they go,
before they meet and become continuous with the
collecting veins of the next venous tree, veins whose
valves are directed in the opposite direction. These
arcades, composed of directional and oscillating veins
that link adjacent venous pedicles, form the first tier
of the Roman aqueduct. Beyond these channels, sen-
tinel ostial valves guard the entry of the next tier of
venous arcades. In our studies, these were the last valves
detected before the capillary bed was reached. They
were rudimentary and were represented in our radi-
ographic studies as small diverticula-like projections
where the mixture was arrested in most cases (see
Fig. 15-41).

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352 I • GENERAL PRINCIPLES

FIGURE 1 5 - 3 6 . Top, Schematic

diagram of the integument and
underlying muscle (shaded) in a limb
illustrating the superficial (S) and
deep (D) venous systems with their
interconnecting network. A large
vena communicans (C) connects
these systems, and the alternative
pathways of four venae comitantes
are shown. The valved veins are dark,
and the oscillating veins are light.
Bottom, Similar diagram represent-
ing other regions where the pre-
dominant venous drainage is by
means of the venae comitantes. Note
in each diagram that oscillating
veins link adjacent territories in the
integument and deep tissues. (From
Taylor CI, Caddy CM, Watterson PA,
Crock JC: The venous territories
[venosomes) of the human body:
experimental study and clinical
implications. Plast Reconstr Surg
1990:86:185.)

•^w

FIGURE 1 5 - 3 7 . Cross-sectional arterial (left) and venous (right) studies of the integument of the breast
(A), thigh (B), and sole of foot (C). In D, the arterial study is of the buttock, with the outer surface of the
gluteus muscle defined with small arrows. The venous study is of the erector spinae and overlying skin.
(From Taylor CI, Caddy CM, Watterson PA, Crock JC: The venous territories [venosomes) of the human
body: experimental study and clinical implications. Plast Reconstr Surg 1990,86:185.)

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image...

«- — v "*T ^F^

JV - < <
.
FIGURE 1 5 - 3 8 . Schematic
diagram to compare with Figure B
15-37, with the site of the deep
fascia indicated in each case
(arrow). Note how the choke arte-
ries are matched by oscillating
veins in each pair. (FromTaylorGI,
Caddy CM. Watterson PA, Crock
JC: The venous territories [veno-
somes] of the human body:
experimental study and clinical
implications. Plast Reconstr Surg
1990;86:185.) D

FIGURE 1 5 - 3 9 . Cross-sectional study

of the arterial supply (left) and venous
drainage (right) of the thigh showing the
course of the cutaneous perforators in
the intermuscular and intramuscular
septa. Note the similarity between the
studies, which are taken at approximately
the same level in different subjects. (From
Taylor CI, Caddy CM, Watterson PA,
Crock JC: The venous territories [veno-
somes) of the human body: experimental
study and clinical implications. Plast
Reconstr Surg 1990:86:185.)

Superficial Lateral femoral

femoral circumflex
venosome venosome

Profunda
Common femoris
femoral venosome
venosome
FIGURE 15-40. Venous map to correspond with Figure 15-39, with accompanying diagram of venosomes. Note
that these territories span from the bone to the skin, that their boundaries lie between or within muscles, and that
these junctions are often represented by oscillating zones in the soft tissues. In the common femoral venosome, a cuta-
neous perforator drains by means of the plexus in the sartorius muscle to the long saphenous vein with valves oriented
along the pathway. This is a good example of the function of the "muscle pump" in this region. (From Taylor CI, Caddy
CM, Watterson PA, Crock JG: The venous territories [venosomesi of the human body: experimental study and clinical
implications. Plast Reconstr Surg 1990;86:185.)

353

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image...

354 I • CENERAL PRINCIPLES

FIGURE 1 5 - 4 1 . A, Schematic representation of a venous perforator showing the primary, secondary, and tertiary
venous arcades. Note the ostial valves that guard the entry of the secondary tier of veins (small arrows). B, A close-
up study of the venous network of the scalp showing the preceding features, except that these veins are devoid of
valves. C, The ostial valves have arrested the radiopaque mixture in this muscle study and appear as small diverticula-
like projections on the side of the veins. (From Taylor CI, Caddy CM, Watterson PA, Crock JC: The venous territories
[venosomes] of the human body: experimental study and clinical implications. Plast Reconstr Surg 1990;86:185.)

Beyond this, the venous network consists of tiers
of progressively smaller interconnecting arcades until
the capillary bed is reached. In some cases, these fine
channels were demonstrated radiologically, especially
in the scalp and occasionally in the limbs. If one reverses
the processes and the venous pathway is traced from
the capillary bed to the parent vein, it can be seen that
anatomically there is a rich system of oscillating veins
that allows the equilibration of flow (and perhaps
pressure) along the way.
MUSCLES ARE PRIME MOVERS OF
VENOUS RETURN
Most surgeons have been preoccupied with the arte-
rial supply of the various muscles used for transfer.
The efferent veins that accompany the arteries and drain
the muscles have been noted and assumed, quite cor-
rectly, to be sufficient to provide an adequate venous
return.
However, this is but half the picture. There are affer-
ent veins entering almost every muscle in the body that
arise from the overlying integument, adjacent muscles,
and underlying bone where muscles are attached. When
the muscles contract, valves in the efferent veins direct
flow toward the heart. During "diastole," valves direct
flow into the muscles by means of their afferent veins.
If the valves in the muscles in the leg become incom-
petent (e.g., as the late result of deep venous throm-
bosis), it would not be difficult to envision the
backpressure effect on the afferent cutaneous veins
entering the muscle and their role in the pathogene-
sis of varicose veins and venous ulceration.
Many veins connect muscle pairs or groups of
muscles as arcades. It is noteworthy that the muscles
with the richest afferent supply were those that filled
most readily with our injection studies. Notable exam-
ples are the gastrocnemius-soleus complex, the quadri-
ceps muscles, the triceps, and the shoulder girdle
muscles, especially the deltoid.

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 image...
SUPERFICIAL VEINS FOLLOW NERVES;
PERFORATING VEINS FOLLOW
PERFORATING ARTERIES
The venous drainage of the skin following investiga-
tion has been found to consist of two parts.
1. A subdermal horizontal network tends to follow
the cutaneous nerves. This is seen in the limbs
in particular, with named cutaneous nerves
following named superficial veins (Color
Plate 15-14).
2. Where perforating veins pass through the deep
fascia in a perpendicular fashion, this occurs with
accompanying arteries. As stated in previous
concepts, this usually occurs at fixed sites
(see Fig. 15-30).
NERVOUS AND VASCULAR SYSTEMS
DEVELOP EMBRYOLOCICALLY
IN HARMONY
This is a rapidly expanding area in medical research.
It has often been thought that either the nervous system
or the vascular system determines the growth of the
other. Recent evidence, however, is showing that rather
than one system's taking the lead, the two systems
develop in harmony and are interdependent (Color
Plate 15-15).
CLINICAL APPLICATIONS
The anatomic information outlined in this chapter
represents an attempt to correlate the efforts of
many workers, including those of Manchot 4,5 and
Salmon.8"10 It aims to provide some concepts to aid in
the design of flaps and incisions, simplifying the
nomenclature and stimulating further research.
Although much is now known about the arterial frame-
work of the body, the venous framework, and the
nervous network, there are still gaps in our knowledge.
Some of the applications of this work and anatomic
research are considered briefly; the details are covered
in other chapters.
The Doppler Probe and Mapping
of Perforators
On the basis of the premise that perforators are always
connected by a network of arteries and corresponding
veins regardless of the dominant axis of each per-
forating vessel, it seems evident that if two adjacent
primary cutaneous perforating arteries can be isolated
clinically with precision, a line drawn between them
should represent the axis of a viable flap.
The Doppler probe allows surgeons to locate
cutaneous perforators with precision in individual
cases. By use of the knowledge that most cutaneous
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15 • VASCULAR TERRITORIES 355
arteries emerge from fixed skin sites as already out-
lined in the section on anatomic concepts (see Color
Plate 15-1), their expected origin can be anticipated
and located rapidly. There is currently renewed inter-
est in these flaps based on the skin vessels, which are
referred to as perforator flaps. A large number of flaps
based distally in the limbs have appeared in the liter-
ature in recent years.67"69
The use of the Doppler probe to locate the origin
of cutaneous perforators is not new and has been used
by many in the past.70,71 It is not necessary in every
case, for obvious reasons. However, its application in
free flap transfer has been found to be invaluable, espe-
cially in siting a small flap. A good example of this is
the osteocutaneous fibular flap, where just a small skin
paddle is required either to monitor the vascular anas-
tomosis or as part of the reconstruction. The Doppler
probe is a quick, simple method for defining the
perforators.
There is a distinct learning curve to the use of the
instrument and a time factor before one becomes
proficient. There are also some limitations in its use.
Obese patients in particular may limit its efficiency for
two reasons. First, the thick cutaneous layer may pre-
clude detection of the perforator as it emerges from
the deep fascia. Second, as adipose tissue increases, the
integument stretches into folds, and the course and
destination of the perforators become distorted. There
is therefore an increased margin for error in siting the
base and axes of the skin flap.
Axes of Skin Flaps
The arterial atlas of the integument details the origin,
course, size, density, and interconnections of the cuta-
neous perforators. It therefore provides for the logical
planning of the base and axis of a skin flap. Some of
the potential flaps available for transfer based on these
perforators are shown in Figure 15-42 as "perforator
flaps."
Cross-sectional studies confirm the reason for
including the outer layer of the deep fascia with flaps
raised in the scalp and in the extremities; in these sit-
uations, the vessels hug the fascia for considerable
distances. If a flap is designed along the course of the
cutaneous nerve, such as the saphenous or the sural
nerve, long safe flaps can be and have been elevated.
Ponton's28 original flaps were designed in this way, and
the saphenous neurovascular flap was planned in a
similar manner. 72
In the loose skin areas of the torso, it is unneces-
sary to include deep fascia because the cutaneous arter-
ies course at an early stage within the integument. They
frequently correspond with the course of the cutaneous
nerve. 73
Conventional flaps in the limbs have been based
proximally or transversely in the past with rigid
image...
356 I • GENERAL PRINCIPLES
length-to-breadth ratios. In the latter case, the base has
been broad. Inclusion of the deep fascia has extended
flap dimensions, and the anatomic rationale has
already been discussed. Flaps in the literature that are
based distally and that may defy many geometric guide-
lines can also be explained.
The arterial perforators radiate in stellate patterns,
and this includes branches that course proximally. The
accompanying veins converge from the same direc-
tions. Hence, if a flap is based distally over such a per-
forating system, it will contain arterial branches that
radiate proximally from it and valved veins that return
to that point.
Another clue to flap design is the site and orienta-
tion of the large subdermal venous channels that are
evident in a lean, well-muscled individual, particularly
in the hyperdynamic state. Frequently, they parallel the
axis of the underlying cutaneous arteries or chain-
linked system of arteries. Another example is the long
axis of veins that is often seen extending obliquely from
the axilla to the groin. On the arterial side, this is
matched by a chain-linked system of arteries that is
the basis of the long thoracoepigastric flap described
by Webster.I6 This arterial axis is provided by the limbs
of the lateral thoracic and thoracodorsal arteries
above, the lateral intercostal perforators in the middle,
and the superficial inferior epigastric and superficial
circumflex iliac cobweb that radiates from below. The
veins that diverge from the nipple, especially to the
axilla and to the parasternal region, provide another
example. Their relationship to the underlying arteries
is well illustrated in Figures 15-6,15-37, and 15-38 and
may serve as a guide in the design of the various breast-
reduction and breast-sharing techniques.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
FIGURE 15-42. Some of the large
axial cutaneous flaps that have been
used or are available based on spe-
cific perforating arteries and their
accompanying perforating veins, as
defined by radiographic studies of
the integument. In the scalp and the
limbs, they should include the deep
fascia. Compare with Color Plate 15-
1 and Figure 15-25. (From Taylor CI,
Palmer JH: The vascular territories
[angiosomes] of the body: experi-
mental study and clinical applica-
tions. Br J Plast Surg 1987; 40:113.)
It follows that longer breast flaps should be based
where the skin is fixed and their axes oriented along
the lines of maximal skin mobility. The farther the dis-
tance between fixed points, the longer the safe dimen-
sions of the flap. There are many instances in which
this applies in practice. For example, long flaps can be
based at the groin, the paraumbilical region, or the
parasternal region of the chest. In considering the
concept of the law of equilibrium, this has applica-
tion to the axis of a flap. The deltopectoral flap of
Bakamjian18 is an excellent example. It is based medi-
ally over the second to fourth intercostal spaces to
embrace the variable sizes of the internal thoracic per-
forators. Designed below and parallel to the clavicle,
it is usually dissected medially from its tip at the shoul-
der. If small perforators are noted over the deltoid
muscle, and in particular from the deltopectoral
groove, the dissection is continued to the flap base on
the assumption that the internal thoracic perforators
will be large. If, however, a large cutaneous perforator
is seen emerging from the deltopectoral groove, this
pedicle is usually ligated, and further dissection of
the flap is delayed for 1 week owing to the possibility
that the adjacent internal thoracic perforators will be
small. This delay procedure is employed because of the
risk of flap necrosis, especially if the flap's tip spans
beyond the point of the shoulder.
Skin Flap Dimensions
Because the blood supply of the integument, both
venous and arterial, has been shown to be a continu-
ous system of linked vascular territories, the survival
length of a skin flap must depend on (1) the caliber
HlWftf'aStfW image...
and length of the dominant vessels on which the flap
is based; (2) the caliber and span of the adjacent cap-
tured artery or arteries, vein or veins; (3) the caliber
and length of the connecting choke vessels; and (4)
an anatomically favorable or unfavorable venous
return.
Where the arterial perforators are large and widely
separated, the territory of each is large and a long flap
can be raised with safety. These flaps are characteris-
tic of the loose skin areas of the torso and the scalp.
Conversely, if the perforators are diminutive and close
together, the territory of each is small. The viable length
of the flap is short unless the supplying source vessel
is included in the design. This is evident in the fixed
skin area of the sole of the foot.
If very large flaps are required or if vessels of a large
caliber are necessary for microvascular anastomoses,
the requirements can be satisfied by chasing the
perforators through the intermuscular septa or the
intramuscular septa to include the underlying source
vessels. The intelligent use of a delay also allows safe
capture of adjacent vascular territories.
When we consider the venous drainage, the large
longitudinal veins in the subcutaneous tissue of
the limbs offer an excellent drainage for proximally
based flaps because their valves are oriented in that
direction. However, in the lower abdomen, the
drainage of proximally based flaps may be anatomi-
cally unfavorable because the valves of the superficial
inferior epigastric veins are directed distally toward
the groin. The undermined flap of a transverse
abdominal lipectomy is a case in point, and perhaps
FIGURE 1 5 - 4 3 . Diagrammatic representation of the
same flap raised with and without a surgical delay to
illustrate the necrosis line and the changes in the choke
vessels. In X, the adjacent territory a is captured with
safety, and the necrosis line occurs at the choke-vessel
interface with vessel b or the one beyond. In Y, vessel
a had been delayed. Note the effect on the choke vessels
and the site of the necrosis line. In Z, vessels a and b
have been delayed in this bipedicled flap. Vessel c is
divided and the tip of the flap elevated at a second
stage to provide the longest flap.
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Dr.Mustafa D.
15 • VASCULAR TERRITORIES 357
fortuitously, the area of the flap in question is ampu-
tated in the procedure.
The scalp veins are mostly free of valves, and hence
flaps based in any direction will drain favorably. In many
regions, however, the venous network consists of ter-
ritories of valved veins oriented in different directions
that are linked by oscillating veins.
The precise mechanism of the necrosis line of a flap
is unknown, although the opening up of arteriovenous
shunts provides a plausible theory. Whatever happens,
it has been shown that the choke vessels on the arte-
rial side and some of the valved territories of the venous
return provide a potential mechanical obstruction to
flow.
The Delay Phenomenon
Skin flap dimensions can be extended by the intelli-
gent use of simple "delay" procedures. The existing
arteries enlarge along the axis of the flap, and this
has been well documented in experimental animal
models (Fig. 15-43). One adjacent anatomic vascular
territory can be captured with safety on the cutaneous
artery at the flap base. Anastomotic vascular keystones,
usually formed by reduced-caliber choke arteries that
link adjacent cutaneous perforators, play an integral
role in the delay phenomenon. When a flap is ele-
vated, these choke vessels, which initially reduce flow
from one arterial territory to the next along the flap,
enlarge to the caliber of the cutaneous arteries they
connect (Fig. 15-44). However, this process of vessel
enlargement is an active event and takes time. It is a
image...

358 I • CENERAL PRINCIPLES

The deep fascia should be included in the design of

the fasciocutaneous flap in those sites where the skin
is relatively fixed to the deep fascia, for example, in the
limbs or the scalp. In these instances, the dominant
cutaneous vessels course on or lie adjacent to the deep
fascia. Although they can be dissected free in some cases,
it is safer or more expedient to include the deep fascia
with the flap. However, where the skin and subcuta-
neous tissues are mobile over the deep fascia, for
example, in the iliac fossae or the breast, it is unnec-
essary to include this fascial layer because the major
cutaneous vessels have already left its surface.
The term septocutaneous is sometimes misleading,
especially when it is used to describe a surgically created
entity rather than a true anatomic structure. This may
occur, for example, where the cutaneous perforators
of a radial or ulnar flap are dissected within an
envelope of loose areolar tissue. Furthermore, the
septocutaneous flap may provide traps for the unwary
surgeon. In some cases, the cutaneous artery and its
accompanying vein leave the underlying source vessels

Control Delay
FIGURE 1 5 - 4 4 . Arteriogram of control (left) and
delayed (right) rectus abdominis muscles of a dog 7 days
postoperatively. Note the dilated choke vessels in the
delayed flap by ligation of the deep inferior epigastric
artery (arrow). (From Dhar SC, Taylor CI: The delay
phenomenon: the story unfolds. Plast Reconstr Surg
1999; 104:2079.)

permanent and irreversible process involving multi-

plication and hypertrophy of the cells in each layer
of the vessel wall, with its maximal effect occurring
between 48 and 72 hours after operation74 (Fig.
15-45). It has been observed that necrosis usually
occurs at the level of the next choke anastomosis
in the arterial network or the one beyond. Surgically,
flap survival can be extended by the strategic division
of vascular pedicles at various time intervals along
the length of the proposed flap—the "flap delay"
procedure.

Fasciocutaneous Flaps Control Delay

The vessel relationship to the different types of
connective tissue achieves special significance when
the surgeon raises a cutaneous flap that includes
the outer layer of the deep fascia (the fasciocutaneous
flap) or when the design involves the intermuscular
septa or the intramuscular septa (the septocutaneous
flap).
FIGURE 1 5 - 4 5 . Arteriogram of control (left) and
delayed (right) rectus abdominis muscle of a dog 12 weeks
after reanastomosis of the previously ligated deep infe-
rior epigastric artery (arrow). Note that the choke vessels
remain tortuous and dilated, revealing that the effect of
the delay is permanent and irreversible. (From Dhar SC,
Taylor CI: The delay phenomenon: the story unfolds. Plast
Reconstr Surg 1999:104:2079.)

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
T%W)»tf<ySd,W image...
and course toward the surface in a surgically favorable
position, adjacent to a true white fibrous intermuscu-
lar septum. This is typical of the blood supply to the
skin of the lateral arm flap, where cutaneous perfora-
tors arise from descending branches of the profunda
brachii vessels and follow the lateral intermuscular
septum toward the skin. This pattern of supply usually
exists where the muscles glide on either side of the inter-
muscular septum.
However, if the muscles attach to either side of the
intermuscular septum, the cutaneous perforator may
have a variable course. This variability is seen in par-
ticular in the lateral aspect of the upper calf. If a com-
pound skin and bone flap is designed at this site over
the lateral intermuscular septum based on the cuta-
neous perforators of the peroneal vessels, (1) these
skin vessels may course directly to the surface, trav-
eling in a favorable position, either adjacent to the
septum or within the substance of the soleus or flexor
hallucis longus muscles, close to their attachments to
the fibula, or alternatively, (2) they may arise indi-
rectly from branches to the soleus or flexor hallucis
muscles as terminal twigs of muscle branches that have
arisen from the peroneal vessels at considerable dis-
tance from the lateral intermuscular septum. In these
cases, a long and laborious intramuscular dissection
of the cutaneous supply will be required to success-
fully raise the flap.
Musculocutaneous Flaps
When skin and deep fascia are firmly bound to the
underlying muscle (e.g., the gluteus maximus and latis-
simus dorsi), the blood supply to the overlying skin is
ensured. At each fixed site over the muscle, vessels
emerge, some large and some small, to supply the
integument. However, when the muscle is mobile
beneath the deep fascia (e.g., the gracilis muscle), the
cutaneous supply is at best tenuous.
In general, musculocutaneous flaps can be raised
safely if the skin paddle is placed over the perforators
of the feeding muscle artery or those in the adjacent
muscle territory (Fig. 15-46). Attempts to capture
territories beyond this, without previous delay, fre-
quently result in vascular insufficiency. This situation
may prevail, for reasons already outlined, in the pec-
toralis major and the lower TRAM flaps.
Depending on the muscle type and the site of the
skin paddle, the venous pathway once again may
become anatomically favorable or unfavorable. In each
case, the venous drainage is thrust on perforators that
drain to the intramuscular plexus of veins. In type I
muscles, the drainage is favorable regardless of the
site of the skin paddle over the muscle because the
venous drainage is in one direction. If the skin paddle
is placed over the distal territory of type II and type
III muscles, the valves of this territory are oriented in
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Dr.Mustafa D.
15 • VASCULAR TERRITORIES 359
the opposite direction to those of the draining pedicle,
and the pathway is anatomically unfavorable. This
problem was highlighted by Costa et al75 in their inves-
tigations of the venous drainage of the lower TRAM
flap.
Many of the direct (primary) cutaneous perfora-
tors arise from the source artery as it courses beneath
or within a muscle (e.g., cutaneous perforators from
the internal thoracic, deep inferior epigastric, or
gluteal vessels). To reach the integument, these per-
forators pass between the muscle fibers, providing
branches en route, before they pierce the overlying deep
fascia to reach the subcutaneous tissue and skin. Inter-
est is currently focused on dissecting the intramuscu-
lar course of these cutaneous perforators to reach their
source vessel origin. This is done to provide large vessels
for microvascular transfer; to eliminate the bulk of
muscle, when appropriate; and to preserve muscle func-
tion, for example, in harvesting a lower transverse
abdominal skin flap on one or more perforators of the
deep inferior epigastric artery,"14 often referred to as
perforator flaps.
However, all cutaneous flaps are based on cutaneous
perforators, whether direct or indirect and regardless
of whether they pass between or through the muscles
to reach the overlying integument. Hence, to confine
the term perforator flap to only those instances in which
the cutaneous vessel emerges from muscle to perfo-
rate the overlying deep fascia is misleading. The term
perforator flap therefore should include anyisland skin
flap, based on a cutaneous perforator, whether it arises
from a source vessel between or within a muscle or other
deep tissue. Some of the early free flaps, for example,
the groin flap, are true perforator flaps, in this instance
based on the superficial circumflex iliac or superficial
inferior epigastric artery.22,72
Composite Flaps
A knowledge of the supply of all the tissues that
constitute each angiosome provides the basis for the
transfer of composite units of skin, muscle, nerve,
tendon, and bone supplied by a single arteriovenous
system. This knowledge has been applied extensively
in free composite tissue transfer (Figs. 15-47 and
15-48).
The vessels within the angiosome interconnect
between the various layers. This interconnection is well
illustrated with the transfer of composite tissue from
the groin region. The direct cutaneous perforators of
the superficial circumflex iliac artery interconnect with
the indirect perforators of the deep circumflex iliac
artery. When a composite osteocutaneous flap is based
on the deep system, the perforators of the deep
circumflex iliac artery capture the territory of the
superficial circumflex iliac artery to perfuse the skin.53
When the superficial system is used, the reverse applies
360 I • GENERAL PRINCIPLES

•
FIGURE 15-46. AThecutaneous
supply from the deep superior epi-
gastric arteries (s), the perforators
of the deep inferior epigastric artery
that are concentrated around the
umbilicus (P), and the radiating
branches of the superficial inferior
epigastric vessels (E) and their rela-
tionship to the skin paddle of the
TRAM flap. B, The angiosome terri-
tories of each source artery with the
outline of the TRAM flap (dotted).
The intercostal (striped) and deep
circumflex iliac (unshaded) territo-
ries are unlabeled. DIEA, deep infe-
rior epigastric artery; DSEA, deep
superior epigastric artery; SIEA,
superficial inferior epigastric artery.
C, The four zones of the TRAM flap
as defined by Carl Hartrampf, shown
here when the flap is designed on
the right rectus muscle (arrow).
B

FIGURE 15-47. Composite muscle-

nerve flap isolated on the radial
vessels. (From Taylor CI: Free vascu-
larized nerve transfer in the upper
extremity. Hand Clinics 1999; 15:673.)

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Dr.Mustafa D.
 image...
FIGURE 1 5 - 4 8 . Composite bra-
chioradialis muscle and superficial
radial nerve flap with two additional
cable nerve grafts in parallel before
reanastomosis in the recipient
forearm. (From Taylor Gl: Free vas-
cularized nerve transfer in the upper
extremity. Hand Clinics 1999; 15:
673.) *»k
to perfuse the anterior segment of iliac crest and the
attached muscles.51
Tissue Expansion
Tissue expansion has increased in popularity since it
was first introduced in 1957 by Neumann 42 and pop-
ularized in 1976 by Radovan 76 for breast reconstruc-
tion. Controlled tissue expansion has since been used
for the reconstruction of all areas of the body in many
diverse situations. The histologic changes evident in
expanded skin lend support to the concept that skin
expansion is in fact a form of delay. This was sup-
ported by Cherry et al,77 who looked at the survival
of expanded and delayed flaps compared with acutely
raised random-pattern skin flaps. Both the expanded
flaps and delayed flaps show increased survival length
compared with unexpanded or undelayed skin flaps.
There was no difference between the expanded or
delayed skin flaps. Angiograms of expanded skin show
evidence of increased vascularity compared with con-
trolled skin.
Sasaki and Pang78 showed an increased total capil-
lary blood flow within expanded and delayed flaps
compared with undelayed skin flaps. Other authors
have shown angiographic evidence of increased caliber
of axial vessels in expanded flaps similar to that seen
in the choke vessels of delayed flaps. Laser Doppler
flowmetry and venous outflow measurement have
again shown increased superficial blood flow in
expanded skin.
Liposuction
Contouring of specific areas of the body by suction
lipectomy has been performed since earlier this century.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
15 • VASCULAR TERRITORIES 361
The procedure involves the removal of localized sub-
cutaneous fat deposits through a small stab incision.
Various methods have been described in the past,
including the deep liposuction as well as the more recent
superficial technique as described by Gasparotti. 79 The
ultrasound-assisted liposuction technique is another
introduction. Regardless of the technique of liposuc-
tion used, the anatomic principle is the same, that is,
the removal of fat deposits between the connective
tissue septa of the subcutaneous layer that contain the
blood vessels supplying the overlying skin.
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chest wall. Br J Plast Surg 1986;39:287.
58. Taylor GI: Foreword. In Manchot C: The Cutaneous Arteries of
the Human Body. Risic J, Morain WD, trans. New York,
Springer-Verlag, 1983.
59. Hunter J: A Treatise on the Blood, Inflammation and Gunshot
Wounds. London, John Richardson, 1794.
60. Tsuge K: Treatment of established Volkmann's contracture.
J Bone Joint Surg Am 1975;57:925.
61. Wei FC, Chen HC, Chuang CC, Noordhoff MS: Fibular
osteoseptocutaneous flap: anatomic study and clinical appli-
cation. Plast Reconstr Surg 1986;78:191.
62. Abbe R: A new plastic operation for the relief of deformity due
to double harelip. Med Rec 1898;53:477.
63. Williams P, Warwick R: Gray's Anatomy, 36th ed. Edinburgh,
Churchill Livingstone, 1980.
64. Last RJ, Tompsett DH: Corrosion cast of the blood vessels of
stillborn babies. Acta Anat 1962;51:338.
65. Johnston TB, Davies IES, Davies F, eds: Gray's Anatomy, 32nd
ed. London, Longmans, 1958.
66. Patten BM: Human Embryology, 3rd ed. New York, Blakiston
Division, McGraw-Hill, 1968.
67. Amarante J, Costa H, Reis J, Soares R: Venous skin flaps: an
experimental study and report of two clinical distal island flaps.
BrJPlastSurgl988;41:132.
68. Costa H, Soutar DS: The distally based island posterior
interosseous flap. Br J Plast Surg 1983;41:221.
 image...
69. Masquclet AC, Beveridge J, Romana C: The lateral supramalle-
olar flap. Plast ReconstrSurg 1988;81:74.
70 Song R, Gao Y, Song Y, et al: The forearm flap. Clin Plast Surg
1982;9:2l.
71 Taylor GI, Doyle M, McCartcn G: The Doppler probe for plan-
ning flaps; anatomical study and clinical applications. Br J Plast
Surg 1989;43:1.
72. Acland RD, Schusterman M, Godina M, et al: The saphe-
nous neurovascular free flap. Plast Reconstr Surg 1981;67:
763.
73. Badran HA, El-Helaly MS, Safe I: The lateral intercostal neu-
rovascular free flap. Plast ReconstrSurg 1984;73:17.
74. Dhar SC, Taylor GI: The delay phenomenon: the story unfolds.
Plast Reconstr Surg 1999; 104:2079.
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15 • VASCULAR TERRITORIES 363
75. Costa MAC, Carriquiry C, Vasconez LO, et al: Study of the venous
drainage of the transverse rectus abdominis musculocutaneous
flap. Plast Reconstr Surg 1987;79:208. '
76. Radovan C: Adjacent flap development using expandable
situation implant. Presented at the annual meeting of the
American Society of Plastic and Reconstructive Surgeons,
Boston, 1976.
77. Cherry GW, Austad E, Pasyk K, et al: Increased survival and
vascularity of random-pattern skin flaps elevated in controlled,
expanded skin. Plast Reconstr Surg 1983;72:680.
78. Sasaki GH, Pang CY: Pathophysiology of skin flaps raised on
expanded pig skin. Plast Reconstr Surg 1984;74:59.
79. Gasparotti M: Superficial liposuction: a new application of the
technique for aged and flaccid skin. Aesthetic Plast Surg
1992;16:141.
COLOR PLATE 1 5 - 1 . Map of the arterial perforators of 0.5 mm or more,
which are color coded to correspond to the underlying parent arteries and course
with the associated perforating veins. They provide the basis for the current
revival of "perforator flaps." Compare with Color Plate 15-2 to identify the parent
(source) arteries of these cutaneous perforators. (From Taylor CI, Palmer JH:
The vascular territories [angiosomes] of the body; experimental study and clin-
ical applications. Br J Plast Surg 1987;40:113.)

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COLOR PLATE 15-2. The angiosomes of the source arteries of the body shaded to corre-
spond to Color Plate 15-1. They are thyroid (1), facial (2), buccal (internal maxillary) (3), oph-
thalmic (4), superficial temporal (5), occipital (6), deep cervical (7), transverse cervical (8),
acromiothoracic (9). suprascapular (10), posterior circumflex humeral (11), circumflex scapular
(12), profunda brachii (13), brachial (14), ulnar (15), radial (16), posterior intercostals (17),
lumbar (18), superior gluteal (19), inferior gluteal (20), profunda femoris (21), popliteal (22),
descending genicular (saphenous) (22a), sural (23), peroneal (24), lateral plantar (25), anterior
tibial (26), lateral femoral circumflex (27), adductor (profunda) (28), medial plantar (29), poste-
rior tibial (30), superficial femoral (31), common femoral (32), deep circumflex iliac (33), deep
inferior epigastric (34), internal thoracic (35), lateral thoracic (36), thoracodorsal (37), posterior
interosseous (38), anterior interosseous (39), and internal pudendal (40). (From Taylor CI, Palmer
JH: The vascular territories [angiosomes] of the body: experimental study and clinical applica-
tions. Br J Plast Surg 1987;40:113.)

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image...

COLOR PLATE 1 5-3. The venosomes of the body. Compare with Color Plate 15-2. (From Taylor
Glp Caddy CM, Watterson PA, Crock JC: The venous territories [venosomes] of the human body:
experimental study and clinical implications. Plast Reconstr Surg 1990;86:185.)

Radial recurrent artery

Radial
artery Profunda brachii artery

Ulnar Ulnar
artery recurrent
artery

Radial recurrent Radial Anterior

COLOR PLATE 15-4. The artery artery interosseous
cutaneous perforators of the BR artery
forearm, color coded to match
the angiosomes. Large and
small skin perforators are indi-
cated by the size of the colored
markers. Compare with Color
Plate 15-2. (From Inoue Y,
Taylor CI: The angiosomes of
Posterior Posterior
the forearm: anatomic study
and clinical applications. Plast ulnar recurrent recurrent Ulnar interosseous
Reconstr Surg 1996;98:195.) artery artery artery artery

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image..

Median artery | Profunda brachii artery

Radial Radial recurrent artery

Ulnar
artery Ulnar recurrent
A artery
Median artery

Ulnar Ulnar Profunda

B artery Anterior recurrent brachii
interosseous artery artery artery
Radial recurrent artery I
Radial artery
l i>

V, Ulnar Ulnar
artery recurrent
artery

COLOR PLATE 1 5-5. The angiosome territories of the superficial (A), middle (B), and
deep (C) forearm flexor muscles. Note that the junctional zone between angiosomes
occurs primarily within the muscles and that most muscles cross at least two angiosomes.
Compare with Color Plates 15-2 and 15-4, which reveals the supply to each muscle from
each angiosome. (From Inoue Y, Taylor CI: The angiosomes of the forearm: anatomic
study and clinical applications. Plast Reconstr Surg 1996;98:195.)

Profunda brachii artery Anterior

Radial recurrent artery
Radial artery interosseous
artery

Interosseous Posterior
recurrent artery interosseous
artery

Anterior
interosseous COLOR PLATE 15-6. The angio-
artery * "
some territories of the superficial (A)
and deep (B) forearm extensor
muscles showing once again that the
junctional zone between angiosomes
lies primarily within the muscles.
Compare with Color Plate 15-2.
(From Inoue Y, Taylor CI: The angio-
somes of the forearm: anatomic
Interosseous Posterior study and clinical applications. Plast
recurrent artery Reconstr Surg 1996;98:195.)
interosseous
artery
B

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image...

Radial
recurrent
artery

Common
extensor

Interosseous
recurrent artery

Anterior interosseous
artery

Radial artery Ulnar

artery

ECRB

Posterior
Interosseous
artery

Anterior Ulnar artery

interosseous
artery

ECRL

EPL
Posterior EDM
branch of
interosseous
anterior
artery
interosseous
artery

C O L O R PLATE 1 5 - 7 . Cross-sectional studies of the forearm at the level of the

head of the radius (A), insertion of the pronator teres (B), and midforearm (C) showing
the angiosomes of the brachial (yellow), radial (blue), ulnar (red), anterior interosseous
(green), and posterior interosseous (orange) arteries. Note that the junctions of the
angiosomes occur within the skin, within muscles (highlighted by asterisk in A but seen
especially in 8), and within bone. The angiosome of the anterior interosseous artery
does not reach the skin until the distal forearm posteriorly (not illustrated) unless it
has a dominant median branch (10% of cases). (From Inoue Y, Taylor CI: The angio-
somes of the forearm: anatomic study and clinical applications. Plast Reconstr Surg
1996;98:195.)

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image...

Popliteal Popliteal
artery artery^*

Medial
Anterior tibial sural Lateral sural
recurrent artery artery artery
Anterior tibial
artery
FDL
PB

Peroneal Peroneal
artery artery

EHL
Peroneal artery
Anterior tibial
artery

COLOR PLATE 15-8. The colored spheres are sited at the points of emer-
gence of the cutaneous perforators from the deep fascia and depict the relative
size of these vessels. EDL, extensor digitorum longus; EHL. extensor hallucis
longus; FDL, flexor digitorum longus; GAS, gastrocnemius; PB, peroneus brevis;
PL, peroneus longus; PT, peroneus tertius; So, soleus; TA, tibialis anterior. (From
Taylor CI, Pan WR: The angiosomes of the leg: anatomic study and clinical appli-
cations. Plast Reconstr Surg 1998; 102:599.)

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image...

Popliteal
artery

Inferior lateral
genicular artery
Inferior medial
genicular artery
Anterior tibial Popliteal
recurrent artery artery

Anterior
tibial artery

- Anterior
recurrent
tibial artery

— Anterior
tibial artery

PB
Peroneal
artery

Anterior
tibial artery

B
COLOR PLATE 15-9. A, Illustration of the anterior muscle group that lies totally within the anterior tibial angio-
some (blue). This angiosome extends to include part of the peroneal muscles. B, Illustration of the lateral muscles and
their supply from the anterior tibial (blue) and peroneal (green) angiosomes. EDL, extensor digitorum longus; EHL,
extensor hallucis longus; PB, peroneus brevis; PL, peroneus longus; PT, peroneus tertius; TA, tibialis anterior. (From
Taylor CI, Pan WR: The angiosomes of the leg: anatomic study and clinical applications. Plast Reconstr Surg 1998; 102:599.)

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 Popliteal
artery \
Popliteal
PLA artery
N
;

Medial
sural artery Lateral Inferior lateral
sural artery genicular artery
Inferior medial
genicular artery
Anterior tibial
artery
TP

Peroneal
artery
Peroneal
artery

A B
COLOR PLATE 15-10. A, The superficial muscle group with its supply from the arteries of the popliteal
(purple), sural (orange), posterior tibial (yellow), and peroneal (green) angiosomes. All muscles cross at
least two angiosomes and receive branches from the source arteries of each. B, The deep muscles and
their supply from the source arteries of each angiosome. Once again, each muscle crosses at least two
vascular territories. FDL, flexor digitorum longus; FHL, flexor hallucis longus; GASTROC, gastrocnemius;
PLA, plantaris; POP, popliteal; SOL, soleus; TP, tibialis posterior. (From Taylor Gl, Pan WR: The angio-
somes of the leg: anatomic study and clinical applications. Plast Reconstr Surg 1998; 102:599.)

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image...

Branches of
sural arteries

Anterior tibial PLA

recurrent
artery

PLA

Anterior tibial
artery

C O L O R PLATE 1 5 - 1 1 . Anterior view of the leg with cross sections at three levels, viewed distally.
They show the angiosomes of the anterior tibial (blue), posterior tibial (yellow), peroneal (green), and
sural (orange) arteries. Note in each case that the angiosome territories extend from the sKin to the
bone and that their borders, defined by anastomotic vessels, meet usually within tissues, especially the
muscles, rather than between them. EDL, extensor digitorum longus; EHL, extensor hallucis longus; FDL,
flexor digitorum longus; FHL, flexor hallucis longus; GASTROC, gastrocnemius; PB, peroneus brevis; PL,
peroneus longus; PLA, plantaris; PT, peroneus tertius; SOL, soleus; TA, tibialis anterior; TP, tibialis pos-
terior. (From Taylor CI, Pan WR: The angiosomes of the leg: anatomic study and clinical applications.
Plast Reconstr Surg 1998; 102:599.)

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image

COLOR PLATE 1 5 - 1 2 . Angiosometerritoriesofthemusclesoffacial

expression and mastication in the face. Compare with Color Plate 15-
13. (From Houseman ND, Taylor CI, Pan WR: The angiosomes of the
head and neck: anatomic study and clinical applications. Plast Recon-
str Surg 2000:105:2287.)

COLOR PLATE 1 5 - 1 3 . The

angiosomes of the head and neck
colored and numbered to match
Color Plates 15-2 and 15-12.
They are internal maxillary (1),
facial (2), ophthalmic (3), super-
ficial temporal (4), posterior auric-
ular (5), occipital (6), transverse
cervical (7), deep cervical (8), infe-
rior thyroid (9), and superior
thyroid (10). The sagittal section
(B) shows the three angiosomes,
vertebral (11), ascending pharyn-
geal (12), and lingual (13), that do
not reach the skin surface. (From
Houseman ND.TaylorCI, Pan WR:
The angiosomes of the head and
neck: anatomic study and clinical
applications. Plast Reconstr Surg
2000:105:2287.)

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COLOR PLATE 1 5 - 1 4 . Arterial (A) and venous (B) studies of the integument
of the upper limb with the axillary (1), lower lateral brachial (2), supraclavicular
(3), intercostobrachial (4), posterior antebrachial (5), medial antebrachial (6),
medial brachial (7), lateral antebrachial (8), dorsal branch of ulnar (9), superfi-
cial radial (10), median (11), and ulnar (12) nerves labeled. (From Taylor Gl,
Gianoutsos MP, Morris SF: The neurovascular territories of the skin and muscles:
anatomic study and clinical implications. Plast Reconstr Surg 1994;94:1.)

COLOR PLATE 15-15. Confocal microscopic study of the developing fore-

limb of a day 7 chick embryo with the arteries fluorescing red and the nerves
fluorescing yellow. The brachial (ba) and digital (d) vessels and the median (m),
interosseous (in), and ulnar (u) nerves are labeled, cnv, supracoracoideus neu-
rovascular bundle. (From Taylor Gl, Bates D, Newgreen DF: The developing neu-
rovascular anatomy of the embryo: a technique of simultaneous evaluation using
fluorescent labeling, confocal microscopy, and three-dimensional reconstruc-
tion. Plast Reconstr Surg 2001 j 108:597.)

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age...
CHAPTER
16
•
Flap Classification and
Applications
STEPHEN J. MATHES, MD • SCOTT L HANSEN, MD
HISTORY
FLAP CLASSIFICATION
Muscle and Musculocutaneous Flaps
Fascial and Fasciocutaneous Flaps
Perforator Flaps
Abdominal Visceral Flaps
FLAP MODIFICATIONS
Tissue Expansion
Segmental Transposition Flaps
Vascularized Bone
Functional Muscle Flaps
Sensory Flap
Combination Flaps
Prelaminated and Prefabricated Flaps
Distally Based Flaps and Reverse-Flow Flaps
Reverse Transposition Flap
Venous Flaps
Microvascular Composite Tissue Transplantation
The use of flaps with an intact blood supply has rev-
olutionized the field of plastic surgery. Today, the recon-
structive plastic surgeon faced with a soft tissue defect
has a plethora of options. The muscle flap, the mus-
culocutaneous flap, the fasciocutaneous flap, and the
various techniques of microvascular composite tissue
transplantation have made possible major advances
in the field of plastic surgery. By applying a precise
knowledge of the anatomy of skin, muscle, bone, and
fascia in planning reconstructive procedures, the
surgeon has the ability to restore form and function
in congenital and acquired defects in most topographic
regions.
Modifications and refinements in flap design offer
considerable variety and versatility in the techniques
available for use in reconstructive surgery. By appli-
cation of the principles of flap design and technique,
it is possible to simplify the approach to the surgical
defect. Coverage, form, and function are the three most
important factors in determining a successful outcome.
Through careful analysis of each individual surgical
defect, the most appropriate method of reconstruc-
tion can be selected. This chapter reviews flap
classification and gives examples of their application.
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FLAP APPLICATIONS
Advantages and Disadvantages of Muscle and
Musculocutaneous Flaps
Advantages and Disadvantages of Fascial and
Fasciocutaneous Flaps
Flap Transposition and Arc of Rotation
Prediction of Skin Territory
Selection of Specific Muscle and Musculocutaneous
Flaps
Selection of Specific Fascial and Fasciocutaneous
Flaps
Regional Application of Muscle and
Musculocutaneous Flaps
PREOPERATIVE AND POSTOPERATIVE MANAGEMENT
Positioning of the Patient
Flap Monitoring Techniques
Complications
HISTORY
The use of flaps for reconstructive plastic surgery dates
to 600 BC, when the earliest recorded application of
pedicled flaps for nasal reconstruction is attributed to
the Sushruta Samhita (translated by Bhishagratna 1 in
1916). The earliest flaps centered on the head and neck
as well as the lower extremity because wounds in these
regions failed to heal by secondary intention. The initial
flaps used would now be considered random-pattern
flaps; they were not based on a specific blood supply
and were used without an understanding of how and
why they worked. Tagliacozzi2 used a distally based
arm flap in a two-staged procedure. His work was pub-
lished in Venice in 1597. Much of this knowledge was
forgotten until the 19th century, when the English
surgeon Carpue 3 successfully used forehead flaps to
reconstruct the noses of two officers. The publication
of Rhinoplastik by von Graefe4 in 1818 further advanced
the use of these techniques. Attention in the early 20th
century remained focused on tubed random flaps. It
was found that the only way to increase survival of
these flaps was to perform a surgical delay. A German
anatomist, Carl Manchot, 5 demonstrated the concept
365
366 • GENERAL PRINCIPLES

of anatomic skin territories SLipplied by consistent
vessels in Die Hautarterien des menschlichen Korpers,
published in 1889. Tansini6 described the island of the
latissimus dorsi musculocutaneous flap in 1906.
Davis,7 crediting Manchot, demonstrated axial and
pedicle muscle and fascial flaps as well as composite
flaps in 1919. McGregor8 introduced the temporalis
flap, which allowed midface and lower face coverage
without the donor site deformity associated with the
previously popular forehead flap. Coverage of the lower
third of the face as well as of oral and esophageal defects
was accomplished by Bakamjian9 with the use of the
deltopectoral flap. The availability of the forehead, tem-
poralis, and deltopectoral flaps changed the approach
to head and neck cancer extirpative surgery with a new
emphasis on immediate reconstruction.
The muscle flap for lower extremity reconstruction
was initially described by Stark10 for coverage of
debridement sites for osteomyelitis. Unfortunately, this
report went unnoticed until Ger" recognized that
the leg muscles are a source of well-vascularized tissue
for leg coverage. Although Owens,12 in 1955, used a
compound flap consisting of the sternocleidomastoid
muscle with overlying skin for head and neck recon-
struction, the concept of musculocutaneous perforat-
ing vessels providing a cutaneous territory for
superficial muscles was first reported by Orticochea13
in 1972. Shortly thereafter, surgeons made significant
contributions toward definition of flaps, expansion,
and use of muscle and musculocutaneous flaps in
reconstructive surgery., Significant contributions
included the concept of cutaneous territory of
superficial muscles14; anatomy of the muscles includ-
ing specific arcs of rotation15,16; applications of muscle
and musculocutaneous flaps for breast,17 chest,18
extremity,19 and head and neck reconstruction20,21; and
microsurgical transplantation. 22 In 1981, Ponten23
recognized the input of septocutaneous perforating
vessels to overlying skin circulation. On the basis of
this observation, the concept of fasciocutaneous flaps
was introduced. Like the muscle flap, the septocuta-
neous flap was initially described in the lower extrem-
ity, but the principle of the fasciocutaneous flap,
based on muscle, fascia, and associated cutaneous
territories, was rapidly applied to all body regions
(Table 16-1).
Starting in the late 1970s, a proliferation of inno-
vative techniques reported in the surgical literature
throughout the world defined new anatomic data and
applications of the muscle, musculocutaneous, fascial,
and fasciocutaneous flap systems. Many of these flap
innovations are cited throughout this new edition
of Plastic Surgery. These advances in flap definition
and application have changed the entire approach to
plastic surgery. With the isolation of the vascular pedi-
cles to muscle- and fascia-based flaps, microsurgical
transplantation may be selected when the ideal flap
is outside of a traditional and safe arc of rotation to
the recipient site (site of reconstruction). With the
definition of musculocutaneous and fasciocutaneous
territories, an expander may be used to enlarge flap
dimensions and still ensure direct closure of the donor
site. The reconstructive ladder,24 introduced in 1982,
was appropriate for use in choosing reconstructive
methods that ensure safety in the reconstructive
process. Now, ideal form and function can be achieved
by complex procedures without compromising safety.
Furthermore, donor site deformity is frequently
avoided because the flap can be precisely tailored or
expanded to fit the defect. In 1997, the reconstructive
triangle was introduced.25 The surgeon may choose the
transposition flap, microsurgical transplantation, or
tissue expansion with the goals of achieving form and
function at the recipient site, avoiding donor site defor-
mity, and providing safety throughout the recon-
structive endeavor. The following information traces

TABLE 16-1 • TIMELINE OF THE DEVELOPMENT OF FLAP SURGERY

600 BC Sushruta Samhita' Pedicle flaps in the face and forehead for nasal reconstruction
1597 Tagliacozzi2 Nasal reconstruction by tubed pedicle flap from arm; described "delay"
of pedicle flap
1896 Tansini157 Latissimus dorsi musculocutaneous flap for breast reconstruction
(post-mastectomy)
1920 Gillies"9 Tubed pedicle flap
1946 Stark10 Muscle flaps for osteomyelitis
1955 Owens12 Compound neck flap
1963 McGregor8 Temporalis flap
1965 Bakamjian530 Deltopectoral flap
1971 Ger" Lower extremity musculocutaneous flap
1972 McGregor and Jackson551 Groin flap
1972 Orticochea13 Musculocutaneous flaps
1977 McCrawetal 14 Musculocutaneous territories
1981 Mathesand Nahai'6 Classification of muscle flaps based on vascular anatomy
1981 Ponten25 Fasciocutaneous flaps

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image...

16 • FLAP CLASSIFICATION AND APPLICATIONS 367

the development of the flap systems, defines the
vascular anatomy, and provides an overview of flap
classifications and applications. The reconstructive
ladder and the reconstructive triangle are compared,
and this serves as a foundation for the selection of
reconstructive options offered throughout this edition.
FLAP CLASSIFICATION
A flap consists of tissue that is mobilized on the basis
of its vascular anatomy. Flaps can be composed of skin,
skin and fascia, skin and muscle, or skin, muscle, and
bone. Because the circulation to the tissue to be mobi-
lized is crucial for flap survival, the development of
flap techniques has depended on defining the vascu-
lar anatomy of the skin and underlying soft tissue. An
early concept of vascular anatomy as it pertained to
flap surgery was the thought that skin circulation is
based on the longitudinal subdcrmal plexus (Fig. 16-
1). A random-pattern flap based on this subdermal
plexus (Fig. 16-2) was designed to allow elevation of
a rectangular flap of skin and subcutaneous tissue with
a length-to-width ratio in the range of 2 to 1.5:1.
Although limited in its reach, the random-pattern flap
can be elevated and rotated to provide viable skin and
subcutaneous tissue to cover an adjacent wound.
Common flaps based on the subdermal plexus include
the bipedicle flap, advancement flaps (i.e., V to Y), and
rotation or transposition flaps (Fig. 16-3).
Historically, attempts to use a random-pattern flap
based on subdermal circulation distant from the
wound site eventually resulted in the introduction of
the tubed pedicle flap. Through a series of delays with
use of the initial bipedicle flap design, the arc of rota-
tion of the skin flap was increased. Alternatively, the
flap was attached to an arm carrier, which later
required shifting the arm carrier of the random-pattern
flap from one body region (donor site) to another
(recipient site) (Fig. 16-4). This use of the random-
pattern flap with multiple delays or the arm carrier
allowed reconstruction of distant complex defects, par-
ticularly in the head and neck region, and coverage of
composite wounds when local tissue was unavailable
or severely damaged. Despite this, the random-pattern
flap provided no new source of circulation on trans-
fer to a distant site. Thus, the success of these flaps ulti-
mately depended on the local wound environment for
nourishment.
Other restrictions of random flaps include the
limited arc of rotation, the proximity of the flap to
the wound, and the associated zone of injury and
decreased bacterial resistance.26 Given the vascular
limitations of the random-pattern flap, investigators
attempted different means by which to maximize the
potential area of a flap, which led to the concept of
flap delay. Although the delay procedure has been used
for several hundred years, it was not until the early
1900s that the concept was recognized- Blair intro-
duced the term delayed transfer in 1921.27 In the 16th
century, Tagliacozzi delayed his upper arm flaps by
making parallel incisions through the skin and sub-
cutaneous tissue overlying the biceps muscle. In 1965,

SKIN CIRCULATION

Subepidermal
Dermal

Subdermal
- Plexuses
Subcutaneous
Fascia Prefascial and
subfascial
Muscle

Musculocutaneous
artery

R
!lTa' Septocutaneous
artery artery
FIGURE 1 6 - 1 . Skin circulation. Because circulation to the transferred tissue is crucial for flap design and sur-
vival, the development of flap techniques has depended on defining the vascular anatomy of skin and underlying
soft tissue. (From Mathes SJ, Nahai F: Reconstructive Surgery: Principles, Anatomy, and Technique. New York,
Churchill Livingstone. 1997.)

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368 I • GENERAL PRINCIPLES

A
Subdermal plexus
(note outline of flap design with Standard arc of rotation
2:1 length:width ratio)
FIGURE 1 6-2. Random-pattern flap. Initially, the subdermal plexus was considered the source of blood supply to
the skin. This network of arterial and venous channels is oriented parallel and adjacent to the skin surface. A random-
pattern flap based on this subdermal plexus was developed to allow elevation of a rectangular flap with a length-to-
width ratio of approximately 2 : 1 . Although limited in reach, this flap could be elevated and rotated to provide viable
skin and subcutaneous tissue to close an adjacent wound. (From Mathes SJ, Nahai F: Reconstructive Surgery: Princi-
ples, Anatomy, and Technique. New York, Churchill Livingstone, 1997.)

using the pig model, Milton 38 investigated the effec-
tiveness of four different methods of delaying a flap.
He found that in developing a bipedicled flap, the best
form of delay was by making two incisions and under-
mining the skin between the incisions. The goal of a
delayed flap is to enhance flap circulation, ensuring
flap survival after advancement, transposition, or
transplantation to a defect site. Flap delay may be used
to increase circulation to the muscle or fascia or to
enhance vascular connections to the overlying cuta-
neous territory or adjacent structures to be included
during flap elevations (tendon, fascia, and bone).
Although delay may be accomplished by biochemical
means to improve flap perfusion, currently the most
effective method to ensure delay is surgical manipu-
lation of the flap. To date, no pharmacologic method
has surpassed the reproducibility of stirgical delay and
the degree to which surgical delay protects against flap
necrosis. 29 There are two theories that describe the
potential mechanism by which the delay phenome-
non prevents skin necrosis. The first is that delay accli-
matizes the flap to ischemia (tolerance), permitting it
to survive with less blood flow than would normally
be required. This theory suggests that vascular delay
causes adaptive metabolic changes at a cellular level
within the tissue.30 The second theory is that delay
improves vascularity by increasing flow through pre-
existing vessels, reorganizing the pattern of blood flow
to more ischemic areas.31,32 On the basis of experi-
mental data, it appears that both of these mechanisms,
either directly or indirectly, contribute to the beneficial
effects of surgical delay. Regardless of the underlying
mechanisms, most experimental work on surgical delay
demonstrates changes at the microcirculatory level.33,34
Surgical flap delay is accomplished in two ways:
standard delay, with an incision at the periphery of
the cutaneous territory or partial flap elevation; and
strategic delay, with division of selected pedicles to the
flap to enhance perfusion through the remaining
pedicle or pedicles.
The technical aspects of standard surgical delay to
enhance circulation are straightforward. The flap
cutaneous territory is outlined, and incisions are
made through all or part of the border of a planned
cutaneous territory (Fig. 16-5). Minimal to partial flap
undermining is performed. The incisions are then
closed. The flap is then elevated after 10 to 14 days. It
has been shown that after 1 week, the blood flow into
the area of delay reaches a maximum. 35
Strategic pedicle delay is accomplished by making
incisions at the border of the planned flap cutaneous
territory. The dissection is deep to either muscle or
fascia, depending on the flap type, to reach pedicles
entering the flap territory. These pedicles are divided

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16 • FLAP CLASSIFICATION AND APPLICATIONS 369

BIPEDICLE FLAP DELAY

Bipedicle delay completed

(note outline of distal
flap division site) Standard arc of rotation
A

ADVANCEMENT FLAP ROTATION FLAP

Rotation Inset

Design of V-Y flap V-Y flap advancement

B
FIGURE 1 6 - 3 . A, Illustration of bipedicle flap delay technique. B, Advancement flap. Note donor site closed
directly. Flap based on underlying perforator vasculature. C, Rotation flap. Note back cut at base of flap or skin
graft for donor site closure. {From Mathes SJ, Nahai F: Reconstructive Surgery: Principles, Anatomy, and Tech-
nique. New York, Churchill Livingstone, 1997.)

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370 I • GENERAL PRINCIPLES

Flap design with flap inset Flap inset on arm carrier Arm carrier transfers chest flap
on upper extremity skin graft to recipient site
B
C

Flap inset on lower Flap base division and

extremity defect final flap inset
E
FIGURE 1 6-4. A to E, Historically, attempts to use a random-pattern flap based on subdermal circulation distant
from the wound site eventually resulted in the introduction of the tubed pedicle flap. The arc of rotation of the skin
flap was increased through a series of delays, or alternatively, the flap was attached to an arm carrier. The flap was
subsequently shifted from the donor site to the recipient site. (From Mathes SJ, Nahai F: Reconstructive Surgery:
Principles, Anatomy, and Technique. New York, Churchill Livingstone, 1997.)

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16 • FLAP CLASSIFICATION AND APPLICATIONS 371

Cutaneous
territory of flap

Delay incision

Delay incision
with partial distal
flap elevation

7
Delay incision
B
FIGURE 1 6 - 5 . Standard delay flap modification. A, Flap cutaneous territory. B, Parallel inci-
sions for flap delay. C, Parallel flap undermining for flap delay. (From Mathes SJ, Nahai F: Recon-
structive Surgery: Principles, Anatomy, and Technique. New York, Churchill Livingstone, 1997.]

and the incision is closed. Second-stage flap elevation
is performed after a 2-week period. Effectiveness of
strategic delay based on ligation of the dominant vas-
cular pedicle was initially demonstrated in the Con-
verse model of the gracilis musculocutaneous flap. 36
This type of delay is usually advocated in patients with
risk factors for flap ischemia (i.e., smoking history,
obesity, radiation therapy, abdominal scar). An example
of an indication for a strategic surgical delay would be
a patient who is to undergo breast reconstruction with
a TRAM flap. It has been shown that high-risk patients
benefit from surgical delay.37 In addition, it has been
shown that delay potentially reduces the incidence of
abdominal wall complications. 38 New techniques for
strategic delay are designed to minimize incision length
and procedure-related morbidity. Endoscopic tech-
niques may allow visualization and division of pedi-
cles with minimal incisions. Interventional radiology
techniques may also be used to occlude dominant or
secondary pedicles to the flap territory to enhance per-
fusion to the remaining flap pedicles.
Although important historically, the delay technique
is used less frequently because of the development of
better techniques, including axial, musculocutaneous,
fasciocutaneous, transposition, and microvascular
free flaps. As with the random-pattern flap, the limi-
tation of the delayed flap is that a parallel blood supply
is not efficient. Flap delay also has disadvantages: a pre-
liminary operation is required; inadvertent injury to
the desired pedicle for flap design is possible; and result-
ant scar tissue at the site of flap delay may impair
subsequent manipulation and inset of the flap at the
recipient site.
The delay phenomenon may occur in part from
a sympatholytic state that results from cutting the
sympathetic innervation to the vasculature and the
subsequent vasodilatation. Drugs that block vaso-
constriction or those that vasodilate may be of theo-
retical value. Attempts have been made to stimulate
the delay phenomenon pharmacologically by manip-
ulating the autonomic nervous system.39 Although
pharmacologic delay is of theoretical importance,
additional studies need to be done to prove its
effectiveness.
The erroneous concept that skin circulation is based
on a longitudinal vascular network independent of
deeper structures delayed the search for new flaps. A
few isolated areas with direct cutaneous vessels allowed
flap elevation without the 2:1 length-to-width ratio
restriction (e.g., median forehead flap). However, the
need for longer flaps without a requisite delay proce-
dure resulted in the identification of flaps with specific
vascular territories based on the course of the superficial
vascular pedicles with an axial alignment (Fig. 16-6).
Axial flaps based on this concept include the lateral
forehead (superficial temporal artery), deltopectoral
(internal mammary branches), superficial groin
(superficial circumflex iliac artery), and dorsal foot
(dorsalis pedis artery) flaps. The development of these
axial flaps has had a tremendous impact on recon-
struction, particularly in the head and neck and upper
extremity.
The longer, nondelayed axial flaps made immedi-
ate reconstruction of defects possible in the head and
neck, groin, and upper extremity and spurred the search
for new flaps based on consistent vascular pedicles in

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372 I • GENERAL PRINCIPLES

Arc to frontal skull

A B
FIGURE 16-6. A, An axial-pattern flap may be based on the superficial temporal artery (D) and its branches. B, An
axial flap based on the superficial temporal artery and parietal branch (temporoparietal flap) may be used to recon-
struct forehead defects. (From Mathes SJ. Nahai F: Reconstructive Surgery: Principles, Anatomy, and Technique. New
York, Churchill Livingstone, 1997.)

the trunk and extremities. Muscle was soon identified
as a source of tissue that could be detached from its
normal origin or insertion and transposed as a flap
based on its major (dominant) vascular supply (Fig.
16-7A). Further analysis of skin circulation, through
anatomic and clinical research, revealed that there
are important musculocutaneous perforator vessels
supplying the overlying skin, altering the approach to
flap design (Fig. 16-7B).'3''5 This eventually led to the
concept that muscles and fascia have distinct vascular
pedicles. The success of muscle flaps in reconstructive
surgery is based on reliable blood supply. With knowl-
edge of the location and subsequent preservation of
the vascular pedicles to muscles, every muscle may be
rotated as a flap.
Muscle and Musculocutaneous
Flaps
In 1981, Mathes and Nahai16 described a classification
system for muscles based on the following anatomic
relationships between the muscle and its vascular
pedicles:
• the regional source of the pedicle entering the
muscle;
• the number and size of the pedicle;
• the location of the pedicle with respect to the
muscle's origin and insertion; and
• the angiographic patterns of the intramuscular
vessels.
This classification system enables the surgeon to cat-
egorize the various muscle and musculocutaneous flaps
into distinctly different, clinically applicable groups
based on the vascular anatomy. There are hwe differ-
ent vascular patterns by which the various muscles are
categorized (Fig. 16-8).
TYPE I: ONE VASCULAR PEDICLE
Type I muscles are supplied by a single vascular pedicle
(Table 16-2).
TYPE II: DOMINANT VASCULAR PEDICLE
A N D MINOR PEDICLE
Type II muscles are supplied by both a dominant and
minor vascular pedicle. The larger dominant vascular

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16 • FLAP CLASSIFICATION AND APPLICATIONS 373

of muscle flap

Muscle flap arc of rotation Musculocutaneous flap arc of rotation

B
FIGURE 1 6-7. A, Design of muscle flap. B, Muscle flap arc of rotation. C, Musculocutaneous flap arc of rotation,
(From Mathes SJ, Nahai F: Reconstructive Surgery: Principles, Anatomy, and Technique. New York, Churchill Living-
stone, 1997.)

pedicle will usually sustain circulation to these muscles dominant vascular pedicles. This vascular pattern
after the elevation of the flap when the minor pedicles permits the muscle to be split, allowing the use of only
are divided. This is the most common pattern of cir- part of the muscle as a muscle or musculocutaneous
culation observed in human muscle (Table 16-3). flap (Table 16-4).

TYPE III: TWO D O M I N A N T PEDICLES TYPE IV: SEGMENTAL VASCULAR

Type III muscles possess two large vascular pedicles
from separate vascular sources. These pedicles either
have a separate regional source of circulation or are
located on opposite sides of the muscle. Division of
one pedicle during flap elevation rarely results in
loss of muscle within its vascular distribution. The
entire muscle will usually survive on one of its two
PEDICLES
Typ? IV muscles are supplied by segmental vascular
pedicles entering along the course of the muscle belly.
Each pedicle provides circulation to a segment of the
muscle. Division of more than two or three of the pedi-
cles during elevation as a flap may result in distal muscle
necrosis (Table 16-5).

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374 I • GENERAL PRINCIPLES

Type IV

Type

~ ^ > ^ ' ^ ' /%

Gluteus maximus

Tensor fascia lata Gracilis Sartorius Lattssimus dorsi

FIGURE 1 6-8. Mathes-Nahai classification of muscle and musculocutaneous flaps. Patterns of vascular anatomy:
type I, one vascular pedicle; type II, dominant pedicle and minor pedicle; type III, two dominant pedicles; type IV, seg-
mental vascular pedicles; type V, one dominant pedicle and secondary segmental pedicles. (From Mathes SJ, Nahai F:
Classification of the vascular anatomy of muscles: experimental and clinical correlation. Plast Reconstr Surg 1981 ;67:177.)

TYPE V: ONE DOMINANT VASCULAR
PEDICLE AND SECONDARY SEGMENTAL
VASCULAR PEDICLES
Type V muscles are supplied by a single dominant
pedicle and secondary segmental vascular pedicles.
These muscles have one large dominant vascular
pedicle near the insertion of the muscle with several
segmental pedicles near the origin. The internal
vasculature can be supplied by either the dominant
or the segmental pedicles, and therefore the muscle
may be elevated as a flap on either vascular system
(Table 16-6).
Fascial and Fasciocutaneous Flaps
A growing knowledge of the source of skin circulation
after the recognition of the muscle and musculocuta-
neous system led to the identification of vascular pedi-
cles emerging between muscles (septocutaneous

TABLE 16-3 • TYPE II VASCULAR PATTERN

MUSCLES
TABLE 1 6-2 • TYPE ! VASCULAR PATTERN
MUSCLES Abductor digiti minimi (foot)
Abductor hallucis
Abductor digiti minimi (hand) Brachioradialis
Abductor pollicis brevis Coracobrachialis
Anconeus Flexor carpi ulnaris
Colon Flexor digitorum brevis
Deep circumflex iliac artery Gracilis
Hamstring (biceps femoris)
First dorsal interosseous
Peroneus brevis
Gastrocnemius, medial and lateral Peroneus longus
Genioglossus Platysma
Hyoglossus Rectus femoris
Jejunum Soleus
Longitudinalis linguae Sternocleidomastoid
Styloglossus
Tensor fascia lata Trapezius
Transversus and verticalis linguae Triceps
Vastus lateralis Vastus medialis

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16 • FLAP CLASSIFICATION AND APPLICATIONS 375

TABLE 16-4 • TYPE III VASCULAR PATTERN TABLE 1 6-6 • TYPE V VASCULAR PATTERN
MUSCLES MUSCLES

Gluteus maximus Fibula

Intercostal Internal oblique
Omentum Latissimus dorsi
Orbicularis oris Pectoralis major
Pectoralis minor
Rectus abdominis
Serratus anterior
Temporalis

perforators or direct septocutaneous branches of

pedicles) and entering the deep fascia. Elevation of the
skin with its deep fascia represented a new vascular
basis for flap design.
A fascial flap consists of fascia detached from its
normal origin or insertion and transposed to another
location (Fig. 16-9). Without the overlying skin and
fat, this represents a delicate flap. A fasciocutaneous
flap, originally called an axial flap, includes the skin,
subcutaneous tissue, and underlying fascia, which may
be distinct from the fascia covering the underlying
muscle (Fig. 16-10). The vascular supply is derived
at the base of the flap from musculocutaneous
TABLE 16-5 • TYPE IV VASCULAR PATTERN
MUSCLES
Extensor digitorum longus
Extensor hallucis longus
External oblique
Flexor digitorum longus
Flexor hallucis longus
Sartorius
Tibialis anterior
major arteries.
The first fascial and fasciocutaneous flaps were
described by Ponten 23 in 1981 for lower extremity
reconstruction and by Tolhurst40 in 1983 for trunk and
axillary reconstruction. Investigations have shown the
fasciocutaneous system to consist of perforating vessels
that arise from regional arteries and pass along the
fibrous septa between muscle bellies or muscle com-
partments. The vessels then spread out at the level of
the deep fascia, both above and below, to form
plexuses, which in turn give off branches to the skin.
In 1975, Schafer41 found three major vascular systems
of the deep fascia: perforating arteries from underly-
ing muscle giving off several radiating branches,
which perforate the fascia before continuing to the
subdermal plexus; subcutaneous arteries running in
the fat and anastomosing frequently with the superficial
plexus of the deep fascia and with each other; and sub-
fascial arteries arising from the intermuscular septa
and running in the loose areolar tissue beneath the
deep fascia and adjoining the deep and superficial
plexus.
These pedicles consist of an artery (generally a
branch of the artery to the specific anatomic region of
the fascia and regional musculature) and paired venae
comitantes that drain into corresponding major

FIGURE 16-9. Fascial flap arc of rotation. A

fascial flap consists of fascia detached from its
normal origin or insertion and transposed to
another location. (From Mathes SJ, Nahai F:
Reconstructive Surgery: Principles, Anatomy,
and Technique. New York, Churchill Livingstone,
1997.) Fascial flap arc of rotation

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376 • CENERAL PRINCIPLES

FIGURE 16-10. Fasciocutaneous flap arc of

Fasciocutaneous flap arc of rotation
rotation. A fasciocutaneous flap, originally called
an axial flap, includes the skin, subcutaneous
tissue, and underlying fascia, which may be dis-
tinct from the fascia covering the underlying
muscle. (From Mathes SJ, Nahai F: Reconstruc-
tive Surgery: Principles, Anatomy, and Technique.
New York, Churchill Livingstone, 1997.}

regional veins. Direct cutaneous and septocutaneous
pedicles are fairly constant in location. There is a greater
variability in location of the musculocutaneous per-
forators. These pedicles provide a vascular basis for
specific fascial or fasciocutaneous flaps. On this basis,
Mathes and Nahai have classified fascial and fascio-
cutaneous flaps as types A, B, and C (Fig. 16-11).25
Anatomic studies demonstrate that the type A fas-
ciocutaneous flaps have a vascular pedicle to the deep
fascia that emerges from a regional source coursing
initially beneath the deep fascia and eventually con-
tinuing superficial to the deep fascia. This pedicle
provides numerous fasciocutaneous perforators to the
skin. Because the pedicle tends to course in a radial

MATHES-NAHAI CLASSIFICATION OF FASCIA/ FASCIOCUTANEOUS FLAPS

Type A
TypeB

TypeC

FIGURE 1 6-1 1. Mathes-Nahai classification of fascial and fasciocutaneous flaps. Patterns of vascular anatomy: type
A, direct cutaneous pedicle; type B, septocutaneous pedicle; type C, musculocutaneous pedicle. (From Mathes SJ,
Nahai F: Reconstructive Surgery: Principles, Anatomy, and Technique. New York, Churchill Livingstone, 1997.)

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16 • FLAP CLASSIFICATION AND APPLICATIONS 377

TABLE 16-7 • TYPE A FASCIAL AND TABLE 16-9 • TYPE C FASCIAL AND
FASCIOCUTANEOUS FLAPS FASCIOCUTANEOUS FLAPS

Deep external pudendal artery Anterior lateral thigh

Digital artery Deltopectoral
Dorsal metacarpal artery Nasolabial
Clutealthigh Median forehead
Great toe (hallux) Thoracoepigastric (transverse abdominal)
Groin Transverse back
Lateral thoracic (axillary)
Pudendal—thigh
Saphenous
Scalp
Second toe
Standard forehead the deep fascia and cutaneous circulation. The design
Superficial external pudendal artery of a fasciocutaneous flap can be based on these dom-
Superficial inferior epigastric artery inant perforating vessels without incorporation of the
Sural artery underlying muscle; this vascular pattern represents the
Temporoparietal fascia type C fasciocutaneous flap. However, increasing
pedicle length will necessitate proximal dissection of
the pedicle through muscle to its regional source or
incorporation of all or part of the muscle in the flap
fashion from its regional source into its distal cuta- design. Type C flaps are generally the anatomic model
neous distribution, the flap is often referred to as an used for the perforator flap in microsurgical compos-
axial flap. The long, relatively superficial course of the ite tissue transplantation (Table 16-9).
dominant pedicle permits evaluation by palpation or Cormack and Lamberty42 also classified fasciocu-
Doppler probe (Table 16-7). taneous flaps based on vascular anatomy. The type A
The type B fasciocutaneous flap has a septocuta- flap is supplied by multiple fasciocutaneous perfora-
neous pedicle, which courses between major muscle tors that enter at the base of the flap and extend
groups in an intermuscular septum or between adja- throughout the longitudinal length. The flap can be
cent muscles. This pedicle is located within the inter- based proximally, distally, or as an island. The type B
muscular septum or the potential space between flap has a single fasciocutaneous perforator, which is
adjacent muscles and supplies a regional fascial vas- of moderate size and is fairly consistent. It is intended
cular system. The largest septocutaneous pedicles are for use as a free flap. The type C flap is based on mul-
dominant pedicles to specific fasciocutaneous flaps and tiple small perforators that run along a fascial septum.
are fairly constant in location (Table 16-8). The supplying artery is included within the flap. It may
In certain regions, larger musculocutaneous per- be based proximally, distally, or as a free flap. The type
forators enter the deep fascia and contribute to both D flap is an osteomusculofasciocutaneous flap and is
based on multiple small perforators, similar to the type
C flap, but also includes a portion of adjacent muscle
and bone. It may be based proximally or distally on a
TABLE 16-8 • TYPE B FASCIAL AND
pedicle or used for microvascular composite tissue
FASCIOCUTANEOUS FLAPS
transplantation (Fig. 16-12).
Anterior lateral thigh
Anterior tibial artery
Deltoid
Perforator Flaps
Dorsalis pedis Further refinements in flap application have led to the
Inferior cubital artery (antecubital) development of perforator flaps. Perforator flaps have
Lateral arm
Lateral plantar artery evolved from musculocutaneous and fasciocutaneous
Lateral thigh flaps without the muscle or fascial carrier. It has been
Medial arm shown that neither a passive muscle carrier nor the
Medial plantar artery underlying fascial plexus of vessels is necessary for flap
Medial thigh survival.43 Advantages of perforator flaps include less
Peroneal artery donor site morbidity, versatility in flap design, muscle
Posterior interosseous sparing (less functional deficit), and improved post-
Posterior tibial artery
Radial forearm operative recovery of the patient.44'47 Disadvantages
Radial recurrent of perforator flaps include the meticulous dissection
Scapular needed to isolate the perforator vessels (resulting
Ulnar recurrent in increased operative time), the variability in the

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378 I • GENERAL PRINCIPLES

General scheme of vascularization

Vascular plexus of the
deep fascia supplying
overlying skin
Fasciocutaneous perforators Subcutaneous vein draining
lying in intermuscular the skin through the
fascial septum superficial venous system
Muscle belly - generally long, thin muscles

Venae comitantes of regional artery

Major regional artery May also receive veins draining down
along fascial septum

Type A -
Type A subcutaneous
pedicle

TypeB
B-modified

TypeC Type

FIGURE 1 6 - 1 2 . A classification of fasciocutaneous flaps. (From Cormack GC, Lamberty BG: The Arterial
Anatomy of Skin Flaps. Edinburgh, Churchill Livingstone, 1986.)

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f image...
16 • FLAP CLASSIFICATION AND APPLICATIONS
TABLE 1 6 - 1 0 • ABDOMINAL VISCERAL FLAP CLASSIFICATION
Flap Type Circulation Pattern
Colon Bowel Type I
Jejunum Bowel Type I
Omentum Omentum Type III
position and size of the perforator vessels, and the ease
with which the vessels can be damaged.48"50
The nomenclature of perforator flaps is confusing
and oftentimes misstated. Perforator flaps have been
designated by their location (e.g., anterolateral thigh
flap), arterial supply (e.g., deep inferior epigastric artery
perforator flap), or muscle of origin (e.g., gastrocne-
mius perforator flap). It has been suggested by Geddes
et al44 that the nomenclature of perforator flaps be stan-
dardized by describing all perforator flaps according
to the main artery of origin. In this system, cutaneous
flaps are divided into either cutaneous flaps or mus-
culocutaneous perforator flaps. Cutaneous flaps
include those previously described as axial, septocu-
taneous, and fasciocutaneous (type A and B fasciocu-
taneous flaps according to Mathes and Nahai).
Musculocutaneous perforator flaps are the type C fas-
ciocutaneous flaps according to Mathes and Nahai,
in which the pedicle to the perforator flap is the dom-
inant or major pedicle to the muscle with its perfora-
tor vessel passing through the muscle to the overlying
fascia, subcutaneous tissue, and skin. Because the
muscle is excluded from the flap, the perforator flap
is anatomically a type C fasciocutaneous flap.
There are many perforator flaps currently used and
others that are of theoretical value. As studied closely
by Taylor and Palmer,51 there are many named perfo-
rating vessels to each angiosome of the body. Accept-
able perforator flap donor sites have four common
features: predictable and consistent blood supply, at
least one large (diameter > 0.5 mm) perforating vessel,
sufficient pedicle length for the required anastomo-
sis, and ability to close the donor site primarily. Com-
monly used perforator flaps are the deep inferior
epigastric artery perforator flap, superior gluteal artery
perforator flap, thoracodorsal artery perforator flap,
anterolateral thigh perforator flap, tensor fascia lata
perforator flap, and medial sural artery perforator
flap.43'44'52'55
Abdominal Visceral Flaps
The abdominal viscera are not easily classified; however,
for the purposes of flap transposition or microvascu-
lar tissue transplantation, the colon, jejunum, and
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379
Size
20 to 25 cm in length
Lumen diameter of 8 cm
7 to 25 cm may be transferred on one pedicle
Lumen diameter of 3 to 5 cm
Variable; up to 40 x 60 cm
omentum fall conveniently into the muscle
classification system (Table 16-10). For microvascular
transplantation, the segment of bowel (jejunum or
colon) is elevated on one vascular arcade with a single
dominant vessel, a type I pattern of circulation. In
unusual circumstances when a longer piece of bowel
extends beyond the vascular territory of one arcade,
two vascular arcades must be included to ensure via-
bility of this longer segment of bowel. In this instance,
the pattern of circulation is type HI (two dominant
arcades or pedicles). It is possible to reconstruct the
esophagus from the base of the tongue to the stomach
with a long segment of jejunum where one pedicle is
revascularized in the upper chest or neck and the second
pedicle is left intact. Other uses of the colon or jejunum
as flaps have been for vaginal reconstruction.
The omentum may be based as a transposition flap
on either the right or left gastroepiploic vessels and is
thus classified as having a type III pattern of circula-
tion. The omentum is also commonly transplanted
microsurgically. The omentum can be used to recon-
struct a wide range of extraperitoneal defects and has
been shown to have immunologic and angiogenic
properties.56"58 Although it is useful for reconstruction,
donor site complications can be significant, includ-
ing abdominal wall infection and hernia.59,60 With the
advances in minimally invasive surgery, the abdomi-
nal viscera can successfully be harvested laparoscop-
ically, obviating the need for a large midline incision,
with a better cosmetic result and less donor site
morbidity.6'-63
FLAP MODIFICATIONS
There has been considerable progress in the clinical
application of muscle and musculocutaneous flaps over
the years. Countless modifications and refinements
in both technique and design have been described in
the continuing quest for the optimal result in recon-
structive surgery. These modifications include tissue
expansion, segmental transposition flaps, vascularized
bone flaps, distally based flaps, reverse transposition
flaps, combination flaps, delayed flaps, and prefabri-
cated flaps. The development of specialized tissue flaps
has provided the surgeon with the ability to restore
TfcWttf'fcttHJW image...

380 I • GENERAL PRINCIPLES

sensation, motor function, and bone structure in the Tissue Expansion

surgical defect. With the use of such complex tissues
as innervated muscle, omentum, intestine, joint, digit,
iliac crest, and various long bones, the surgeon can
produce, in the words of McDowell,6"1 "a few harpsi-
chords, rather than so many logs—recognizable, new,
artistic and fully acceptable noses, cheeks, chins,
necks, legs, and arms rather than indistinguishable
globs and blobs of transported tissue in those areas."
Skin and soft tissue adjacent to the defect arc preferred
for the closure of the defect because of the similarity
in skin color, texture, and contour. Design of local
advancement flaps will frequently allow use of adja-
cent tissue, particularly if there is skin excess in the
donor area (Fig. 16-13). A rotation or advancement
flap frequently requires either a back-cut or skin graft

Vastus lateralis

FIGURE 16-1 3. Tensor fascia lata (TFL) flap for abdominal wall reconstruction. A, Anterior view of abdomen demon-
strates extensive defect after resection for synergistic gangrene with skin graft coverage on exposed viscera. B, Lateral
view of extensive abdominal fascial defect. C, Bilateral tissue expanders in place (900 cm5 total saline fill) in territory
of TFL flaps. D, Skin grafts excised from viscera; skin island for TFL flap design (14 x 35 cm). Expander fascia extends
from anterior midline to posterior lateral thigh. E, Diagram of position of expanders beneath the territory of the TFL
and arterial and lateral deep fascia. F, Expander fascia and skin island will reach superior abdomen and allow direct
donor site closure.

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image...

16 • FIAP CLASSIFICATION AND APPLICATIONS 381

FIGURE 1 6 - 1 3 , cont'd. G, Left

TFL musculofasciocutaneous flap
transposed into defect. Expanded
fascial component of flap provides
fascial coverage of abdominal defect
between remaining edges of internal
and external oblique muscles.
H, Postoperative view at 6 months
demonstrates stable coverage and
restoration of fascial continuity over
complex abdominal defect. Donor site
of left leg was closed directly. /, Post-
operative view at 1 year demon-
strates intact fascial reconstruction
of abdominal wall by expanded TFL
flap. J, Lateral view demonstrates
intact abdominal wall fascia. [A, C,
and H from Steinwald PM, Mathes
SJ: Management of the complex
abdominal wall wound. Adv Surg
2001:35:77. C from Mathes SJ,
Steinwald PM, Foster RD, et al:
Complex abdominal wall reconstruc-
tion: a comparison of flap and mesh
closure. Ann Surg 2000:232:586.)

at the donor site. The size of the defect or the sur-
rounding zone of injury often prevents the use of
adjacent tissue, which is frequently not available for
wound closure or composite defect reconstruction. In
lhe.se circumstances, tissue expansion may allow the
use of the desired adjacent tissue for reconstruction.
Tissue expansion is an effective method for enlarging
the cutaneous territory of superficially located muscle
and fascial flaps (Figs. 16-14 and 16-15). Although it
is most commonly used to increase the cutaneous flap
territory, the principle of tissue expansion may also
be applied to all soft tissues, including fascia and
peripheral nerve. Neumann 65 is credited with the first
modern report of this technique in 1957. Radovan 66
further described the use of this technique for breast
reconstruction in 1976.
Technically, the tissue expander is inserted under
the skin as a mechanism for increasing skin dimen-
sions to provide sufficient skin circumference for
designing an advancement or transposition flap. If a
fasciocutaneous flap is planned, the expander is placed
below the deep fascia. If a musculocutaneous flap is
planned, the expander is placed beneath the deep
surface of the muscle. The expander should not be
placed directly beneath the dominant vascular pedicle
at its point of entrance into the flap territory to avoid
injury to the pedicle during the expansion process.
Although immediate skin expansion is possible, delayed

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I • GENERAL PRINCIPLES

skin graft

B
FIGURE 1 6 - 1 4 . A, Design of extended territory of deltopectoral
flap. B, Distal flap elevated from deltoid muscle and Silastic sheet or
expander placed beneath flap for delay technique.

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l W t t f ' t f c f t f W image...

16 • FLAP CLASSIFICATION AND APPLICATIONS 383

~-C<-\>;N

D
FIGURE 16-1 A, cont'd. C, Expander allows dual purpose of flap
delay and increased dimension for distal flap territory. D, Delayed del-
topectoral flap allows increased arc of rotation to midface.
Continued

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384 I • GENERAL PRINCIPLES
skin graft
expansion is usually performed before flap elevation.
During a selected time, usually 6 weeks to 3 months,
the expander is injected with saline at 2-week inter-
vals. Once the desired amount of expansion has been
achieved, the expander is removed and the modified
flap skin territory is recruited for reconstruction.
Safe tissue expansion depends on surgical judgment
regarding its usefulness for a specific problem. The
benefits of local surrounding tissues in reconstructive
surgery are well recognized; however, this tissue is
frequently injured because of its proximity to the
traumatic or surgical defect, obviating the ability to
use this tissue. Failure of tissue expansion is usually
attributable to inadequate stability of skin and
associated soft tissue during the expansion process.
Failure of the expander is signaled by wound dehis-
cence followed by expander exposure and infection.
Unlike failure of flap transposition or transplantation
techniques, expander failure is not generally associ-
ated with increased wound complexity or donor site
problems.67,68
Segmental Transposition Flaps
A muscle can be split, and a portion in continuity with
the dominant or major vascular pedicle can be used
as a transposition flap. Techniques of muscle splitting
to preserve tissue and function have been described.
The remaining muscle with its origin and insertion is
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FIGURE 16-14, cont'd. E, Delayed flap
inset into midface defect. The donor site is
covered with skin grafts at later flap inset. The
proximal flap is returned to the original donor
site.
maintained to preserve function. Alternatively, the
entire muscle may be split and used to cover two defects
simultaneously. Frequently, only a part of the muscle
in proximity to the dominant vascular pedicle is
elevated for microvascular transplantation.
The skin territory may also be modified and split
into two separate skin islands or elevated with only a
segment of the muscle flap. However, the skin terri-
tory must include vascular connections through mus-
culocutaneous perforating vessels from the segmental
flap (Figs. 16-16 and 16-17).
The latissimus dorsi has been described as a muscle
that can be segmentally transferred. This muscle has
a consistent proximal bifurcation of its neurovascular
supply into a medial and lateral subunit. For example,
in the reconstruction of the cervical esophagus, the
latissimus dorsi musculocutaneous flap can be split
into two skin paddles that can be used for lining
and skin coverage.,6,25,69"71 Segmental latissimus dorsi
transfer has also been used in facial reanimation and
for coverage of long soft tissue defects of the lower
extremity.72"74
The basis for splitting the pectoralis major muscle
was demonstrated by Tobin75 in 1985. The pectoralis
has three segmental neurovascular subunits: the
clavicular, the sternocostal, and the external subunit.
These can be surgically split and independently trans-
ferred on vascular pedicles from the thoracoacromial,
internal mammary, and lateral thoracic vessels.76
 linage...

16 • FLAP CLASSIFICATION AND APPLICATIONS 385

FIGURE 1 6-1 5. Delayed deltopectoral flap for left midfacial reconstruc-

tion. A, Patient with Corlin syndrome (nevoid basal cell carcinoma syndrome).
Left midface resection is planned for extensive basal cell carcinoma. B, Flap
delayed with elevation of extended flap territory over deltoid muscle. C, Six
weeks after delay flap elevated. D, Flap base preserves fasciocutaneous per-
forating vessels (type C) from internal mammary vessels. £, Extended arc of
rotation allows flap inset into midface. F, Postoperative view at 2 years. The
patient subsequently underwent resection of basal cell carcinoma of the right
lower third of the face with immediate reconstruction with right pectoralis
major musculocutaneous flaps. Note thin coverage of left midface provided
by deltopectoral fasciocutaneous flap, as compared with the bulk and less
optimal color match associated with a right pectoralis major skin island.
Continued

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T^Wttf'SdtfMf image..

386 • GENERAL PRINCIPLES

FIGURE 16-15, cont'd. G, Donor site delayed for deltopectoral flap demonstrates stable coverage provided by
skin grafts distally and reinset at medial two thirds of flap proximally. H, Lateral view reveals midface coverage with
deltopectoral flap. /, Right lateral view reveals lower third face coverage with pectoralis major musculocutaneous flap.

Arc to sacrum Arc to sacrum

B
FIGURE 16-16. Gluteus maximus segmental muscle transposition. A, Superiorhalfofgluteusmaximus
muscle (arc to sacrum). B, Inferior half of gluteus maximus muscle. (From Mathes SJ, Nahai F: Recon-
structive Surgery: Principles, Anatomy, and Technique. New York, Churchill Livingstone, 1997.)

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image...

6 • FLAP CLASSIFICATION AND APPLICATIONS 387

A B

FIGURE 1 6 - 1 7 . Function preservation muscle flap design.

A, Chronic sinus track communicates with spinal canal at site
of prior myelomeningocele closure. The patient has recur-
rent episodes of meningitis. B, Sinus track excised. The supe-
rior half of the gluteus maximus muscle is elevated as a flap
based on superior gluteal vessels. The inferior half of the
muscle's origin, insertion, innervation, and pedicle (inferior
gluteal vessels) is preserved. C, Superior gluteal muscle flap
arc of rotation into sacral defect. D, Muscle flap inset into
defect donor site and overlying skin closed directly. E, Post-
operative view at 3 years demonstrates successful closure
of defect with stable coverage and no further infections. Note
donor site closure of superior right buttock.

Splitting of the pectoralis major muscle into segments Vascularized Bone

has been performed when the segmental transfer of
a single intercostal portion of the pectoralis muscle,
based on a single medial perforating branch of the
internal thoracic artery, is required for chest wall and
neck reconstruction (Figs. 16-18 and 16-19).77 The
concept of segmental transposition of muscle allows
transplantation of independent neuromuscular units
(segments of muscle innervated by a single nerve
fascicle).78
Bone is vascularized through endosteal and periosteal
sources (Fig. 16-20). The complex blood supply of bone
is based on nutrient vessels entering the bone directly
and through vascular connections between muscles
and bone, typically where the muscle has a large, fleshy
bone origin or insertion. Muscles with all five patterns
of circulation have vascular connections between
the muscle fibers and the periosteum. However, the

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I • GENERAL PRINCIPLES

FIGURE 16-1 8. A and B, Pectoralis major muscle flap segmental transposition

with function preservation. (From Mathes SJ, Nahai F: Reconstructive Surgery:
Principles, Anatomy, and Technique. New York, Churchill Livingstone, 1997.)

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TeWftf "Sel tf«f image-

IS • FLAP CLASSIFICATION AND APPLICATIONS 389

FIGURE 1 6 - 1 9 . Tibialis anterior muscle flaps split for segmental transposition with function preservation.
A, Segmental flap with preservation of tendon continuity with proximal intact muscle. B, Posterior advancement
flap. C, Anterior turnover flap. (From Mathes SJ, Nahai F: Reconstructive Surgery: Principles, Anatomy, and
Technique. New York, Churchill Livingstone, 1997.)

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390 I • GENERAL PRINCIPLES
FLAP VASCULAR CONNECTIONS TO BONE
FIGURE 16-20. Flap vascular connections to bone.
Studies related to flap design have demonstrated vascu-
lar connections to adjacent bone in many body regions.
Both muscle and fascial flaps have vascular pedicles with
either periosteal or direct nutrient branches to bone. (From
Mathes SJ, Nahai F: Reconstructive Surgery: Principles,
Anatomy, and Technique. New York, Churchill Livingstone,
1997.)
incorporation of vascularized bone with the transpo-
sition flap is generally not feasible because the point
of entrance of the dominant vascular pedicle into the
muscle determines the point of flap rotation. The bone
attachments are usually located beyond the point of
rotation. An example of a transposition bone flap is
the vascularized radial bone graft based on the 1,2 or
4,5 intercompartmental supraretinacular branches
of the radial artery for carpal bone reconstruction. 79
Another example of a rotational flap with bone is the
pectoralis major muscle with periosteal vascular con-
nections to the fifth anterior rib at the site of muscle
origin (Figs. 16-21 and 16-22). Historically, this has
been used for reconstruction of the irradiated
mandible. 80
Vascularized bone is useful in muscles suitable for
microvascular transplantation or in those muscles
designed for transposition when the vascular attach-
ments to bone are distal to the point of rotation. The
most commonly transferred bones are the fibula
based on the peroneal artery (Figs. 16-23 and 16-24),
the iliac crest based on the deep circumflex iliac artery
(Fig. 16-25), the scapula based on the circumflex scapu-
lar or thoracodorsal arteries (Figs. 16-26 and 16-27),
and the radius based on the radial artery.
The patterns of circulation to the scapula and radius
are classified according to the parent flap, which con-
sists of the vascular supply and associated soft tissue
component (e.g., scapular and radial forearm flaps).
These bones are always transposed as an integral part
of the parent flap. The fibula and the iliac crest,
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however, are most often transferred as bone only
without a soft tissue component. Classification of the
iliac crest as having a type I vascular pattern reflects
its dependence on surrounding muscles as well as direct
osseous vessels from the deep circumflex iliac artery.
The fibula is classified as having a type V vascular
pattern because of the dominant nutrient pedicle into
the proximal bone from the peroneal artery and the
segment at the origin of periosteal pedicles along the
length of the bone (standard segmental pedicles). This
type V pattern of circulation permits osteotomies to
be performed to separate the bone into distinct, inde-
pendently vascularized segments (Table 16-11).
Certain type A and type B fasciocutaneous flaps may
be elevated with bone. The regional vascular source of
the flap also provides nutrient vessels to the neigh-
boring bones. A segment of bone maybe included with
the fascial or fasciocutaneous flap when it is designed
either for transposition or for microvascular trans-
plantation (e.g., radial forearm and temporoparietal
fascial flaps).
Functional Muscle Flaps
Release of the origin or insertion of the muscle trans-
position flap will result in loss of muscle function.
However, many of the muscle flaps may be designed
for both coverage and functional muscle transfer. For
function to be preserved, the motor nerve must be
preserved along with dominant vascular supply, the
muscle must be reattached to a new bone or tendon
across a joint, and the muscle must exert a direct force
on its new point of attachment. Muscles suitable for
use as transposition flaps or microvascular compos-
ite tissue transplantation, providing both coverage and
function, include the latissimus (Figs. 16-28 and 16-
29), gluteus maximus (segmental) (Fig. 16-30),
gracilis, gastrocnemius, and serratus muscles. Restora-
tion of the original muscle length-to-width ratio and
repair of the motor nerve to a suitable receptor motor
nerve at the recipient site are essential for restoration
Text continued on p. 405
TABLE 16-11 • BONE VASCULAR
CLASSIFICATION
Bone Blood Supply Flap Type
Fibula Peroneal artery V*
Iliac crest Deep circumflex iliac artery I*
Scapula Circumflex scapular or B*
thoracodorsal arteries
Radius Radial artery B*
'Bone associated wiih musculocutaneous flap.
'Bone associated with fasciocutaneous flap.
TeWttf'aelCiW image...

16 • FLAP CLASSIFICATION AND APPLICATIONS 391

FIGURE 1 6 - 2 1 . Muscle flap modification with vascularized bone. A, Pectoralis major muscle with periosteal vas-
cular connections to fifth anterior rib at site of muscle origin. B, Arc of rotation of osseous muscle flap to head and
neck region. (From Mathes SJ, Nahai F: Reconstructive Surgery: Principles, Anatomy, and Technique. New York,
Churchill Livingstone, 1997.)

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392 I • GENERAL PRINCIPLES

FIGURE 1 6 - 2 2 . Osteocutaneous flap design. A, The patient required flap coverage of lower third face with
simultaneous mandible replacement. Design of pectoralis major musculocutaneous flap incorporates sixth ante-
rior rib. B, Deep surface of pectoralis major musculocutaneous flap with muscle attachments to periosteum of
rib to provide vascularized rib graft for mandible reconstruction. C, Lateral view of lower third facial defect at
site of resection of osteoradionecrosis of anterior mandible. Note that the right pectoral major osteomusculo-
cutaneous flap is elevated and ready for transposition to facial defect. D, Postoperative 6-month anterior view
demonstrates mandible coverage of lower third facial defect with simultaneous central mandible reconstruc-
tion. E, Lateral view demonstrates excess bulk of osteomusculocutaneous flap due to necessity of preserving
muscle attachment to vascularized rib.

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image...

16 • FLAP CLASSIFICATION AND APPLICATIONS 393

FIGURE 1 6 - 2 3 . Fasciocutaneous flap with vascularized

bone. Fibula flap with peroneal fasciocutaneous flap shows
vascular anatomy. (From Mathes SJ, Nahai F: Recon-
structive Surgery: Principles, Anatomy, and Technique.
New York, Churchill Livingstone, 1997.)

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394 I • GENERAL PRINCIPLES

I
FIGURE 16-24. See legend on opposite page.

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image...

16 • FLAP CLASSIFICATION AND APPLICATIONS 395

FIGURE 1 6 - 2 4 . Microvascular transplantation of fibula

for mandible reconstruction. A, Preoperative view of
patient with an ameloblastoma of the right horizontal
ramus of the mandible. B, Radiograph demonstrates an
ameloblastoma in the right lateral mandible. C, Specimen
consisting of right mandibulectomy. D, Design of skin island
of fibular fasciocutaneous flap (type B, peroneal artery).
E, Flap includes segment of vascularized fibular and sep-
tocutaneous skin territory based on peroneal artery and FIGURE 1 6 - 2 5 . Deep circumflex iliac artery compos-
associated veins. F, Flap inset with skin island used for ite flap. A, Marking for incision of standard osseous flap.
oral lining and fibula inset to replace right horizontal and Continued
vertical rami. Plates support osteotomy sites of vascu-
larized bone and are inset into right parasymphyseal and
vertical ramus of mandible. C, Postoperative view at 1
year reveals stable intraoral coverage provided by skin
island. H, Postoperative anterior view at 1 year demon-
strates intact reconstructed right mandible. /, Lateral
postoperative view demonstrates adequate mandible pro-
jection. J, Donor site view demonstrates stable coverage
of donor site with skin grafts. The patient is fully ambu-
latory with no disability at the donor site.

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396 I • GENERAL PRINCIPLES

FIGURE 1 6 - 2 5 , c o n t ' d . 8, Division of external oblique aponeurosis and identification ofvascular pedicle.
C, Division of internal oblique and transversus muscles with lateral dissection of pedicle. D, Release of
tensor fascia lata and gluteus medius for full-thickness osseous flap. E, Completion of dissection. (From
Mathes SJ, Nahai F: Reconstructive Surgery: Principles, Anatomy, and Technique. New York, Churchill
Livingstone, 1997.)

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image...

16 • FLAP CLASSIFICATION AND APPLICATIONS 397

FIGURE 1 6 - 2 6 . Independent vascularized segments of

scapula based on circumflex scapular and thoracodorsal pedi-
cles, s, subscapular artery; D, dominant pedicle: circumflex
scapular artery; t, thoracodorsal artery; a, angular branch of
thoracodorsal artery. (From Mathes SJ, Nahai F: Reconstruc-
tive Surgery: Principles, Anatomy, and Technique. New York,
Churchill Livingstone, 1997.)

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398 I • CENERAL PRINCIPLES

- FICURE 16-27. Microvascular transplantation of a fasciocutaneous flap with vascularized

scapula for mandible reconstruction. A Preoperative anterior view of a patient presenting with
squamous cell carcinoma. Right oral mucosa is invading mandible. B, Intraoral view of tumor.
C, Extirpative defect after right hemimandibulectomy and incontinuity from a radical neck dis-
section. D, Design of skin island may vary according to required location of skin in relation to
the vascularized segment of bone. E, Osteofasciocutaneous flap dissected on vascular pedicle
of the circumflex scapular artery and venae comitantes. Note skin island and vascularized bone
on separate vascular pedicles to provide inset for vascularized bone and floor of mouth cov-
erage, f. Vascularized bone placed into mandibular defect.

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6 • FLAP CLASSIFICATION AND APPLICATIONS 399

G H

K
FIGURE 1 6 - 2 7 , cont'd. G, Postoperative view at 3 months after immediate facial recon-
struction. Skin island of scapular flap provides stable lower third facial coverage. H, Submental
view demonstrates position of skin island and restoration of mandibular continuity with vas-
cularized scapula. /, Posterior trunk demonstrates donor site direct closure. J, Upper extrem-
ity abduction maintained at donor site. K, Postoperative intraoral view reveals stable coverage.

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image...

400 • GENERAL PRINCIPLES

FIGURE 1 6 - 2 8 . Functional muscle transfer. A, Utis-

simus dorsi muscle with sutures placed at specific inter-
vals to determine in situ flap length.

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 16 • FLAP CLASSIFICATION AND APPLICATIONS

FIGURE 1 6 - 2 8 , cont'd. B, Release of origin and insertion for flap trans-

position. C, Flap inset for biceps function restoration. Note preservation of
thoracodorsal pedicle and motor nerve and length restored at site of flap
inset. (From Mathes SJ, Nahai F: Reconstructive Surgery: Principles, Anatomy,
and Technique. New York, Churchill Livingstone, 1997.)

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402 I • GENERAL PRINCIPLES

FIGURE 1 6 - 2 9 . Functional muscle transposition.

A, Patient lost arm flexors in avulsion accident. B, Design of
latissimus dorsi muscle with skin island for functional muscle
transposition to restore arm flexion. C, Anatomic dissection
demonstrates arc of rotation of latissimus dorsi muscle for
coverage of functional transfer to upper extremity. D, Muscle
insertion reinset to anterior shoulder girdle at coracoid
process. Muscle length is preserved with origin reinset in
bicipital aponeurosis and radial tuberosity. E, Postoperative
anterior view at 1 year demonstrates stable coverage pro-
vided by latissimus dorsi musculocutaneous flap. F, Lateral
view demonstrates functioning muscle transfer and restored
elbow flexion.

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TeWttf'aStfW image...

16 • FLAP CLASSIFICATION AND APPLICATIONS 403

FIGURE 1 6 - 3 0 . Flap selection for simultaneous coverage and

reconstruction of functional defect. A, This patient has chronic pelvic
hernia after abdominal-perineal resection, including removal of pos-
terior vaginal wall, pelvic musculature, and perineal skin. B, Inferior
half of left gluteus maximus musculocutaneous flap based on infe-
rior gluteal artery and associated venae comitantes is elevated. Inner-
vation of superior half and inferior half of muscle flap is maintained
through the preserved inferior gluteal nerve. Continued

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404 I • GENERAL PRINCIPLES

FIGURE 16-30, cont'd. C, Posterior vaginal mucosal lining reconstructed with local flap turnover based on deep
external pudendal artery and associated venae comitantes. D, Insertion of inferior half of muscle is inset into con-
tralateral sacrum to maintain functional length of muscle flap. Skin island replaces missing perineal skin. E, Post-
operative view at 1 year demonstrates stable pelvic coverage and functional repair of pelvic hernia. F, Combined deep
external pudendal fasciocutaneous and inferior half of gluteus maximus musculocutaneous flaps allow simultaneous
single-stage vaginal reconstruction. (From Mathes SJ, Eshima I: The principles of muscle and musculocutaneous flaps.
In McCarthy JG, ed: Plastic Surgery. Philadelphia, WB Saunders. 1990:379.)

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image...

16 • FLAP CLASSIFICATION AND APPLICATIONS 405

of transplanted muscle function at its new inset site
(see Fig. 16-28).
The latissimus dorsi muscle flap has been used to
provide neodiaphragmatic motion for repair of recur-
rent congenital diaphragmatic hernias, to restore knee
function after resection of the quadriceps mechanism
in the lower extremity, to restore elbow and shoulder
motion in the upper extremity, and to restore oral and
nasal function after head and neck tumor ablation (see
Fig. 16-29).8'*84
Sensory Flap
Specific sensory nerves are identified in the cutaneous
territory of many of the flaps available for recon-
structive surgery. Both musculocutaneous and fas-
ciocutaneous transposition flaps may be designed to
incorporate the sensory nerve in the flap base. If the
cutaneous nerve does not enter the flap base in prox-
imity to the vascular pedicle, it is also possible to divide
the sensory nerve during flap elevation and then sub-
sequently coapt the nerve to a suitable sensory nerve
at the recipient site.
Muscle flaps with intact motor nerves or with reanas-
tomosis of the motor nerve to suitable motor or sensory
nerves at the recipient site appear to retain protective
sensibility, possibly through nerve fibers of propriocep-
tion. Maintenance of protective sensation is essential for
hands, feet, and other weight-bearing areas. Another
common area in which sensate flaps are used is the oral
cavity, and this potentially improves postoperative intra-
oral function.85'87 Harris et al88 state that reconstruc-
tion of weight-bearing areas should provide adequate
contour for normal footwear, thick durable skin, pro-
tective sensation, and solid anchorage to the deep struc-
tures to resist shearing forces (Figs. 16-31 and 16-32).

FIGURE 1 6 - 3 1 . Sensory flap (type B). A, Deltoid flap with vascular pedicle: posterior humeral circumflex artery
and vein and humeral circumflex sensory nerve to cutaneous territory. B, Flap elevated for composite tissue trans-
plantation. (From Mathes SJ, Nahai F: Reconstructive Surgery: Principles, Anatomy, and Technique. New York, Churchill
Livingstone, 1997.)

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image...

406 • GENERAL PRINCIPLES

a
i

- '

IP^aMHH
1 PPM
•
"^r 1
^^| ^^L
^^^k
^xB
'
1 h^.

3rt'i>i. • -1 .1' _ — «1
•L.'. * \/, "*£

FIGURE 1 6 - 3 2 . See legend on opposite page.

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image...

16 • FLAP CLASSIFICATION AND APPLICATIONS 407

FIGURE 1 6 - 3 2 , cont'd. Sensory flap modification. A, Plantar surface of foot at site of avulsion injury and subse-
quent skin graft on remaining calcaneus. Skin grafts have not provided stable coverage. B, Cutaneous territory of
deltoid flap at donor site on right upper extremity. Preoperative markings are shown for the deltoid flap based on
external landmarks, including line a-b between acromion and medial epicondyle. Line c-d is located in groove between
posterior deltoid and triceps muscle. Intersection point s denotes location of exit point of septocutaneous pedicle, the
posterior circumflex humeral artery and lateral cutaneous branch of circumflex humeral nerve. C, Deltoid neurosen-
sory fasciocutaneous flap elevated for microvascular composite tissue transplantation to foot defect. D, Flap inset at
3 months. The flap pedicle is repaired to the posterior tibial artery and vein, the sensory nerve is repaired to branches
of the saphenous sensory nerve. £and F, Postoperative views at 1 year. Crosshatched markings on flap indicate areas
of sensibility in flap cutaneous territory. The flap has provided stable coverage with preservation of sensibility on the
posterior plantar surface of the foot. (From Mathes SJ, Nahai F: Reconstructive Surgery: Principles, Anatomy, and
Technique. New York, Churchill Livingstone, 1997.)

Studies have shown benefits of protective sensation for
ankle and heel reconstruction both with rotational flaps
and by microvascular tissue transfer.89"91
Combination Flaps
Two muscle flaps frequently share a common regional
source for their dominant artery and vein. Both flaps
may be elevated simultaneously and either transposed
as a regional flap or transplanted by microvascular
surgery based on the common regional artery and vein.
This technique permits a flap design with the ability
to cover large defects or use of two or more flaps for
specialized coverage. The subscapular artery and vein
are a common regional source for the dominant pedi-
cles to Iatissimus dorsi muscle or musculocutaneous
flap, serratus anterior muscle flap, and scapular fas-
ciocutaneous flap; all three flaps may be transposed

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408 I • GENERAL PRINCIPLES

Scapular flap

Serratus
anterior
Latissimus dorsi

Superficiaf
inferior
epigastric
flap

a = axillary artery and vein

b = crossing branch for serratus muscle
c • circumflex scapular artery and vein
s • subscapular artery and vein Standard
groin flap
t = thoracodorsal artery and vein
A

ci - superficial circumflex iliac artery and vein

e = superficial inferior epigastric artery and vein
/ = superficial femoral artery and vein
B
F I G U R E 1 6 - 3 3 . Combination flap modification. A, Common vascular connections between subscapular artery and
vein to dominant pedicle to latissimus dorsi, serratus anterior, and scapular flaps. B, Common vascular connections
between the superficial circumflex iliac artery and groin flap a n d the superficial inferior epigastric artery and inferior
abdominal flap. (From Mathes SJ, Nahai F: Reconstructive Surgery: Principles, Anatomy, and Technique. New York,
Churchill Livingstone, 1997.)

or transplanted on this single artery and vein (Fig. 16-
33). Clinically, the subscapular system provides many
varieties of useful combination flaps.92,93 Another
example is the gluteal thigh flap, which is an inferior
gluteal musculocutaneous flap with a posterior fas-
ciocutaneous extension.94"96 The more subtle charac-
teristics of each tissue component enable the surgeon
to tailor the flap precisely to the specifications of the
individual defect. Combined flaps have been further
divided into Siamese, conjoint, and sequential flaps.97
Siamese flaps have multiple flap territories, depend-
ent on some common physical junction, yet each
retains its independent vascular supply. Conjoint flaps
have multiple independent flaps, each with an inde-
pendent vascular supply but linked by a common
source vessel. Another variety of a combined flap is a
sequential flap, which is defined as multiple inde-
pendent flaps, each with an independent vascular
supply and artificially linked by a microanastomosis.
Prelaminated and
Prefabricated Flaps
Flap prelamination, a term coined in 1994, involves
surgical manipulation of a flap that requires partial
to complete elevation and suturing of the flap to form
structures at the site of the reconstruction.98 This tech-
nique may also incorporate new tissues into the flap
territory, establishing a multilayered flap. When these
structures at the donor site have healed, flap trans-
position or transplantation is performed. With suture
lines or various grafts healed at the time of flap inset,
complex reconstructions are theoretically accom-
plished with less risk of complications at the recipi-
ent site. Flap prelamination techniques are used for
flaps in head and neck reconstruction. Baudet et al99
and Pribaz et al100 have used prelamination techniques
on the forearm for nasal and central face reconstruc-
tion. Although it is useful, many reconstructive

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16 • FLAP CLASSIFICATION AND APPLICATIONS
surgeons still prefer to perform secondary procedures
after successful initial flap inset rather than flap
prelamination at the donor site.
Another form of flap manipulation is termed pre-
fabrication. Prefabrication provides a new dominant
vascular pedicle to structures for subsequent trans-
position or transplantation. A suitable artery and vein
are selected and buried in fascia or subcutaneous tissue
in the planned flap territory. A large pedicle to an adja-
cent muscle is frequently used. The pedicle and a small
segment of muscle are elevated and inset beneath the
proposed flap site. In 6 weeks, the flap based on the
new vascular pedicle is elevated and either transposed
or transplanted by microsurgery. This technique for
prefabrication is not always reliable for establishing a
new dominant pedicle to a flap territory. With the
numerous options available for safe flap selection, this
technique of flap prefabrication is rarely used.101
Distally Based Flaps and Reverse-
Flow Flaps
Certain muscles can be elevated on minor or second-
ary segmental pedicles. Muscles with type II circula-
tion can be based on the minor pedicle (Table 16-12).
To accomplish this, one must divide the dominant vas-
cular pedicle and transpose the muscle distally, based
on the lesser pedicle. In designing a distally based flap,
one must consider that the minor pedicles differ in
size and location and therefore can be unreliable.
Without a prior strategic delay (preliminary division
of the dominant pedicle), only a segment of the muscle
based on the minor pedicle will survive. If the wound
requiring coverage is traumatic, the minor pedicle may
be located within the zone of injury (i.e., distal third
of the lower extremity). Prior delay of the muscle by
selective division of the dominant vascular pedicle will
provide more reliable muscle circulation and will
permit use of the cutaneous territory of the proximal
muscle if a musculocutaneous flap is planned.22
TABLE 1 6 - 1 2 • DISTALLY BASED FLAPS
Abductor digiti minimi
Anterior tibial artery
Dorsalis pedis
External oblique
Gastrocnemius
Gracilis
Hemisoleus
Peroneal artery
Peroneus brevis
Posterior tibial artery
Soleus
Vastus lateralis
Vastus medialis
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409
Fasciocutaneous flaps may also be designed as dis-
tally based flaps. The deep fascia receives specific blood
supply through direct cutaneous, septocutaneous,
and musculocutaneous pedicles. For example, type B
fasciocutaneous flaps frequently have multiple pedi-
cles located sequentially along the axis of the inter-
muscular septum (e.g., posterior tibial, anterior tibial,
and peroneal fasciocutaneous flaps). Although the
specific territory of a type B fasciocutaneous flap may
have a larger pedicle proximally in the extremities, it
is possible to base the flap distally on isolated septo-
cutaneous pedicles. Similarly, the cutaneous territory
of a type C fascial flap is usually based on a specific
large musculocutaneous, perforating pedicle. The
presence of an isolated musculocutaneous pedicle in
the distal flap will allow distally based transposition
of a fasciocutaneous flap.
Although distally based flaps are often termed
reverse-flow flaps, not all distally based flaps have
reverse flow, since perforating vessels spread out radi-
ally in the subcutaneous tissues. Thus, a flap may be
oriented such that flow is antegrade and yet the pedicle
may be based proximally, distally, medially, or later-
ally. A number of clinically useful reverse-flow flaps
have been described since the original description in
1995, including the distally based radial forearm
fasciocutaneous flap, a posterior interosseous flap,
and a reversed first dorsal metacarpal artery flap used
in hand reconstruction.102 The distally based radial
forearm flap relies on retrograde flow through the deep
palmar arch and associated venae comitantes with the
rotation point of the reverse flap at the level of the
wrist (Fig. 16-34). Examples of reversed flow flaps used
for lower extremity reconstruction are sural fascio-
cutaneous flaps based on perforators from the per-
oneal artery and reversed flexor hallucis longus flaps
based on retrograde flow through the peroneal
artery. [03,104
Reverse Transposition Flap
A muscle flap based on a minor pedicle is defined as
a distally based flap. However, it is possible to elevate
the regional artery and vein with the flap, including
both minor and major pedicles. With division of the
proximal regional artery and vein and transposition
of the flap in a distal direction opposite the standard
arc of rotation, a reverse transposition is accomplished.
This flap modification requires reversal of flow within
the regional artery and vein to the flap and may
adversely affect distal perfusion by the division of a
major regional vessel. A soleus muscle flap based on
minor pedicles from the posterior tibial artery and
vein located in the distal third of the lower extremity
would be classified as a distally based flap. An example
of a reverse-flow flap is the soleus muscle flap based
on the distal pedicle from the posterior tibial artery
410 I • GENERAL PRINCIPLES

Standard arc to antecubital fossa

A

Arc of reverse flap to palmar surface of hand

B
FIGURE 16-34. Radial forearm flap. A, Standard arc to antecubital fossa. B, Arc of reversed flap to palmar surface
of hand. (From Mathes SJ, Nahai F: Reconstructive Surgery: Principles, Anatomy, and Technique. New York, Churchill
Livingstone, 1997.)

and vein. The flap is transposed distally with proxi-
mal division of the posterior tibial artery and vein
(Fig. 16-35).
Type V muscles have two arcs of rotation. The stan-
dard arc is based on the major vascular pedicle (i.e.,
thoracodorsal artery and venae comitantes for the latis-
simus dorsi muscle and thoracoacromial artery and
venae comitantes for the pectoralis major muscle). The
second arc of rotation is based on a series of second-
ary pedicles that provide a reverse arc of rotation (i.e.,
posterior intercostal and lumbar arteries and venae
comitantes for the latissimus dorsi muscle and
branches of the internal mammary artery and venae
comitantes for the pectoralis major muscle). The
reverse arc of rotation for the latissimus dorsi muscle
was described by Bostwick et al105 in 1980. The use of
the latissimus dorsi muscle flap has been shown to be
a reliable method of closure for complex back wounds
in patients with spinal cord exposure or exposed ver-
tebral hardware.106
A direct fasciocutaneous flap (type B) may be
designed as a reverse-flow flap. After a dominant
regional pedicle to the flap is divided, the flap is ele-
vated with the divided dominant pedicle for trans-
position in the opposite direction from the source of
the divided dominant pedicle. The blood supply to
the flap will depend on reversal of flow in its major
pedicle. For example, after division of the proximal
radial artery and vein, the radial forearm flap can be
elevated with its radial artery and venae comitantes
and transposed distally to the hand as a reverse flap
(Fig. 16-36).
In a type B flap, the proximal regional source for a
septocutaneous pedicle may be divided and the flap
and its regional vascular pedicle rotated distally as a
reverse transposition flap. This technique also requires
reversal of flow within the regional pedicle. For
instance, the dominant pedicles to the leg (anterior
tibial artery and venae comitantes, posterior tibial artery
and venae comitantes, and peroneal artery and venae
comitantes) may be divided proximal to the point of
entrance of the dominant pedicle to the fasciocuta-
neous flap territory. Septocutaneous branches from the
dominant sources of blood flow to the leg may be main-
tained and serve as a basis for design of a reverse trans-
position flap for distal coverage of leg wounds.

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 16 • FLAP CLASSIFICATION AND APPLICATIONS 411

FIGURE 1 6 - 3 5 . Reverse transposition fasciocutaneous flap modification. A, Posterior tibia fasciocuta-

neous flap (type B) elevated after ligation of posterior tibial artery and vein superior to proximal septocu-
taneous pedicle to cutaneous territory. B, Distal flap transposition based on reverse flow through posterior
tibial artery and venae comitantes. Note that this technique may jeopardize leg circulation if the remaining
leg vessels have been subjected to vascular disease or trauma. (From Mathes SJ, Nahai F: Reconstructive
Surgery: Principles, Anatomy, and Technique. New York, Churchill Livingstone, 1997.)

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image..

412 I • GENERAL PRINCIPLES

FIGURE 1 6-36. Reverse transposition fasciocutaneous flap modification. A, Radial forearm flap (type B) ele-
vated after ligation of proximal radial artery and venae comitantes. B, Distal flap transposition based on reverse
flow in radial artery and venae comitantes. (From Mathes SJ, Nahai F: Reconstructive Surgery: Principles,
Anatomy, and Technique. New York, Churchill Livingstone, 1997.)

Venous Flaps Microvascular Composite Tissue

A venous flap is defined as a composite flap of skin,
subcutaneous tissue, and other tissues such as nerve,
tendon, and bone that uses a subcutaneous vein for
the arterial inflow and venous outflow. Nakayama107
first described these flaps in 1981. Three types of
venous flap have been identified (Fig. 16-37). m Type
I is a unipedicled venous flap; a single cephalad vein
is the sole conduit for perfusion and drainage. These
flaps can be proximally or distally based. Type II is a
bipedicled venous flap with a vein entering (caudal
end) as well as leaving (cephalad end) the flap. The
flow of blood is from the caudal to cephalad end.
Type III is an arteriovenous venous flap that is per-
fused by a proximal artery and drained by a distal
vein. These flaps have had success in hand recon-
struction. Available small, thin flaps with defined arte-
rial inflow and venous outflow are limited. Thus, when
local flaps are not available, arterialized venous free
flaps provide a good solution for successful soft tissue
reconstruction.109
Transplantation
With the ability to repair vessels less than 2 mm in
diameter, it became apparent that microvascular
transplantation was possible. Microvascular compos-
ite tissue transplantation has been termed free flap
because the tissue is transplanted from one part of
the body to another. Since flaps are now designed on
known vascular pedicles, transplantation of compos-
ite tissue from the donor site to a distant site is pos-
sible by re-establishment of flap circulation through
anastomosis of the flap arterial and venous pedicles
to suitable receptor vessels in proximity to the defect.
Reliable anastomosis of vessels with external lumen
diameters of 0.5 to 2 mm is possible with patency
rates of 95% or better (Fig. 16-38).'10 The ability to
transplant a flap to a distant site eliminates the need
to select a flap with an arc of rotation that reaches
the defect. The surgeon is thus able to transfer com-
posite tissue by flap suitability for defect coverage
rather than by proximity to the defect. This technique

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image...
16 • FLAP CLASSIFICATION AND APPLICATIONS
FIGURE 1 6 - 3 7 . Classification of venous flaps.
A, Type I. Schematic drawing of unipedicled venous
flap. B, Type II. Schematic drawing of bipedicled
venous flap. C, Type III. Schematic drawing of arte-
riovenous venous flap. (From Thatte MR, Thatte
RL: Venous flaps. Plast Reconstr Surg 1992;91:
747.) B Type II
is most suited for the type I, II, and V muscles, given
the nature of the pedicles. Common muscles trans-
ferred include the latissimus, rectus abdominis,
gracilis, and serratus. Common fasciocutaneous and
perforator flaps transferred include the lateral arm flap,
anterolateral thigh flap, deep inferior epigastric artery
perforator flap, and superficial inferior epigastric
artery flap.
When a microvascular anastomosis is used as part
of a rotational flap, it is termed supercharging. Super-
charging is a method of augmenting the blood supply
to a large pedicled flap that may extend beyond the
boundary of a single pedicle. For example, the supe-
riorly based unipedicled TRAM flap may be super-
charged by anastomosis of the inferior epigastric vessels
to the thoracodorsal vessels in the axilla."1,112
FLAP APPLICATIONS
Whether a clinical problem is simple or difficult, the
traditional approach has been to use the reconstruc-
tive ladder to guide surgical reconstruction (Fig. 16-
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Dr.Mustafa D.
413
Cephalad vein
Type I
Cephalad vein
Caudal vein
39). The choice of reconstructive options ranges from
simple to complex.
The concept of the reconstructive ladder was pro-
posed to establish priorities for technique selection
based on the complexity of the technique and the defect
requirements for safe wound closure. The ladder pro-
vides a systematic approach to wound closure, empha-
sizing selection first of simple and then of complex
techniques, depending on local wound requirements
and complexity. Direct closure represents the simplest
and most straightforward technique. Direct closure
may be precluded by the size of the wound or the con-
sequences of wound tension at the closure site, result-
ing in malalignment of adjacent tissues. When this
occurs, a more complex closure technique, such as a
skin graft that uses distant skin for defect coverage, is
required.
The simpler techniques, including skin grafts and
local flaps, may allow defect closure. However, these
techniques may not provide optimal results in terms
of form and function. The more complex procedure
often achieves superior results. The goals of form and
 I • GENERAL PRINCIPLES

Fasciocutaneous flap elevation Distant donor accent debridement

completed completed and suitable arterial and venous
receptor vessels isolated
B

Revascularization of flap with end-to-side

artery and end-to-end venous anastomosis
between flap and receptor vessels

Close-up view

FIGURE 1 6-38. Microvascular composite tissue transplantation of fasciocutaneous flap. A, Fas-

ciocutaneous flap elevation completed. B, Distant donor site debridement completed and suitable
arterial and venous receptor vessels isolated. C, Revascularization of flap with end-to-side artery and
end-to-end venous anastomosis between flap and receptor vessels. (From Mathes SJ, Nahai F: Recon-
structive Surgery: Principles, Anatomy, and Technique. New York, Churchill Livingstone, 1997.)

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image...
16
RECONSTRUCTIVE LADDER
Complex Distant flap
Local flap
Skin grafts
Simple Direct closure
FIGURE 16-39. Reconstructive ladder. The concept of
the reconstructive ladder was proposed to establish pri-
orities for reconstructive technique selection based on
the complexity of the technique and the defect require-
ments for safe wound closure. The reconstructive ladder
provides a systematic approach to wound closure empha-
sizing selection of simple to complex techniques based
on local wound requirements and complexity. (From
Mathes SJ, Nahai F: Reconstructive Surgery: Principles,
Anatomy, and Technique. New York, Churchill Livingstone,
1997.)
function may best be served by more complex
approaches, including regional or distant flaps, tissue
expansion, and microvascular transplantation. A new
paradigm, the reconstructive triangle, is thus more
appropriate in light of the more sophisticated options
available today (Fig. 16-40). This emphasizes the
selection of a technique that safely achieves a success-
ful reconstruction and restores form and function.
Increased experience has led to the safe use of tech-
niques such as flap transposition, microvascular com-
posite tissue transplantation, and tissue expansion.
The surgeon should now consider the reconstructive
triangle to select the optimal technique to achieve
predetermined reconstructive goals without donor
site complications.
Safety in reconstructive surgery is generally meas-
ured in terms of immediate success of wound cover-
age or defect reconstruction. With the identification
of specific vascular pedicles to muscle and fascia, flap
reliability is significantly improved. Safe and reliable
muscle or musculocutaneous and fascial or fasciocu-
taneous flaps have been described for use in all areas
of the body. When design is properly based on the
precise vascular territory of their vascular pedicles, the
majority of flaps survive transposition to a defect
within the standard flap arc of rotation.
Certain situations will decrease flap safety. Flap loss
may result when the defect is located beyond the stan-
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• Fu\p CLASSIFICATION AND APPLICATIONS 415
dard arc of rotation, causing excessive tension on the
vascular pedicle. Defect size beyond the vascular ter-
ritory of the flap pedicle may result in either an inap-
propriate increase in flap dimensions or excessive flap
tension at the inset site. Selection of a flap with a pedicle
location in the zone of injury or use in patients with
preexisting vascular compromise may result in failure.
Flap modifications, including segmental and distally
based designs, are also subject to vascular compro-
mise and potential loss. Thus, flap safety is determined
on the basis of design and assessment of the specific
reconstructive requirements.
The technique selected for defect closure or com-
posite reconstruction should restore normal shape or
contour. Tissue expansion is ideal for this purpose
because the skin and soft tissue next to the defect have
the same thickness, texture, and color. Unfortunately,
this tissue is frequently damaged or unavailable for
use as either an advancement or transposition flap.
Although the initial experience with the musculo-
cutaneous flap resulted in safe wound closure, the
excessive bulk was often unsightly. Frequently, a
muscle flap with a skin graft provided a superior
restoration of form at the recipient site. With the
identification of muscle and fascial units suitable for
design as either a standard transposition or a micro-
vascular composite tissue transplantation, the surgeon
may select the flap best suited for defect closure. When
a skin island is required, the surgeon may select a flap
with a thin layer of overlying subcutaneous tissue (i.e.,
radial forearm flap) or may plan secondary flap revi-
sion by direct excision or suction-assisted lipectomy
to improve flap contour in thicker flaps. The avail-
ability of numerous flap donor sites allows selection
Flaps
Microsurgery Tissue Expansion
FIGURE 1 6 - 4 0 . Reconstructive triangle. The recon-
structive triangle is a new paradigm more appropriate
than the reconstructive ladder for the sophisticated recon-
structive options now available. The individual surgeon's
judgment, experience, and familiarity with the various tech-
niques and flaps ultimately influence the selection of recon-
structive techniques. The reconstructive triangle is a
systematic approach to care of the patient through key
phases of management: defect analysis, assessment of
surgical options, identification of surgical goals, execu-
tion of the operative procedure, and result analysis or
outcome evaluation. (From Mathes SJ, Nahai F: Recon-
structive Surgery: Principles, Anatomy, and Technique.
New York, Churchill Livingstone, 1997.)
416 I • CENERAL PRINCIPLES
of a technique for either standard transposition or
microvascular composite tissue transplantation that
best restores form for defect coverage or composite
reconstruction.
Form preservation at the donor site should also
in fluence flap selection. When possible, the donor site
should be closed directly. Use of a flap that requires a
skin graft for donor site closure is justified when the
flap harvested is clearly superior to alternative flaps
for the defect. If it is possible to stage the flap eleva-
tion with preliminary insertion of a tissue expander,
an increase in both the cutaneous flap dimensions for
defect closure and the adjacent skin territory for donor
site direct closure may be accomplished. Although the
ultimate form at the flap recipient site remains the
primary basis for flap selection, deformity due to loss
of form at the donor site should be avoided when pos-
sible. Thus, reconstructive balance is achieved with
selection of a tissue source to restore the defect or defor-
mity while form and function are preserved at the
donor site.
In an effort to minimize donor site morbidity, many
surgeons have evaluated the utility of endoscopic
harvest of muscle flaps. Minimally invasive techniques
for harvest of several muscles have been described.
These include the latissimus dorsi, rectus abdominis,
gracilis, rectus femoris, external oblique, and gastroc-
nemius muscles. In addition to the endoscopic harvest
of muscles, laparoscopic techniques are frequently used
to harvest the omentum. This has been a significant
advance because the benefits include decreased scar-
ring, less postoperative pain, and theoretically less
donor site morbidity.113'115
Stability of the closure represents the most impor-
tant long-term consideration at the site of defect
coverage. For this reason, flap coverage is frequently
selected despite the simplicity of split-thickness skin
grafts for some defects that may ultimately require a
flap at a later date. With selection of a reliable flap design
and use of a standard technique for transposition or
microvascular transplantation, flap coverage will
provide stability at the defect site without necessarily
increasing the risk or compromising safety.
Specialized functions at the site of reconstruction
include hair growth, sensibility, skeletal support (bone),
and motion (animation). Techniques of reconstruc-
tion must consider these specialized requirements.
Although function restoration may require staged pro-
cedures, especially for a composite defect, it is often
possible to restore all functional requirements with a
single procedure.
Tissue expansion can increase the surface area of
specialized skin, especially hair-bearing scalp. Inser-
tion of a tissue expander at the defect edge will not
interrupt the sensory innervation of the planned flap.
Both skin and subcutaneous tissues of the expanded
advancement or transposition flap will provide the
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appropriate match for defect closure with resultant
optimal form and function.
The cutaneous territory flaps based on muscle or
fascia will not provide normal sensibility unless a
specific cutaneous nerve to this territory is incorpo-
rated in the flap design. With the exception of defects
on weight-bearing surfaces and in areas of special-
ized function, including the hand, face, and oral cavity,
the sensory innervated flap is not critical for stabil-
ity and function. In weight-bearing areas where motor
and sensory function remains intact except at the
site of the defect, a well-vascularized flap without
excessive bulk will generally provide stable coverage
and restore function. However, a well-vascularized flap
will not provide functional restoration for defects
located in weight-bearing areas where sensory func-
tion is completely absent. For example, flap coverage
of a pressure sore defect associated with spinal cord
transection will be subject to recurrent ulceration
unless a coordinated program of patient education
and pressure avoidance is instituted. Efforts to design
a neurosensory flap by incorporating a sensory
nerve in the flap cutaneous territory or through
intervening nerve grafts after both flap transposition
and transplantation may be required for functional
preservation.
Restoration of skeletal support is essential for
functional restoration in the head, chest, and extrem-
ities. The surgeon has the option of providing flap cov-
erage followed by staged skeletal reconstruction or of
providing both flap and vascularized bone simulta-
neously. Studies of human vascular anatomy related
to flap design have demonstrated vascular connections
to adjacent bone in many body regions. Thus, both
muscle and fascial flaps have vascular pedicles with
either periosteal or direct nutrient branches to bone.
Although prosthetic materials are safely used in con-
junction with flaps, vascularized bone is preferred, par-
ticularly for mandible and long bone reconstruction.
However, standard bone grafting techniques are also
reliable, especially if stable flap coverage is provided.
Techniques involving bone osteotomy and lengthen-
ing will frequently allow skeletal restoration, especially
if stable wound coverage is provided through flap cov-
erage. Because of the complexity of flap design when
vascularized bone is included, microvascular trans-
plantation of composite flaps is preferred to regional
transposition flaps with vascularized bone. When use
of a vascularized bone is planned, donor site bone
instability and associated loss of form and function
should be avoided.
Restoration of muscle function at the site of recon-
struction may also be required. After release of its origin
or insertion, the muscle will no longer perform its
intended function. However, flap technique may
include preservation of the motor nerve to the muscle
flap. Preservation of motor nerve innervation, along
VeWS^yfltfW image...
16 • FLAP CLASSIFICATION AND APPLICATIONS
with re-establishment of the muscle origin, insertion,
or both, can maintain normal muscle tension across
the defect site. When local or regional muscle flaps are
unavailable, a distant muscle may be transplanted by
microvascular techniques that include coaptation of
the muscle motor nerve with a suitable receptor motor
nerve at the recipient site. Proper selection of donor
muscles of appropriate size and shape can restore
muscle function at the defect site.
Function preservation at the donor site represents
an important consideration, particularly with use of
a muscle flap or a flap with vascularized bone. A
regional muscle should not be used if adjacent muscle
groups are absent or injured, especially if it is feasible
to transplant a distant flap microsurgically. When pos-
sible, function-preserving techniques for muscle trans-
position are advocated. It is frequently possible to use
a segmental muscle flap based on a reliable vascular
pedicle that allows preservation of the remaining
muscle with intact origin and insertion.
Advantages and Disadvantages of
Muscle and Musculocutaneous
Flaps
Selection of the most appropriate reconstructive
method can be difficult. Careful consideration must
be given to all the possible methods of repair, and the
advantages and disadvantages of each technique must
be weighed accordingly.
The advantages of muscle and musculocutaneous
flaps include the following:
• The vascular pedicles are specific and reliable.
• The vascular pedicle is often located outside the
surgical defect, which can be particularly impor-
tant for wounds with an extensive zone of injury
beyond the actual wound (e.g., after irradiation,
trauma).
• The muscle provides bulk for deep, extensive
defects and protective padding for exposed vital
structures (e.g., tendons, nerves, vessels, bones,
and prostheses).
• Muscle is malleable and can be manipulated (e.g.,
folded on itself) to produce a desired shape or
volume.
• Well-vascularized muscle is resistant to bacterial
inoculation and infection." 6
• Reconstruction by use of muscle or musculocu-
taneous flaps is often a one-stage procedure.
• Restoration of function, whether motor or
sensory, is possible with certain flaps.
• The reliability and availability of muscle and mus-
culocutaneous flaps make them an excellent
alternative means of reconstruction when the
closure method of choice for a particular defect
is unavailable or inadequate.
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417
The disadvantages of muscle and musculocutaneous
flaps include the following:
• The donor defect may lose some degree of
function.
• The donor defect may be aesthetically undesirable.
• Reconstruction with muscle or musculocutaneous
flaps may provide excessive bulk, leaving an aes-
thetically unacceptable result.
• Muscle or musculocutaneous flaps may atrophy
over time and thus fail to provide adequate cov-
erage.
• Removal of the muscle or musculocutaneous flap
may result in contour deformities at the donor
site.
The preservation of function can be extremely
important when nonexpendable muscles are used as
flaps. The techniques of function preservation gener-
ally involve transposing part of the muscle without
completely interrupting the origin or insertion of the
donor muscle. For example, the transposition of the
superior half of the gluteus maximus muscle for sacral
coverage in the ambulatory patient can be performed
without loss of thigh extension or hip stability because
the remainder of the gluteus maximus is functionally
intact.117'1'8
Advantages and Disadvantages of
Fascial and Fasciocutaneous Flaps
The advantages and disadvantages of fascial and fas-
ciocutaneous flaps are somewhat similar to those of
muscle flaps, although there are a few exceptions.
The advantages include the following:
• They are thin and pliable.
• Blood supply is reliable and robust.
• Donor site morbidity is minimal in regard to
function.
• They are muscle sparing.
• They have the ability to restore sensation.
• There are many potential donor sites.
The disadvantages include the following:
• They lack bulk for deep defects.
• They are technically more challenging (pedicle
dissection; many require microvascular anasto-
mosis).
• There are size limitations.
• The arc of rotation is limited.
• Donor site may require skin graft closure, result-
ing in donor site deformity.
Flap Transposition and Arc of
Rotation
Numerous pedicle flaps are available for transposition
to cover or to reconstruct specific defects. When a trans-
image...
418 I • GENERAL PRINCIPLES
position flap is elevated, the dominant vascular pedicle
to the flap is preserved. A factor that may prevent suc-
cessful flap transposition is the flap's arc of rotation.
The arc of rotation of a muscle is determined by the
extent of elevation of the muscle from its anatomic
bed and the ability of the muscle to reach adjacent areas
without devascularization. The mobility of a muscle
depends on the number of vascular pedicles and the
location of the dominant vascular pedicle relative to
the muscle's origin and insertion (Fig. 16-41). The area
covered by the arc of rotation varies among individ-
uals. On the basis of the flap length distal to the point
of rotation and the length of the vascular pedicle, a
safe standard arc of rotation is measured for each flap.
A modified arc of rotation is also available by
refinements in design and specific modifications of the
flap. Precise knowledge of the safe standard and
modified arc of rotation is necessary to avoid loss of
the flap from excessive tension or damage to the pedicle
from overzealous dissection.
In general, the arc of rotation is inversely propor-
tional to the number of vascular pedicles. If a muscle
has a large number of pedicles, it usually has a limited
FIGURE 1 6 - 4 1 . Arc of muscle rotation (latissimus
dorsi). (From Mathes SJ, Eshima I: The principles of muscle
and musculocutaneous flaps. In McCarthy JC, ed: Plastic
Surgery. Philadelphia, WB Saunders, 1990:379.)
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arc of rotation. Type IV muscles, such as the sartorius
and tibialis anterior, are examples of muscles with mul-
tiple segmental vascular pedicles and limited arcs of
rotation. Similarly, the location of the dominant vas-
cular pedicle relative to the muscle's origin and inser-
tion greatly determines the arc of rotation. The closer
the dominant vascular pedicle is to either the origin
or insertion of the muscle, the greater the arc of rota-
tion. The points of rotation for types I, II, III, and V
muscles are generally located at one end or the prox-
imal third of the muscle. For example, type V muscles,
such as the pectoralis major and latissimus dorsi,
have their major vascular pedicle near their insertion
and correspondingly have a wide arc of rotation.
Certain muscles, such as type V muscles, have two arcs
of rotation. The first arc of rotation is based on the
major blood supply; the second is based on the sec-
ondary segmental vascular pedicles. Reverse arc of
rotation refers to the degree of transposition of a flap
based on its secondary segmental vascular pedicles
(Fig. 16-42).
The fasciocutaneous flap's standard arc of rotation
is determined by the extent of elevation of the deep
fascia from its normal anatomic position to reach adja-
cent defects. The point of rotation is based on the site
of entrance of the dominant vascular pedicle into the
fascia. The fascial or fasciocutaneous flap is elevated
to the point of entrance of the flap pedicle, and the
fascia and overlying skin distal to this point are
rotated into the defect. In a type A fasciocutaneous
flap, the flap is elevated to include the direct cutaneous
pedicle. A standard arc of rotation is achieved with
the flap elevated to the proximal edge of the flap ter-
ritory. When the flap is designed as a fascial skin island,
the arc of rotation can be increased with proximal dis-
section of the axially directed pedicle.
The standard arc of rotation for a type B flap is
determined by elevating the flap to the point of
entrance of the septocutaneous pedicle at the flap base.
Proximal dissection of the septocutaneous pedicle to
its junction with regional vessels will increase the flap's
arc of rotation. This increased extension, however, is
often not as great as what can be achieved with a type
A flap because the pedicle dissection is generally deep
between muscle groups, which prevents a wider arc
of rotation.
The type C flap is elevated to the muscle surface at
the site of penetration of the musculocutaneous
pedicle. Dissection of the pedicle through muscle to
the regional vessels will increase the arc of rotation. It
is also possible to include a segment of muscle with
the fasciocutaneous flap design.
Prediction of Skin Territory
The successful use of the overlying skin in a muscu-
locutaneous flap depends on the skin's blood supply.
T%W>«J<a«H5,W image...

16 • FLAP CLASSIFICATION AND APPLICATIONS 419

FIGURE 1 6 - 4 2 . Predictionofarcofrotation.A Flapanatomy

showing origin (o), insertion (i), and dominant vascular pedicle
(p). The arrow indicates point of entrance of pedicle to flap. The
regional pedicle artery and vein (r) are shown. B, Arc of rota-
tion of flap elevation to point of entrance of vascular pedicle to
flap. Applications of the flap are based on standard arcs of rota-
tion. C, Extended arc of rotation based on flap elevation with
dissection of pedicle to regional source. D, Extended arc of rota-
tion based on flap elevation with pedicle dissection and release
of proximal fascia and muscle origin or insertion. (From Mathes
SJ, Nahai F: Reconstructive Surgery: Principles, Anatomy, and
Technique. New York, Churchill Livingstone, 1997.)

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420 I • GENERAL PRINCIPLES
Advances in the anatomic study of the cutaneous
vascular system have revealed three distinct vascular
patterns supplying the skin: direct cutaneous vessels,
which are specific vessels in the subcutaneous fat
that run parallel to the skin surface; musculocuta-
neous perforators, which arise from underlying
muscle; and fasciocutaneous vessels, which are specific
vessels that arise from regional vasculature and
extend through intermuscular spaces into the over-
lying fascia.
The major blood supply to the skin varies by region.
Skin overlying the broad, flat muscles of the trunk (e.g.,
the latissimus dorsi) is largely dependent on the mus-
culocutaneous perforating arteries. Skin overlying the
thin, narrow muscles (e.g., the gracilis) is largely
dependent on the fasciocutaneous perforating vessels.
Each musculocutaneous perforating artery nour-
ishes a certain territory of skin. There can be much
overlap, depending on the complexity of the skin's inter-
connecting vascular system. By appreciating this vas-
cular system, the surgeon can safely design the skin
territory of the flap.
All muscles, with the exception of the type I group,
require the division of vascular pedicles for flap trans-
position. Muscles with type II or type IV patterns
require division of minor or segmental pedicles for
flap elevation. Doing so may compromise the corre-
sponding skin territory. Type III muscles have two
large vascular pedicles arising from separate vascular
sources. The entire skin overlying the muscle often
survives on either of the pedicles. Type V muscles are
the most versatile because the skin islands can be based
on either the proximal major pedicle or the second-
ary segmental pedicles. Type I muscles are reliable
because the blood supply generally supports all the
overlying skin.
In general, each superficial muscle supplies the skin
lying directly over it, and the skin territory may be
safely extended 3 to 4 cm beyond the borders of the
underlying muscle. The additional skin is supported
by various anastomotic networks in the subcutaneous
tissues. In certain patients, there appears to be a degree
of axiality in the musculocutaneous perforators that
anastomose with the cutaneous vessels. This anatomic
arrangement enables an even larger territory of skin
to be safely elevated. For example, in the extended
deep inferior epigastric musculocutaneous flap
described by Taylor et al" 9 in 1983, certain paraum-
bilical musculocutaneous perforators from the infe-
rior epigastric artery course superoiaterally in the line
of the intercostal spaces, anastomosing with the lateral
cutaneous branches of the intercostal system. This
arrangement enables the skin island to extend over
the costal margin toward the tip of the scapula. Gott-
lieb et al120 stated that the skin island of this flap could
extend as far as the posterior axillary line, certainly a
considerable distance from the borders of the under-
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lying muscle. As modifications and refinements in the
musculocutaneous flap continue, it is certain that
various other extended skin territories, supported by
the intricate anastomoses of the cutaneous, muscu-
locutaneous, and fasciocutaneous systems, will be
discovered.
Selection of Specific Muscle and
Musculocutaneous Flaps
After the decision has been made to use a muscle or
musculocutaneous flap, the specific muscle must be
chosen. General guidelines to assist in the selection of
a muscle are as follows.
1. Ideally, the muscle should be adjacent to the
defect.
2. The muscle should be of sufficient size and
bulk to cover the defect. The final design of the
flap should occur only after the defect is
completely defined. When tumor exposure Or
wound debridement is required, the defect is
often much larger and deeper than initially
anticipated. By final design of the flap after
debridement, costly errors in inadequate cov-
erage can be avoided. If the defect is unstable
or the margins are unclear (tumor pathology
not available), wound packing or temporary
skin graft coverage is recommended. One
must also take into consideration that a
significant amount of atrophy occurs if the
origin, insertion, or motor nerve of the muscle
is disrupted.
3. The muscle should be expendable. There are
often synergistic muscles that can compensate
for the loss of the selected muscle so that the
donor site is not impaired. However, if no
synergistic muscle groups are available, either
techniques to preserve donor muscle function
(e.g., muscle splitting) should be employed or a
different muscle chosen.
4. The status of the vascular pedicle that will
sustain the proposed flap must be known
prcoperatively. Selective arteriography must
be considered if there is a history of previous
surgery in proximity to the vascular pedicle
of the proposed muscle flap or if muscle paral-
ysis is noted on physical examination. Earlier
division of the motor nerve may also have
included ligation of the vascular pedicle. Clin-
ical situations in which evaluation by arteriog-
raphy is particularly useful include, for example,
the sural artery (gastrocnemius) after knee
surgery, the transverse cervical artery (trapez-
ius) after neck and shoulder surgery, and the
thoracodorsal artery (latissimus dorsi) after
axillary surgery.
image...
16 • FLAP CLASSIFICATION AND APPLICATIONS
5. The donor defect must be carefully considered.
Some patients do not accept the use of a skin
graft at the donor site, and certain muscles are
more likely than others to require grafts for
closure. Likewise, some patients prefer one scar
site to another (e.g., the abdominal scar of the
TRAM flap versus the back scar of the latissimus
dorsi flap in breast reconstruction).
6. The cutaneous territory of the proposed flap
must be of sufficient size and of acceptable
texture. The harvested skin should be an accept-
able match to the recipient site (e.g., not hair
bearing).
7. If restoration of sensation or motor function is
necessary, a select number of muscle, musculo-
cutaneous, and fasciocutaneous flaps are avail-
able. Common examples of muscles that provide
sensation or restore function are the serratus
muscle, rectus abdominis, and latissimus
dorsi.122'126
8. Osteomusculocutaneous flaps are available for
defects in need of vascularized bone in addition
to soft tissue. Examples include the trapezius
flap with vascularized clavicle and scapular
spine,127-129 pectoralis major flap with vascular-
ized rib, iliac osteomusculocutaneous flap
based on the ascending and transverse branches
of the lateral circumflex femoral system,132,133 and
latissimus dorsi-scapular osteomusculocuta-
neous flap.134-'35
9. The operation should be technically straight-
forward.
Selection of Specific Fascial and
Fasciocutaneous Flaps
General guidelines for choosing a specific fascial or
fasciocutaneous flap are similar to those for selection
of muscle and musculocutaneous flaps, with a few
exceptions. The fascial or fasciocutaneous flap must
be in proximity to the defect if a rotational flap is
planned. The planned flap must be of sufficient size
and bulk to reconstruct the defect. Fascial and fascio-
cutaneous flaps are ideal for areas that do not require
bulk. The vascular supply of the area must be assessed
preoperatively. If a fasciocutaneous flap is planned, the
perforating vessels should be assessed with a Doppler
probe preoperatively so that the skin island can be accu-
rately designed. The results of the Doppler study may
determine a specific fasciocutaneous flap to be used.
The donor defect should be considered. This can gen-
erally be closed primarily (fascial flap) but may require
a skin graft if the skin island is large. Restoration of
sensation with fasciocutaneous flaps is possible. Exam-
ples include the lateral arm flap,136 radial forearm flap,137
deltoid flap,138 anterolateral thigh flap, 139 and tensor
fascia lata flap.140
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421
Regional Application of Muscle and
Musculocutaneous Flaps
HEAD AND NECK RECONSTRUCTION
REGIONAL FLAPS
Temporalis
Sternocleidomastoid
Platysma
DISTANT FLAPS
Pectoralis major
Trapezius
Latissimus dorsi
MICROVASCULAR FLAPS
Radial forearm
Rectus abdominis
Latissimus
Scapular
Abdominal viscera (omentum, jejunum, colon)
Perforator flaps
Radical cancer surgery or traumatic injury can produce
massive defects in the head and neck. Whereas many
simple defects can be adequately treated with direct
closure, local scalp flaps, or skin grafts, the more com-
plicated defect requires a larger reconstruction. The
muscle, musculocutaneous, and fasciocutaneous flaps
play a major role in these reconstructions. Historically,
large surgical defects of the head and neck were
managed with staged reconstruction. Currently, the
most common reconstruction involves microvascular
tissue transfer.
The primary applications of the muscle or mus-
culocutaneous flap in head and neck reconstruction
include provision of tissue bulk for a significant
defect (e.g., after hemimandibulectomy); protective
coverage of vital structures (e.g., the carotid artery);
provision of skin for intraoral lining and coverage;
and provision of skin for skull, facial, and neck
defects.
The local muscle and musculocutaneous flaps for
head and neck reconstruction include the temporalis,
sternocleidomastoid, and platysma flaps.
The temporalis muscle is a type III, fan-shaped,
bipcnniform muscle. Transposition of the muscle as a
turnover flap is especially useful for coverage of the
orbit, superior maxilla, and ear.
The sternocleidomastoid is a type II muscle, first
described in head and neck reconstruction by
Owens12 in 1955. This flap has historically been used
for intraoral and pharyngeal reconstruction. Other
uses have included augmentation of soft tissue
defects of the upper neck and jaw, protective cover-
age of major vessels, and closure of pharyngocutaneous
fistulas.141"143 However, of all the musculocutaneous
flaps used for head and neck reconstruction, the ster-
nocleidomastoid is considered the least reliable,20,143
Vtft*,ttf(9elCiW image...

422 I • GENERAL PRINCIPLES

The platysma is a type II, thin, broad, sheet-like
muscle extending over the entire anterior and lateral
aspects of the neck. The use of the platysma as a mus-
culocutaneous flap was first described in 1887 by
Gersuny, m who employed it in reconstruction of a full-
thickness defect of the cheek. The platysma has been
used for intraoral, lip, lower midface, and anterior neck
reconstruction. Because of the thinness of the platysma
muscle, the reconstructive surgeon must be particu-
larly careful to avoid disrupting the muscle fibers during
the dissection and placing undue tension on the vas-
cular pedicle after transposition of the flap (Fig. 16-43).

. . - • .

^A _^, ^ '
£ ^ '-
' ^^5

FIGURE 16-43. Platysma musculocutaneous flap for intraoral cov-

erage. A, Left buccal mucosal defect at site of tumor extirpation. Note
skin island design over inferior territory of ipsilateral platysma muscle.
B, Muscle elevated with skin island, with attachment to mandible pre-
served. C, Arc of rotation of platysma muscle flap to lower third of
face, buccal sulcus, and lateral oral cavity. The flap is based on a pedicle
from the facial artery and associated veins. D, Flap transposed beneath
mandible into oral cavity; skin island noted at lateral oral commissure.
E, View of flap inset with skin island extending from oral commissure
to the anterior tonsillar pillar, providing coverage of buccal lateral
cavity. F, Postoperative view at 3 months demonstrates viable skin
island providing stable coverage. C, Postoperative lateral view demon-
strates donor site closure. The flap provides intraoral coverage with
excess bulk. (From Mathes SJ, Nahai F: Reconstructive Surgery: Prin-
G ciples, Anatomy, andTechnique. New York, Churchill Livingstone, 1997.}

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image...
16 • FLAP CLASSIFICATION AND APPLICATIONS
The distant muscle and musculocutaneous flaps in
head and neck reconstruction include the pectoralis
major, trapezius, and latissimus dorsi flaps.
The pectoralis major is a type V, large, broad muscle.
Its use as a musculocutaneous flap was first described
in 1968 by Hueston and McConchie 145 as part of a com-
pound deltopectoral flap. In 1977, Brown et al18
described the use of the pectoralis major as a flap in
mediastinal coverage. In 1979, Ariyan21 introduced the
pectoralis major musculocutaneous flap for head and
neck reconstruction (Figs. 16-44 and 16-45). During
the ensuing years, the pectoralis major musculocuta-
neous flap proved more valuable than the deltopec-
toral flap and supplanted it as the primary flap (other
than microvascular tissue transplantation) in head and
neck reconstruction (Fig. 16-46).
The common applications of the pectoralis major
musculocutaneous flap in head and neck reconstruc-
tion include the following: external resurfacing of the
skin of the face and neck; intraoral and pharyngeal
lining; carrying vascularized rib and skin in mandibu-
lar reconstruction; and reconstruction of the esoph-
agus. M 6 , 5 ° Historically, the pectoralis major
musculocutaneous flap has been one of the most ver-
satile flaps used in head and neck reconstruction.
The trapezius, a type II muscle, is less widely used
than the pectoralis major muscle, yet its superior
FIGURE 1 6 - 4 4 . Pectoralis major
flap. Standard arc to middle third of
face. {From Mathes SJ, Nahai F: Recon-
structive Surgery: Principles, Anatomy,
andTechnique. New York, Churchill Liv-
ingstone, 1997.)
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423
location and wide anterior arc of rotation make it a
valuable musculocutaneous flap.14,36 Modifications in
design have enabled the trapezius muscle to be used
as distinctly different upper and lower musculocuta-
neous flaps. 151 The various clinical applications of the
trapezius flap have included lower facial reconstruc-
tion, especially the ear and parotid regions; lateral upper
face and scalp (occipital and temporal) repair152; ante-
rior and posterior neck reconstruction 153 ; orbital
reconstruction with the use of an extended flap154,155;
and pharyngoesophageal reconstruction. Historically,
the trapezius has also been used as an osteomusculo-
cutaneous flap, incorporating either the lateral aspect
of the clavicle or the spine of the scapula (Figs. 16-47
andl6-48). 1 5 6
The latissimus dorsi is a type V muscle originally
described as a superiorly based flap by Tansini157 in
1896. Since the first description, there have been numer-
ous modifications and refinements of the flap. His-
torically, the latissimus dorsi musculocutaneous flap
has been used in head and neck reconstruction for large
defects or when previous irradiation or surgery pre-
cluded other flaps. Since Quillen et al158 reported the
use of the latissimus dorsi as a transposition island flap
in 1978 to cover the mandible and neck after resection
of a tumor, various other clinical applications of the
Text continued on p. 430
Standard arc to middle third of face
 I • GENERAL PRINCIPLES

FIGURE 16-45. Pectoralis major flap foir head and neck reconstruction. A, Preoperative
view of patient with squamous cell carcinoma involving right lateral oral cavity and invading
into mandible. B, Preoperative intraoral view of invasive squamous cell carcinoma. C, Speci-
men after right hemimandibulectomy and, in continuity, a radical neck dissection. D, Intraoral
defect after radical tumor extirpation. E, Design of skin island for right pectoralis major mus-
culocutaneous flap. F, Pectoralis major musculocutaneous flap elevated with division of the
muscle fibers or origin and insertion with preservation of vascular pedicle, thoracoacromial
artery, and associated veins.

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 16 • FLAP CLASSIFICATION AND APPLICATIONS 425

FIGURE 1 6 - 4 5 , c o n t ' d . G, Pectoralis major arc of rotation into neck and lower third of
face. H, Illustration of pectoralis major muscle flap for reconstruction of oral cavity defects.
Note that the skin island and anterior surface of the muscle rotate into the oral cavity after
the flap is transposed from the chest to the head. (From Mathes S: The pectoralis major flap.
In Stark RB, ed: Plastic Surgery of the Head and Neck. New York, Churchill Livingstone, 1985:949.)
/, Postoperative view at 6 months demonstrates flap coverage of radical neck defect and minimal
bulk in lower third of face. J, Postoperative intraoral view demonstrates stable oral coverage
of resection defect.

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image...

426 I • GENERAL PRINCIPLES

ifrW

FIGURE 16-46. See legend on opposite page.

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image...

16 • FLAP CLASSIFICATION AND APPLICATIONS 427

FIGURE 1 6 - 4 6 , cont'd. Pectoralis major musculocutaneous flap for reconstruction of a pharyngoesophageal

fistula in a patient presenting with radiation necrosis and failed deltopectoral flap. A, Preoperative view. The patient
had recurrent squamous cell carcinoma of the larynx after primary radiation therapy, which necessitated laryngec-
tomy. Complications secondary to poor wound healing resulted in right-sided carotid rupture and necrosis of the
anterior cervical esophageal wall. B, The deltopectoral flap failed to provide stable coverage, d, site of deltopectoral
flap inset; e, anterior wall defect of the pharynx-cervical esophagus extending to the site of the tracheostomy. C, Del-
topectoral flap excised; pharyngeal-cervical esophageal defect (e) debrided. The left pectoralis major musculocuta-
neous flap is elevated with a distal vertical skin island, a, superior aspect of skin island; b, inferior aspect, D, After
flap transposition to the neck, the skin island is inset in the defect with the superior edge of the skin island sutured
to the esophagus at the level of the trachea; the inferior portion is placed into the superior aspect of the pharyngeal
defect. E, One month after reconstructive surgery, the patient demonstrated normal pharyngeal-esophageal conti-
nuity. F, Close-up view demonstrates stable coverage provided by skin grafts on the exposed deep surface of the
pectoralis major muscle. (From Mathes S: The pectoralis major flap. In Stark RB, ed: Plastic Surgery of the Head and
Neck. New York, Churchill Livingstone, 1985:949.)

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428 | • GENERAL PRINCIPLES

Arc to face and anterior neck

FIGURE 16-47. Trapezius flap. Arc to face and anterior neck.
(From Mathes SJ, Nahai F: Reconstructive Surgery: Principles,
Anatomy, and Technique. New York, Churchill Livingstone, 1997.)

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image...

16 • FLAP CLASSIFICATION AND APPLICATIONS 429

FIGURE 1 6 - 4 8 . Vertical trapezius musculocutaneous flap for head and neck recon-
struction. A, The patient has a recurrence of lateral mandible squamous cell carci-
noma. She has previously undergone tumor resection with right radical neck dissection.
B, Intraoral view of recurrent anterior tonsillar fossa squamous cell carcinoma. C,
Right trapezius muscle denervated during prior radical neck dissection. Selective
angiogram confirms that the transverse cervical artery and its descending branch are
intact despite prior neck dissection with division of cranial nerve XI (accessory nerve),
tc, transcervical artery; m, internal mammary artery. D, Descending branch fills,
confirming intact pedicle for denervated trapezius muscle, d, descending branch of
transverse cervical artery. E, With patient in supine position, tumor resection with
mandibulectomy is performed. F, With patient turned to lateral decubitus position,
vertical trapezius musculocutaneous flap is designed. Continued

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430 I • GENERAL PRINCIPLES

FIGURE 16-48, cont'd. G, Arc of rotation of vertical trapezius musculocutaneous flap to

upper face, midface, and lower third of face. With denervated muscle, the flap is thin but the
vascular pedicle is intact. H, Postoperative view at 6 months demonstrates stable direct closure
of cutaneous defect. /, Postoperative lateral view at site of closure of facial defect. J, Postop-
erative intraoral view demonstrates skin island trapezius musculocutaneous flap providing stable
intraoral coverage.

muscle have been described. In fact, the latissimus dorsi
musculocutaneous flap was used frequently in intra-
oral and pharyngeal reconstruction.159 Other uses of
the latissimus dorsi muscle in head and neck recon-
struction have included reconstruction of defects of
the posterior neck, shoulder, anterior neck, lower face,
occipital scalp, and intraoral-pharyngoesophageal
regions.
Microvascular tissue transplantation in head and
neck reconstruction has become the reconstruction
of choice in most centers. The use of microsurgery
has allowed the surgeon to achieve superior recon-
structive results with regard to form and function.
Various muscle, musculocutaneous, and fasciocuta-
neous flaps are used in head and neck reconstruction,
depending on the defect as well as the surgeon's pref-
erence. Large midface defects are often reconstructed
with rectus abdominis musculocutaneous flaps. 160
The rectus provides muscle bulk to fill large three-
dimensional defects and has a large skin island for
external coverage.161 Intraoral defects can often be
closed with a radial forearm flap, restoring a functional
oral cavity.162 Partial or total glossectomy defects have
been reconstructed with good results by the radial
forearm flap, rectus abdominis muscle flap, latissimus
dorsi muscle flap, gracilis muscle flap, and anterolat-
eral thigh flap.163,164 Large scalp defects are effectively
managed by transfer of the latissimus dorsi muscle
flap or omental free flap in combination with a split-
thickness skin graft. The latissimus has been widely
used because of its large surface area, long vascular
pedicle, and reliability (Fig. 16-49).165'166 Although it
is not as commonly used, the omentum can provide
stable coverage of large scalp defects.60 The required
laparotomy increases the donor site morbidity. When
the patient has undergone a prior laparotomy, adhe-
sion may complicate flap harvest.
BREAST RECONSTRUCTION
REGIONAL FLAPS
Pectoralis major
Serratus anterior
Pectoralis minor

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 16 • FLAP CLASSIFICATION AND APPLICATIONS 431

^ * « *

' — ^
. '

D
FIGURE 1 6 - 4 9 . Segmental transplantation of latissimus dorsi muscle with function preser-
vation. A, Osteoradionecrosis of skull, the site of a prior craniotomy. B, Debridement of non-
viable infected bone and dura. C, Site of skin island on ipsilateral anterior latissimus dorsi
muscle. D, Deep surface of free flap demonstrates random portion of skin island, a, random
portion of skin island; p, vascular pedicle. Continued

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 I • GENERAL PRINCIPLES

FIGURE 1 6 - 4 9 , cont'd. E, Segmental transplantation of latissimus dorsi preserves edge

of posterior muscle (a-b) with intact vascular pedicle and motor nerve, c-d, former location
of anterior edge of latissimus dorsi muscle. F, Immediately after flap inset. (The free flap is
vascularized by end-to-side anastomosis of anterior branch of thoracodorsal artery and venae
comitantes to superficial temporal artery and vein.) G, Postoperative view at 3 months demon-
strates stable wound coverage with function preserved at donor site. {A to C from Mathes SJ,
Vasconez LO, Rosenblum ML: Management of the difficult scalp and intracranial wound. Clin
Plast Surg 1981;8:331. 0 to F from Mathes SJ, Nahai F: Clinical applications for muscle and
musculocutaneous flaps. St. Louis, CV Mosby, 1982.)

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16 • FLAP CLASSIFICATION AND APPLICATIONS
DISTANT FLAPS
Rectus abdominis
Latissimus dorsi
MICROVASCULAR FLAPS
Rectus abdominis
Deep inferior epigastric perforator
Superficial inferior epigastric artery
Superior gluteal perforator
Inferior gluteal perforator
Gluteus maximus
Muscle and musculocutaneous flaps have had a
tremendous impact on breast reconstruction and have
provided women with superior cosmetic results after
mastectomy. Less aggressive surgical treatments of
breast cancer, such as the modified radical mastectomy,
skin-sparing mastectomy, and lumpectomy, have
replaced the classic radical mastectomy as the treat-
ment of choice for breast cancer. This change in
approach has resulted in smaller defects and more local
tissue available for use in reconstruction. In addition,
more women with premalignant disease or with a
family history of breast cancer are undergoing pro-
phylactic mastectomy and immediate reconstruction.
Local muscles available in breast reconstruction are
the pectoralis major, pectoralis minor, and serratus
anterior. These muscles are especially important for
patients who undergo prosthetic implant or expander
insertion. For patients with an intact pectoralis major
muscle and adequate overlying skin, the submuscular
(subpectoral or subserratus-pectoral) placement of a
prosthetic implant is a common reconstructive tech-
nique. 167 The pectoralis minor and serratus muscles
can also assist in implant coverage and are generally
used in addition to the pectoralis major muscle.'68*170
The distant muscles available in breast recon-
struction are the latissimus dorsi, the rectus abdominis,
and a variety of other muscles transferred microsur-
gically, including the gluteus and fasciocutaneous per-
forator flaps (deep inferior epigastric perforator and
superficial inferior epigastric artery). Distant muscu-
locutaneous or fasciocutaneous flaps are usually indi-
cated for patients with inadequate local tissue,
unacceptable overlying skin, or radiation damage.
Tansini157 described the earliest version of the latis-
simus flap. Since then, this muscle has become one of
the most versatile flaps in plastic and reconstructive
surgery. The advantages of the latissimus flap are that
it has a reliable vascular supply and skin island and
ultimately provides an acceptable cosmetic result.171
The major drawback in use of the latissimus dorsi
muscle for breast reconstruction is that a prosthetic
implant is usually required to provide adequate pro-
jection because the musculocutaneous flap by itself is
generally too thin.172 The extended latissimus dorsi flap
has been described; it provides additional soft tissue,
thus obviating the need for implants. 173 In addition,
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433
the latissimus dorsi donor scar is often unsightly, and
the seroma rates are high (Figs. 16-50 and 16-51).174
The rectus abdominis is a type III muscle that com-
monly supplies a generous amount of abdominal fat
and overlying skin. As a musculocutaneous flap, the
rectus abdominis has proved to be one of the most valu-
able options for breast reconstruction. Variations in flap
design have produced different types of rectus abdo-
minis musculocutaneous flaps (e.g., vertical, transverse,
bipedicled, superiorly based, and inferiorly based
flaps). The flap was initially described based on its supe-
rior pedicle, the superior epigastric artery and venae
comitantes, with a vertical skin island. Subsequently,
its use based on the inferior pedicle, the deep inferior
epigastric artery, was reported.175 In 1982, Hartrampf
et al176 described a technique that changed the entire
approach to breast reconstruction. By alignment of the
skin island in a transverse direction, between the umbili-
cus and pelvis, the rectus abdominis musculocutaneous
flap provided skin and soft tissue for breast recon-
struction with improved abdominal contour. The
transverse rectus abdominis musculocutaneous
(TRAM) flap is now considered the musculocutaneous
flap of choice for breast reconstruction (Fig. 16-52).
The indications for use of the TRAM flap in breast
reconstruction include a patient in need of additional
soft tissue and overlying skin who has a moderate
amount of lower abdominal tissue; a patient who
prefers autologous tissue reconstruction without the
use of a prosthetic implant; a patient who prefers a
lower abdominal donor scar rather than a back scar;
and a patient who has had an unacceptable result after
undergoing other reconstructive methods (Figs. 16-
53tol6-55). 1 7 7
The relative contraindications to use of the TRAM
flap include an extremely thin patient who has little
lower abdominal tissue, a nulliparous patient in her
childbearing years, a patient with a history of abdom-
inal wall herniation, an extremely obese patient, a heavy
smoker, and a patient with lower abdominal scars. An
absolute contraindication for a superiorly based trans-
position TRAM flap for breast reconstruction is prior
division of its superior pedicle, usually related to a supe-
rior transverse laparotomy incision.
Advantages of the flap include the following:
• It provides sufficient bulk so that a prosthetic
implant usually is not required.
• The suprapubic horizontal donor scar is aes-
thetically acceptable.
• Transposition of the flap can be performed with
the patient in a single operative position.
• The skin dimensions are larger than those avail-
able with the latissimus dorsi flap.
• Asimultaneousabdominoplasty is accomplished
with direct donor site closure.
Text continued on p. 440
434 I • GENERAL PRINCIPLES

Arc after release of muscle insertion

B
FIGURE 16-50. Latissimus dorsi flap. A, Arc to anterior thorax with insertion intact. B, Arc after release of muscle
insertion. (From Mathes SJ, Nahai F: Reconstructive Surgery: Principles, Anatomy, and Technique. New York, Churchill
Livingstone, 1997.)

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16 • FLAP CLASSIFICATION AND APPLICATIONS 435

FIGURE 1 6 - 5 1 . Latissimus dorsi musculocutaneous flap for breast reconstruction. A, Preoperative view after
modified radical mastectomy for breast carcinoma. B, Postoperative view after breast reconstruction by a latis-
simus dorsi musculocutaneous flap with silicone gel implant. The nipple was reconstructed with a full-thickness skin
graft. C Oblique view. D, Lateral view. Note the donor site scar. (From MathesSJ, Eshima I: The principles of muscle
and musculocutaneous flaps. In McCarthy JG, ed: Plastic Surgery. Philadelphia, WB Saunders, 1990:379.)

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436 I • GENERAL PRINCIPLES

MATHES 1977 EVER 1970 ROBBINS1979

0

MARINO 1981 HARTRAMPF 1982 DINNER 1982

Aim

^IK

LEJOUR 1982 HARTRAMPF 1982 GANDOLFO 1982

HARTRAMPF 1982 ELLIOT 1983 DINNER 1983

FIGURE 16-52. Various designs of superiorly pedicled TRAM flaps. (From

Cormack GC, Lamberty BC: The Arterial Anatomy of Skin Flaps. Edinburgh,
Churchill Livingstone, 1986.)

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16 • FLAP CLASSIFICATION AND APPLICATIONS 437

FIGURE 1 6 - 5 3 . Flap selection for contour defects. A, This patient has a left modified radical mastectomy defect.
B, Design of contralateral TRAM flap based on the superior epigastric artery and associated venae comitantes for au-
togenous breast reconstruction. C, Flap transposed 90 degrees to contralateral chest wall defect to provide soft tissue
and skin for breast reconstruction. The abdominal fascial defect is reconstructed with Prolene mesh. D and E, Post-
operative views at 1 year demonstrate results of single-stage breast reconstruction with direct closure of donor defect
and adequate autogenous tissue to achieve breast mound projection. (From Mathes SJ, Nahai F: Reconstructive Surgery:
Principles, Anatomy, and Technique. New York, Churchill Livingstone. 1997.)

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438 • GENERAL PRINCIPLES

FIGURE 1 6 - 5 4 . TRAM flap for breast reconstruction. A, The

patient has recurrent breast cancer after right lumpectomy and
radiation therapy. She desires autogenous reconstruction after
mastectomy. B, Preoperative design of transverse skin island for
TRAM flap. C, Left TRAM flap transposition to right mastectomy
defect. The lateral third of the rectus abdominis muscle is pre-
served at the donor site for partial function preservation. D, Post-
operative anterior view at 1 year demonstrates right autogenous
breast reconstruction with TRAM flap. E, Lateral view demon-
strates normal abdominal contour at donor site and adequate
breast projection and symmetry with contralateral breast.

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16 • FLAP CLASSIFICATION AND APPLICATIONS 439

FIGURE 1 6 - 5 5 . TRAM flap for breast reconstruction. A, Preoperative anterior view after left radical mastec-
tomy and adjuvant radiotherapy. B, Preoperative lateral view. C, TRAM flap before insetting. Note the donor
site at the bottom. D, Prolene mesh is used to reinforce anterior fascial closure. Note that the point of rotation
of the rectus muscle is at the left costal margin. Continued

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440 I • GENERAL PRINCIPLES
FIGURE 16-55, cont'd. E, Postoperative anterior view. F, Postoperative lateral view. (From Mathes SJ, Eshima
I: The principles of muscle and musculocutaneous flaps. In McCarthy JC, ed: Plastic Surgery. Philadelphia, WB
Saunders, 1990:379.)
The major disadvantage of the TRAM flap is the
potential risk of abdominal hernia or weakness after
the use of the single or bilateral rectus muscles for the
flap harvest.178
The long-term effect of the loss of one or both
rectus abdominis muscles has been the subject of many
investigations.179 Most studies report qualitative rather
than quantitative data with regard to the postopera-
tive strength of the abdominal wall. However, studies
are beginning to show qualitative deficits of abdom-
inal wall muscle loss.180 Overall, the majority of
patients resume normal activities without physical
limitations after use of the TRAM flap for breast
reconstruction.
Reconstruction of the breast with microvas-
cular tissue transplantation has become the primary
method in some centers. Several musculocutaneous
flaps have been described, with the rectus abdominis
being the most common.181 In addition, the superior
and inferior gluteus maximus musculocutaneous
flaps have been used for breast reconstruction.182,183
In addition to musculocutaneous flaps, perforator
and fasciocutaneous flaps are being used more fre-
quently. Perforator flaps have been advocated because
of frequent use and the theoretical advantage of less
morbidity at the donor site. They include the deep infe-
rior epigastric perforator flap, the superior gluteal artery
perforator flap, the inferior gluteal artery perforator
flap, and the superficial inferior epigastric artery
flap.184''86
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MEDIASTINUM
REGIONAL FLAPS
Pectoralis major
DISTANT FLAPS
Rectus abdominis
Latissimus dorsi
Omentum
MICROVASCULAR FLAPS
Latissimus dorsi
The most common reason for reconstruction of the
mediastinum is infection after median sternotomy.
Although the incidence of infection after median ster-
notomy is low, reported from 0.4% to 6.9%, the mor-
bidity and mortality are significant.187 The treatment
of an infected median sternotomy wound depends on
the extent of the infection and the amount of tissue
necrosis. Historically, the standard therapy for an
infected median sternotomy wound included debride-
ment and closed tube irrigation. Muscle flap coverage
was generally reserved for wounds recalcitrant to stan-
dard therapy. Now, it is generally accepted that early
muscle flap transposition decreases morbidity, and
therefore the use of a muscle flap should always be
considered for the treatment of median sternotomy
wounds.
The preferred local muscle for mediastinal cover-
age is the pectoralis major. In 1980, Jurkiewicz et al188
described the use of the pectoralis major muscle flap
image...
16 • FLAP CLASSIFICATION AND APPLICATIONS
to obliterate the sternal-mediastinal dead space. The
pectoralis major can be mobilized in several ways.
The muscle can be transposed either on the dominant
thoracoacromial pedicle or as a turnover flap on the
segmental secondary vascular pedicles (perforating
vessels from the internal mammary artery and vein).
Nahai et al189 described a modified technique of the
turnover flap that preserves the lateral third of the
muscle based on the dominant vascular pedicle and
its motor nerves. The advantage of this technique is
the preservation of the anterior axillary fold. The
pectoralis muscle flap remains the mainstay of treat-
ment in both adults and children with sternal wound
infections. m'in
Depending on the size of the defect, the surgeon
can use one or both pectoralis major muscles for cov-
erage.193 If additional coverage is needed, the rectus
abdominis can be used along with the pectoralis major
muscles to cover the inferior aspect of the wound. 194
Used as either a muscle or musculocutaneous flap, the
rectus abdominis muscle is a reliable source for infe-
rior mediastinal coverage; as well, it provides the ability
to fill a large dead space.195,196 In considering the use
of the rectus abdominis muscle, it must be noted that
the superior epigastric artery is the continuation of
the internal mammary artery inferior to the sternum
that should be avoided during debridement of the
sternal wound. Furthermore, the use of the internal
mammary artery as a coronary artery bypass graft may
adversely affect perfusion of the superiorly based rectus
abdominis flap, which precludes the use of the rectus
flap on that side. Collateral circulation to the internal
mammary vessels distal to the site of ligation during
coronary bypass will generally allow adequate perfu-
sion through the superior epigastric artery and vein
for superior transposition to the mediastinum (Figs.
16-56 to 16-58).
The omentum is an alternative source of tissue avail-
able to be transferred for mediastinal reconstruction;
it may be used solely or in combination with another
flap. 197 The omentum can be based on the right or left
gastroepiploic vessels. In view of the risk of exposing
the peritoneum to a contaminated field, however, the
omentum is generally reserved for patients in whom
the pectoralis major and rectus abdominis muscles are
unavailable.198 The harvest of the omentum has been
achieved laparoscopically to lower the potential
abdominal wall morbidity.199
The latissimus dorsi provides another alternative
muscle or musculocutaneous flap for coverage of the
upper mediastinum.200 Its use is usually indicated when
the pectoralis major is absent or damaged by previ-
ous incisions or radiation therapy.201 The advantage
of using the latissimus dorsi muscle or musculocuta-
neous flap is that the vascular pedicle and the donor
site are distant to the infected area.202 The disadvan-
tages include the inconvenience of obtaining a muscle
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441
flap from the back and that the latissimus dorsi muscle
may be too thin for the deeper, more extensive medi-
astinal defects. The latissimus dorsi can also be trans-
ferred microsurgically to sternal wound defects.203
CHEST WALL AND PULMONARY CAVITY
REGIONAL FLAPS
Pectoralis major
Latissimus dorsi
Serratus anterior
DISTANT FLAPS
Rectus abdominis
Omentum
MICROVASCULAR FLAPS
Latissimus dorsi
Rectus abdominis
Reconstruction of the chest wall is challenging. Abla-
tive surgery for neoplasm, infection, radiation damage,
and trauma can produce extensive full-thickness chest
wall defects. Furthermore, many of the patients in need
of reconstruction have previously undergone some
form of chemotherapy or high-dose irradiation
for their primary disease. Wound healing can
therefore be severely compromised at the time of
reconstruction.
Historically, methods of chest wall reconstruction
consisted of various random and tube flaps that often
required several stages before completion. Currently,
the reconstruction of the chest wall is successfully
accomplished without the need for delay or staged pro-
cedures. Partial-thickness defects with viable muscle
at the wound bed can be managed with skin grafting;
larger full-thickness defects require flap reconstruc-
tion. In addition to flap reconstruction, Prolene mesh
is indicated for chest wall reconstruction to provide
stability and support for the overlying flap when there
is significant loss of chest wall continuity.204,205
The pectoralis major and latissimus dorsi muscles
and musculocutaneous flaps are the most commonly
used in chest wall reconstruction (Fig. 16-59). Larson
and McMurtrey^stated that the pectoralis major mus-
culocutaneous flap is the flap of choice for defects of
the lower neck and upper third of the sternum,
whereas the latissimus dorsi musculocutaneous flap
is preferred for wounds of the anterior chest wall that
will require removal of two or three ribs and resection
of less than 8 cm of skin. In these authors* series of 53
flaps in 50 patients, the musculocutaneous flap alone
provided adequate support and stability. Fascia, ribs,
and prosthetic mesh were not needed for support.
The use of the latissimus dorsi flap in a patient who
has previously undergone a thoracotomy decreases
the reliability of the pedicle and safety of subsequent
ipsilateral flap transposition, although previous
Text continued on p. 446
442 I • GENERAL PRINCIPLES

Arc to anterior mediasti

A

Arc to sternum and anterior mediastinum
B 1997.)
FIGURE 1 6 - 5 6 . Pectoralis
major flap. ^, Standard arc to ante-
rior mediastinum based on thora-
coacromial pedicle.fi, Turnover arc
to anterior mediastinum based on
perforator vessels from internal
mammary artery and associated
veins. (From Mathes SJ, Nahai F:
Reconstructive Surgery: Princi-
ples. Anatomy, and Technique-
New York, Churchill Livingstone,

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T^WK^aaciWimage...

16 • FLAP CLASSIFICATION AND APPLICATIONS 443

FIGURE 1 6 - 5 7 . Bilateral pectoralis major muscle flaps for mediastinal reconstruction. Flap rotation was based
on the major vascular pedicle—type V muscle. A, Chronic mediastinal wound infection 14 months after a myocar-
dial revascularization procedure. B, Wound debridement included removal of bilateral costal cartilages and the medial
third of both clavicles. The bilateral pectoralis major muscle flaps were elevated for wound coverage. The arrows
indicate the site of the vascular pedicle (thoracoacromial artery). C Bilateral pectoralis major muscle flaps provide
coverage at the site of the mediastinal and cartilage debridement. D, Postoperative view at 2 years. The patient has
stable chest wall coverage without recurrent infection. (From Mathes S: Muscle flaps and thoracic problems: cov-
erage of a chronic and infected mediastinal wound. In Kittle CF, ed: Current Controversies in Thoracic Surgery.
Philadelphia, WB Saunders, 1986:246.)

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TfeWt^<aelcrw image...

444 I • CENERAL PRINCIPLES

FIGURE 16-58. Pectoralis major muscle flap for coverage of a mediastinal defect. Flap rotation was based on the
segmental secondary vascular pedicles—type V muscle. A, Diabetic patient with an anterior mediastinal infection
after a coronary artery bypass graft (left internal mammary artery). B, After complete debridement of the left sternum
and partial debridement of the right sternum, the right pectoralis major muscle was elevated on the segmental vas-
cular pedicles from the right internal mammary artery, the muscle was split at the fourth intercostal space into two
flaps (a and b). C, Flap a was placed into the superior anterior mediastinum. Flap b completed coverage of the infe-
rior mediastinal defect. D, Postoperative view at 6 months. (From Mathes SJ, Eshima I: The principles of muscle and
musculocutaneous flaps. In McCarthy JC, ed: Plastic Surgery. Philadelphia, WB Saunders, 1990:379.)

FIGURE 16-59. Pectoralis major muscle flap transposition with split rib grafts for anterior chest. A, Preoperative
anterior view of patient presenting with sternal tumor. B, Radiographs demonstrate soft tissue tumor involving ante-
rior chest and sternum. C, Specimen after resection of sternum and bilateral costal cartilages. D, Anterior chest wall
defect including absence of sternum and costal cartilages. E, Split ribs provide bone support for bilateral pectoralis
major muscle flaps. F, Postoperative view at 2 years demonstrates stable chest wall reconstruction. C, Postoperative
view demonstrates full range of motion with bilateral pectoralis major muscle flaps in continuity with split rib grafts for
anterior chest reconstruction.

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16 • FLAP CLASSIFICATION AND APPLICATIONS 445

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446 I • GENERAL PRINCIPLES
thoracotomy is not an absolute contraindication. In
fact, Scheflan et al207 reported that a standard antero-
lateral thoracotomy, which separates the latissimus
dorsi into an upper third and lower two thirds, does
not preclude the subsequent use of the muscle as a
flap. More recently, the latissimus dorsi muscle has been
used successfully in patients who had undergone pre-
vious posterolateral thoracotomy.208 The upper third
of the latissimus dorsi muscle, based on the thora-
codorsal pedicle, may be used to cover superior antero-
lateral chest wall defects. The lower two thirds of the
muscle, based on its secondary pedicles from the
paraspinal perforators, can be used as a reverse latis-
simus dorsi flap with or without the overlying skin to
cover inferolaterai and posterior chest wall defects. Early
work by McCraw et al209 and Bostwick et al105 was instru-
mental in the development of the reverse latissimus
dorsi flap. Latissimus dorsi muscle and musculocuta-
neous flaps have proved invaluable in the treatment
of numerous chest wall and pulmonary cavity disor-
ders, including Poland syndrome,210,211 spina bifida
defects,212,215 and diaphragmatic hernias.214,215
The serratus anterior muscle can also be useful as
a local muscle flap for chest wall and pulmonary cavity
reconstruction.The serratus muscle has a constant and
reliable vascular pedicle and a long arc of rotation.216
Arnold et al217 described its use in reconstruction of
the chest wall, closure of bronchopleural fistulas, and
reinforcement of tracheal reconstructions. The serra-
tus may be surgically split, thereby using only a
portion for reconstruction.76
The rectus abdominis muscle is a distant muscle or
musculocutaneous flap for chest wall reconstruction.
Larson et al206 showed that the rectus abdominis mus-
culocutaneous flap is particularly useful for large chest
wall defects. The availability of the flap is dependent
on the status of the internal mammary arteries.
Miyamoto et al218 favored the rectus abdominis mus-
culocutaneous flap over the latissimus dorsi in chest
wall reconstruction because of its convenience (the
patient can remain in one position intraoperatively)
and the ease of elevation and subsequent closure of
the donor site. In addition, it is thought that in situa-
tions when up to three ribs are removed and recon-
structed with mesh, the rectus shows a distinct
advantage given its thickness, which minimizes the risk
of a resultant flail chest wall.219 Large defects of the
chest wall within the arc of rotation of the rectus can
be reconstructed. The rectus abdominis muscle may
be used as a transverse or vertically oriented muscu-
locutaneous flap.220
If the internal mammary vessels have been
manipulated, the rectus flap is often transferred
microsurgically.221
The omentum is also used for chest wall recon-
struction. The omentum can be harvested laparo-
scopically, obviating the need for a large abdominal
incision. When it is used as a transposition flap, the
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omentum can be based on either the right or left gas-
troepiploic vessels. The omentum has a large surface
area, obliterates dead space, is pliable, and contains
angiogenic and immunogenic properties. The use of
the omentum in chest wall reconstruction secondary
to osteoradionecrosis, cancer ablation, and chronic
wounds is well established.59
ABDOMINAL WALL
REGIONAL FLAPS
Rectus abdominis
External oblique
DISTANT FLAPS
Tensor fascia lata
Latissimus dorsi
Rectus femoris
MICROVASCULAR FLAPS
Tensor fascia lata
Latissimus dorsi
Rectus femoris
Anterolateral thigh
Groin
In reconstruction of abdominal wall defects, the sur-
gical objective is to provide soft tissue coverage in addi-
tion to re-establishing the abdominal wall integrity.
To plan safe and reliable techniques for wound closure,
it is helpful to classify complex wounds by location
and the status of the overlying skin and soft tissue cov-
erage. In regard to location, the abdominal wall
is divided into four zones: zone 1A, upper midline
defects with extension across the midline; zone IB,
lower midline defects with extension across the midline;
zone 2, upper quadrant defects; and zone 3, lower quad-
rant defects (Fig. 16-60 and Table 16-13).
The two muscles available for local flaps are the
rectus abdominis and the external oblique. The rectus
abdominis muscle or musculocutaneous flap is the flap
of choice for unilateral abdominal wall defects. In 1977,
Mathes175 described the use of the rectus abdominis
musculocutaneous flap for reconstruction of an
abdominal wall defect. Parkash and Ramakrishnan22'
reported the use of a rectus abdominis musculocuta-
neous island flap for coverage of an extensive
radionecrotic abdominal wall ulcer that had been resist-
ant to conservative therapy. In 1983, Taylor et al119
described the extended deep inferior epigastric flap,
which consists of an inferiorly based rectus abdominis
musculocutaneous flap with a superolateral fasciocu-
taneous extension. With this larger skin territory, exten-
sive defects of the abdomen as well as those of the groin
and thigh have been successfully treated.
The rectus may be released from its lateral attach-
ments to achieve midline abdominal wall closure.
Several variations have been described. One variety,
termed separation of components, involves separation
of the external oblique fascia with an incision just
*&W>ttf<y«ltf,W image...
16 • FLAP CLASSIFICATION AND APPLICATIONS
FIGURE 16-60. A and B, Reconstruc-
tive zones of the abdomen (see Table 16-
13). (From Mathes SJ, Steinwald PM,
Foster RD, et al: Complex abdominal wall
reconstruction: a comparison of flap and
mesh closure. Ann Surg 2000:232:586.)
lateral to the linea semilunaris, allowing a plane to
develop between the external and internal oblique
muscles.223 This permits medial mobility of the rectus
abdominis muscle. Other variants of sliding myofas-
cial partitions or releases have been used successfully
to reconstruct the abdominal wall.175,224 Alternatively,
the rectus may be used as a turnover flap to achieve
closure.225
The external oblique muscle may be used to recon-
struct absent or deficient rectus fascia.226 The external
oblique musculocutaneous flap is an alternative local
flap, useful for reconstruction of small, full-thickness
upper abdominal wall defects.227'229 The external
oblique musculofascia may also be expanded and
advanced centrally to repair abdominal wall
defects.230'231
The distant muscle and musculocutaneous flaps
used in abdominal wall reconstruction include the latis-
simus dorsi, tensor fascia lata, and rectus femoris flaps.
Transposition of the latissimus dorsi musculocuta-
neous flap is a reliable technique for superolateral
abdominal wall defects.232,233 This flap is particularly
TABLE 16-13 • FLAPS FOR ABDOMINAL RECONSTRUCTION BY LOCATION (ZONE)
Flaps
Latissimus dorsi
Rectus abdominis Superiorly based
Inferiorly based
Advancement
External oblique advancement
Tensor fascia lata Transposition
Expansion
Rectus femoris
Modified fromMathesSJ,SteinwaIdPM,FosterRD,etai:Cornplex abdominal wall rcconstruction:acomparisonofflapand mesh closure. AnnSurg2000;232:586.
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447
c1 :
2 2
3 3
\ ^
* - • "T t
useful in traumatic defects, burn injuries, and post-
extirpative defects.234"236 The latissimus dorsi can also
be transferred microsurgically to cover central abdom-
inal defects.237 This flap may also be reinnervated and
has shown enough contractile capacity and strength
to adequately replace the function of the missing
abdominal wall muscles (Fig. 16-61).238
The use of the tensor fascia lata (TFL) as a muscu-
locutaneous and musculofascial flap is indicated for
lower abdominal wall reconstruction. Wangensteen239
initially described use of this flap for lower abdomi-
nal wall closure. The unique qualities of the TFL flap
include the large amount of vascularized fascia and
skin and the low donor site morbidity.240*242 The TFL
is most commonly used as a rotational flap, although
success as a free flap has been demonstrated. 243 As a
rotational flap, the arc of rotation is limited to the lower
abdominal wall, whereas when it is used as a free flap,
any region of the abdominal wall may be reconstructed
(Fig. 16-62).244
The rectus femoris musculocutaneous flap is a
dependable alternative flap for abdominal wall recon-
Zones
M IB 2 3
X
X X
X
X
X X
X X X X
X X
448 I • GENERAL PRINCIPLES

V.

FIGURE 1 6 - 6 1 . Latissimus dorsi musculocutaneous flap for zone 2 abdominal wall reconstruction. A, Pre-
operative view of radiation necrosis defect in left upper quadrant after hepatic cancer resection, B, Debride-
ment includes resection of necrotic abdominal wall and costal cartilages. C, Elevation of ipsilateral latissimus
dorsi muscle with associated skin island for transposition to abdominal wall defect. D, Postoperative view at 1
year demonstrates stable coverage with closure of defect, (From Steinwald PM, Mathes SJ: Management of
the complex abdominal wall wound. Adv Surg 2001 ;35:77.)

struction.245,246 Variations of the rectus femoris flap, large defects and to avoidstaged reconstruction. Common
including the use of fascial extensions and tissue expan- flaps microsurgically transferred to the abdomen
sion, have been described to extend its arc of rota- include the latissimus dorsi flap, anterolateral thigh
tion.247,248 However, it tends to be bulkier than theTFL flap, groin flap, TFL flap, and rectus femoris flap.251"2
flap and has greater donor site morbidity. Leg exten-
sion may be adversely affected with the use of this flap, GROIN AND PERINEUM
although subsequent studies show no appreciable
REGIONAL FLAPS
effect.247,249 In certain instances, the rectus femoris flap
Sartorius
is preferred to the TFL flap. An example would be the
use of the rectus femoris to treat a radionecrotic ulcer DISTANT FLAPS
involving the lower abdominal wall, given the need Gracilis
for muscle bulk to fill the defect (Fig. 16-63).250 Tensor fascia lata
Microvascular composite tissue transplantation to Rectus femoris
the abdomen, although uncommon, is a potential Rectus abdominis
reconstructive option. This may be the best option for Gluteus maximus

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 16 • FLAP CLASSIFICATION AND APPLICATIONS 449

FIGURE 1 6 - 6 2 . TFL musculocutaneous flap for zone 3 abdominal wall reconstruction. A, Right
lower quadrant fascial defect after dehiscence that followed renal transplantation. B, Arc of rotation
of standard TFL musculocutaneous flap to inferior abdominal wall defect. C, Postoperative view demon-
strates TFL musculocutaneous flap reconstruction that provides autogenous fascia for fascial recon-
struction and skin island for abdominal coverage. D, Lateral view demonstrates direct donor site
closure and site of flap inset into abdominal wall.

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 *

I • GENERAL PRINCIPLES

FIGURE 16-63. Rectus femoris musculocutaneous flap with intraperitoneal mesh for management of
chronic type II, zone 1B defect- A, Preoperative anterior view of woman with radiation necrosis of infe-
rior abdominal wall after radiation treatment for bladder carcinoma. B, Intraperitoneal Prolene mesh
restores fascial continuity after wound debridement and cystectomy with ileal loop urinary diversion. C,
Left rectus femoris musculocutaneous flap. Transposition will provide coverage of mesh and restore skin
continuity. D, Postoperative view at 2 years demonstrates stable coverage and closure of fascial defect.
(From Steinwald PM, Mathes SJ: Management of the complex abdominal wall wound. Adv Surg 2001 ;35:77.)

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image...

6 • FLAP CLASSIFICATION AND APPLICATIONS 451

Reconstruction of the groin and perineum is often indi-
cated for defects due to trauma, tumor resection, and
infection. The wounds can be extensive and because
of their proximity to the anus and urethra are sus-
ceptible to fecal and urinary contamination. In addi-
tion, wounds involving the groin may expose the
femoral vessels. Vascular prosthetic grafts and adjunc-
tive radiation therapy in the cancer patient can further
compound the problem.
The sartorius is a type IV muscle with multiple seg-
mental vascular pedicles that limit its arc of rotation.
The division of one or two of the most proximal pedi-
cles, however, enables the superior aspect of the sar-
torius muscle to be transposed medially into the groin.
This technique is used for coverage of exposed femoral
vessels and prosthetic vascular grafts.256
The gracilis is a type II muscle that has both an ante-
rior and posterior arc of rotation. Anteriorly, the muscle
can be used for groin and perineal reconstruction;
posteriorly, ischial and perirectal defects can be recon-
structed.257*259 Other common uses of the gracilis muscle
and musculocutaneous flap include reconstruction of
the vagina, penis, scrotum, and anal sphincter (Fig.
16-64).22-260-262
The tensor fascia lata is particularly useful for groin
and perineal reconstruction.263,264 It can be used as either
a musculocutaneous flap or a musculofasciai flap. The
tensor fascia lata is also used in vulvar reconstruction
and recurrent inguinal hernia reconstruction.2"10
The rectus femoris is useful for coverage of the groin
and perineum.265,266 It is a large, bulky muscle that has
an arc of rotation similar to that of the tensor fascia
lata. Despite its reliability and desirable bulk, this
muscle is generally used as an alternative flap in the
ambulatory patient, given the potential functional
deficit associated with its harvest, although more recent
evidence suggests that the results of the reconstruc-
tion appear to outweigh the loss of strength.240,267
The rectus abdominis muscle or musculocutaneous
flap based on its inferior pedicle provides a reliable
flap for defects of the anterior pelvis and groin.175,250,268
Its wide arc of rotation and abundant blood supply

FIGURE 1 6 - 6 4 . Bilateral gracilis and gluteal thigh flaps for reconstruction of a radiation defect of the perineum.
A, Necrotic lesion of the perineum and sacral cavity after radiation therapy and abdominoperineal resection for
carcinoma of the rectum. The wound extended from the perineum into the pelvic cavity at the level of the peri-
toneal reflection. B, Bilateral gracilis (g) and gluteal thigh (f) fasciocutaneous flaps elevated for wound coverage.
C, After de-epithelialization of the distal half of both gluteal thigh flaps, which were used to fill the pelvic cavity
and to provide skin coverage. The arrows denote the site of flap de-epithelialization; f, skin surface of the gluteal
thigh flap. D, Stable wound coverage 1 year after repair. The flap donor sites were closed primarily. (From Mathes
SJ, Hurwitz DJ: Repair of chronic radiation wounds of the pelvis. World J Surg 1986; 10:274.)

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TWffWaatfw image...

452 I • GENERAL PRINCIPLES

through the inferior epigastric vessels make it an excel-
lent reconstructive flap for this region. The vertical
rectus abdominis musculocutaneous flap is useful for
large, irradiated defects in the perineum (Figs, 16-65
and 16-66).'2*269'270
The gluteus maximus muscle provides stable cov-
erage for pelvic and perineal defects. Its large mass is
particularly useful for obliterating pelvic dead space
and coveringperineal wounds; it is also useful for rectal
sphincter reconstruction.271,272 The gluteus maximus
fasciocutaneous V-Y advancement flap is reliable for
extensive vulvectomy and recurrent rectal cancer
defects.273,274 The gluteal thigh flap, described by
Hurwitz,94 includes the inferior part of the gluteus

Arc to groin and perineum

Arc to internal pelvis

B
FIGURE 16-65. Rectus abdominis flap. A, Arc to groin and perineum. 8, Arc to internal pelvis. (From
Mathes SJ, Nahai F: Reconstructive Surgery: Principles, Anatomy, and Technique. New York, Churchill Liv-
ingstone, 1997.)

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 16 • FLAP CLASSIFICATION AND APPLICATIONS 453

*NiM

FIGURE 1 6 - 6 6 . Rectus abdominis musculocutaneous flap

for groin coverage. A, Left groin defect after radical groin dis-
section for recurrent melanoma. B, Design of transverse skin
island for right rectus abdominis musculocutaneous flap for
left groin coverage. C, Donor site closed directly. The flap is
inset over the previously irradiated groin defect. D, Postop-
erative view demonstrates stable coverage at left groin and
right superior flap donor site.

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454 I • GENERAL PRINCIPLES
maximus muscle and a large cutaneoLis territory of the
posterior thigh that is supplied by the descending
branch of the inferior gluteal artery. The gluteus
maximus musculocutaneous and gluteal fasciocuta-
neous flap is particularly useful for reconstruction of
deep perineal and pelvic defects.95,275
LOWER EXTREMITY
REGIONAL FI.APS
Gastrocnemius
Soleus
DISTANT FLAPS
Cross-leg
MICROVASCULAR FLAPS
Latissimus dorsi
Rectus abdominis
Gracilis
Fibula
Omentum
Reconstruction of the lower extremity remains
particularly challenging. Defects including exposed
joints and prostheses, infected bone, and fractures are
common. Furthermore, the availability of adequate soft
tissue for coverage is limited, particularly in the lower
third of the leg.
Two local sources of muscle or musculocutaneous
flaps are available for reconstruction of the leg, the gas-
trocnemius and the soleus muscles. The use of distant
flaps involves microvascular transplantation of various
muscles, depending on the size of the wound and the
surgeon's preference. Many muscles have been
described, including the gracilis, latissimus dorsi,
and rectus abdominis. Cross-leg flaps are also avail-
able but have largely been supplanted by either
local muscle flaps or microvascular composite tissue
transplantation.
The gastrocnemius is a type I muscle consisting of
a medial and a lateral head. Each head has a wide arc
of rotation based on its single vascular pedicle (medial
or lateral sural vessels). The gastrocnemius muscle or
musculocutaneous flap is the flap of choice for cover-
age of the knee and for coverage of exposed bone or
orthopedic hardware involving the upper two thirds
of the leg.276,277 Defects of the middle third of the leg
can also be reconstructed with the gastrocnemius
muscle.278"280 In patients with radical knee debridement
with loss or disruption of the extensor mechanism,
the gastrocnemius can be used to restore knee func-
tion (Figs. 16-67 and 16-68).281
The soleus muscle flap is used for reconstruction
of defects involving the middle third of the leg. The
soleus muscle is the prime ankle plantar flexor, and it
serves to stabilize the ankle in ambulation by oppos-
ing dorsiflexion.282 Because of compensatory mecha-
nisms, the use of the soleus muscle as a flap does not
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impair function at the donor site. Function-preserv-
ing technique, such as muscle splitting, is recommended
if the soleus is used in a patient who does not have a
functional medial and lateral gastrocnemius
muscle.:a',,:s4 Defects of the proximal third can be
reached by the soleus, but this requires extensive mobi -
lization of the muscle.285 In the lower third of the leg,
the soleus muscle can be used as a proximally or dis-
tally based flap. In this region, however, the soleus
muscle flap is generally used for smaller defects (Figs.
16-69 and 16-70). Larger defects require microvascu-
lar tissue transplantation.
Microvascular tissue transplantation has had a
significant impact on lower extremity reconstruction.
Muscles such as the latissimus dorsi, rectus abdominis,
and gracilis have been used successfully to reconstruct
extensive post-extirpative and traumatic defects.286"288
Other useful flaps include the fibula flap, based on the
peroneal vessels to reconstruct large tibial defects, and
the omentum, which provides a large area of well-vas-
cularized and malleable tissue.289,290 Advances in lower
extremity microsurgery now offer better functional and
sensate reconstructions.82
In certain individuals, microvascular tissue trans-
plantation is not possible. For those patients, alterna-
tive methods of reconstruction include the
fasciocutaneous, random-pattern, and cross-leg flaps.
Various local fasciocutaneous flaps have also been
identified and are of clinical utility. In 1981, Ponten23
described several fasciocutaneous flaps that are useful
in the repair of soft tissue defects on the lower leg.
Examples include the anterior tibial artery flap, per-
oneal artery flap, sural flap (proximally or distally
based), posterior tibial artery flap, and saphenous
flap.291,292 The distally based sural flap has proved useful
in coverage of defects at the lower leg and foot in both
adults and children.293'294
FOOT
REGIONAL FLAPS
Flexor digitorum brevis
Abductor hallucis
Abductor digiti minimi
DISTANT FLAPS
Cross-foot
MICROVASCULAR FLAPS
Gracilis
Latissimus
Rectus abdominis
Serratus
Defects of the foot are most often due to trauma
or the long-standing effects of underlying systemic
disorders, such as diabetes mellitus and peripheral
vascular disease. These wounds can be extremely
Text continued on p. 462
 16 • FLAP CLASSIFICATION AND APPLICATIONS 455

B
FIGURE 1 6 - 6 7 . Gastrocnemius flap. A and B, Arc to knee and upper third of leg. (From
Mathes SJ, Nahai F: Reconstructive Surgery: Principles, Anatomy, and Technique. New
York, Churchill Livingstone, 1997.)

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456 I • GENERAL PRINCIPLES

FIGURE 16-68. Gastrocnemius musculocutaneous flap for knee and proximal third of tibia defect. A, The patient
sustained a close-range gunshot wound. The defect after debridement of the left knee is shown. B, Medial gastrocne-
mius musculocutaneous flap elevated with division of both origin and insertion, preserving the sural artery and asso-
ciated veins to muscle flap. The transverse skin island is designed at the distal portion of the muscle flap. C, Arc of
rotation of medial musculocutaneous flap to knee and proximal third of the leg. D, Flap is passed through tunnel to
anterior tibial defect. E, Muscle portion of flap is inset into the defect. The skin island provides stable cutaneous cov-
erage and will serve as cover for later knee joint replacement. F, Early postoperative result demonstrates stable cov-
erage at flap inset site. C, Postoperative view at 3 years after prosthetic knee joint replacement demonstrates stable
coverage provided by the gastrocnemius musculocutaneous flap.

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A&WWafltfW image...

16 • FLAP CLASSIFICATION AND APPLICATIONS 457

A B
FIGURE 1 6 - 6 9 . Soleus flap. A and B, Arc to middle third of leg, medial approach.
Continued

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VtJWttf^KltSW image...

458 • GENERAL PRINCIPLES

FIGURE 1 6 - 6 9 , c o n t ' d . C and D, Arc to middle third of leg, lateral approach. E and
F, Arc to middle of leg, hemisoleus flap.

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Tt&Waed'Tee image...

16 • FLAP CLASSIFICATION AND APPLICATIONS 459

FIGURE 1 6 - 6 9 , cont'd. C and H, Arc to lower third of leg, hemisoleus flap. (From
Mathes SJ, Nahai F: Reconstructive Surgery: Principles, Anatomy, and Technique. New
York, Churchill Livingstone, 1997.)

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460 I • GENERAL PRINCIPLES

Origin Origin

Insertion

FIGURE 1 6 - 7 0 . Distally based flap modification. A, Soleus (type II) flap based on the dominant pedi-
cles, proximal branches of the posterior tibial (pt) and peroneal (pe) arteries. B, Radiographic view.
Note distal minor pedicles (arrows) on inferior portion of muscle.

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TekPW'SadW image...

16 • FLAP CLASSIFICATION AND APPLICATIONS 461

'

\ • *

F
FIGURE 1 6 - 7 0 , cont'd. C, Chronic wound of the distal third of the leg with exposed fibula and absent per-
oneal musculature. 0, Distal soleus muscle is elevated from the lateral approach; arrows, medially located minor
pedicles to distal muscle. E, Arc of rotation of the distal portion of the soleus with medial muscle continuity main-
tained. F, Skin grafts are applied to the exposed muscle belly. Postoperative view at 9 months reveals stable
wound coverage. (From Mathes SJ, Nahai F: Classification of the vascular anatomy of muscles: experimental and
clinical correlation. Plast Reconstr Surg 1981;67:117.)

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462 I • GENERAL PRINCIPLES

difficult to treat and often are best left uncovered

until the underlying disease is treated (e.g., by revas-
cularization). For some patients with severe, irreversible
underlying systemic disease, local conservative wound
care mav he the only appropriate form of therapy.
When reconstruction is necessary, several issues
must he addressed, such as the size of the defect and
the patients vascular, neurosensory, and weight-
bearing status. For small defects, skin grafts are often
the procedure of choice, provided there is adequate
protective soft tissue within the bed of the defect. For
small defects involving weight-bearing areas, axial
innervated skin flaps and fasciocutaneous flaps have
been successful in providing stable coverage.89,292 For
the deeper, more extensive foot defect, a muscle or mus-
culocutaneous Hap is usually necessary. The local
muscles available for use as flaps are the flexor digito-
runi brevis, the abductor hallucis, and the abductor
digiti minimi. These muscles are small and are inad-
equate for larger defects. The use of a distant muscle
(e.g., cross-foot flap) or microvascular composite tissue
transplantation is usually necessary for coverage of any
major wound (those with excessive size and depth or
with component loss).
Mathes et al15 demonstrated the anatomy of the
flexor digitorum brevis for use as a flap in 1974. It is
a type II muscle that measures approximately 1 0 x 4
cm. This muscle was then shown to be clinically useful
to cover a calcaneal defect in 1974 by Vasconez et al.19
In 1980, Hartrampf et al295 described a modification Arc to heel
of this technique, using the muscle as an island flap FIGURE 1 6 - 7 1 . Flexor digitorum brevis flap. Arc to
that increased the arc of rotation. As an island flap heel. (From Mathes SJ, Nahai F: Reconstructive Surgery:
based on the lateral plantar artery, the flexor digito- Principles, Anatomy, and Technique. New York, Churchill
rum brevis muscle reaches the malleolus and can cover Livingstone, 1997.)
the entire posterosuperior aspect of the heel pad. The
authors recommended that the patency of both the
dorsalis pedis and the tibialis posterior arteries be vascular supply.15 Based on this vascular pedicle, the
confirmed before the lateral plantar artery is divided. abductor hallucis can be elevated as a muscle or mus-
In patients who have occlusion of either the dorsalis culocutaneous flap, and it can reach defects just infe-
pedis or the tibialis posterior artery, the lateral plantar rior to the medial malleolus as well as defects of the
artery serves as a vital conduit of collateral flow and proximal medial aspect of the dorsum of the foot. Like
should not be divided for flap use. The flexor digito- the lateral plantar artery, the medial plantar artery
rum brevis, when transposed as a muscle flap, may should not be divided if either the dorsalis pedis or
provide stable coverage and is of benefit in both the posterior tibial artery is occluded. The abductor
diabetic and nondiabetic patients (Figs. 16-71 and hallucis muscle flap may be distally based to recon-
16-72).296'297 struct forefoot defects.300
The retrograde lateral plantar artery flap was The abductor digiti minimi is a type II muscle with
described by Reiffel and McCarthy298 in 1980. The branches of the lateral plantar artery as its dominant
flap is fashioned by dividing the lateral plantar vessels vascular pedicle.I5 This small muscle based on its dom-
proximally; the plantar fascia and the flexor digito- inant pedicle can reach defects adjacent to the lateral
rum brevis muscle can be elevated as a flap based on malleolus. However, because of its size, the flap is
distal retrograde flow. This flap is particularly useful limited in its ability to provide coverage of larger
for coverage of medial and lateral metatarsal head defects. In 1985, Yoshimura et al301 reported the use
defects.299 of a distally based abductor digiti minimi muscle flap.
The abductor hallucis is a type II muscle with This muscle flap based distally on the communica-
branches of the medial plantar artery as its dominant tion between the lateral plantar artery and the plantar

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image...

16 • FLAP CLASSIFICATION AND APPLICATIONS 463

FIGURE 1 6 - 7 2 . Flexor digitorum brevis musculocu-

taneous flap for heel coverage. A, Level V melanoma of
heel. B, Defect after wide local excision of calcaneus in
ambulatory patient. C, Flexor digitorum brevis elevated;
calcaneus partially resected. D, Arc of rotation of flap
over posterior calcaneus. E, Muscle flap inset. The tendon
of the flexor digitorum brevis is sutured into the Achilles
tendon, and the donor site is closed directly. F, Post-
operative view at 1 year demonstrates muscle flap with
skin graft closure. The patient was ambulatory with stable
coverage. (From Mathes SJ, Nahai F: Clinical applica-
tions for muscle and musculocutaneous flaps. St. Louis,
CVMosby. 1982.)

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464 I • GENERAL PRINCIPLES

arch can be used to cover small defects of the distal PRESSURE WOUNDS
half of the foot. The abductor digiti minimi may be REGIONAL FLAPS
harvested with the lateral calcaneal artery sensate skin Gluteus maximus
flap to cover plantar heel wounds. 302
For extensive foot defects> microvascular tissue DISTANT FLAPS
transfer is the procedure of choice given the lack of Tensor fascia lata
local tissues. The gracilis, latissimus dorsi, rectus Gracilis
abdominis, and serratus muscles have proved effec- Hamstrings
tive.WV3W In addition to muscle flaps, fasciocutaneous Omentum
flaps such as the anterolateral thigh flap and radial The gluteus maximus is a regional flap commonly used
forearm flap have been used successfully.139,306,307 Alter- for the surgical treatment of pressure sores. It is a type
native methods include the cross-leg and cross-foot III muscle, and it is the flap of choice for reconstruc-
flaps (Fig. 16-73). 30MBt tion of deep sacral and ischial pressure sores. Func-

v^**

FIGURE 16-73. Microvascular transplantation of the gra-

cilis muscle for foot reconstruction. A, Post-traumatic defect
on the plantar surface of the right heel with exposed cal-
caneus. Attempts at local wound care and skin grafting were
unsuccessful. B, Gracilis muscle prepared for microvascu-
lar transplantation, p, medial femoral circumflex artery and
paired venae comitantes; s, obturator nerve. C, Gracilis
muscle after revascularization by microvascular repair of
the pedicle end-to-side with the posterior tibial vessels. D,
Two-year postoperative view. The combination of muscle
flap with skin graft provided satisfactory contour with the
adjacent plantar foot surface. E, Close-up view of the recon-
structed heel demonstrates stable coverage in a fully ambu-
latory patient. (From Stevenson TR( Mathes SJ: Management
of foot injuries with free-muscle flaps. Plast Reconstr Surg
1986:78:665.)

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 16 • FLAP CLASSIFICATION AND APPLICATIONS 465

tion-preserving techniques, such as bilateral advance-

ment flaps using only the superior halves of the gluteus
maximus for sacral coverage, are recommended for the
ambulatory patient."8,310"'11 Variations in technique,
including the sliding gluteus maximus flap, the trans-
position gluteus maximus flap, and island flaps based
on musculocutaneous perforating vessels (muscle
preserving,), have been described.Sl'3M The sliding flap
is indicated for small sacral defects, whereas the trans-
position flap (unilateral or bilateral) is generally
appropriate for larger defects because it has a greater
range of coverage. For extensive pressure sores, the
gluteal thigh flap has also been useful.94,95,315"317
Three distant muscles used in the reconstruction
of pressure sores are the tensor fascia lata, the gracilis,
and the hamstrings. The tensor fascia lata (TFL) is a
type I muscle that is useful for reconstruction of
trochanteric pressure sores.241,316'318 It is also a reliable
alternative flap for ischial defects because of the fol-
lowing advantages: there is relatively low donor site
morbidity, especially in an ambulatory patient; the
flap provides vascularized, durable fascia; and the
flap can provide sensibility in certain instances.
Several investigators have described the use of the
innervated TFL flap, based on the lateral femoral cuta-
neous nerve (L2-3), for reconstruction of ischial FIGURE 1 6-74. Gracilis flap. Arc of rotation to per-
defects. They have reported successful restoration of ineum. (From Mathes SJ, Nahai F: Reconstructive Surgery:
protective sensibility without recurrence of pressure Principles, Anatomy, and Technique. New York, Churchill
ulceration in paraplegic patients with lesions below Livingstone, 1997.)
the L3 level.240'319,320
The major disadvantage of the TFL flap is its rel- The gluteus maximus muscle (type III) is well sit-
ative thinness, a problem for the deeper pressure sore. uated for coverage of both sacral and ischial pressure
In 1981, Scheflan318 described a technique to increase sores. There are a number of modifications for its
the bulk of the TFL flap. By de-epithelialization of the design and use for both ischial and sacral pressure sores.
distal aspect of the flap and folding of the inferior In general, it is preferable to use segmental transpo-
portion of the flap underneath, part of the flap gains sition, reserving the superior half of the muscle based
bulk. Used as a "sandwich" the modified flap can on the superior gluteal artery and associated venae
usually fill the deeper defect. Modifications in the comitantes for the sacral sore and the inferior half based
design of the TFL flap have been described in an on the inferior gluteal artery and associated venae
attempt to minimize the donor site morbidity. Prob- comitantes for the ischial sore.
lems such as dog-ears, excessive tension at wound For the sacral sore, the cutaneous territory of the
closure, skin necrosis at certain wound margins, and superior half of the muscle may be used as a V-Y
need for skin grafts have prompted techniques such advancement flap, or the skin island may be designed
as the bilobed TFL flap321 and the V-Y retroposition distally (near the muscle insertion) for use as a trans-
TFL flap.322,323 These modifications appear to facili- position flap or proximally (near the muscle origin)
tate donor closure in certain instances. in V-Y advancement. For V-Y advancement, the supe-
The gracilis is a type II muscle, first described in rior half of the muscled origin and insertion is divided
1972 by Orticochea13 for use as a musculocutaneous so the composite of muscle plus the overlying soft tissue
flap. In the treatment of pressure sores, the gracilis is will cover the debridement site of the sacral decubi-
used primarily to repair the ischial defect.324,325 Use of tus. Although perforating vessels will allow bilateral
the gracilis does not preclude the future use of the V-Y advancement of the skin island with release of
gluteus maximus or the posterior thigh flap if the ulcer the muscle, adequate well-vascularized soft tissue and
recurs. The muscle can be elevated with the patient muscle are required to provide a long-lasting stable
prone, but the distal muscle should be located before coverage over the sacrum (Figs. 16-76 and 16-77).
the skin island is incised to ensure the correct local- When it is used as a transposition flap, the skin island
ization of the skin overlying the muscle (Figs. 16-74 and underlying muscle are transferred 180 degrees to
and 16-75). provide sacral coverage. It is not necessary to divide

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image...

466 I • CENERAL PRINCIPLES

FIGURE 1 6 - 7 5 . Gracilis musculocutaneous flap for ischial

pressure sore coverage. A, The patient presented with deep
left ischial and superficial right ischial pressure sores.
B, Debridement of left ischial pressure sore including partial
ischiectomy. The left thigh mark denotes center of cutaneous
territory of gracilis muscle. C, Gracilis muscle with overlying
skin territory is elevated to ischium. The pedicle with medial
femoral circumflex artery and associated veins is preserved.
Distal half of skin island is de-epithelialized. D, Postoperative
view at 6 months demonstrates left ischial sore provided with
stable coverage by gracilis musculocutaneous flap.

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image...

t6 • FLAP CLASSIFICATION AND APPLICATIONS 467

FIGURE 1 6-76. Cluteus maximus-gluteal thigh flap. A, V-Y segmental muscle advancement (supe-
rior half of gluteus maximus muscle). Flap advancement for sacral coverage. B, V-Y segmental muscle
advancement (inferior half of gluteus maximus muscle). Flap advancement for sacral coverage. (From
Mathes SJ, Nahai F: Reconstructive Surgery: Principles, Anatomy, and Technique. New York, Churchill
Livingstone, 1997.)

the superior muscle origin, although partial to com-
plete release of the origin allows easier flap inset over
the sacrum (Fig. 16-78; see also Fig. 16-16A).
The inferior half of the gluteus maximus is ideal
for ischial sore coverage. The skin island is designed
near the muscle insertion. After splitting of the muscle,
the muscle and overlying skin island are easily rotated
90 degrees to the ischial defect. The condensed bulk
of the muscle and its specific cutaneous territory
provide stable coverage at the ischial site of recon-
struction (Fig. 16-79; see also Fig. 16-16B).
The hamstrings, consisting of the biceps femoris,
semimembranosus, and semitendinosus, are a group
of muscles of the posterior thigh. These muscles orig-
inate from the ischial tuberosity, although the biceps
femoris also has a short head originating from the linea
aspera of the femur. As a group, these muscles are useful
in the reconstruction of ischial pressure sores. Used
as a transposition flap, depending on the size of the
defect, one or more of the hamstring muscles may
provide ischial coverage. Hurteau et al326 described V-
Y advancement of the hamstring musculocutaneous
flap for reliable coverage of the ischial pressure sore.
A triangular island of skin overlying the hamstring
muscles is designed with the base of the triangle at
the inferior margin of the ischial defect. The hamstring
muscles are divided distal to the skin island, and the
entire muscle group is mobilized superiorly. The
origins of the hamstring muscles are detached from
the ischium, thus enabling further advancement, and
the flap is sutured into place. Long-term results reveal
stable coverage of ischial pressure sores.327
PREOPERATIVE AND
POSTOPERATIVE MANAGEMENT
Preoperative management is critical to the success of
a reconstruction. Education of the patient is of par-
ticular importance. Expectations of operative outcome
may differ considerably between the surgeon and the
patient. For example, the patient may not realize
the size of the donor scar or that a skin graft will be
taken. By thoroughly discussing the procedure with
the patient preoperatively, the surgeon can avoid these
misunderstandings.
A complete physical examination provides valuable
information. Evidence of previous incisions, muscle
atrophy, comorbid conditions, and vascular supply and

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468 I • GENERAL PRINCIPLES

FIGURE 1 6 - 7 7 . Gluteus maximus musculocutaneous flap for treatment of a sacra! pressure sore. A, Preopera-
tive view of a sacral pressure sore in a quadriplegic patient. B, Wound debridement included excision of the sinus
and the infected outer table of the sacrum. C, Right superior gluteus maximus musculocutaneous flap elevated and
based on the superior gluteal artery and veins. The muscle origin and superior half insertion are incised to permit
flap transposition into the sacral defect. The donor site is closed directly after V-Y advancement of the muscle flap.
D, Postoperative view at 6 months demonstrates stable wound coverage at the site of the sacral pressure sore.
(From Mathes SJ, Eshima I: The principles of muscle and musculocutaneous flaps. In McCarthy JG, ed: Plastic
Surgery. Philadelphia, WB Saunders, 1990:379.)

wound analysis may assist the surgeon in selecting the
most appropriate reconstruction. Additional diagnostic
measures (e.g., selective arteriography to delineate the
vascular anatomy) maybe indicated, depending on the
physical findings.
Wound analysis includes assessment of the defect
in terms of location, size, and physical components.
When the defect involves a significant percentage of
the body surface area (e.g., burns or giant hairy nevus),
the reconstructive options maybe limited to skin grafts
for acute coverage (e.g., burns) or sequential tissue
expansion for elective reconstruction (e.g., giant hairy
nevus). The components of a given defect may include
one or all of the following: skin, nerves, mucosa, fascia,
subcutaneous tissue, cartilage, muscle, bone, and
vessels. Each component affects function and form at
the defect site. Selection of a reconstructive option is
based on the feasibility and relative importance of
replacing each component of the defect.
Wound analysis must also include the vascular
status and bacteriology of exposed structures. Prior
surgical procedures, trauma, infection, radiation
therapy, or a combination of these factors may have
caused vascular injury and decreased circulation in all
structures within the potential zone of injury. Assess-
ment of the vascular status may be accomplished by
noninvasive means, such as Doppler ultrasonography
and magnetic resonance angiography, or by invasive
studies, such as arteriography. Selective arteriography
may be helpful to evaluate the transverse cervical artery

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 16 • FLAP CLASSIFICATION AND APPLICATIONS 469

FIGURE 1 6 - 7 8 . Superior half of gluteus maximus musculocutaneous flap for sacral cov-
erage. A Sacral pressure sore. B, Debridement of sacral pressure sore including resec-
tion of exposed outer table of sacrum. C, Elevation of superior half of gluteus maximus
musculocutaneous flap with split of mid-muscle and release of superior half of muscle's
insertion. D, Arc of rotation of flap to sacrum. E, Muscle inset directly into defect. The
donor site is closed directly with a small area of muscle flap skin grafted to avoid tension
at the donor site closure. F, Postoperative view at 6 months demonstrates stable cover-
age at sacral defect reconstruction site.

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image...

470 I • GENERAL PRINCIPLES

-.*•

C D
FIGURE 1 6 - 7 9 . Inferior half of gluteus maximus musculocutaneous flap for ischial coverage. A, Right ischial
pressure sore. B, Right ischial pressure sore debridement including left ischiectomy. The skin island is designed
over the distal cutaneous territory of the inferior half of the gluteus maximus muscle. C The gluteus maximus
muscle is split, and the inferior half of the muscle insertion is divided. D, Postoperative view at 1 year demon-
strates stable coverage at inset site of inferior half of gluteus maximus musculocutaneous flap for ischial pres-
sure sore reconstruction.

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Dr.Mustafa D.
image..
16 • FLAP CLASSIFICATION AND APPLICATIONS
in the patient with a history of radical neck dissection
or in the patient with a history of peripheral vascular
disease or trauma to the lower extremity before the
harvest of a fibular flap.
A careful assessment should be made of the extent
of debridement required to remove nonviable struc-
tures subject to bacterial invasion and impaired vas-
cularity. Inability to accurately predict the amount of
debridement required may necessitate sequential
wound debridement with subsequent wound obser-
vation and bacterial culture of the wound. When
regional vascular insufficiency involving the wound
site is observed, preliminary or simultaneous vascu-
lar procedures may be required in conjunction with
wound debridement and coverage.
The design of the flap is of paramount importance.
The final design of a flap intended for standard trans-
position, staged expansion, or microvascular trans-
plantation should be based on the actual defect size.
The original design of the flap has an impact on future
procedures if the defect should recur or require further
revisions. In general, flap design is delayed until ade-
quate wound debridement or tumor resection is
accomplished. If simultaneous flap elevation and
resection are performed, the flap design should allow
for the maximal defect size. If tissue expansion is used,
the expander advancement or transposition flap should
be elevated and advanced to the potential defect site
before the resection is performed. Repeated expansion
will be necessary if adequate tissue is not available to
cover the defect made at the resection site.
Prior incisions or trauma may either damage the
vascular pedicle or disrupt vascular connections
between the muscle or fascia and overlying skin. Selec-
tive arteriography is recommended to determine
the patency of the planned flap pedicle. Prior eleva-
tion of a random cutaneous flap represents a relative
contraindication to design of this skin as a musculo-
cutaneous or fasciocutaneous flap. Experimental
data have demonstrated successful elevation of a
musculocutaneous flap after an interval of 3 weeks
following separation of the skin territory from the
underlying muscle. Although clinical use of a previ-
ously elevated rotation flap as an island musculocu-
taneous flap after an interval of 6 months has
been reported, alternative flaps are preferred when
possible. Other considerations include whether the
patient has had suction lipectomy in the area of
flap harvest and the reliability of the local venous
drainage.
Identification of high-risk patients is important. Sys-
temic factors such as tobacco use, obesity, cardiovas-
cular disease (e.g., hypertension, peripheral vascular
disease), immunosuppression, and pulmonary disease
must be taken into account. These critical factors will
influence the selection of patients and flaps as well as
the success and durability of the final result.
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471
Tobacco use decreases skin circulation and is asso-
ciated with an increased risk of flap failure. Cessation
of smoking for 6 to 8 weeks before flap transportation
is recommended. In patients who require an emergency
flap procedure or who refuse to stop smoking, flap
design should not include a skin segment extending
beyond the primary territory of the muscle or fascial
flap.
Obesity may result in decreased reliability of the
cutaneous territory of muscle or fascia. Furthermore,
the thick flap has a reduced arc of rotation. A wide skin
island is recommended in the obese patient to ensure
incorporation of perforating vessels between muscle
or fascia and overlying skin.
In certain circumstances, flap selection may depend
on the reliability of the flap. Muscles with a single vas-
cular pedicle (type I), two dominant pedicles from
different vascular sources (type III), or a dominant
vascular pedicle with a secondary segmental pedicle
(type V) represent the most reliable patterns of muscle
flap circulation for a muscle or musculocutaneous flap.
Muscles with a dominant and single or multiple minor
pedicles (type II) or segmental pedicles (type IV) are
less reliable because the vascular pedicles to the distal
part of the muscle must be divided to achieve an ade-
quate arc of rotation. Similarly, fasciocutaneous flaps
with direct cutaneous (type A) orseptocutaneous (type
B) pedicles represent the most reliable pattern of cir-
culation. The fasciocutaneous flap based on pedicles
through muscle (type C) usually has several pedicles
at the flap base that may be less reliable.
Design of a skin island on a broad flap base is prefer-
able to design of a skin island on a narrow flap base.
Furthermore, design of the skin island at the midpor-
tion of the flap closer to the site of entrance of the
dominant vascular pedicle is preferable to design of a
skin island at the most distal aspect of the flap.
Positioning of the Patient
When possible, the patient is positioned to allow visu-
alization of both the donor and recipient sites. If this
is not possible, initial positioning should provide
optimal visualization of the recipient site if a major
resection is required.
Careful padding of the potential pressure sites is
necessary to avoid injury to normal structures. Areas
subject to pressure include the scalp, elbow, breast,
hip, sacrum, and feet. Axillary and chest padding is
recommended when the patient is placed in the lateral
decubitus and prone positions. A beanbag is also
helpful in maintaining appropriate positioning of the
patient without excessive pressure at sites of bone
prominences. During long procedures involving
microvascular composite tissue transplantation,
pressure sites should be checked for proper padding
midway through the procedure. Excessive abduction
472 I • GENERAL PRINCIPLES
of the upper extremity should be avoided to prevent
brachial plexus stretch injury.
Postoperative flap management is of equal
importance to the success of a reconstruction. The
maintenance of proper positioning, temporary im-
mobilization, and proper dressing of the wound are
critical.
Pressure on the flap base is to be avoided during
the postoperative period. When possible, the area of
the flap inset is elevated, as in head and neck and
extremity reconstruction. If the area of the flap lacks
protective sensation, the site of reconstruction is
placed in a nondependent position. Use of an air-
tluidized bed is recommended to avoid pressure on
dependent areas in patients with spinal cord injury.
Constricting bandages are avoided, particularly in
the area of the flap base, where pressure on the flap
pedicle may compromise flap circulation. The flap is
observed for potential circulatory problems during the
initial postoperative period. Those patients undergo-
ing head and neck reconstruction with microvascular
tissue transplantation should have strict orders to have
nothing placed circumferentially around the head or
neck. Nasal cannulas, oxygen masks, eyeglasses, and
tracheostomy collars should be avoided because of the
risk of pedicle compression.
Excessive motion in the area of the flap inset is to
be avoided by padding of areas adjacent to the flap
inset site. In extremity reconstruction, the use of a
plaster splint to immobilize the joint proximal and distal
to the flap inset site is recommended. Circular casts
are avoided because of the risk of pressure associated
with postoperative edema and difficulty in observing
flap circulation.
A closed suction drain system is generally used at
both the donor and recipient closure sites. Drains are
not removed until the patient is mobilized because the
resultant motion may temporarily increase the risk of
seroma formation. Drains in proximity to a tissue
expander or prosthetic implants are a potential source
of infection and are removed as quickly as possible.
When seroma drainage decreases to 20 mL in a 24-
hour period, the closed drainage system is removed.
When possible, drainage systems are removed by post-
operative day 10 to avoid potential wound contami-
nation through the drain exit site.
Perioperative antibiotics are recommended when
flaps are inset at the site of contaminated defects. If an
expander or permanent implant insertion site has a
history of prior infection, perioperative antibiotics are
also recommended. Cultures of the wound site will
determine the necessity for postoperative antibiotic
therapy. Continued use of postoperative antibiotic
therapy should be based on wound cultures and selec-
tion of culture-specific antibiotic agents.328
Prolonged bed rest is avoided when possible after
reconstructive surgery. With the exception of those
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Dr.Mustafa D.
undergoing reconstruction of the perineum and lower
extremity, most patients are ambulatory after the first
postoperative day. Elevation and immobilization of
upper and lower extremities are generally recom-
mended for 10 days followed by no weight bearing for
up to 6 weeks. Weight bearing at the site of flap inset
for pressure sore coverage is avoided for up to 4 weeks.
Range-of-motion exercises at the donor site are encour-
aged when wound healing is complete, usually by post-
operative day 7 to 10, to avoid joi nt stiffness and muscle
weakness.
If the patient has difficulty regaining function at
either the donor or recipient site, a physical therapy
program is recommended. Pain management for
patients treated for complex defects may require con-
sultation with a pain specialty clinic and psychiatrist.
Occupational therapy is indicated for patients unable
to return to their jobs. A multispecialty approach to
patients who have undergone cancer treatment is essen-
tial to provide tumor surveillance and adjuvant therapy
when indicated. Patients at risk for wound recurrence,
particularly after closure of a pressure sore, and
patients with spinal cord injury require instruction in
avoidance of pressure and shear forces at the site of
flap reconstruction and assistance in obtaining devices
(i.e., wheelchair with appropriate padding) to avoid
future skin injury.
Postoperative use of anticoagulation is largely sur-
geon dependent and is usually of concern in microvas-
cular tissue transplantation. Common postoperative
regimens include daily aspirin, heparin, or dextran.
Aspirin inactivates platelets by blocking cyclooxyge-
nase. Heparin is an antithrombin III inhibitor. Dextran
decreases platelet adhesiveness, inhibits platelet
aggregation, and decreases blood viscosity. The use of
these medications varies among surgeons.
Flap Monitoring Techniques
Postoperative monitoring of muscle and musculocu-
taneous flaps is a critical component in the care of
these patients. Many techniques have been developed
to monitor flaps and have primarily focused on those
flaps transferred microsurgically. These monitoring
methods assess the patency of the small-vessel
microanastomosis. The goal is to discover any problem
with the anastomosis early enough to salvage the flap.
Musculocutaneous flaps that have not been divided
from their vascular pedicle are generally monitored
with clinical observation. Clinical observation gener-
ally involves assessment of skin color, tissue turgor,
temperature, and capillary refill.
Complications
Complications with the use of muscle and musculo-
cutaneous flaps fall into three categories: judgment,
image....
16 • FLAP CLASSIFICATION AND APPLICATIONS
technique, and patient management. The most
common complications include seroma, hematoma,
superficial skin necrosis, wound separation, inadequate
coverage of the defect, infection, and partial or com-
plete loss of the flap. By analyzing these complications
in relation to judgment, technique, and patient man-
agement, the surgeon should be able to understand
the cause of each complication to prevent subsequent
complications.
Errors in surgical judgment are usually due to inad-
equate preparation, inadequate flap design, or inade-
quate knowledge of anatomy.
Inadequate preparation is characterized by pro-
ceeding with a reconstructive procedure without
having sufficient resources to perform the operation.
For example, a surgeon may be asked to evaluate an
elderly patient who has an extensive nonhealing ulcer
involving the distal third of the leg. The surgeon rec-
ommends microvascular transplantation of a muscle
flap yet forgoes a preoperative arteriogram, even
though the patient has significant risk factors for
peripheral vascular disease. Intraoperatively, adequate
recipient vessels cannot be found, and the flap is there-
fore aborted. This underscores the importance of
preoperative preparation, especially if the diagnostic
study has a direct impact on the surgical procedure
planned.
Inadequate flap design is usually due to the surgeon's
failure to account for every aspect of the surgical defect.
The flap should not be designed and elevated before
debridement of the wound. Premature flap elevation
will not be based on precise assessment of the defect
size and may result in a significantly larger wound and
an inadequately small flap. The flap should be designed
and elevated only after the defect is completely estab-
lished.
Inadequate knowledge of surgical anatomy may
result in damage to the vascular pedicle during dis-
section, which can lead to failure of the flap. In addi-
tion to directly injuring the vascular pedicle, the surgeon
can indirectly injure a pedicle by using a flap whose
vascular pedicle is within the zone of injury, as in defects
involving infection and radiation necrosis. Vascular
pedicles within this environment may be compromised.
For example, in a distally based flap, the minor pedicle
is usually close to the defect and may be affected by
the underlying cause of the defect. For this reason, a
distally based flap is less reliable than the muscle flap
that is based on its dominant, major, or segmental sec-
ondary vascular pedicles. Through an appreciation of
these subtle anatomic differences, proper flap selec-
tion and safe flap transposition can be achieved. It is
imperative that the surgeon understand the precise
anatomy of the muscle and musculocutaneous flap and
the relationship to its vascular pedicle.
Surgical technique directly affects the outcome of
any procedure. The handling of tissue, particularly vas-
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Dr.Mustafa D.
473
cular pedicles, is of utmost importance to the success
of the flap. Vessels can be injured at any stage of the
operation and are subject to spasm, kinking, shear-
ing, and twisting. One preventive measure is the place-
ment of temporary sutures between the skin of the
flap and the underlying muscle or fascia to prevent
shearing of the musculocutaneous perforating vessels.
Another technique is to avoid skeletonization of the
vascular pedicle unless it is absolutely necessary to
prevent spasm and injury. Last, in flaps that are tun-
neled beneath skin bridges, it is important to avoid a
tourniquet effect produced by the potentially con-
strictive skin bridge. The tunnel dimension should be
twice the size of the portion of the flap within the
tunnel.
Ultimate flap loss can be due to intrinsic or extrin-
sic reasons. Flap loss due to intrinsic reasons is largely
caused by inadequate blood supply, which is the most
common reason for flap compromise. Flap compro-
mise due to extrinsic circumstances includes infection,
hypotension, and vasoconstricting agents such as
pressors. Compression or tension on the flap due to
hematoma is another extrinsic cause of flap compro-
mise. Exploration of the flap should be expeditious
when failure is suspected.
Donor site complications include fluid collections
due to dead space (seroma, hematoma), wound sepa-
ration, infection, and injury to adjacent structures
during flap harvest.
Errors in patient management are a common cause
of postoperative complications. For patients under-
going a muscle or musculocutaneous flap transposi-
tion, the most common errors of management are
inadequate attention to the patient's underlying
medical conditions, inadequate assessment or man-
agement of intravascular volume status, and inadequate
surveillance of flap viability and perfusion.
The safety and reliability of muscle and musculo-
cutaneous flaps have been repeatedly demonstrated.
Such successes now encourage surgeons to choose a
more complex procedure than a simple one, especially
if form and function can be improved. For example,
in the reconstruction of a defect involving the lower
leg, the soleus and gastrocnemius provide reliable and
safe closure. However, the aesthetic and functional
results maybe unacceptable to certain patients. In these
patients, a more sophisticated technique (e.g.,
microvascular composite tissue transplantation) is
appropriate and may be the procedure of choice.
Microvascular tissue transplantation is clearly indicated
as the procedure of choice for certain defects. In fact,
microvascular composite tissue transplantation to
reconstruct head and neck defects has revolutionized
the field and has allowed both functional and aes-
thetically pleasing results for large extirpative defects.
The quality of the result is far greater than the risk
involved.
VtJWttf^elCiW image...
474 • CENERAL PRINCIPLES
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16 • FLAP CLASSIFICATION AND APPLICATIONS
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T-eWttf^d'^imaqe...
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image
480 I • GENERAL PRINCIPLES
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288. Vranckx JJ, Misselyn D, Fabre G, et al: The gracilis free muscle
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294. Sharma GN, Nepram SS: Sural artery flap: a dependable solu-
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297. Sakai N, Yoshida T, Okumura H: Distal plantar area recon-
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review of 25 cases of transfer to traumatic extremity wounds.
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of sole and heel defects with free tissue transfers. Ann Plast
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308. Acikel C, Celikoz B, Yukscl F, Ergun O: Various applications
of the medial plantar flap to cover the defects of the plantar
foot, posterior heel, and ankle. Ann Plast Surg 2003:50:498.
309. Atiyeh BS, Al-Amm CA, El-Musa KA, et al: Distally based sural
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310. Fischer J, Arnold PG, Waldorf J, Woods JE: The gluteus maxi-
mus musculocutaneous V-Y advancement flap for large sacral
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312. Lee HB, Kim SW, Lew DH, Shin KS: Unilateral multilayered
musculocutaneous V-Y advancement flap for the treatment
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314. BaranCN,CelebiogluS,CivelekB,SensozO:TangentiaIlysplit
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316. Foster RD, Anthony JP, Mathes SJ, et al: Flap selection as a
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V-Y retroposition flap. Ann Plast Surg 1981;6:34.
*&Wttf t aatfW image...

16 • FLAP CLASSIFICATION AND APPLICATIONS 481

323. Siddiqui A, Wiedrich T, Lewis VL Jr: Tensor fascia lata V-Y
retroposition myocutaneous flap: clinical experience. Ann Plast
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Ann Surg 1983:198:420.
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Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
image...
CHAPTER
17
•
Flap Physiology
NICHOLAS B. VEDDER, MD
WHAT IS A FLAP?
REGULATION OF FLAP BLOOD FLOW
FLAP FAILURE
REPERFUSION INJURY AND THE ROLE OF
NEUTROPHILS
Neutrophil-Endothelial Adhesion
Integrin-lg-like Ligand Adhesion
Selectin-Carbohydrate Adhesion
Regulation of Neutrophil Adhesion
Blocking PMN-Endothelial Adhesion in In Vivo Models
of Neutrophil-Mediated Reperfusion Injury
Nitric Oxide
WHAT IS A FLAP?
Flaps are the essence of plastic surgery. The ability to
successfully conceive, design, execute, and manage a
flap is what defines a plastic surgeon. What distin-
guishes a flap from a graft is an intrinsic blood
supply that is responsible for a flap's viability; a graft
must rely on diffusion until its vascularity becomes
re-established. An intrinsic vascularity confers tremen-
dous flexibility and potential, allowing a flap to supply
critical vascularized coverage to complex defects and
to restore form and function in nearly unlimited ways.
Because the viability of a flap depends on its intrin-
sic vascularity, fully understanding and being able to
optimize the vascular physiology of a flap can make
the difference between success and failure.
As in all tissues, the vascular supply of a flap includes
both macrocirculation and microcirculation com-
ponents. Both of these are subject to intrinsic and
extrinsic factors that can dramatically influence per-
fusion and hence viability. The anatomy of the macro-
circulation is used to define and design a flap. The
major arterial inflow and venous outflow of a flap con-
stitute the foundation from which the microcircula-
tory beds then provide nutrition and oxygen and carry
away carbon dioxide and waste products, thus forming
the basis of cellular metabolism throughout the flap.
It is at the microcirculatory level—the arterioles, cap-
illaries, venules, and arteriovenous anastomoses—
where this exchange occurs and where most of the
control of perfusion occurs.
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ISCHEMIC PRECONDITIONING AND THE DELAY
PHENOMENON
ISCHEMIC INJURY AND APOPTOSIS
NEOVASCULARIZATION
FLAP MONITORING
THERAPEUTIC INTERVENTIONS TO IMPROVE FLAP
VIABILITY
Taylor1'5 has eloquently demonstrated that the
blood supply to potential flaps involves a continuous
three-dimensional network of vessels not only in the
skin but also in all tissue layers. The anatomic terri-
tory of a source artery in the skin and deep tissues, in
most cases, gives rise to what has been described as
the angiosome concept. Arteries closely follow the con-
nective tissue framework of the body. The primary
supply to the skin is by direct cutaneous arteries, which
vary in caliber, length, and density in different regions.
This primary supply is reinforced by numerous small
indirect vessels, which are terminal branches of arter-
ies supplying the deep tissues. Careful anatomic
studies have shown an average of 374 major perfora-
tors in the human subject, revealing that there are many
more potential skin flaps yet to be defined. The angio-
somes defined in this way are the tissues available for
composite transfer.
One of the primary functions of skin is ther-
moregulation, which is accomplished through the
regulation of skin blood flow. Heat is dissipated by
increasing skin blood flow and is conserved by decreas-
ing skin blood flow. The primary regulation of blood
flow to skin is at the arteriolar level. It is here that
sympathetic tone regulates flow through the precap-
illary sphincters, arterioles, and arteriovenous anas-
tomoses. When the precapillary sphincters constrict
in response to either local or systemic sympathetic
tone, blood flow is forced to bypass the capillary bed
through arteriovenous anastomoses. In addition, a
number of other factors come into play in regulating
483
484 I • GENERAL PRINCIPLES

flap blood flow. These include the systemic central A. Viable random flap
blood pressure and cellular factors within the micro-
circulation involving the endothelium, platelets, and
white blood cells.
The normal blood flow to skin is approximately
20 mL per 100 g of tissue; it is significantly higher for
muscle.6 This is consistent with the different meta-
bolic demands of skin and muscle, with muscle having
much higher demand for oxygen and metabolites.
Because flap viability depends on this critical balance
between blood flow and metabolic demand, it is impor- B. Extended random flap with distal necrosis
tant to keep the tissue-specific requirements in mind
in designing, executing, and manipulating blood flow
to optimize flap survival.
Because effective microcirculatory perfusion is
dependent on its proximity to the nearest nutrient
vessel, flaps that are based on an axial nutrient vascu-
lar system will be much more reliable than flaps that
are not. Random flaps are those not based on a dom-
inant nutrient vascular system but instead are supplied
by flow through the subdermal or subfascial plexus. C. Axial flap with viable distal random component
As a result, random flaps are much less reliable than
axial flaps, and their length is limited to a short dis-
tance from the pedicle origin. The portion of an axial
flap that extends beyond the axial vessel is random in Ax
nature. The single most important factor in classify-
ing flaps, therefore, is whether they are axial or random
in nature (Fig. 17-1).7 Although this chapter focuses
on the physiology and pathophysiology of flaps as well
FIGURE 1 7 - 1 . Random versus axial flaps. The impor-
as methods of improving flap physiology, by far the tance of axial perfusion of a flap is illustrated. Panel A
most important factor in successful flap survival is shows the reliable perfused area of a flap based on purely
proper flap design. random perfusion (R) from the vascular pedicle (black
circle). Panel B shows a random flap designed beyond the
limits of reliable random perfusion, resulting in distal flap
necrosis. Panel C shows the benefit of designing a flap
REGULATION OF FLAP based on an axial pedicle. The length of reliable flap per-
BLOOD FLOW fusion includes the same length of reliable random per-
fusion (R) plus the length of the axial pedicle (Ax). (© 2003
Regulation of cutaneous blood flow occurs at two levels, Nicholas Vedder.)
systemic and local (Table 17-1). Systemic control is, in
turn, exerted through both neural regulation and
humoral regulation.6 Of these, neural regulation is
predominant. Neural regulation is exerted primarily Local control of blood flow, or autoregulation, is
through sympathetic fibers and cc-adrenergic recep- important to many tissue beds throughout the body,
tors that induce vasoconstriction; (3-adrenergic re- especially those with high metabolic rates, such as skele-
ceptors, on the other hand, induce vasodilation. In tal muscle, ft letabolic factors that affect skin blood flow
addition, serotonergic receptors, located at arteriove- at the local level include hypercapnia, hypoxia, and
nous anastomoses, also induce vasoconstriction. acidosis, all of which cause vasodilation. In addition,
Together, these work to regulate the vascular smooth a number of physical factors affect the regulation of
muscle tone at the level of the arterioles and arteri- blood flow. Increased tissue perfusion pressure can
ovenous anastomoses. trigger a "myogenic reflex," resulting in vasoconstric-
Humoral regulation occurs through the action of tion in an effort to maintain constant capillary blood
systemic vasoactive substances on their specific recep- flow, independent of arterial perfusion pressure. Local
tors, such as that of epinephrine and norepinephrine hypothermia also decreases local blood flow by acting
on a-adrenergic receptors. Other systemic vasocon- directly on the vascular smooth muscle to cause vaso-
strictors include serotonin, thromboxane A2, and constriction, whereas local hyperthermia has the
prostaglandin F2a. Counteracting vasodilators include opposite effect.
prostaglandin B|, prostaglandin I2 (prostacyclin), his- Rheologic factors can have an effect on flow, but
tamine, bradykinin, and leukotrienes C4 and D4. typically only under abnormal conditions. Profound

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Dr.Mustafa D.
image...
TABLE 17-1 • REGULATION OF FLAP BLOOD FLOW
Regulation
Scope Category Agent
Systemic Neural Sympathetic fibers
Neural Sympathetic fibers
Neural Sympathetic fibers
Humoral Norepinephrine, epinephrine
Humoral Serotonin, thromboxane A2,
prostaglandin F2a
Humoral Prostaglandin E,, prostaglandin
l2 (prostacyclin), histamine,
bradykinin, leukotrienes Gv
and I).-,
Rheologic Anemia
Rheologic Polycythemia, sickle cell
Local Hypercapnia, hypoxia, acidosis,
hyperthermia
Myogenic reflex
Hypothermia
anemia can improve rheologic properties and increase
flap blood flow; in some studies, it has been shown to
improve distal flap survival,8 but other studies have
shown little or no effect on flap survival, perhaps
because the rheologic improvement is offset by dimin-
ished oxygen delivery.9 Abnormally elevated rheologic
factors as in polycythemia or sickle cell disease can,
however, seriously compromise perfusion and viabil-
ity, especially at the marginal portions of a flap. It is
under conditions and in areas of marginal perfusion
that rheologic factors can play a significant role and
may be amenable to intervention.
Most of the same concepts apply to perfusion reg-
ulation in muscle flaps, although with some notable
exceptions. Although muscle tissue has a much higher
capillary density than skin, arteriovenous shunts are
absent. Muscle, like other organs of high metabolic
demand, is highly dependent on autoregulation to
maintain a level of blood flow commensurate with the
current metabolic demands. Epinephrine, rather than
causing vasoconstriction as it does in skin, causes arte-
riolar vasodilation in muscle beds as part of the
fight or flight response. Because muscle is not a ther-
moregulatory organ like skin, temperature has much
less effect on blood flow.
The endothelium plays a critical role in the regu-
lation of blood flow both through the direct release
of vasoactive substances 10 and through its effect on
the circulating white blood cells and platelets. This
latter effect, a response to injury, can play a significant
physiologic role in altered flap circulation, as discussed
later.
The action of elevating a flap produces profound
changes and disrupts the carefully balanced equilib-
rium that regulates blood flow to tissue. There is an
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Dr.Mustafa D.
17 • FLAP PHYSIOLOGY 485
Mediator Effect
cc-Adrenergic receptors Vasoconstriction
p-Adrenergic receptors Vasodilation
Serotonergic receptors Vasoconstriction
a-Adrenergic receptors Vasoconstriction
Varied Vasoconstriction
Varied Vasodilation
Hemodilution Increased blood flow
Sludging Diminished blood flow
Varied Vasodilation
Increased tissue perfusion Vasoconstriction
Vasoconstriction
immediate loss of sympathetic innervation that results
in a spontaneous discharge of vasoconstricting neu-
rotransmitters. 6 Combined with the drop in perfusion
pressure from physical removal of inflow vessels, the
result is that peripheral portions of the flap become
acutely ischemic. What occurs at the level of the micro-
circulation in this peripheral area during the next 24
hours will determine what proportion of the flap will
survive. Banbury et al" describe a triphasic, dynamic
response in the peripheral microcirculation of thecre-
master muscle flap. An initial acute hyperadrenergic
phase is followed by a nonadrenergic phase, with
significant vasodilatation, then a sensitized phase, with
increased capillary perfusion and hyperresponsiveness
to vasoactive substances.
The hemodynamic, anatomic, and metabolic
changes that follow flap elevation ultimately determine
the outcome. Hemodynamic changes have been the
most intensely examined. A number of excellent
studies using labeled microspheres have been carried
out, including those by Palmer, Nathanson, Kerrigan,
and others. l2"I6These studies showed that although flow
at the base of a pedicle flap is preserved after eleva-
tion, flow at the tip of the flap often drops to less than
20% of normal, usually within the first 6 to 12 hours.
Flow gradually returns to approximately 75% of
normal within I to 2 weeks and to 100% by 3 to 4
weeks.
At the same time that flow is gradually returning
to the ischemic portion of the flap by longitudinal flow
from the pedicle, additional flow is also returning
by inosculation and neovascularization from the bed.
This is a significant factor in very thin flaps, such as
those used in animal models of experimental flaps;
however, it is much less important in the thicker flaps
image...
486 I • GENERAL PRINCIPLES
generally used clinically. This difference must be kept
in mind in interpreting experimental flap studies,
which ideally should use a barrier between the flap
and the bed to remove this confounding variable.
Musculocutaneous flaps, which consist of a cuta-
neous component perfused by perforator vessels from
the underlying axial muscle flap, take on the perfusion
benefits of the underlying axial muscle flap. Gottrup
et al17 showed that musculocutaneous flaps have an
early and continuous increase in blood flow after
elevation, whereas random skin flaps have an early
decrease. Random flaps, however, develop a subsequent
lasting increase in flow. Tissue oxygen tensions are also
significantly higher in musculocutaneous flaps than
in random-pattern flaps up to 6 days after elevation
and are higher in the proximal portions than in
the distal portions in each flap type. This difference
between proximal and distal flap is greater in the
random-pattern flap than in the axial muscle or mus-
culocutaneous flap, as one would expect. Differences
in patterns of oxygen delivery to random versus mus-
culocutaneous flaps may in part explain the greater
reliability of musculocutaneous flaps when they are
used in the presence of infection and why muscle or
musculocutaneous flaps provide better bacterial killing
function in the setting of infection.18"20
The events after flap elevation can be summarized
as follows. Initially, nutrient vessels and sympathetic
nerves are severed. During the first 12 to 18 hours,
flow diminishes dramatically, especially in the distal
portion of a flap, because of a combination of decreased
perfusion pressure from the acute loss of inflow
vessels as well as the release of sympathetic vasocon-
strictors and the progressive leukocyte-mediated
endothelial injury. If the distal portion is to survive,
sufficient nutrient flow must exist by 6 to 12 hours,
depending on the type of tissue involved; otherwise,
this tissue will ultimately die. As sympathetic neuro-
transmitters are depleted during the ensuing 12 to 24
hours, and as inosculation from the flap bed occurs
in 2 to 3 days, flap perfusion is gradually restored.
However, in distal portions of the flap that are severely
ischemic at 6 to 12 hours, the returning flow only
contributes to the reperfusion injury that will ulti-
mately result in microvascular shutdown and tissue
necrosis, as the dead tissue is actively separated from
the living.
FLAP FAILURE
What causes the distal or peripheral portion of some
flaps to fail, whereas the entire flap survives in other
instances? The answer is multifactorial and elusive. Of
course, the composition of the flap is a critical factor
in determining both its inherent blood flow and its
tolerance to ischemia. Skin flaps, although they may
normally have much less blood flow than muscle flaps,
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have much lower metabolic requirements than muscle
flaps do and are far more tolerant of periods of ischemia
than muscle flaps are. Many studies addressing flap
survival have focused on the delay phenomenon (dis-
cussed later) because it is one of the few predictable
and clinically applicable methods of improving distal
skin flap viability. Early studies by Reinisch21 suggested
that arteriovenous shunting played an important role
in determining distal flap viability and that in acutely
elevated flaps, distal arteriovenous shunting prevented
adequate nutrient flow to the capillary bed. Delayed
flaps, on the other hand, were thought to have under-
gone a closure of the distal arteriovenous shunts,
thereby maintaining nutrient flow. A number of sub-
sequent studies, however, including those of Kerrigan,
Sasaki, and Pang,22"24 have conclusively demonstrated
that arteriovenous shunting plays little role in deter-
mining distal flap viability. Instead, distal flap necro-
sis is a result of simply inadequate end flow due to
either vasoconstriction of the small arterioles or per-
fusion pressure drop-off at a sufficient distance from
the pedicle vessels.
After elevation, the proximal surviving portion of
a pedicle flap has reduced blood flow as a result of sym-
pathectomy, catecholamine release, and local response
to injury. In the distal portion, however, the local
ischemia results in maximal vasodilation, yet inade-
quate perfusion pressure from the proximal portion
may fail to produce adequate perfusion distally. In this
way, inadequate arterial inflow is ultimately the cause
of distal flap failure.14,15'22
Khiabani and Kerrigan25 have described a significant
difference in the response of experimental skin flaps
versus muscle flaps to ischemia and reperfusion. In
flap skeletal muscle, an early hyperemic phase during
reperfusion maintains a significant blood flow to all
regions, including the area of the flap that is destined
for necrosis. In flap skin, however, there is a marked
decrease in flow rates. These differences have impor-
tant implications for the intravascular delivery of ther-
apeutic agents to improve flap viability, described later.
The relative importance of arterial versus venous
insufficiency as the primary cause of pedicle flap failure
has been examined and debated extensively. It has
clearly been shown that sufficient reduction in venous
outflow can produce flap necrosis despite adequate
arterial inflow.7 In free tissue transfers, venous occlu-
sion is more common than arterial occlusion and can
certainly result in flap failure if it is not corrected
quickly. In most pedicle flaps, however, the two are
closely linked, and any venous insufficiency in the face
of impaired arterial inflow will lead to significant tissue
necrosis. In experimental models of primary venous
and arterial ischemia, it appears that venous ischemia
is more deleterious.26"28 Similarly, in models of sec-
ondary ischemia, it has been observed that secondary
ischemia is more deleterious than primary ischemia
image...
and that venous insufficiency causes more damage than
equivalent arterial insufficiency.29
Kerrigan et al30 described three situations in which
global flap ischemia can occur: a flap designed too
large for its intrinsic blood supply, arterial thrombo-
sis, and venous thrombosis. For random and axial
pedicle flaps, thrombosis is usually secondary to the
development of a low-flow state at the level of the
microcirculation, caused by improper flap design,
ischemia-reperfusion injury (discussed later), sys-
temic factors affecting the microcirculation (e.g.,
hypotension, sepsis, smoking, vasoconstrictors), or
physical compression of the flap (e.g., from improper
inset, kinking, hematoma). For free flaps, however, axial
arterial or venous thrombosis, leading to total flap loss,
is often the result of thrombosis originating at the site
of the microvascular anastomosis. This is usually a
result of poor technique, allowing prothrombotic
adventitia or media to be exposed to the luminal blood
flow, with subsequent platelet and fibrin deposition,
rather than having a smooth endothelial lining across
the anastomosis. For this reason, antiplatelet and
antithrombotic therapy is mostly confined to microvas-
cular flaps, as discussed later.
The metabolic changes that follow flap elevation,
particularly in the distal ischemic portion of the flap,
are numerous and extreme. Ischemic tissue undergoes
a conversion to anaerobic metabolism with a rapid
depletion of levels of oxygen, glucose, and ATP, along
with a concomitant increase in levels of carbon dioxide
and lactic acid. Prostacyclin and thromboxane levels
are significantly elevated. Glucose and glycogen
consumption increases in the ischemic but viable
portions of a flap in proportion with the degree of
ischemia; glucose consumption peaks around day 3
and returns to normal by day 7.31,32
Associated with the conversion to anaerobic metab-
olism is the markedly increased production of toxic
superoxide radicals.32*35 These toxic oxygen radicals
can cause direct cytotoxic effects, but probably more
important, they are a trigger for local acute inflamma-
tion, adherence and accumulation of leukocytes, and
subsequent endothelial injury, with the subsequent cel-
lular events leading to microvascular shutdown. Levels
of the body's key protective enzyme superoxide dis-
mutase are decreased in the distal portions of acute
flaps as the enzyme is consumed in converting super-
oxide to oxygen in a tissue-protective mechanism. 34
Much attention has been devoted to the concept
that during reoxygenation after ischemia, xanthine
dehydrogenase is converted to xanthine oxidase, which
catalyzes the conversion of hypoxanthine (formed from
the degradation of ATP during ischemia) plus oxygen
to form xanthine, with the production of superoxide
anion as a byproduct. 36 Superoxide anion can lead to
the formation of other oxygen radical species and result
in direct cellular injury. During the ischemic period,
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Dr.Mustafa D.
7 • FLAP PHYSIOLOGY 487
cell energy levels fall, disrupting the ion gradients and
allowing calcium to enter the cytoplasm. Calcium then
activates a cytosolic enzyme that transforms xanthine
dehydrogenase, in endothelial cells, into xanthine
oxidase, which can reduce molecular oxygen into
oxygen radicals. While xanthine oxidase is being gen-
erated, ATP is being degraded to AMP and ultimately
hypoxanthine as the cell undergoes anaerobic metab-
olism. Hypoxanthine is a substrate in the generation
of oxygen metabolites by xanthine oxidase. Thus,
during the ischemic period, two of the three princi-
ples involved in radical formation are generated. Once
oxygen is reintroduced during reperfusion, the reac-
tion proceeds forward and the radicals, primarily
superoxide anion, hydrogen peroxide, and hydroxyl
radical, are produced (Fig. 17-2). Exposure of plasma
to enzymatically generated oxidants37,38 or of endothe-
lial cells to hypoxia39 can also elicit the production of
neutrophil chemoattractants in vitro. Similarly, tissue
hypoxia and reperfusion in vivo have been shown to
promote neutrophil sequestration, an effect that is
blocked by lipoxygenase inhibitors'10 or free radical
scavengers.41
Once the metabolites are produced, injury is
believed to occur in one of two ways. The first is by
-
direct reaction of superoxide radical with the endothe-
lial membrane, causing lipid peroxidation, disruption
of membrane proteins, increased cell permeability, and
consequently cytoplasmic swelling and dysfunction.
The second mechanism is through the chemotactic
property of oxygen metabolites, primarily superoxide
anion, which causes neutrophil migration into the
reperfused area, with the neutrophils actually causing
the tissue destruction. Plasma exposed to superoxide
ATP
I
AMP
I xanthine
dehydrogenase
Adenosine
I Ca
H
Protease
Inosine xanthine
I oxidase
Hypoxanthine -O2
Xanthine
O
Reperfusion
FIGURE 1 7 - 2 . Oxidant generation with ischemia and
reperfusion. During reoxygenation after ischemia, xan-
thine dehydrogenase is converted to xanthine oxidase,
which catalyzes the conversion of hypoxanthine (formed
from the degradation of ATP during ischemia) plus oxygen
to form xanthine, with the production of superoxide anion
as a byproduct. Superoxide anion can lead to the forma-
tion of other oxygen radical species and result in direct
cellular injury. (© 2003 Nicholas Vedder.)
488 I • GENERAL PRINCIPLES
anion in vitro becomes potently chemotactic for
neutrophils. Interestingly, this chemotactic activity is
inhibited by superoxide dismutase but not catalase.37
Many studies have examined oxygen metabolites
and their effect on tissue injury. The distal, ischemic
areas of experimental flaps have been found to have
markedly increased levels of xanthine oxidase as well
as of malonyldialdehyde, another indicator of free
radical formation.42'44 In experimental flaps, a single
dose of superoxide dismutase has been shown to
increase survival of random flaps from 38% to 76%. 45
These findings have been confirmed by other investi-
gators46 and include studies with allopurinol, a xan-
thine oxidase inhibitor,47'51 and deferoxamine, an iron
chelator and free radical scavenger.44 However, the clin-
ical significance of these studies is questionable because
xanthine oxidase levels in human tissue are 7« those
of rats, used in most of these studies.
Free radicals also play an important role in
hematoma-related flap necrosis. Hemoglobin and
iron catalyze the chemical reactions that lead to the
production of highly destructive free radicals, in par-
ticular the hydroxyl radical. Deferoxamine, by chelat-
ing the iron component and acting as a free radical
scavenger, has been shown to enhance experimental
flap survival in the presence of flap hematoma. 52
Another mechanism for reperfusion injury in-
volves arachidonic acid derivatives. The activation of
lipoxygenase yields leukotriene B4) a potent chemoat-
tractant, which can induce superoxide anion genera-
tion and degranulation in neutrophils. Activated
neutrophils, in turn, produce leukotrienes and per-
petuate the inflammatory reaction. Similarly, the
action of cyclooxygenase, in the setting of ischemia,
results in the generation of thromboxane and
prostaglandins. Thromboxane A2 is a potent vaso-
constrictor and induces platelet aggregation. Prosta-
cyclin (prostaglandin I2), on the other hand, is a potent
vasodilator and inhibitor of platelet aggregation.
Numerous experimental flap studies have therefore
focused on altering arachidonic acid metabolism- Both
prostacyclin53 and the prostacyclin analogue iloprost
have been shown to improve experimental flap sur-
vival.54 There has even been a report of successful flap
salvage with use of iloprost.55 Prostaglandin Ii, which
has similar vasodilatory and antiaggregation effects,
has also been shown to have beneficial effects on flap
survival.56,57 By use of an inhibitory approach, throm-
boxane synthase inhibitors have been successful in
improving flap survival in several experimental flap
studies.58,59
REPERFUSION INJURY AND
THE ROLE OF NEUTROPHILS
Ischemia-reperfusion injury forms the basis of many
important clinical disorders, including myocardial
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Dr.Mustafa D.
infarction, stroke, vascular disease, organ transplan-
tation, and shock. Ischemia-reperfusion injury is par-
ticularly relevant to the field of plastic surgery, in which
altered perfusion leading to cellular and tissue organ
injury is one of the major causes of complications.
There is evidence that a significant proportion of the
tissue damage triggered by ischemia may frequently
be a consequence of events associated with reperfu-
sion of ischemic tissues, that is, reperfusion injury.
Studies have shown a close association between tissue
neutrophil (PMN) accumulation and tissue injury in
this setting and have also demonstrated injury reduc-
tion by depletion of circulating PMNs, suggesting
an important role for PMNs in ischemia-reperfusion
injury.60 The rapid intravascular accumulation of neu-
trophils can lead to progressively decreased perfusion
and may represent the "no-reflow" phenomenon 6 'or,
more precisely, a "diminishing-reflow" phenomenon
associated with ischemia and reperfusion.62
There are several mechanisms whereby activated
PMNs may cause injury in the setting of ischemia-
reperfusion. First, adherent, activated PMNs can cause
direct endothelial injury, resulting in loss of vascular
integrity, edema, hemorrhage, and thrombosis (Fig.
17-3). Another possible mechanism involves microvas-
cular occlusion and further ischemia resulting from
adherence and accumulation of aggregates of PMNs
within the vessel lumen.
Neutrophil-Endothelial Adhesion
Neutrophil adherence to endothelium plays a pivotal
role in neutrophil-mediated vascular and tissue
injury.63'66 Observations of the microcirculation by
intravital microscopy have illuminated a sequence of
events involved in neutrophil adhesion to endothe-
lium.67*69 At the site of inflammation, neutrophils are
first seen to leave the laminar flow stream and to roll
along the endothelium of adjacent postcapillary
venules. This is followed by firm adherence to the
endothelium, which arrests the neutrophil, followed
by diapedesis and emigration. Once the neutrophils
are firmly adherent to the endothelium, a protected
microenvironment develops beneath the adherent neu-
trophil in which its proteases, oxidants, or other toxic
products can cause injury to the endothelium, inac-
cessible to circulating anti-inflammatory or anti-
oxidant agents.70 At the interendothelial junctions,
neutrophils then crawl between the endothelial cells
and emigrate into the surrounding tissues. This adher-
ence-dependent loss of microvascular integrity can
result in edema formation, hemorrhage, or thrombo-
sis, and the resulting vascular injury may ultimately
be responsible for tissue and organ dysfunction or
death.
There has been remarkable progress in the char-
acterization of the specific proteins involved in this
 17 • FLAP PHYSIOLOCY 489

Rolling - Activation - Adherence - Injury

FIGURE 1 7 - 3 . Neutrophil activation, adherence, and injury. Diagrammatic

representation of the sequential events that occur at a site of neutrophil-
mediated microvascular injury. Initial selectin-carbohydrate-mediated rolling
along the surface of the endothelium and tethering of neutrophils, where local
agonists then stimulate integrin-lg superfamily ligand-mediated firm adherence,
lead to neutrophil-mediated endothelial injury with loss of vascular integrity,
edema, hemorrhage, and thrombosis. Another mechanism involves microvas-
cular occlusion and further ischemia resulting from adherence and accumula-
tion of aggregates of neutrophils within the vessel lumen. (© 2003 Nicholas
Vedder.)

critical adherence interaction (Fig. 17-4). The molec-
ular structures of these proteins have been defined,
and much has been learned about their functions
through in vitro as well as in vivo study.63,64'71"73 These
adhesion molecules are currently classified into two
major categories, the leukocyte integrins and their
ligands on endothelial cells that are members of the
immunoglobulin (Ig) superfamily74 and the selectins
and their carbohydrate counterstructures. The inte-
grin-Ig-Iike Iigand interaction mediates the steps of
firm adhesion of neutrophils to endothelium at sites
of inflammation, diapedesis, and emigration. The
selectin receptors are lectin-containing proteins that
recognize specific carbohydrate counterstructures,
expressed on glycoproteins. Selectin receptors appear
to be responsible for the initial transient adhesion
of neutrophils that occurs at sites of inflammation,
manifested as "rolling." Once slowed by selectin-
carbohydrate interactions, local inflammatory stim-
uli subsequently activate the neutrophils to produce
firm adhesion through the integrin-Ig-like Iigand
interaction.
Integrin-ig-Iike Ligand Adhesion
The CD11/CD18 complex is a leukocyte membrane
glycoprotein complex, localized to the leukocyte
surface, that plays a major role in mediating leuko-
cyte adhesiveness. The three CD 11 a chains and the
CD 18 p chain have been cloned and shown to be
members of the integrin superfamily of adhesion
receptors comprising the (32 subclass that is restricted
to leukocytes.72,74 It has been shown that normal,
unstimulated neutrophils exhibit a very low level of
basal adherence. After stimulation, there is a marked
increase in neutrophil adherence to endothelium. Addi-
tion of monoclonal antibodies directed to functional
epitopes of CD1 lb or CD18 essentially eliminates this
increased adhesiveness in vitro and in vivo and pre-
vents PMN-mediated endothelial and microvascular
injury.63'64'75
The integrin heterodimer most responsible for firm
adhesion in neutrophils appears to be CD1 lb/CD18
(Mac-1, M o l , CR3). 76 The mechanism by which
CDllb/CD18 augments neutrophil adhesiveness in
response to stimulation is not entirely clear. In unstim-
ulated neutrophils, CDllb/CD18 exists both on the
cell surface and in far greater quantities within the sec-
ondary or tertiary granules. On stimulation, these
granule contents translocate to the cell surface, result-
ing in a 3- to 10-fold increase in surface-associated
CDllb/CD18. This increase in surface expression,
however, is neither necessary nor sufficient to cause
increased adhesiveness.77 Instead, the primary mech-
anism appears to be an activation of surface receptors
that produces a conformational change resulting in a
high-avidity binding to Iigand through what is known
as inside-out signaling.78 The molecular basis for avidity
modulation of the fi 2 integrin receptor has not been
fully defined but is dependent on interactions of inte-
grin cytoplasmic domains with adaptor molecules and
the cytoskeleton.79

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Dr.Mustafa D.
490 I • GENERAL PRINCIPLES

Neutrophil-Endothelial Adhesion Receptors

PECAM-1

E-selectin P-selectin

FIGURE 17-4. Molecular basis of leukocyte-endothelial adhesion. Diagrammatic representation of

the known neutrophil-endothelial adhesion receptors. The P2 integrin receptors on neutrophils, LFA-1
(CD11a/CD18) and Mac-1 (CD1 lb/CD18; both represented as aP dimers), bind to intercellular adhe-
sion molecules (ICAMs). Endothelial E-selectin (CD62E) and P-selectin (CD62P; represented with their
N-terminal lectin domain, epidermal growth factor domain, multiple complement-regulatory repeat
sequences, transmembrane domain, and cytoplasmic domain) bind to carbohydrate ligands, particularly
sialyl Lewis x antigen (SLex; CD 15s), expressed on glycoproteins of neutrophils, with PSCL-1 being the
primary ligand for P-selectin. L-selectin (CD62L) on neutrophils binds to carbohydrate ligands on endothe-
lium in systemic vasculature and also presents SLex to E-selectin and P-selectin. [© 2003 Nicholas
Vedder.l

Endothelial counterstructures for CD l i b / C D 18
include ICAM-1 (intercellular adhesion molecule 1;
CD54), a member of the Ig superfamily.72'74 ICAM-1
is expressed at low levels on resting endothelium in
vitro and in vivo, and it is up-regulated during a period
of hours in response to inflammatory stimuli. Mono-
clonal antibodies to ICAM-1 are effective at inhibit-
ing neutrophil adherence to endothelium in response
to inflammatory stimulation in vitro, although gen-
erally less effective than monoclonal antibodies to
CDIlborCDIS.68
Selectin-Carbohydrate Adhesion
Selectin receptors and their carbohydrate counter-
structures are the other major category of adhesion
molecules involved in neutrophil-endothelial adhe-
sion.80 Recent in vitro and in vivo evidence suggests
that selectin-mediated adhesion plays an important
role in the initial rolling of neutrophils along the
endothelium at sites of inflammation. The three
selectin receptors are L-selectin (CD62L; LAM-1, Leu-
8, or LECAM-1), E-selectin (CD62E; ELAM-1), and
P-selectin (CD62P; GMP-140, PADGEM, or CD62).
E-selectin is localized to endothelial cells, P-selectin is
found on platelets as well as on endothelial cells, and
L-selectin is expressed only on leukocytes. Binding
occurs between the lectin domain and the specific car-
bohydrate counterstructure on either the neutrophil
(in the case of E-selectin and P-selectin) or the
endothelial cell (in the case of L-selectin). For E-selectin
and P-selectin receptors, the sialyl Lewis x (SLex; CD 15s)
antigen is a major counterstructure. 81
P-selectin is only minimally expressed on the
surface of unstimulated endothelium in vivo, but it is
rapidly induced within minutes of stimulation. 80 This
initial increased surface expression does not require
de novo synthesis because P-selectin is stored within
the Weibel-Palade bodies and is quickly translocated
to the cell surface in response to stimulation. 82 P-
selectin-mediated adhesion provides an ideal mech-
anism for initially slowing neutrophils at sites of
inflammation so that stimulation can occur, leading
to firm, integrin-mediated adhesion and subsequent
diapedesis or, under some conditions, to direct
endothelial injury.
Unlike P-selectin, L-selectin is constitutively
expressed on the neutrophil in the basal state and is
rapidly shed from the surface in response to stimula-
tion. 73 AJthough E-selectin shares the same binding
properties as the other selectins, its time course of
induction in vitro is notably different, requiring de novo
protein synthesis, and therefore it does not reach peak
surface expression for 4 to 6 hours. 80

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Dr.Mustafa D.

Regulation of Neutrophil Adhesion
In the normal, healthy state, there is minimal or no
adherence interaction between circulating neutrophils
and endothelium. After an inflammatory stimulus,
such as ischemia and reperfusion, there is initially rapid
induction of selectin-mediated rolling at the site of
inflammation. Factors released as part of the early
inflammatory process, such as thrombin, histamine,
and oxidants, can initiate P-selectin expression and
thereby induce leukocyte rolling; whereas cytokines
generated later, such as interleukin-1 and tumor
necrosis factor-a, can induce L-selectin ligand or E-
selectin. This initial rolling allows the neutrophils
to directly contact the endothelium of the inflamed
vessels, where subsequent activation of integrin recep-
tors by various agonists produces firm adherence.73,83,84
Lipid mediators such as platelet-activating factor
(PAF), chemotactic peptides such as C5a, and
chemokines such as interleukin-8 may play important
roles in initiating integrin/ICAM-1-mediated adhe-
sion. In vitro, PAF is expressed on the endothelial surface
along with P-selectin in response to thrombin, hista-
mine, or oxidizing agents. PAF can in turn result in
up-regulation and activation of neutrophil integrins,
leading to the second step of firm adhesion. This effect
can be blocked by inhibiting either P-selectin or the
PAF receptor, suggesting that a coordinated or "jux-
tacrine" process is involved.85 In a musculocutaneous
flap ischemia-reperfusion model, PAF inhibition has
been shown to reduce neutrophil accumulation and
to improve both skin and muscle survival.86
In the setting of ischemia-reperfusion, it is known
that oxygen-derived free radicals are generated at the
time of reperfusion.38,87 These free radicals can initi-
ate the process of selectin-mediated adhesion through
rapidly increasing the surface expression of P-selectin,
followed by release of PAF, and subsequent integrin-
mediated adhesion. 88 The potential role of oxygen free
radicals in initiating this process has been demon-
strated both in vitro and in vivo.89,90 Interleukin-8 has
also been shown to be involved in the process of PMN
recruitment in ischemia-reperfusion. 91
Blocking PMN-Endothelial
Adhesion in In Vivo Models
of Neutrophil-Mediated
Reperfusion Injury
Monoclonal antibodies directed against specific ad-
hesion proteins have been found to be effective at
inhibiting neutrophil accumulation and neutrophil-
mediated injury in a number of animal models of
reperfusion injury. The first such study used a CD 18
monoclonal antibody to examine the role of neu-
trophils in feline gut reperfusion injury.92 Antibody-
mediated adherence blockade significantly reduced the
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Dr.Mustafa D.
17 • FLAP PHYSIOLOGY 491
increase in plasma leakage that normally follows intes-
tinal ischemia and reperfusion. CD 18 monoclonal anti-
body was also shown to be effective in reducing organ
injury and improving survival in the whole animal
ischemia-reperfusion injury that occurs with hemor-
rhagic shock and resuscitation. 93
A pedicle flap model using the rabbit ear, isolated
on its central vascular pedicle, demonstrated that
blocking neutrophil aggregation and neutrophil adher-
ence to endothelium with CD 18 monoclonal antibody
can markedly reduce reperfusion-associated edema
formation, a functional measure of endothelial
integrity, as well as tissue necrosis in pedicle flaps (Fig.
17-5).62 Of note in this study was that the degree of
protection against endothelial, microvascular, and
tissue injury was the same whether antibody was
administered before ischemia or after ischemia but
immediately before reperfusion. This finding indicates
that neutrophil-mediated injury in this model of
ischemia-reperfusion occurs at the time of reperfu-
sion, as activated neutrophils flood the vascular bed,
causing diffuse endothelial and tissue injury. This was
the first study to demonstrate that the neutrophil-
mediated injury associated with ischemia-reperfusion
was in fact a reperfusion injury, that is, a consequence
of events that follow the reperfusion of previously
ischemic tissue. Subsequent studies indicate that
significant protection can still be achieved when
administration of blocking antibody is delayed up to
4 hours after reperfusion.94,95
Similar results have since been obtained in iso-
lated skin/composite flaps with P-selectin antibody
as P-selectin expression is increased in ischemia-
reperfusion,96 with L-selectin antibody, 97 with SLe*
oligosaccharide, 98 and with E-selectin and L-selectin
blockade in musculocutaneous flaps.99 In these studies,
P-selectin surface expression was shown to increase
soon after reperfusion, and blockade with P-selectin
antibody effectively inhibited neutrophil adherence and
accumulation as well as the associated tissue injury.
Anti-ICAMl antibody has also been shown to reduce
experimental composite tissue ischemia-reperfusion
injury.100 These results are consistent with the theory
that leukocyte rolling precedes firm attachment, that
rolling is mediated by P-selectin or L-selectin in
ischemia-reperfusion, and that blocking either of
these molecules or CD 18 is sufficient to prevent reper-
fusion injury. Synthetic inhibitors of neutrophil rolling
have also been examined. Fucoidin, a nontoxic neu-
trophil rolling inhibitor,has been shown to limit tissue
injury in a dose-dependent manner by inhibiting
neutrophil rolling when it is administered before
reperfusion in an experimental flap model.101
The p 2 integrin-mediated neutrophil adhesion has
also been shown to play an important role in skeletal
muscle ischemia-reperfusion injury, although the
window of protection, as expected, is much shorter
TfcWttf'aelClW image...

492 I • GENERAL PRINCIPLES

• *

B
-

• *

u
•

S
FIGURE 17-5. Blocking leukocyte adhesion reduces reperfusion injury. A comparison of tissue injury in rabbits
treated with saline [A and C) or anti-CD 18 monoclonal antibody [B and D) just before reperfusion after 10 hours
of complete ischemia. This comparison was made 24 hours after initial ischemia. Severe neutrophil-associated
vascular injury with dense intravascular and extravascular neutrophil accumulation and evidence of vascular
destruction with parenchymal hemorrhage is seen in controls and is blocked by CD 18 antibody treatment. Some
of the smaller vessels were occluded by neutrophil aggregates and thrombus. The end result of this microvas-
cular injury is significant tissue necrosis.

than for skin and subcutaneous tissue. With 4 hours
of ischemia, a significant benefit in muscle survival
was seen in animals treated with CD 18 monoclonal
antibody before reperfusion, but no improvement was
seen with 6 hours of ischemia, leading to the conclu-
sion that leukocytes are important mediators of skele-
tal muscle reperfusion injury and that treatment with
CD 18 monoclonal antibody can limit reperfusion
injury after a moderate ischemic insult.102 Inhibition
of neutrophil adherence with CD 18 monoclonal anti-
body has also been shown to prevent the increase in
vascular permeability and resistance that occurs in
skeletal muscle after ischemia and reperfusion.103
Random flaps (and the random component of
axial flaps) are a model of "gradient" ischemia in
that tissue is progressively ischemic from the base of
the flap toward the tip with an "ongoing" ischemia-
reperfusion injury present. In this setting, too, neu-
trophil-mediated injury appears to play a major role
in flap necrosis. In a rabbit random cutaneous flap
model, CD 18 monoclonal antibody was shown to
reduce random flap necrosis by two thirds, suggesting
that increased neutrophil adhesiveness plays an impor-
tant role in the tissue injury involving the ischemic
"at-risk" area of random flaps and that transient,
specific inhibition of leukocyte adherence by CD 18
monoclonal antibody can markedly improve random
flap viability (Fig. 17-6).'04
Although there maybe an intuitive concern regard-
ing the potential infection risks of therapeutic block-
age of leukocyte adherence, experimental studies have
shown that these risks can be prevented with appro-
priate prophylactic antibiotics.105,106 This has been
borne out in clinical trials of antiadhesion therapy.
Hyperbaric oxygen has long been used in the treat-
ment of difficult wounds and ischemic tissues, includ-
ing flaps. Recent evidence suggests that an important
mechanism of action of hyperbaric oxygen is through
reducing neutrophil adhesion to postcapillary venules,
an effect that is in part mediated by CD18.107 Other

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Dr.Mustafa D.
image...

17 • FLAP PHYSIOLOGY 493

: .
vT '•

r -*--

D
FIGURE 1 7-6. Leukocyte role in gradient reperfusion injury of random flaps. Gross appearance of random
dorsal skin flaps in rabbits at 14 days. A, A representative control animal. B, A representative animal that
received anti-CD 18 monoclonal antibody at the time of flap elevation, with markedly improved gradient perfu-
sion and flap survival. The distal portion of control flaps at 24 hours. C, Histologic evidence of intense intravas-
cular and extravascular neutrophil accumulation with endothelial injury, loss of vascular integrity, edema,
hemorrhage, and cellular necrosis, whereas specimens from CD 18 antibody-treated animals (D) were devoid
of neutrophils with markedly attenuated endothelial injury, leading to the differences seen at 14 days.

methods of reducing neutrophil response have also
been described, such as the immunosuppressive agents
FK506 and cyclosporine, which have also been shown
to improve experimental flap survival when they are
administered before ischemia. 108"'H The advantages,
however, of using an antibody or similar agent to
specifically target neutrophil adhesion at the time of
reperfusion are clear; such therapy is specific and
immediate and can be performed after ischemia,
at the time of reperfusion, with efficacy equal to
pretreatment.
Another receptor, platelet-endothelial cell adhesion
molecule 1 (PECAM-1 [CD31]), has also been shown
to be involved in neutrophil-endothelial interac-
tions. 1 12 PECAM-1 is found on the surface of platelets,
at endothelial intercellular junctions, and it has been
shown to play an important role in transendothelial
emigration of phagocytes and their migration through
the subendothelial matrix. PECAM-1 inhibition
through administration of antibodies to PECAM-1 has
been shown to provide partial protection against
ischemia-reperfusion injury, again in a rat flap
model.113
Mast cells may also be involved in the multistep
recruitment of neutrophils into postischemic tissue.
Cordeiro et a l m found that diphenhydramine and
cimetidine, H, and H 2 blockers, respectively, protected
against ischemia-reperfusion injury in a rat epigastric
island skin flap model. Their results suggest that mast
cells, through their release of histamine, are involved
in the damaging process of ischemia-reperfusion
injury.
Nitric Oxide
Another compound that has been shown in vitro to
inhibit neutrophil adhesion is nitric oxide, initially
known as endothelium-derived relaxing factor. It is
produced in multiple sites, including the endothelium
and polymorphonuclear leukocytes, and is synthesized

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Dr.Mustafa D.
494 I • CENERAL PRINCIPLES
from L-arginine by the enzyme nitric oxide synthase.
Because nitric oxide is a labile gas, it is difficult to
administer directly. Instead, a nitric oxide precursor
is usually used, such as L-arginine, which in the pres-
ence of nitric oxide synthase is converted to nitric
oxide.115 Competitive inhibitors of nitric oxide syn-
thase also exist, the most commonly used being N-
nitro-L-arginine methyl ester (L-NAME). Several
experimental studies in myocardium, lung, bowel,
brain, and kidney have demonstrated the protective
effect of nitric oxide and L-arginine in the setting of
ischemia-reperfusion, concomitant with their ability
to inhibit neutrophil adhesion, which is thought to be
a primary mechanism of protection.116"120 Studies
have shown that this mechanism appears to be medi-
ated in part by down-regulation of specific cell adhe-
sion molecules, including ICAM-1, E-selectin, and
P-selectin.12M24A number of experimental flap studies,
including muscle, skin, and musculocutaneous flaps,
have shown that administration of nitric oxide pre-
cursors, such as L-arginine, or nitric oxide donors, such
as SIN-1, to ischemic flaps before reperfusion protects
against ischemia-reperfusion injury and decreases
flap neutrophil counts and that this effect can be
reversed with competitive inhibitors of nitric oxide
ISCHEMIC PRECONDITIONING
AND THE DELAY PHENOMENON
The only reliable and regularly practiced method of
improving flap viability is the delay procedure, which
involves partially elevating a flap, inducing a level of
ischemia in the distal portion of the flap that does not
cause necrosis yet "conditions" the tissue so that the
flap will survive after later elevation, whereas distal
necrosis would occur if the flap were elevated acutely
in its entirety. Naturally, much flap research during
the past half-century has focused on trying to eluci-
date the mechanisms responsible for the delay
phenomenon. Most early studies of the delay phe-
nomenon, dating to Germany in 1933, described
anatomic changes in the vessels of the flap with lon-
gitudinal reorientation of the small vessels in line with
the long axis of the flap, increase in vessel size, and
increase in the number of small vessels in the sub-
dermal plexus.I31,IM There may also be a role played
by neovascularization (i.e., the growth of new blood
vessels) in the delay phenomenon. The relative con-
tribution of physical changes in the microcirculation
versus physiologic changes at the cellular level (con-
ditioning) remains unclear. Certainly, physical changes
require days or weeks to occur, whereas cellular
changes can occur much more rapidly. This of course
has a practical impact on the timing of a delay pro-
cedure. Dhar and Taylor133 suggest that the primary
event is dilation of existing vessels within the flap, not
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Dr.Mustafa D.
ingrowth of new vessels. They observed an initial
period of vasoconstriction that resolved within 3 hours
postoperatively, followed by an active and progressive
dilation of choke vessels that was most dramatic
between 48 and 72 hours. They further observed that
the choke vessel dilation seen in the delay period is a
permanent and irreversible event and is an active
process associated with both hyperplasia and hyper-
trophy of the cells in all layers of the choke artery wall,
with a resultant increase in caliber of these vessels.
Taylor's studies also suggest that a surgical delay can
safely add at least one anatomic vascular territory to
the length of a flap.134 Animal studies suggest that a
period of as little as a few days can provide significant
flap protection, whereas longer delay periods are
required in the clinical setting, with the traditional
period being 2 to 3 weeks.135
The traditional delay procedure involves incising
both sides of the flap and undermining the flap from
its bed while leaving the distal end of the flap intact.
The distal end of the flap is then divided after an appro-
priate period and the flap transferred. Myers and
Cherry136 showed that for a delay procedure to be suc-
cessful, the axial vessel must be divided as part of the
delay. This concept suggests that partial ischemia plays
a critical role in inducing later protection against
ischemia. When it is performed in this manner, the
traditional delay procedure improves flap viability in
the distal, ischemic area of the flap, allowing a much
longer flap to be harvested than would otherwise be
possible without a delay procedure. Axial flaps with
large random components, such as the transverse rectus
abdominis myocutaneous flap, have also been shown
to have improved distal vascularity and tissue survival
when they are delayed.137 Is not clear, however, that
the traditional delay procedure provides protection
against complete ischemia. Milton138 showed that
delayed flaps tolerated complete ischemia for only half
the time that previously delayed flaps did. Especially
in the setting of free tissue transfer, having a method
of preconditioning the tissue to ischemia, thereby
enhancing viability, could be of great value. The
current focus of much flap research is now in the area
of ischemic preconditioning.
Ischemic preconditioning is a process whereby
tissue is subjected to a brief period of nonlethal
ischemia (Table 17-2). This process confers on the
tissue a resistance to damage by subsequent prolonged
ischemic events. The phenomenon of ischemic pre-
conditioning was first described by Murry et al in
a model of myocardial ischemia-reperfusion, in which
it was shown to reduce infarct size in rat myocardium.
It has also been shown to improve survival of exper-
imental muscle and musculocutaneous flaps.140,141
This protective effect is manifested in two separate
phases, early and late. The early phase is effective imme-
diately after ischemic preconditioning and lasts up to
image...
TABLE 17-2 • ISCHEMIC PRECONDITIONING
Preconditioning Modality Preconditioning Phase
Delay procedure Early and late
Adenosine Early
Monophosphoryl lipid A Mimics late
Remote preconditioning Early and late
Heat Late
4 hours, whereas the late phase becomes effective
approximately 24 hours after ischemic precondition-
ing and lasts for 72 hours. 142
The mechanism by which ischemic precondition-
ing protects tissue is still not fully understood. Rees
et al143 demonstrated that the increase in neutrophil
and neutrophil products seen in experimental distal
random flaps was associated with distal flap necrosis
and that preconditioning with a delay procedure
reduced neutrophil accumulation and was associated
with improved distal flap survival. A number of
authors have proposed that cytoprotection involves
activation of protein kinase C (PKC), which causes
phosphorylation of proteins such as the K+-ATP chan-
nels.144"146 This concept is supported by studies demon-
strating that adenosine administration mimics the
effects of ischemic preconditioning and that adeno-
sine receptor antagonists can block this protective
effect.147,148 Pang et al149 demonstrated a protective effect
of ischemic preconditioning in pig latissimus dorsi
muscle, although protection required at least three
cycles of 10 minutes of ischemia followed by 10 minutes
of reperfusion—significantly more than required for
cardiac muscle protection. Forrest150 observed that as
with myocardium, adenosine administration improved
the ischemic tolerance of muscle flaps in the pig.
Hopper et al151 further investigated the mechanisms
of ischemic preconditioning in the pig latissimus
muscle and found that the protective effect of ischemic
preconditioning was blocked by PKC inhibitors and
was mimicked by PKC activators. In addition, they
found that K+-ATP channel antagonists also attenu-
ated the anti-infarction effect of ischemic precondi-
tioning, suggesting that PKC plays a central role in the
anti-infarction effect of ischemic preconditioning in
pig latissimus muscle flaps, most likely through a
PKC-K + -ATP channel signal transduction pathway.
Another potential method of pharmacologic
preconditioning is with the synthetic compound
monophosphoryl lipid A, which mimics the late phase
of preconditioning. This compound, which has been
used clinically in cardiac bypass surgery, has been shown
to produce the same beneficial effects as ischemic pre-
conditioning in experimental random skin flaps and
pedicled skeletal muscle flaps.152,153
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17 • FLAP PHYSIOLOCY 495
Mechanism
Neovascularization, choke vessel dilation, vessel
reorientation
Protein kinase C (PKC) activation
PKC-K+-ATP transduction^)
Increased heat shock protein
Although it is intriguing to contemplate a phar-
macologic method of preconditioning, potential side
effects, such as hypotension with adenosine, may pre-
clude its use. The possibility of remote ischemic pre-
conditioning has therefore been studied as a potentially
clinically applicable technique. 154 It has been demon-
strated in pigs that three cycles of 10 minutes of remote
limb occlusion with a tourniquet, followed by 10
minutes of reperfusion, significantly reduced the
extent of necrosis in latissimus dorsi muscle flaps com-
pared with ischemic controls. This protective effect of
remote preconditioning was blocked by a mitochon-
drial ATP-sensitive Kf channel inhibitor, suggesting
that the effector mechanisms against infarction
might be similar for local and remote ischemic
preconditioning. 155
Moreover, ischemia is not the only form of stress
that can be used for preconditioning. Heat and the
production of heat shock proteins have long been
recognized as preconditioning processes. Several
investigators have shown that heat shock and recov-
ery can be used to increase survival of experimental
flaps, with increased expression of heat shock proteins
inthefiapskin. , 5 6 - , M
The precise mechanisms involved in ischemic pre-
conditioning are the subject of ongoing investigation.
A better understanding of these mechanisms may lead
not only to improvement in mechanical precondi-
tioning techniques but also to the development of other
preconditioning techniques. Such techniques could
prove valuable in the clinical setting, reducing
ischemia-related tissue injury and potentially expand-
ing our reconstructive potential.
ISCHEMIC INJURY
AND APOPTOSIS
Whereas the events described in the preceding section
may be involved in intermediate steps, it is likely that
cytoprotection involves events at the gene level as well.
Apoptosis is the process of programmed cell death
and is mediated at the molecular level. It results from
the activation of a caspase cascade that causes DNA
strand breaks, which can be identified by DNA lad-
dering in a terminal deoxyribonucleotidyl transferase-
*»?**> t#<aeldW image...
496 I • GENERAL PRINCIPLES
mediated deoxyuridine triphosphate-digoxigenin
nick-end labeling assay, also known as a TUNEL assay.
Maser et al159 observed that hypoxia induced by pre-
conditioning appears to trigger apoptosis, evidenced
by DNA laddering seen in panniculus carnosus muscle
harvested 24 hours after ischemic preconditioning.
This laddering was not seen in tissue that had not been
exposed to a preconditioning event. A number of the-
oretical explanations alone or in combination may
explain the cytoprotection afforded to composite
tissue by apoptosis. Programmed death of a portion
of the cells that will be exposed to the oxygen- and
nutrient-poor environment associated with relative
ischemia may allow the remaining cells to survive by
limiting the number of cells competing for limited
resources. Another possible mechanism may involve
activation of protein kinase C, which in turn causes
phosphorylation of the inhibitory factor IKB. Under
normal circumstances, IKB prevents N F K B (a cyto-
protective transcription factor) from exerting its effect
on the cell's DNA. Phosphorylation of IKB allows up-
regulation of N F K B , which may lead to production of
cytoprotective proteins.160
Apoptosis has also been implicated in ischemic
injury as distinguished from reperfusion injury
described previously. It has become apparent from
numerous clinical trials of anti-leukocyte adhesion
therapy targeting reperfusion injury in the clinical
setting that with longer ischemic periods, there is
an ischemic injury that can overwhelm therapy that
merely targets the reperfusion injury. Apoptosis
and specifically the role of caspases in the process of
apoptosis have become central areas of investigation.
Free radical activation, a key component of ischemia-
reperfusion, causes the activation of caspases.161 Studies
of brain, spinal cord, and cardiac ischemia have found
a role for caspases as part of the injury mechanism
(reviewed in reference 162).Theanti-apoptotic protein
Bcl-2 and its family members have been shown to
inhibit oxidative cell death.163 In addition, Bcl-2 family
members have been shown to be cytoprotective in
ischemic injury to cells.161 Bcl-2 is closely linked with
inhibition of mitochondria-initiated apoptosis, which
seems to be involved in some models of ischemic
injury.164 These findings indicate that Bcl-2 might have
an important regulatory role in ischemic damage
during flap loss and could be targeted to help prevent
this phenomenon.
Iwata et al165 examined caspase inhibition in mouse
muscle ischemia-reperfusion injury, using the pan-
caspase inhibitor z-VAD and comparing this with anti-
CD 18 antibody treatment. They found that although
anti-CD18 treatment provided protection for ischemic
periods of 60 minutes or less, it was not effective with
longer periods of ischemia. Longer periods of ischemia
resulted in apoptosis, which caspase inhibition effec-
tively reduced, concomitantly protecting muscle
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Dr.Mustafa D.
viability with ischemic periods as long as 120 minutes.
This concept suggests that targeting apoptosis and the
caspase cascade may ultimately provide a powerful
method of limiting ischemia-reperfusion injury and
improving flap viability.
NEOVASCULARIZATION
The identification and characterization of a number
of growth factors in recent years provide yet another
potential method of improving flap vascularity and
viability. Current evidence suggests that neovascular-
ization is mediated by a wide range of angiogenic
growth factors, with vascular endothelial growth
factor one of the most important angiogenic factors
in vivo. Although some early studies with basic fibro-
blast growth factor showed no effect in promoting neo-
vascularization in a flap model,166 subsequent studies
in an ischemic flap model showed that basic fibro-
blast growth factor enhanced the development of vas-
cular connections between the bed and the flap,
improved pedicle flap distal perfusion, and protected
marginally perfused areas from necrosis.167,168 Similar
benefits have also been demonstrated with vascular
endothelial growth factor or vascular endothelial
growth factor cDNA in animal models.169"171
FLAP MONITORING
Because of the unpredictability of flap viability, careful,
regular flap monitoring is paramount to success
(Table 17-3). Detection of compromised perfusion at
an early stage is critical to the ability to intervene, to
correct problems, and to save a flap. The ideal flap
monitoring system should be simple, reliable, repro-
ducible, and sensitive and should reflect the condi-
tion of the entire flap. In certain situations, such as
buried flaps or free flaps, the monitoring system itself
may need to be buried, or the monitored area of the
flap may need to be used as a small window to the
overall flap status. Limited access to the flap may lead
to faulty assessment. The optimal monitoring method
may also differ, depending on the type of flap (e.g.,
skin versus muscle versus bone or pedicled versus free).
Certainly, the "gold standard" of all monitoring
systems is direct clinical observation. For skin flaps,
assessment of the skin color compared with the adja-
cent normal skin color and evaluation of capillary refill
after pressure and release or scratching of the skin with
an instrument can provide a valuable and reliable
assessment of flap viability. A pink color that returns
within 1 to 2 seconds after pressure and release indi-
cates a healthy flap, whereas a pale color without cap-
illary refill can represent arterial insufficiency. A dusky
color with exceptionally brisk refill can represent
venous congestion. Probably the most reliable clini-
cal indicator of flap status is the color of the blood
image...

17 • FU\P PHYSIOLOGY 497

TABLE 17-3 • F1J\P MONITORING

M o n i t o r i n g Modality Advantages Disadvantages

Clinical examination Quick, easy Dark blood at distal end can be confused with
venous congestion
Fluorescein Used at time of elevation Can underestimate amount of tissue that will survive
Objective Cumbersome to do in serial fashion
Can be done quantitatively
Temperature Simple Variations with ambient environment
Differential thermometry good for Lags behind vascular compromise
buried or muscle flaps
Transcutaneous oxygen Simple, rapid, continuous Cutaneous version subject to systemic factors
pH monitoring Continuous Experimental, not widespread
Rapid change with arterial and
venous occlusion
Photoplethysmography Rapid, precise Shallow penetration (1-2 mm)
Differentiates arterial and venous Not widespread
compromise
Near-infrared Continuous Bulky, expensive
spectroscopy Deep penetration (10cm)
Laser Doppler Continuous, noninvasive Shallow penetration (1-2 mm)
Sensitivity to position changes
Sensitivity to temperature changes
Small sample area
Ultrasound Doppler Simple Difficulty separating signals from other vessels
Deep penetration
Implantable version sensitive and
specific for flap compromise

that oozes from the flap after sticking it with a needle.
Bright pink oozing reflects a healthy flap, whereas dark
purplish oozing reflects compromised perfusion or
venous insufficiency. In the distal random portion of
a flap, inadequate arterial perfusion can also result in
a deoxygenated, purplish color.
Fluorescein has long been used to assist the
direct assessment of skin perfusion.172"17'1 Fluorescein
is usually administered as an intravenous bolus
(15mg/kg); then, after 20 minutes, the tissue is exam-
ined with an ultraviolet lamp. Adequately perfused
tissue fluoresces, whereas inadequately perfused tissue
is not seen with the ultraviolet lamp. In general, fluores-
cein testing underestimates the amount of tissue that
will ultimately survive. It is most useful in evaluating
a flap at the time of elevation or in evaluating trau-
matically elevated flaps. This technique can be used
in a quantitative fashion known as dermofluorome-
try, whereby a fiberoptic light is used to measure and
quantify the dermal fluorescence. 175 When it is com-
bined with serial fluorescein injections, this technique
can be used for continuous flap monitoring. Its suc-
cessful use has been reported in a number of clinical
flap scenarios, both pedicled and free.176,177 Thomson
and Kerrigan178 discussed the interpretation of the dye
fluorescence index used in dermofluorometry and
found that at 2 and 5 hours after flap elevation, the
optimum dye fluorescence index thresholds are 7%
and 27%, respectively.
Temperature monitoring is one of the oldest and
simplest indirect methods of assessing flap blood flow.
Surface temperature, however, is subject to the vari-
ables of the local external environment and, addi-
tionally, responds slowly to vascular compromise.
Nevertheless, Khouri and Shaw179 described their
experience with surface temperature monitoring in
more than 600 free flaps, describing a sensitivity of
more than 90% and a positive predictive value of 75%.
A potentially more reliable method of temperature
monitoring is differential thermometry. With this tech-
nique, thermocouple probes are placed proximal and
distal to a microvascular anastomosis, and the tem-
perature differential is recorded. This is particularly
applicable for muscle flaps or buried flaps. 180,181 These
methods, nevertheless, also suffer from being indirect
measures of perfusion, subject to local environmen-
tal variables.
A number of monitoring methods based on meas-
urement of various aspects of flap metabolism have
also been described. Measurement of transcutaneous
oxygen tension is one of the oldest methods of assess-
ing metabolic flap viability. This test uses a heated
electrode placed on the skin surface and measures
trends over time. Serafin et al182 demonstrated that

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Dr.Mustafa D.
498 I • GENERAL PRINCIPLES
the transcutaneous Po 2 monitor provides safe, reli-
able monitoring of peripheral oxygenation in the
microcirculation that is rapid, continuous, and non-
invasive. Others report similar success in application
of this method clinically.183 This method is, however,
subject to many other systemic factors affecting oxygen
transport and tissue oxygenation.
A more refined method of tissue Po 2 monitoring
uses an optochemical, oxygen^sensing electrode
(Oxygen Optode) that is inserted in the subcutaneous
tissue of the flap to provide continuous monitoring of
tissue oxygen tension.184,185 In one series, this method
correctly identified failing flaps in all cases.
Continuous pH monitoring is another method of
assessing metabolic function in flaps. It uses a minia-
turized glass pH probe that allows the continuous
measurement of subcutaneous tissue pH. A rapid fall
in tissue pH is seen in response to either arterial or
venous occlusion.186 Changes in muscle and subcuta-
neous pH appear to be similar during arterial or venous
occlusions. Although it is thought that pH monitor-
ing can be a reliable experimental tool, it has never
reached widespread clinical application.187
Photoplethysmography measures fluid volume by
detecting variations in light absorption by the skin. It
uses a light-emitting diode to transmit light into a
tissue. Reflected light from hemoglobin in the dermal
capillary red blood cells is received by a photo detec-
tor and is analyzed as light intensity along a frequency
spectrum, removing noise and allowing a means to
distinguish between perfused and nonperfused tissues.
A limitation of this method is that it measures flow
in tissues only to a depth of 1 to 2 mm. One of the
oldest monitoring methods, it has undergone a number
of modifications over the years.188 Current systems use
a green light-emitting diode and in clinical series have
been reported to provide a rapid, precise method with
which to determine flap ischemia and to differentiate
venous compromise versus arterial compromise in
flaps almost immediately after the onset of an ischemic
insult.189 Their use, however, has never achieved wide-
spread acceptance.
Near-infrared spectroscopy is a new method of con-
tinuous tissue monitoring that works by measuring
the oxyhemoglobin and deoxyhemoglobin concen-
trations in tissue up to 10 cm deep. Studies have shown
that it is able to differentiate reasonably accurately
between arterial, venous, and total vascular occlusion
in a flap. The equipment is bulky and expensive,
however, and clinical experience is limited.190
Probably the most widely accepted adjunct to the
clinical assessment of vascular perfusion uses the
Doppler effect to measure the velocity of blood flow,
as first described by Strandness.191 The two main types
of Doppler instruments are the ultrasound Doppler
probe and the laser Doppler probe. The ultrasound
Doppler study uses reflected sound waves to measure
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Dr.Mustafa D.
the flow of blood cells within the larger arteries and
veins of tissues. The laser Doppler study, on the other
hand, measures the frequency shift of light rather than
sound and, as such, has a limited penetration of only
1 to 2 mm.
Laser Doppler study is almost exclusively confined
to measurement of skin blood flow. A laser light probe
is affixed to a specific area of the skin and produces a
voltage output proportional to the total flux of red
blood cells in the small volume of tissue sampled. In
general, the laser Doppler study provides relative
voltage readings rather than absolute measures of flow
rates, although some conversion can be made to actual
flow rates, depending on the tissue sampled. This
method, too, can provide continuous noninvasive
monitoring of flaps. A number of studies have
described its successful use in clinical flap monitor-
ing. Hallock192 evaluated the clinical threshold for tissue
viability with the laser Doppler flowmeter and found
that a value of 30% of baseline generally predicted
flap survival. A number of studies have correlated laser
Doppler readings with ultimate tissue viability.193,194
In one study, the sensitivity and specificity were found
to be 93% and 94%, respectively.195 There are, however,
a number of limitations with this technique that
significantly limit its clinical utility, including sensi-
tivity to minor changes in the probe position and angle
on the tissue surface with the patient's movement as
well as sensitivity to temperature changes and the fact
that only a small amount of tissue is sampled at any
one time.
Conventional Doppler ultrasonography, in clini-
cal use for more than 40 years, is one of the simplest,
most direct, and most reproducible methods of eval-
uating flow in the major arteries and veins of axial
flaps. By use of a standard ultrasound probe, vessels
several centimeters deep can easily be evaluated. A
typical arterial signal has a classic triphasic pattern; a
venous signal is lower pitched and continuous, varying
with the respiratory cycle and easily augmented with
gentle pressure on the flap. Because compression or
occlusion of the axial artery or vein is the most
common cause of flap failure, conventional Doppler
ultrasonography is an ideal method to monitor and
identify problems at an early stage. When normal arte-
rial inflow and flow through the flap are compromised,
the arterial signal will lose its normal triphasic pattern
and become more "water-hammer" in nature or dis-
appear. When venous outflow is compromised, the
continuous low-pitched sound of the venous signal
will be absent or muted, and the ability to augment
venous flow by gentle compression of the flap will be
lost.
A potential limitation of conventional Doppler
ultrasonography, especially when it is used to monitor
free flaps, is the inherent difficulty in separating the
flap signal from signals coming from adjacent normal

vessels deep to the flap. To address this issue, minia-
ture implantable Doppler probes have been developed
that can be surgically placed on the effluent vein of a
free flap to continuously monitor venous outflow,
which, because of the closed system of a free flap, can
provide nearly instant notification of either arterial
or venous occlusion.196 Studied in a series of 135 con-
secutive free flaps, this method had a sensitivity of
100% in identifying flaps that required re-exploration,
with a false-negative rate of 3 % . With its early
identification of arterial or venous compromise, this
method allowed early re-exploration and 100% flap
salvage.197 Because this is a simple and direct method
of monitoring axial blood flow, this technique is
becoming the standard method of monitoring free
flaps.
THERAPEUTIC INTERVENTIONS
TO IMPROVE FLAP VIABILITY
By far the most important factors in optimizing flap
viability are proper flap selection and design, metic-
ulous debridement and preparation of the bed, careful
flap elevation and inset, and close postoperative clin-
ical monitoring (Table 17-4). No drug, device, monitor,
or maneuver can overcome poor planning or poor
technical execution. In particular, selecting and de-
signing a reliable axial flap with robust, large-vessel
arterial and venous flow to the majority of the flap
and ensuring the patency of this large-vessel flow
through careful dissection and inset will go a long
way toward ensuring reconstructive success. The final
stages of flap inset and dressing application, as well
TABLE 17-4 • THERAPEUTIC INTERVENTIONS
Intervention Benefits
Hypothermia Reduces metabolic rate
Prolongs ischemia window
Delay procedure Ischemic preconditioning
Effective during reperfusion
Steroids Membrane stabilizer
Anti-inflammatory
Edema reduction?
Dextran Volume expansion
Decreased platelet adhesion
Inhibition of platelet aggregation
Aspirin Inhibition of platelet aggregation
Vasodilation (higher doses)
Heparin Inactivates clotting factors
Improves patency
Leeches Inject hirudin
Vasodilation
Mechanical decompression
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17 • FLAP PHYSIOLOGY 499
as postoperative positioning, are particularly impor-
tant to prevention of compromised perfusion. Some-
times, a single poorly placed suture or piece of tape
or gauze can lead to tightness or kinking, resulting in
the loss of just that portion of the flap required to
cover the critical portion of the defect. Particularly
for microsurgical flaps, if, at the end of the proce-
dure, one believes "it's probably OK" it is not, and
one should take the time to ensure that everything is
as perfect as possible before leaving the operating
room. Careful postoperative monitoring is critical too,
as only early intervention can be successful in salvaging
flaps from mechanical causes of ischemia, such as
hematoma, compression, kinking, or anastomotic
thrombosis.
There are, however, a number of metabolic factors
that should be addressed before any elective flap
surgery to optimize flap physiology, including careful
control of blood pressure and the patient's tempera-
ture and review of all medications. In situations in
which systemic hemodynamics are compromised,
such as sepsis, and when patients are taking vasoac-
tive medications, such as nicotine, ephedrine, or illicit
drugs (particularly cocaine), elective flap surgery
should be postponed until these conditions can be
reversed. Smoking has long been known to adversely
affect survival of flaps as a result of its systemic vaso-
constrictive effect.198,195 This is particularly true in
microsurgery, in which uncontrolled vasospasm can
lead to thrombosis with total flap loss. It is generally
recommended, therefore, that patients stop smoking
completely for several weeks before and after flap
surgery.200
Risks
Increases number of procedures
Systemic, infectious risks
Anaphylaxis
Pulmonary edema
Excessive volume expansion
Bleeding
Bleeding, hematomas
Bleeding
Infection
500 I • GENERAL PRINCIPLES
Temperature can have a profound effect on micro-
circulatory perfusion as well as tissue tolerance to
ischemia and the severity of the reperfusion injury
process. As part of the normal thermoregulatory phys-
iology of skin, hypothermia can clearly result in
microcirculatory vasoconstriction and decreased tissue
perfusion. On the other hand, hypothermia is also pro-
tective against the injury effects of ischemia and reper-
fusion. It is well known that cooling ischemic tissue
will dramatically reduce the metabolic rate and
markedly prolong the period of ischemia that can still
result in successful reperfusion. In the case of digits,
which contain no muscle, this period can be measured
in days. For muscle, of course, the safe ischemic window
is much less, only 2 hours at 34°C or 5 hours at 26°C
in one study.201 Even mild hypothermia can provide
significant protection, although interestingly, mild
hypothermia has a far greater impact during the reper-
fusion phase than during ischemia and is associated
with a reduction in neutrophil accumulation and neu-
trophil-mediated tissue injury.202 This suggests that the
common practice of actively warming reperfused
ischemic tissue, such as a free flap, may be ill-advised.
Whenever there is concern about the potential via-
bility of a planned flap, especially if the flap is designed
to contain a large random component, some form of
ischemic preconditioning should be employed. This
could be achieved with a standard delay procedure,
by selective pedicle ligation if more than one axial
pedicle exists, or by repeated courses of pedicle clamp-
ing. The possibility of employing remote ischemic pre-
conditioning, as previously described, is intriguing but
has not yet reached widespread clinical applicability.
In addition, a number of pharmacologic agents have
been reported to have varying degrees of efficacy in
improving perfusion and survival of flaps, both at the
microcirculatory level and at the macrocirculatory level
of a free flap anastomosis. Many of these have shown
significant efficacy in experimental studies as described
in the previous sections but have not yet shown pre-
dictable clinical efficacy; therefore, few are in wide-
spread clinical use. It is hoped, however, that some of
the promising therapies currently under investigation
will someday provide important adjuncts to flap
surgery.
Steroids have been used both experimentally and
clinically in flap surgery. Their effect as a membrane
stabilizer and nonspecific anti-inflammatory agent
points to a mechanism of action similar to targeted
antineutrophil strategies described earlier, although
without the same specificity or efficacy. Experimen-
tally, systemic steroids have shown mixed results in
improving flap viability.203'205 There is a general clin-
ical impression that steroids reduce flap edema, but
this has not been critically examined, and the risks of
systemic steroid administration, especially the infec-
tious risks, seem to outweigh the potential benefits.
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Dr.Mustafa D.
The more commonly used classes of pharmaco-
logic agents are the rheologic agents and anticoagu-
lants. Johnson and Barker206 and Conrad and Adams207
have reviewed the mechanisms of the anastomotic and
microcirculatory responses to thrombosis and provide
rationales for therapy. Dextran, a polysaccharide syn-
thesized by bacteria from sucrose, was first developed
as a volume expander and has since been shown to
have myriad salutary effects, including decrease of
platelet adhesiveness, inhibition of platelet aggrega-
tion, and decrease of blood viscosity. In a hyper-
thrombotic model of an arterial inversion graft,
dextran was shown to nearly double microvessel
patency.208 It is produced as both a 70,000 molecular
weight and the more commonly used 40,000 molec-
ular weight formulation and is usually administered
as a continuous intravenous infusion during the flap
procedure and continuing for several days postoper-
atively. Allergic reactions, including anaphylaxis and
excessive volume expansion, lead to pulmonary edema,
especially in elderly or compromised patients. For this
reason, a small test dose is usually administered before
infusion, and its use in elderly patients is relatively
contraindicated. Although some clinical studies
support the use of dextran in flaps and in micro-
surgery,209 there have been no prospective random-
ized clinical trials to document its efficacy.
Aspirin is also commonly used in flap surgery, espe-
cially microsurgical flaps, again because of its effect
in blocking platelet aggregation and vascular throm-
bosis. This effect occurs by inhibition of platelet-
derived cyclooxygcnasc, which produces thromboxane,
a potent vasoconstrictor and platelet aggregator. At
higher doses, aspirin also inhibits endothelial cyclooxy-
genase, which produces prostacyclin, a vasodilator and
inhibitor of platelet aggregation. The ideal dose to
inhibit thromboxane, without inhibiting prostacyclin,
is thought to be 50 to 100 mg, easily provided by a
single 81-mg baby aspirin, although a single 325-mg
tablet is also probably reasonable.210 Unlike dextran,
aspirin does not have rheologic effects, so its primary
benefit is antithrombotic, leading it to be more com-
monly used for microsurgical flaps rather than for
improving distal perfusion, for which dextran is often
employed.
Heparin is the most widely used antithrombotic in
both medical and surgical applications. It is an
antifibrin agent that works by binding to antithrom-
bin III, which then inactivates a number of clotting
factors, including thrombin. In flap surgery, it has been
used both systemically and as a topical irrigant at the
time of anastomosis. In prothrombotic experimental
models, it improves patency twofold to fourfold.21
In a large clinical trial of myocardial thrombolysis,
heparin doubled the coronary patency rate compared
with control.212 Because of the extremely high risk of
clinically significant hematoma formation with flap
ltJWttf'yadW image...
surgery, however, systemic heparin is usually reserved
for microvascular applications when an intraopera-
tive thrombosis occurs and requires mechanical clear-
ing. Topical irrigation with heparinized saline is a
widely used technique in microsurgery, and its use in
concentrations of 100 units/mL has some support in
the clinical literature. 213 Because of the low risk of
topical anastomotic heparin irrigation, it has become
standard microsurgical technique; however, the largest
prospective series to examine various methods of pre-
venting microsurgical thrombosis showed no outcome
benefit of topical heparin irrigation. 2 H This study, the
largest prospective flap study published (493 flaps), is
particularly revealing in that no therapeutic inter-
vention other than subcutaneous heparin showed a
significant effect on outcome. This study was followed
by a large prospective clinical trial of anastomotic irri-
gation with tissue factor plasminogen inactivator, a
natural protein that combines with tissue factor and
factors Vila and Xa to inhibit coagulation. Although
promising in experimental studies, this agent also
showed no significant benefit in the controlled clini-
cal trial. 215
Leeches have been used for a variety of indications
since ancient times, and they have clearly found a
current application in the treatment of flap compli-
cations. 216,217 Medicinal leeches, Hirudo medicinalis, are
specifically bred for medical applications and are com-
monly used to relieve venous congestion in flaps and
especially replantations. Their beneficial effects are
several: injection of hirudin, an extremely potent
inhibitor of the conversion of fibrin to fibrinogen that
does not require antithrombin III for activation and
therefore can be used in cases of antithrombin III
deficiency; potent vasodilation effect; injection of
hyaluronidase, which helps the spread of hirudin
through the tissues; and mechanical creation of
decompressive venous bleeding through the skin. T h e
most significant risks of leech therapy are excessive
bleeding and Aeromonas hydrophila infection, for
which prophylactic antibiotics should be administered
for the duration of treatment.
In summary, there are many promising potential
therapies currently b e i n g investigated that m a y
someday be employed clinically to improve flap phys-
iology and flap viability, allowing expanded flap appli-
cations. Nevertheless, there is no substitute for proper
flap design and technical execution. It is hoped,
however, that some of the promising therapies cur-
rently under investigation will someday provide impor-
tant adjuncts to flap surgery.
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196. Swartz WM, Jones NF, Cherup L, Klein A: Direct monitoring
of microvascular anastomoses with the 20-MHz ultrasonic
Doppler probe: an experimental and clinical study. Plast Recon-
str Surg 1988;81:149-161.
197. Kind GM, Buntic RF, Buncke GM, et al: The effect of an
implantable Doppler probe on the salvage of microvascular
tissue transplants. Plast Reconstr Surg 1998;101:1268-1273,
discussion 1274-1275.
198. Rees TD, Livcrett DM, Guy CL: The effect of cigarette smoking
on skin-flap survival in the face lift patient. Plast Reconstr Surg
1984;73:911-915.
199. Chang LD, Buncke G, Slezak S, Buncke H J: Cigarette smoking,
plastic surgery, and microsurgery. J Reconstr Microsurg
1996;12:467-474.
200. Chang DW, Reece GP.Wang B, et al: Effect of smoking on com-
plications in patients undcrgoingfreeTRAM flap breast recon-
struction. Plast Reconstr Surg 2000;105:2374-2380.
201. Eckert P, Schnackerz K: Ischemic tolerance of human skeletal
muscle. Ann Plast Surg 1991;26:77-84.
202. CornejoCJ,KierneyPC,VedderNB,WinnRK:Mildhypother-
mia during reperfusion reduces injury following ischemia of
the rabbit car. Shock 1998;9:116-120.
203. Mes LG: Improving flap survival by sustaining cell metabo-
lism within ischemic cells: a study using rabbits. Plast Recon-
str Surg 1980;65:56-65.
204. Nancarrow JD: Augmentation of island flaps by preoperative
cell membrane stabilisation: an experimental study in rats. Br
] Plast Surg 1981;34:212-214.
205. Nakatsuka T, Pang CY, Neligan P, et al: Effect of glucocorti-
coid treatment on skin capillary blood flow and viability in
cutaneous and myocutaneous flaps in the pig. Plast Reconstr
Surg 1985;76:374-385.
206. Johnson PC, Barker JH: Thrombosis and antithrombotic
therapy in microvascular surgery. Clin Plast Surg 1992; 19:799-
807.
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207. Conrad MH, Adams WP Jr: Pharmacologic optimization of
microsurgery in the new millennium. Plast Reconstr Surg
2001;108:2088-2096, quiz 2097.
208. Rothkopf DM, Chu B, Bern S, May JW Jr: The effect of dextran
on microvascular thrombosis in an experimental rabbit
model. Plast Reconstr Surg 1993;92:511-515.
209. Pomerance J.Truppa K, Bilos ZJ, et al: Replantation and revas-
cularization of the digits in a community microsurgical prac-
tice. J Reconstr Microsurg 1997;13:163-170.
210. Weksler BB, Pelt SB, Alonso D, et al: Differential inhibition
by aspirin of vascular and platelet prostaglandin synthesis
in atherosclerotic patients. N Engl J Med 1983;308:800-
805.
211. Greenberg BM, Masem M, May JW Jr: Therapeutic value of
intravenous heparin in microvascular surgery: an experimental
vascular thrombosis study. Plast Reconstr Surg 1988;82:463-
472.
212. Bleich SD, Nichols TC, Schumacher RR, et al: Effect of heparin
on coronary arterial patency after thrombolysis with tissue
plasminogen activator in acute myocardial infarction. Am J
Cardiol 1990;66:1412-1417.
213. Das SK, Miller JH: Current status of topical antithrombotic
agents in microvascular surgery. Microsurgery 1994; 15:630-
632.
214. Khouri RK, Coolcy BC, Kunselman AR, et al: A prospective
study of microvascular free-flap surgery and outcome. Plast
Reconstr Surg 1998;102:711-721.
215. Khouri RK, Sherman R, Buncke HJ Jr, et al: A phase II trial
of intraluminal irrigation with recombinant human tissue
factor pathway inhibitor to prevent thrombosis in free flap
surgery. Plast Reconstr Surg2001; 107:408-415, discussion 416-
418.
216. Lee C, Mehran RJ, Lessard ML, Kerrigan CL: Leeches: con-
trolled trial in venous compromised rat epigastric flaps. Br J
Plast Surg 1992;45:235-238.
217. Batchelor AG, Davison P, Sully L: The salvage of congested
skin flaps by the application of leeches. Br J Plast Surg
1984;37:358-360.
 image...

CHAPTER

18•
Principles and Techniques of
Microvascular Surgery
FU-CHAN W E I , MD • SINIKKA SUOMINEN, MD, PhD

HISTORY MICROANASTOMOSIS
DEFINITION Suturing Technique
End to End
BENEFITS AND DISADVANTAGES Sleeve Anastomosis
LEARNING CURVE End to Side
Microvascular Crafts
TOOLS Size Discrepancy
Surgical Microscopes Flow in Free Flaps
Magnifying Loupes Ischemia Time
Microinstruments Anastomotic Failure
TECHNIQUES FREE FLAP SURCERY
Requirements Advantages and Disadvantages
Planning Timing
Approach and Exposure
Preoperative Considerations
Choice of Recipient Vessels
Dissection Techniques Microvascular Anesthesia
Preparation of Vessels Special Techniques and Flap Design Modifications
Vasospasm Monitoring Flaps
Anastomosis Sequence Results
Future

HISTORY experiments of Jacobson and Suarez9 demonstrated

In 1552 Pare described the possibility of vascular repair,
but the first report of clinical use was decades later,
1759, by Hallowell, who successfully sutured a brachial
artery lesion.1 The progress was slow until the turn of
the 20th century. The first vascular anastomosis was
described by J.B. Murphy in 1897, 2 andin 1902 Alexis
Carrel performed vascular end-to-end anastomosis
using a three-stay suture technique. 3 These techniques
were further developed by Carrel's coworker Charles
Guthrie, 4 and Carrel was awarded the Nobel Prize in
1912 for his achievements in vascular surgery and organ
transplantation. 1 The later discovery of an anticoagu-
lant by McLean5 in 1916 and the final purification of
heparin by Charles and Scott6 set the basis for clinical
vascular surgery.
The compound microscope was invented by
Zacharias Janssen in 1590/ but it was not until 1921
that it was first used in a surgical setting by the Swedish
otologist OlofNylen. 8 Its potential for repair of small
vessels was not appreciated for decades until the
successful microvascular repair of vessels as small as
1 mm in diameter. Replantation became the first clin-
ical application of microvascular surgery. In 1964,
Malt10 successfully replanted an arm of a 12-year-old
boy run over by a train. This was soon followed by
several other procedures performed around the world.1
The first digital replantation was performed by Tamai
in 1965 with use of an operating microscope, 1 and the
first successful toe to thumb transfer was performed
byCobbettinl968. 1 2
The first experimental free composite tissue trans-
plantation (the term free flap was subsequently adopted
to indicate revascularization of a flap completely trans-
planted from its donor site) was performed on a dog,
based on the superficial epigastric vessels, and pub-
lished by Krizek et al13 in 1965. The first report of the
use of a free flap in a human was published in 1971,
but the operation had been performed several years
earlier in Bombay, India, by Antia and Buch,14 who
used a free dermolipomatous groin flap to fill a
facial defect. The procedure was complicated by an

507

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Dr.Mustafa D.
TeWR^aacfWimage...
508 I • GENERAL PRINCIPLES
infection, and at least partial necrosis of the flap
occurred. The first completely successful free flap oper-
ation in a human was performed in 1970 in Oakland,
California, by McLean and Buncke15 with use of
omentum for a large scalp defect. This was soon fol-
lowed by transfer of the first composite flap, a groin
flap, by Daniel and Taylor16 in January 1973 and
repeated 2 months later by O'Brien,17 both in Mel-
bourne, Australia. Advances in free flap surgery were
rapid from then on, and the clinical use of free microvas-
cular flaps has been possible for more than 30 years.
The first decade was spent on experimenting with new
flaps as well as expanding the indications for free tissue
transfer, and to date an endless variety of flaps have
been described.
During the 1980s, free microvascular flap proce-
dures became routine surgery, and as surgical skill
improved and better donor sites were identified, the
failure rate decreased.18,19 The success rate today ranges
from 95.9% to 99%,20'25 whereas in earlier series it
ranged from 74% to 91%. 1 8 Still, failures and vascular
complications continue to occur, even in experienced
hands. A technical error can be blamed in many cases,
but sometimes there is no obvious reason for flap
failure.
During the late 1980s and the 1990s, research on
microvascular surgery transferred its focus from flap
anatomy and survival toward refinements and flap
choice. A free flap should contain the right compo-
nents and fulfill the functional requirements of the
reconstructed defect. It must match the recipient site
not only in size but also in texture, form, and color. As
more and more free flaps are performed as elective oper-
ations, donor morbidity becomes less tolerable and the
appearance of the donor site must remain inconspic-
uous. The greater variety of free flaps allows the avoid-
ance of major donor site problems, but all flaps leave
a donor defect of some kind. Donor site problems may
diminish in the future, however, with the development
of new minimally invasive and endoscopic harvesting
methods. The studies on tissue engineering and flap
prefabrication will certainly introduce new options in
flap design.
DEFINITION
The word microscope comes from the Greek words
mikros (meaning "small") and skopein (meaning "to
view").7,26 Microsurgery, subsequently, means surgery
with the aid of a microscope; inside the field of plastic
surgery, the term includes microvascular surgery,
microneural surgery, microlymphatic surgery, and
microtubular surgery. The term microsurgery is widely
used also inside ophthalmology, neurosurgery, otology,
and dermatology, to name but a few. Microvascular
surgery is a more defined term referring to coaptation
of small vessels performed under illumination, and in
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a clinical setting it is often used synonymously with
the term reconstructive microsurgery, referring to both
free tissue transplantations and replantations.
BENEFITS AND DISADVANTAGES
Microsurgery is a fundamental tool in reconstructive
surgery today. It allows an almost unlimited choice of
the reconstructive methods, replacement of lost tissue
with similar components, and optimal selection of
donor site with minimal morbidity. For the individ-
ual patient, this may mean faster recovery and mobi-
lization or restoration of otherwise lost function. Fast
and adequate coverage with well-vascularized tissue
reduces the risk of infection, helps avoid development
of chronic infections, and allows early postoperative
management of the recipient site (e.g., physical therapy,
irradiation). A free flap reconstruction is essentially a
single-stage procedure, whereas pedicled flaps may, in
some instances, require two operations (one for trans-
fer, one for inset) with an uncomfortable waiting period
in between. Several studies have demonstrated the
cost-effectiveness of microsurgical reconstruction as
opposed to more traditional methods of flap trans-
position. Kroll et al27 showed microsurgical head and
neck reconstructions to be more economical than
regional flaps, and Grotting et al28 suggested that a free
transverse rectus abdominis myocutaneous (TRAM)
breast reconstruction costs less than a pedicled one.
Microsurgical lower extremity reconstructions have
been demonstrated to be less expensive than local or
cross-leg flaps.29 The psychological benefits of restor-
ing the body image have been documented. 30
Microsurgery is a powerful and attractive tool, but
the mere ability to perform a free flap docs not mean
that it should be used in every case. The decision to
use a free flap should be made only after exclusion of
other simpler reconstruction options, carefully weigh-
ing the pros and cons in each individual case. One must
also bear in mind Mathes and Nahai's metaphor of
a reconstructive ladder.31 This implies that a simpler
method is not necessarily always the best, and in selec-
tive cases it is justified to jump over some steps in the
reconstructive ladder. The simplest feasible procedure
may not prove to be the best in the long term.32 For
example, in many cases, it is justifiable to choose a free
TRAM or a deep inferior epigastric perforator flap
over the simpler methods of pedicled TRAM flap or
endoprosthesis, and the final choice should be made
together with the patient.
The principal disadvantage of free tissue trans-
plantation is the need for special resources and
technical expertise. Microsurgery cannot be per-
formed without first making some investments in
special instruments, preferably a microscope, and it
requires specially trained personnel both in the oper-
ating room and in the postoperative care unit. A
TeWR^SeldW image...
18 • PRINCIPLES AND TECHNIQUES OF MICROVASCULAR SURGERY
sufficient and steady volume of microsurgery is nec-
essary to maintain the skills of both the surgeons and
the assisting personnel. Because microsurgical proce-
dures tend to be lengthy, ranging from 4 to more than
12 hours, a two-team or even three-team approach is
preferable. It is not advisable for a single surgeon to
maintain a microsurgery unit; there should be enough
trained surgeons to ensure a prompt re-exploration if
the principal surgeon is temporarily unavailable. At a
more personal level, the lengthy operations, the fear
for the rare but possible complete flap failure, the sub-
sequent need for continuous alertness, and the reop-
erations at early morning hours are strenuous for both
the surgeons and their families and require sacrifices
in daily life. In a bigger unit, the responsibilities can
beshared to ease the workload of an individual surgeon.
LEARNING CURVE
Retrospective studies indicate that a critical factor
influencing success rates of microvascular surgery is
the surgeon's operative experience. 18 Surgeons with a
high success rate have gone through a learning curve,
and a major determinant between success and failure
is individual operative technique. Several studies
have addressed the issue of operative experience. Early
success rates are markedly lower (between 72% and
91%) and rise to 96% to 97% when experience is
gained.18,33 This, however, cannot be fully attributed
to experience only because microvascular techniques,
materials, and instruments have evolved concomitandy.
A study on the first year of clinical experience of three
microvascular head and neck surgeons yielded a
success rate of 97.5%, showing that well-trained junior
microvascular surgeons can achieve survival rates
comparable to those of experts. 33
TOOLS
Surgical M i c r o s c o p e s
HISTORY
In the late 1800s, a German machinist by the name of
Carl Zeiss started mass production of high-quality
microscopes. They soon became an integral part of lab-
oratory research, but the first surgical microscope was
designed, built, and used by a Swedish otologist, Carl
Nylen, in the 1920s. He used first a monocular micro-
scope for rabbit labyrinthine fenestrations and later a
binocular microscope in human cases of chronic otitis
and pseudofistula formation. 8 His chief, Holmgren,
reported the first microsurgical fenestration for
otosclerosis with use of a stereoscopic operating
microscope.34
The first diploscope, a stereoscopic microscope for
simultaneous use by two surgeons, was designed by
Hans Littman of the Zeiss company on the request of
vascular surgeon Julius Jacobson.7 The second piece
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509
was delivered to a plastic surgeon, Jim Smith of New
York, for use in peripheral nerve repair.35
In 1960, at the American College of Surgeons Forum,
Jacobson and Suarez9 presented a series of successful
small-vessel anastomoses with use of this operating
microscope. A plastic surgeon, Harry J. Buncke, was
in the audience. He had been struggling in attempt-
ing repair of 1- to 2-mm vessels without a microscope.
He now adopted the operating microscope to his lab-
oratory, and the world's third diploscope was purchased
by Buncke in 1962.7'"
TIPS FOR USE
The operating microscope allows the magnification
to be changed up to 40x during the different stages
of surgery. Most models have a foot control panel
for focusing and zooming; some manufacturers have
placed these functions in the handles. The head of the
microscope should be easily tiltable and the light inten-
sity changeable. An advantage over loupes is that the
surgeon and the assistant can view the same field, and
most models allow a television monitor to be connected
to the microscope for teaching purposes. The proce-
dures can also be videotaped, or a camera can be
installed for pictures through the microscope.
However, all microscopes are big and clumsy,
require space, and at the same time limit the surgeon's
choice of position. Ceiling-mountable microscopes
require less space but are confined to a single operat-
ing theater and thus are often impractical in busy
centers. Ideally, the microscope should be easily
adjustable and provide the assistant with an equal view;
unfortunately, most microscopes do not allow as much
adjustability to the assistant's binoculars as to the
surgeon's, although this has been improved in the
newest models. In fact, the assistant is often left in an
awkward and uncomfortable position after the ideal
position for the surgeon has been achieved, so the assis-
tant would benefit from more flexibility. Another dis-
advantage is that unless a monitor is used, the magnified
operative field is viewed simultaneously by only two
of the surgical team, usually leaving the assisting nurse
without a proper view of the procedure.
It is wise to spend some time thinking about the
ergonomics of microsurgery (Fig. 18-1). The micro-
scope must be good and easily adjustable, and one must
take time to place it well. The seat must be adjustable,
and one should sit in a slightly forward-leaning posi-
tion with feet apart, forming a load-bearing triangle
that ends at floor level.36 The upper extremities must
be fully supported to allow them to relax, thus omit-
ting tremor. This is not always easy, but it can often be
achieved by piling folded sheets on which to rest the
arms. Last, the surgeon must be fam iliar with the micro-
scope as well as with its operation and adjustment to
achieve an ideal view of the operative field.
510 14 GENERAL PRINCIPLES
FIGURE 1 8 - 1 . Comfortable and ergonomic position-
ing during microvascular surgery.
Magnifying Loupes
Loupes are widely used in surgical and dental proce-
dures to enhance visualization, allowing precise
dissection of tissues. Loupe use is advocated on the
grounds of cost-effectiveness, portability, and opera-
tor freedom.37
Some microsurgeons opt to use loupes also for
microanastomosis; in experienced hands, they pro-
vide an alternative to the operating microscope for
microvascular anastomosis of vessels 1.0 mm or more
in diameter. A retrospective study of 200 consecutive
free microvascular tissue transplantations compared
the performance of free tissue transplants with 3.5x
loupes and with the operating microscope.25 The micro-
scope was required for performing vascular anasto-
moses on children and on vessels of 1.5 mm or less in
diameter. There was no difference in outcome between
the two groups, with free flap success rates of 99% for
both the loupe and the microscope groups. Despite
these studies, most centers still use the microscope with
its greater range of magnification and light sources.
TYPES
Basically two types of loupes suitable for surgery are
commercially available, the compound (Galilean)
loupes and the prismatic loupes (often referred to as
wide-angle loupes). As opposed to single-lensed drug-
store magnifying glasses, the compound loupes consist
of two magnifying lenses separated by air. The image
quality of compound loupes tends to become distorted
around the edges at magnifications above 2.5x. This
disadvantage, however, is counterbalanced by their
relatively low cost and light weight.38 A new version
of Galilean loupes, the Ultralight loupes, weigh only
10 g. These 2.5x or 3.2x loupes, with self-adjustable
working distance, are snap-fit coupled to the user's own
glasses.
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The prismatic loupes provide higher optical quality
because of a Schmidt prism, which lengthens the path
of light through a series of mirror reflections inside
the loupe.38 They can provide a wider field of view and
a longer depth of field or working distance, but they
are 30% to 40% heavier and more expensive than com-
pound loupes.38
TIPS FOR USE
The next step is to choose suitable magnification. For
hand surgery and dissection of flaps, a magnification
of 2.5x is usually suitable; but if loupes are to be used
for anastomosis, the larger magnifications of 3.5x or
4.5x might be more suitable. The size of the field viewed
through the system as well as the length of the in-focus
distance will decrease with increasing magnification
while the weight of the loupes increases. Loupes with
a magnification higher than 4.5x tend to be too heavy
for daily use, resulting in tension of the neck and con-
sequent trembling of the head.
After the type of loupe is selected, a few optical fea-
tures need to be individually adjusted. Most loupes
need to be fixed to a certain workinglength determined
by the owner, usually between 30 and 55 cm (12 to 20
inches) .The working angle and the position of the lens
in the plane of the user's face are usually customized
at the initial fitting of the loupes, although some models
are self-adjustable.
Loupes come in many different designs. A matter
of thought may be whether to purchase loupes that
are fixed to the lenses or the flip-up type. The flip-up
or snap-fit types permit cheaper changing of the lenses
if the surgeon's vision changes because the glasses are
one's prescription glasses and can be handled by any
optician.
Microinstruments
MATERIALS AND MAINTENANCE
Most microinstruments are made of heat-hardened
stainless steel, which is more resistant to wear and tear
than are the antimagnetic materials like titanium or
other steels. Magnetization of steel instruments can
cause annoyance, and they should be stored on demag-
netized or nonmagnetic shelves. If an instrument
becomes magnetized, passing it through a coil demag-
netizer will help.
All instrument manufacturers give instructions for
maintenance, and it is extremely important to follow
them to ensure maximal performance of the microin-
struments. It is advisable to store the microinstruments
in specially designed instrument cases (Fig. 18-2). One
should avoid using them for anything but the actual
microsurgery because they are easily damaged; all blood
clots, suture pieces, and the like should be constantly
washed off by the nurse during surgery.
 image...
18 • PRINCIPLES AND TECHNIQUES OF MICROVASCULAR SURCERY
FIGURE 1 8 - 2 . A basic set of microinstruments and
clamps in a storage case.
TYPES
Scissors
Microvascular scissors and needle holders are spring
loaded to allow finer movements. Scissors that are
designed for dissecting have a rounded tip and curved
blades; when held closed, they can be used as a dis-
secting probe. Those designed for stripping of adven-
titia have straight blades that are pointed at the tip,
and they are also used for cutting microsutures of less
than 8-0. Microvascular scissors come with flat or round
handles, according to the surgeon's preference, and in
different lengths ranging from 10 to 18 cm. There are
also fine-toothed scissors designed specifically for
cutting nerves.
Needle Holders
Microvascular needle holders are spring loaded and
can be delicately maneuvered between the index finger
and the thumb like a pencil. They come in different
lengths, with flat or round handles and straight or
curved tips. Angulated forceps can also be used as needle
holders. Some needle holders come with a ratchet-
lock, designed mainly for convenience for parking the
needle or for passing the needle to the surgeon, not
for use while suturing- The unlocking type is easier to
use in inexperienced hands. The locking type requires
more practice because it easily damages the fine
needle, which consequently loses its shape, and the
locking and unlocking movements can cause unin-
tended damage to the tissues handled.
Forceps
The jeweler's forceps were originally designed by the
Swiss Dumont factory and are characterized by a flat
handle and sharply narrowing tips. They are further
classified by the width of the contact surface, the nar-
rowness, and the overall configuration. No. 2 forceps
have wide jaws and can be used as needle holders. No.
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511
5 forceps have very fine tips and are suitable for tissue
handlingand thus are commonly used in microsurgery.
No. 7 forceps have curved jaws (Fig. 18-3).
Microforceps are also available with round handles,
and some prefer them to the flat handles because they
are more easily rotated. The most commonly used
forceps are smooth tipped, but the forceps can also be
toothed, curved, or equipped with a hole in the tip for
better grasping. Forceps specifically designed for tying
knots or for dilating vessel ends are also available.
Clamps
Jacobson, in his historical first microanastomoses, used
bulldog clamps. These, however, were far too big
for 1-mm vessels, and during the early years, several
pioneers of microsurgery developed their own
modifications of microclamps. The clamps developed
by Henderson and O'Brien 39 in 1970 are described
by the inventors as not suitable for vessels less than
1.5 mm. 40 The type designed by Acland41 in 1974
has been further developed and is still commercially
available, as is the device of two clamps incorporated
into a sliding bar developed by Tamai in 1972. l
Modifications of both are now available from many
suppliers. Clamps are ideally atraumatic and have
sufficient closing pressure to prevent bleeding and slip-
page but not damage the vessel wall. To optimize the
pressure, clamps are available in a variety of sizes for
different vessel diameters (Fig. 18-4) and separate
designs for arteries and for veins. Handling the small
clamp maybe difficult, especially in constricted spaces,
so special clamp appliers are available to ensure the
accurate placement and removal of the clamps without
damage to the vessels.
Bipolar Coagulator
The development of a bipolar coagulator by a neuro-
surgeon, Malis, in 1956 promoted further development
of microsurgery because a completely bloodless field
was now attainable. 1 The bipolar coagulator produces
FIGURE 1 8 - 3 . A set of jeweler's forceps, numbers 1,
3, 4, 5, and 7.

512 I • GENERAL PRINCIPLES
44 tt n » § v B
II
A B
heat damage only within a very small area between the
instrument tips. Its power setting must be optimized;
too much power results in spreading of the heat. In
microsurgery, the bipolar coagulator is preferred to a
monopolar coagulator because it allows more precise
coagulation of bleeders without damage to the sur-
rounding tissues. Some surgeons like to use it for dis-
section instead of a knife or scissors, and it is particularly
useful in coagulating small branches of the donor or
recipient vessels in place of vascular clips.36 Bipolar scis-
sors are now commercially available.
Using Microinstruments
Microinstruments should be held like a pencil, with
pulp to pulp pinch. The end of the instrument is sup-
ported by the thenar web (Fig. 18-5). The movement
should come mainly from the fingertips; the hand
should remain still for firm control. The position must
be comfortable and the forearms well supported to
avoid trembling and fatigue. For smooth changing of
the instruments under the microscope, one can allow
the assistant or the nurse to control the instruments,
or the instruments can be positioned in an area where
the hand can pick them up without moving the view
from the operating field.
MICROSUTURES
Buncke11 describes making his first microneedle by
drilling a hole in a 75-|im stainless steel wire. This needle
held a single strand of silk and was used to replant a
FIGURE 18-5. Pulp to pulp pinch allows delicate control
of a microneedle holder.
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Dr.Mustafa D.
•
s
i FIGURE 18-4. As A series of
microvascular approximator
clamps. B, Single clamps of
varying sizes.
rabbit's ear by anastomosis of 1-mm vessels. Soon a
commercially available needle was developed by
Acland,42 working with the Springler-Tritt company.
Since then, microsurgical sutures with attached needles
have been developed in different sizes and tensile
strengths (7-0 to 12-0). The most widely used suture
materials in microsurgery are nonresorbable like silk,
polyamide, and polypropylene, but resorbable suture
materials like polyglyconate43 are currently being
studied. The needles attached to the sutures also come
in different sizes, with variations on curvature and tip
design. Microneedles are typically shaped as % of a
circle but are also available as a half-circle or straight,
with round, tapered, or spatula-shaped tips. Needle
diameters range from 30 to 150 urn.
ANASTOMOTIC DEVICES
In 1962, Nakayama44 introduced an anastomotic device
consisting of two metallic rings and interlocking pins
that remains in situ as a permanent implant. The
Unilink system, which was developed by Ostrup and
Berggren in 1986,45 and the 3M and ACE coupling
devices were adaptations of this ring-pin device, which
is currently on the market under the name of Microvas-
cular Anastomotic System. The system consists of a
high-density polyethylene ring and stainless steel pins
that are implanted with a reusable anastomotic instru-
ment. The ring-pin device has the advantage of not
disturbing the intima in the anastomosis and has
yielded excellent patency rates of up to 100%.46"48 The
rings come in a variety of sizes from 1 to 2.5 mm in
diameter, allowing the coaptation of vessels ranging
from 0.8 to 3 mm, and the device is suitable for both
end-to-end and end-to-side anastomosis.
In an experimental comparison of venous anasto-
mosis with use of this device, the sleeve technique, or
the standard end-to-end technique, the patency rates
were 100%, 80%, and 95%, respectively.46 The anas-
tomosis time was only 3.6 minutes with the Unilink
system compared with 12.3 minutes with the conven-
tional suture technique. In an invited discussion of this
paper, Shaw47 reported that in more than 500 clinical
venous anastomoses by use of this method, he and his
colleagues completed the anastomosis in 2 to 5 minutes
with a patency rate of 99.5%. It has also been used in
end-to-side anastomosis of veins in head and neck free
 image...
18 • PRINCIPLES AND TECHNIQUES OF MICROVASCULAR SURGERY
flap reconstruction,119 but a complication of device
exposure in a previously irradiated patient has been
reported.118 To resolve the disadvantage of the ring's
remaining in situ after healing of the anastomosis, a
biodegradable ring has been developed and has been
used experimentally, achieving patency rates of 92.9%50
to 100%.51 The ring was completely absorbed at 30
weeks after anastomosis.
The nonpenetrating microvascular stapler, first
introduced by Kirsch et al52 in 1992, uses nonpene-
trating titanium clips applied in an interrupted, evert-
ing fashion. The clips come in four sizes ranging from
0.9 to 3.0 mm. In an end-to-end anastomosis, two stay
sutures are first placed at 180 degrees to facilitate the
eversion of vessel walls during clip placement; a special
everting forceps and experienced assistant are needed.
In an end-to-side anastomosis, four sutures are rec-
ommended, sutures at the heel and toe and two stay
sutures at the 3- and 9-o'clock positions. Yamamoto
et al53 reported clinical use of these staples* with a mean
anastomosis time of 12 minutes. Cope et al54 have
reported a 100% patency rate of 153 anastomoses of
both veins and arteries with use of the same device. A
comparative scanning electron microscopic study of
sutured and stapled anastomoses revealed no major
differences between them. 55
All anastomotic devices are essentially for healthy
vessels only; the veins should be pliable and the arter-
ies soft to allow eversion of the vessel wall.48 The vessel
ends should be approximately of the same size and
thickness.
FUTURE METHODS
Methods to glue or to weld a union of two vessels seem
attractive and have been intensively studied experi-
mentally. Lasers have long been advocated56; however,
despite intensive experimental investigation, their use
in clinical practice remains scarce. Different laser types
(neodymium:yttrium-aluminum-garnet, 5 6 carbon
dioxide,57 argon, and most recently diode lasers58,59)
have been used. Laser-activated protein solders have
been introduced to achieve more strength. 58 In an
experimental setting, a diode laser-assisted carotid
artery end-to-end microanastomosis provided an
equal survival rate with a contralateral suture anasto-
mosis with a shorter anastomosis time, and scanning
electron microscopy showed faster healing on the laser
side.59 Although the later studies have promising
results on tensile strength, the fear of possible weak-
ening at the site of the anastomosis and consequent
pseudoaneurysm formation has so far prevented the
clinical use of laser welding.
Fibrin glue has been used to seal an anastomosis,
both experimentally 60 and in small clinical series of
r
VCS, Auto Suture, Tokyo, Japan.
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Dr.Mustafa D.
513
digital replantations. 61,62 It is advocated to shorten the
anastomosis time because it allows the use of fewer
sutures than without a sealant. Although in these studies
it resulted in a fast union without compromising
the patency rate,61 it has not achieved popularity in
clinical use, partly because of the fear that glue will
accidentally enter the vessel lumen.
Other experimentally studied methods of anas-
tomosis include cyanoacrylate glue63 and cylindrical
or T-shaped intravascular stents. 64,65 An external
metallic ring has been suggested to keep the cylin-
drical form of a sutured anastomosis and to avoid
through-stitching. 66
TECHNIQUES
Requirements
The first step in training for microsurgery is in the lab-
oratory. The usual sequence is to start by first getting
acquainted with the use of microinstruments under
magnification by suturing stretched gloves or Silastic
tubes. Then, the trainee usually sutures vessels with-
out blood flow, for example, pig's coronaries, before
moving on to the rat. Ideally, one should be supervised
by an experienced colleague and perform consecutive
anastomoses in animals until confidence and a satis-
factory patency rate are achieved.
The preconditions of good microsurgical work are
a calm disposition and patience. As in all surgery, the
surgeon must be able to concentrate on the ongoing
procedure, without unnecessary interruptions and
other obligations. Microsurgery is detailed and pre-
cious work and cannot be hurried.
One should, however, not work too long at a stretch,
and it is justified to take a break during long sessions
under the microscope. Today, some reconstructive sur-
geons prefer to use magnifying loupes for routine free
flap surgery and for vessels larger than 2 mm in diam-
eter. These allow more flexibility in positioning of both
the patient and the surgeon.
Planning
In microsurgery, good planning is worth the time spent
on it. Choosing the easiest and most comfortable access,
the right incisions, and the right positioning of the
patient becomes easier with experience. It is extremely
important to be comfortable during the procedure;
comfort relates directly to success.36
Insetting of the flap must be considered before anas-
tomosis. After the blood flow is restored, the flap will
swell and bleed, and insetting becomes increasingly
difficult.This is especially true in head and necksurgery,
in which the flap is often positioned in tight spaces
with limited visibility. On the other hand, bleeders
are easier to control before final inset. Insetting before
514 I • GENERAL PRINCIPLES
anastomosis allows more accurate judgment of pedicle
length; tension or redundancy can be avoided, and the
positioning of the pedicle and the anastomosis becomes
easier.
Approach and Exposure
The incisions and the patient's positioning should be
planned to allow minimal changing of position during
surgery. A two-team approach can cut the operating
time in half and should always be considered. In recon-
structive tumor surgery, even a three-team approach
is possible if there are enough available personnel.
One team does the resection and is later replaced
by another team that prepares the recipient site for
microsurgery. A third team can raise the predesigned
flap simultaneously.
Choice of Recipient Vessels
The key for success is use of healthy vessels of reason-
able size, with good outflow. A healthy vessel has a soft
wall and a vascular sheath that is easily dissectible.
Traumatized or irradiated vessels are difficult to
expose, and the dissection may result in bleeding or
even disruption of the vessels or their branches. This
iatrogenic trauma can further enhance the chance of
thrombosis.
It is often necessary, especially in the lower extrem-
ity, to assess the quality of the recipient vessels pre-
operatively. This is especially important in trauma
patients if there is suspicion of injury to the vessels as
well as in patients with atherosclerotic disease or
advanced diabetes. Clinical examination and palpa-
tion of peripheral pulses seem reliable; several studies
have shown that preoperative angiography does not
add relevant information if the pedal pulses are pal-
pable.67,68 However, normal findings on angiography
do not necessarily ensure good vessels.68 When there
is clinical suspicion of vessel damage, ankle/brachial
pressure index, systolic toe pressure, and hand-held
Doppler auscultation can help make a decision as to
whether angiography is needed.
The anastomosis should be made without tension,
and the length of the flap's pedicle is a factor limit-
ing the choice of recipient vessels. Vein grafts have
been shown to reduce success rates and are not a
primary choice, although a vein graft is better than
use of damaged vessels even if they are close to the
flap recipient site. Mobilizing the vessels gives more
length and makes the anastomosis easier, but exten-
sive mobilization may result in redundancy of vessel
length, and this in turn may lead to kinking or twist-
ing of vessels.
When there is no expendable pedicle with adequate
anterograde arterial inflow (e.g., due to arteriosclero-
sis or extensive injury of the recipient site), an end-to-
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Dr.Mustafa D.
side anastomosis to a major vessel or a venous graft
from a proximal healthy artery is an appropriate solu-
tion. However, should a long vein graft pass through
severely scarred soft tissue, or after a failed end-to-side
anastomosis with good distal arterial reflux, the use of
reversed arterial flow may be considered.69
Dissection Techniques
During dissection of recipient vessels and the flap
recipient site, hemostasis must be maintained. Bleed-
ing is controlled by vascular clips or bipolar coagu-
lation. If possible, it is convenient to use a tourniquet
during flap elevation or vessel exposure, but one
should release it before anastomosis to ensure reli-
able recipient flow. Perivascular hematoma should be
avoided because it has been shown to cause vasospasm
and flow disturbances, to prolong vessel wall ischemia,
and to increase the local inflammatory response.70
Hemostasis is aided by irrigation, which not only
cleans the view but also keeps the vessels moist and
prevents damage from drying. This is easily achieved
by use of 5- to 10-mL syringes with short metallic
needles or pliable plastic needles to produce a vigor-
ous splash. Too much irrigation of course results in
flooding, and drainage of the wound must be arranged
either by gauge or small-tipped gentle suction. During
the anastomosis procedure, irrigation is usually
achieved with a heparin solution (5000 to 50,000 U
in 500 mL lactated Ringer solution), which is changed
to normal saline or lactated Ringer solution after the
vascular repair is finished. However, although some
studies warrant this practice,71 others suggest that a
vehicle without any additives may be just as effective
as heparin solution.72
Preparation of Vessels
The vessel wall consists of three principal layers. The
innermost tunica intima is formed by a single layer of
endothelium resting on a basal lamina. Above this is
a thin subendothelial layer consisting of connective
tissue adjacent to the internal elastic lamina that sep-
arates the tunica intima from the tunica media. The
tunica media consists mainly of smooth muscle cells
and is the thickest layer of the arterial wall, whereas it
is much thinner in veins and sometimes almost indis-
tinguishable. It is again covered by the external elastic
membrane, and the outer layer of the vessel wall is the
tunica adventitia. This is loose areolar connective tissue
that contains the vasa vasorum, which nourish the vessel
wall.73 The veins consist of the same layers as the arter-
ies, but the layers are less defined, especially the media
(Fig. 18-6).
The key to vessel dissection is advancement in the
perivascular plane between the vessel and its vascular
sheath. Once the sheath is divided, it can be retracted
T-ek^s^elciWimage...
18 • PRINCIPLES AND TECHNIQUES OF MICROVASCULAR SURCERY
FIGURE 1 8 - 6 . Cross sections of a medium-sized artery
and vein. Note the difference in thickness of the vessel
wall and especially the tunica media.
by gentle pulling and then be cut and removed. Most
prefer to use blunt but narrow-tipped scissors for this
dissection; others prefer the knife or the bipolar coag-
ulator.36 Vessel branches are divided and either coag-
ulated or ligated with metallic vascular clips. This is
usually performed with loupes for magnification.
The vessels are dissected free for as long a segment
as is needed to ensure good positioning and a ten-
sionless anastomosis and to allow placement of the
clamps so that the anastomosis can be rotated freely.
After that, a higher magnification by either loupes or
the microscope is required. The vessels are cut sharply
at the desired level where the vessels are judged healthy
and where the vein does not have a valve close by.
The clamps are placed so that the vessel ends are in the
middle with enough space to freely maneuver the
needle.
It is customary to place a pliable nonadherent sheet
as a background to separate the vessels from the under-
lying field of a similar color; sponge-like materials are
also used. The color of the background sheet is the
surgeon's choice; many opt to use bright colors like
blue or green to provide better contrast, and it is pos-
sible to place a suction drain under the background
sheet or sponge. Anastomosis in a deep hole can be
made easier, vessel length permitting, if the vessels are
lifted to a higher position by stacking (e.g., moist gauze
underneath the background sheet). Placement of
moist white surgical dressing around the field of vision
helps not only to keep the field cleaner but also to find
lost needles.
Adventitia is routinely removed from the vessel ends
to improve visualization of vessel walls and to ensure
accurate suture placement. Some prefer to peel it away
bluntly with microforceps, but this rough manipula-
tion can result in vasospasm and focal intimal destruc-
tion. Sharp dissection with scissors is a less harmful
method not affecting the media or intima (Fig. 18-
7).74,75 However, it has been shown that neither blunt
nor sharp dissection removes significant amounts of
true adventitia; both remove only the larger collagen
fibers and leave a meshwork of smaller fibers on the
vessel wall.74 Nevertheless, tidying the vessel ends before
anastomosis seems warranted, and sharp dissection
leaves the vessels essentially unharmed. However,
because tunica media of small veins can be almost
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Dr.Mustafa D.
515
FIGURE 1 8 - 7 . Sharp trimming of adventitia.
nonexistent, it is advisable to remove only the adven-
titia that overhangs the vessel ends.
Vasospasm
Good outflow of the recipient vessel is necessary for
the anastomosis to stay open. This can be ensured by
selecting as healthy a vessel as possible, but dissection
and manipulation of the vessels may result in
vasospasm. The mechanisms behind vasospasm are
unclear, but vasoactive substances and sympathetic
innervation play a role. If the vessel is left untouched
for a few minutes, it usually regains its natural diam-
eter. If the surgeon is too impatient to wait, an attempt
can be made to relieve the vasospasm by topical appli-
cation of 2% lidocaine or papaverine (30 mg/mL).
Papaverine is an opium alkaloid that has direct action
on smooth muscle. The vasodilatory mechanism of
lidocaine remains unclear; in fact, lidocaine can be a
vasoconstrictor at low concentrations.76 Some studies
indicate that lidocaine 2% is not effective enough alone
and suggest that its concentration be increased up to
20% or even that it be combined with papaverine.77
Lidocaine is not significantly absorbed from the
wound, and systemic effects are unlikely.78
Stripping of adventitia usually helps relieve
vasospasm because of both a sympathectomy effect
and the mechanical thinning of the vessel walls, allow-
ing them to dilate more freely. Dilatation of healthy
vessels can be done either mechanically with intralu-
minally introduced metallic standard-sized dilators or
by intraluminal irrigation (Fig. 18-8), but caution is
necessary, especially in arteriosclerotic vessels. Vessel
ends can be dilated with specially designed dilator
forceps or simply by use of blunt-tipped microneedle
holders or a blunt forceps (Fig. 18-9).
Stable and thorough anesthesia is a requirement;
hypovolemia, pain, and low core temperature (<36°C)
can result in vasospasm. The patient's temperature
should be constandy monitored and adequate hydra-
tion maintained. The wound should be kept moist with
516 I • GENERAL PRINCIPLES
FIGURE 18-8. Irrigation of the vessel lumen.
irrigation because drying of the vessels also promotes
vasospasm*
Anastomosis Sequence
Either the artery or the vein can be repaired first, but
the optimal order is yet to be established. Vessel posi-
tion naturally helps determine the sequence, and the
deeper or the more difficult will be repaired first. If
the vessels are at an equally good position, repair of
the artery first seems logical because it shortens the
warm ischemia time. However, this results in bleeding
of the flap, which can disturb the anastomosis of the
vein. Bleeding is further enhanced by venous conges-
tion because a vascular clamp is required on the vein
during its repair. Venous congestion of the flap can be
avoided either by performing the venous anastomo-
sis first or by clamping the repaired artery until venous
repair is complete. Both methods, obviously, delay
revascularization of the flap. In an experimental
attempt to address this problem, Thomson et al79 per-
formed anastomoses in the rat with four groups of
either artery or vein first, clamped or not clamped. They
had a high incidence of failure in all groups. The highest
was in the group in which the artery was repaired first
and left undamped. They attributed this to venous
congestion of the flap. Clinical observations are con-
FIGURE 18-9. Gentle dilatation of the vessel end.
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Dr.Mustafa D.
tradictory; at Chang Gung Memorial Hospital, where
more than 700 free flaps are performed per year, the
artery is routinely repaired first and left undamped,
but the vein is clamped during its repair. No clinical
problems have been noticed from the temporary venous
congestion. If the pedicle has two comitant veins,
venous congestion can be avoided by letting one comi-
tant vein stay open during anastomosis of the other,
leaving it to drain into a gauze or away from the oper-
ating field.
Although two venous anastomoses may seem to be
more fail-safe in case of anastomotic failure, a single
venous anastomosis provides greater flow inside a single
vessel lumen with adequate drainage, reduced
operative time, and no additional morbidity. In a series
of 43 free radial forearm flaps, Futran and Stack80
showed equivalency of single and dual venous anas-
tomosis with respect to flap survival.
MICROANASTOMOSIS
According to Acland,36 the principal faults that lead to
anastomotic failure are tearing, leaking, narrowing,
through-stitching, and inclusion of adventitia. Tearing
occurs when there is too much tension and distance
between the vessel ends. It can also be caused by too
meticulous stripping of adventitia; the veins of the head
and neck region are especially fragile. Leaking occurs
when there is too big a gap between sutures, or there
is a tear or a tiny unnoticed branch near the anasto-
motic site. Even a small leak will be covered by a throm-
bus, precipitating the formation of an intraluminal
thrombus.81 Narrowing of the lumen can be caused by
oversized bites, entangling knots with one another,
or continuous suturing that is too tight. Through-
stitching entails taking a bite of the back wall with the
suture, thus obstructing the lumen. This can be
avoided by keeping the vessel lumen open by irriga-
tion and lifting the vessel wall with a microforceps.
The needle tip should point upward, not downward.
Inclusion of adventitia is a result of inadequate vessel
preparation. Loose adventitia may prolapse into the
lumen.
Suturing Technique
The aim is to place the smallest number of sutures
needed to achieve a leakproof anastomosis. Each
suture can lead to potential trauma, and too tight a
closure may be even worse than a leaking one.
The needle is grasped just beyond its midpoint, and
a microforceps can be used to provide gentle coun-
terpressure while the needle penetrates the vessel wall
(Fig. 18-10). The size of a bite is determined by the
thickness of the wall and by the thickness of the needle
and suture. As a rule, the distance between two sutures
should be the same as the bite size.
lt&Vttf'aeicme image...
18 • PRINCIPLES AND TECHNIQUES OF MICROVASCULAR SURGERY
FIGURE 1 8 - 1 0 . Entry of the needle tip with delicate
counterpressure from the forceps.
The first throw should be double to ensure that it
maintains the intended tightness, and then two single
throws follow to complete the knot (Fig. 18-11).Tight-
ening must be done under vision, not by feel, and should
stop when the two vessel edges meet. The knots should
result in accurate alignment of the intima. Good knots
are tied so that they are parallel to the cut surface, and
sutures are placed symmetrically within equal distances
from each other. Suture ends are cut short to prevent
entry into the lumen and removed or irrigated away
from the view. Loose ends mimic the one to be tied
and can result in the loss of a suture.
End to End
PLACING THE CLAMPS
Bleeding disturbs the view, and both vessel ends should
be clamped. Although some microsurgeons prefer to
use single clamps, which allow more freedom in sutur-
ing, it is advisable for a beginner to use double approx-
imator clamps to hold the two vessel ends. This ensures
tension-free repair at the anastomotic site and prevents
vessel tearing from too tight suture attempts. Flipping
of the clamps easily turns the vessels and makes it just
FIGURE 18-11. Tying the knot with a double throw.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
517
as simple to repair the back wall as it is to repair the
front wall. The cleaned vessel ends are placed in the
clamps so that at least a length equal to the vessel's
diameter is projecting from each clamp. A sliding-type
double clamp will allow the distance between vessels
to be adjusted. Before the first suture is placed, it is
best to gently dilate the vessel ends by placing either a
closed blunt forceps or a needle holder inside the lumen;
the instrument is then opened slowly to dilate the vessel,
with care taken not to damage the intima.
INTERRUPTED
End-to-end anastomosis with interrupted sutures is
by far the most common method. It is simple and can
be used for both veins and arteries. The arteries have
a higher intraluminal pressure and tend to require more
sutures than the veins do.
In Carrel's original technique, three stay sutures were
placed in triangulation (Fig. 18-12). This was later
modified by Cobbett, who placed only two sutures
at 120-degree angles, thus making a longer back wall
and a shorter front wall. This supposedly lessens the
chance of through-suturing the back wall. These
can also be placed as stay sutures so that an assistant
may hold them if necessary. However, when a double
approximator clamp is used, the stay sutures are not
necessary. Two sutures are placed at a 180-degree angle
to ensure equal placement of vessel ends (Fig. 18-13).
The in-between sutures are then placed and tied indi-
vidually. To maintain a reliable view of the vessel edges,
it is advisable to leave the last two or three stitches untied
until the last one is in place. Open gaps between sutures
can be closed with superficial partial-thickness sutures
I/
FIGURE 18-1 2. The placement of three stay sutures
at 120 degrees results in triangulation of the lumen; two
stay sutures at 180 degrees result in biangulation.
l ^ t t f ^ S t f f e e image...
518 I -t GENERAL PRINCIPLES
FIGURE 18-13. End-to-end anastomosis with inter-
rupted suturing technique.
to avoid through-stitching. Once the suturing seems
complete, the clamp is temporarily released. If any
serious leakage sites are revealed, the clamp is re-
applied and more sutures are placed.
OPEN LOOP
An experienced surgeon may opt to place all the sutures
of an entire wall continuously but leave loose loops
between the sutures (Fig. 18-14). Tying is started from
the first suture and the threads are cut, resulting in an
interrupted closure. This technique is faster because
there is no need to change instruments during suture
placement. However, the loops can easily get tangled
if they are too large, and an inexperienced surgeon may
lose more time managing the scrambled loops.
CONTINUOUS
Continuous suture technique for end-to-end vascu-
lar anastomosis has been cautioned against because of
the risk of vessel constriction,82 but it can be faster than
interrupted sutures as well as more hemostatic. The
continuous technique is more suitable for vessels larger
than 2 to 3 mm in diameter and becomes more
FIGURE 1 8 - 1 4 . End-to-end anastomosis with the open
loop technique.
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Dr.Mustafa D.
technically challenging at diameters closer to 1 mm.
It is recommended to first place two stay sutures at 160
to 180 degrees and then to perform a running suture
for both walls separately, thus avoiding a purse-string
effect. Hudson et al8i reported an experimental study
of continuous end-to-end suturing of veins with 100%
patency. Cordeiro and Santamaria84 reported a clini-
cal series of 410 continuous microanastomoses with
a success rate of 97.5%, with both veins and arteries
and end-to-end or end-to-side repair.
Sleeve Anastomosis
Sleeve anastomosis, introduced by Lauritzen85 in 1978,
is a variant of the end-to-end technique,"end-in-end";
it is reported to reduce anastomosis time because only
a few stitches are needed. This entails telescoping the
vessels by use of two extraluminal sutures that pull one
vessel inside the other (Fig. 18-15). Theoretically, fewer
sutures lead to less vessel trauma, but low patency
rates reported by Sully86 resulted in the technique's not
gaining popularity despite contradictory results by
others. The sleeve technique was suggested to be limited
to vessels with size discrepancy. A modification of
"hemi-invagination" by Riggio et al,87 however, yielded
patency rates of 95% to 100%. They modified the orig-
inal technique by a side-cut of the overlapping vessel
and the addition of a stitch in its apex, thus dilating
the vessel to facilitate anastomosis of vessels of equal
size.K7
End to Side
End-to-side anastomosis is performed when it is
judged important to preserve the continuity of the
recipient vessel or when there is considerable size
or wall thickness mismatch between the vessels. An
arterial end-to-side anastomosis provides access to a
higher and more reliable arterial pressure than end-
to-end anastomosis does and lessens the chance of
vasospasm. Arterial flow through the anastomosis is
FIGURE 1 8 - 1 5 . Sleeve anastomosis.
image...
18 • PRINCIPLES AND TECHNIQUES OF MICROVASCULAR SURGERY
A B
FIGURE 1 8 - 1 6 . End-to-side anastomosis. A, Cutting a hole on the wall of the recipient vessel. B, Posterior wall
completed.
determined by the type of flap used. Preserving the
continuity of the recipient vessel may help maintain
adequate flow through the anastomosis and thus help
prevent thrombosis.
End-to-side anastomosis requires first making a hole
in the recipient vessel wall. There are many ways to
make an arteriotomy or venotomy in the recipient
vessel. Some like to cut a triangular or elliptical hole;
others merely cut a longitudinal slit with a sharp blade.
There are also special devices available for more con-
trolled puncturing or cutting of a hole. A useful method
is to grasp the vessel wall with a specially designed
clamp, then cut a hole around the clamp with a No.
11 scalpel.
Two stay sutures are usually placed at the opposing
ends of the anastomosis. It is advisable to do the back
wall first, because it is the most difficult, using the
desired technique, interrupted or continuous sutures
or clips (Fig. 18-16). The anastomosis is then com-
pleted by closing the front wall.
In an experimental study of 104 rats, there were no
differences in vessel patency between an end-to-side
hole and an end-to-side slit technique.88 However, in
small vessels less than 1.5 mm, the slit technique is tech-
nically easier. Samaha et al89 examined the fate of more
than 2000 clinical microvascular anastomoses and
found the end-to-end and end-to-side microvascular
techniques to be equally effective when properly
applied.
Microvascular Grafts
VEIN GRAFTS
Increased choices in flap type and location as well as
technical refinements in performing microsurgical
anastomoses have diminished the need for vein grafts,
especially in head and neck surgery. Many authors state
that they try to avoid vein grafting by proper planning
and selecting flaps with a long vascular pedicle.18,90
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519
Several studies have found a correlation between inter-
position vein grafting and free flap failure,21,91,92 but an
analysis of 93 vein grafts in free flaps by Germann and
Steinau93 showed a success rate of 96.2%. The use of
vein grafts has also been associated with hematomas.21
It is possible that the additional anastomoses increase
the potential for thrombosis. Vein grafting is, however,
often performed in particularly difficult conditions
(e.g., large trauma or otherwise poor-quality vessels,
which can independently lead to flap failure). Others
advocate the use of vein grafts in reoperations and claim
it is safer to use a vein graft than poor-quality vessels.94
Poor recipient site vessel selection has been cited as an
important cause of flap failure.18
The indications for a vein graft include a short
pedicle, tension at the site of anastomosis, consider-
able size mismatch, and the need to place the anasto-
mosis away from an injured area. Good hemostasis is
particularly important if a vein graft is used because
it will receive its vascularization from the recipient bed.
A hematoma might impair this as well as cause spasm
of the recipient vessels.70
If the vessel length is not adequate and a vein graft
will be needed, an arteriovenous loop might be con-
sidered.95 This is made either by a long loop from the
recipient vein, suturing it to the recipient artery, or by
anastomosis of a long vein graft between the future
recipient vessels. Both procedures provide a tempo-
rary arteriovenous shunt that is left to mature during
flap harvest. The vein or vein graft is then divided in
the middle and used as the recipient vessels. In the
extremities, the saphenous or cephalic vein can be used
to design such a loop.
If there is an arterial or venous defect at the recip-
ient site, a flow-through flap can be designed to bridge
the defect; the radial forearm, the latissimus dorsi, and
the anterolateral thigh are especially suitable because
of the nature of their vascularization and large-caliber
vessels.
TfcWttf'SeldW image...

520 I • GENERAL PRINCIPLES

It is advisable to harvest the vein graft cautiously,

with use of loupes, and to ligate all small branches care-
fully because the quality of the graft is prognostic of
its patency. The longer the graft, the more important
is the handling of the vessel. Long grafts are suscepti-
ble to vasospasm, and the adventitia should be removed
along the whole length of the graft. Although superficial
subcutaneous veins are tempting and easily located,
their wall is thin and they have many valves, so it is
wiser to use the stronger major superficial vessels like
the cephalic or saphenous veins. A common mistake
is to use too long a segment; when placed under arte-
rial flow, the vein graft will stretch and may easily result
in redundancy and even kinking.

ARTERIAL GRAFTS
At present, microarterial grafts appear to have no
significant advantages over vein grafts,96 although the
clinical use of the radial artery as a coronary artery
graft is established.97,98 Ongoing experimental research
in the field of arterial graft preservation is promising,
however, with use of glutaraldehyde, cryopreserva-
tion," and freeze-drying100 aimed at eliminating the
need for graft harvesting.
SYNTHETIC GRAFTS
Synthetic small-caliber vascular grafts are being studied
but are still at the experimental phase. Some of those
being studied are polytetrafluoroethylene grafts and
polyurethane tubes. To improve their patency, various
anticoagulant drugs have been tested, or the tubes have
been coated on the inner surface with antithrombotic
agents.101*103 It seems necessary to maintain high blood
flow through the prosthesis, and creation of an arte-
riovenous fistula distal to the graft has been suggested.103
Porcine aortas have been successfully seeded in vitro
with human endothelial cells, which grew to a mono-
layer under flow conditions,104 and hydrostatic pres-
sure has been used to facilitate adenovirus-mediated
gene transfer into vein grafts for intraoperative genetic
engineering.105 Tissue engineering of vascular grafts
seems promising for application in the clinical
situation.104'106
Size Discrepancy
Size discrepancy between the vessel ends is not un-
common and can often be handled simply by dilating
the smaller vessel to match the larger. The same effect
can be achieved by taking wider bites of the bigger
vessel. It is also possible to enlarge the circumference
of the smaller lumen by either cutting the vessel end
obliquely or making a longitudinal side-cut (Fig. 18-
17). Some have advocated a wedge resection of the
bigger vessel to reduce its size, but it is generally advis-
able to try to widen the smaller lumen. An end-to-side
C
13 ^
FIGURE 1 8 - 1 7 . Size discrepancy of vessels. A, Smaller
vessel dilated to match the bigger. B, Smaller vessel cut
obliquely to increase its diameter. C, A longitudinal side-
cut of the smaller vessel.
anastomosis maybe chosen to overcome large (>1:3)
size mismatch, or a vein graft may be used. A side branch
of the larger vessel is sometimes of more suitable size.
A discrepancy in the thickness of the vessel walls can
be overcome by taking a full bite of the thinner vessel,
but including only the inner layers of the thicker wall.
Flow in Free Flaps
There are many reasons that the flow in a free flap is
not similar to the flow in the same intact pedicle. First,
all minor pedicles and capillaries supplying arterial
blood or venous outflow have been cut, and all blood
transfer is through the pedicle. Motor nerves to the
muscle have been cut, resulting in loss of muscle tone,
and the pedicle is skeletonized and cut, thus disrupt-
ing the sympathetic nervous system around the vessels.
Dissection of the pedicle may also have resulted in
vasospasm or trauma.
Poiseuille's law states that flow is directly propor-
tional to the pressure and radius of the vessel and
inversely proportional to the viscosity. The flow in the
pedicle is mainly determined by the needs of the flap
itself,107 but it is also affected by cardiac output and
systemic vascular resistance. Cardiac output is volume
dependent, as described by the Frank-Starling curve.
Hypovolemia results in reduction of cardiac preload
and subsequently in reduction of cardiac output. A

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Tt&*>ttf<y0Ci,Kf image...
8 • PRINCIPLES AND TECHNIQUES OF MICROVASCULAR SURGERY
prospective study of 86 free flaps that measured intra-
operative transit time in the donor and recipient arter-
ies indicated that blood intake of a free microvascular
flap depends more on the specific tissue components
of the flap than on the recipient artery flow.107 In low-
flow arteries, the flow increased to the level of the initial
donor artery flow after anastomosis. The initial intake
of blood is low in flaps that consist mainly of adipose
tissue, like the TRAM flap, and high in fasciocutaneous
flaps like the radial forearm flap that may even act as
a shunt.
During free flap transfer, the sympathetic fibers sur-
rounding the pedicle are invariably cut, resulting in
sympathetic denervation of the flap. This leads to loss
of vascular tone and decreased resistance but serves to
the surgeon's advantage because increased blood flow
not only helps keep the microanastomosis open but
also promotes wound healing. Animal studies have
shown that surgical stripping of adventitia and con-
sequent sympathectomy of the donor vessels of free
flaps result in changes in the microcirculation, vasodi-
latation, increased capillary flow, and hypersensitivity
to topical vasoactive agents.108,109 A prospective clini-
cal study addressed the same issue in noninnervated
free latissimus dorsi muscle flaps and demonstrated
that blood flow in the pedicle and in the recipient artery
of a free muscle flap increases after surgery while the
resistance index decreases."0 However, as the motor
nerve is cut, a part of the vasodilatation may also be
attributed to loss of muscle tone.
Ischemia Time
Ischemia time (the time between the interruption and
the re-establishment of blood supply) is of frequent
concern to the microsurgeon. Gurleket a l m reviewed
results for 700 free flaps used for breast or head and
neck reconstruction. Flaps that failed had a mean
ischemic time of 111 minutes, whereas flaps that sur-
vived had a mean ischemic time of 91 minutes, but the
difference was not statistically significant. They con-
cluded that ischemic time is irrelevant to flap survival,
provided ischemia is not prolonged past 3 hours or to
the point at which the no-reflow phenomenon occurs.
This conclusion is supported by other retrospective
studies.92
Experimental studies indicate that heparin offers
protection from ischemia-reperfusion injury when it
is introduced into the vascular network either before
or during the ischemia period. This has been studied
by perfusion with heparinized or citrated blood or
heparinized normal saline.112'"4 Other experimentally
used substances include the vasodilators nitrendipine
and prostacyclin, the thrombolytic agents urokinase
and streptokinase, the free radical scavengers defer-
oxamine and superoxide dismutase,'' 5 and their com-
binations, to name but a few. There are, however, no
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521
clinical applications so far, although there is a report
of continuous intra-arterial infusion of prostaglandin
Ei and heparin to salvage a free flap subject to the no-
reflow phenomenon." 6
Anastomotic Failure
TESTING FOR PATENCY
Patency can usually be detected by simple observation.
If true pulsating is seen distal to the anastomosis, the
artery is patent. A closed artery will present "kicking"
pulsations proximal to the anastomosis. If the recipi-
ent vein fills well and has a natural round diameter, it
is probably patent. This is further confirmed by the
color of tissue bleeding distal to the anastomosis. In
cases of venous occlusion, the bleeding will be dark
and more profuse. If there is doubt about the patency,
an empty-and-refill test (or the milking test) can be
performed by gently occluding the vessel with two
jeweler's forceps and then moving the second one
downstream, thus emptying the vessel. The test must
be done delicately to avoid injury to the intima. The
first one is then released, and venous flow should be
seen refilling the emptied segment. However, a flap
bleeding profusely may have good color despite venous
occlusion because it is drained by bleeding. Thus, hemo-
stasis must be obtained before the efficacy of venous
return is evaluated. The patency of an artery can usually
be easily confirmed by the occurrence of venous
backflow through the pedicle. If the venous return is
of low flow, it can be difficult to confirm patency; some-
times a small side branch of the recipient vein can be
temporarily opened to demonstrate flow through the
anastomosis.
In a large multicenter study, the incidence of intra-
operative thrombosis was 8.3%, and it was observed
more frequently in musculocutaneous flaps or when
vein grafts were needed.21
MECHANISMS OF THROMBOGENESIS
Thrombosis may be caused by changes in the intralu-
minal flow, the vessel's endothelium, or the coagula-
tion system, but it is often a result of many different
factors. Changes in flow can be due to external
mechanical compression from tension, twisting,
kinking, or compression of the vascular pedicle after
the anastomosis is completed. Intraluminal turbulence
caused by irregularities of the vessel's shape or its
endothelium is also thrombogenic and maybe due to
atherosclerosis. Valves or dead-end pouches near the
anastomosis should be avoided. The endothelium of
damaged vessels is highly thrombogenic, and surgical
precision is a key factor in minimizing damage to
the vessels during dissection and anastomosis. With
more manipulation, the risk of thrombus formation
increases.
522 I • GENERAL PRINCIPLES
ABNORMALITIES IN THE
COAGULATION PATHWAYS
Pregnancy complicates microvascular surgery because
of the pregnancy-associated hypercoagulable state; the
risk of thromboembolic disease increases considerably
during pregnancy.117 Pregnancy is a relative con-
traindication to microvascular surgery, and if a strong
indication warrants the surgery, thromboprophylaxis
is necessary. Leong and Granick118 described a preg-
nant woman who required microvascular tissue trans-
fer to salvage her leg. The patient was hypercoagulable
and consumed large amounts of heparin during the
surgery.
It has also been suggested that patients with active
cancer are hypercoagulable compared with other
patients81 and that thromboprophylaxis should be con-
sidered. Screening for coagulation disorders like acti-
vated protein C resistance is expensive and has been
found to be of no value in clinical practice.119
PHARMACOLOGIC AGENTS
Vasoactive Agents
Endothelin-l is a potent endogenic vasoconstrictor
released by the vascular endothelium, and its ex-
perimental injection has been shown to induce flap
failure.120 In a study of pedicled TRAM flaps, high
plasma endothelin-l concentrations were found to be
associated with peripheral vasoconstriction.121 Calcium
antagonists, like felodipine, have been advocated to sup-
press endothelin-1 release and subsequently to reduce
vasospasm during microvascular surgery. However, in
a clinical study of patients undergoing a microvascu-
lar TRAM flap breast reconstruction, preoperatively
administered felodipine had no effect on periopera-
tive endothelin-l levels, temperature changes, or flap
skin blood flow.122
Endothelial cells produce prostacyclin, a vasodila-
tor that also has a platelet antiaggregant effect. Prosta-
cyclin and its synthetic derivatives iloprost and cicaprost
have been infused intraoperatively with favorable
results in cases of recurrent perioperative thrombo-
sis123 and in an experimental setting.12'1 However, topical
application of prostacyclin has been shown to have a
thrombogenic effect.125 Vascular endothelial growth
factor, a potent angiogenic agent with a suspected role
in the protection of endothelium, has had a bene-
ficial effect on flap survival in a model of ischemia-
reperfusion injury.126
Animal studies have implicated that flap flow is not
dependent on total cardiac output alone. In a porcine
model, sodium nitroprusside, in a dose causing a 30%
decrease in systemic vascular resistance and arterial
pressure, caused a severe reduction in free flap blood
flow despite maintaining cardiac output.127 In the same
study, systemic phenylephrine in a dose increasing the
systemic vascular resistance and arterial pressure by
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Dr.Mustafa D.
30% had no adverse effects on blood flow in free latis-
simus dorsi musculocutaneous flaps, but Cordeiro et
al128 had a contradictory result in another pig model,
in which phenylephrine clearly decreased rectus
abdominis muscle flap flow. They also studied the
effects of dopamine and dobutamine and found that
dopamine did not affect total flap flow at either low
or high doses despite increasing cardiac output, but
dobutamine increased both flap flow and cardiac
output.128
This hypothesis is further supported by a clinical
placebo-controlled study of the effects of dopamine
and dobutamine (both at 8 ug/kg/min) on blood flow
in an elevated but not yet detached free TRAM flap
with intraoperative measurements of transit time in
both the pedicle and the recipient artery.129 This study
showed that dopamine may act as a vasoconstrictor
even at concentrations below 10 ug/kg/min, at which
it is traditionally thought not to do so. Even if
dopamine increased both the cardiac output and sys-
temic blood pressure, it did not increase blood flow to
the flap or in the recipient artery and even had an
adverse effect in some patients. Dobutamine, on the
contrary, increased cardiac output and decreased the
systemic vascular resistance as expected. This resulted
in a significantly increased flow in both the pedicle
and the recipient artery, with little effect on systemic
blood pressure. In conclusion, systemic blood pres-
sure does not always correlate with blood flow to the
flap, nor does cardiac output alone. The results of these
studies caution against the use of dopamine during
microvascular anesthesia; dobutamine seems a safer
choice if a vasoactive agent is needed.
The effect of vasoactive agents after a free flap is
detached and anastomosed remains to be studied.
Anticoagulative Agents
Controversy still surrounds the use of anticoagulation
in the form of dextran, heparin, and fibrinolytics and
the effectiveness of aspirin in improving anastomotic
patency, but they are all in clinical use.21,130 In fact,
whereas no studies have conclusively shown that any
anticoagulant improves the patency rates of microvas-
cular anastomoses, several large clinical series have
failed to show any correlation between the use of anti-
coagulants and flap failure.21,130,131 If anticoagulation
is to be used, several questions remain: what agent to
give, when to give it and for how long, and whether to
give it topically or systemically.
Heparin was the first anticoagulant described. It
reduces platelet aggregation, activates antithrombin III,
and lowers blood viscosity. Studies have suggested that
it may also protect against reperfusion injury through
a direct effect on the microvascular endothelium, inde-
pendent of its systemic effect.112 Heparin is routinely
used topically to irrigate vessels during microvascular
surgery, but although infusion of low-dose heparin has
image...
18 • PRINCIPLES AND TECHNIQUES OF MICROVASCULAR SURGERY
been shown to improve flap salvage132 and an inter-
national survey of anticoagulation practice found that
postoperative low-molecular-weight heparins reduced
risk of anastomotic thrombosis,21 the routine use
of unfractionated heparin as an intravenous antico-
agulant has mostly been abandoned because of the
significant risk of bleeding and hematomas.130 Kroll et
al studied 517 flaps retrospectively and found that
the use of low-dose heparin had no correlation with
hematoma or bleeding, whereas high-dose heparin
increased their incidence. In an experimental
study comparing unfractionated heparin and low-
molecular-weight heparin, both improved anastomotic
patency, but hematomas developed only in the unfrac-
tionated heparin group.133 In the recent decade, low-
molecular-weight heparins have become the most
widely used anticoagulants,21 although they are usually
administered to prevent deep venous thrombosis
rather than to maintain anastomotic patency.
Aspirin is an antiplatelet agent that at a low dose of
50 to lOOmg selectively inhibits thromboxane while
preserving prostacyclin function.134 Low-dose aspirin
has been shown to have a beneficial effect on anasto-
mosis patency and capillary perfusion in an experi-
mental setting,135 but no clinical studies have been
performed to address its effect on free flap patency.
However, it is in wide clinical use,21,131 bleeding and
gastritis being the most common side effects. Both
dextran and aspirin have also been given postopera-
tively to inhibit platelet aggregation and to limit throm-
bus formation.
Dextran is a polysaccharide synthesized from
sucrose and produced as a 40,000 or 70,000 molecu-
lar weight polymer. It has several mechanisms of action,
such as inhibiting platelet aggregation and function,
modifying the structure of fibrin, and acting as a volume
expander.131 Dextran is in wide clinical use during
microvascular surgery21,130,131 despite the lack of any
clinical proof of its efficacy. However, in experimen-
tal studies, it has been beneficial to anastomotic
patency.l36 Although most patients who receive dextran
have no problems, particularly after hapten inhibition
by dextran 1 infusion, several serious complications
have been attributed to dextran use,137 such as adult
respiratory distress syndrome.138 The serious nature
of these complications and the fact that several large
clinical studies have failed to show a cause-and-effect
relationship between the use of dextran and flap loss
or prevention of thrombosis21,130"132 call into question
the routine use of dextran in microsurgery.
FREE FLAP SURGERY
Advantages and Disadvantages
Reconstructive surgery aims to restore both cosmesis
and function. This goal is achieved by transplantation
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523
FIGURE 1 8 - 1 8 . A failed free flap. A musculocutaneous
latissimus dorsi flap failed despite several revasculariza-
tion attempts.
of tissue as similar as possible to replace the missing
components. The advantages of free microvascular flap
techniques over the more conventional methods are
well documented. Free flap surgery offers freedom of
choice of donor tissue and can be applied when there
is no tissue available locally or the most similar tissue
is at a distant site. Free flaps can be designed to meet
the specific requirements of the recipient site in size,
form, and tissue components. When many donor
sites are available, the one with least donor morbidity
can be chosen. Free flaps are well perfused, and for
example, free TRAM flaps have been shown to have
better cutaneous blood flow and less edge necrosis than
pedicled TRAM flaps do.139
When all goes well, the advantages of microvascu-
lar free flaps are clear, but although rare, the most feared
complication of total failure is a catastrophe both for
the patient and for the surgeon (Fig. 18-18). The
benefits of a microvascular reconstruction have to be
weighed against the risks of a long operation and a
long rehabilitation period, taking into account the
patient's general condition and underlying illnesses.
The length of the operation is a disadvantage in itself,
and even if time can be reduced by working with two
teams, operation theater capacity may sometimes be
a limiting factor. Microsurgery requires a reasonably
sized unit to ensure 24-hour re-exploration possibil-
ities, and it is not recommended to do it alone.
Timing
Timing of free flap surgery has been an ongoing subject
of debate for years. It is mainly determined by the indi-
vidual surgeon's assessment; however, it also depends
on the local health care system and the facilities as well
as cultural issues. The nomenclature is also not agreed
on; some define acute reconstruction of trauma as the
interval ranging from emergency or immediate pro-
cedures within 24 hours to urgent procedures done
within 72 hours, whereas others have suggested that
image..

524 I • GENERAL PRINCIPLES

the first 24 hours be called primary.140 In reconstruc-

tion of traumatic defects, lower infection rates have
been reported for the acute phase compared with the
late phase; others"" report no significant increase in
the incidence of infections if reconstructions are
delayed by 72 hours141,1" or even up lo 5 days.143 Pro-
ponents of delaying the reconstruction by a few days
as opposed to immediate reconstruction argue that the
viability of an extremity can be better assessed, the
reconstructive procedure can be planned more pre-
cisely, and the procedure can be done during the day
under better operating conditions.141,143
Immediate radical debridement followed by ade-
quate soft tissue cover within a reasonable time, deter-
mined by the systemic condition of the patient and
the nature of the injured extremity, seems a safe and
effective method for treatment of severe injuries, but
immediate cover must be considered if vital structures
are exposed. Emergency free flap transfer may salvage
a limb or a finger, and although it helps improve
the functional and aesthetic results, it also shortens
possible hospital stay.144
In tumor reconstruction, the definition is clear:
immediate reconstruction is performed in the same
operation as tumor removal, whereas delayed recon-
struction is performed in a second operation at a later
stage. Insertion of osseointegrated dental implants
after mandibular reconstruction with vascularized
composite bone grafts is usually done months after
the reconstructive surgery. However, primary place-
ment of implants into the new mandible during the
initial reconstructive surgery allows better access to the
bone and easier determination of interdental rela-
tionships, and oral rehabilitation can be attained faster
(Fig. 18-19).145 Selection of patients for this combined
procedure is based on the pathologic nature of the
mandible and the need for and timing of radiother-
apy. Other factors influencing the decision are the soft
tissue and bone requirements, the number of
osteotomies needed, the rigid fixation method to be
used, and the surgeons familiarity with the use of FIGURE 18-19. Osseointegrated teeth. A The intra-
osseointegrated implants. operative insertion of osseointegrated implants to a free
fibula flap. B, Implants visible in the mouth floor. C, Final
result with new teeth in place.

Preoperative Considerations
EVALUATION OF THE PATIENT
Chief among the causes of free flap failure is inade-
quate preoperative planning.18 This starts with proper
selection of the patient, assessment of the condition
and possible complications, establishment of priori-
ties, and setting of goals for the reconstruction. The
flap and the recipient vessels are chosen with concern
regarding the donor site. It must provide enough tissue,
comprise all the required components, and at the same
time have minimal donor sequelae. The tissue avail-
able must be slightly bigger than required, with a slightly
longer pedicle than required. Larger vessels are more
forgiving than are small ones. Preparation must be
made for unforeseen problems, and it is wise always
to have a backup plan ready.
RisH Factors
Risk factors can be related to the patient, acquired,
or related to the nature of the injury or disease. In an
elective situation, some acquired risk factors can be
reduced preoperatively; for example, the patient can
be encouraged to lose weight, to stop smoking, or to

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18 • PRINCIPLES AND TECHNIQUES OF MICROVASCULAR SURGERY
join an alcohol withdrawal program. However, not all
risk factors can be eliminated, and they must be weighed
against the possible benefits of the free flap recon-
struction and its timing.
Tobacco smoking has been suspected of being a risk
factor in patients undergoing free flap transplantation.
Animal studies have shown that tobacco smoking has
a negative effect on the survival of pedicled flaps
and wound healing and that it is detrimental to free
flap survival.146 Several clinical studies have, however,
demonstrated the contrary, namely, that cigarette
smoking has no effect on free flap survival.121 A study
by Chang et al147 showed an increased donor site mor-
bidity and a higher incidence of mastectomy flap necro-
sis in smokers undergoing free TRAM flap breast
reconstruction.
Alcohol abuse is common among head and neck
cancer patients in the Western Hemisphere, and pro-
phylactic therapy to prevent the occurrence of alcohol
withdrawal syndrome should be considered. Patients
who experience alcohol withdrawal syndrome are more
likely than other patients to suffer non-flap-related
complications.148
Irradiation impairs the quality of tissues and vessels
and may predispose the flap to failure. It has had no
effect on flap survival in several clinical studies,
however.24,149,150 In a retrospective analysis of 226 irra-
diated head and neck reconstructions and a case-
control study of failed flaps, Mulholland et al150 found
that postoperative infection and time delay between
radiation and surgery were the only factors correlat-
ing with free flap failure. However, Singh et al24 found
that patients with prior radiation exposure have a
significantly higher risk for development of compli-
cations at the recipient site.
It has been suggested that elderly patients present
with a high risk of perioperative morbidity and mor-
tality. However, several studies have shown that the
incidence of surgical complications21,151 and success
rates in the elderly are similar to those in the general
population. Age alone is not a contraindication to free
tissue transfer. Kroll et al91 evaluated 854 free flaps in
which age played no role in flap survival. In a study of
head and neck patients, an age of more than 70 years
did not increase the rate of surgical complications,
but medical complications were more common.152
However, old patients may be more sensitive to the
effects of prolonged anesthesia and are likely to have
more severe complications.24 Bonawitz et al153 reported
an almost threefold increase in the free flap failure rate
between an elderly (>60 years) and a younger age group.
Despite this finding, they concluded that age should
not be a contraindication in free flap surgery.
Free flaps can be safely performed in children.154"157
Free vascularized joint and toe to hand transfers are
established methods for the correction of congenital
hand malformations in children,158 and children who
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525
had toe to hand transfer after traumatic amputations
have been reported to achieve normal growth.155 Free
fibula transfer has been used for mandibular recon-
struction in children,159 and a donor morbidity study
with 8 years of follow-up revealed no significant donor
problems.160
Obesity clearly increases the risks of microvascu-
lar surgery. In a multicenter study of 23 centers, obesity
was associated with increased hematoma or hemor-
rhage.21 Chang etal161 analyzed their experience of 936
TRAM flap breast reconstructions and found that
although the majority of obese patients had success-
ful outcome, the incidence of flap loss and of compli-
cations in the form of hematoma, seroma, infection,
and hernia was significantly higher than in the normal-
weight patients. They concluded that morbidly obese
patients are at very high risk for flap failure and that
breast reconstruction should be avoided in these
patients.
The necessity of routine angiography in evaluation
of the vasculature of recipient legs before microsurgi-
cal free tissue reconstruction remains controversial.67
A prospective study of 33 patients found that if at least
one palpable pedal pulse was available, the preopera-
tive angiography did not add relevant information, but
in two cases, despite a normal angiogram, there was
underlying vascular scarring that resulted in change
of recipient vessels.68 The authors concluded that pre-
operative angiography is indicated only when both
pedal pulses are not palpable and that normal preop-
erative angiographic findings do not guarantee the pres-
ence of vessels suitable for anastomosis. Many centers,
however, still require preoperative angiography if
vascular disease or injury is suspected on the basis
of extremity trauma or symptoms of vascular
insufficiency.
THROMBOPROPHYLAXIS
Deep venous thrombosis and pulmonary embolism
present small but significant risks for surgical patients;
fatal pulmonary embolism occurs in 0.1% to 0.8% of
general surgery patients and in 4% to 7% of patients
undergoing open reduction of hip fracture.162 As in
any major surgery, the patient's risk factors must be
evaluated, and mechanical thromboprophylaxis in the
form of compression stockings, intermittent pneumatic
compression, and comfortable positioning on the oper-
ating table is applied according to the national guide-
lines. Adequate hydration must also be maintained.
The use of chemical thromboprophylaxis must be
weighed against the possibility of hemorrhagic com-
plications. The use of anticoagulants in free flap surgery
is controversial, and the reason for using them varies;
some use them with the hope of enhancing flap success,
others for thromboprophylaxis. A survey of 73
microvascular centers by Davis in 1982 reported the
image...
526 I • GENERAL PRINCIPLES
use of 21 different antithrombotic agents, and several
centers used none at all. A similar survey was conducted
10 years later by Salemark,130 and still consensus was
lacking; eight agents, either single or combined, were
in use. He found a statistical difference in the frequency
of anastomotic thrombosis between the centers using
anticoagulants and those that did not, but no differ-
ence in final success rate. In a study of 23 microvas-
cular centers, the use of antithrombotic drugs showed
no effect on outcome, but postoperative subcutaneous
low-molecular-weight heparin was associated with a
lower incidence of anastomotic thrombosis.21 Many
centers use low-molecular-weight heparin routinely,
not to prevent microvascular thrombosis but for pro-
phylaxis of deep venous thrombosis. The risk of deep
venous thrombosis is significantly lower in the East
Asian population, and thromboprophylaxis has been
considered unnecessary.I63 Some studies challenge this
concept,164,165 although no studies have addressed the
risk in microsurgery.
Microvascular Anesthesia
A stable anesthesia is a prerequisite of microvascular
surgery. Adequate fluid management includes slight
hemodilution to facilitate the maintenance of high
cardiac output and low systemic vascular resistance.166
The choice of fluids is important because flaps are sus-
ceptible to development of edema due to their lack of
lymphatic drainage. Crystalloids can be used for basic
fluid replacement, but synthetic colloids (pentastarch
or hydroxyethyl starch167) are preferred for the replace-
ment of plasma constituents.166
Blood flow in the donor and recipient arteries is of
concern to the microvascular surgeon. This is pre-
dominandy determined by cardiac output and systemic
vascular resistance and is not always reflected by sys-
temic blood pressure. Cardiac output depends on
cardiac preload, which can be lowered either by hypo-
volemia (blood loss, inadequate fluid replacement) or
by vasodilatory agents. Many factors including the anes-
thetic agents affect systemic vascular resistance, but
adequate pain control and core temperature moni-
toring help prevent peripheral vasoconstriction and
vasospasm. It is extremely important to keep the patient
from cooling during the long surgery by use of
warming blankets, warm infusion fluids, and warm
and humidified inspired gases.
Epidural anesthesia causes both sensory and sym-
pathetic block that may be advantageous in free flap
surgery. An experimental study168 has suggested caution
in its use because extradural block causes a decrease
in cardiac output, mean arterial pressure, and micro-
circulatory blood flow, and a clinical study by the same
group has confirmed this.169 However, epidural anes-
thesia has been clinically used with good results.170,171
Inberg et al156,170 combined regional anesthesia
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(brachial, spinal, and epidural blocks) with bupiva-
caine in toe to hand transfers and found that because
of plexus block, the skin temperature in the operated
hand was higher than in the contralateral hand. Scott
et al171 compared a combination of epidural and general
anesthesia to general anesthesia alone in patients under-
going free flap transfer to the lower extremities and
found epidural supplementation to be advantageous.
Special Techniques and Flap
Design Modifications
ENDOSCOPIC TECHNIQUES
Endoscopically assisted harvest of free tissue requires
smaller incisions and leaves a more acceptable scar
at the donor site than does the conventional open
method. However, the procedure also requires special
instrumentation and training of the personnel, and as
in any new method, the surgeon needs to undergo a
learning curve, so the first operations will be length-
ier than usual. In a series of 22 gracilis muscle flaps,
Lin et al172 found that the endoscopically assisted group
had a shorter incision length (mean, 6.5 cm) compared
with the conventional group (15.5cm). The endo-
scopically assisted method was fast; the gracilis muscles
were harvested within 40 minutes. A donor site mor-
bidity comparison between the endoscopically assisted
and the traditional latissimus dorsi muscle flap harvest
revealed no statistically significant differences in the
incidence of postoperative hematoma, seroma, or
wound infection. However, a patient questionnaire
revealed that the endoscopically assisted group expe-
rienced less pain, and their overall satisfaction was
significantly higher.173 Another endoscopically har-
vestable flap is the rectus abdominis,174 which can be
harvested by either a transperitoneal or an extraperi-
toneal approach.
Experimental and clinical cases document that the
omentum and jejunum can be harvested successfully
as a free flap with laparoscopic assistance.175 Coronary
artery anastomoses of a porcine heart have been per-
formed endoscopically with a microsurgical robotic
system.176 Robotic technology may enable the devel-
opment of a truly endoscopic approach to microsurgery
(see Chapter 40).
PERFORATOR FLAPS
A perforator flap is defined as a flap based on a mus-
culocutaneous perforating vessel that is direcdy visu-
alized and dissected free of surrounding muscle until
adequate pedicle length is obtained. The key idea with
perforator flaps is to achieve better accuracy in recon-
struction while at the same time minimizing donor
site morbidity. The technique allows inclusion of only
the specific components required for the reconstruc-
tion. A cutaneous flap is septocutaneous when it is based
image...
18 • PRINCIPLES AND TECHNIQUES OF MICROVASCULAR SURGERY
FIGURE 1 8 - 2 0 . A septocutaneous anterolateral thigh
free flap.
on a vessel traveling in the intermuscular septum (Fig.
18-20), and the same skin island becomes a perfora-
tor flap when it is based on direct musculocutaneous
perforators that have been dissected free of all muscle
tissue (Fig. 18-21). The strongest advantage may be
the alleviation of concern about anatomic variations
because the planning is retrograde and starts from the
distal end of the vascular tree. It is possible preopera-
tively to trace the desired perforator by pencil Doppler
probe and to design the flap accordingly.177 The vessel
is then visualized at the level of the fascia and dissected
in a retrograde fashion until the desired pedicle length
and caliber are reached. This method allows complete
freedom in the choice of flaps. "Freestyle free flaps"178
can be designed almost anywhere, as long as there is a
willingness to use small-caliber vessels. The perfora-
tor or the septocutaneous vessel is followed until it joins
the source artery, and at most times the vessels are
divided at this higher level to achieve vessels of suit-
able caliber.
Koshima179,180 has introduced the concept of divid-
ing the pedicle of a perforator flap at a level above the
fascia. This truly minimizes donor site morbidity
because the fascia remains intact and the muscle does
FIGURE 1 8 - 2 1 . A perforator flap; the musculocuta-
neous pedicle has been dissected free of muscle.
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527
not need to be touched. This, however, leaves the vessels
with diameters of less than 1 mm, and anastomosis to
such vessels is supramicrosurgery. The pedicle will also
be very short, and for practical reasons it will be difficult
for such flaps to achieve popularity.
CHIMERIC FLAPS
A chimeric flap refers to a flap with separate compo-
nents that are linked to each other because they all derive
from the same source vessel.181 The separate compo-
nents can be individually maneuvered and placed in
a three-dimensional manner to accomplish an optimal
one-stage reconstruction of compound defects. A
typical combination for head and neck reconstruction
is an anterolateral thigh flap and vascularized iliac bone
graft based on the lateral circumflex femoral system
and the deep circumflex iliac system182 (Fig. 18-22)
as well as the flaps based on the subscapular arterial
system.183 The same effect can also be achieved by
joining several flaps together in a flow-through fashion,
for example, by combining an anterolateral or antero-
medial thigh flap with a vascularized fibular graft for
composite oromandibular defects.184
The latissimus dorsi muscle can be split into
hemiflaps sequentially linked to reconstruct a long
slender defect or two separate, longitudinally located
adjacent defects.18' The hemiflaps can also be com-
pletely separated for simultaneous reconstruction of
two distant defects.186
REFINEMENTS
The choice of donor tissue is based on the require-
ments of the recipient site, and with the wide range of
naturally occurring flaps available, an almost ideal solu-
tion can often be found. Table 18-1 compares the most
common donor sites used for composite mandibular
reconstruction and highlights the typical factors to be
FIGURE 1 8 - 2 2 . A chimeric flap: an anterolateral thigh
flap with a separate vastus lateralis muscle flap from the
same pedicle. A free groin flap is to be attached to the
distal end of the anterolateral thigh flap in flow-through
manner.
528 I • GENERAL PRINCIPLES

TABLE 18-1 • COMPARISON OF VARIOUS DONOR SITES FOR COMPOSITE MANDIBULAR

RECONSTRUCTION

Bone Soft Tissue

Length Quality Contourability Availability Flexibility in Flexibility in
Flap Contouring Insetting
* *« **

•
• • • •

•
»

•
Fibula

»
*
•
* » ** *
Ilium » » »
*
Scapula * * ** **

*
Radius * • **

considered: the availability of bone and soft tissue and
the contourability of the bone as well as the flexibility
of the positioning of the soft tissues.
The restoration of functional mobility and sensi-
bility are principal factors in determining donor site
tissue, especially in reconstruction of the hand.
However, in complex or large soft tissue defects, cover
is the primary goal, and standard flaps like the lateral
arm or radial forearm flap that provide protective sen-
sibility can be used.187 For soft tissue defects of the
fingers, the best sensibility is obtained by use of tissue
either from the palmar surface of the hand itself or
from the toes. The glabrous skin and pulp of the great
toe have high sensibility; especially use of the trimmed
great-toe technique results in a thumb similar in
size and shape to the contralateral normal thumb
(Fig. 18-23).
New flaps are constantly being developed in search
of the optimal tissue replacement for each defect. The
free medialis pedis provides good thickness, texture,
and color matching for hand and digit resurfacing.
\ long neurovascular pedicle, is the most commonly used
-
FIGURE 18-23. The final result of a trimmed great toe
to thumb transfer.
»
*
Moreover, in a defect with a vascular gap, it can be used
as a flow-through flap to provide both cover and vessel
continuity in a one-stage procedure; the size of the
feeding vessels of the flap matches that of the digital
vessels well, and it consists of glabrous skin rich in nerve
endings, so it has good potential for sensory recov-
ery.188 Other flaps that are suitable for flow-through
include the radial forearm flap,189 the latissimus dorsi
flap, and the anterolateral thigh flap.
The anterolateral thigh flap has become one of the
most widely used flaps in recent years because of its
great versatility (Fig. 18-24).190,19' It has a pedicle of
suitable size and can be used as a flow-through flap. It
can be a musculocutaneous or a chimeric flap, includ-
ing either a small portion of the vastus lateralis muscle
or even the entire muscle, but it can also be made into
an ultrathin perforator flap raised at a suprafascial level.
The skin island can be anything from a few centime-
ters to the entire lateral portion of the thigh.
INNERVATED FREE FLAPS
The fact that cutaneous nerves as well as the motor
nerves of muscles are always accompanied by a paral-
lel system of arteries and veins was known as early as
1892 by Quenu and Lejars.32 Functioning free muscle
transplantation implies the use of an innervated
muscle flap to replace previously lost function (e.g.,
after facial paralysis or brachial plexus injury). The gra-
cilis muscle,192 because of its expandability, shape, and
and can be harvested endoscopically.193 If a larger
muscle is needed, for example, for reconstruction after
soft tissue sarcoma ablation, the latissimus dorsi, the
rectus femoris, and the tensor fascia lata can be used.194
Some sensory recovery occurs even in noninner-
vated free flaps, although the recovery is significantly
better if the flap is innervated.195 Experimental studies
have shown that a skin graft will regain sensory inner-
vation if it is placed over an innervated muscle flap,
but if a free flap is not innervated, the skin graft also
remains denervated.196 Sensory innervated flaps like
the radial forearm flap and the anterolateral thigh
flap have been advocated especially in intraoral

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TeWftf'aelcrKf image...
.

18 • PRINCIPLES AND TECHNIQUES OF MICROVASCULAR SURCERY 529

300-J

255
250-

200-

150-

100- 99

50- 44

2 1 1 0 1 5
FICURE 1 8 - 2 4 . The use of the anterolateral o - - I I 1 1 1 t=
T=3 1 ' I I
thigh free flap at the Chang Cung Memorial
Hospital. 1991 1993 1995 1997 1999

reconstruction,197 and several studies have shown the conventional free flaps and thinned flaps to the lower
superiority of return of sensibility compared with non- extremities, the survival rate was the same, but 11 of
innervated flaps.195,198,199 However, because some spon- 15 of the conventional flaps versus 5 of 15 of the thinned
taneous sensory recovery occurs and none of these flaps required secondary revisional surgery.204
studies has large enough patient numbers, they have
so far not been able to show any benefit in speech or PREFABRICATED FLAPS
swallowing.195'199
Prefabrication of flaps aims for greater refinement in
Sensory reinnervation of the reconstructed breast reconstruction by custom-making flaps to fulfill the
is a relatively new concept as satisfactory spontaneous individual requirements. This means designing flaps
return of sensibility occurs.200 However, if the lower with only the required tissue components and identi-
abdominal flap is raised as a perforator flap (deep infe- fying new donor sites while minimizing donor mor-
rior epigastric perforator), a sensory nerve can be dis- bidity. Instead of doing secondary corrective procedures
sected free and reconnected to a cutaneous nerve in to a standard flap, the transferred item is finished before
the axilla.201 This seems to increase the quality and quan- the final free flap stage is entered.
tity of sensation.202
The several clinical types of prefabrication205 include
tissue expansion, delay, vascular induction, and pre-
THIN FLAPS transfer grafting (also called prelamination). The sim-
The primary goal of reconstructive microsurgery has plest is pretransfer tissue expansion to augment the
traditionally been filling of the defect with complica- necessary tissues and to enlarge the size of a flap. This
tion-free healing, but this is no longer applicable today. also facilitates primary donor site closure. The size
The aim is to achieve as much as possible in one stage.
Because most of the available flaps are thick and bulky,
secondary revisions are often needed. The concept of
thinning flaps before transplantation has arisen from
the understanding of their vascular supply and from
the increasing experience with perforator flaps. Skin
is nourished by a subdermal plexus arising from an
axial vessel, and a cutaneous flap can be raised without
the fascia at a level above the deep fascia (Fig. 18-25).
Once a sizable perforator is encountered, the fascia is
incised and the pedicle followed to the source vessels.
Thinning should be performed before the vascular
pedicle is divided.203 This not only results in a thinner
flap but also helps reduce donor site morbidity because
fascial integrity can easily be restored. Preoperative
Doppler mapping of perforators helps in designing FIGURE 1 8 - 2 5 . Suprafascial dissection of a free
a suitable skin island.203 In a study comparing anterolateral thigh flap. Note the perforator vessels arising
through the fascia.

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530 I • GENERAL PRINCIPLES
of an area nourished by a known vessel can also be
enlarged by pretransfer delay of a cutaneous flap.206
Vascular induction by implantation of vascular pedi-
cles allows the design of more discrete donor flap sites
or in areas of skin excess, thus also minimizing donor
morbidity.207,208 It is possible to establish new flaps with
the desired components from areas that do not have
defined axial vessels. The technique was in fact first
used in local flaps; in 1971, Orticochea described vas-
cular implantation into the retroauricular conchal skin
for later pedicled nasal reconstruction.209,210
Prelamination entails the formation of new multi-
layered tissue combinations by either skin grafting
or implanting the donor site with bone, cartilage, or
mucosa.211 The forearm is the most common site for
prelamination, most typically used to build a new nose
or a double lined flap for intraoral reconstruction.2"
The newly made, well-designed subunit, however, will
become a victim of the contractile forces of healing,
swelling, and scarring, which often cause suboptimal
results.210
Flap prefabrication is a subject of intense experi-
mental research. In a rat model, the maturation of the
prefabricated flap has been accelerated with vascular
endothelial growth factor.212 The clinical implications
are still relatively scarce; the prefabrication process
implies that the patient must undergo at least one or
more preparatory surgeries before the actual flap trans-
fer. The surgeon and the patient must invest more
time and effort than in a conventional free flap, and
a large variety of naturally occurring free flaps are
now available that satisfy identified reconstructive
requirements.
VENOUS FLAPS
First described in an animal model by Koshima et al214
in 1991, venous flaps are clinically limited in use. They
are small because the risk of edge necrosis is propor-
tional to the increasing size of the flap.213 Arterialized
venous flaps offer a long vascular leash without
sacrifice of any donor artery,213,21,1 but a pure venous
flap is nourished by venous blood alone. An arterial-
ized venous flap may cause an arteriovenous fistula,
which may lead to systemic manifestations or a steal
syndrome.
Monitoring Flaps
Free flap success is enhanced by the rapid identification
of postoperative free flap ischemia at an early stage to
permit successful intervention and flap salvage. Early
recognition of such problems, within 8 to 12 hours,215
is crucial, but we still lack an ideal "foolproof" moni-
toring method. The ideal method should be harmless
to both the flap and the patient, be accurate and reli-
able, and provide fast recognition of circulatory
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Dr.Mustafa D.
changes. It should also be simple to use and easy to
interpret as well as inexpensive. Various monitoring
strategies have been developed, but not a single one is
uniformly accepted. Most flaps can be safely moni-
tored by clinical observation and surface temperature
monitoring. A skin island is often added to buried flaps
for monitoringpurposes.216Apart of the jejunum flap
can temporarily be left exteriorized and excised later
after serving its purpose. Buried flaps that lack an exter-
nal component present a challenge and require more
sophisticated monitoring devices.
The majority of thrombi occur within the first 2
postoperative days, and salvage rates go down the later
the thrombosis occurs.217 Arterial thrombi tend to occur
on the first postoperative day, whereas venous thrombi
can occur later. The cost-effectiveness of postopera-
tive monitoring of free flaps is greatest during the first
2 days, after which it decreases significantly.217 In a study
of 750 free flaps monitored with conventional methods,
such as clinical observation, hand-held Doppler ultra-
sonography, surface temperature probes, and pinprick
testing, Disa et al218 found that ischemia in the non-
buried flap was usually detected early, but the buried
ones presented symptoms later in the form of wound
complications.
CLINICAL METHODS
Most centers rely on experienced nursing staff to rec-
ognize compromised flaps by observation of clinical
signs of skin color, capillary refill, fullness, and bleed-
ing. Pinprick testing can be used to observe the color
of capillary bleeding. Measurement of surface tem-
perature with a surface temperature probe is easy and
inexpensive218 and, in a series of 600 free flaps by Khouri
and Shaw, was 98% sensitive and 75% predictive of
vascular compromise. Acland219 promoted this tech-
nique in the early 1980s and stated that a temperature
between 30°C and 32°C was marginal and that a tem-
perature below 30°C was indicative of flap failure.
Comparison of the temperature of the flap to that
of the surrounding skin or comparison between
two measurements is also used to detect vascular
compromise.215
ULTRASONOGRAPHY
Hand-held pencil Doppler probes (low-frequency
continuous ultrasonography),218 implantable high-
frequency pulsed Doppler probes, and the laser Doppler
have all been used. Yuen and Feng,22 in a study of 232
microvascular flaps, found that the laser Doppler
flowmeter detected vascular compromise in all 13 cases
with no false-positive or false-negative results. An
experimental comparative study of oxygen tension
measurements and laser Doppler study showed that
both methods could distinguish arterial from venous
occlusion.220 Although oxygen tension measurements
image...
18 • PRINCIPLES AND TECHNIQUES OF MICROVASCULAR SURGERY
were slightly slower in response than laser Doppler
measurements, the values were more reliable. Color
Doppler ultrasonography readily distinguishes between
thrombosis and vasoconstriction, but it requires expe-
rienced personnel and cannot be used for continuous
monitoring.
OTHER METHODS
Measurements of transcutaneous oxygen, pulse oxime-
try, hydrogen clearance technique,"21 and near infrared
spectroscopy222 have been used. Photoplethysmogra-
phy allows the waveforms to be transmitted by
telephone to a remote station, permitting them to be
interpreted by the surgeon at home. Green light pho-
toplethysmography analyzes the light reflecting from
hemoglobin as a way to distinguish between perfused
and nonperfused tissue.223 Computed thermography
has good potential for intraoperative and bedside
monitoring of free flaps.
Microdialysis,anewpromisingbut invasive method
for flap monitoring, can distinguish between arterial
and venous occlusion.224 A small double-lumen catheter
is inserted into the flap tissue, and perfusion fluid is
slowly pumped through the catheter. The dialysate,
equilibrated with the extracellular fluid, is analyzed
for lactate, glucose, and glycerol concentrations, allow-
ing early detection of ischemia.225 The probe can be
left in place for 3 days. Another invasive method is the
implantable tissue oxygen probe.226
The idea of an implantable Doppler probe was intro-
duced in 1988 by Swartz et al,227 who secured the probe
in place, attaching it to a Gore-Tex mesh wrapped
around the vessel. Swartz228 later reported having moved
on to use of a silicone cuff to secure the probe; however,
the cuff remains in place after removal of the probe.
The idea has been modified by Kind et al,229 who use
absorbable Vicryl mesh to secure the probe. Both report
excellent results in their hands, but no comparative
studies have been published.
Results
SURVIVAL
As free flaps have become routine surgery, failures have
become rare and success rates range from 96% to
100%.18,33,54 In the 1980s, the literature concentrated
on describing new flaps and the technical aspects of
free tissue transfer (e.g., the anastomosis technique).
The introduction of flaps as reliable as the latissimus
dorsi or radial forearm flap has helped to bring failure
rates down. The availability of more reliable donor sites
with large-caliber vessels has created an intermediate
status between true microsurgery and vascular surgery,
termed micromacrosurgery. Micromacrosurgery can
be performed without a microscope, with use of only
loupes.
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531
Although the surgeon's operative experience is a
critical factor, and many anastomotic problems can be
traced to technical errors like kinking or compression,
mere surgical skill cannot guarantee success. What
seems like a perfect anastomosis between two healthy
vessels may still fail. Failure is often due to an error in
overall craftsmanship, poor planning, poor choice of
flap or vessels, or poor timing.18
VASCUU\R COMPLICATIONS
Re-exploration rates in free flap surgery range from
6% to 25%.21,23 Thrombosis of the arterial anas-
tomosis is the most common finding in reopera-
tions.18'20'94'215'230 Technical failure in anastomosis and
thrombogenic injury to the epithelium can result in
"primary thrombosis"at the anastomosis site. Kinking
or compression of vessels due to hematoma or edema
can lead to decreased inflow and "secondary throm-
bosis." Partial primary anastomotic thrombosis can
seed microemboli to the flap and cause secondary
thrombosis. The incidence of primary thrombosis
decreases as the surgeon increases in experience.
Re-exploration salvage rates of 54% to 100% have
been reported.21 In cases in which anastomotic revi-
sion is not enough, Fogarty thrombectomy230 or clot
lysis with antithrombotic agents has been recom-
mended. Leeches can be used in cases of poor venous
outflow.
COMPLICATIONS
Complication rates vary between 24% and 55% for
different subtypes of free flaps23,152,161; they are
naturally more frequent in emergent lower extremity
reconstruction and head and neck surgery but rare in
elective breast reconstruction. In head and neck micro-
surgery, the complication rates vary between 28% and
55%,24,152 with multiple complications occurring in
10.5%. Singh et al24 studied 200 patients who under-
went microvascular transplantation and found that
prior radiation treatment, anesthesia time of more than
10 hours, and preexisting medical conditions were asso-
ciated with an increased risk for complications. These
findings were confirmed in a similar series by Hoff-
mann et al.231 In Singh's study, comorbidity and age
older than 70 years correlated with increasing com-
plication severity. General complications, systemic or
psychiatric in nature, occur in 14% to 23% of the
patients24,231 and again are more common in patients
older than 70 years.152
Recipient site complications have been reported as
15%; history of prior radiation therapy is associated
with increased risk.24 Reported hospital stays vary
between 16 and 20 days for head and neck recon-
struction23,24 and up to 82 days for lower extremity
trauma142; the development of complications increased
the median hospital stay by 7.5 days.24
532 I • GENERAL PRINCIPLES
DONOR SITE COMPLICATIONS
All flaps leave some donor morbidity, and the possi-
ble benefits of free flap transplantation must outweigh
its sequelae. The incidence of donor site complications
varies between 5.5% and 31 O/Q.24-232-234 Early donor prob-
lems are associated with wound healing (hematoma,
seroma, and wound dehiscence)232,233 and seem to be
more common in obese patients161 and in smokers.147
Hematoma formation can occur with any flap; large
dead spaces like the latissimus dorsi donor site are espe-
cially susceptible to seroma formation.232,233 Wound
dehiscence occurs with tight closure, typically with the
TRAM, gracilis, scapular, and dorsalis pedis flaps.233,235
Long-term morbidity includes problems with form,
function, or pain.
If the donor site has to be covered by split skin graft-
ing, it will leave a cosmetic defect as, for instance, the
radial forearm233,236 and dorsalis pedis flaps do.237 Many
patients with radial forearm flaps are unhappy with
the cosmetic result238; dissatisfaction with the aesthetic
outcome is reportedly higher among women than
among men.239 Delayed skin graft healing can lead to
exposed tendons; a prospective study of 100 patients
with radial forearm flaps showed delayed healing in
22% of patients and tendon exposure in 13%.238 Donor
site morbidity of the radial forearm flap can be
significantly reduced by use of the suprafascial dis-
section technique (Fig. 18-26),240,241 which optimizes
the skin graft take; as the fascia is preserved, the size
of the donor defect remains smaller, and there is no
tenting of the musculofascial structures. It also allows
easier preservation of the superficial radial nerve
and the thenar cutaneous branch of the lateral ante-
brachial nerve (Fig. 18-27).
FIGURE 18-26. Suprafascial dissection of a radial
forearm flap. B.R., brachioradialis tendon; F.C.R., flexor
carpi radialis tendon; arrowhead, branch of the lateral
antecubital nerve; closed arrow, superficial branch of the
radial nerve; open arrow, lateral antecubital nerve. (From
Chang CN, Miller G, Halbert CF, et al: Limiting donor site
morbidity by suprafascial dissection of the radial forearm
flap. Microsurgery 1996;17:136-140.)
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FIGURE 18-27. The donor site of asuprafascially ele-
vated radial forearm flap; arrows point to a branch of the
lateral antecubital nerve and the superficial branch of the
radial nerve.
Latissimus dorsi transfer can result in functional
impairment of the shoulder,233,242,243 and serratus
anterior elevation may cause scapular winging.244
TRAM,245,246 iliac crest,247 or groin flap233 elevation can
result in abdominal wall weakness and hernia forma-
tion, and the iliac crest flap may lead to gait problems.247
Free flaps that include bone (radial forearm, fibula,
iliac crest) leave a fracture-susceptible donor site,
impaired function, and contour irregularity.233,247
Painful neuromas or numbness can be encountered
on the lateral arm,248 radial forearm, iliac crest,247 or
groin flap249 donor sites, and free fibula transfer can
result in a temporary peroneal nerve palsy. Hypesthe-
sia of the cutaneous territory of the obturator nerve
has been reported in patients with gracilis free flaps.250
The most feared complication of free fibula harvest is
compartment syndrome.251
Future
In the last 30 years, free flap surgery has become routine,
but the basic principles of microsurgery have changed
very little. Most surgeons still use the original tech-
niques of interrupted end-to-end suturing with the
aid of a microscope, and because the results are good,
many see no reason for change, even if, for example,
the devices for anastomosis have proved to be faster
and as reliable as the traditional techniques.46"48 The
search for new techniques continues, and in time they
will probably gain more popularity.
More and more emphasis is put on minimizing
donor sequelae, and this has led to the rapid develop-
ment of minimally invasive and endoscopic surgery.
The endoscope is used not only to facilitate flap harvest
through a smaller incision but also as an alternative to
a microscope, allowing the surgeon and the whole team
to see the magnified anastomosis on a screen instead
of through the binoculars. Endoscopic surgery is closely
linked to the development of robotics, and coronary
image...
18 • PRINCIPLES AND TECHNIQUES OF MICROVASCULAR SURGERY
artery anastomoses of a porcine heart have already been
performed endoscopically with the aid of a microsur-
gical robotic system. 17
T h e prefabrication of flaps has already been dis-
cussed, but tissue engineering will surely provide us
with new possibilities in the form of tissue manufac-
turing or guided regeneration of tissues. 252 Tissue
engineering of vascular grafts has true potential for
application in the clinical situation, 104,106 and culture
of vascularized bone 2 0 5 has been attempted. Biomo-
lecular medicine is advancing in the study of gene
regulation of biologic mechanisms a n d has already
produced clinically available growth factors to promote
w o u n d healing. 252
For an optimal result to be reached, the coopera-
tion of multiple specialties is necessary, which will also
bring new indications and applications for free flap
surgery. By combining knowledge and effort, patients
who were previously deemed inoperable can n o w be
surgical candidates, for example, by the combination
of microvascular muscle flap transfer with vascular
reconstruction for salvage of legs with ischemic tissue
loss or w o u n d complications after bypass surgery. 253
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3. Carrel A: La technique des anastomoses vasculaires et de la
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4. Guthrie C: Blood Vessel Surgery and Its Applications. New
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5. McLean J: The thromboplastic action of cephaline. Am J Physiol
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6. Charles A, Scott D: Studies on heparin L The preparation of
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culocutaneous flaps in pigs. Plast Reconstr Surg 1997; 100:945.
169. Erni D, Banic A, Signer C, et al: Effects of epidural anaesthe-
sia on microcirculatory blood flow in free flaps in patients
under general anaesthesia. Eur J Anaesthesiol 1999:16:692.
170. Inberg P, Tarkkila PJ, Neuvonen PJ, et ah Regional anesthesia
for microvascular surgery: a combination of brachial plexus,
spinal, and epidural blocks. Reg Anesth 1993:18:98.
171. Scott G, Rothkopf D, Walton R: Efficacy of epidural anesthe-
sia in free flaps to the lower extremity. Plast Reconstr Surg
1993:91:673.
172. Lin CH, Wei FC, Lin YT: Conventional versus endoscopic free
gracilis muscle harvest. Plast Reconstr Surg 2000:105:89.
173. Lin CH, Wei FC, Levin LS, et al: Donor-site morbidity
comparison between endoscopically assisted and traditional
harvest of free latissimus dorsi muscle flap. Plast Reconstr Surg
1999:104:1070.
174. Miller M, Robb G: Endoscopic techniques for free flap harvest.
Clin Plast Surg 1995:22:755.
175. Saltz R: Endoscopic harvest of the omental and jejunal free
flaps. Clin Plast Surg 1995;22:747.
176. Stephenson ER Jr, Sankholkar S, Ducko CT, et al: Robotically
assisted microsurgery for endoscopic coronary artery bypass
grafting. Ann Thorac Surg 1998;66:1064.
177. Giunta R, Geisweid A, Feller AM: The value of preoperative
Doppler sonography for planning free perforator flaps. Plast
Reconstr Surg 2000; 105:2381.
178. Asko-Seljavaara S: Free style free flaps. Presented at the 7th
Symposium of the International Society of Reconstructive
Microsurgery, New York, 1983.
179. Koshima I, Inagawa K, Yamamoto M, Moriguchi T: New micro-
surgical breast reconstruction using free paraumbilical per-
forator adiposal flaps. Plast Reconstr Surg 2000;106:61.
180. Koshima I,MoriguchiT,Fukuda H,et al: Free, thinned,paraum-
bilical perforator-based flaps. J Reconstr Microsurg 1991 ;7:313.
181. Hallock GG: Simultaneous transposition of anterior thigh
muscle and fascia flaps: an introduction to the chimera flap
principle. Ann Plast Surg 1991;27:126.
182. Koshima I, Yamamoto H, Hosoda M, et al: Free combined com-
posite flaps using the lateral circumflex femoral system for
repair of massive defects of the head and neck regions: an intro-
duction to the chimeric flap principle. Plast Reconstr Surg
1993:92:411.
183. Germann G, Bickert B, Steinau HU, et al: Versatility and
reliability of combined flaps of the subscapular system. Plast
ReconstrSurg 1999;103:1386.
184. Ao M, Asagoe K, Maeta M, et al: Combined anterior thigh flaps
and vascularised fibular graft for reconstruction of massive
composite oromandibular defects. Br J Plast Surg 1998;51:350.
185. Lin CH, Wei FC: Widely split latissimus dorsi muscle flaps for
reconstruction of long soft-tissue defects in lower extremities.
Plast Reconstr Surg 2000;105:706.
image.
18 • PRINCIPLES AND TECHNIQUES OF MICROVASCULAR SURCERY
186. Chiang YC, Wei FC: Simultaneous coverage of two separate 211.
defects with two free hemiflaps harvested from one latissimus
dorsi muscle. Plast Reconstr Surg 1995;95:385.
187. Halbert CF, Wei FC: Neurosensory free flaps. Digits and hand. 212.
Hand Clin 1997:13:251.
188. Wong SS, Wang ML, Su MS, et al: Free medialis pedis flap as
a coverage and flow-through flap in hand and digit recon- 213.
struction. j Trauma 1999;47:738.
189. Chiang YC, Chen FC, Hsieh M J, et al: Reconstruction of a large
thoracoabdominal wall defect with a flow-through forearm 214.
flap and a latissimus dorsi-groin flap. Plast Reconstr Surg
1997;100:1240. 215.
190. Kimata Y, Uchiyama K, Ebihara S, et al: Versatility of the free
anterolateral thigh flap for reconstruction of head and neck 216.
defects. Arch Otolaryngol Head Neck Surg 1997; 123:1325.
191. Demirkan F, Chen H, Wei F, et al: The versatile anterolateral
thigh flap: a musculocutaneous flap in disguise in head and 217.
neck reconstruction. Br J Plast Surg 2000;53:30.
192. ChungDC, Carver N, Wei FC: Results offunctioning free muscle
transplantation for elbow flexion. J Hand Surg Am 1996; 218.
21:1071.
193. Doi K, Hattori Y, Soo-Heong T, et al: Endoscopic harvesting
of the gracilis muscle for reinnervated free-muscle transfer. 219.
Plast Reconstr Surg 1997; 100:1817.
194. lhara K, Shigetomi M, Kawai S, et al: Functioning muscle trans- 220.
plantation after wide excision of sarcomas in the extremity.
Clin Orthop 1999;358:140.
195. Netscher D, Armenia A, Meade R, et al: Sensory recovery of
innervated and non-innervated radial forearm free flaps: func- 221.
tional implications. J Reconstr Microsurg 2000;16:179.
196. Bayramicli M, Jackson I, Herschman B: Innervation of skin
grafts over free muscle flaps. Br J Plast Surg 2000;53:130. 222.
197. Kimata Y, Uchiyama K, Ebihara S, et al: Comparison of inner-
vated and noninnervated free flaps in oral reconstruction. Plast
Reconstr Surg 1999;105:1307. 223.
198. Kuriakose M, Loree T, Spies A, et al: Sensate radial forearm
free flaps in tongue reconstruction. Arch Otolaryngol Head
Neck Surg 2001;127:1463. 224.
199. Mah S, Durham J, Anderson D, et al: Functional results in oral
cavity reconstruction using reinnervated versus nonreinner-
vated free fasciocutaneous grafts. J Otolaryngol 1996;25:75. 225.
200. Shaw W, Orringer J, Ko C, et al: The spontaneous return of
sensibility in breasts reconstructed with autologous tissue. Plast 226.
Reconstr Surg 1997;99:394.
201. Yap L, Whiten S, Forster A, et al: The anatomical and neuro-
physiological basis of the sensate free TRAM and DIEP flaps. 227.
Br J Plast Surg 2002;55:35.
202. Blondeel P, Demuynck M, Mete D, et al: Sensory repair in per-
forator flaps for autologous breast reconstruction: sensational
or senseless? Br J Plast Surg 1999;52:37. 228.
203. Kimura N, Satoh K: Consideration of a thin flap as an entity
and clinical applications of the thin anterolateral thigh flap.
Plast Reconstr Surg 1996;97:985. 229.
204. Ohjimi H, Taniguchi Y, Kawano K( et al: A comparison of thin-
ning and conventional free-flap transfers to the lower extrem-
ity. Plast Reconstr Surg 2000;105:558. 230.
205. Khouri R: Principles of flap prefabrication. Clin Plast Surg
1992;19:763.
206. Abbase E, Shenaq S, Spira M, et al: Prefabricated flaps: exper- 231.
imental and clinical review. Plast Reconstr Surg 1995;96:1218.
207. Morrison WA, Penington AJ, Kumta SK, et al: Clinical appli-
cations and technical limitations of prefabricated flaps. Plast 232.
Reconstr Surg 1997;99:378.
208. Pribaz J, Fine N, Orgill D: Flap prefabrication in the head and 233.
neck: a 10-year experience. Plast Reconstr Surg 1999;103:808.
209. Orticochea M: A new method for total reconstruction of the 234.
nose: the ears as donor areas. Br J Plast Surg 1971;24:225.
210. Pribaz JJ, Weiss DD, Mulliken JB, et al: Prelaminated free flap
reconstruction of complex central facial defects. Plast Recon- 235.
str Surg 1999:104:357.
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Rath T, Millesi T, Millesi-Shobel G, et al: Mucosal prelamina-
tion of a radial forearm flap for intraoral reconstruction.
J Reconstr Microsurg 1997; 13:507.
Li Q, Reis E, Zhang W, et al: Accelerated flap prefabrication
with vascular endothelial growth factor. J Reconstr Microsurg
2000;16:45.
Galumbeck M, Freeman BG: Arterialized venous flaps for recon-
structing soft-tissue defects of the extremities. Plast Reconstr
Surg 1994:94:997.
Koshima I, Soeda S, Nakayama Y: An arterialized venous flap
using the long saphenous vein. Br J Plast Surg 1991:44:23.
Jones N: Intraoperative and postoperative monitoring of free
flaps. Clin Plast Surg 1992;19:783.
Furuta S, Hataya Y, Ishigaki Y, et al: Monitoring the free radial
forearm flap in pharyngo-oesophageal reconstruction. Br J Plast
Surg 1997:50:40.
Kroll SS, Schusterman MA, Recce GP, et al: Timing of pedicle
thrombosis and flap loss after free-tissue transfer. Plast Recon-
str Surg 1996:98:1230.
Disa JJ, Cordeiro PG, Hidalgo DA: Efficacy of conventional
monitoring techniques in free tissue transfer: an 11 -year expe-
rience in 750 consecutive cases. Plast Reconstr Surg 1999; 104:97.
Acland R: Discussion of: Experience in monitoring the circu-
lation in free flap transfers. Plast Reconstr Surg 1981;68:554.
Liss AG, Liss P: Use of a modified oxygen microelectrode and
laser-Doppler flowmetry to monitor changes in oxygen tension
and microcirculation in a flap. Plast Reconstr Surg 2000;
105:2072.
Machens HG, Mailaender P, Reimer R, et al: Postoperative blood
flow monitoring after free-tissue transfer by means of the hydro-
gen clearance technique. Plast Reconstr Surg 1997;99:493.
Thorniley MS, Sinclair JS, Barnett NJ, et al: The use of near-
infrared spectroscopy for assessing flap viability during recon-
structive surgery. Br J Plast Surg 1998;51:218.
Futran ND, Stack BC Jr, Hollenbeak C, et al: Green light pho-
toplethysmography monitoring of free flaps. Arch Otolaryn-
gol Head Neck Surg 2000; 126:659.
Rojdmark J, Heden P, Ungerstedt U: Comparison of flap
ischaemia induced by arterial or venous occlusion in pigs with
the aid of microdialysis. Eur J Plast Surg 2000;23:278.
Udcsen A, Lontoft E, Kristensen SR: Monitoringof free TRAM
flaps with microdialysis. J Reconstr Microsurg 2000; 16:101.
Wechselberger G, Rumer A, Schoeller T, et al: Free-flap mon-
itoring with tissue-oxygen measurement. J Reconstr Micro-
surg 1997;13:125.
Swartz W, Jones N, Cherup L, et al: Direct monitoring of
microvascular anastomoses with the 20-MHz ultrasonic
Doppler probe: an experimental and clinical study. Plast Recon-
str Surg 1988:81:149.
Swartz W: Discussion to: The effect of an implantable Doppler
probe on the salvage of microvascular tissue transplants. Plast
Reconstr Surg 1998;101:1274.
Kind G, Buntic R, Buncke G, et al: The effect of an implantable
Doppler probe on the salvage of microvascular tissue trans-
plants. Plast Reconstr Surg 1998;101:1268.
Wheatley MJ, Meltzer TR: The role of vascular pedicle
thrombectomy in the management of compromised free tissue
transfers. Ann Plast Surg 1996;36:360.
Hoffmann J, Ehrenfeld M, Hwang S, et al: Complications after
microsurgical tissue transfer in the head and neck region.
J Craniomaxillofac Surg 1998;26:255.
Colen SR, Shaw WW, McCarthy JG: Review of the morbidity
of 300 free-flap donor sites. Plast Reconstr Surg 1986:77:948.
Mahoney J: Complications of free flap donor sites. Microsurgery
1995;16:437.
Hallock GG: Complications of the free-flap donor site from
a community hospital perspective. J Reconstr Microsurg
1991;7:331.
Hallock GG: Relative donor-site morbidity of muscle and fascial
flaps. Plast Reconstr Surg 1993;92:70.
538 I • GENERAL PRINCIPLES
236. Suominen S, Ahovuo J, Asko-Seljavaara S: Donor site mor-
bidity of radial forearm flaps. A clinical and ultrasonographic
evaluation. Scand J Plast ReconstrSurg Hand Surg 1996;30:57.
237. Rautio J, Asko-Seljavaara S, Harma M, et al: Free flaps for
reconstruction of the foot. Handchir Microchir Plast Chir
1989:21:227.
238. Richardson D, Fisher S, Vaughan D, et al: Radial forearm flap
donor site complications and morbidity: a prospective study.
Plast ReconstrSurg 1997;99:109.
239. Bardsley AF, Soutar DS, Elliot D, et al: Reducing morbidity in
the radial forearm flap donor site. Plast Reconstr Surg
1990;86:287.
240. Chang SC, Miller G, Halbert CF, et al: Limiting donor site mor-
bidity by suprafascial dissection of the radial forearm flap.
Microsurgery 1996;17:136.
241. LuWB,WeiF,ChangS,etal:Donorsitemorbidityaftersuprafas-
cial elevation of the radial forearm flap: a prospective study
in 95 consecutive cases. Plast Reconstr Surg 1999;103:132.
242. Fraulin FOG, Louie G, Zorilla L, et al: Functional evaluation
of the shoulder following latissimus dorsi muscle transfer. Ann
Plast Surg 1995:35:349.
243. Salmi A, Tuominen R, Tukiainen E, et al: Morbidity of donor
and recipient sites after free flap surgery. Scand J Plast Recon-
str Hand Surg 1995:29:337.
244. Derby LD, Bartlett SP, Low DW: Serratus anterior free-tissue
transfer: harvest-related morbidity in 34 consecutive cases and
a review of the literature. J Reconstr Microsurg 1997;! 3:397.
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Dr.Mustafa D.
245. Suominen S, Asko-Seljavaara S, von Smitten K, et al: Seque-
lae in the abdominal wall after pedicled or free TRAM flap
surgery. Ann Plast Surg 1996:36:629.
246. Suominen S, Asko-Seljavaara S, Kinnunen J, et al: Abdominal
wall competence after free transverse rectus abdominis mus-
culocutaneous flap harvest: a prospective study. Ann Plast Surg
1997:39:229.
247. Forrest C, Boyd B, Manktelow R, et al: The free vascularised
iliac crest tissue transfer: donor site complications associated
with eighty-two cases. Br J Plast Surg 1992;45:89.
248. Graham B, Adkins P, Scheker LR: Complications and mor-
bidity of the donor and recipient sites in 123 lateral arm flaps.
J Hand Surg Br 1992:17:189.
249. Graf P, Biemer E: Morbidity of the groin flap transfer: are we
getting something for nothing? Br J Plast Surg 1992;45:86.
250. Deutinger M, Kuzbari R, Paternostro-Sluga T, et al: Donor site
morbidity of the gracilis flap. Plast Reconstr Surg 1995;95:1240.
251. Saleem M, Hashim F, Babu Manohar M: Compartment syn-
drome in a free fibula osteocutaneous flap donor site. Br J Plast
Surg 1998:51:405.
252. Lorenz HP, Hcdrick MH, Chang J, et al: The impact of bio-
molecular medicine and tissue engineering on plastic surgery
in the 21st century. Plast Reconstr Surg 2000:105:2467.
253. Lepantalo M, Tukiainen E: Combined vascular reconstruction
and microvascular muscle flap transfer for salvage of ischaemic
legs with major tissue loss and wound complications. Eur I
Vase Endovasc Surg 1996:12:65.
image...
CHAPTER
19 •
Principles of Tissue Expansion
Louis C. ARCENTA, MD • MALCOLM W. MARKS, MD
HISTORY OF TISSUE EXPANSION
BIOLOGY OF TISSUE EXPANSION
Epidermis
Dermis
Muscle
Vascularity of Expanded Tissue
Ultrastructure of Expanded Tissue
Molecular Basis for Tissue Expansion
The Source of Increased Tissue from Expansion
IMPLANT TYPES
BASIC PRINCIPLES
Implant Inflation
TISSUE EXPANSION IN SPECIAL CASES AND SPECIFIC
ANATOMIC SITES
Burns
Tissue Expansion in Children
Expansion of Myocutaneous Flaps
Expanded Full-Thickness Skin Grafts
Reconstruction of the Head and Neck
Tissue expansion is based on the observation that
all living tissues respond in a dynamic fashion to
mechanical stresses placed on them. In normal body
growth, the skin and soft tissue envelopes respond to
growth of the skeleton. A fetal skull is induced to
increase in size by the development of the underly-
ing brain. Skin and subcutaneous tissue grow over
the gravid abdomen and will serially do so in subse-
quent pregnancies. Histologically normal skin and
mucosa will grow over benign and malignant tumors,
demonstrating the focal ability of these structures to
respond to stimuli that are clearly nongenetic. Prim-
itive tribes in Africa purposely increase the size of
lips and earlobes with larger and larger metallic and
wooden rings.
Therapeutic attempts to induce tissue growth by
mechanical stimuli have evolved during the past 20
years. All of these techniques involve the application
of an external physical force that distorts the cell mem-
brane for the purpose of producing new tissue. Tissue
expansion involves the placement of a prosthesis that
is gradually enlarged by the addition of saline. Such
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Reconstruction of the Scalp
Male Pattern Baldness
Reconstruction of the Forehead
Reconstruction of the Lateral Face and Neck
Nose Reconstruction
Periorbital Reconstruction with Expanded
Full-Thickness Grafts
Reconstruction of the Ear
Postmastectomy Breast Reconstruction
Tissue Expansion in the Irradiated Chest Wall
The Hypoplastic Breast
Expansion of the Trunk
Expansion in the Extremities
COMPLICATIONS AND THEIR MANAGEMENT
Infection
Implant Exposure
Compromise and Loss of Tissue at the Time of Flap
Rotation
Implant Failure
mechanically induced tissue expansion allows recon-
struction by an entirely new approach: donor tissue is
generated in situ and used for reconstruction without
compromise of innervation, vascularity, or external
physical appearance.
Codvilla, Matev, and others applied the same prin-
ciples to bone.1,2 By the application of distraction force
to fractured bone,new bone was generated.These prin-
ciples have been applied to the craniofacial skeleton
as well as to most of the long bones of the body.3,4
Vacuum-assisted closure uses an identical principle to
apply force on the surrounding cells in a wound, result-
ing in the induction of new tissue and closure of the
wound.5
HISTORY OF TISSUE EXPANSION
Early attempts at bone lengthening resulted in con-
comitant but poorly recognized induction of growth
of adjacent soft tissue. Neumann6 purposely induced
soft tissue growth with a subcutaneously implanted
balloon in an attempt to reconstruct an external ear
539
540 I • GENERAL PRINCIPLES

deformity. His work, unfortunately, was treated as anec-
dotal and generally forgotten. Radovan and Austad7,8
simultaneously evolved the concept of purposeful soft
tissue expansion with use of an implanted silicone
balloon. Radovan's device contained a self-sealing valve
through which saline was periodically injected to
increase size of the prosthesis. Without animal or
laboratory studies, he immediately began clinical
trials. His initial work was a significant departure
from accepted techniques; it was initially greeted with
skepticism.
Austad's prosthesis was devised as a self-inflating
device using osmotic gradients driven by salt placed
within the expander. His work was largely experimental
and was critical to elucidating the underlying physi-
ology of tissue expansion.
Encouraged by Grabb's editorial after Radovan's
publication in 1982, the technique was rapidly
and widely applied to create new dimensions in re-
constructive surgery.9"14 Large studies subsequently
confirmed the safety and effectiveness of this
technique.
BIOLOGY OF TISSUE EXPANSION
Extensive information is available regarding the biology
of tissue expansion (Fig. 19-1). Following animal exper-
iments,15,16 studies on human tissue, both during the
period of expansion and postoperatively, have also been
performed.17 Studies of the effects of tissue expansion
on nerve, muscle, and bone have also been published.
Epidermis
Statistical analysis of multiple sites over the implant
and its periphery has revealed an increase in epider-
mal thickness during the process of expansion. Early
after placement of the prosthesis, significant thick-
ening of the epidermis is evident. This is also seen
in sham-controls and may, in part, represent post-
operative edema. Within 4 to 6 weeks, epidermal
thickness generally returns to initial levels, but
some increase in thickness persists for many months.
Hair follicles and accessory skin structures are com-
pressed but show no evidence of degeneration. Animal

2& «'• * °
*& £) -

cs&z&vx — -:'—?.

" 4
\

FIGURE 1 9 - 1 . Right, Low-power view of tissue over an implant at 4 weeks demonstrating intact normal-appearing
stratified squamous epithelium, slight compression of the hair follicles, moderate atrophy of the panniculus carnosus
muscle, and well-formed fibrous connective tissue capsule. Left, Normal nonexpanded tissue. Note the thickness of
the panniculus carnosus muscle compared with that of the treated animal on the right (x200).

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image...

19 • PRINCIPLES OF TISSUE EXPANSION 54

studies demonstrate that there may be an increase in

number of hairs and density proportional with expan-
sion. Clinically, individual follicles do not appear to
be reproduced, but data are still lacking.18 Melanocytic
activity is increased during expansion but returns to
normal within several months after completion of
reconstruction.

Dermis
The dermis decreases rapidly in thickness over the entire
implant during expansion. Thinning is most pro-
nounced in the first several weeks after implant place-
ment and persists for the entire period of expansion.
Dermal thinning persists at least 36 weeks after expan-
sion is completed in human tissue.19
A dense fibrous capsule is formed around the
implant, which becomes less cellular over time. The
capsule is thickest at 2 months of expansion. Pro-
gressive collagenization with well-organized bundles
develops during 3 months. No evidence of dysplastic
changes or loss of normal cell maturation has been
observed. Dystrophic calcification may occur when a
hematoma resolves or when the prosthesis is repeat-
edly traumatized.
Expanded tissue demonstrates a quantitative
increase in collagen content of the dermis. After
expansion, the relative proportions of type I and type
III collagen are not significantiy changed in the dermal-
epidermal or subcutaneous-capsular interface.20
Mitotic activity in the capsule fibroblast is maximum
about 96 hours after expansion. The application of a
constant pressure beyond 96 hours results in progres-
sive decrease in mitotic activity. These studies suggest
that cell proliferation and resultant growth and dif-
ferentiation of the extracellular matrix may be con-
trolled by an appropriate cycle pressure change in the
expander.21
Muscle
Muscle atrophies significantly during the process of
expansion, whether the prosthesis is placed above or
below a specific muscle (Fig. 19-2). The effects on
human muscle after expansion during breast recon-
struction have demonstrated occasional histologic
ulceration. Focal muscle fiber degeneration with glyco-
gen deposits and mild interstitial fibrosis have been
noted. Some muscle fibers show disorganization of the
myofibrils in the sarcomeres.22 Animal studies on the
histomorphologic changes in skeletal muscle suggest
that the expansion of skeletal muscle is not a stretch-
ing process but rather a growth process of the muscle
cell accompanied by an increase in the number of sar-
comeres per fiber. Expanded skeletal muscle repairs
normal muscle architecture, vasculature, and function
after the prosthesis is removed.23 Muscle mass returns
cf> ,
FIGURE 19-2. High-power view of atrophic panniculus
carnosus muscle (arrow) and the adjacent edematous con-
nective tissue 2 weeks after implantation (x400).
to normal levels after removal of the device in human
studies.
The effect of expansion on underlying cranial
bone has been studied in the animal model.24 There
is a decrease in bone thickness and volume in cranial
bone beneath the expander, but bone density is unaf-
fected. An increase in bone volume and thickness
occurs predominantly at the periphery of the expander.
Osteoplastic bone resorption occurs beneath ex-
panders, and a periosteal inflammatory reaction is
seen at the periphery of the expander. Craniosynos-
tosis has not been induced clinically or experimen-
tally. Cranial bone appears to be significantly more
affected than long bone is. Long bone remodeling
begins within 5 days after removal of the expander,
and the long bone is completely normal within 2
months.
Vascularity of Expanded Tissue
The robust vascularity of expanded tissue was clini-
cally evidenced long before laboratory work quanti-
tated its presence (Fig. 19-3). It has been clinically and
histologically demonstrated that a large number of new
vessels are formed adjacent to the capsule.
The content of collagen fibers in existing vessels
initially decreases after expansion. Elastic fibers in
existing blood vessels initially increase, probably as a
response to mechanical stress.

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542 I • GENERAL PRINCIPLES
FIGURE 19-3. Transillumination of expanded human
skin demonstrating intense increase in arterioles and
venules with a dense interconnecting capillary bed. The
proliferation of capillary bed renders the overlying skin
erythematous.
Angiogenesis probably occurs secondary to ischemia
of the expanded tissues. The number of cells express-
ing vascular growth factor is significantly higher than
in nonexpanded similar tissue.25
The increase in vascularity affords expanded tissue
significant functional benefits. Animal studies26 have
shown that flaps elevated in expanded tissue have
significantly greater survival areas compared with
acutely raised and delayed flaps (Fig. 19-4). Similar
studies employing labeled microspheres have demon-
strated an increase of flap survival as well as an increased
blood flow in the expanded tissue.14
Ultrastructure of Expanded Tissue
Electron micrographic studies have confirmed the rel-
atively innocuous nature of soft tissue expansion.27 The
epidermis demonstrates a reduction of intercellular
distance and a significant decrease in the undulation
of the basal lamina compared with normal. The
dermis displays large, compact bundles of collagen
fibers oriented in an orderly parallel fashion over the
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implant surface. Active fibroblasts are identified in the
expanded dermis, and intercellular collagen is identified
in these cells. Myofibroblasts develop in the deep dermis
adjacent to the capsule. Skeletal muscle demonstrates
pressure atrophy with increased mitochondria and
abnormal rearrangement of sarcomeres. Small blood
vessels within the skeletal muscle, however, appear
normal.
Molecular Basis for
Tissue Expansion
The application of mechanical stress to living cells
affects various cell structures and signaling pathways
that are highly integrated (Fig. 19-5).28 Several in vitro
stretching systems have been used to better understand
the molecular events that occur.29
Mechanical deformation forces involve several cel-
lular mechanisms including the cytoskeleton system,
extracellular matrix, enzyme activation, secondary
messages, and ion channels (Fig. 19-6). These
closely integrated cascades are theorized to explain
the generation of new tissue through mechanical
stimulation.30
The cytoskeleton that uniformly exists in the cell
plays a critical role in mediating the transformation
of extracellular mechanical force to intracellular events.
Intracellular tension and cell structure are maintained
by a system of microfilaments within the cytoplasm.
These microfilaments act to transduce signals to adja-
cent cells and play a critical role in initiating trans-
duction cascades within the cell.
Protein kinase C plays a pivotal role in signal trans-
duction. Mechanical strain on cell walls activates inos-
itol phosphatase, phospholipase A2t phospholipase D,
and other messengers. Activation of these components
results in protein kinase C activation. Protein kinase
C is associated with nuclear proteins, suggesting that
intracellular signals can be transmitted to the nucleus.
Protein kinase C activation has been noted in human
cells subjected to strain in vitro.
Many growth factors, including platelet-derived
growth factor and angiotensin II, play a role in strain-
induced cell growth.31 Platelet-derived growth factor
has a well-documented effect of stimulating cutaneous
cell proliferation. Transforming growth factor-P pro-
duction has also been demonstrated in stretch in vitro
models and has been implicated in extracellular matrix
products. Extensive laboratory studies now under
way are attempting to quantitate and determine inter-
relationships of these two complex molecules. These
growth factors and mechanical strain appear to share
several common pathways downstream of the cellu-
lar membrane molecules, such as the cytoskeletal system
and protein kinase families.
Studies have demonstrated that strain-induced cell
proliferation is matrix dependent. 32 Mechanical stress
image...

19 • PRINCIPLES OF TISSUE EXPANSION 543

A B
FIGURE 1 9-4. Barium-injected radiograph of vessels in a random-pattern skin flap in a pig (A) and an expanded flap
in the same animal model (B). A dramatic increase in the vascularity of the expanded flap is evident. (From Cherry CW,
Austad ED, Pasyk KA, et al: Increased survival and vascularity of random-pattern skin flaps elevated in controlled,
expanded skin. Plast Reconstr Surg 1983;72:680.)

deforms the extracellular matrix, which induces IMPLANT TYPES

changes in adhesion complexes such as integrins.
Mechanical strain has been shown to produce alter-
ations in integrin expression.33 These integrins become
effective pathways to mediate extracellular signals to
intracellular molecules.
The Source of Increased Tissue
from Expansion
The increase in skin surface area over the expander
includes normal skin brought in from adjacent areas
as well as new skin generated by increased mitosis.34
Autoradiographic studies using radiated thymi-
dine have demonstrated increased mitotic activity
in the epidermis directly overlying the expansion.35
Serial inflations of the prosthesis result in serial
increases in tritiated thymidine uptake. With deflation
of the implant, a significant decrease in the rate of
the epidermal mitosis below normal baseline occurs.
A wide variety of off-the-shelf and custom implants
of any shape are available from manufacturers.
Radovan's initial expander consisted of a silicone
prosthesis with two valves, each connected to the main
reservoir by silicone tubing. One valve was used for
injection; the other was used as a means to withdraw
fluid. Technologic improvements resulted in a single
valve for both purposes.
The filling reservoir may be incorporated directly
into the prosthesis. Such devices have the advantage
ofavoiding the remote port. The valve in the integrated
prosthesis can be difficult to palpate. Magnetic and
ultrasonic devices can be useful when the valve is
difficult to locate, and metal-finding devices have been
designed. Breast reconstruction with these prostheses
has become popular.
Self-inflating expanders containing osmotic sub-
stances that cause the migration of extracellular water
through the silicone membrane have also been devised.

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Dr.Mustafa D.
544 I • GENERAL PRINCIPLES

w
EGF, PDGF Focal Adhesion Plaques
Extracellular Matrix
FIGURE 19-5. Effects of tissue expansion on surrounding tissue. Strain-induced responses are
mediated by growth factors, such as platelet-derived growth factor, that are known to stimulate
cutaneous cell proliferation. Other growth factors, such as transforming growth factor-p, may stim-
ulate extracellular matrix production. Membrane-bound molecules including protein kinase play a
key role in regulating intracellular signaling cascades. (From Takei T, Mills I, Arai K, Sumpio B:
Molecular bases for tissue expansion: clinical implications for surgeon. Plast Reconstr Surg
1998;101:247.)

None is commercially available at this time. Such
devices have the theoretical benefit of continuous
slow inflation of the prosthesis. Recently released self-
expanding prostheses have rapid fill times and are rel-
atively small in surface area. Minimizing office visits,
less pain, and more rapid expansion are potential
benefits.
Prostheses that expand differentially into any
specific shape, rather than the usual round, are avail-
able. Differential expanders have found most use in
reconstruction of the breast where ptosis and projec-
tion are desired. Low-profile implants that accordion
on themselves were designed to eliminate fold flaw
erosion early in the expansion process. These implants
have not achieved wide acceptance.
Expanders incorporating both saline and silicone
in double-lumen implants have also been devised.
These expanders have been used primarily in breast
reconstruction when a "permanent" prosthesis is
desired.36*38 Such implants have the potential of elim-
inating the second stage of breast reconstruction. Prob-
lems with silicone gel prostheses, however, made these
devices less widely used.
Attempts have been made to incorporate surface
textures and geometries on the expander surface to
immobilize the expander and to decrease capsular
contracture. Textured silicone expanders as well as
polyurethane-covered implants have been devised.
Both of these have the advantage of allowing less capsule
formation to occur and more rapid expansion to
be achieved. Polyurethane-coated implants, despite
significant advantages, are no longer available. New
expanders with surface-bound macromolecules are
being developed and will be available in the future.
These devices will attempt to speed expansion by min-
imizing adjacent scar formation. Molecules that will
form a bacterial-hostile environment are also being
devised. These will decrease "slime" for motion around
implants, thus decreasing the ability of bacteria to resist
systemic antibiotics.
BASIC PRINCIPLES
Tissue expansion is a protracted procedure that may
involve temporary but significant cosmetic deformity.
In general, tissue expansion is well tolerated by emo-
tionally stable patients of all ages. Noncompliant or
mentally impaired patients are obviously poor candi-
dates. Smokers have a higher risk of complications.
Tissue expansion is generally best performed as a

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Dr.Mustafa D.
 image...

PRINCIPLES OF TISSUE EXPANSION 545

Mechanical stimulation
Extracellular |
I N
Adhesion complex / Integrin

Cell membrane Tyrosine kinase

G-protein Talin / Vinculin
cAMP/PKA

1/ PGEj

Protein synthesis

Oxygen tension

MEKK/MEK

i
MAPK/JNK/P38

Proliferation
FIGURE 19-6. Schematic of possible signal transduction pathways induced by mechanical strain. Transduction path-
ways are activated by numerous strain-induced signals transmitted through various membrane receptor or membrane
ion channels. Terminal enzymes activated by these intracellular cascades transduce these signals into the nucleus.
cAMP, cyclic adenosine monophosphate; DAG, diacylglycerol; IP3, inositol 1,4,5-triphosphate; JNK, c-Jun amino ter-
minal kinase; MAPK, mitogen-activated kinases; MEK, MAPK kinase; MEKKf MAPK kinase; PCE2, prostaglandin E2;
PKA, protein kinase A; PKC, protein kinase C; PLC, phospholipase C.

secondary reconstructive procedure rather than in the
acute trauma period. Expansion can be performed adja-
cent to an area of an open wound before definitive
closure but at the risk of infection, extrusion, and less
than optimal results. Tissue expansion is best suited
to those patients who require definitive optimal cov-
erage when time is not of the essence.
The key to successful expansion is meticulous plan-
ning before any incision is made. The proposed type
of flap—advancement, rotation, or interpositional—
that is to be expanded should be carefully considered
to minimize risk and to optimize cosmetic recon-
struction. The simpler the flap, the less the potential
for complication. The length and position of result-
ant scars significantly determine the overall cosmetic
postoperative result. Ideally, planning is done so that
aesthetic units are reconstructed and scars are in min-
imally conspicuous locations.
The size ofthe implant selected should closely relate
to the size and shape ofthe donor surface. An implant
equal to or slightly smaller than the donor area is
selected. Less importance is placed on the specific
volume ofthe implant than on the overall base size of
the device. Hyperinflation of the prosthesis is easily
accomplished to several times the manufacturer's des-
ignated volume with minimal risk. The wide variety
of size and shapes of implants available off-the-shelf
will accommodate most donor sites. On occasion, a
custom-fabricated implant may be necessary.
The choice of an integrated or distal inflation port
should be considered. Remote filling ports have the
advantage of minimizing the risk of implant puncture
during inflation. The filling port should be localized
in subcutaneous tissue where it is easily palpable and
under stable skin. Bone prominences are avoided. The
prosthesis tubing should avoid the incision through
which the implant is placed and should not traverse
joints. It is occasionally possible to position a filling
port in a relatively anesthetic area to minimize
discomfort.

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546 I • GENERAL PRINCIPLES
Remote filling ports can be placed external to the
skin. These are particularly useful when parents or non-
medical personnel are to inflate the device. In such cases,
the connecting tubing should be tunneled a significant
distance from the prosthesis. Cultures of implants
with external valves revealed an 82% colonization
rate. Unless permanent implants are to be placed, this
colonization is well tolerated and produces few
complications.
Expanders are usually placed beneath the skin and
subcutaneous tissue above fascia. When the subcuta-
neous tissue is thin or the risk of extrusion significant,
prostheses may be placed under muscle. In general,
multiple small expanders are better than one large
expander. Inflation of multiple prostheses proceeds
more rapidly and complications are fewer. Multiple
expanders also allow the surgeon to vary the plan for
reconstruction after expansion has been achieved.
The prosthesis is placed through an incision that
will minimize the risk of compromise for flap devel-
opment. Optimally, incisions are incorporated into
tissue that will become one margin of the flap. Radial
incisions are preferred by some surgeons to minimize
tension on the suture line and to avoid extrusion.
Implant Inflation
Implants should be partially inflated immediately after
wound closure. This allows closure of "dead space" to
minimize seroma and hematoma formation. It also
smoothes out the implant wall to minimize risk of fold
extrusion. Enough saline is placed to fill the entire dis-
section space without placing undue tension on the
suture line. Tension on the suture line will be greater
when incisions are parallel to the direction of expan-
sion and less when incisions are perpendicular to the
direction of expansion.
Serial inflation usually starts 1 to 2 weeks after initial
placement, although inflation schedules can be indi-
vidualized to the specific case and the tolerance of the
patient. Inflation reservoirs seal best when a 23-gauge
or smaller needle is used. A 23-gauge butterfly intra-
venous needle is especially useful; it allows the patient
some motion without dislocation of the needle.
Frequent small-volume inflations are better toler-
ated and are physiologically more suited to develop-
ment of adequate overlying tissue than are large
infrequent inflations. For practical purposes, most pros-
theses are inflated at weekly intervals. On occasion,
accelerated inflation schedules may be followed.39 In
children with external ports, small-volume inflation
at 2- to 3-day intervals is well tolerated. Individual
inflations proceed until the patient experiences dis-
comfort or blanching of the overlying skin. In hypoes-
thetic areas, objective changes in flap vascularity must
be evaluated with particular care. Although a variety
of pressure transducers, oxygen tension monitors, and
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Dr.Mustafa D.
other devices are available as adjuncts to inflation,
objective inspection of the patient's response is usually
a reliable indicator of appropriate inflation. Serial
inflations proceed until an adequate amount of soft
tissue has been generated to accomplish the specific
surgical goal.
Overinflation is helpful when permanent implants
are to be placed, particularly in breast reconstruction.
Overinflation of 20% to 30% is usual so that after per-
manent implant placement, some ptosis of the breast
can be developed. In general, the breast is expanded
for approximately 4 to 6 months before the perma-
nent implant is placed. Long-term studies indicate
that this may not be as useful as originally thought,
however, because contraction gradually occurs.40
TISSUE EXPANSION IN SPECIAL
CASES AND SPECIFIC
ANATOMIC SITES
Burns
The use of tissue expansion in reconstruction of burns,
particularly about the scalp and face, has revolution-
ized treatment of these patients. Because there is almost
always a paucity of tissue after burns, reconstruction
should be carried out after all burns have thoroughly
healed and scars have matured. Planning is particu-
larly important in these cases so that once flaps are
rotated, suture lines are not parallel to previous scars.
Significant late distortion and contracture may result
in excessive scars placed in burned tissue, particularly
in the facial area.
Skin that has suffered a partial-thickness burn or
that has been scarred by adjacent burns is attenuated
and is more susceptible to expansion.41 Incisions can
be placed in previous scars, but the scar should be
mature and relatively thick so that extrusion does not
occur. The placement of multiple prostheses of smaller
volume is better than one large prosthesis. Periopera-
tive antibiotics and meticulous preparation are always
used in burn patients because the incidence of infec-
tion is higher in these patients.
Tissue Expansion in Children
Skin and soft tissue are always thinner in children than
in the adult. They are probably better vascularized but
less resistant to trauma. Tissue expansion has a higher
complication rate in children than in the adult.42 This
is particularly true in the head and neck area with the
exception of the scalp. Expansion of the facial areas
and neck can be particularly difficult. After age 5 years,
most children are able to cooperate adequately, and
complication rates decrease. In many children, an exter-
nal reservoir is used to minimize the amount of trauma
required with injections. Application of EMLA to the
image...
skin over the buried injection port is also helpful in
minimizing discomfort. Small-volume inflation at fre-
quent intervals is especially useful in children because
the amount of pain generated is considerably less. As
in all cases, planning should be done meticulously so
that the flaps generated will result in anatomic unit
reconstruction as much as possible. With growth, con-
tracture may occur, particularly about the mouth and
around the orbits, and revision will be required.
Expansion of Myocutaneous Flaps
Myocutaneous flaps are the standard of care for the
treatment of large defects, particularly when bone and
vital structures are involved. The territories of stan-
dard flaps are well described. These territories can be
considerably enlarged by placing an expander beneath
the standard myocutaneous flap, and an extremely
large flap can be developed during a short period.
Expansion increases the vascularity of the flap and
allows a large adjacent random area to be carried with
the original flap. 43 The vascular pedicle of such flaps
remains intact and may in fact be elongated, thus
allowing flaps to be transferred farther. Myocutaneous
flaps, such as the latissimus dorsi and pectoralis, can
be expanded to almost double their surface area, allow-
ing coverage from almost any defect on the abdomen
or thorax. 44
One edge of the myocutaneous flap is selected for
implant placement, and care is taken not to injure the
vascular pedicle. Expanders of up to 1000 mL can be
placed beneath such flaps and rapidly expanded. The
expanded myocutaneous flap generated can then be
transferred either as a pedicled flap or as a free flap.
Bilateral latissimus dorsi myocutaneous flaps can be
expanded and moved to the midline to cover large
meningoceles or the vertebral column. The expansion
prostheses in these cases are placed under the latis-
simus dorsi muscle through incisions in the lateral
margin of the muscle. Such expanded flaps not only
provide coverage of other donor defects but preserve
the function of the muscle.
Expanded Full-Thickness
Skin Grafts
Full-thickness skin grafts are particularly useful in
resurfacing areas of the face and hands. The limited
areas from which full-thickness grafts can be harvested
without creation of a donor defect make their use
infrequent. The placement of a large tissue expander
beneath the donor site can result in a full-thickness
graft that can easily cover large areas of the face or the
entire hand or foot. Expanded full-thickness grafts
are extremely resilient and have been shown to grow
in children over time. The rate of contracture is
significantly less than that of split-thickness grafts.
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Dr.Mustafa D.
19 • PRINCIPLES OF TISSUE EXPANSION 547
The best color matches are generated when the full-
thickness graft is harvested as close as possible to the
recipient site. Care must be taken so that hair-bearing
tissue is not transferred to an area that normally has
no hair. The periorbital area and the area around the
mouth are particularly well suited to reconstruction
with expanded full-thickness grafts harvested from the
supraclavicular area.
Expanders with a surface area equal to the donor
site are placed through peripheral incisions. The pros-
thesis is then inflated to an adequate volume. A tem-
plate is then made of the recipient site and transferred
to the expanded donor area, and the full-thickness graft
is harvested. The graft harvested should be approxi-
mately 10% to 15% larger than the recipient area to
allow some contracture. The prosthesis is then removed
and the donor site closed primarily. Closing of the
donor site should be done so that the resulting scar is
as innocuous as possible. The capsule is left intact.
Expanded full-thickness skin grafts require more
immobilization in the recipient site than split-
thickness skin grafts do. A bolster dressing or ideally
a VAC sponge dressing is required. The graft is sutured
in place and a VAC sponge placed over the graft; 125
mm Hg of negative pressure is maintained for 4 days.
Successful take of such grafts with this technique is
extremely high.
Reconstruction of the Head
and Neck
The head and neck area contains many specialized
tissues that must be matched appropriately to achieve
optimal aesthetic reconstruction. Aesthetic recon-
struction is maximized by mobilization of adjacent local
tissues rather than by transfer of distant tissues with
poor match of color, texture, or hair-bearing capabil-
ity. Tissue expansion allows optimal aesthetic recon-
struction by use of a similar adjacent tissue area to
reconstruct a defect without creation of a donor site.10,45
The face can be subdivided into five tissue-specific
areas. The scalp is unique in that it contains specific
hair-bearing qualities that cannot be mimicked by any
other tissue of the human body. The forehead is a con-
tinuation of the scalp but is specific in that it has thick
skin containing a large number of sebaceous glands,
but no hair. The nose is embryologically related to the
forehead, and the color, texture, and sebaceous gland
content closely mimic the forehead. The lateral cheek
areas, neck, and upper lip have fewer sebaceous glands;
the skin is thinner, and the hair-bearing pattern is
significantly different in quality and quantity from that
on the remainder of the body. The skin of the perior-
bital areas is extremely thin and pliable, containing a
minimal number of sebaceous glands.
Because of the limited amount of tissue on the
human face, procedures must be planned carefully and
548 I • GENERAL PRINCIPLES
reconstruction accomplished correcdy at the first
attempt. Correct planning should take into consider-
ation the area and shape of the defect, quality of the
remaining tissue of the aesthetic unit, preexisting scars,
and reconstructive needs of other areas of the head
and neck. All alternatives for potential reconstruction
should be carefully considered before the placement
of any prostheses. If there is a chronic infection, the
presence of fistulas, or the need to reconstruct facial
mass, other reconstructive alternatives may be better
suited.
Reconstruction of the Scalp
Tissue expansion is the ideal procedure for recon-
struction of scalp defects (Fig. 19-7).46 Expansion of
the scalp is well tolerated and is the only procedure
that allows development of normal hair-bearing tissue
to cover the areas of alopecia. The amount of scar and
deformity generated is considerably less than with pre-
vious procedures, such as serial reduction and complex
rotation flaps.
Although some animal studies have demonstrated
an increase in hair follicles during tissue expansion,
our clinical experience is that no significant number
of new follicles are formed. Rather, existing follicles
are redistributed to a larger surface area. Because of
the finite number of follicles, attempts should be made
to redistribute them as homogeneously as possible. To
accomplish this, large or multiple expanders, expand-
ing large areas of the remaining scalp, produce the best
results. Hair follicles can be separated by a factor of 2
without producing noticeable thinning. The darker the
hair, the more visible the thinning. Individuals who
have large defects and require extreme expansion may
achieve better results by lightening of the hair with
dyes.
Although there is considerable overlap in the vas-
cular territories of the scalp, the incorporation of one
or more major vessels of the scalp optimizes recon-
struction. Flaps should be well vascularized to ensure
maximum growth of hair. Planning is therefore of
importance, as is consideration of scar and previous
areas of trauma. Advancement or rotation flaps achieve
the best results, particularly when the anterior hair-
line is reconstructed. Simultaneous expansion and
mobilization of the forehead may also help achieve a
normal hairline. When multiple defects or large defects
exist, multiple expanders under most of the normal
hair-bearing scalp are almost always better than one
large expander.
Previous scars and incisions can be used for place-
ment of the prostheses. Once the galea is encountered,
dissection can proceed widely with a blunt dissector.
It is not unusual to mobilize most of the remaining
scalp so that the prostheses are well accommodated.
Individual pockets are not necessary for multiple
Bin kilometrelik bir yolculuk ilk adimla baslar.•
Dr.Mustafa D.
expanders, but care should be taken to fix the inflation
reservoirs so that they do not migrate into a common
pocket. Prostheses with incorporated parts can also
be used but can be uncomfortable because of their
bulk. Inflation reservoirs can be placed at the vertex
of the scalp or in the forehead. Care should be taken
not to place them where pressure is applied during
sleep.
Expansion of the scalp is initially uncomfortable.
It is best to use frequent small saline injections as
opposed to infrequent large injections. After several
weeks, the scalp loosens, and large amounts of saline
can be infused without difficulty. Most scalp expan-
sions can be accomplished in 6 or 8 weeks, particu-
larly when multiple expanders are used. In children,
some erosion of the skull can be evidenced on radi-
ography and occasionally clinically. Increased thick-
ness of the subcutaneous tissue at the edge of the
implant space is frequently palpable. Experimental
work as well as clinical observation shows that this
resolves once the expander has been removed. Expan-
sion should best be delayed in children until they are
approximately 1 year of age. By this time, the skull is
solid enough that significant erosion is not a cause for
concern.
Once adequate expansion has been achieved, the
prostheses arc removed through the incisions through
which they were originally placed or the margin of
the flap to be moved. Flaps should be designed for
advancement, transposition, or rotation. Every attempt
should be made to minimize transection of the major
vessels of the scalp; this will allow faster healing and
better regeneration of hair follicles. Large areas of the
scalp are mobilized and positioned by temporary
staples. Dog-ears are left in place because they subside
over time. Removal or cutting of capsule and galea
should be avoided. Monofilament absorbable sutures,
such as Monocryl, are used to tack the flaps in posi-
tion. The wounds are then closed with subcuticular
Monocryl sutures, which are left in place until they
dissolve. This minimizes scar formation, hair loss, and
retraction.
When large areas of the scalp must be resurfaced,
it may be impossible to achieve an adequate amount
of tissue with one expansion. In these cases, serial
expansion can be accomplished (Fig. 19-8). After the
initial expansion, flaps are advanced as far as possi-
ble. Lesions or areas of alopecia are excised only after
the flap has been advanced. The expander is then left
in place under the flap, and after several months, the
scalp is re-expanded. Adults tolerate three or four
sequential expansions without difficulty. Infants and
children may thin excessively after two expansions;
an interim of 8 to 12 months is optimal for a later
expansion.
In growing children, scars frequently widen over
time. These require revision when they become a
image

FIGURE 19-7. A A young woman with

a split-thickness skin graft of one quarter
of the scalp after excision of a nevus. A
single 450-mL expander was placed under
the entire left scalp. B, At the second pro-
cedure, the flap was advanced and the
split-thickness skin graft removed in a
single stage.

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Dr.Mustafa D.
550 I • GENERAL PRINCIPLES

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I'eVtfttf'SeldW image...
cosmetic problem, optimally after 16 to 18 years of age.
Scalp that has been vigorously expanded may lose some
hair follicles, but these usually regrow. Twelve months
should pass before any areas of alopecia are con-
sidered permanent. Long-term studies have demon-
strated no detrimental growth of the skull in children
who have been expanded in infancy (Fig. 19-9).
Male Pattern Baldness
Tissue expansion can be used as an adjunct for scalp
reduction or the development of flaps for male pattern
baldness.47"49 Expansion allows the homogeneous dis-
tribution of the remaining hair follicles and reduces
scalp tension so that reductions are achieved under
less tension.
In patients with vertex baldness, the remaining tem-
poral and occipital scalp can be expanded during 2
months. Expanders are placed through incisions that
would normally be used for scalp reduction. Cosmetic
deformity during this process may be significant after
the first several weeks. At the second procedure, the
scalp is advanced as far as possible and the area of
alopecia removed.
Individuals who are unable to accept the deformity
that occurs with single large expansions can be seri-
ally expanded and undergo serial scalp reduction. In
these patients, the prosthesis is inflated until defor-
mities become visible. The expanders are deflated and
the hair-bearing flaps advanced as far cephalad as pos-
sible. The prostheses are left in place, and a second or
third expansion is carried out until the entire bald area
is removed.
Expansion can also be used to greatly increase the
size of standard transposition flaps. Simple expansion
and advancement in cases of anterior baldness produce
a straight and unnatural hairline. Transposition flaps,
as described by Juri and others, result in a more normal
hairline. They are limited in size and may require
multiple delays to ensure adequate hair viability.50
Expanders placed beneath the temporoparietal area can
dramatically increase the size of Juri flaps and increase
their safety. Bilateral flaps, one transposed behind the
other, will cover the entire forehead and a significant
portion behind it. The bilateral advancement trans-
position flap is especially efficacious in transposing a
large amount of hair to the forehead.51
FIGURE 1 9-8. A, A child born with a giant hairy nevus
occupying one third of the scalp. B, The remaining normal
scalp was expanded, allowing removal of more than half
of the lesion. C, The original expander was left in place
and 4 months later re-expanded, removing the remain-
ing lesion. D, The patient is shown 1 year after expan-
sion. E, The patient 10 years after expansion with stable
hairline and normal hair distribution.
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Dr.Mustafa D.
19 • PRINCIPLES OF TISSUE EXPANSION 551
Reconstruction of the Forehead
The forehead is anatomically and histologically iden-
tical to the scalp with the exception of the number of
hair-bearing follicles. Reduction or gain of 15% to 20%
of the surface area of the forehead is not readily ap-
parent with appropriate hair styling. The aim of
reconstruction to the forehead should be to achieve
symmetric brow position and a normal hairline.
Prostheses are usually placed in the forehead
through an incision in the scalp. The prostheses are
placed beneath the frontalis muscle because this plane
is safe and a well-vascularized flap can be developed.
Multiple expanders are usually necessary so that ade-
quate tissue can be mobilized and still leave the brows
in an appropriate symmetric position. Expansion is at
first difficult and uncomfortable, but as in the scalp,
once a certain point is reached, the expansion proceeds
rapidly. Flaps may be developed in any direction but
are usually simple advancements. The adjacent scalp
should be mobilized at the same time so that a normal
hairline can be reconstructed.
If the entire forehead must be reconstructed, an
expanded full-thickness graft from the neck is optimal.
These grafts are secured in place with negative-
pressure devices for at least 4 days.
Expansion of the forehead is useful in many cran-
iofacial anomalies with low hairlines. Expansion of the
remaining forehead is accomplished and moved into
a cephalad direction. The intervening hair-bearing scalp
is excised. Fixation of the expanded forehead to the
underlying skull with small screws reduces the amount
of retraction.
Reconstruction of the Lateral Face
and Neck
The lateral facial areas and neck contain essentially
the same type of skin. This skin has hair-bearing poten-
tial, is relatively thin, but contains numerous oil and
sebaceous glands. It is much thinner than the fore-
head and nose. Expansion of the neck can be accom-
plished to develop a large Mustardd-type rotation flap
for facial reconstruction. In children, there is a higher
risk of extrusion problems in expansion of this area
of the face (Fig. 19-10). In adults, such reconstruc-
tion can be accomplished with relative ease. The flap
is based inferiorly and medially. The prosthesis is
inserted through a preauricular face lift-type incision.
The platysma should not be incorporated because
this exposes the marginal mandibular nerve to trauma
and restricts flap advancement. Reservoirs are usually
placed in the neck or behind the ear. The pros-
thesis is then inflated as tolerated by the patient.
Despite placement of the prosthesis over the carotid
artery and jugular vein, few complications have been
encountered.
552 I • GENERAL PRINCIPLES

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T W K ^ d d w image...
Once an adequate amount of tissue has been gen-
erated, the Mustarde flap is elevated. This is done
through a preauricular incision that is carried in front
of the hair-bearing scalp and then onto the lateral
orbital area above the lateral canthus. The flap is then
rotated medially and superiorly to cover whatever areas
of the cheek require resurfacing. In general, it is best
to rotate this flap and secure it in place with tempo-
rary staples before the recipient area is excised. The
medial scar in this flap is best not carried beyond the
lateral commissure because scars below that area tend
to distort the mouth. The flap is suspended both medi-
ally and laterally at a level above the canthi so that ectro-
pion does not develop. If coverage is required for the
periorbital area, this is done as a separate aesthetic unit
graft, usually a full-thickness graft from the supra-
clavicular area.
The lower half of the face and the neck are aes-
thetically the same unit. Hair distribution, sebaceous
gland density, and skin thickness are similar. Defects
of the lower face and neck can be interchangeably recon-
structed by expanding either the lower face or the neck.
The neck is expanded superficial to the platysma
muscle, and despite placement of the prosthesis directly
above major arteries and veins, complications are few.
Most frequently, the neck is expanded and the flap
advanced into the lower face. Bony reconstruction of
the mandible and maxilla can be performed with grafts
placed beneath the expanded flap.
Bilateral expanders are usually placed in the range
of 400 to 500 mL. Once an adequate amount of tissue
is generated, the flaps can be brought superior to cover
the lower edge of the face, medial to cover the central
portion of the neck> or laterally in the neck as needed
(Fig. 19-11). When flaps are brought from the neck
FIGURE 19-9. A, An infant was born with severe aplasia
cutis congenita involving the scalp, skull, and derma,
leaving exposed brain. B, The brain was covered imme-
diately after birth with two large scalp-forehead advance-
ment flaps. Absence of the cranium prevented the patient
from attending school. C, At age 4 years, the flaps were
separated from the underlying brain; a reinforced poly-
ethylene sheet was secured to the cranial defect, an
expander was placed over the sheet, and the scalp was
expanded during 3 months. D, The cranium was recon-
structed with multiple split rib grafts within the expanded
capsule. E, One year later, the scalp was re-expanded to
more than 1000 mL over the reconstructed cranium. The
skin graft was excised, and the scalp and forehead flaps
were repositioned appropriately. The reconstructed skull
suffered no ill effect during the re-expansion. F, One year
postoperatively, the patient has an intact skull, normal
scalp, and normal forehead coverage. This patient has
been stable with no secondary procedure for 14 years
after the reconstruction.
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Dr.Mustafa D.
19 • PRINCIPLES OF TISSUE EXPANSION 553
into the face, it is important to secure the flap with
permanent sutures to the deep muscles at the com-
missures of the mouth. If this is not accomplished,
incontinence may develop later. Form-fitting neck
collars may be necessary to secure the expanded flap
in place over the neck after a portion of it has been
brought onto the face.
Nose Reconstruction
Reconstruction of major defects of the nose, includ-
ing total nose reconstruction, maybe facilitated by pre-
expanding the forehead skin. Previously, inadequate
amounts of tissue and difficulty closing the forehead
could be anticipated. When total nose reconstruction
is performed, expansion of the forehead allows the
development of large flaps that are well vascularized
as well as primary closure of the donor site. Because
the color and texture of the forehead are ideally suited
to reconstruction of the nose, this procedure makes
reconstruction of any nasal defect possible. Any of the
standard forehead flaps can be employed in conjunc-
tion with expansion. If lining is also necessary, expan-
sion of a forehead or Converse scalping flap develops
enough tissue to allow folding of the expanded tissue
on itself.
The supraorbital and supratrochlear vessels are
located by Doppler examination, and the nasal flap is
based on either of these axial vessels. Prostheses are
best placed beneath the frontalis muscle through an
incision in the hair. Expansion of the entire forehead
with a 400- to 600-mL prosthesis generates an ade-
quate amount of tissue for total nose reconstruction
and primary forehead closure. At the second proce-
dure, the expander is removed and the flap, including
the capsule, is rotated inferiorly. Approximately 2 cm
above the supraorbital rim, the posterior capsule is
incised, and development of the flap is continued in a
subperiosteal plane. This allows mobilization of the
flap into the orbit, almost down to the canthus.
Bony and cartilaginous supporting structures of the
nose are critical to avoid contraction of the expanded
tissue. Early experience in use of expanded forehead
tissue was unsuccessful because the underlying bony
and cartilaginous structure was not adequate. A cranial
bone graft or rib graft is taken to reconstruct the dorsum
of the nose. This is secured to the remaining nasal bone
or by a plate to the skull. The nasal cartilage is recon-
structed with cartilage from the conchal bowl bilater-
ally. Thinly carved rib cartilage is also useful if the ear
cartilage is inadequate. Nasal stents are used for 3 to
4 months to maintain a patent airway while the flap
matures.
The forehead flap is divided and inset approximately
2 weeks after rotation. Some swelling and contracture
of tissue may occur, but major touch-ups are infre-
quent (Fig. 19-12).
image...

554 ! • GENERAL PRINCIPLES

y r c

FIGURE 19-1 0. A, A 4-year-old child with a giant hairy nevus of the face. The neck was expanded to 450 mL with
a prosthesis above the platysma in the neck. B, A Mustarde cheek rotation flap was rotated to the aesthetic unit of
the lateral face. C, At a third procedure, the remaining nevus in the nasolabial fold and nose was primarily excised.
Nevus remaining on the lower eyelid was reconstructed with an expanded full-thickness graft from the neck. No other
reconstructive procedures were necessary in this child, who is now 17 years of age. (From Argenta L Controlled tissue
expansion in reconstructive surgery. Br J Plast Surg 1984;37:520.)

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Dr.Mustafa D.
 9 • PRINCIPLES OF TISSUE EXPANSION 555

FIGURE 19-1 1, A, This young man sustained extensive burns over the face, but the neck was largely spared.
B, Bilateral large expanders were placed in the neck, and the entire neck and upper chest were expanded dramati-
cally. C, The area of burned skin over the lower face was excised and the neck flap advanced superiorly. The capsule
was secured firmly to the muscle on the lateral commissures to minimize later distortion of the mouth. D, The patient
2 years later. The upper lip has been reconstructed as an aesthetic unit from temporoparietal flaps.

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
556 i • GENERAL PRINCIPLES

FIGURE 19-1 2. A, This woman had her nose resected for a mucosa melanoma. Three years later, reconstruction
was begun by placement of a 450-mL expander in the forehead. B, At the second procedure, the infrastructure of the
nose was made with a cantilever bone graft and bilateral conchal cartilage grafts. C, The forehead flap was turned
down in the subperiosteal plane to the level of the medial canthus. D, The distal third of the flap was markedly thin so
that the skin could be turned on itself to recreate nasal lining. E and F, The patient 11 years after reconstruction with
a functional breathing nose.

Periorbital Reconstruction with recommended. Replacement of aesthetic units—the

Expanded Full-Thickness Grafts
The periorbital area contains skin that is soft and pliable.
It contains few glands and no hair. Unfortunately, there
is little tissue in the periorbital area that can be expanded
or moved easily.
When significant areas require reconstruction, full-
thickness skin grafts from expanded donor sites are
entire periorbital area or the upper or lower perior-
bita—gives the best result. Grafts should be harvested
from skin as close to the orbit as possible. The supra-
clavicular area contains soft pliable skin that mimics
the orbital skin.
An expander is placed subcutaneously in the supra-
clavicular area above the platysma. When an adequate
expansion is achieved, a template of the recipient site

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Dr.Mustafa D.
VtSWttf'SelcrKf image...
is increased 15% to 20% and then harvested from the
expanded donor site. The expander is then removed
and the donor site closed primarily.
The expanded skin graft is thinned to dermis and
sutured to the recipient site. The site is immobilized
with tie-over dressing or a negative-pressure device.
Long-term results have been remarkable in that this
tissue grows with children, scar is minimal, and sec-
ondary reconstruction is infrequent.
Reconstruction of t h e Ear
Most cases of microtia and trauma ear deformities can
be reconstructed without expansion. Expansion is
helpful when there is insufficient skin and soft tissue
for reconstruction. As with all ear reconstructions,
a child should be approximately 6 years of age before
reconstruction is begun. A custom or rectangular
expander is placed beneath the remaining non-hair-
bearing tissue adjacent to the remnant.52 The prosthesis
is then expanded and left in place for approximately
3 months. This allows significant thinning of the over-
lying skin and tissue maturity that will result in minimal
secondary distortion due to contracture.52
The expansion prosthesis is best placed through an
incision in the postauricular hair-bearing tissue, pre-
serving the temporoparietal fascia for possible later
needs. Once adequate tissue has been generated, the
framework is reconstructed with carved costal carti-
lage with some exaggeration of the bulk of the
infrastructure. This minimizes distortion because it
conforms to the cartilage. Silicone and other synthetic
frameworks give excellent initial results; they are
fraught with late complications. In general, autologous
tissues are recommended for ear reconstruction.
Postmastectomy Breast
Reconstruction
Breast reconstruction techniques have continued to
evolve during the last decade, and with refinements
in the techniques for autologous tissue transfer, the
aesthetic standards for breast reconstruction have
increased. Tissue expansion, however, remains an
important modality in breast reconstruction because
of its simplicity compared with some of the more
complex procedures available for autologous tissue
transfer. Use of tissue expansion and breast implants
remains the most common method for postmastec-
tomy reconstruction in the United States. With
continued refinements in surgical technique for
mastectomy, preservation of the pectoralis major
muscle and its innervation, less radical excision of skin
with skin-sparing mastectomy, and preservation of the
inframammary fold, more patients with qualitatively
good chest wall skin and soft tissue are suited to expan-
sion techniques. Only small-breasted women are
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Dr.Mustafa D.
19 • PRINCIPLES OF TISSUE EXPANSION 557
candidates for placement of a breast implant without
pre-expansion, so that most postmastectomy patients
may at least be considered candidates for reconstruc-
tion with tissue expansion.
Placement of an expander prosthesis for breast
reconstruction is a simple, straightforward procedure.
It adds little operative time after mastectomy in the
case of immediate reconstruction and does not prolong
the postmastectomy hospitalization. Delayed recon-
struction with a tissue expander can be done as an out-
patient procedure or with minimal hospitalization. It
is ideally suited to both elderly patients and those who
wish a minimal postoperative recovery. Tissue expan-
sion allows ideal color and texture match of the recon-
structed breast with the remaining chest wall because
the breast is generated from existing chest wall skin.
Breast reconstruction with tissue expansion tech-
nique usually requires two operative procedures. In
the first procedure, the tissue expander is placed
through the original mastectomy scar, avoiding addi-
tional scarring. Removal of the tissue expander and
placement of the permanent implant are also accom-
plished through a straightforward approach and can
be done under general or local anesthesia in an out-
patient setting. If the expander is less than ideally posi-
tioned, the second procedure will be more complicated,
requiring capsulotomy or capsulectomy. After place-
ment of the permanent implant, there is some shift-
ing and settling of the reconstructed breast; in most
instances, nipple reconstruction is best delayed for
several months. The most significant inconvenience
of reconstruction with tissue expansion relates to the
frequent visits required to expand the device fully.
Patients are seen weekly, and this process usually con-
tinues for 2 months. If the patient has a large con-
tralateral breast, inflation may need to continue longer.
THE EXPANDER DEVICE
In recent years, expanders with an integrated valve have
become the expanders of choice. The valve is located
subcutaneously in the upper pole of the breast. It is
easily palpable and has a metal backing to prevent injury
to the attached expander. The integrated valve avoids
the need for a separate pocket laterally and subcuta-
neous tunnels for the connecting tube. It avoids the
complications associated with a distal port, including
rotation and extrusion of the port, and mechanical
problems related to the connecting tubing, such as
kinking and leaking.
The textured silicone implant has been an impor-
tant advance in breast reconstructed by tissue expan-
sion. It is imperative that the expander be placed in
the ideal position to match the contralateral breast.
The textured surface enables tissue ingrowth and adher-
ence of the capsule, which in turn immobilizes the
implant. The immobility of the textured implant
558 I • GENERAL PRINCIPLES
enables a more anatomic expansion of the overlying
tissue and enables more expansion in the inframam-
mary fold area to help establish a fold with some degree
of ptosis. Differential expanders to develop projection
and ptosis are also available. Long-term studies,
however, reveal that implants tend to assume a round
shape over time regardless of the original geometry.
SURGICAL TECHNIQUE
Correct positioning of the expander reduces the need
for secondary reconstructive procedures. It is impor-
tant that the inframammary fold and the extent of
underminingbe marked with the patient in an upright
position in permanent ink before induction of
anesthesia.
Radovan's initial technique placed the expander in
the subcutaneous space above the pectoralis muscle.53
As with all reconstructions in this plane, the frequent
result was a firm, round breast with less than an ideal
cosmetic appearance. Most surgeons currently place
expanders and prostheses beneath the chest wall
muscle.54'57
Breast reconstruction expanders may be partially
or totally submuscular. Complete submuscular cover
requires elevation of the pectoralis major muscle, the
anterior edge of the serratus anterior muscle, and the
origin of the anterior rectus abdominis muscle. If
the implant is placed only under the pectoralis, the
pectoralis major muscle is elevated, and the lower third
of the pocket includes only skin and subcutaneous
tissue. Most authors agree that subpectoral placement
is sufficient for secondary breast reconstruction.58 In
the case of immediate breast reconstruction, complete
muscle coverage is more important because it com-
pletely isolates the implant from the overlying mas-
tectomy wound. Should there be skin necrosis with
loss of mastectomy flaps, wound dehiscence, or delayed
healing—especially in previously irradiated chest
walls—or a cellulitis, a totally submuscular implant
may be salvaged, whereas a partially submuscular
implant will be lost.
General anesthesia is preferred, although local
anesthesia with sedation can be tolerated by some
patients. The hands are positioned on the iliac crest,
thus removing tension from the pectoralis muscle and
facilitating dissection beneath it. The most lateral aspect
of the patient's original mastectomy scar is used for
placement of the expander. Dissection is carried down
to the pectoralis muscle, which is split in the direction
of its fibers several centimeters from the lateral border.
Splitting of the muscle allows better closure than can
usually be achieved by dissecting laterally to the lateral
margin of the muscle. Dissection beneath the pectoralis
is done bluntly down to the level of the serratus, where
dense adhesions occur and require sharp dissection.
Electrocautery is usually employed at this point. A
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Dr.Mustafa D.
round inflatable prosthesis of appropriate size is
placed. The base of the prosthesis should be slightly
larger than the base of the opposite breast. The base
size of the prosthesis is more important than its actual
volume because the prosthesis may be overinflated. If
prostheses with distant reservoirs are used, the inflation
reservoir is ideally placed in the subcutaneous space
in the axilla or beneath what will be the patient's
brassiere line. The muscle is closed with absorbable
sutures, and saline is infused until mild tension of
the overlying musculature is observed. Subcuticular
monofilament sutures are used for skin closure and
left in place for at least 1 month.
Inflation follows the general plan for expansion as
previously described. Inflation of the expander is ini-
tiated 7 to 10 days after placement. The patient returns
at weekly or biweekly intervals for serial percutaneous
inflation with a 23-gauge butterfly needle if a remote
port is used or a 21 -gauge needle for an integrated valve.
Care is taken at each inflation not to overinflate the
expander, causing unnecessary discomfort. The
expander should be inflated until the overlying skin
and subcutaneous tissues feel firm. If the patient expe-
riences significant discomfort, saline is withdrawn until
the patient is comfortable. During this period, the over-
lying skin frequently becomes hyperemia This usually
resolves after inflation has been completed. After vol-
umetric symmetry with the opposite side is achieved,
hyperinflation of at least 250 to 400 mL is carried out.59
If a large amount of ptosis is to be developed or exten-
sive repositioning of the breast is necessary, additional
hyperinflation may be required. The fully expanded
prosthesis should be left in place for 3 to 4 months so
that natural ptosis of the breast will develop and sym-
metry with the mature breast on the opposite side will
evolve. Expanders may be left in place for many months
or even years before being exchanged for permanent
implants.60
PLACEMENT OF THE PERMANENT
IMPLANT
The permanent silicone or saline implant is placed at
a second procedure. Sufficient saline is removed from
the expansion prosthesis immediately before surgery
to achieve symmetry with the opposite side. The volume
of the remaining implant can be measured and an
appropriate prosthesis chosen.
An incision is made through the original mastec-
tomy scar. It is continued down through pectoralis
muscle and capsule to the tissue expander. The
expander is then removed. Management of the capsule
depends on how well the expander was positioned,
the location of the inframammary fold, the shape
and projection of the stretched soft tissues, and the
degree of capsular contraction. The capsule may be
removed through complete capsulectomy, partial
image...

9 • PRINCIPLES OF TISSUE EXPANSION 559

capsulectomy, or capsulotomy in the places that the
capsule is restrictive.
If repositioning of the inframammary fold or
definition of the fold is required, an incision is made
at the projected inframammary fold (Fig. 19-13). This
allows ptosis by infolding and uplifting of the expanded
tissue and advancement of the lower abdominal
flap.61,62 The expander is deflated to volume symme-
try with the opposite side, and the inframammary fold
is moved up or down so that the apices of the breasts
are on an equal level. The capsule is left intact unless
the prosthesis needs to be repositioned. Stable recon-
struction of the inframammary fold can be achieved
by tacking the anterior capsule to the posterior chest
wall capsule so that the new breast is at the same level
as the opposite side. Permanent large sutures are usually
required for stability. The abdominal skin is under-
mined above the fascia and is advanced superiorly into
the inframammary cleavage to close the posterior wall
defect. An appropriate binder is placed across the supe-
rior aspect of the breast to prevent the implant from
being displaced in a cephalad direction. Vigorous
massaging begins 5 days after the procedure.
EXPANSION OF A MUSCLE FLAP
A patient may require transfer of a latissimus dorsi
muscle or myocutaneous flap in combination with
tissue expansion. In most instances, a simple implant
can be used in conjunction with the latissimus dorsi
flap. If, however, the chest wall skin is too tight for a
sufficiently large implant to match a large, ptotic con-
tralateral breast, the latissimus flap can be transferred
to cover a tissue expander. The tissue expander can
then be inflated, and once sufficient laxity of chest wall
skin and soft tissues develops, the permanent implant
is placed beneath the latissimus dorsi muscle.
After removal of large areas of skin graft or abnor-
mal skin, the amount of skin transferred in a flap may
be insufficient to achieve symmetry with the opposite
side. In these instances, the expander prosthesis can
be replaced beneath the latissimus dorsi as well as a

FIGURE 1 9 - 1 3 . The technique

of designing a ptotic breast by
moving the inframammary fold.
A, The prosthesis is overex-
panded to make an excess
amount of tissue. B, The position
of the desired breast fold (point
B) is determined on the thoracic
wall. C, Through an inframam-
mary incision (point C), the
expander is removed and a per-
manent device placed. The skin
and soft tissue are moved supe-
riorly and sutured to point B.
D, The abdominal wall is under-
mined above the fascia and
advanced into the inframammary
defect.

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Dr.Mustafa D.
560 • GENERAL PRINCIPLES

transverse rectus abdominis flap to provide additional
volume as needed.
Expansion can also be employed to salvage cases
in which transverse rectus myocutaneous flap recon-
struction is inadequate. This is not infrequent in bilat-
eral reconstruction in thin patients. If more breast
volume is desired than is available with the abdomi-
nal tissue, an expander is placed behind the flap. It is
then gradually expanded to achieve desired volume.
Expansion should be delayed until the transverse rectus
abdominis muscle flap has matured 4 to 6 weeks.
IMMEDIATE POSTMASTECTOMY BREAST
RECONSTRUCTION
The inframammary folds should be marked with the
patient in an upright position before introduction of
general anesthesia for the mastectomy and expander
placement. The mastectomy should be accomplished
in a fashion that maximizes local control, with careful
attention, however, to preservation of skin and sub-
cutaneous tissue, especially in the inframammary fold
area. In recent years, with the advent of skin-sparing
mastectomy, general surgeons are much more consci-
entious in preservation of skin. If too much skin is
spared, however, unnecessary dog-ears and sagging may
result, requiring the plastic surgeon to trim excess skin
on completion of expander placement.
After completion of the mastectomy, a submuscu-
lar pocket is dissected for placement of the tissue
expander. The muscle incision can be made in one of
two locations. If a muscular fascial layer has been well
preserved after mastectomy, incision can be made par-
allel to the pectoralis major fibers. By use of sharp and
blunt dissection, the pectoralis major muscle is lifted
off the underlying chest wall and pectoralis minor
muscle. Dissection is continued inferiorly beneath the
origin of the rectus abdominis muscle and laterally
beneath the serratus anterior muscle. Alternatively,
an incision can be made at the lateral border of the
pectoralis major or parallel to the fibers of the serra-
tus anterior muscle. The dissection is continued down
to the rib, and from this lateral position, a pocket is
dissected inferiorly, superiorly, and medially, lifting the
pectoralis major origin of the rectus abdominis muscle
and the origin of the serratus anterior muscle.
Regardless of the location of the muscle incision,
care must be taken not to dissect the serratus anterior
too far laterally, which will allow displacement of the
implant into the axilla. If the fascia at the junction of
the pectoralis major and rectus abdominis muscles has
been violated during mastectomy, complete submus-
cular closure can be difficult. In general, a small ex-
posure of the implant is of no consequence. Larger
exposure can be covered with a transposition or rota-
tion of anterior rectus abdominis fascia.
The incisions are closed with absorbable suture. Sep-
arate suction drainage of the mastectomy site and the
submuscular pockets is placed. The expander is inflated
with sufficient volume to obliterate dead space, stop-
ping short of excessive tension on the wound closure
(Fig. 19-14).

A B
FIGURE 19-1 A. Immediate breast reconstruction was achieved by placement of a total muscular tissue expander
at the time of mastectomy. A, The prostheses were expanded during 2 months with slight overinflation, B, The patient
5 years after permanent implant placement and nipple reconstruction.

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image...
Antibiotics are given perioperatively and contin-
ued until all drains are removed postoperatively.
Inflation of the expander is initiated after healing of
the mastectomy incision 2 to 3 weeks postoperatively.
If there is a complication related to the mastectomy
flap, such as skin necrosis or wound separation, the
expander is deflated until these complications of
wound healing have been controlled.
Adjunct chemotherapy is used more aggressively
today than in previous years. Postoperative chemother-
apy does not affect mechanical expansion. The patient
will be making frequent visits for chemotherapy and
oncologic follow-up, so inflations should be scheduled
such that the patient is not inconvenienced with exces-
sive visits to the physician. Patients who are experi-
encing nausea and malaise with chemotherapy may not
desire inflations during these periods, and visits should
be worked around the patient's general well-being.
Inflation is postponed if leukopenia below 2000 occurs.
If the patient requires adjunctive radiation because
of close or questionable resection margins, this can be
done with the tissue expander in place. The integrated
valve with metal backing does not alter radiation deliv-
ery protocols. Radiation treatments are usually started
several months after mastectomy so that the patient
can receive postoperative chemotherapy. The expander
is slowly inflated during this postoperative interval.
Inflations are discontinued during radiotherapy and
then reinitiated 6 to 12 weeks after radiation, depend-
ing on the quality of skin and subcutaneous tissue.63
PERMANENT EXPANSION PROSTHESES
Several prostheses designed to avoid a second proce-
dure have been developed.38 The expander is intended
to remain in place as a permanent breast prosthesis
after expansion has been accomplished. Experience
with these devices has been favorable. The prosthesis
is placed in a position identical to that in secondary
or immediate breast reconstruction. The reservoir is
usually located cither below the brassiere line or in the
axilla. The expander is inflated and hyperinflated by
at least 200 mL for 3 months. The excess fluid is removed
to make a more naturally ptotic breast.
In approximately 50% of patients, a second proce-
dure to reposition the prosthesis or to redefine the
inframammary fold is thus avoided. The expansion
device is especially useful in women who have a min-
imally or mildly ptotic breast and whose inframam-
mary fold is not well defined. The inflation reservoir
and tubing maybe removed in a brief office procedure
under local anesthesia.
The permanent expander prosthesis is a bilumen
implant. The outer lumen is filled with silicone; the
inner layer is inflated as saline is injected through the
distal port. The implant was not available for a number
of years owing to the controversies related to silicone
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19 • PRINCIPLES OF TISSUE EXPANSION 561
implants but is now again commercially manufactured.
Because the implant is designed to be left in place per-
manently, it is especially beneficial in the reconstruc-
tion of congenital breast deformities in adolescent
patients. The design of the prosthesis provides a more
natural aesthetic expansion than is available with many
of the temporary expanders.
The term permanent expander must be used with
caution. As with any device containing silicone gel, there
are potential problems, such as rupture and leak, that
would require replacement of the implant.
Tissue Expansion in the Irradiated
Chest Wall
Chest wall irradiation is an important modality in the
management of breast cancer.64 Reconstructive breast
surgeons are often faced with surgical procedures com-
plicated by chest wall irradiation. Patients with irra-
diated chest walls fall into one of three groups: patients
who have had previous lumpectomy and radiation with
recurrence and are now candidates for a mastectomy
and immediate reconstruction; patients with mastec-
tomy followed by adjunctive radiation who are now
candidates for delayed reconstruction; and patients who
have undergone mastectomy and immediate placement
of a tissue expander and postoperatively are noted to
have inadequate margins and require irradiation over
the tissue expander. There is a significantly higher com-
plication rate in irradiated patients treated with tissue
expansion and implant. A 32.5% incidence of late cap-
sular contracture has been noted. Patients who are
seeking secondary reconstruction after chest wall irra-
diation should seriously be considered for autologous
tissue reconstruction rather than tissue expansion.
Patients who already have a tissue expander in place
after primary reconstruction are a more difficult
group, however. Our experience has been that favor-
able outcome is common enough that we would not
advise removal of the tissue expander and alternative
reconstructive measures. It is best to proceed with
inflation of the tissue expander in the early postoper-
ative course, during which time many patients are
receiving chemotherapy. Inflations are discontinued
during radiation and reinstituted 6 weeks after com-
pletion of radiation when the appearance and texture
of chest wall skin improve. There is, however, a higher
incidence of capsular contracture, extrusion, and pain,
and aesthetic results are less favorable in irradiated
patients. In these instances, the patient may be a can-
didate for removal of the implant and reconstruction
with autologous tissue.
The Hypoplastic Breast
Acquired breast and chest wall deformities may be due
to burns, trauma, surgery, or radiation with injury to
562 I • GENERAL PRINCIPLES
the prepubescent female breast bud. Systemic factors
may be responsible for bilateral hyperplasias and
hypoplasias, and diagnosis of their etiology may
require consultation with pediatricians, endocrinolo-
gists, or gynecologists. Most cases of congenital uni-
lateral hypoplasia are idiopathic and include hypoplasia
of one breast, total aplasia of one breast, or hypoplasias
in conjunction with underlying chest wall deformities
as seen in Poland syndrome. Unilateral hypoplasia
varies from a smaller well-formed breast to total absence
of the breast with variable hypoplasias or aplasia of
the nipple and areola. If a hypoplastic nipple-areola
complex is present, it will usually lie in a cephalad posi-
tion relative to the contralateral breast. Tissue expan-
sion has played an important role in the reconstruction
of both acquired and congenital breast hypoplasias.
Management of the deformity depends on the degree
of breast asymmetry, the nature of the deformity, the
quality of the chest wall soft tissues, and the age of the
patient at presentation.
THE FULL AND MATURE BREAST
The breast develops from the mammary ridge at
puberty. The pituitary gonadotropins stimulate the
ovary's secretion of estrogen and progesterone, which
in turn stimulates the budding of the ducts and devel-
opment of secreting acinar tissue. The normal breast
continues to develop, achieving full growth by 18 to
19 years of age. The breasts will continue to change
throughout life secondary to hormonal changes and
weight changes. At the time of presentation, the degree
of breast hypoplasia is determined and characterized
as minor hypoplasia with a normal nipple-areola
complex, moderate to severe hypoplasia, and total
breast aplasia. The nipple-areola complex will be
normal, hypoplastic, displaced, or aplastic. Mild breast
hypoplasias may be corrected with simple placement
of a breast implant, but more severe hypoplasias and
aplasias with nipple-areola displacement are best
treated with initial placement of a tissue expander.
A tissue expander is placed through cither an infra-
mammary or axillary incision into the subpectoral
space. If the pectoralis muscle is absent, the deformity
is likely to be associated with Poland syndrome (dis-
cussed later). The type of expander placed includes
smooth and textured wall implants, implants with inte-
grated valves, and expanders with distal ports, depend-
ing on one's preference. The prosthesis is expanded at
2-week intervals initially. As the expander is inflated
and the overlying skin relaxes, the cephalad-displaced
nipple-areola complex will descend. The slower the
expander is inflated, the better the nipple-areola will
descend. A slow expansion also minimizes develop-
ment of striae. The expander is overinflated to a volume
at least 40% larger than the desired volume of the per-
manent implant. The expander is left in place forscveral
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Dr.Mustafa D.
months after the final inflation to allow development
of additional ptosis.
The permanent implant is introduced at a second
procedure. An incision is made through the original
incision used to place the expander. The expander is
removed, and a capsulectomy is carried out if needed.
The inferior portion of the capsule may be tacked to
the rib periosteum to better delineate the inframam-
mary fold. A permanent implant is selected to achieve
symmetry with the contralateral side. Alternatively, if
a permanent expander prosthesis has been used, the
prosthesis is inflated to several hundred milliliters larger
than the desired final volume. The expander prosthe-
sis is allowed to remain overinflated for several months.
In the office, saline is then withdrawn to achieve sym-
metry with the contralateral breast. An incision is made
over the distal port, and the port with attached tubing
is removed when desired.
THE IMMATURE BREAST
The use of tissue expanders has been beneficial in the
management of young adolescents presenting with
breast asymmetry. 65 This is a critical stage in the ado-
lescent's psychosocial development. Failure to address
the problem during this time of intense social pres-
sures and self-awareness of a developing physique can
result in psychological problems. These patients do not
need full maturity for reconstruction.
A subpectoralis muscle plane is elevated through a
small axillary incision. A 700-mL or larger expander
prosthesis is placed in the subpectoral plane beneath
the hypoplastic breast. An expander with an integrated
valve or distal port is positioned. If a distal port pros-
thesis is used, the inflation reservoir is placed in the
lateral thoracic wall or upper abdomen below the infra-
mammary fold. The prosthesis is then inflated at in-
tervals appropriate to maintain symmetry with the
developing breast on the contralateral side. The slow
expansion will cause the areola to enlarge, and the
nipple-areola complex will progressively be displaced
caudally to a more normal position. The adolescent
can continue with normal activities, participation in
sports, and other physical endeavors.
Once development of the contralateral breast has
stabilized, usually between 18 and 19 years of age, the
expander is removed. Definitive reconstruction is
achieved as previously described for correction of the
mature breast.
THE TUBEROUS BREAST
Expansion is a useful technique in the correction
of the hypoplastic tuberous breast. Through an in-
framammary or periareolar approach, the tuberous
breast is lifted off the underlying pectoralis fascia. Radial
cuts are made through the breast tissue to expand the
base of the breast, and a tissue expander is introduced
image...
in the submammary plane. Inflation and expansion
are achieved as previously discussed. Once adequate
expansion has been achieved, the expander is removed
and replaced with the permanent prosthesis. Alterna-
tively, a permanent expander device is used and
overinflated by several hundred milliliters. Several
months after completion of the inflation, fluid is
removed to achieve symmetry with the contralateral
side, and the port and attached tubing are removed.
CORRECTION OF POLAND SYNDROME
Poland syndrome involves not only abnormal devel-
opment of the breast but also thoracic wall deformi-
ties, deformities of the upper extremity, and vertebral
anomalies. Uniform to all cases of Poland syndrome
is an absence of the sternal head of the pectoralis major
muscle. There is also an associated deficiency of sub-
cutaneous tissue, hypoplasia, aplasia, or malposition
of the nipple-areola complex and deficiency of breast
tissue. There may be an abnormality of the anterior
ribs and costal cartilages and deficiencies of the
muscles of the scapular area including the latissimus
dorsi.
A mild deformity characterized by breast hypopla-
sia or aplasia is corrected with initial placement of a
tissue expander through a transaxillary approach. A
700-mL or larger expander is used. Once full expan-
sion has been achieved during a 3- to 4-month period,
the tissue expander is removed and a permanent breast
implant placed. Ideally, if there is an adequate latis-
simus dorsi muscle, the latissimus dorsi muscle is
transposed to cover the breast prosthesis. The inser-
tion of the latissimus dorsi is taken down and trans-
posed anteriorly on the humerus to form an anterior
axillary fold. Alternatively, the tissue expander can be
placed at an initial operation and covered immedi-
ately with a latissimus dorsi muscle transposition.
Once expansion has been completed, the expander is
removed and the permanent breast implant intro-
duced. More severe cases of Poland syndrome char-
acterized by contour depression of the ribs will require
both osteotomy and repositioning of the ribs or a
custom, solid Silastic implant. The latissimus dorsi
muscle is transposed, and the anterior axillary fold is
reconstructed by transposition of the insertion over
the custom Silastic implant. The breast contour is
reconstructed with tissue expansion followed by per-
manent breast implant.
In the immature girl with Poland syndrome,
expanders are placed at the onset of contralateral breast
development through a small incision in the axilla. The
implant is gradually inflated until development of the
contralateral breast has stabilized. The expander is
inflated slowly to maintain symmetry with the devel-
oping contralateral breast. In the final months, the
expander is overinflated by 200 to 300 mL and then
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19 • PRINCIPLES OF TISSUE EXPANSION 563
removed and replaced with the permanent implant. If
a latissimus dorsi muscle is available, it is transposed
at this time to cover the breast prosthesis (Fig. 19-15).
Expansion of the Trunk
The trunk and abdomen are well suited to tissue expan-
sion in individuals of all ages. Large prostheses can be
either placed above the fascia or incorporated between
muscle planes in the abdomen or on the back. Because
of the large adjoining surface area from which tissue
can be recruited, large prostheses can be placed and
flaps quickly expanded (Fig. 19-16). Incorporation of
the latissimus dorsi, pectoralis major, or rectus muscles
allows development of an expanded myocutaneous
flap. Prostheses placed between layers of the abdomi-
nal wall have been used to develop large flaps for
abdominal wall reconstruction. 66 Multiple expanders
around a specific defect minimize the distortion
during the process of expansion, and sufficient tissue
for completion of the reconstruction develops more
rapidly. Expansion of the trunk with large prostheses
may produce significant deformity and discomfort.
Expansions of the back and buttocks are particularly
difficult for the patient because of interference with
everyday functions of living. Fortunately, expansion
in such areas can be rapidly expedited with multiple
prostheses.
Large deformities, such as burns, giant hairy nevi,
and other congenital anomalies, may require multiple
serial expansions. In such cases, the expanders arc
inflated maximally and the flaps advanced. The pros-
theses are left in place, and re-expansion is carried out
in the subsequent weeks. In the abdomen, two or three
serial expansions are usually well tolerated, even in
children.
Expansion in the Extremities
Skin and soft tissues of the extremities tolerate tissue
expansion well.67 Tissue defects resulting from con-
genital abnormalities, tumor, or trauma can be cor-
rected. The capsule that develops adjacent to the
expander has a resilient surface that can be transposed
over joints and tendons to decrease adhesions.
Multiple expanders are usually recommended.
They are best placed axially to the defect. Placement
of prostheses on a long axis of the extremity is less
optimal, and a greater amount of expansion is neces-
sary. The use of multiple expanders in the extremity
has the advantages of less distortion, less compromise
of everyday life activity, and more rapid development
of tissue. Functional impairment, even when the pros-
theses are placed directly over vessels and nerves, is
unusual. Occasional transitory neurapraxias have
been described in the lower extremity but are un-
common in the upper extremity. If such discomfort
564 I • GENERAL PRINCIPLES

*•

FIGURE 1 9-1 5. A, A female patient with Poland syndrome at 14 years of age. 8, A tissue expander is placed through
an axillary incision and gradually inflated during 4V2 years to retain symmetry with growth of the opposite side. C, At
18 years of age, the expander was removed. A latissimus dorsi muscle was transferred to the anterior chest wall and
placed over a permanent implant- 0, The patient has excellent symmetry, projection, softness, and nipple location.
(From Argenta L, Vanderkolk C, Friedman R, Marks M: Refinements and reconstruction of congenital breast deformi-
ties. Plast Reconstr Surg 1985;76:74.)

or neurapraxia develops, the prostheses should be
deflated and then reinflated at a much slower rate.
Standard rectangular and round prostheses usually
suffice. In areas such as the hand or foot, custom
implants can be fabricated. The dorsum of the hand
and foot lends itself well to expansion, whereas the
palm and plantar areas are particularly painful and
resistant to expansion.
The upper leg is easily expanded because of the
thickness of skin and underlying subcutaneous tissue.
Complications are infrequent. Below the knee, inflation
carries significant risks, particularly after crush injuries
or when large areas of traumatized skin surround the
defect. Clean isolated defects, such as those that follow
local tumor excisions, are better reconstructed with
expansion. Multiple small expanders are recommended

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Dr.Mustafa D.
image...

19 • PRINCIPLES OF TISSUE EXPANSION 565

~^7

FIGURE 1 9 - 1 6 . Separation of ischiophagus twins was accomplished by first pre-expandingthe trunk skin, both ante-
riorly and posteriorly. At a second procedure, the patients were divided (arrow), and the hemipelvis of each side was
brought together with the opposite side by closing the pelvic ring over expanded soft tissue.

to minimize the risks of implant loss. If cellulitis or
tissue compromise occurs, the prosthesis should be
deflated or removed. In general, individuals who
have suffered major crush or degloving trauma to the
extremity are better treated with function-restoring
microvascular and myocutancous flaps, rather than
attempting excessive aesthetic reconstructions with
tissue expansion.
Expanded full-thickness grafts harvested from the
abdomen are extremely versatile in reconstruction of
the foot and hand. These grafts are stable over time
and can be harvested as a single graft. Reasonable pro-
tection and sensation return to these grafts over time.
COMPLICATIONS AND THEIR
MANAGEMENT
Initial attempts at tissue expansion were associated
with a high rate of complication. As more experience
accumulated, however, the incidence dramatically
decreased. Complication rates are directiy proportional
to the number of expansion procedures performed
and the experience of the surgeon.68 Most complica-
tions incurred during tissue expansion are relatively
minor and do not interfere with completion of the
procedure.
Infection
As with the placement of any prosthesis in the human
body, infection is possible. The introduction of bac-
teria in the perioperative period is the most common
cause of early infection. The area to be reconstructed
should be stable, and there should be no open wounds
at the time that the procedure is undertaken. Areas
susceptible to lymphedema, such as traumatized lower
extremities, carry a significantly higher rate of infec-
tion. Areas of copious lymphatic drainage, such as the
neck and the groin, also tend to accumulate lymphatic
fluid around the prosthesis and are more susceptible
to infection. These areas should be drained with suction
drains until all excess drainage stops. Antibiotics are
given as long as the drain remains in place.
Late infections are usually the result of iatrogenic
introduction of bacteria during the course of inflation.
The inflation procedure should be performed under
sterile conditions in the office. Povidone-iodine
(Betadine) is used to prepare the injection site.

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566 I • GENERAL PRINCIPLES
Many infections can be well tolerated by the patient
and can be difficult to detect. More than 80% of pros-
theses with externalized ports were found to have col-
onized the expander capsule, with some degree of
infection present. Externalized ports are contraindi-
cated when a permanent prosthesis is to be used. This,
however, did not affect outcome unless permanent
implants or bone grafts were placed in the expanded
tissue.
Some erythema may occur over all expansion
prostheses. Significant pain, warmth, and systemic
symptoms such as fever and chills suggest significant
infection. If the infection occurs in the perioperative
period or early course of expansion, the prosthesis
should be removed and the wound irrigated. The pro-
cedure is aborted, and a second attempt is made 3 or
4 months after healing. If infection occurs late in the
course of expansion, the prosthesis can be removed
and the expanded tissue advanced after irrigation of
the infected cavity. Permanent implants should not be
placed when Gram stain of the expander space reveals
bacteria.
Implant E x p o s u r e
Implant exposure can occur early in the postoperative
period or after a protracted course of expansion. Expo-
sure early after placement is almost universally related
to inadequate dissection or an excessively large pros-
thesis that impinges on wound closure. Undermining
should be sufficient so that the prosthesis is easily
accommodated and the wound can be closed in mul-
tiple layers. The inflation tubing should be maintained
at a site away from the incision, as should the inflation
valve.
Late exposure is usually related to excessively rapid
and overzealous inflation. There are few instances in
which rapid expansion is indicated. Tissue expansion
is basically an aesthetic procedure and should be carried
out judiciously to achieve optimal cosmetic results. If
implants begin to become exposed late in the course
of expansion, multiple rapid fillings are done to gen-
erate adequate tissue. Reinforcement of the compro-
mised overlying skin with paper tape is sometimes
helpful.
Avoidance is the best solution to implant exposure.
Tissues that are compromised, such as grossly trau-
matized lower extremities and irradiated and burned
tissues, must be approached with caution.
Treatment of the exposed implant depends on the
timing of exposure. If the prosthesis becomes exposed
soon after placement, it is best to remove it and
return 3 to 4 months later to replace it. If minimal or
late exposure occurs, the procedure can continue. Paper
tape or antibiotic creams are placed over the exposed
area, and expansion is continued. Most flaps survive
and do well even with some exposure of the implant.
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Compromise and Loss of Tissue at
the Time of Flap R o t a t i o n
Tissue expansion exerts changes on living tissue similar
to the phenomenon of flap delay. Expanded flaps are
almost universally more robust than nonexpanded
flaps. One should attempt to maintain a significant
axial vessel in the expanded tissue to ensure vascular-
ity. The debate as to whether epinephrine-containing
solutions predispose delayed or expanded flaps to
compromise continues, and until this is resolved,
epinephrine-containing solutions are best avoided at
the reconstructive procedure.
Implant Failure
Early implants carry a high risk of failure. Improve-
ments in design of expanders and associated ports
have significantly reduced the incidence of mechani-
cal failure. However, the use of an excessively large
needle or inadvertent puncture of the implant can lead
to deflation. The implant reservoir should be entered
at a 90-degree angle because this maximizes sealing of
the valve. If there is any question about the location
of the inflation reservoir, radiologic or sonographic
techniques may be helpful.
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31. Wilson E, Mai Q, Sudhir K, et al: Mechanical strain induces
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loan? J Plast Surg 1986:68:63.
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struction. J Plast Surg 1989:84:607.
37. Becker H, Cohen I, Scheflan M: Breast reconstruction after
modified radical mastectomy. South Med J 1982;75:1335.
38. Becker H: Breast reconstruction using an inflatable breast implant
with detachable reservoir. J Plast Surg 1984;73:678.
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41. Neale H, High R, Billmore D, et al: Complications of controlled
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eliminate large scalp defects. Ann Plast Surg 1985;12:305.
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tion, 2nd ed. New York, Marcel Dekker, 1987:519-561.
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pattern baldness. Ann Plast Surg 1993:31:385.
52. Tanino R, Miyasaka M: Reconstruction of microtia using tissue
expanders. Clin Plast Surg 1990;I7:339.
53. Radovan C: Breast reconstruction after mastectomy using the
temporary expander. J Plast Surg 1982;69:195.
54. Argenta L, Marks M, Grabb W: Selective use of serial expan-
sion in breast reconstruction. Ann Plast Surg 1983; 11:188.
55. Seckel B, Hyland W: Soft tissue expander for delayed and
immediate breast reconstruction. Surg Clin North Am
1985:65:383.
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immediate reconstruction of the breast following modified
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61. PennisiV: Makinga definite inframammary fold under a recon-
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in reconstruction of congenital breast deformities. J Plast Surg
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1984;74:493.
image...
CHAPTER
20 •
Repair and Grafting of Dermis,
Fat, and Fascia
THOMAS R. STEVENSON, MD • THOMAS P. WHETZEL, MD
DERMIS
History
Autogenous Dermis
Allograft Dermis
FAT
History
Autogenous Free Fat Graft
Dermis-Fat Craft
During the last decade, the grafting of dermis, fat, and
fascia has continued to increase in importance along
with the need to improve contour or to restore func-
tion. Grafts of these autogenous components were
historically used to replace deficits of like kind, such
as fascial grafts to repair inguinal hernias or fat to fill
orbital fatty deficits. Dermis was used for structural
support similar to fascial grafts for hernia repair or
ligament reinforcement. The immediate sequela to
these surgical procedures was the problem of variability
in the resorption of these autogenous tissues. During
the last century, attempts have been made to quantify
resorption for each of the tissues or combination of
tissues, such as the dermis-fat grafts. If only the per-
centage of fat or dermis that would "take" or revas-
cularize in any given anatomic region were known,
one could achieve some level of predictability of the
final result. However, the historical problem of auto-
genous grafting of dermis, fat, and fascia has been one
of wide variability in long-term retention of the graft
volume. Accordingly, vascularized grafts or flaps were
developed in parallel with the improvements in micro-
surgical techniques in the 1970s and 1980s. Vascular-
ized grafts, which demonstrated minimal resorption,
had significant limitations in their general applicability
to common reconstructive or cosmetic situations
because of their large size and pedicle requirements.
Currently, the greatest need in plastic surgery for
autogenous grafting is in the reliable replacement or
augmentation of subcutaneous volume. Much atten-
tion is now being focused on augmentation of sub-
cutaneous volume to restore loss of volume from
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Free Fat Flaps
Free Fat Injection
FASCIA
History
Indications and Use
Harvesting
Outcomes
normal aging in many areas of the face. Replacement
of lost subcutaneous volume in contour depressions
after liposuction or other acquired deformities is also
an area of increasing interest. The grafting of free fat
by injection and its harvesting by cannula continue
to progress as an offshoot of the development of lipo-
suction in the 1980s. Fat is much more available than
dermis or fascia and can easily be removed with a
cannula. Still, free fat has historically been the tissue
least able to re-establish a vascular connection with
the recipient site. A scientific and controlled evalua-
tion of durability and predictability of this grafting
process continues to evolve with frequent publications
and presentations. Finally, the search for a grafting
material that does not require a harvest at all, with
elimination of a donor site, is an area of active
progress and evaluation. The current use of acellular
allogeneic dermis that is processed from cadaveric
human skin is timely.
DERMIS
History
Autogenous dermal grafts were first described in 1913
as a substitute for fascia in hernia repair and as tendon
grafts in the repair of severed tendons.' Shordy after-
ward (1914), they were used clinically to augment soft
tissue depressions in the nasal tip, ear, and cheek.2
Although most dermal grafting was performed for
hernia repair, dermal grafts were also used to rein-
force extra-articular ligaments in the knee joint,
569
570 I • GENERAL PRINCIPLES
temporomandibular joint, fingers, and elbows. Suc-
cessful use of the dermal graft primarily in Germany
throughout the 1920s and 1930s led to its adoption
in the United States by Cannaday3,4 >" the 1940s.
Dermal grafts were used in the treatment of anky-
losis of the mandible, repair of stenotic bronchial tubes,5
and patchingof major diaphragmatic defects.Through-
out the 1960s, dermal grafts were used to protect
the carotid artery, to repair dural defects and replace
articular disks after meniscectomy of the temporo-
mandibular joint, and to provide cosmetic soft tissue
augmentation of the face and nasal dorsum.
Much information has become available in regard
to the use of dermal grafts during the last few decades;
however, the limitations of variable long-term per-
sistence and availability of inconspicuous donor sites
remain as obstacles. In an attempt to escape these draw-
backs, acellular allogeneic dermis (AlloDerm) emerged
as a promising soft tissue replacement in the mid-
1990s.6 AlloDerm is processed from cadaveric human
skin. Antigens are removed, leaving the dermis and
extracellular matrix intact. AlloDerm has been used so
far in skin grafting of burn wounds, lip augmentation,
repair of nasal septal perforations, intraoral resurfac-
ing, and facial soft tissue augmentation. The long-term
effectiveness of AlloDerm continues to be evaluated.
B phia, WB Saunders, 1990:520.)
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
Autogenous Dermis
INDICATIONS
Autogenous dermal grafts without adherent fat are
typically used for augmentation of minimal soft tissue
defects. These include some saddle nose deformities,
depressed scars, nasolabial folds, and limited or asym-
metric lip deformities. Dermal grafts are employed for
coverage of exposed carotid arteries after neck dis-
section.7 Dermal autografts have also been used in lieu
of synthetic mesh for closure of abdominal fascial
defects after transverse rectus abdominis myocuta-
neous (TRAM) flap harvest.8
HARVESTING
Dermal grafts may be harvested in any location,
typically like a donor site for a full-thickness graft;
however, unlike with a full-thickness graft, theskin color
match with the recipient site will not be a considera-
tion. This includes the groin, the gluteal fold or lateral
gluteal region, the submammary region in women, the
lower abdomen, the preauricular and postauricular
regions, and the supraclavicular area in some instances
(Fig. 20-1). Use of the area surrounding a preexisting
scar is often desirable. The graft as outlined on the skin
with a surgical marker will be approximately 259 o
FIGURE 2 0 - 1 . Common dermis-
fat graft donor sites. A, Suprapu-
bic and subiliac sites. X designates
the iliac spines. B, Gluteal crease
site. X designates the ischial
tuberosity. (From Chiu DTW, Edgar-
ton BW: Repair and grafting of
dermis, fat, and fascia. In McCarthy
JC, ed: Plastic Surgery. Philadel-
image...
20 • REPAIR AND GRAFTING OF DERMIS, FAT, AND FASCIA
smaller when it is resting on the back table because of
immediate contraction. The graft should accordingly
be planned to be about 25% larger than the size of the
true defect. The grafts are typically harvested in an ellip-
tical pattern, and the donor site is closed in a linear
fashion. The epidermis can be removed from the graft
either before it is removed from the donor site with a
scalpel or scissors or after harvest with a Reese drum
dermatome. In either method, care must be taken to
ensure complete removal of epidermis to prevent future
epidermoid cyst formation. The fat that is adherent to
the reticular dermis can be trimmed with scissors before
graft placement (Fig. 20-2).
Grafts can be placed into subcutaneous tunnels by
pulling them through with sutures, or they can be
directly sutured into place with an open defect. If the
vascularity of the recipient site is excellent, such as the
nasal dorsum, a double layer of dermal graft may be
used. Revascularization of a double layer or greater
amount of grafts requires a correspondingly better
recipient bed blood supply.
Complications are poor graft take with resorption
of the graft and subsequent infection. Hematoma,
inadequate fixation, or wound infection can also lead
to loss of the graft.
OUTCOMES
The outcome of dermal grafting in animals and
humans is well documented. 9 "" Human dermal grafts
undergo an inosculation period similar to other skin
grafts, with evidence of early vascularization of the graft
by the fourth day.12 Whereas the sebaceous glands typ-
ically disappear within several weeks, the sweat glands
survive permanently and continue to function.
Although the sweat gland ducts end blindly at the
surface of the graft, they continue to produce secre-
tions that are internally absorbed by adjacent capil-
laries (Fig. 20-3). I3 The hair follicles generally disappear
within several months of dermal grafting, but they may
produce microscopic epidermoid cysts after the first
2 weeks. The accumulating keratin and epithelial debris
of the hair follicles cause the epithelial wall of the
FIGURE 2 0 - 2 . Dermis graft con- Epidermis
tains the deeper layer of the papil-
lary dermis and the entire reticular
layer of the dermis along with a
minimal amount of adherent subcu- Dermis
taneous fat and indigenous subepi- graft
dermal extensions of the epithelial
appendages. (From Chiu DTW,
Edgarton BW: Repair and grafting
of dermis, fat, and fascia. In
McCarthy JG, ed: Plastic Surgery. Subcutaneous
Philadelphia, WB Saunders, 1990: fat
509.)
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
571
microcyst to stretch and become necrotic. A foreign
body reaction including giant cells eventually leads to
replacement fibrosis (Fig. 20-4).
The fate of dermal allografts implanted in rats across
class II histocompatibility antigens is similar to that
of human autografts. Dermis buried in a subcutaneous
pocket shows absence of adnexal structures but a
well-maintained dermal framework at 39 days after
implantation. 14
Allograft Dermis
SOURCE
Acellular allogeneic dermis (AlloDerm) is produced
from human cadaveric allograft skin by the LifeCell
Corporation. During the skin processing, immuno-
genic components that include all viable cells are
extracted, leaving acellular dermis and extracellular
matrix intact. The entire epidermis and all of the
dermal cells are removed during a freeze-drying
process. The resultant matrix has undamaged colla-
gen types IV and VII, elastin, and laminin present,
documented by electron microscopy (Fig. 20-5).
Immunohistochemical staining demonstrates absence
of class I and class II antigens. Strict protocols are
observed to prevent transmission of diseases. Donors
are screened by history for risk factors or clinical
evidence of viral hepatitis types B and C and human
immunodeficiency virus. Serologic testing is per-
formed for viral hepatitis types B and C, human
immunodeficiency virus 1 and 2, human T-lym-
photropic virus 1, and syphilis. The acellular and
porous dermal matrix allows ingrowth and coloniza-
tion by host fibroblasts and endothelial cells.15
AlloDerm is supplied in sterile freeze-dried sheets
that are rehydrated in isotonic saline for 5 minutes
before use. The rehydration makes them soft and
pliable. An injectable micronized form of AlloDerm
has been developed and is undergoing clinical inves-
tigation. 16 The micronizing is performed by cutting
the AlloDerm sheets into 2.0 x 1.2-cm pieces with a
No. 15 blade. The strips are then homogenized in liquid
Dermis-
fat graft
572 I • GENERAL PRINCIPLES

* » . , " . ••
'. " : J J .

>V* : •'"•--.

FIGURE 2 0 - 3 . A Human autogenous

dermal graft buried subcutaneously for 4
years. The essentially normal secretory coil
of sweat gland is shown. (Hematoxylin and
eosin stain; magnification xl 20.) 8, From
the same section as A. The greatly dilated
excretory duct containing a secretion cast
in its lumen (above) is shown with its asso-
ciated sweat gland (below). (Hematoxylin
and eosin stain; magnification x75.) (From
Chiu DTW, Edgarton BW: Repair and graft-
ing of dermis, fat, and fascia. In McCarthy
JC, ed: Plastic Surgery. Philadelphia, WB
Saunders, 1990:511.)

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
image...

20 • REPAIR AND CRAFTINC OF DERMIS. FAT, AND FASCIA 573

FIGURE 2 0 - 4 . A, Human autoge-

nous dermal graft buried subcutaneously
for 4 years. The dark granules represent
sites of succinic dehydrogenase activity
inside the cells of a surviving sweat gland.
Succinic dehydrogenase, an enzyme in
the Krebs citric acid cycle, is essential
for the vital processes of mammalian
cells. (Neotetrazolium method; magnifi-
cation x300.) 8, Human autogenous
dermal graft buried subcutaneously for
5 months. An epidermoid cyst derived
from a hair follicle is shown at an inter-
mediate stage of disintegration. The
epithelial lining is becoming thinned after
the accumulation of keratohyaline debris
inside the cyst. There is considerable sur-
rounding reactive fibrosis. (Hematoxylin
and eosin stain; magnification x2IO.)
(From Chiu DTW, Edgarton BW: Repair •
and grafting of dermis, fat, and fascia.
In McCarthy JG( ed: Plastic Surgery. w ? > '
Philadelphia, WB Saunders. 1990:512.)

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
574 I • GENERAL PRINCIPLES
nitrogen to produce microfractures rather than shred-
ding of the AlloDerm ultrastructure. They are freeze-
dried and stored in vacuum-sealed containers. At the
time of clinical use, they are rehydrated, centrifuged,
and rehydrated again to a final volume of 0.5 mL con-
taining approximately 150 mg of AlloDerm per mil-
liliter. The median particle size of AlloDerm is 123 Jim.
INDICATIONS
The clinical use of AlloDerm was first reported in 1995
for the treatment of full-thickness burns. 6 It appears
that when skin grafts are placed over AlloDerm on an
open wound, there is a similar time frame and graft
take characteristic of skin grafts without the use of
AlloDerm. This suggests rapid ingrowth of tissue with
AlloDerm. There also does not appear to be much evi-
dence of rejection or adverse reaction to the implant.17
According to the manufacturer, some surgeons have
used AlloDerm as a patch for fascial defects, such as
of the anterior rectus sheath in TRAM flap procedures
(Fig. 20-6).
AlloDerm has been used in the treatment of
depressed facial soft tissue defects,18 for the correc-
tion of nasal contour deformities,19,20 for intraoral
FIGURE 2 0 - 6 . Intraoperative view of patient's lower
abdomen during a TRAM flap procedure shows lower
abdominal skin retracted superiorly with a sheet of Allo-
Derm sewn into fascial defect margins of the anterior rectus
sheath {leftside). The umbilical stalk is seen in the upper
portion. (Photograph courtesy of Lee Colony, MD.)
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Dr.Mustafa D.
FIGURE 2 0 - 5 . Hematoxylin and
eosin-stained sections of allograft
skin (left) and AlloDerm (right). Note
the absence of cellular material in
the AlloDerm and the maintenance
of extracellular matrix structural
integrity. (Photographs courtesy of
LifeCell Corporation, Branchburg, NJ.)
resurfacing,21 for septal perforation repair,22 for lip aug-
mentation, ' and in the treatment of burn wounds.
It has also been used in conjunction with fat injec-
tions. The micronized form has been injected behind
the ear as part of a clinical investigation.16
USES
A common use of AlloDerm is lip augmentation. The
procedure is performed with regional blocks (infra-
orbital and mental nerves) as well as direct local anes-
thesia infiltration of the lips. Two 5-mm incisions are
made approximately 1 cm from the oral commissure
on either the upper or lower lip. A Bunnell tendon passer
is placed through the lip in the plane superficial to the
orbicularis muscle at the junction of the dry and wet
mucosa. A single standard 3 x 7-cm sheet of Allo-
Derm can be used for the upper and lower lips, divided
longitudinally into two thirds for the upper lip and
one third for the lower lip. The portion of the Allo-
Derm sheet for the upper lip is then pulled through
the tunnel and trimmed at its ends, and the wounds
are closed with chromic sutures. Care is taken not to
fixate the graft. Early results of this procedure (<2 years)
in 47 patients demonstrated no infection, exposure,
or hematoma. Three grafts of the 47 underwent
significant resorption within the first 12 months. A
patient questionnaire with 38% response showed a 53%
overall satisfaction rate, although 71% of the patients
said they would repeat the procedure. The most fre-
quent complaint was inability to appreciate a significant
postoperative difference (Fig. 20-7).23
x ~~*y t
x >
A B
FIGURE 2 0 - 7 . A, Preoperative lips. B, Postoperative
result at 6 months after AlloDerm insertion by the tech-
nique described in the text. (Photographs courtesy of Rod
Rohrich, MD.)
image...
20 • REPAIR AND GRAFTING OF DERMIS, FAT, AND FASCIA
One clinical study reported the use of AlloDerm
to augment facial defects in both adults and children.
Cleft lip-nasal deformities of the columella and ala as
well as post-traumatic soft tissue depressions of the
right commissure, chin, and nasolabial areas were aug-
mented. Techniques used were primarily tunneling of
theAlloDerm graft beneath the depression and fixation
with a 5-0 Vicryl suture. Some traumatic scars were
excised and closed with Z-plasties. Before final closure,
the AlloDerm graft was inserted into the pocket of the
wound. Follow-up in this study ranged from 6 to 20
months. Ten of the 11 patients had an average follow-
up of 13 months. Stability of the grafts was good.
Antibiotics were given postoperatively for 3 days. Rejec-
tion, mobilization, absorption, and extrusion of the
grafts were not seen.18
AlloDerm serves as a readily available onlay graft
in both primary and secondary rhinoplasty. The grafts
are useful for dorsal augmentation, correction of an
overresected dorsum, and coverage of an irregular
dorsum (Fig. 20-8). They can also be used to cover
5fc_
K:
^mm^gf
K
B k
tl
FIGURE 2 0 - 8 . A and C, Preopera- ; -
tive nasal dorsal defect. B and D, Post- T
operative result after 8 months with
placement of AlloDerm graft to the
nasal dorsum. (Photographs courtesy
of Rod Rohrich, MD.1
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
575
autogenous grafts (an open roof) and to camouflage
the inverted V deformity (collapsed lateral walls) .Allo-
Derm was not useful as a supporting graft except at
the piriform aperture in patients with cleft lip.19 Other
similar uses in rhinoplasty are coverage of osseo-
cartilaginous irregularities and elimination of the
adhesions between nasal bones and overlying skin
in secondary rhinoplasty to achieve a smooth nasal
dorsum. 20 There appears to be little reaction to Allo-
Derm, and tissue incorporation is good. Long-term
results, generally defined as 2 years, are good. However,
partial resorption of the grafts continues to be a
significant feature of the grafts. In the study by
Gryskiewicz,19 45% of the patients showed partial
graft resorption (defined as 50% or less) by 1 year
postoperatively.
OUTCOMES
AlloDerm as an implantable dermal matrix provides
a template for fibrous ingrowth, resulting in an
' • • -
/ * \
m
J&1
•
L - •' J H S J
4 M.
, ^ /
T
576 I • GENERAL PRINCIPLES
integrated graft that is not rejected. In a rabbit ear
model, vessel ingrowth was visible at the borders of
the grafts in 3 days and within the collagen bundles
of the grafts by 7 days. After 28 days, single-layer grafts
were structurally intact, with identifiable vessels
throughout the collagen bundles. There was no volume
loss.24 AlloDerm appears to be tolerated well from early
clinical reports. There have been no documented
reports of transmission of human immunodeficiency
virus or other viruses from AlloDerm. It can be used
for almost any area as long as there is adequate blood
supply to support the graft. AlloDerm survival in less
vascular areas is unknown. The benefit of eliminat-
ing a donor site is significant, especially in children.
The evaluation of long-term stability of the grafted
material continues.
FAT
History
Autogenous fat transplantation in humans was
reported as early as the late 1800s. Neuber is gener-
ally recognized as the first to use free fat autografts.
In 1893, he repaired a cosmetic defect around the orbit
by fat transplantation.26 Neuber stressed the use of mul-
tiple small grafts because he had previously failed with
the use of large fat grafts. In the early 20th century,
fat was transplanted for obliteration of orbital defects
after enucleation, in treatment of hemifacial atrophy,
and for enlargement of small breasts.27 In the 1960s
and 1970s, free autogenous fat grafts were used to fill
the dead space left behind after frontal sinus obliter-
ation.28 Grafts of fat were also used to cover dura during
lumbar spine operations29 as well as to cover nerves
and tendons. Free dermis-fat grafts have been used
throughout the 1900s for correction of soft tissue
deficits of the face. Leaf and Zarem30 brought atten-
tion to the technique of filling facial contours with
dermal fat grafts in 1972. They stressed gentle han-
dling of the tissues to reduce resorption and confirmed
previous studies demonstrating no significant cyst for-
mation from buried dermis. Dermal fat grafts are still
advocated for small to moderate soft tissue defects of
the face, such as with Romberg disease as described
by Mordick31 in 1992. Another use is for retro-
mandibular depressions after parotid resection or other
acquired or congenital soft tissue depressions.
With the growing use of dermis-fat grafts and the
observed phenomenon of variable resorption of the
grafts, different theories were proposed to explain their
ultimate fate after clinical implantation. One theory
was that fat grafts behave like bone grafts, which
undergo cellular death and are gradually replaced
by new cells of the same type.32 Others were less opti-
mistic and believed that fat is gradually replaced by
fibrous connective tissue. Two theories of fat survival
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Dr.Mustafa D.
eventually emerged as described by Billings and May.33
Proponents of the"host replacement theory"believed
the lipid material in transplanted cells would be taken
up by histiocytes that eventually replace the fat cells.
Peer34 opposed this theory and proposed instead the
"cell survival theory." This theory holds that trans-
planted fat cells survive, if vascularized, and histiocytes
remove, not replace, nonvascularized fat cells (Fig. 20-
9). Billings and May have described the behavior of fat
grafts during the days and weeks after transplantation.
During the first 3 days, there is extensive infiltration
of inflammatory cells, including plasma cells, lym-
phocytes, and eosinophils, without reaction of the
adipose cells or their surrounding stroma cells. By the
fourth day, small graft vessels have joined local host
vessels, and an increased number of eosinophils and
foreign body giant cells appear. At this point, progressive
fat degeneration proceeds, depending on the number
of fat cells that revascularize successfully. The process
of fat cell breakdown and inflammatory cell absorp-
tion peaks at 2 months. Progressive but slower fat
absorption occurs during the following months. Fat
that survives the process and is present at 1 year appears
to remain stable indefinitely (Fig. 20-10).
The unpredictability of the final fat volume that
remained after 1 year led to the standard technique of
"overcorrecting" the defect by 20% to 40%. Because
of this difficulty with dermis-fat grafts, surgeons
embraced the development of free tissue fat trans-
plantation in the 1970s. Early free tissue transfers of
omental fat were used for many purposes, including
resurfacing of scalp defects and restoration of contour
in hemifacial atrophy. The evolution of this technique
has resulted in free fascia-fat flaps or fasciocutaneous
free flaps such as the scapular flaps that are de-
epithelialized and used beneath the skin to augment
facial defects. The advantage of these flaps is less mobil-
ity of the transplanted fat at the recipient site and greater
ease of flap contouring during the inset. Finally, with
the advent of liposuction techniques in the 1980s, the
injection of fat aspirates represents the latest technique
for transplantation of autogenous fat tissue. Current
research in fat transplantation has similarly begun to
focus on the cellular level. The preadipocyte may be
the way to achieve fat transplantation without
significant volume loss. The preadipocyte is a con-
nective tissue cell that is virtually identical to a fibro-
blast but takes up lipid as it develops to become a mature
adipose cell. Tissue culture techniques have demon-
strated that the preadipocyte is a unique cell with the
ability to synthesize lipid material.35 Van and Roncari
transplanted preadipocytes from the rat epididymis
into an intramuscular location and saw a fat pad
develop at the intramuscular location. Billings and May
suggest that ischemia and poor cellular nutrition after
fat grafting cause mature fat cells to undergo necrosis
or to return to a more primitive cellular state as a
image...

20 • REPAIR AND CRAFTING OF DERMIS, FAT, AND FASCIA 577

1 until 4 days 4 days

Fat cell

Trapped °*<f>
poly **• Host cell
undergoing Graft
vessel exudate
diapeaes/s
Anastomosis
y \ bloodvessel B Host
Vessel

10 th day 30 days

Degenerating
fat cell H' istiocytes

H/stiocyh£ 9
:.

U
C3 ^ Host cell
exudate. Host cell
Penefra ting exudate.
host capillary

3 until 4 months 1 until 13 years

SurvivinQ
Fat ceil
Histiocytes
Fat cell .
absorbed

t qlobuk Fibroblasts

FIGURE 2 0 - 9 . A to F, The contrasting fate of two adipose cells in an autogenous human fat
transplant. The fat cell on the right fails to survive transplantation, and its fatty content is
removed by host histiocytes and other host cells. The fat cell on the left survives transplanta-
tion and constitutes part of the apparently normal adipose cells seen in the grafted area 1 year
or more after transplantation. The drawings are based on a series of autogenous human fat
grafts removed and examined histologically. (From Chiu DTW, Edgarton BW: Repair and graft-
ing of dermis, fat, and fascia. In McCarthy JC, ed; Plastic Surgery. Philadelphia, WB Saunders,
1990:517.)

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
578 • GENERAL PRINCIPLES
" • •
preadipocyte. With revascularization, the preadipocytes
that remain may mature into adipocytes but in a smaller
volume because of the loss of many mature cells after
transplantation. In the future, a surgeon may be able
to transplant preadipocytes that could develop into
mature fat cells without the loss of volume currently
seen in the transplantation process.
It is perhaps useful to divide fat grafting into four
categories. These arc free adipose tissue transplanta-
tion of fat cells and their stromal tissues (autogenous
free fat graft), transplantation of adipose tissue with
a dermal carrier (dermis-fat graft), transplantation of
free fat as a microvascular graft (free fat flap), and trans-
plantation of free fat aspirate from a suction harvest
technique (free fat injection).
Autogenous Free Fat Craft
Free fat grafts are used today much as they were
throughout the 1900s. They are transplanted for filling
of dead spaces in small well-vascularizcd areas or the
restoration of contour defects throughout the head and
neck. Dead spaces that are filled include the frontal
sinus after exenteration, the skull base after acoustic
neuroma resection, and the denuded dura mater
during lumbar spine operations. Fat is harvested from
the abdominal wall or a site that may already be in a
surgical field at the time of transplantation. There is
some evidence to suggest that gentle handling of the
grafts reduces loss of graft volume in the postopera-
tive period. The fate of these grafts in clinical use is
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Dr.Mustafa D.
FIGURE 2 0 - 1 0 . A, Autogenous human fat graft
buried in muscle for 21 days. Note the surviving fat
cells and large histiocytes. The histiocytes are resorb-
ing fat cells that have failed to survive. B, Autoge-
nous human fat graft buried in muscle for 40 days.
Note that there are surviving fat cells and that large
histiocytes are removing broken-down fat. C, Autog-
enous human fat graft buried in muscle for 14 months.
Note the normal-appearing fatty tissue. Craft loss
was approximately 50% of its volume. D, Autoge-
nous human fat graft buried in muscle for 13 years.
Its appearance is that of normal fatty tissue. Craft
loss was approximately 50% of its volume. (From
Chiu DTW, Edgarton BW: Repair and grafting of
dermis, fat, and fascia. In McCarthy JC, ed: Plastic
Surgery. Philadelphia, WB Saunders, 1990:518.)
variable, however, with different surviving volumes
after 1 year. There is some literature supporting the
long-term survival of fat grafts along the lumbar spine
by follow-up computed tomographic scans.29 Reported
complications from these transplants are relatively few,
although four instances of aseptic lipoid meningitis
due to subarachnoid fat migration from autologous
fat grafting have been documented after acoustic
neuroma resection. M
Dermis-Fat Graft
Dermis-fat grafts are indicated for conditions that
include reconstruction of facial and forehead contour
defects,37,38 orbital reconstruction of the anophthalmic
socket,39 coverage of nerves and tendons,40 and lip aug-
mentation. Dermis-fat grafts have even been used in
closure of palatal fistulas,41 cosmetic treatment of first
web space atrophy,12 and coverage of auricular carti-
lage grafts in cleft lip rhinoplasty.43 The uses of dermis-
fat grafts generally fall into three functional categories:
augmentation of small contour defects, provision of
a barrier between nerves and skin, and prevention of
adhesions around gliding surfaces.
HARVESTING
Dermis-fat grafts are usually harvested from the same
areas as full-thickness skin grafts are. These include
the lower abdomen, the suprapubic or periumbilical
regions, the gluteal or inframammary folds, the
TUWfiS'SeitfW image...

20 • REPAIR AND GRAFTING OF DERMIS, FAT, AND FASCIA 579

subiliac crest, and even the forearm for hand surgery

purposes. An ellipse of skin with dimensions appro-
priate to fill the recipient defect is outlined. The epithe-
lium can be removed by sharp excision with a scalpel
or dermabrasion. In general, it is easier to remove the
epithelium before the graft is detached; however, the
epithelium can be removed after detachment with a
Reese drum dermatome that attaches the skin to the
drum with an adhesive on the articular surface. The
remaining ellipse of dermis and subcutaneous fat is
incised to a level of 2 cm of maximum thickness and
removed as a single block of tissue. The donor site is
then closed in layers primarily. The graft is inset into
the recipient site as a single block after tailoring. Hemo-
stasis must be fastidious because hematomas are likely
to prevent graft take.

OUTCOMES
Experimental studies of dermis-fat grafts in pigs
demonstrated 33% loss of graft volume by 8 weeks.44
The volume loss was primarily attributable to fat.
Revascularization of dermis was noted microscopi-
cally, but no vessels were seen extending into the fat
(Fig. 20-11). This was presumably the reason for fat
loss. Other investigators have confirmed that the fat
tends to disappear in the porcine model over time (10
weeks).45 In humans, the historical work of Peer46,47 is
still the primary source of information about graft sur- B
vival. His studies performed in the 1950s concluded FIGURE 2 0 - 1 1. A, Autogenous human dermis-fat
that 45% of fat volume in dermis-fat grafts is lost graft buried 4 days on pull-out sutures. Note the absence
during 1 year. Interestingly, his work also showed that of cell infiltration, the unruptured fat cells, and the empty
patients who gained weight in the postoperative graft blood vessel (xlOO). B, The same graft showing an
area with two blood vessels engorged with red blood cells
period after graft transplantation had increased graft and adjacent adipose cells (x400). (From Chiu DTW, Edgar-
volume at follow-up. These studies have led to the ton BW: Repair and grafting of dermis, fat, and fascia. In
general guideline that dermis-fat grafts should be McCarthy JC, ed: Plastic Surgery. Philadelphia, WB
designed to overcorrect defects by 40%. Saunders, 1990:518.)

Free Fat Flaps
Free fat flaps are covered in greater depth in Chapter
16; however, the free omental flap is the single flap
consisting only of fat that can be transplanted by micro-
surgical technique. The free omental flap has been used
with varying success in the treatment of facial atrophy
and Romberg disease (Fig. 20-12). It has also been used
for scalp resurfacing. The omental flap is transplanted
as a pedicled flap based more commonly on the right
gastroepiploic artery for mediastinal reconstruction48
or less commonly on the left gastroepiploic vessels for
pelvic reconstruction (Fig. 20-13).49
Free Fat Injection
HISTORY
Soon after the introduction of liposuction in the 1980s,
the problem of contour depressions appeared. Surgeons
treated these depressions by free fat injection aug-
mentation. As early as 1983, Chajchir50 began presenting
work on liposuction fat grafts in the face. Illouz51
reported the fat cell "graft" as a new technique to fill
depressions in 1986. By the end of the 1980s, studies
were beginning to look at the effects of mechanical
stress on harvested adipocytes and at the long-term
survival of injected fat.52 Coleman53 most notably
recommended in the 1990s that fat be concentrated
by centrifuge and used in multiple planes throughout
the face.
INDICATIONS
The indications for the use of injected autologous fat
continue to expand. Fat can essentially be injected for
tissue augmentation in any subcutaneous location
where there is atrophy or missing tissue. The most
common indication is for facial augmentation. This

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Dr.Mustafa D.
T ^ t ^ y a c r f S P image...

580 I • GENERAL PRINCIPLES

if'

B
FIGURE 2 0 - 1 2. A, Adult patient with right hemifacial microsomia and significant soft tissue defects. B, Intraoper-
ative view of the same patient after harvesting of free omental fat flap. The thin omental free flap has been spread over
the facial areas, where it will be inset under the patient's skin after vascular anastomosis. C, Postoperative result at
11 months after inset of free omental flap.

includes effacement of the nasolabial folds54 and aug- HARVESTING

mentation of the lips, malar region, and cheek. The
fat injections can correct depressions or fatty deficits
due to lipodystrophy syndromes and atrophic areas.
Depressions of the abdominal wall, flanks, buttocks,
back, or thighs after liposuction can be improved
by fat injection. Reductive liposuction and fat aug-
mentation may be performed simultaneously. Fat
injection has been used not only over the torso and
face but also for augmentation of the paralyzed vocal
cord,55 for treatment of sphincteric incontinence by
perianal injection,56 and for penile augmentation. Some
authors report the use of fat augmentation through
injection to restore volume to the dorsum of the hands.
Breast augmentation with fat injection continues to
be unsatisfactory because of calcifications and the
inability to achieve survival of a significant volume of
fat injected.
Strict sterile technique must be observed when fat is
harvested.57 Lactated Ringer solution with 1:400,000
epinephrine is infiltrated bluntly through a stab
incision before harvesting. A 10-mL disposable
Luer-Lok syringe attached to a two-holed blunt
cannula is used to harvest the fat. Suction is applied
at a minimal negative pressure by slowly drawing
back on the plunger of the 10-mL syringe in a gradual
manner. The syringe that is filled with fat is then
spun in a centrifuge at 3000 rpm for 2 to 3 minutes,
or if time permits, it can be allowed to separate
by sedimentation. The material in the centrifuge
separates into three layers, of which the middle
layer is the usable subcutaneous tissue (Fig. 20-14).
The refined, concentrated fat is then transferred
to a 1-mL or 3-mL Luer-Lok syringe for injection

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20 • REPAIR AND CRAFTING OF DERMIS, FAT, AND FASCIA 581

C D
FIGURE 2 0 - 1 3. A, Patient with draining sternal wound after cardiac surgery and
previous attempt at closure with debridement and local muscle flaps. B, Sternal
wound has been debrided and irrigated. Pedicled omental fat flap is brought through
the laparotomy incision. The abdominal fascia is closed securely around pedicle
base after inset. C, Omental fat flap reaches to superior aspect of wound near base
of neck. O, In this patient, a meshed skin graft was applied to the surface of the
omental fat graft. A tension-free closure was obtained with adequate soft tissue
coverage of the heart and mediastinal structures. Uneventful healing was obtained.

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582 I • GENERAL PRINCIPLES

FIGURE 2 0 - 1 4 . A, Harvested subcutaneous material is placed into a centrifuge and spun for 3 minutes at
3000 rpm. B to C, This separates into levels on the basis of density. The oil layer is decanted. D, The Luer-Lok cap
is then removed, and the aqueous components are allowed to drain. E and F, A cottonoid surgical strip is inserted
for at least 4 minutes into the barrel of the syringe to wick any remaining oil. (Photographs courtesy of Sydney Coleman,
MD.)

(Fig. 20-15). The fat is injected through a blunt-tipped
18-gauge cannula. Small 1- or 2-mm incisions are
made with a No. 11 blade, the cannula is advanced
through the tissues, and the fat is injected during with-
drawal through the tissues. Approximately 7 8 mL is
placed evenly over the length of the tunnel formed
by the 18-gauge cannula.
Each single injection should be placed into a new
tunnel at the site of fat implantation.57 The grafted fat
should be deposited as tiny fractions of a milliliter,
lining up like peas in a pod, with avoidance of oblong
or spherical configurations. Fat is placed through hun-
dreds of passes of the blunt-tipped cannula and is
layered at multiple levels in a three-dimensional
manner. Augmentation over the malar or mandibu-
lar regions begins initially next to the bone. Sequen-
tially, more superficial layers are placed. It is believed
that fat placed in this way will result in good long-
term survival of the grafts. However, because the injec-
tant contains some lidocaine, blood, and oil, which
will be resorbed, some overcompensation is coordi-
nated into the operative plan (Fig. 20-16).57
OUTCOMES
The degree to which injected fat grafts survive at their
recipient sites remains shrouded in controversy.
Although it is widely acknowledged that fat trans-
planted by injection can achieve long-term survival,
it is the reliability and predictability of results thathave
remained elusive for many surgeons.
Although undercorrection implies that the surgeon
did not place enough graft material, resorption is
another plausible explanation when this untoward
sequela occurs. Overcorrection is another problem that
can be encountered with fat injection. This is a more
difficult problem to solve. Prolonged edema can be seen
with fat injection. Although most edema resolves in
the first 2 weeks, swelling and induration may be
observed up to 1 year. Necrosis and migration of grafted
tissue can occur. For necrosis to be avoided, multiple
small passes should be used instead of large deposits.
Migration tends to occur around areas of fibrous attach-
ment, such as scars and retaining ligaments. Injection
around the attachments builds higher pressure or
tension around the graft, allowing it to migrate to lower
pressure areas. Lack of feathering of the grafts around
specific folds or lines may result in lumpy-appearing
deposits. Infections may occur, sometimes the result
of unnoticed perforations of the oral mucosa.
Complications arising from fat injection are not
common but can be serious. Fat injection into the
glabellar region has resulted in three reports of patients
with unilateral loss of vision.58 In one patient, there

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Dr.Mustafa D.
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20 • REPAIR AND GRAFTING OF DERMIS, FAT, AND FASCIA 583

FIGURE 2 0 - 1 5. Refined fat is transferred from the 10-mL syringes into I -rnL Luer-Lok syringes. The 1 -mL syringes
should be filled in an oblique upward direction to avoid air bubbles (above). Placing an index finger over the Luer-
Lok controls the column of fat as it slips down the syringe (below). The plunger is then replaced and advanced to
remove the dead space. (Photograph courtesy of Sydney Coleman, MD.)

was a coincident middle cerebral artery embolism. It
was presumed that fat injected into the facial artery of
these patients reached the orbital and cerebral arter-
ies in a retrograde fashion. Two other instances of facial
fat injections resulting in devastating complications
have been reported. In one patient who had injection
into the nasolabial folds, lower lip, and chin, global
aphasia and mild right sensorimotor hemiparesis
developed 7 hours after surgery. A magnetic resonance
imaging scan demonstrated infarction in the course
of the left middle cerebral artery and multiple fat emboli
in the right retinal artery. The infarction resulted in
permanent fluent speech aphasia. Another patient who
had autologous fat injected into the periorbital areas
for correction of crow's-feet under local anesthesia
experienced left eye pain and violent headaches and
became stuporous and unresponsive. She had com-
plete flaccid right hemiplegia and global aphasia with
deviation of the head and eyes toward the left. Selec-
tive angiography of the left carotid artery confirmed
occlusion of the left ophthalmic artery. Magnetic res-
onance imaging demonstrated infarctions in the left
cerebral hemisphere. The patient regained the ability
to walk and had improvement of the global aphasia
but remained permanently blind in the left eye. The
conclusion of these reports recommended caution in
injecting regions of the face supplied by internal carotid
artery flow.
Coleman, S9 writing in the Aesthetic Surgery Journal,
addressed the issue of arterial occlusion from injec-
tion of soft tissue fillers. He reviewed several reports
of blindness, stroke, and skin necrosis after injection
of soft tissue fillers. He speculated that a needle or
cannula used to inject soft tissue filler can acciden-
tally perforate the wall of one of the distal branches
of the ophthalmic artery. Many superficial arteries of
the face, such as the supraorbital, supratrochlear, dorsal
nasal, and angular artery of the nose, are distal
branches of the ophthalmic. Filler may be pushed
retrograde through the ophthalmic artery, traveling
as a column proximally past the origin of the retinal
artery. As the surgeon stops pressure on the syringe
plunger, the arterial systolic pressure propels small
amounts of the filler into the retinal artery. Another
route for high-pressure filler to take is into the inter-
nal carotid; it subsequently embolizes, causing stroke.
The same filler can embolize the arterial supply of
mucous conjunctiva or skin, resulting in necrosis. He

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584 I • GENERAL PRINCIPLES
relays in his article that blindness, stroke, and skin
necrosis have been reported after injection of only
0.5 mL of filler into the region of the nasal bridge.
Coleman suggests that the use of larger blunt cannu-
las, vasoconstriction by epinephrine at that injection
site, and injection of 0.1 mL of filler of less per pass
are practical ways to limit these complications. Sharp
cannulas, small cannulas, and needles are more likely
to perforate arterial walls and in his opinion are to be
avoided.59
Fat injection to correct a left-sided groin defect has
caused cyst formation with pearl-like fat lobules. The
volume of fat injected was 40 mL, and 5 months post-
operatively, a 3 X 10-cm cyst containing pearl-like fat
lobules was removed from the region.60
A giant liponecrotic pseudocyst has been reported
10 months after breast augmentation with fat injec-
tion. A 10 x 8-cm pseudocystic mass with fibrocalcific
walls, fat necrosis, and cystic formations of an oily fluid
was removed.61
A complication related to fat injections of the penis
for augmentation has been reported.62 Four stages of
fat injection were performed on a 34-year-old man
each time for presumed resorption. The abdomen and
buttocks were used as donor sites. During a period of
6 months, the fat was resorbed in an irregular manner,
leaving the patient with a mushroom-shaped penis.
The penis was explored surgically, and numerous small
(2 to 3 mm) yellowish globules that had the appear-
ance of caviar were discovered in a bursa-like sac. The
cavities also contained a yellowish fluid consistent with
serum or liquefied fat.
Fat grafts that do not take may become lined with
fibrotic tissue and persist in this state indefinitely. A
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FIGURE 2 0 - 1 6 . A, From two or
three separate 2-mm incisions,
numerous passes are made to place
minuscule tunnels of fat. From the
same incision, tat is gradually placed
over the entire planned area. After
a radiating network of tunnels has
been placed through one incision (S,
such as the cheek), a similar network
of tunnels is made from another site
(C such as the temple). D, Fat is pri-
marily placed when the cannula is
withdrawn. [Photograph courtesy of
Sydney Coleman, MD.)
subsequent infection of this material might theoreti-
cally require debridement and antibiotics to resolve
the infection.
FASCIA
History
In the early 1900s, McArthur63 performed the first
reported fascial free graft transfer. These were nonvas-
cularized grafts consisting of strips of external oblique
aponeurosis that were used as biologic sutures to repair
inguinal hernias. Fascial strips of autogenous fascia
lata were later used as slings to correct facial nerve
palsy.64 These techniques, popularized by Blair65 in the
1920s, continue to be used today. The fascial tissue of
the tensor fascia lata has been used for repair of joints,
reconstruction of the thoracoabdominal wall, repair
of dural defects, repair of penile chordee, facial rean-
imation, and brow lift suspensions. With a greater
understanding of the blood supply of the fascia lata,
it was used as a pedicled musculocutaneous flap for
local repairs, such as of trochanteric pressure sores,
lower abdominal defects after tumor excision, and
bladder exstrophy. In the 1970s, free tissue transplan-
tation allowed use of this large source of fascia (tensor
fascia lata) in a vascularized form throughout the
human body. The advantages of the free flap are the
ability to extend its use for supraumbilical or distant
repairs, such as of the pharynx, and its survival in con-
taminated or relatively ischemic environments. Other
fascial flaps include the temporoparietal fascial flap
and the radial forearm flap. The lateral arm, anterior
thigh, and posterior calf are described donor sites.
image...
20 • REPAIR AND GRAFTING OF DERMIS, FAT, AND FASCIA
Indications and Use
Surgeons can repair abdominal wall fascial defects with
several forms of fascia or prosthetic mesh. Tensor fascia
lata may be used as a free graft, as a pedicled flap, or
as a vascularized free flap. Free tensor fascia lata grafts
maybe used if there is a defect of fascia only with well-
vascularized, adequate local soft tissue coverage.
Wounds should additionally be clean or only lightly
contaminated. Free fascial grafts are also useful as onlay
grafts when the primary fascia repair may be tenuous. 66
Free tensor fascia lata may be used in the epigastrium
or in lieu of two pedicled flaps. The vascularized tensor
fascia grafts in either pedicled or free form are prefer-
able in defects with heavier colonization or relatively
ischemic native tissues. In general, the pedicled tensor
fascia lata flap is used for lower abdominal defects of
limited size requiring both fascia and soft tissue cov-
erage. Technical points given by Carlson et al66 include
use of absorbable Vicryl mesh under flaps to provide
protection during the initial postoperative period. In
this series, of six free tensor fascia lata flaps performed,
fascial dehiscences occurred in two patients in whom
Vicryl mesh was not used. Their patients were kept at
bed rest for 5 days after the procedure, and when pos-
sible, they did not use the distal third of the flap because
of high necrosis rates. Although tensor fascia lata
myocutaneous flaps can be harvested within 5 cm of
the knee joint, delay may prevent tip necrosis.
New approaches to the abdominal wall defect
include techniques using local musculofascial flaps that
have the advantage of providing innervated musculo-
fascial support. The main requirement of this tech-
nique, known as the components method of closure,
is that the anatomic components of the abdominal wall
must be intact. These components are the rectus muscle
and its sheaths and the oblique muscles and their
aponeuroses. The technique is limited to midline
defects less than 20 cm wide. The recruitment of mus-
culofascial tissue at the superior abdomen near the
xiphoid and the lower abdomen near the pubis is not
as great. After wide subcutaneous undermining, the
external oblique fascia is incised and released lateral
to its condensation at the rectus abdominis border, sep-
arating it from the underlying internal oblique muscles.
If more release of the abdominal musculofascial units
is needed, the posterior rectus sheath is incised and
the rectus muscle is elevated from the posterior rectus
sheath (Fig. 20-17). 67
Facial palsy has been treated historically with
fascial strips used either as static slings to resuspend
facial components or as connectors between active
muscles and the paralyzed facial components. Fascial
strips are typically harvested from the fascia lata and
inserted either around the oral commissure or around
the lateral canthus of the eye. This can be done in stages,
first as an initial procedure to allow tissue incorpora-
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Dr.Mustafa D.
585
tion into the fascial graft at the oral commissure, for
example, followed by a secondary procedure ro connect
the active muscle components to the original fascial
graft. Alternatively, all of the fascial grafting can be
done as a one-stage procedure.
Fascial free grafts have also been used for aug-
mentation of nasal or facial defects. As with dermal
grafts, the fate of the grafts is variable. When it is used
for augmentation of small areas, such as the glabella,
fascia can be harvested from the external surface of
the temporalis muscle. Other uses include the closure
of nasal septal defects and the repair of urethral
fistulas.
The fascia just superficial to the deep temporal
fascia, or the temporoparietal fascia, is supplied by
the superficial temporal artery and vein. The tem-
poroparietal fascial flap has been used in numerous
clinical situations during the last 2 decades. As a local
pedicled flap, it has been used to cover exposed eai
cartilage or cartilage frameworks fabricated for micro-
tia repair. Although the flap is relatively thin, it is usually
covered with a skin graft when it is used for otologic
purposes, and the final result is not as delicate as one
would like. As a free flap, the temporoparietal fascial
flap can provide a thin coverage for gliding surfaces,
such as extensor tendons on the hand or foot
dorsum. The temporoparietal fascial flap has also been
used for coverage of Achilles tendon and orbital
reconstruction.
Harvesting
The harvesting of a fascia lata graft may be performed
at the lateral aspect of the thigh by an open approach
for large grafts or a more closed technique for long,
thin grafts. For a strip of fascia 10 to 15 mm wide, a
small incision can be made over the iliotibial tract above
the knee joint. A transverse incision exposes the fascia.
Two incisions are made parallel to the fibers of the
fascia lata as wide as the desired graft. The two inci-
sions are joined at right angles, with the transverse
incision raising a small flap of fascia lata. The end of
the fascial strip is passed through the stripper, and the
fascial flap is secured with a clamp. Traction is placed
on the fascia, pulling it toward the knee. The stripper
is pushed proximally under the subcutaneous tissue
of the thigh toward the muscle belly of the tensor fascia
lata as it strips the fascia parallel along its fibers. Some
strippers have a guillotine-type mechanism that can
be activated to sever the upper end of the graft. The
small cutaneous wound may be sutured, and a com-
pressive dressing can be applied to the leg. The result-
ing fascial graft can be divided into multiple strips
along its long axis. Desiccation of the grafts should be
avoided (Fig. 20-18). Techniques for elevation and
transplantation of the tensor fascia lata flap are dis-
cussed in Chapter 16.
586 I • GENERAL PRINCIPLES

FIGURE 2 0 - 1 7. Technique of abdominal closure by use

of components separation. A, Large chronic abdominal wound
cannot be closed because of fascial defect in midline. Clamps
are on edges of fascia at margins of wound with exposed
bowel and omentum visible. B, Fascial wound edges can be
brought together without tension after release of external
oblique fascia near lateral border of rectus abdominis muscle.
C, Fascial edges of abdominal wound are sewn together
without tension. This completes the fascial closure of the
abdominal wound. Placement of drains above the fascia and
skin closure conclude the operation. (Photographs courtesy
of Michael S. Wong, MD.)

Outcomes directly sutured beneath the skin without a fascial inter-

Fascial grafts demonstrate variations in survival. As
early as 1924, Gallie and Le Mesurier68 reported newly
formed vascular tissue around free grafts used for hernia
repair after 3 weeks. More recently, vascularization was
demonstrated by fluorescein angiography at 3 and 6
weeks.69 In contrast, transplantation of fascia into
corneas has shown little reaction after 4 to 6 weeks.70
Studied years after transplantation, strips used for ptosis
repair showed relatively little survival and incorpora-
tion of the graft.71 Other authors demonstrated revas-
cularization of fascia when it is placed as a single layer
between two layers of vascular tissue but no revascu-
larization when the fascia is folded (two fascial layers
together) or placed on bone. The collagen matrix of
the fascia, however, was maintained in all experimen-
tal conditions.72 Another study in rats demonstrated
that the interposition of a free fascial graft between an
isolated vascular pedicle and overlying skin stimulates
more vascularization to the skin than does a pedicle
position graft.73 It appears that fascial grafts can achieve
vascularization in certain good or ideal conditions;
however, even when conditions are poor, significant
structural integrity remains for a relatively long time.
Vascularized fascial flaps such as the tensor fascia
lata flap and the temporoparietal flap can have excel-
lent postoperative results; however, each flap has
certain areas of difficulty. Nahai74 reported his expe-
rience with 60 tensor fascia lata flaps, of which 37 were
used for pressure sore reconstruction. He found the
tensor fascia lata flap to be reliable for groin and lower
abdominal wall reconstruction. O'Hare75 reported four
pedicled tensor fascia lata flaps for large abdominal
wall defects. Of his three extended pedicled tensor fascia
lata flaps, two required revision for tip necrosis.
Carlson66 reported nine instances of pedicled tensor
fascia lata flaps for abdominal wall repair. Two of these
nine flaps had greater than 50% necrosis, and a third
had tip necrosis. The author of this study recom-
mended delay for the extended pedicled or free tensor

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20 • REPAIR AND CRAFTING OF DERMIS, FAT, AND FASCIA 587

FIGURE 2 0 - 1 8. A, Patient with large right lower quadrant hernia. Hernia sac covered by skin grafts. B, Right
lower quadrant fascial defect repaired with mesh. C, Outline of tensor fascia lata myocutaneous flap on right
thigh. D, Elevation and rotation of tensor fascia lata myocutaneous flap to right lower abdominal defect. E, Inset
of flap into right lower quadrant defect of abdomen. F, Postoperative follow-up of tensor fascia lata flap to right
lower quadrant defect at 2 years after surgery.

fascia lata flap. The overall complication rate of 48%
for this series of 27 patients underscores the difficulty
of reconstructing these challenging abdominal wall
defects.
Dissection of the temporoparietal flap must be
meticulous. Vessels are initially identified in the preau-
ricular region, and the large superficial temporal vein,
lying directly beneath the preauricular incision, must
not be injured. According to Upton,' who described
15 patients with Achilles tendon defects, the variations
of the superficial temporal vessels should be recog-
nized and a template of required tissue oudined directly
over the vessels. Of the 12 patients receiving tem-
poroparietal fascial flaps for Achilles coverage, one flap
had partial loss, one flap had delayed healing, and three
flaps had delayed take of the skin graft. Woods77

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588 I • GENERAL PRINCIPLES
described 21 patients with temporoparietal fascial flaps
for lower extremity reconstruction. O n e flap was com-
pletely lost 10 venous thrombosis (4.8%), four patients
had partial (between 20% and 40%) flap loss (20%),
and four patients had transient d o n o r site alopecia
(20%). I lowever, all patients were performing weight-
bearing ambulation within 1 m o n t h of surgery, and
no patient required the use of modified footwear.
SUMMARY
Autogenous tissue grafting is increasing in importance
as the need to fill contour deficits increases. D e r m i s
and fascia were originally used for structural repairs,
which progressed to the filling of minor contour irreg-
ularities. T h e fat graft has also been widely used for
contour irregularities and the filling of volume deficits
because of its ample availability. However, the problem
of graft resorption with free fat led to the develop-
m e n t of several techniques to enhance graft p e r m a -
nence. Small blocks of free stromal fat combined with
dermis, constituting the dermal fat graft, demonstrate
better but unpredictable survival, depending on the
blood supply and anatomic location of the recipient
site. T h e development of microsurgical techniques led
to the free fat flap, which brought blood supply with
the transplanted fat. Donor site morbidity, limited
d o n o r flaps, and large size requirements of the trans-
planted fat flap units make this practical for only
selected indications. Injection of free fat by needle and
cannula is currently being refined as a useful and prac-
tical technique because of its broader application with
limited donor site morbidity. Multiple deposits of small
beads of fat in well-vascularized tissues have been stated
to achieve long-term survival. Also, off-the-shelf grafts
with immunogenic tolerance, such as AlloDerm, are
currently gaining in popularity. D e m a n d for minimal
augmentation of acquired deformities, such as sub-
cutaneous atrophy with aging, is driving development
of these techniques. We can anticipate the introduc-
tion of many more of these autogenous or acellular
grafts in the future. Cellular research in many areas,
such as with the preadipocyte, may provide new ways
to fill defects or to replace tissues in the future. T h e
historical problems of variable graft resorption and
unpredictable volume retention of these grafts as well
as the refinement of their indications for use will con-
tinue to be evaluated over the long term.
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Aesthetic Surg Q 1996;16:196-201.
18. Achauer BM, VanderKam VM, Celikoz B, Jacobson DC:
Augmentation of facial soft-tissue defects with Alloderm
dermal graft. Ann Plast Surg 1998;41:503-507.
19. Gryskiewicz JM, Rohrich RJ, Reagan BJ: The use of AlloDerm
for the correction of nasal contour deformities. Plast Reconstr
Surg 2001;107:561-570.
20. Jackson IT, Yavuzer R: AlloDerm for dorsal nasal irregularities.
Plast Reconstr Surg 2001;107:553-558.
21. Rhee PH, Friedman CD, Ridge JA, Kusiak J: The use of processed
allograft dermal matrix for intraoral resurfacing. Arch Oto-
laryngol Head Neck Surg 1998;124:1201-1204.
22. Kridel RW, Foda H, Lunde KC: Septal perforation repair with
acellular human dermal allograft. Arch Otolaryngol Head Neck
Surg 1998;124:73-78.
23. Rohrich RJ, Reagan BJ, Adams WP, et al: Early results of ver-
milion lip augmentation using acellular allogeneic dermis: an
adjunct in facial rejuvenation. Plast Reconstr Surg 2000; 105:409-
418.
24. Eppley BL: Revascularization of acellular human dermis (Allo-
derm) in subcutaneous implantation. Aesthetic Surg J 2000;
20:291-295.
25. Castor SA, To WC, Papay FA: Lip augmentation with AlloDerm
acellular allogenic dermal graft and fat autograft: a compari-
son with autologous fat injection alone. Aesthetic Plast Surg
1999;23:218-223.
26. NeuberGA: Fettransplantation.Verh Dtsch GesChir 1893;22:66.
27. Lexer E: Free transplantation. Ann Surg 1914;60:166.
28. Schenck NL: Frontal sinus disease. III. Experimental and
clinical factors in failure of the frontal osteoplastic operation.
Laryngoscope 1975;85:76-92.
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20 • REPAIR AND GRAFTING OF DERMIS. FAT, AND FASCIA
29. Bryant MS, Bremer AM, Nguyen TQ: Autogeneic fat transplants
in the epidural space in routine lumbar spine surgery. Neuro-
surgery 1983;13:367-370.
30. Leaf N, Zarem HA: Corrections of contour defects of the face
with dermal and dermal-fat grafts. Arch Surg 1972;105:715-
719.
31. Mordick TG II, Larossa D, Whitaker L: Soft-tissue reconstruc-
tion of the face: a comparison of dermal-fat grafting and vas-
cularized tissue transfer. Ann Plast Surg 1992;29:390-396.
32. Neuhof H: The Transplantation of Tissues. New York, Apple-
ton, 1923.
33. Billings E Jr, May JW Jr: Historical review and present status of
free fat graft autotransplantation in plastic and reconstructive
surgery. Plast Reconstr Surg 1989;83:368-381.
34. Peer LA: The neglected free fat graft. Plast Reconstr Surg
1956;18:233.
35. Van RL, Roncari DA: Complete differentiation in vivo of
implanted cultured adipocyte precursors from adult rats. Cell
Tissue Res 1982;225:557-566.
36. Ricaurte JC, Murali R, Mandell W: Uncomplicated postopera-
tive lipoid meningitis secondary to autologous fat graft necro-
sis. Clin Infect Dis 2000;30:613-615.
37. Davis RE, Guida RA, Cook TA: Autologous free dermal fat graft.
Arch Otolaryngol Head Neck Surg 1995;121:95-100.
38. Lapierc JC, Aasi S, Cook B, Montalvo A: Successful correction
of depressed scars of the forehead secondary to trauma and
morphea en coup de sabre by en bloc autologous dermal fat
grafts. Dermatol Surg 2000;26:793-797.
39. BonavolonaG.Tranfa F,SaliconeA,Strianese D: Orbital dermis-
fat graft using periumbilical tissue. Plast Reconstr Surg
2000;105:23-26.
40. McClinton MA: The use of dermal-fat grafts. Hand Clin
1996;12:357-364.
41. VanDeput JJ, Droomgmans B, Tranner JC: Closure of palatal
fistulas using a dermis-fat graft. Plast Reconstr Surg 1995;
95:1105-1107.
42. Ghobadi F, Zangeneh M, Massoud BJ: Free fat autotransplan-
tation for the cosmetic treatment of first web space atrophy.
Ann Plast Surg 1995;35:197-200.
43. Nakakita N> Sezaki K, Yamazaki Y, Uchinuma E: Augmentation
rhinoplasty using an L-shaped auricular cartilage framework
combined with dermal fat graft for cleft lip nose. Aesthetic Plast
Surg 1999;23:107-112.
44. SawhneyCP,BanerjeeTN,ChakravartiRN:Bchaviorof dermal
fat transplants. Br J Plast Surg 1969;22:169-176.
45. Mackay DR, Manders EKt Saggers GC, et ah The fate of dermal
and dermal-fat grafts. Ann Plast Surg 1993;31:42-46.
46. Peer LA: Loss of weight and volume in human fat grafts with
postulation of a "cell survival theory." Plast Reconstr Surg
1950;5:217.
47. Peer LA: The neglected "free fat graft," its behavior and clinical
use.AmJSurgl956;92:40.
48. Wormon IL III, Maragh H, Pozez A, Guerraty AJ: Use of the
omentum in the management of sternal wound infection after
cardiac transplantation. Plast Reconstr Surg 1995;95:697-
702.
49. KusiakJF,RosenblumNG:Neovaginal reconstruction after exen-
teration using an omental flap and split-thickness graft. Plast
Reconstr Surg 1996;97:775-783.
50. Chajchir A: Liposuction fat grafts in face. Presented at the 11th
Annual Symposium on Aesthetic Plastic Surgery, University of
Guadalajara, November 7,1983.
51. Illouz YG: The fat cell graft: a new technique to fill depressions
[letter to editor]. Plast Reconstr Surg 1986;78:122.
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589
52. Chajchir A, Benzaquen I: Fat-grafting injection for soft-tissue
augmentation. Plast Reconstr Surg 1989:85:921-934.
53. Coleman S: Long-term survival of fat transplants: controlled
demonstration. Adv Plast Surg 1995;19:421-425.
54. Guyuron B: The armamentarium to battle the recalcitrant
nasolabial fold. Clin Plast Surg 1995;22:253-264.
55. Bauer CA, Valentino J, Hoffman HT: Long-term result of vocal
cord augmentation with autogenous fat. Ann Otol Rhinol Laryn
gol 1995;104:871-874.
56. Shafik A: Perianal injection of autologous fat for treatment of
sphincteric incontinence. Dis Colon Rectum 1995;38:583-587.
57. Coleman SR: Facial recontouring with lipostructure. Clin Plast
Surg 1997;24:347-367.
58. Feinendcgen DL, Baumgartner RW, Vuadens P, et al: Autolo-
gous fat injection for soft tissue augmentation in the face: a safe
procedure? Aesthetic Plast Surg 1998;22:163-167.
59. Coleman SR: Avoidance of arterial occlusion from injection of
soft tissue fillers. Aesthetic Surg J 2002;22:555-557.
60. Mandrckas AD, Zambacos GJ, Kittas C: Cyst formation after fat
injection. Plast Reconstr Surg 1998;102:1708-1709.
61. Castello JR, Barros J, Vazquez R: Giant liponecrotic pseudocyst
after breast augmentation by fat injection. Plast Reconstr Surg
1999;103:291-293.
62. Leithauser LC, Gilbert E, Barton J: Complications of fat graft-
ing to the penis. Ann Plast Surg 1995;34:173-175.
63. McArthur LL: Autoplastic sutures in hernia and other diseases.
JAMA1904;43:1039.
64. Kischner M: Ober freie Sehnen- und Faszientransplantation.
BeitrKlinChirl909;65:472.
65. Blair VP: Notes on the operative corrections of facial palsy. South
Med J 1926;19:116.
66. Williams JK, Carlson GW, deChalain T, et al: Role of tensor
fasciae latac in abdominal wall reconstruction. Plast Reconstr
Surg 1998;101:713-718.
67. Girotto JA, Ko MJ, Redctt R, et al: Closure of chronic abdomi-
nal wall defects: a long-term evaluation of the components
separation method. Ann Plast Surg 1999;42:385-395.
68. Gallie WE, Le Mesuricr AB: The use of transplants of fascia as
living sutures in the treatment of hernia. Arch Surg 1924;9:516.
69. Disa JJ, Klein MH, Goldberg NH: Advantages of autologous
fascia versus synthetic patch abdominal reconstruction in exper-
imental animal defects. Plast Reconstr Surg 1996;97:801-806.
70. Crawford JS: Nature of fascia lata and its fate after implanta-
tion. Am J Ophthalmol 1969;67:900-907.
71. Orlando F, Weiss JS, Beyer-Machule CK, et al: Histopathologic
condition of fascia lata implant 42 years after ptosis repair. Arch
Ophthalmol 1985;103:1518-1519.
72. Das SK, Davidson SF, Walker BL, Talbot PJ: The fate of free
autogenous fascial grafts in the rabbit. Br J Plast Surg 1990;
43:315-317.
73. Guriinluoglu R, Bayramicli M, Dogan T, et al: Use of fascial
grafts as an interface in flap prefabrication: an experimental
study. Ann Plast Surg 1999;43:42-48.
74. Nahai F, Hill HL, Hester TR: Experiences with the tensor fascia
lata flap. Plast Reconstr Surg 1979;63:788-799.
75. O'Hare PM, Leonard AG: Reconstruction of major abdominal
wall defects using the tensor fasciae latae myocutaneous flap.
Br J Plast Surg 1982;35:361-366.
76. Upton J, Baker TM, Shoen SL, Wolfort F: Fascial flap coverage
of Achilles tendon defects. Plast Reconstr Surg 1995;95:1056-
1061.
77. Woods JMIV, Shack RB, Hagan KF: Free temporoparietal fascia
flap in reconstruction of the lower extremity. Ann Plast Surg
1995;34:501-506.
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CHAPTER
21
•
Repair and Grafting of Tendon
PHYLLIS CHANG, MD
ANATOMY
Tendons
HISTOLOGY AND BIOCHEMISTRY
Myotendinous and Osteotendinous Junctions
Light Microscopic Appearance of Tendon
TENDON NUTRITION
TENDON AND CRAFT HEALING
Stages of Tendon Healing
Extrinsic Versus Intrinsic Healing
Modulators of Tendon Healing
ANATOMY
Tendons
Tendons are glistening white anatomic structures
interposed between muscles and bones. They trans-
mit the force created in muscle to bone and make joint
movement possible. Tendons may be surrounded by
a bed of loose areolar tissue called paratenon, or they
may reside within a tunnel of dense fibrous tissue, the
tendon sheath.
PARATENON
In areas not subjected to mechanical stress, the
paratenon encases the tendon in loosely arranged con-
nective tissue consisting essentially of type I and type
III collagen fibrils, some elastic fibrils, and an inner
lining of synovial cells. The tendon is bathed in a fluid
environment similar to synovial fluid (Fig. 21-1).
Nestled within the paratenon, the entire tendon is
covered by the epitenon (also called mesotenon), a
fine, loose connective tissue sheath containing the
vascular, lymphatic, and nerve supply. The epitenon
extends deeper into the tendon between the tertiary
bundles of collagen fibrils as the endotenon. Together,
the paratenon and epitenon are sometimes called the
peritendon (Fig. 21-2). u
TENDON SHEATH
The classic two-layered synovial tendon sheath is
present only in certain tendons as they pass areas of
increased mechanical stress. These sheaths span an area
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CLINICAL APPLICATION
Repair of Tendon Laceration
Variables That Affect the Outcome of Tendon Repair
Tenolysis
Tendon Grafting
TENDON SUBSTITUTES
Allograft
Synthetic Graft Replacements
from the metacarpal heads to the midportion of the
distal phalanges. The outer layer is the fibrotic (liga-
mentous) sheath; the inner layer is the synovial sheath,
which consists of thin visceral and parietal sheets. The
parietal layer is not unlike the synovial lining of a joint;
it allows smooth gliding of tendon as well as provides
synovial fluid nutrition. The annular and cruciate
pulleys in these fibrous sheaths provide mechanical
advantage as they hold tendons close to the bone while
allowing acute flexion of the interphalangeal joints (Fig.
21-3).3,4 The key pulleys that inhibit bowstringing of
flexor tendons are located at the proximal portion
of the proximal phalanx (A2 pulley) and at the mid-
portion of the middle phalanx (A4 pulley).
BLOOD SUPPLY
Within the hand, tendons are vascularized along the
entire length in a longitudinal pattern. The different
sources are vessels that enter the palm and extend down
intratendinous channels, vessels that enter from the
proximal synovial fold in the palm, segmental vessels
that develop from paired digital arteries and enter
tendon sheaths as vincula, vessels that enter the
osseous insertions of the tendon, and vessels at the
musculotendinous junction. By and large, the major-
ity of these vessels supply the dorsal or posterior surface
of tendon.
A tendon in an area of low compression is vascu-
larized by small vessels that enter at multiple levels from
the surrounding areolar tissue. Blood flow is low,
averaging less than 10 mL per 100 g per minute.5 In
591
image...

592 I • GENERAL PRINCIPLES

Collagen provides tendon with tensile strength; ground

Paratenon
FICURE 2 1 - 1 . The paratenon at the forearm is a filmy,
homogeneous material containing mucopolysaccharide
components that facilitate the gliding motion. The
paratenon is composed of fine collagen fibers arranged
as a loosely laced network that contributes to its pliabil-
ity. (From Chu DTW, Edgerton BW: Repair and grafting of
tendon. In McCarthy JG, ed: Plastic Surgery. Philadelphia,
WB Saunders, 1990:527-545.)
contrast in compressed areas, such as across a joint
space, nutrition comes from the segmental vincula.
Within the digital sheath, both profundus and sub-
lines tendons have relatively avascular segments over
the proximal phalanx; the profundus has an additional
short avascular zone over the middle phalanx. In these
avascular zones, tendons must rely on synovial fluid
pumping for nutrition.6*10
HISTOLOGY AND BIOCHEMISTRY
The basic elements of tendon are collagen bundles
(70%), cells, and ground substance or extracellular
matrix, a viscous substance rich in proteoglycans.
substance provides structural support for the collagen
fibers and regulates the extracellular assembly of pro-
collagen into mature collagen. Proteoglycans regulate
tissue strength because they determine the size and
packing of collagen fibrils."
The collagen fibril diameter in the adult tendon typ-
ically ranges from 100 to 200 nm, but this will vary
with tissue loading. With increasing tensile loads, there
is a shift toward higher fibril diameter.12 Tenocytes (or
fibrocytes), flat tapered cells sparingly distributed
among the collagen fibrils, synthesize both the ground
substance and the procollagen building blocks of
protein.
Collagen is arranged in hierarchical levels of increas-
ing complexity beginning with tropocollagen, a triple-
helix polypeptide chain. Each tropocollagen is
composed of helical arrangement of two Ctl(I) and
one a2(I) collagen chains.13 These helical molecules
of tropocollagen in turn unite into fibrils, fibers
(primary bundles), fascicles (secondary bundles) that
spiral into tertiary bundles, and finally the tendon itself
(Fig. 21-4).
Myotendinous and
Osteotendinous Junctions
The myotendinous junction is a highly specialized
anatomic region in the muscle-tendon unit where
tension generated by muscle fibers is transmitted from
intracellular contractile proteins to extracellular con-
nective tissue proteins (collagen fibrils).

Paratenon Tendon

Mesotenon Nutrient vessel

FICURE 21 - 2 . The multilayered paratenon forms a barrier between the tendon and
the surrounding structure and serves as a source of nutrition through the vincular
vessels. The mesotenon is the part of the paratenon draped over the nutrient vessels
functioning as an umbilicus. Its pliability and length allow the tendon to glide and yet
maintain continuous perfusion. (From Chu DTW, Edgerton BW: Repair and grafting of
tendon. In McCarthy JG, ed: Plastic Surgery. Philadelphia, WB Saunders, 1990:527-
545.)

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image...

21 • REPAIR AND CRAFTING OF TENDON 59 "6

• •

FIGURE 2 1 - 3 . Lateral (top) and palmar (bottom) views of a finger depict the components of the digital flexor sheath.
The sturdy annular pulleys (Al, A2, A3, A4, and A5) are important biomechanically in keeping the tendons closely
applied to the phalanges. The thin, pliable cruciate pulleys (CI, C2, and C3) collapse to allow full digital flexion. The
palmar aponeurosis pulley (PA) adds to the biomechanical efficiency of the sheath system. (From Strickland JW: Devel-
opment of flexor tendon surgery: twenty-five years of progress. J Hand Surg Am 2000;25:214-235.)

Triple-helical Quarter-
tropocollagen stagger
molecules lines

Alpha chain Tropocollagen Fibril with 64-nm Collagen fiber with Tendon with
quarter stagger crimp structure spiraling fibers
of 300-nm tropocollagen
molecules
FIGURE 2 1 - 4 . Hierarchy of tendon structure. (From Amadio PC: Tendon and ligaments. In Cohen IK, Diegelmann
RF, Lindblad WJ, eds: Wound Healing: Biochemical and Clinical Aspects. Philadelphia, WB Saunders, 1992.)

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image...
594 I • GENERAL PRINCIPLES
The osteotendinous junction is a specialized region
in the muscle-tendon unit where the tendon inserts
into a bone. In the osteotendinous junction, the vis-
coelastic tendon transmits the force into a rigid bone.
The region has been described as containing four light
microscopic zones: tendon, fibrocartiiage, mineralized
fibrocartiiage, and bone.1H
Light Microscopic Appearance
of Tendon
Normal tendon consists of dense, clearly defined par-
allel and slightly wavy collagen bundles. Collagen has
a characteristic reflective appearance under polarized
light. Between the collagen bundles, there is a fairly
even sparse distribution of cells with thin wavy nuclei.
There is an absence of stainable ground substance and
no evidence of fibroblastic or myofibroblastic pro-
liferation. Tendon is supplied by a network of small
arteries oriented parallel to the collagen fibers in the
endotenon, which is a continuation and invagination
of the outer epitenon (Fig. 21-5).
TENDON NUTRITION
Tendons receive nutrition from both vascular and sy-
novial systems. Synovial fluid diffusion provides rapid
delivery of nutrients by imbibition, whereby fluid is
pumped into small conduits in the tendon surface
during digital flexion and extension. In the absence of
vascular inflow, diffusion alone can provide adequate
FIGURE 21 - 5 . Cross section of a tendon showing the
arrangement of the fasciculi and vascular bundles. (From
Braithwaite F, Brockis JG: The vascularization of a tendon
graft. Br J Plast Surg 1951 ;4:130.)
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nutrition for tendon healing.1316 The relative contri-
bution of these two sources is difficult to determine
clinically. However, for rapid tendon healing and func-
tional gliding to be achieved, it is important to pre-
serve the integrity of these two nutritional sources.
Compromise to either vincula or digital sheath will
result in less than optimal healing.17'19
TENDON AND GRAFT HEALING
Stages of Tendon Healing
The stages of tendon and graft healing model normal
wound healing. Initially, the stage of inflammation lasts
48 to 72 hours after repair. The strength of the tendon
repair is almost entirely supplied by the suture. A
fibrin clot fills the space between tendon, or between
tendon and graft, while macrophage and inflamma-
tory cells join the repair site. Cells originating from
the extrinsic peritendinous tissue, the epitenon, and
the endotenon migrate to the wound, and the mor-
phologic appearance changes to that of fibroblasts.
These cells proliferate and begin collagen production.
The fibroblastic or collagen-proliferation stage lasts
5 days to 4 weeks, when scar is deposited. The scar
tissue is composed of random collagen fibrils, with type
I and type III collagen, along with increased water, DNA,
and glycosaminoglycan content. Fibroblast numbers
peak at 2 to 3 weeks, then decrease. At this time, there
is relative weakness in the healing tendon ends, and
strength of repair is dependent on the construct and
strength of the holding suture.
During the maturation or remodeling stage, the par-
allel,longitudinally oriented collagen fibers merge with
the disorganized scar and impart a portion of their
normal physiologic stress through the scar, which may
help organize the initial random network of new col-
lagen fibers. Cross-linking of fibers also imparts an
increase in tensile strength. By 3 to 4 months, the remod-
eling process is complete. 20
Extrinsic Versus Intrinsic Healing
Controversy used to exist in determining whether the
extrinsic cells (coming from peritendinous tissue) or
intrinsic cells (coming from within the tendon, such
as tenocyte, endotenon, or epitenon) produced new
collagen. Previous knowledge presumed that tendons
were incapable of self-healing and that nutrients
came from surrounding adhesions. Numerous authors
have now shown that intrinsic healing is indeed a
pathway to tendon healing.2'"25 The relative contri-
bution of extrinsic and intrinsic cells to tendon
healing is dependent on level of initial injury, quality
of surgical repair, and postoperative regimen. As a
rule, intrinsic cellular healing results in less adhesion
formation.
ftWWafltfW image...
Modulators of Tendon Healing
In the hope of enhancing tendon healing, investiga-
tors are looking at the role of soluble polypeptides in
the cellular events of tendon healing. The agents under
study include growth factors, hormones, and chemo-
tactic factors such as fibronectin.26"30 Other researchers
have looked into the role of different modalities
applied externally in tendon healing. Nessler31 and
Fujita32 examined the effect of direct-current electri-
cal stimulation; Nelson 33 and Greenough 34 looked at
pulsed electromagnetic fields, with some positive
effects on an experimental model.
The beneficial effect of ultrasound therapy has been
discussed by several authors. Clinical and experimen-
tal studies suggest that ultrasound may also limit adhe-
sions, assisting in ultimate functional outcome.35"38
Investigations suggest that nonsteroidal anti-
inflammatory agents may decrease adhesion forma-
tion.39,40 Unfortunately, Kulick's study 39 also resulted
in decreased breaking strength of repaired extensor
tendons.
Another area of active interest is the use of
hyaluronic acid in decreasing tendon adhesions. Some
experimental results have been promising, with no
adverse effect on tendon tensile strength.41*43 An initial
clinical trial by Hagberg44 showed no improvement in
total active movement, but a later laboratory study45
suggested that hyaluronic acid's efficacy is affected by
both the concentration and the molecular weight of
the preparation.
CLINICAL APPLICATION
Repair of Tendon Laceration
COALS
The goals of tendon repair and grafting are to achieve
tendon healing and to attain effortless gliding to allow
full joint motion. The finger flexors must glide approx-
imately 3 to 3.5 cm to provide full finger motion, and
an additional 3 cm of glide is taken up at the wrist.46
The challenge has been to repair both flexor tendon
and the surrounding sheath, which is 1 mm away, and
have both heal without being encased in a single scar
mass. Unfortunately, one of the most common com-
plications of tendon repair is limited joint motion
secondary to adhesions.
INDICATIONS
As knowledge of tendon healing has advanced,
Bunnell's47 original principle of avoiding primary
repair of zone II injuries, between the distal palmar
crease and insertion of the sublimis tendon, has given
way to immediate primary repair. Particular indica-
tions for primary tendon repair are tendon lacerations
in clean wounds with intact soft tissue, digital
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21 • REPAIR AND GRAFTING OF TENDON 595
replantation, and tendon injury with concomitant
bone fractures in which fixation is stable enough to
allow immediate motion of joints.
TIMING OF REPAIR
Matev,48 Schneider,49 and others50,51 have shown that
primary repair of tendon injury within the flexor sheath
may be performed in a delayed fashion without com-
promise to outcome. Gelberman's review,52 however,
suggested that better biomechanical results can be
achieved with immediate repair of tendon injury
compared with repairs delayed 7 or 21 days.
GUIDELINES FOR REPAIR
Surgical technique and tissue handling are critical to
the quality of the result after tendon repair. Meticu-
lous atraumatic technique is necessary to avoid tendon
or tendon sheath injury and injury to the blood
supply.53 Because the blood supply to tendons in the
sheath lies dorsally, strangulation is avoided by place-
ment of core sutures in the relatively avascular, ante-
rior portion of the tendon. Repeated efforts to retrieve
a retracted tendon may result in trauma to the tendon
or sheath, and one should not hesitate to extend the
exposure. Trail54 evaluated several suture materials
for flexor tendon repairs and determined that 4-0
monofilament polypropylene or braided polyester
sutures are reasonable choices. Barrie et al55 recom-
mended that 3-0 suture be considered for tendon
repairs when early active motion is planned. Suture
method for tendon repair should not be unduly
complex, and there should be a smooth edge between
cut ends.
The repaired tendon must not bulge outside the
confines of the tendon sheath. The circumferential, epi-
tcndinous suture performs two functions. It avoids
exposing the cut ends of tendons, minimizing extrin-
sic healing by adhesions and the development of gap
formation, and adds to the tensile strength of the
repair.56,57 Several authors 58,59 have advocated the place-
ment of the epitenon suture first, as a technique to
align the tendon ends, to provide stability during repair
and to keep the free ends from fraying. Papandrea 60
compared two methods of Kessler suture repair of
tendons and reported a 22% increase in tensile strength
when the epitenon rather than the core suture was
placed first.
Variables That Affect the Outcome
of Tendon Repair
BLOOD SUPPLY
Vascularity is a critical factor determining the final
result after tendon repair. Hypovascularity is reflected
in decreased matrix synthesis in the tendon, decreased
tensile strength and motion, and greater adhesion
596 I • GENERAL PRINCIPLES
formation. In cases of severe injury, with damage to
vincula or when sublimis tendon was excised, the results
of tendon repair were worse.17,61
PRESERVATION AND RECONSTRUCTION
OF THE FLEXOR SHEATH
The critical elements that must be preserved within
the flexor sheath are the A2 and A4 pulleys. They
provide the moment arm for digit flexion and inhibit
bowstringing (Fig. 21-6).62 Repair of the fibrous flexor
sheath restores the closed synovial space for nutrition
and lubrication. The technical requirements for recon-
struction may be challenging. With sheath repair, there
are additional pitfalls, including excessive scarring, loss
of vascularity, and limitation of tendon gliding.63,64 In
some cases, then, better results may be achieved by
excising portions of the sheath to avoid impingement
on motion, triggering, and adhesion.
EARLY MOTION AND TENSILE STRESS
Early controlled postoperative motion improves
tendon tensile strength and excursion.65 This salutary
effect is thought to be secondary to increased intrin-
sic healing, increased collagen formation, facilitated
pumping ofsynovial fluid, and possible disruption of
early vascular budding and adhesion formation. The
tensile stress initiated by early motion has been shown
FIGURE 2 1 - 6 . The retinacular pulley system prevents
bowstringing of the flexor tendon. A, A five-pulley system
is optimal, with pulleys bridging each side of the metacar-
pophalangeal and proximal interphalangealjointsand lying
proximal to the distal interphalangeal joint. B, Disruption
of the key pulleys allows bowstringing. (From Strickland
JW: Development of flexor tendon surgery: twenty-five
years of progress. J Hand Surg Am 2000;25:214-235.)
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to increase the rate and organization of collagen
synthesis.66
Gelberman and Woo67 have suggested that early
passive motion will stimulate maturation and strength-
ening of the tendon scar, whereas Aoki et aloS propose
that active mobilization will increase the tensile
strength of the repair. Excellent clinical results were
achieved by Chow et al69 by adaptation of a palmar
pulley into the splint along with early motion. Further
improvement in the technique of postoperative mobi-
lization is recommended by Zhao et al70 when imme-
diate passive digit flexion is combined with synergistic
wrist extension to lessen adhesion formation.
Initiation of early motion to achieve better tendon
healing is a two-edged sword; gaps of scar tissue
between the cut ends continue to occur with high
frequency. Gap formations may disrupt the normal
length-tension relationship of tendon, resulting in
lower grip strength, or increase the rate of tendon
rupture.
Schuind et al71 reported an in vivo study of tensile
demands on flexor tendons performed during open
carpal tunnel release. The normal index flexor requires
a maximum force of 3 N (0.3 mgf) for passive motion,
about 15 N (1.5 mgf) for low active grip, 30 N (2.9 mgf)
for strong active grip, and up to 118N (12 mgf) for
tip pinch. These numbers are often-quoted guidelines
for needed breaking strength of tendon repair to with-
stand the forces encountered during postoperative early
motion protocols. Gill et al72 proposed that any early
active motion protocol should have a tendon pull-out
strength of greater than 30 N. Their rationale is that
one should also factor in decreased tendon strength
in the early weeks after repair and also increased gliding
resistance at the repair site.
Momose et al73 tested several suture methods for
both breaking strength and gliding resistance. Their
data demonstrated that the often-used low breaking
strength and low gliding resistance technique of the
modified Kessler repair (combined with epitendinous
suture) is adequate for the commonly used passive
mobilization protocol. For active mobilization proto-
cols, some of the multistrand repairs they tested
demonstrated higher breaking strength without pro-
ducing higher gliding resistance than in less robust
repairs.
Improvements in Suture Technique
Myriad core suture techniques have been developed
to minimize gap formation and to avoid rupture with
early postoperative motion, especially active motion.
Biomechanical testing in numerous four-strand and
six-strand repairs attests that the strength of a flexor
tendon repair is roughly proportional to the number
of suture strands that cross the repair site.74"78 Winters
et al79 tested a newly developed eight-strand repair
with 4-0 Supramid and compared its biomechanics
image...

21 • REPAIR AND GRAFTING OF TENDON 597

with that of the two-strand Kessler-Tajima suture and
the four-strand modified Savage repair. At 6 weeks,
the motion of the eight-strand repair was less than
that of the other techniques. Strickland 9 comprehen-
sively reviewed many of these studies and determined
that any locking or cruciate four-strand core suture
in combination with circumferential epitenon suture
should withstand light, composite grip. Strickland sug-
gested that the cruciate four-strand suture repair
described by McLarney et al80 comes closest to the
ideal suture for flexor tendon repair. McLarney et al
showed that the cruciate repair is stronger than other
four-strand repairs; it is relatively easy to perform,
taking time similar to the two-strand Kessler suture,
and places the knots outside the laceration site
(Fig. 21-7).
The advantages of achieving greater tensile strength
and decreased gap formation with multistrand repairs
must be weighed against possible increase in bulk of
the tendon, increased gliding resistance within the
sheath, potential compromise of vascularity, and
increased operating time. Zhao 81 compared the
modified Kessler suture with a multistrand technique
and determined that high-friction suture techniques
may cause more adhesion formation under passive
postoperative therapy.
In summary, uncontrollable factors that affect
outcome are the extent of soft tissue and flexor sheath
injury and the vascular supply to the injured tendon
ends. Controllable factors that affect the outcome of
tendon repair are the amount of stress placed on the
repair (postoperative regimen), surgical technique, and
type of suture repair.
Tenolysis
When tendon adhesions inhibit motion of the digit,
better function may be gained through tenolysis.

Modified Kessler Interlock suture

A E

7 \ m. ,J> _— *

s !
x Augmented Becker
Kessler-Tajima
B F

\ r
• : : \

.1\$:
J V
Double loop Six-strand Tang

H
F I G U R E 2 1 - 7 . Various core tendon repairs. A, Modified Kessler. B, Kessler-Tajima. 79 C, Tsuge. 102 D, Double loop. 7 4
E, Interlock suture. 7 8 F, Augmented Becker. 7 6 C, Cruciate. 8 0 H, Six-strand Tang. 7 8 Continued

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598 I • GENERAL PRINCIPLES
% ,,
A X"izzz-fzz: •• » zf\-:::::x Xi
fX x::::::::r='' ' :.::::::x >?
jX xz:zzzzz\zz,J ^ " i z z - x x>
Six-strand modified Savage
I
Double modified Tsuge
J the joint. Contraindications for grafting entail an
if'""fl ff
Eight-strand ^ ^
K careful, graduated mobilization.
FIGURE 21 - 7 , cont'd. /, Six-strand modified Savage.68
J, Double modified Tsuge.78 K, Eight-strand.79
Tenolysis may be performed after primary tendon
repair, after tendon grafting, or after two-staged tendon
grafting. This should not be attempted until tissue equi-
librium, that is, suppleness of soft tissue as well as of
joints, is achieved. The patient's passive motion should
exceed his or her active motion, but regardless, surgery
should be considered when there is a plateau in therapy.
The optimal time may be 3 to 4 months after initial
tendon repair. Wray et al82 reported a study of chicken
flexor tendons in which tenolysis performed at 12
and 16 weeks after tenorrhaphy resulted in increased
tendon vascularity without adversely affecting the
strength of the tendon repairs.
Tenolysis is optimally performed under initial local
anesthesia to allow the patient to actively flex the digits
and to confirm adequate release of all adhesions teth-
ering the tendon. Tenolysis should be considered an
exploratory procedure, for in addition to lysis of tendon
adhesions, the patient should be prepared to have
primary repair of tendon laceration, primary graft,
two-staged graft, capsulotomy, or even joint arthro-
desis. Should tenolysis fail, it may become necessary
to remove the repaired tendon and replace this with
a tendon graft. A graft that is thin enough may survive
through imbibition of synovial fluid, particularly if it
is passed through an intact or repaired sheath. A thick
graft, however, must become revascularized from sur-
rounding tissue, often from surrounding adhesions,
and is susceptible to central necrosis.
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Tendon Grafting
INDICATIONS
Single-staged tendon grafts should be used if tendon
ends cannot be approximated. This situation may be
encountered if the proximal stump of flexor tendon is
necrotic during late repair.
REQUIREMENTS FOR TENDON GRAFTING
Before tendon grafting, there must be complete wound
healing, with adequate soft tissue coverage. There must
be an absence of edema and induration. The skeletal
alignment must be satisfactory and stable, and opti-
mally, there should be full range of passive motion of
absence of any of these elements, adherent extensor
tendons, planned capsulotomy for stiff joints, and the
need for pulley reconstruction.83
To achieve success in tendon grafting, Pulvertaft84
listed the following requirements: mobile digit with
minimal scarring and at least one digital nerve intact;
meticulous surgical technique; cooperative patient; and
TWO-STAGED TENDON GRAFTING
(INITIAL INDUCTION OF
TENDON SHEATH)
Indications
Two-staged tendon grafting is indicated in severely
scarred wound beds, as in digits with bone exposure.
It may be indicated with simultaneous fracture fixation
and when flexor and extensor tendons must be
repaired. An injured tendon bed that might provide
poor nutrition to a tendon graft is considered a
candidate for two-staged repair. Initial induction of
tendon sheath with use of a Silastic rod might be per-
formed in conjunction with needed repair of the A2
or A4 pulley. Other indications include joint stiffness,
when capsulotomy is planned, or where local finger
flaps are needed to provide soft tissue coverage in severe
crushing injuries. Two-staged tendon grafts may be
indicated in failed zone II flexor tendon repairs. Before
embarking on two-staged tendon grafting, one must
be sure of the patient's proper cooperation and moti-
vation for therapy after surgery.
Timing Considerations for Two-Staged
Tendon Graft
The initial stage consists of removal of scarred tissue;
reconstruction of key pulleys; repair of digital nerve;
and then placement of a pliable tendon rod, composed
of a woven Dacron spacer that is encased in silicone,
within the tendon pulleys.
After a minimum period of 3 months, a pseu-
dosheath will have formed around the silicone rod as
a foreign body reaction, providing a surface for the
image...

21 • REPAIR AND GRAFTING OF TENDON 599

future autologous tendon graft to glide on. As the tem-

porary rod is removed, the ultimate goal in two-staged
tendon grafting is survival of the tendon graft within
the pseudosheath before vascular adhesions are formed.
As a general principle, tendon grafts are not mobilized
until 3 weeks postoperatively, after the transplanted
tendon has obtained sufficient vascularity from its
bed.85

DONOR SITES FOR TENDON GRAFTS

Potential tendon donors should have adequate length,
be in a superficial location for ease of harvest, have
little or no functional loss, and be thin enough to
become revascularized yet strong enough to move the
digit. In order of preference,86,87 potential tendon donors
are the following:
Palmaris longus Advantage: easy access, no func-
tional loss, and good caliber for digital flexors.
Disadvantage: may be absent in 10% and may
be too short for fingertip to wrist grafts.
Plantaris Advantage: long tendon, with no func-
tional loss; easily braided if a thicker graft is
required. Disadvantage: requires a second oper-
ative site, and there is no test to determine its
presence beforehand. It maybe missing in 20%
of cases, and if it is not present on one side, only
one in three will have a plantaris tendon on the FIGURE 21 -8. The anatomic relationships of the plan-
taris tendon. (Modified from White WL: Tendon grafts: a
other side (Fig. 21-8). M consideration of their source, procurement, and suitabil-
Extensor digitorum longus Advantage: reliable ity. Surg Clin North Am 1960;40:403.)
source of graft from the second, third, and fourth
toes and may provide a long, many-tailed graft
without injury to epitenon. Disadvantage: pos-
sible flexion deformity of the toes.
Sakellarides91 reported 80% excellent to good results
Extensor indicis proprius Advantage: within the in a series of 50 patients who had replacement of chronic
same operative field. Disadvantage: short length; zone II profundus tendon lacerations, delayed more
may lead to a small extensor lag. than 6 weeks, with thin tendon grafts. These were either
Flexor digitorum superficialis Not really recom- transplanted plantaris tendon or palmaris longus
mended; harvest may cause proximal interpha- tendon.
langeal joint hyperextension and may decrease
Wehbe et al92 reviewed long-term results of 150
flexion power.
fingers having two-staged flexor tendon graft. Range
Spare parts Tendon graft harvested from an of motion improved an average of 74 degrees when
irreparably injured structure. the metacarpophalangeal, proximal interphalangeal,
and distal interphalangeal joints were considered. Joint
RESULTS OF TENDON GRAFT range of motion plateaued 3 months after tendon graft-
ing. If clinical results are less than optimal, consid-
Kraemer et al,89 in a review of 220 consecutive grafts, eration should be given to further tenolysis or
reported an incidence of 1.1% tendon graft disrup- capsulotomy.
tion for one-staged tendon grafts compared with an
incidence of 7.6% graft disruption in two-staged
tendon grafts. One incredible report 90 described the TENDON SUBSTITUTES
complication of transplantation of the median nerve
as a tendon graft in four cases. This serves as a somber Allograft
reminder of the importance of careful identification Because of the paucity of cellular elements in tendon,
of nerve during dissection and clinical determination tendon allografts would be expected to have relatively
of the presence or absence of the palmaris longus low antigenicity. This is thought to decrease the risk
tendon preoperatively. of fibrosis from immunologic reaction.

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Tew>t#<aeltft$f image...
600 I • GENERAL PRINCIPLES
Various methods, including freezing, refrigeration,
lyophilization, trypsin, irradiation, and cialit,93 have
been experimentally applied to decrease antigenicity.
Zhang et al94 gained good motion with fieeze-dried
allograft rendon combined with partial sheath graft-
ing in a chicken model.
Clinical reports of successful allograft transplanta-
tion for tendon reconstruction have been sparse,
however. Liu9: treated 35 patients with refrigerated
flexor tendon allografts in two-staged grafting to replace
a silicone rod. Only 8% had good total active motion,
and 71 % tiad a fair result. Asencio et al96 reported a 5-
year follow-up of two cases of human composite flexor
tendon allograft with improved function.
Tissue engineering may play a role in providing bio-
logic substitutes for tendon. He et al97 presented results
of a complex of polydioxanone suture, fibroblasts, and
human amnion extracellular matrix engineered to
replace a tendon defect in a rabbit model. The tensile
strength at 3 months was 8 1 % of the normal tendon.
Synthetic Graft Replacements
Tendon replacements made of Dacron, expanded
polytetrafluoroethylene, carbon fiber, and woven
nylon have been considered for use.5 The three major
considerations involve biocompatibility, material prop-
erties of the implant and ability to withstand repeti-
tive stress, and fixation of the implant. These synthetic
products are presently limited to investigational,
salvage procedures.
One difficulty with synthetic grafts is lack of
control of scar formation, especially scar tissue, which
develops beyond the margin of the intended pseu-
dosheath. This exuberant scar would generally lead to
limited finger motion, but Ketchum98 presented a case
report of a silicone implant functioning as an active
tendon flexor after 25 years. In this patient, Silastic
rods were placed as a late procedure, after revascular-
ization and nerve grafting of a volar distal forearm
injury. At the time of exploration for secondary
tendon grafting, the original implants were never
removed because of exuberant scar tissue at the wrist
level. Twenty-five years later, flexor tendons and this
"active" tendon implant were functioning well.
Just as these synthetic grafts may cause a foreign
body reaction, risking scar and adhesion formation,
the inert qualities of these materials also lead to limited
ingrowth fixation. This increases the risk of rupture
of the repair with continued, repetitive stress. Such
limitations exist for both tendon-bone and tendon-
muscle fixations. Indeed, even when autologous tissue
is repaired at the tendon-bone junction, there is
delayed healing.99 Hunter,100 in studying this problem,
developed a prototype of an "active implant" silicone
rod with a porous titanium juncture at either end.
Woven bone ingrowth into the distal titanium plug
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was observed after placement into a drill hole in the
distal phalanx. In addition, cortical bone graft was
sandwiched with the titanium implant at the proxi-
mal muscle interface. The construct has bone graft
growing into the porous titanium and muscle growing
into the bone graft. This concept of strengthening the
distal attachment of tendon graft with a prefabricated
bone graft is supported by Singer et al,101 who showed
that the strength of union of the prefabricated bone-
tendon graft was double that of the conventional bone-
tendon graft junction. A major reason for the lack of
development of a successful active synthetic flexor
tendon implant is the weakness of the tendon-bone
and tendon-muscle interface.
CONCLUSION
To achieve optimal results in tendon repair and graft-
ing, one must respect tendon blood supply, preserve
the integrity of the flexor sheath, and apply techniques
that limit formation of adhesions. With meticulous
tissue handling, the tendon repair must be strong
enough to withstand selected early motion protocol.
Any "ideal"suture repair of the future, whether four-
strand, six-strand, or cruciate, with use of 3-0 or 4-0
suture, braided permanent synthetic suture, or double-
strand loop suture, 102 must be easy to use and learn,
not be time-consuming, have high breaking strength
and low gliding resistance, and maintain the viability
and vascularity of the tendon. One might also strongly
consider aligning the cut ends with the circumferen-
tial epitenon suture first,64 burying the knots away from
the cut surfaces, and using a double-strand suture to
decrease tissue handling.
In the 1990s, much research was devoted to bio-
mechanical properties of new suture techniques,
developed to increase strength of tendon repair, and
toward documenting the advantages of early active
motion stress. We may now have come full circle with
a report by Silva et al.103 With use of a canine model,
their results indicate that passive motion protocols that
produce a moderate amount of tendon excursion
(2 mm) at low levels of force (5 N) are sufficient to
inhibit adhesion formation and to promote healing.
Furthermore, they found that increases in excursion
or force beyond these levels do not accelerate the
healing process. In light of these data, it will be inter-
esting to see the clinical results of four- and six-strand
flexor tendon repair in a series of patients compared
with the modified Kessler repair. To assess successful
repair of tendon, Strickland104 suggests that excellent
be defined as 75% to 100% of normal and good be
defined in the range of 50% to 75% of normal.
In this new millennium, we should look forward to
reports on clinical utility of multistrand suture repair105;
comparison of tendon excursion, and rupture rates,
in active versus passive rehabilitation protocols106;
image...
clinical utility of allograft or tissue-engineered cell
transplants for tendon replacement; development of
active synthetic tendon grafts with effective techniques
for securing these tendons at the bone and muscle inter-
face; and application of biologic factors, such as gene
therapy 107 or growth factors,26"30,108 to enhance tendon
healing.
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63. Lister G: Pitfalls offlexor tendon surgery. Hand Clin 1985;1:140.
64. Saldana MJ, Ho PK, Lichtman DM, et al: Flexor tendon repair
and rehabilitation in zone II: open sheath technique versus
closed sheath technique. J Hand Surg Am 1987;12:1110-1114.
65. Gelberman RH, Botte MJ, Spiegelman JJ, Akeson WH: The
excursion and deformation of repaired flexor tendons treated
with protected early motion. J Hand Surg Am 1986;11:106-
110.
66. SlackC,FlintMH,ThompsonBM:Theeffectoftensionalload
on isolated embryonic chick tendons in organ culture. Connect
Tissue Res 1984;12:229-247.
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67. Gelberman RH, Woo SLY: The physiological basis for appli-
cation of controlled stress in the rehabilitation of flexor tendon
injuries. J Hand Ther 1989;2:66-70.
68. Aoki M, Kubota H, Pruitt DL, Manske PR: Biomechanical and
histological characteristics of canine flexor repair using early
postoperative mobilization. J Hand SurgAm 1997;22:107-114.
69. Chow JA, Thomes LJ, Dovellc S, et al: A combined regimen of
controlled motion following flexor tendon repair in no man's
land. Plast Reconstr Surg 1987;79:447-453.
70. Zhao C, Amadio PC, Momose T, et al: Effect of synergistic
wrist motion on adhesion formation after repair of partial flexor
digitorum profundus tendon lacerations in a canine model in
vivo. J Bone Joint Surg Ain 2002;84:78-84.
71. Schuind F, Garcia-Elias M, Cooney WP 3rd, An KN: Flexor
tendon forces: in vivo measurements. J Hand Surg Am
1992;17:291-298.
72. Gill RS, Lim BH.Shatford RA.etal: A comparative analysis of
thesix-strand double-loop flexor tendon repair and three other
techniques: a human cadaveric study. J Hand Surg Am 1999;
24:1315-1322.
73. MomoseT, Amadio PC.Zhao CF, et al: Suture techniques with
h igh breaking strength and low gliding resistance: experiments
in dog digitorum profundus tendon. Acta Orthop Scand
2001;72:635-641.
74. Lee H: Double loop locking suture: a technique of tendon repair
for early active mobilization. Part I. Evolution of technique
and experimental study. J Hand SurgAm 1990;15:945-952.
75. Noguchi M, Seiler JG 3rd, Gelberman RH, et al: In vitro bio-
mechanical analysis of suture methods for flexor tendon repair.
J Orthop Res 1993;11:603-611.
76. Greenwald DP, Hong HZ, May JW Jr: Mechanical analysis of
tendon suture techniques. J Hand SurgAm 1994;19:641-647.
77. Wagner WF, Carroll C 4th,Strickland JW, et al: A biomechanical
comparison of techniques of flexor tendon repair. J Hand Surg
Am 1994;19:979-983.
78. Tang JB, Gu YT, Rice K, et al: Evaluation of four methods of
flexor tendon repair for postoperative active mobilization. Plast
Reconstr Surg 2001;107:742-749.
79. Winters SC, Gelberman RH, Woo SL, et al: The effects of mul-
tiple-strand suture methods on the strength and excursion of
repaired intrasynovial flexor tendons: a biomechanical study
in dogs. J Hand Surg Am 1998;23:97-104.
80. McLarney E, Hoffman H, Wolfe SW: Biomechanical analysis
of the cruciate four-strand flexor tendon repair. J Hand Surg
Am 1999;24:295-301.
81. Zhao C, Amadio PC, Momose T, et al: The effect of suture
technique on adhesion formation after flexor tendon repair
forpartial lacerations in a canine model. JTrauma2001;51:917-
921.
82. Wray RC, Moucharefied B, Weeks PM: Experimental study of
the optimal time for tenolysis. Plast Reconstr Surg 1978;61:184.
83. Weeks PM, Clement RW: Basic principles of tendon grafting.
In Georgiade NG, ed: Essentials of Plastic, Maxillofacial, and
Reconstructive Surgery. Baltimore, Williams 8c Wilkins, 1987:
77-90.
84. Pulvertaft RG: Indications for tendon grafting. In Hunter JM,
Schneider LH, Mackin EJ, Callahan AD, eds: Rehabilitation of
the Hand: Surgery and Therapy, 3rd ed. St. Louis, CV Mosby,
1990:414-416.
85. Lister GD: Flexor tendon. In May JW Jr, Littler JW, eds: The
Hand. Philadelphia, WB Saunders, 1990:4516-4564.McCarthy
JG, ed: Plastic Surgery; vol 7.
86. Chu DTW, Edgerton BW: Repair and grafting of tendon. In
McCarthy JG, ed: Plastic Surgery. Philadelphia, WB Saunders,
1990:527-545.
87. Lister G: Indications and techniques for repair of the flexor
tendon sheath. Hand Clin 1985;1:85-95.
88. Harvey FJ, Chu G, Harvey PM: Surgical availability of the plan-
taris tendon. J Hand Surg Am 1983;8:243-247.
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89. Kraemer BA, Young VL, Grassc P, Weeks PM: Characteristics
and management of flexor tendon graft disruption. Br J Plast
Surg 1987;40:258-263.
90. Vastamaki M: Median nerve as free tendon graft. J Hand Surg
Br 1987;12:187-188.
91. Sakellarides HT, Papadopoulos G: Surgical treatment of the
divided flexor digitorum profundus tendon in zone 2, delayed
more than 6 weeks, by tendon grafting in 50 cases. ] Hand Surg
Br 1996;21:63-66.
92. Wehbe MA, Hunter JM, Schneider LH, Goodwyn BL: Two-
stage flexor-tendon reconstruction: ten-year experience. J Bone
Joint Surg Am 1986;68:752-763.
93. Seiffert KE: Preserved grafts in reconstructive surgery. Trans-
actions of the Fifth International Congress of Plasticand Recon-
structive Surgeons, 1971. Australia, Butterworths, 1971.
94. Zhang YL, Wang SL, Gao XS: Experimental study of allogenic
tendon with sheath grafting in chicken [in Chinesel. Zhong-
guo Xiu Fu Chong Jian Wai Ke Za Zhi (Chinese J Reconstr
Plast Surg) 2001;15:92-95.
95. Liu TK: Clinical use of refrigerated flexor tendon allografts to
replace a silicone rubber rod. J Hand Surg Am 1983;8:881-
887.
96. Asencio G, Abihaidar G, Leonardi C: Human composite flexor
tendon allografts. A report of two cases. J Hand Surg Br 1996;
21:84-88.
97. He QY, Chen BL, Wang ZB, Li QH: Repair of flexor tendon
defects with complex of fibroblasts and human amnion extra-
cellular matrix (HA-ECM). Chin Med J 2002;115:542-545.
98. Ketchum LD: Twenty-five-year follow-up evaluation of an
active silicone/Dacron tendon interposition prosthesis: a case
report. J Hand Surg Am 2000;25:731 -733.
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21 • REPAIR AND GRAFTING OF TENDON 603
99. Silva MJ, Boyer MI, Ditsios K, et al: The insertion of the
canine flexor digitorum profundus tendon heals slowly fol-
lowing injury and suture repair. J Orthop Res 2002;20:447-
453.
100. Hunter JH, Aulicino PL: Salvage of scarred tendon system using
passive and active Hunter tendon implants. In Jupiter JB, ed:
Flynn's Hand Surgery, 4th ed. Baltimore, Williams & Wilkins,
1991:300-324.
101. Singer D, Doi K, Morrision WA, et al: Comparative study of
the use of prefabricated bone tendon grafts and convention
tendon grafts in flexor tendon reconstruction. J Hand Surg
1989;14:830-836.
102. Tsuge K, Yoshikazu I, Matsuishi Y: Repair of flexor tendons by
intratendinous tendon suture. J Hand Surg Am 1977;2:436-
440.
103. Silva MJ, Boyer MI.Gelberman RH: Recent progress in flexor
tendon healing. J Orthop Sci 2002;7:508-514.
104. Strickland JW: Flexor tendon surgery. Part 1. Primary flexor
tendon repair. J Hand Surg Br 1989;14:261-272.
105. Kitsis CK, Wade PJ, Krikler SJ, et al: Controlled active motion
following primary flexor tendon repair: a prospective study
over 9 years. J Hand Surg Br 1998;23:344-349.
106. Small JO, Brennan MD, Colville J: Early active mobilization
following flexor tendon repair in zone 2. J Hand Surg 1989;
14:383-391.
107. Gerich TG, Kang R, Fu FH, et al: Gene transfer to the rabbit
patellar tendon: potential for genetic enhancement of tendon
and ligament healing. Gene Ther 1996;3:1089-1093.
108. Rohrich RJ.Trott SA, Love M, et al: Mersilene suture as a vehicle
for delivery of growth factors in tendon repair. Plast Recon-
str Surg 1999;104:1713-1717.
image...
CHAPTER
22
•
Repair, Regeneration, and
Grafting of Skeletal Muscle
GEORGE H. RUDKIN, MD • TIMOTHY A. MILLER, MD
HISTORY
ANATOMY AND PHYSIOLOGY
RESPONSE OF MUSCLE TO INJURY
Denervation
Reinnervation
Electromyography
Tenotomy
Ischemia
MUSCLE REPAIR AND REGENERATION
HISTORY
Nonvascularized free grafts of skin, cartilage, bone,
nerve, and tendon are routinely transferred with
success. Before the introduction of microsurgical free
tissue transfer, however, the transfer of muscle tissue
was extremely limited. It was commonly held that
the metabolic demands of this tissue precluded free
grafting.1 Although it currently has limited applica-
tions, nonvascularized free muscle grafting has been
studied extensively. Such research has contributed to
the understanding that successful muscle transfer
involves complex variables of tension, innervation, and
blood supply. Experimental and clinical evidence
demonstrates that altering any of these variables, even
in situ, results in the compromise of muscle function
or death. Although advances in microsurgery have
made the transfer of vascularized muscle grafts com-
monplace, the successful restoration of muscle func-
tion remains one of the greatest challenges in plastic
surgery.
ANATOMY AND PHYSIOLOGY 2-4
Muscle may be classified according to anatomy (stri-
ated versus smooth), innervation (voluntary versus
autonomic), or function. Skeletal muscles generate
force and movement and are under voluntary control.
Located in the walls of hollow organs, smooth muscles
also generate movement and function to maintain
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THE NONVASCULARIZED MUSCLE GRAFT
Experimental Studies
Clinical Applications
THE VASCULARIZED GRAFT
Facial Reanimation
Extremity Reconstruction
Cardiomyoplasty
Anal and Genitourinary Reconstruction
Electrical Stimulation
organ dimensions against applied loads. Cardiac
muscle has properties of both smooth and skeletal
muscle.
Accounting for 45% to 50% of the human body
weight, skeletal muscle is composed of specialized cells
called myofibers (Fig. 22-1). Each individual myofiber
is a cellular syncytium, containing multiple nuclei
beneath an outer sarcolemmal membrane. Myofibers
can be up to 80 \im in diameter and sometimes several
centimeters in length; they are separated by a space
termed the endomysium. In turn, the myofibers are
arranged in fascicles and surrounded by a connec-
tive tissue layer called the perimysium. The whole
muscle is covered in a third connective tissue layer, or
epimysium.
Studied with the electron microscope, the myofiber
is found to be composed of parallel myofibrils, each 1
|Xm in diameter. The basic contractile unit within each
myofibril is the sarcomere, consisting of an array of
thick and thin filaments. The arrangement of these fil-
aments accounts for the striated appearance of skele-
tal muscle. Thick and thin filaments are composed of
myosin and actin protein, respectively. These proteins
are responsible for transducing chemical energy into
mechanical energy during muscle contraction. The
myofibrils lie within the sarcoplasm, which consists of
cytoplasm and cellular organelles. Numerous mito-
chondria, which supply the adenosine triphosphate
necessary for contraction, are located between the
myofibrils.
605
606 I • GENERAL PRINCIPLES

Structure of
Skeletal Muscle

mitochondrion
sarcoplasmic
T-tubule reticulum
sarcolemma
J.

satellite
cell

myofibril

sarcomere
FIGURE 2 2 - 1 . Skeletal muscle is composed of myofibers, covered in a sarcolemmal membrane. The myofiber is
composed of parallel myofibrils, each 1 u.m in diameter. The myofibrils lie within the sarcoplasm, which consists of cyto-
plasm and cellular organelles. Mitochondria, which supply the adenosine triphosphate necessary for contraction, are
located between the myofibrils. The basic contractile unit within each myofibril is the sarcomere, consisting of an array
of thick and thin filaments that are made of myosin and actin protein, respectively. Tubular extensions of the sar-
colemma, known as T tubules, extend deep into the myofiber, allowing depolarizing stimuli to spread and causing the
sarcoplasmic reticulum to release calcium into the cell. This in turn activates the myosin-actin contractile mecha-
nism, resulting in shortening of the muscle. The satellite cell, or adult myoblast, is believed to be involved in muscle
regeneration.

Skeletal muscle fibers contract in small groups called
motor units, which consist of one motor neuron and
the muscle fibers it innervates. Fibers in each motor
unit have distinct histochemical properties and elec-
trophysiologic activities.5 Each fiber within this group
is innervated by a single alpha motor neuron, which
terminates in a specialized nerve ending termed a neu-
romuscular junction, the motor end plate. The release
of acetylcholine at this junction induces a wave of depo-
larization (action potential) within the muscle fiber.
Tubular extensions of the sarcolemma, known as T
tubules, extend deep into the myofiber, allowing the
stimulating wave of depolarization to spread and
causing the sarcoplasmic reticulum to release calcium
into the cell. This in turn activates the myosin-actin
contractile mechanism, ultimately resulting in the
shortening of the muscle.
Several muscle fiber types are distinguishable on
the basis of morphologic, histochemical, and physi-
ologic criteria. The nomenclature regarding the dis-
tinction of these fibers is confusing at best and of
limited practical importance to the plastic surgeon.
A summary follows: Skeletal muscles in mammals
consist of twitch-type fibers, which produce phasic
contractions. Slow fibers produce tonic contractions
and are seen in mammals only in the extrinsic muscles
of the ear and in the extraocular muscles. Twitch-type
fibers are further classified into slow oxidative, fast
glycolytic, and fast oxidative varieties. Slow oxidative
(type 1) and fast oxidative (type Ila) have a high myo-
globin content, which is responsible for their "red"
coloration. Fast glycolytic (type lib) fibers have a low
myoglobin content and are therefore "white." Metab-
olism of the red fibers is generally aerobic, whereas

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22 • REPAIR, REGENERATION, AND CRAFTINC OF SKELETAL MUSCLE
white fibers can also function anaerobically. In
humans, most muscles contain a mixture of fiber types,
oriented in a mosaic fashion on cross section. One
fiber type may predominate in some muscles. The
soleus in the cat and in humans, for example, con-
tains almost entirely slow oxidative fibers. On the basis
of the heterogeneous nature of fiber content, differ-
ent muscles can provide a spectrum of contraction-
relaxation speeds.
The force and velocity of muscle contraction
depend both on the number of sarcomeres and
myofibrils in the muscle cell and on the orientation
of the myofibers within the muscle. The arrangement
of myofibers within a muscle varies. Some muscles are
composed of fibers that are oriented parallel to the
long axis of the muscle (sartorius, flexor carpi radi-
alis). Others consist of shorter fibers that course
obliquely to the long axis (e.g., the bipennate rectus
femoris muscle, whose fiber arrangement resembles
a feather). Still others are arranged in a radial or tri-
angle shape (pectoralis minor). The parallel arrange-
ment maximizes shortening capacity and velocity.
Arrangements that place the myofibers at an angle to
the tendons enhance force generation at the expense
of velocity.
With the exception of the facial muscles and anus,
most striated muscle is covered by fascia and is
attached to the skeleton by tendons and aponeuroses.
In general, the origin is the proximal or more fixed
attachment; the insertion is the attachment to the distal
skeleton that is moved by the muscle. The origin and
insertion of each skeletal muscle determine its resting
tension, which is a crucial parameter in muscle func-
tion and must be considered in muscle reconstruction. 6
The anal sphincter and muscles of facial expression
are distinctive in that they insert on the dermis and
have no fascia.
Muscles demonstrate specific patterns of vascular
anatomy, 7 which play an essential role in flap selection
for reconstructive surgery. Muscles may demonstrate
a single vascular pedicle (type I), a dominant and a
single pedicle or multiple minor pedicles (type II), two
dominant pedicles from different sources (type III),
segmental pedicles (type IV), or a dominant pedicle
with secondary segmental pedicles (type V).
RESPONSE OF MUSCLE
TO INJURY
Denervation
After severance of the motor nerve, muscle atrophies
and is eventually replaced by fibrous tissue. When a
motor nerve is cut, muscle fasciculation occurs; irreg-
ular contractions are caused by the release of acetyl-
choline from the degenerating distal axon. Several days
after denervation, fibrillation begins, characterized by
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607
spontaneous, repetitive contractions that reflect a
supersensitivity of the denervated muscle to acetyl-
choline. Progressive atrophy ensues after 3 to 4 months,
followed by gradual replacement with fat and con-
nective tissue after I to 2 years.3
Reinnervation
Reinnervation of either a denervated muscle or a free
or vascularized muscle graft can be accomplished by
one of three mechanisms: surgical nerve repair of a
severed nerve, with use of a donor nerve or graft if
necessary; sprouting of nerves from adjacent normal
muscle, or "muscle neurotization"; or implantation of
nerve directly into the muscle.
In clinical situations in which a motor nerve is not
available, muscle neurotization predominates; this has
been observed clinically.8,9 After a pharyngeal flap, for
example, there is often reanimation of surrounding
soft palate musculature. 10 For an Abbe lip flap, the
source of reinnervation of the flap after transposition
is the adjacent orbicularis oris muscle. By histochem-
ical and electromyographic methods, muscle neurot-
ization has also been documented in the laboratory."
Muscle neurotization takes place over the entire surface
of the muscle; it is therefore difficult to test for func-
tional recovery of the denervated muscle because it is
intimately adherent to surrounding muscles. It is gen
erally agreed, however, that this process is not as effi-
cient as nerve repair or nerve-muscle implantation.11"15
Fascia almost certainly acts as a barrier to muscle neu-
rotization. Most reports of successful nonvascularized
free muscle grafts in humans have occurred in the
reconstruction of facial and anal muscles, neither of
which have fascial coverings. Direct muscle neuroti-
zation, or the implantation of a motor nerve into a
muscle, has been used clinically when the distal nerve
stump has been avulsed or the muscle is severely
damaged.16'18
Reinnervation is the single most important aspect
of muscle repair. This process takes time, however, even
when surgical neurorrhaphy is performed. After pro-
longed denervation, progressive muscle atrophy and
fibrosis eventually make attempts at reinnervation
unsuccessful. It is likely that different muscles undergo
atrophy at different rates. It has been observed that
intrinsic muscles of the hand often atrophy quickly
within months after denervation, yet successful rein-
nervation of facial muscles has been reported 1 year
after facial nerve injury.19,20 There seems little ques-
tion, however, that the longer the period of denerva-
tion, the more unsuccessful is the reinnervation
process.
The number of available motor axons is important
in the recovery of muscle force after denervation. 21
Studies reporting rapid reinnervation of small muscles
by large numbers of regenerating axons describe
608 l • GENtRAL PRINCIPLES
nearly complete recovery of muscle force,22,23 whereas
studies involving large muscles and few axons demon-
strate force deficits.24'28 During reinnervation ofden-
ervated muscle, motor unit remodeling occurs,
with axons reinnervating larger numbers of motor
units.,2,29"31 However, if the number of axons is severely
reduced, these compensatory mechanisms cannot
eliminate force deficits.21 Electrical stimulation ofden-
ervated muscle has been used experimentally as a means
of preserving functional capacity while awaiting rein-
nervation32 and seems conceptually attractive.
The nerve dictates the properties of the muscle it
innervates, influencing its contractile, histochemical,
and biochemical properties.33"36 Experimentally, nerve
to a slow muscle is able to convert a fast muscle to
a slow type,37 whereas fast muscle nerve exerts
an incomplete control over the properties of slow
muscle.33-34,36 Because the proportion of different fiber
types in a muscle determines its contractile proper-
ties, this plasticity of muscle during reinnervation may
have functional significance. A high degree of func-
tional and structural plasticity has been demonstrated
after free neurovascular transfer of the latissimus dorsi
to reconstruct quadriceps muscle function at late
follow-up (10 years),"3 with the muscle fiber pattern
being donor motor nerve dependent.
Evaluating the extent of muscle reinnervation is dif-
ficult. In experimental models in which biopsy is fea-
sible, choline acetyltransferase levels correlate closely
with the level of reinnervation.38 After reinnervation,
histologic examination may also reveal that "type
grouping" replaces the normal intermingled mosaic
pattern of fibers in skeletal muscle. Because the motor
nerve input to a muscle determines its fiber type, type
grouping—the appearance of unusually large groups
of fibers of the same histochemical type—is seen after
reinnervation as a consequence of axonal sprout-
ing and is evidence of reinnervation.39 In clinical
situations in which biopsy is not possible, how-
ever, one must rely on clinical examination and
electromyography.
Electromyography
As in the brain and heart, there is electric potential
within skeletal muscle. This is normally discharged on
voluntary activity only. At rest, muscle is electrically
silent; other than the slight irritability seen on inser-
tion of the monopolar electrode, no activity is seen.
Denervated muscle (whether due to nerve severance
or neurapraxia) consistently demonstrates a fibrilla-
tion pattern and positive sharp waves. Evidence of rein-
nervation is seen as the appearance of large polyphasic
units (Fig. 22-2).2 When muscle strength cannot be
objectively measured, as in facial reanimation, elec-
tromyography is the only effective means of muscle
function evaluation.40
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Tenotomy
Altering the normal length of a given muscle adversely
influences function. After an unrecognized tendon lac-
eration and the reduction in resting length that follows,
atrophy, fibrosis, and loss of normal elasticity are seen
within a few weeks of injury. On histologic examina-
tion, the muscle fibers decrease in cross-sectional area
and shorten in length, thus Iimitingstrength.41 Increas-
ing the length of a muscle and applying excessive stretch
have similar effects.42 Even without alterations in resting
tension, tenotomy and repair alone have been shown
to produce force deficits in animal models.43 Although
atrophy plays a role, the mechanisms behind these
deficits are not understood.
The studies of Terzis et al44 demonstrated the impor-
tance of resting tension on muscle function. Tenotomy
was found to be more damaging than severance of the
nerve and blood supply, followed by immediate micro-
scopic repair. Experimentally, reduction in resting
tension produces a loss in muscle strength and weight.45
Such experimental findings indicate that when a
muscle is grafted, a reduction of the resting tension
may be as significant an insult as denervation. There-
fore, in clinical situations in which muscle transplants
are required, variations in physiologic muscle length
imposed by the specific demands of the recipient area
may have substantial effects on the functional outcome.
Ischemia
Muscle is extraordinarily sensitive to anoxia because
of its high metabolic demands. In situations of extrem-
ity replantation after trauma, muscle is the time-
limiting tissue. Successful replantation after 33 hours
of warm ischemia has been reported for digits, which
contain no muscle.46 However, it seems generally agreed
that after 6 hours of normothermic ischemia for large
muscles, successful replantation is unlikely. Cooling of
the amputated part improves survival of muscle tissue,
however, and hand replantation has been reported after
54 hours of cold ischemia.47
During vascularized free tissue transfer, the reper-
fusion of ischem ic tissue may be associated with "reper-
fusion injury." Despite a technically successful vascular
anastomosis, some transferred tissue may not reper-
fuse. Such a failure of microvascular perfusion is termed
the no-reflow phenomenon, first described by Ames
in a rabbit brain model.48 No-reflow is thought to be
related to three main pathophysiologic processes:
intracellular calcium overload, oxygen free radical-
mediated damage, and altered arachidonic acid metab-
olism.49 The first tissue irreversibly injured by these
processes is thought to be the endothelium. The rela-
tive contribution of each of these processes to the devel-
opment of no-reflow in ischemic muscle remains
unknown. A variety of strategies designed to alleviate
this phenomenon have been evaluated experimentally
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22 • REPAIR, REGENERATION, A N D GRAFTINC OF SKELETAL M U S C L E 609

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15:50:48
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B
FIGURE 2 2 - 2 . Electromyography tracings. A, Denervated muscle—spike form fibrillation and positive waveform fib-
rillation. B, Early reinnervation—polyphasic, long-duration motor units. (A and B courtesy of Steven E. Levine, MD,
PhD, Los Angeles, Calif.)

in muscle, including ischemic preconditioning50 and
pharmacologic intervention.49
When a large bulk of muscle is ischemic, as in limb
replantation or revascularization, the re-establishment
of flow to the ischemic part may release toxins that have
systemic effects.5' "Replantation toxemia" is associated
with the release of products of muscle breakdown
(rhabdomyolysis) into the circulation, including myo-
globin, and large quantities of lactic acid—the product
of anaerobic metabolism. The release of these agents
into the systemic circulation may be associated with
shock and multisystem organ failure.52 Cooling of the
amputated part reduces the release of muscle enzymes
into the systemic circulation.53 In cases of prolonged
ischemia, prophylactic fasciotomy must be considered.51
MUSCLE REPAIR
AND REGENERATION
Skeletal muscle has the potential for repair after injury
or disease.54,5'1 Muscle has a regenerative capability after
crush injuries and lacerations55 7 and after infection
such as typhus.54,58 The extent of regeneration after
injury and whether this process can be enhanced remain
unclear.
Although muscle lacerations are common in clin-
ical practice, the study of functional recovery after
injury has been minimal. In an animal model,
completely lacerated muscles have been shown to
recover approximately 50% of their ability to produce
tension and to contract against a minimal weight
at 80% of normal. After partial lacerations of the
muscle, 60% of tension production and normal
shortening were observed.59 In this study, the muscle
laceration was noted to heal by scar formation,
but the extremities of the animals used were not
immobilized after injury. The portion of the muscle
distal to the transection showed microscopic evidence
of denervation atrophy: small, irregular-shaped muscle
cells with central positioning of the nuclei and an
increased amount of fibrous tissue. The denervated
segment did not stretch during contraction,

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610 I • GENERAL PRINCIPLES
probably because of the increased content of fibrous
tissue.
Kaariainen60 developed an experimental model
of laceration injury in the soleus of the rat. During
the repair of a complete transection, regenerating
myofibers penetrated into the connective tissue scar
and formed new myotendinous junctions around day
14, restoring functional continuity across the lacera-
tion. Within 14 days, the scar becomes stronger than
the muscle on mechanical testing. Significant atrophy
occurred, probably owing in part to inactivity and distal
denervation. After 14 days, the weakest point is the
atrophic muscle, with rupture occurring at myotendi-
nous junctions. Although stress (tensile strength per
cross-sectional area) reached 96% by day 56, atrophy
led to low failure loads. This suggests that during recov-
ery active mobilization may be important in restor-
ing normal muscle size and strength.
Innervation is vital to the muscle regeneration
process. After injury, regenerative activity begins but
does not continue unless a nerve is present.61,62 With
no vascular repair performed, palmaris longus muscles
have been grafted in the rhesus monkey with and
without surgical repair of the median nerve. Muscle
fibers regenerated in all grafts in which neural repair
was done but in only three of eight autografts without
nerve repair.63 In the rat, sensory reinnervation was
shown to preserve the same degree of muscle bulk as
motor reinnervation. 64
THE NONVASCULARIZED
MUSCLE GRAFT
Experimental Studies
Since the early investigations of muscle grafting
without neurovascular repair, controversies have been
common. Ziclonko (1874) first attempted the trans-
fer of skeletal muscle, placing it into the lymph sac of
a frog.65 The muscle tissue underwent rapid necrosis.
Shortly thereafter, Gluck (1881) claimed success, and
the controversy began.66 During the next 80 years, most
attempts at muscle grafting failed. Although some inves-
tigators observed that muscle possessed regenerative
capabilities,54,57 others observed resorption of the graft
followed by fibrous replacement, regardless of host site.1
It was generally agreed that muscle could not be grafted
successfully.67
Studitsky performed some of the earliest and most
extensive laboratory work on free muscle grafting in
Russia. In 1960, Studitsky and Bosova68 successfully
performed free autografts of skeletal muscle, trans-
ferring the middle third of the gastrocnemius of
the rat. A regenerative capacity of muscle was later
described when "minced" muscle (1-mm cubes) was
found to re-form the rat gastrocnemius muscle after
removal, provided the tendon insertion and nerve were
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left in place.6V,7l> Studitsky also introduced the concept
of preoperative denervation. He found that denervat-
ing the muscle 2 to 4 weeks before transplantation
improved survival, perhaps by lowering the metabolic
rate of the muscle tissue. The beneficial effect of pre-
denervation to improve graft survival has not been
substantiated in laboratory conditions.71,72 However,
predenervation has usually been employed when
nonvascularized muscle grafts are used clinically.
The histologic features of nonvascularized free
muscle grafts have been studied in several animal
species and demonstrate a consistent pattern (Fig. 22-
3).2,73 This pattern is likely to be seen in all muscle
grafts to some extent. Within hours after grafting, all
muscle fibers die of ischemic necrosis with the excep-
tion of a thin rim of cells around the periphery of the
graft. These fibers (<5% of the total) apparently survive
by diffusion of fluid from the recipient site. Vascular
ingrowth begins to penetrate the graft within 2 days,
bringing with it leukocytes and macrophages, 74 which
remove the dead sarcoplasm but leave the basal
laminae intact. After a few days, a cross section of a
free muscle graft discloses three distinct zones: (1) a
peripheral rim of surviving muscle fibers, which is adja-
cent to (2) a ring of muscle regeneration surrounding
(3) a core of necrotic fibers that have not yet been
removed by the macrophages. Regeneration of new
muscle is first noted 3 days after grafting in the small-
est and most extensively studied graft, the extensor dig-
itorum longus of the rat, which weighs 100 mg.71,72 The
first evidence of regeneration appears at the edge of
individual necrotic muscle fibers, where round cells
are noted. 75 These round cells produce myofilaments
and fuse into multinucleated myotubes that mature
into muscle fibers, eventually forming a fascicular
pattern.
The size of the graft is a critical factor in deter-
mining the extent of regeneration. 2 Complete regen-
eration occurs throughout the entire muscle in the
rat extensor digitorum longus (100 mg) 71 and the
rabbit flexor digitorum sublimis (1.5 g). A core of
necrosis, which is later replaced by scar, has been
observed in the cat extensor digitorum longus (3.5 g)
and the monkey palmaris longus (4.5 g).63,76 Attempts
to transfer larger (50 g) muscle grafts in dogs have
uniformly failed.77 ' The failure of central regenera-
tion in larger grafts suggests that a critical graft radius
exists through which vascular ingrowth must pene-
trate to provide nourishment to residual myogenic
cells before necrosis.
Young age of the recipient is also associated with
enhanced muscle regeneration. Muscle grafts in young
rabbits regenerate at a faster rate and become more
completely reinnervated than do those of mature
animals.73,75 Grafts from old rats placed into young ones
develop greater tension on functional testing, compared
with those of the reverse graft exchange.71 Superior
l ^ W t ^ ' y e l t f l ^ image...

22 • REPAIR, REGENERATION, AND GRAFTING OF SKELETAL MUSCLE 611

FIGURE 2 2 - 3 . A 6-day-old,
nonvascularized muscle graft in a
3-month-old rabbit. The edge of
the graft is at the lower right in
both photos. The central zone
(C) of the graft demonstrates a
homogeneous pattern of necrotic,
anucleate muscle cells. The inter-
mediate zone (I) is highly cellular
and demonstrates maturing myo-
tubes, suggestive of regeneration.
In the peripheral zone (not shown),
fibers that appear to have survived
the grafting procedure are seen.
(From Cedars MG, Das SK, Roth
JC, Miller TA: The microscopic
morphology of orthotopic free
muscle grafts in rabbits. Plast
ReconstrSurg 1983;72:179.)

reinnervation, and perhaps revascularization, may
occur in the younger animal. Dynamic tension (allow-
ing excursion of the muscle graft) has also been shown
to enhance the muscle regenerative process after non-
vascularized grafting.80 This result is not unexpected
because it is well documented that muscle force is
important in the maintenance of muscle mass, even
in normal muscle tissue.81
Muscle regeneration is believed to involve activa-
tion of the dormant stem cell known as the adult
myoblast or "satellite cell" identified by Mauro in
1961.82*84 Located between the basement membrane
and plasma membrane (plasmalemma) of the myo-
fiber, these cells are observed throughout muscle
tissue by electron microscopy. Satellite cells compose
2% to 35% of cell nuclei, depending on the age of the
animal. 85 The number of satellite cells increases during
the first 3 weeks after denervation86"88 but severely
decreases after prolonged denervation periods. 89 When
muscles are grafted, the satellite cell is thought to be
more resistant to ischemia than are mature muscle
fibers and initiates the regeneration process once neo-
vascularization occurs. This resistance to ischemia may
be due to a low metabolic rate, related to a relative lack
of cytoplasm. 90,9 ' The factors that stimulate the regen-
eration process are only partially understood. Some
factor associated with the grafting of muscle, perhaps
ischemia, initiates myogenesis.
The satellite cell may also have a significant func-
tion in the reinnervation of chronically denervated
muscle tissue. In a rat model, the implantation of non-
vascularized free muscle grafts was shown to improve

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612 I • GENERAL PRINCIPLES
muscle regeneration and recovery after reinnervation
that followed prolonged denervation (3 months). 92 The
mechanism is thought to involve the introduction of
new satellite cells, which are depleted after long periods
of denervation. Such a strategy might ultimately be
used clinically to improve results after delayed nerve
grafting.
Clinical Applications
In 1971, Thompson 93 reported the first successful free
muscle grafts in humans when palmaris longus grafts
were transferred in an attempt to reanimate the face
after seventh nerve palsy. Predenervation, performed
3 weeks before grafting, was believed to be essential,
as was the atraumatic transplantation of the entire
muscle length. Success was attributed to the survival
of muscle fibers within the graft rather than to muscle
regeneration.
Thompson's success generated renewed interest in
free muscle grafts. The effective use of free muscle grafts
for patients with facial palsy and in the reconstruction
of the anal sphincter was soon reported.13,94"97 Most
techniques relied on the placement of the muscle graft
over normal muscle, in the expectation that muscle
neurotization would provide innervation. The pre-
denervated palmaris longus muscle was used most
commonly. To reconstruct the oral sphincter, the muscle
belly of the graft was divided and sutured over both
the paralyzed and the normal orbicularis oris muscles.
Support and elevation of the oral commissure were
obtained by fixing the tendon to the zygomatic arch.
The electromyographic studies of Hakelius and
Stalberg98 documented graft function, employing
single-fiber techniques. Such documentation is the
exception rather than the rule in clinical reports.
Although muscle grafting was often beneficial in
reconstructing eyelid and oral sphincter function, it is
not clear that the observed motion was due to con-
traction of the muscle graft. A failed graft could func-
tion effectively as a static or passive sling, tightening
as the adjacent normal muscle contracted." Failures
in free muscle grafting were also documented."' 99
Despite early successes for patients with facial nerve
palsy,13,93 other techniques have proved more reliable
for the treatment of this entity. Ultimately dependent
on revascularization from the recipient bed, non-
vascularized grafts are limited in size and therefore
in strength. The survival of muscle tissue is vastly
improved when it is transferred with a neurovascular
pedicle, and microsurgery now allows the remote trans-
fer of large, vascularized grafts. Free nonvascularized
muscle grafts cannot be considered a reliable, consis-
tent reconstructive technique at this time.
Whereas it would be easy to dismiss nonvascular-
ized free muscle grafting as of historical interest only,
variations on this concept may one day prove useful
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Dr.Mustafa D.
in circumstances that are not as yet completely defined.
We are in a time in which many "absolutes" in med-
icine are being challenged. For example, the scarring
of the heart that results from myocardial infarction
has traditionally been taken as evidence that cardiac
myocytes are incapable of cell division. Recently,
however, evidence has been presented suggesting that
human cardiac myocytes are capable of division after
myocardial infarction.100 An increased mitotic index
has been demonstrated in myocytes adjacent to
recently infarcted areas. Such proliferating cells could
derive from resident cardiomyocytes or from circu-
lating stem cells. One may conceive of therapeutic
strategics designed to enhance this phenomenon,
potentially transplanting stem cells as cellular"muscle
grafts."
Thus, with the introduction of tissue engineering,
"muscle grafting" may take on entirely new dimen-
sions. Myoblast cell grafting into heart muscle may
provide a novel approach to the treatment of cardiac
failure. Embryonic cardiomyocytes, skeletal myoblasts,
or marrow-derived mesenchymal stem cells, by intra-
mural injection or arterial delivery, might serve to
augment cardiac function of the injured heart.101 Stable
incorporation of such muscle cell grafts has been doc-
umented experimentally in animals,102 and graftinghas
been shown to enhance ventricular function in injury
models.103 Transplanted myoblast cells have also been
used successfully to treat muscular dystrophies in
104
mice.
In the future, we may anticipate muscle grafting that
goes beyond cellular therapies. Although current tech-
niques of autogenous muscle transfers have proved very
useful, limited donor tissue exists, and donor site
morbidity may also present problems. The ability to
prefabricate muscle with use of tissue engineering
techniques is extremely appealing. In theory, at least,
one might be able to generate muscle conforming to
the specific requirements of a defect, Attempts to engi-
neer muscle tissue have been made by use of different
strategies.105,106 Saxena et al105 described the use of
myoblasts harvested from neonatal rats to make
skeletal muscle constructs. Myoblasts were combined
with biodegradable polymers and implanted into the
omentum of syngeneic adult rats. After 6 weeks,
myoblasts were found to have organized along the
strands of the polymer matrix, forming "neomuscle-
like" strands.
Hedrick et al106 have used a fibroblast-like popula-
tion of cells harvested from liposuctioned fat as a novel
source of cells for tissue engineering. These "processed
lipoaspirate" or PLA cells are of mesodermal or mes-
enchymal origin and can be stimulated to differenti-
ate along a myogenic lineage (Fig. 22-4). The use of
fat as a source of autologous stem cells represents
another option in tissue engineering strategies; the cells
are easy to obtain and abundant.
 image...

22 • REPAIR, REGENERATION, AND GRAFTING OF SKELETAL MUSCLE 613

FIGURE 2 2 - 4 . Advances in tissue engineer-

ing may provide novel approaches to "muscle
grafting." Experimentally, undifferentiated stem
cells have been isolated from liposuctioned fat
and undergo myogenic differentiation on culture
in a myogenic medium; note multinucleated
myotubule/>y.lmmunohistochemical staining is
demonstrated for myosin, which is specific for
human skeletal muscle (B). (Photographs cour-
tesy of Drs. Marc Hedrick, Peter Lorenz, and
Prosper Benhaim, Laboratory for Regenerative
Bioengineering and Repair, UCLA Division of
Plastic and Reconstructive Surgery, Los Angeles,
Calif.) B

THE VASCULARIZED GRAFT little residual functional disability, reduction of

In 1970, Tamai et al107 transferred the rectus femoris
muscle in dogs and documented the histologic, histo-
chemical, and electromyographic events that followed.
These studies firmly established for the first time that
entire muscles could be successfully moved to a new
anatomic position by immediate microscopic revas-
cularization and neural repair.2 This method was soon
used clinically with satisfactory results in the recon-
struction of forearm defects108*110 and in the reanima-
tion of the face after seventh nerve injury.10,20'111
Microneurovascular free muscle transfer is now a well-
established technique for the surgical management of
a variety of functional muscle disorders.
The principles defined in these pioneering efforts
can be summarized as efforts to expedite the techni-
cal aspects of the procedure and to maximize rein-
nervation potential: selection of a donor muscle with
a single artery and nerve that can be removed with
the length of ischemia time, and proximal neural
repair.2,100 Subsequently, refinements in donor muscle
selection have been made, with emphasis placed on
obtaining functional characteristics that closely par-
allel the specific anatomic deficit. Strength and range
of motion are considered among the most important
dynamic attributes.110,112 Fiber length of the donor
muscle is important in determining range of motion,
and strength is proportional to cross-sectional area of
the muscle.
Facial Reanimation
Reanimation of the paralyzed face has been described
with use of gracilis (Fig. 22-5),10'114,115 extensor digito-
rum brevis,111,116 pectoralis minor," 2,117 rhomboideus
major,118 rectus femoris,119 latissimus,120"123 latissimus-
scrratus,124 rectus abdominis, 125,126 and abductor hal-
lucis.' 27,128 One- and two-stage procedures are

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image...

614 • GENERAL PRINCIPLES

FIGURE 2 2 - 5 . Vascularized gracilis muscle graft for facial reanimation. This patient suffered from Bell palsy and
developed partial facial paralysis (A). Reconstruction with a cross-facial nerve and subsequent gracilis muscle graft
was performed [B, 7 months after gracilis flap). (Photograph courtesy of Dr. William Shaw, UCLA Division of Plastic
and Reconstructive Surgery, Los Angeles, Calif.)

described; two-stage procedures rely on a cross-facial
nerve graft to supply innervation.
Unique anatomic and physiologic characteristics of
the facial musculature make facial reanimation chal-
lenging. Lacking fascia and well-defined tendons, the
facial muscles consist of small motor units. In their
native position, the muscles used to reanimate the face
consist of larger motor units compared with the facial
muscles. Therefore, the neuronal input required by
these muscles is far exceeded by the reinnervation
potential of the facial nerve.129 As such, delicate facial
movements are difficult to reproduce. The recon-
struction of the multiple functions of the facial muscles
by a single donor muscle is difficult. For adequate rean-
imation of the paralyzed face, the upper, middle, and
lower facial muscles need to be addressed separately.
Dividing a single muscle graft into different parts
according to the territories of their nerve supply, as
suggested by Manktelow and Zuker, 13° does not ensure
independent function. Overlapping of nerve territo-
ries may result in "mass movements."131
Another one of the difficulties that arises in facial
reanimation is the bulk of the muscle that is trans-
ferred, which may compromise facial appearance. 12
Some atrophy does occur from the effects of tempo-
rary denervation, the loss of resting length, and the
effect of tenotomy. 45 Still, a question may be raised as
to whether these donor muscles are too large in volume
to reconstruct small facial muscles such as the muscle
responsible for smiling, the zygomaticus major, which
is approximately 5 cm in length and shortens 1.5 to
2 cm during smiling.130 To reconstruct this compara-
tively small muscle, a portion of the gracilis muscle,
centered on the neurovascular pedicle, has been used
as a "minitransfer."114,130 The same principle has been
used for the segmental transfer of latissimus, serratus,
and rectus abdominis. 12°-122'125-127'132
Extremity Reconstruction
In 1973, surgeons at the Sixth People's Hospital in
Shanghai transplanted portions of the pectoralis major
to the forearm to restore finger flexion after Volkmann
ischemic contracture. 108 In addition to soft tissue
coverage, vascularized free muscle grafts have found
widespread application in extremity reconstruction.
Functioning microneurovascular free muscle transfer
has become an option for reconstruction in cases of

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image...
22 • REPAIR, REGENERATION, AND GRAFTING OF SKELETAL MUSCLE
Volkmann ischemia/33*135 severe crushing or traction
injury with major muscle loss and nerve trauma,136,13
avulsion injury,'38 tumor resection,139 and brachial
plexus injury.140"142 The most common applications in
the upper extremity are reconstruction of finger
flexion-extension and restoration of biceps and deltoid
function. Functional muscle reconstruction of the
lower extremity is also described.113'139 Selection of
patients, selection of an appropriate donor muscle,
appropriate skin coverage, and postoperative rehabil-
itation contribute to the success of the procedures-
Speed and extent of reinnervation of the transplanted
muscle depend on the choice of recipient nerve, the
patient's age, and the occurrence of postoperative
vascular complications. 139
Guidelines for muscle selection include suitable neu-
rovascular anatomy, adequate strength and range of
muscle excursion, suitable gross anatomy to fit the
defect (muscle length, location of the neurovascular
bundle, and tendon availability), and minimal func-
tional and cosmetic donor defect.144 The gracilis, latis-
simus dorsi, pectoralis major, rectus abdominis, and
rectus femoris have been used as donor muscles. Staged
reconstruction of the forearm flexors (usually flexor
digitorum profundus) and extensors (usually ex-
tensor digitorum communis) has been described.138
Important technical considerations include revascu-
larization, reinnervation, balanced tendon fixation,
muscle positioning at optimum tension, and adequate
flap coverage.144 Determination of optimum tension
is based on the assumption that a muscle's most pow-
erful contraction begins at its maximum excursion. To
re-establish optimum tension at the recipient site, Frey's
technique 45 may be used. With the donor muscle in
situ, the patient is manipulated to place the donor
muscle on maximum stretch. A silk suture is placed
along the long axis of the donor muscle before it is
harvested. During resuturing of the muscle in a het-
erotopic position, the suture should ideally be stretched,
thus re-establishing the desired tension. Alternatively,
markers are placed on the donor muscle at regular
intervals and are later used to position the muscle at
maximum excursion in the recipient site.
Functioning free muscle transfer is usually per-
formed in an elective setting, after healing of bone and
soft tissue has occurred. The failure rate (inadequate
muscle power) of functioning free muscle transfer is
high in acute open wounds, 143 in which the injured
wound bed may promote scarring, and where healthy
donor motor nerves may be difficult to identify.
Cardiomyoplasty
The dynamic cardiomyoplasty was first used clinically
in 1985 by Carpentier. 145 In this technique, devised as
a treatment for end-stage heart failure, the failing heart
is wrapped with a paced skeletal muscle (latissimus
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Dr.Mustafa D.
615
or pectoralis) to provide ventricular assistance. Early
descriptions used pedicled muscle flaps,146 but free
latissimus grafts have more recently been used exper-
imentally and may offer specific functional advan-
tages.'47 Chronic electrical stimulation, performed
during a period of weeks before transfer, allows the
conversion of the skeletal muscle graft from "fast-
twitch" to "slow-twitch" muscle, thereby achieving
fatigue resistance.148 This conditioning makes use of
the capacity of muscle to adapt, as is seen in athletic
training for endurance. A variety of simulation pro-
tocols have been used experimentally, but it is common
clinically to use short bursts of high-frequency stim-
ulation for a period of weeks. Although more than 800
patients worldwide have undergone this procedure
since its inception, there is still controversy about the
way in which cardiomyoplasty works. Its main bene-
fits may derive from a "girdling" action of the muscle,
which prevents further enlargement of the ventricles
and may reduce them in size.149
Anal and Genitourinary
Reconstruction
Although technically a muscle transfer and not a true
graft, the gracilis muscle has been used in functional
anal and genitourinary reconstruction.150"152 Chronic,
low-frequency electrical stimulation of the ncosphinc-
ter may be delivered by implantable devices, with
functional improvement of incontinence. The gluteus
maximus has also been used in reconstruction of the
anal sphincter, both with and without implantable pulse
generators for electrical simulation, and may offer some
advantages over graciloplasty.'53,154 Other muscles have
also been used for this purpose.' 55
Electrical Stimulation
Electrical stimulation of skeletal muscle has been used
clinically in situations that require the muscle to con-
tract at the recipient site, such as in cardiomyoplasty
and anal or genitourinary neosphincter formation. In
conventional electrical stimulation, the target muscle
is stimulated to contract in a nonphysiologic all-or-
none fashion, which results in muscle fatigue. To over-
come this problem, electrical stimulation protocols
have been developed that train the target muscle during
several weeks and make it fatigue resistant. Chronic,
low-frequency stimulation is known to decrease fatigue
in fast-twitch muscle; this has been shown to cor-
relate with changes in blood flow and capillary
structure within the stimulated muscle tissue. 156
Interestingly, mild electrical stimulation may also
increase blood flow in chronically ischemic muscles,
as demonstrated in an ischemic hindlimb model in
the rat.157 Another alternative protocol to avoid fatigue
uses segmental stimulation with multiple electrodes.
T$k*>ttf<9elclW image.
616 I • GENERAL PRINCIPLES
T h i s m e t h o d is t h o u g h t to s t i m u l a t e t h e m u s c l e in a
m o r e physiologic m a n n e r , allowing c o n t i n u o u s force
g e n e r a t i o n while s i m u l t a n e o u s l y allowing p o r t i o n s of
t h e m u s c l e t o rest a n d t o reperfuse. 1 5 8
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image.
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98. Hakelius L, Stalberg E: Elect romyographical studies of free auto-
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99. Nicolai JP: Free muscle grafting in facial paralysis. Br J Plast
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100. Beltrami A, Urbanek K, Kajstura J, et al: Evidence that human
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102. Leor J, Patterson M.QuinonesM.etal: Transplantation of fetal
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103. Scorsin M, Hagege AA, Marote F, et al: Does transplantation
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109. Schenck RR: Free muscle and composite skin transplantation
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110. Manktelow RT, McKee NH: Free muscle transplantation to
provide active finger flexion. J Hand Surg 1978;3:416.
111. O'Brien BM, Franklin JD, Morrison WA: Cross-facial nerve
grafts and microneurovascular free muscle transfer for long
established facial palsy. Br J Plast Surg 1980;33:202.
112. Harrison DH: The pectoralis minor vascularized muscle graft
for the treatment of unilateral facial paralysis. Plast Reconstr
Surg 1985;75:206.
113. Fansa H, Plogmeier K, Feistner H, Schneider W: Plasticity and
function—the fate of a free, neurovascular muscle graft ten
years post-reconstruction. I Reconstr Microsurg 1997; 13:551.
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agement of facial palsy with microvascular free-muscle
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115. Sassoon E, Poole M, Rushworth G: Reanimation for facial palsy
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flap. J Reconstr Microsurg 1985;2:7.
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simus dorsi flap: a segmentally innervated muscle for facial
reanimation. Microsurgery 1988;9:36.
122. Harii K, Asato H.Yoshimura K, et al: One-stage transfer of the
latissimus dorsi muscle for reanimation of the paralysed face:
a new alternative. Plast Reconstr Surg 1998:102:941.
123. Wei W, Zuoliang Q, Xiaoxi L, ct al: Free and split latissimus
dorsi muscle transfer in one stage for facial reanimation. Plast
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124. Ueda K, Harii K, Yamada A: Free vascularized double muscle
transplantation for the treatment of facial paralysis. Plast
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125. Hata Y, Yano K, Matsuka K, et al: Treatment of chronic facial
palsy by transplantation of the neurovascularized free rectus
abdominis muscle. Plast Reconstr Surg 1990;86:1178.
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using the abductor hallucis muscle. Presented at the third joint
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rovascular free abductor hallucis muscle transplantation for
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132. Derby LD, Bartlett SP, Low DW: Serratus anterior free-tissue
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155. Girsch W, Rab M, Mader N, et al: Considerations on stimu-
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667.
image...
CHAPTER
23 •
Repair, Grafting, and
Engineering of Cartilage
MARK A. RANDOLPH, MAS • MICHAEL J. YAREMCHUK, MD
ANATOMY, PHYSIOLOGY, AND PHYSICAL PROPERTIES
SOURCES OF CARTILAGE CRAFTS
Autografts
Perichondria! and Periosteal Grafts
Allografts and Xenografts
Preservation Techniques
Cartilage is a relatively simple but highly specialized
connective tissue consisting of chondrocytes embed-
ded in an extracellular matrix composed primarily
of proteoglycans, collagen, and water.1 Unlike bone,
which has great regenerative potential, cartilage has
no internal vascular network and therefore possesses
limited innate ability for repair and regeneration. 2 ' 4
Consequently, injury to cartilage often results in scar
formation leading to permanent loss of structure and
function.5'12 Nutrition by diffusion rather than through
a vascular network, however, allows cartilage to be easily
transferred to repair sites and to be used in a multi-
tude of ways. For example, autologous cartilage can
be sculpted into delicate structures like an ear or fill
defects and restore contour in areas throughout the
face.13'15 Although the availability and clinical use of
alloplastic implants have accelerated at an exponen-
tial rate, autologous cartilage remains one of the most
prevalent and versatile tissues for facial reconstruc-
tion.16 Furthermore, the relatively simple structure of
cartilage has allowed significant progress in "engi-
neering" it in the laboratory. 17
Cartilage can be divided into categories according
to the composition of the matrix and its biologic role
in the body (Color Plate 23-1). Hyaline cartilage, which
is rich in type II collagen, can be found in the ribs, in
the trachea, and covering the articulating surfaces of
bones where it functions as a gliding surface and shock
absorber for skeletal elements.1,18 Elastic cartilage,
which contains elastin, occurs in tissues such as the
external ear, the epiglottis, and portions of the larynx. 3
Fibrocartilage, which is rich in type I collagen fibers,
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
CARTILAGE INJURY AND HEALING
TISSUE ENCINEERINC OF CARTILAGE
Cells and Cell Sources
Scaffolds
Other Considerations for Engineering of Cartilage
can be found in tissues that are subjected to tensile
forces, like the outer portion of intervertebral disks,
the knee menisci, and certain ligament and tendon
attachments to bone. 18 Specialized cartilage tissues, like
those in the epiphyseal growth centers of long bones,
contain highly specialized chondrocyte elements that
precisely control elongation and mineralization of
growing bones. 18 The structural and mechanical char-
acteristics as well as the normal biologic function of
each of the diverse cartilages should be considered in
choosing cartilage graft material or attempting to
engineer replacement tissue.
Cartilage grafting for some indications has been suc-
cessful, whereas other applications have been fraught
with difficulties and complications.M'19,20 Although car-
tilage grafts are often effective when they are used to
design or to improve contour under the skin, they have
had limited success in joint reconstruction, where they
are subjected to mechanical forces and distributed
load.9,21 In facial reconstruction, the biggest drawback
of large cartilage grafts is their tendency to warp or to
change shape over time.22"24 This may be due to the
presence of perichondrium or to the nonuniform com-
position of the matrix that can affect the shape when
it is placed into a defect. When cartilage grafts are used
for joint reconstruction where they are subject to
significant mechanical forces, graft availability and
ability to adhere or heal to the defect have been prob-
lematic. For some indications, the difficulty remains
in finding appropriate cartilage graft material; for
others, obstacles are related to graft design, shaping,
or fixation.
621
622 I • GENERAL PRINCIPLES
One option for acquiring an unlimited supply of
cartilage graft material while avoiding donor site mor-
bidity has been the use of allogeneic or xenogeneic
sources. Despite their use during the past century
or more, cartilage allografts have performed poorly
overall.21,25,26 Although cartilage is nonvascular and the
chondrocytes are believed to be protected by their extra-
cellular matrix from direct cellular immune attack by
the recipient, cartilage allografts undergo resorption
over the long term.26,27 Various methods have been
developed to preserve and to decrease the antige-
nicity of allogeneic cartilage, such as freezing and
lyophilization, but the outcomes are not significantly
improved with these techniques.
One of the most promising new avenues for carti-
lage repair and reconstruction is to use tissue engi-
neering techniques to generate new cartilage tissue.17,28
Because cartilage is not reliant on a direct vascular
supply, engineering of cartilage has been more suc-
cessful than the engineering of more complex vascu-
lar organs like the liver that perform vital metabolic
functions. Investigations into mesenchymal stem cells
from bone marrow that can be stimulated toward a
chondrogenic lineage and reports of deriving chon-
droprogenitor cells from fat lipoaspirates describe
promising routes for obtaining cells with less donor
site morbidity than by use of autologous cartilage
sources.29"31 Advances in polymer technology, in both
the manufacture of synthetic polymers and the
refinement of naturally occurring polymers, has
permitted rapid development of techniques for
engineering of cartilage tissues.32 Moreover, the
combination of suitable chondroprogenitor cells with
polymers containing growth factors that promote
chondrogenesis could permit controlled engineering
of desired cartilage tissue.
Fundamental concepts of cartilage biology, repair,
grafting, and tissue engineering are covered in this
chapter. Those readers seeking detailed information
on specific techniques for nasal and ear reconstruc-
tion are referred to Chapters 53,54, and 72.
ANATOMY, PHYSIOLOGY, AND
PHYSICAL PROPERTIES
Cartilage is widely distributed throughout the human
body and is composed of a combination of connec-
tive (or skeletal) tissue cells and their associated extra-
cellular matrix. Cartilage is a biphasic material, with
a solid matrix phase consisting of a dense collagen
network suspended in a gel of proteoglycans and an
interstitial fluid phase.33 The interstitial fluid phase gives
cartilage unique viscoelastic properties by the free flow
of water and electrolytes through the extracellular
matrix and allows the nourishment of chondrocytes
through diffusion.34 Cells, which compose only a small
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Dr.Mustafa D.
percentage ( 1 % to 12%) of the volume in cartilage
tissue, are encased within the extracellular matrix.
Without a vascular network, the chondrocytes must
rely on diffusion through the matrix for the delivery
of oxygen and nutrients and the removal of waste prod-
ucts. Hence, the metabolic requirements of chondro-
cytes are much less than those of cells in vascular tissues
and organs. Entrapped within the extracellular matrix,
the chondrocytes continuously produce various
extracellular macromolecules, including collagen, gly-
cosaminoglycans, and elastin,each of which is integrally
related to the biomechanical properties of cartilage.35
Cartilage derives from the mesoderm in the
developing embryo. In young animals, cartilage grows
through interstitial proliferation by chondrocyte
mitosis within the tissue or by appositional growth
of perichondrium-derived cells in those tissues sur-
rounded by perichondrium. As the cells proliferate,
they are arranged into subunits of chondrocytes
(called chondrons) surrounded by a multilaminated
matrix (Color Plate 23-2).36 In the chondron, the peri-
cellular matrix is rich in proteoglycans and hyaluronic
acid. Proteoglycans, which have negative molecular
charges, are responsible for tissue hydration and aid
in the resistance to compressive mechanical forces
applied to joints. These qualities derive generally from
the large aggregating proteoglycans, such as chondroitin
4-sulfate, chondroitin 6-sulfate, dermatan sulfate, and
keratin sulfate. There are also small nonaggregating
proteoglycans found in the matrix, such as biglycan
and decorin, the purpose of which is not fully eluci-
dated. The interterritorial matrix of the chondron is
rich in collagen as well as proteoglycans and other non-
collagenous proteins. The predominant type of colla-
gen in hyaline and elastic cartilage is type II with smaller
quantities of type VI, type IX, type XI, and other types
(Table 23-1). In fibrocartilage, however, the predom-
inant collagen is type I (as much as 90%) with
lesser quantities of type II, type III, and type V.
Noncollagcnous proteins, such as the elastin found in
elastic cartilage, in combination with collagen are
capable of sustaining tension applied to elastic carti-
lage in distraction.
The functional demands of the various cartilage
tissues are related directly to the biologic function
and the mechanical demands placed on the tissue,
specifically compressive, shear, or tensile forces.1,37
Hence, the specific organization of the various matrix
components of cartilaginous tissues is related directly
to the temporal and spatial functional demands on
the tissue, both static and dynamic. In general, these
functional demands pertain to (1) the protection and
support of related nonskeletal tissues and organs,
(2) the articulations between skeletal elements, and
(3) the dynamic processes related to skeletal growth.1
Because of these differences among the structural
image...

23 • REPAIR, GRAFTING, AND ENGINEERING OF CARTILACE 623

TABLE 23-1 • CARTILAGE TYPES AND RESPONSE TO INJURY

Type Function Location Response to Injury

Hyaline Dissipates loads Joints, rib cage, trachea Limited intrinsic healing; regeneration only with
adjacent invasion of bone to permit bleeding and
infiltration of cells
Elastic Provides support Ear, larynx Limited intrinsic healing; scar formation by cells
infiltrating from surrounding tissue
Fibrocartilage Transfers loads Intervertebral disks, Limited regeneration by scar formation
meniscus

demands of cartilage tissues, the biochemical compo-
sition of the extracellular matrix, which confers specific
biomechanical properties, is different among the
diverse cartilage tissues in the body. For example, artic-
ular cartilage is an extremely important mechanical
entity in joint function, playing an important role in
lubrication and wear by providing a fluid-filled, wear-
resistant surface, where one diarthrodial element slides
over the other.38 Other types of cartilage tissues fulfill
mechanical function as well, although different from
that of the articulating surfaces of joints. Cartilage of
the intervertebral disk acts as a load transmitter and
shock absorber between bony vertebral bodies by trans-
ferring axial compressive forces into tangential ones,
the energy of which is then absorbed and dissipated.39,40
The functional roles of cartilage in the trachea, nose,
ribs, ears, and pharynx involve maintaining form and
resisting deformation while providing some degree of
flexibility.41
The extracellular matrix tends to change with age
and injury or as the result of metabolic disease. For
example, collagen content of the extracellular matrix
tends to increase with increasing age, whereas the pro-
teoglycan content decreases. As a result of these and
other changes, the cartilage matrix increases in
stiffness and, in some cases, becomes calcified. Most
notably, the ribs tend to mineralize with age, making
it more difficult to use rib cartilage in the elderly to
reconstruct cartilage defects.16 Traumatic injury or
metabolic disorders can lead to debilitating arthritis,
particularly in aged patients. 2
Flexibility is an essential biomechanical property
for cartilage repair and grafting in the cranium (ear
and nose). Current approaches for ear reconstruction
with use of autologous or homologous transplants or
alloplastic implants can produce well-shaped auricu-
lar frameworks, but the structures are generally
inflexible.19,42,43 Furthermore, the physical demands on
cartilage in its native position may not be favorable for
reconstruction of unrelated anatomic features. For
example, the flexibility of cartilage in the rib cage may
not be equivalent to the flexibility needed for ear or
nasal reconstruction. Rib cartilage that has been
sculpted to form an external ear or a dorsal nasal
implant can often twist or warp, leading to an unsat-
isfactory clinical result (Fig. 23-l). 22 ' 24 To this end, there
has been considerable interest in creating a flexible yet
sturdy framework for use in ear reconstruction.
In those cartilage tissues having a perichondrium,
the perichondrium plays an important role in the

FiCURE 2 3 - 1 . Specimen of rib cartilage after retrieval from a nasal implant showing warping of the implant.

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
image...
624 • GENERAL PRINCIPLES
mechanical qualities of grafts harvested from such
tissues.44''15 The perichondrium forms a fibrous capsule
consisting of two zones, an outer fibrous zone and an
inner cellular zone. The outer zone consists of dense
lamellae of collagenous and elastic fibers and blends
with the surrounding connective tissue. The inner zone
blends smoothly with the subperichondrial cartilage
and can serve as a source of progenitor cells in carti-
lage grafts, particularly in young patients. The inner
zone is usually thicker in the developing tissues of juve-
niles but is nearly absent in adult tissues.46 In addition,
this specialized connective tissue layer has several func-
tions, including providing nutrients to cartilage
through its blood supply,46,47 regulating the growth
region of cartilage proliferation and differentiation,48
and promoting cartilage repair and regeneration.44,49
Studies in our laboratory have examined the func-
tion of perichondrium in relation to the biomechan-
ics and support of ear cartilage. We hypothesized that
ear flexibility is the result of the biomechanical prop-
erties of the cartilage matrix, the perichondrium, and
the binding of these two elements. Results from our
studies of native swine ear cartilage demonstrate that
the presence of perichondrium is essential for confer-
ring flexibility to the auricular cartilage (Fig. 23-2). 45
Intact perichondrium prevents fracture of porcine ear
cartilage when it is subjected to forceful biomech-
anical testing and torsion. These studies support the
conclusion that providing a perichondria! layer is
important for conferring flexibility to engineered car-
tilage tissue intended for craniofacial reconstruction.
To simulate a perichondria! layer when cartilage is
FIGURE 2 3 - 2 . Cartilage from swine ear undergoing forceful bending to demonstrate the role of the perichondrium.
The specimen in A has perichondrium preserved on the convex surface and does not fracture on bending. The speci-
men in B has had the perichondrium removed and fractures easily when bent.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
engineered, expanded polytetrafluoroethylcne (ePTFE)
is used as a structural component. 45 These results are
covered in more detail in the sections on tissue engi-
neering of cartilage.
SOURCES OF CARTILAGE CRAFTS
Autografts
Cartilage relies on diffusion through the matrix for
the cells to receive nutrients; therefore, it can be trans-
ferred to a multitude of recipient sites with relative
ease. Some grafts are harvested as pure cartilage
grafts, whereas others can be composites like peri-
chondrocutaneous grafts. The rib, nasal septum, and
ear are the most common sources of autologous car-
tilage graft material for craniofacial reconstruction
(Fig. 23-3). I6 Most important, fresh autologous grafts
easily survive transplantation procedures and do not
appear to resorb over time. For joint reconstruction,
cartilage or osteochondral grafts can be harvested from
uninvolved sites in the joint and transferred to the
defects.9'50
COSTAL CARTILAGE GRAFTS, The largest source
of autologous cartilage graft material is the rib cage
(see Fig. 23-3). Rib cartilage is extremely versatile and
can easily be sculpted into various shapes for many
uses. The primary disadvantages of use of rib carti-
lage are the relatively invasive procedure required for
harvesting grafts and the progressive calcification of
the cartilage in older patients. 16 Nonetheless, rib car-
tilage has been used successfully as onlay grafts to
image...

23 • REPAIR, GRAFTING, AND ENGINEERING OF CARTILAGE 625

U;-'.Helicar Rim •'•.•.'*'• '•";:./' • ^

irtV.v"-.'-'*
•v.*"•'•-"•
• • ~
-, HelicalCrus-.':-.;-.
• . • • • • » • • • • •
'•'.'

' . * • • ; , • • • • • * . * • , - • • . ./

*r^Coricha '•"..'.

FIGURE 2 3 - 3 . Cartilage grafts for craniofacial reconstruction and augmentation are commonly har-
vested from the external ear, the nasal septum, and the rib.

correct saddle nose and malar and mandibular contour
deformities. It can also be carved into intricate struc-
tures, such as the external ear.16,51,52 According to prin-
ciples described by Gibson, 25 however, internal stress
within rib cartilage can cause grafts to twist and warp.
Therefore, balanced cross-sectional carving and
scoring of grafts must be employed to achieve favor-
able outcomes.
deviations (Fig. 23-5). Without careful attention to
the perichondrium and taking action to counteract
the potential to curl, the perichondrium can warp and
twist cartilage grafts and lead to unacceptable clini-
cal results.

AURICULAR CARTILAGE GRAFFS. Significant por-

tions of the conchal cartilage can be harvested as
a conchal cartilage graft and as a composite full-
thickness wedge without causing deformity of the
donor site (see Fig. 23-3). I6,53 The ear can also serve as
a useful donor site for perichondrial grafts and com-
posite grafts of skin, perichondrium, and cartilage (see
later) (Fig. 23-4). Like costal cartilage, auricular
cartilage is extremely versatile and can be sculpted
into a variety of shapes.14,16 Auricular cartilage grafts
have been employed for partial ear construction, nasal
reconstruction, primary and secondary rhinoplasty,
and even reconstruction of the inverted nipple and
Montgomery glands.54
The perichondrium on auricular cartilage as well
as rib cartilage can wreak havoc on clinical outcomes.
Pure cartilage has little tendency to curl, whereas grafts
with a perichondrial layer can warp significantly.
Bergman and Stenstrom 55 theorized that the peri- f ! f JoK"&o>J M.p.
chondrium causes the cartilage to curl. If it is con-
FIGURE 2 3 - 4 . The ear has several favorable sites for
trolled by scoring or scratching, curling can be used the harvest of composite grafts including skin, perichon-
to correct prominent ears and to straighten nasal drium, and cartilage.

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
image...
626 • GENERAL PRINCIPLES
B
FIGURE 2 3 - 5 . Schematic drawing of scoring of the nasal septum to correct nasal
deviation.
NASAL CARTILAGE GRAFTS. Septal cartilage grafts
can be harvested as pure cartilage obtained by sub-
mucosal dissection or as a chondromucosal graft. In
harvesting of septal cartilage, however, care must be
exercised to avoid secondary deformity. To prevent nasal
collapse, an L-shaped septal strut should be preserved
to provide nasal support. Septal cartilage grafts have
been used successfully in primary and secondary rhino-
plasty.57"59 The grafts can be used as struts and layered
grafts or crushed up and used for filler.59 As a com-
posite chondromucosal graft, septal cartilage can be
used in eyelid reconstruction to restore support and
the mucosal lining of the eyelid.60
Perichondria! and Periosteal Grafts
Noncartilage tissue, such as perichondrium or perios-
teum, can also be transferred to regenerate or to restore
cartilage. Perichondrium is a rich source of chon-
droprogenitor cells and has the potential to generate
new cartilage matrix when it is stimulated in its native
bed, either mechanically or by inflammatory media-
tors. This was originally observed in treatment of
patients for pectus excavatum, in which subperi-
chondrial removal of cartilage demonstrated new car-
tilage formation, presumably from the perichondrium
left behind.61 Studies on the etiology of "cauliflower
ear" by Skoog and colleagues also pointed to disrupted
perichondrium as the source of this unpredictable
chondrogenesis.62"64 Because perichondrium is capable
of generating new cartilage, subsequent work by Skoog
and others attempted to channel this regenerative
capacity into cartilage reconstruction in the ear,
trachea, and joints.65"69
Perichondrial grafts are generally obtained from
rib or the posteromedial auricular surface. Harvest-
ing perichondrium from both ears can provide
significant amounts of graft tissue for some indica-
tions, although the rib is a more generous source.
In the young patient, both sources are acceptable for
generating neocartilage. In the older patient, however,
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
- r * . j o H » v » i M.p.
the perichondrium from rib has the propensity to
form bone. Perichondrial grafts can be difficult to
harvest in any site and are unpredictable in the
amount and form of cartilage that is generated.
Although the potential clinical use of perichondrial
grafts as a source of cartilage received considerable
attention in the 1970s, technical difficulties in harvest
and in transfer and unpredictable yield have limited
their clinical utility.
Periosteum also has some innate capacity to form
cartilage, given the appropriate conditions. Salter and
O^riscoll7,70 have studied the cartilage-forming capac-
ity of periosteum extensively, particularly for use in
restoring articular joint surfaces. Like the chon-
droprogenitor cells in the perichondrium, a popula-
tion of pluripotent cells in the cambium layer of
periosteum can be driven to chondrogenesis under
certain conditions. The avascular nature of diarthro-
dial joints may create a low-oxygen environment that
favors chondrogenesis over osteogenesis by these
pluripotent cells. The orientation of periosteum as well
as of perichondrium has been the subject of many
experimental studies. O'Driscoll70 favors orienting the
cambium layer to face the joint surface with the belief
that the progenitor cells in the cambium layer will be
driven to chondrogenesis and form a new joint surface.
Upton et al71 also thought that this orientation is more
favorable with perichondrial grafts. Long-term clini-
cal results with use of either perichondrium or perios-
teum are not yet available for conclusions to be drawn
on efficacy of the technique.
Allografts and Xenografts
Transplantation of allogeneic (or homologous) and
xenogeneic cartilage has had variable success, both clin-
ically and experimentally.72,73 Autologous (or syngeneic)
grafts survive longer than allografts, which in turn
survive longer than xenografts.25,71,74 Graft survival
appears to depend on the strength of the immune reac-
tion generated. Cartilage is often referred to as an
image...
23 • REPAIR, CRAFTING, AND ENGINEERING OF CARTHAGE
immune-privileged tissue like the cornea and epider-
mis, however, because fresh cartilage grafts theoreti-
cally do not have chondrocytes exposed to the host's
immune system. This may be due to the encapsula-
tion of the chondrocytes in an extracellular matrix
without any vascular conduits. The proteoglycan sub-
units, link protein, and collagen are weakly antigenic
by comparison to the leukocyte cell surface antigens.
As a result, fresh cartilage allografts appear to be weakly
antigenic from a cellular immunology standpoint. Fur-
thermore, there is considerable homology of collagen
molecules between species that may down-regulate the
immune response to xenograft cartilage matrix as well
as to allografts. However, allogeneic cartilage grafts have
performed poorly over the long term, 72 the cause of
which is most likely to be related to an immune reac-
tion by the host.75*78
Fresh cartilage allografts were used extensively
in the early to mid 1900s for craniofacial reconstruc-
tion and augmentation with favorable early results.79
Because the chondrocytes in the allograft are
encased in an extracellular matrix without vascular
channels, they are not susceptible to cell-mediated
rejection by the host. Thus, the cells can persist for a
significant period in their own microenvironment. In
fact, several clinical reports have demonstrated viable
chondrocytes in the first year or two after transplan-
tation. 25 Studies by Hagerty et al,26 however, demon-
strated that the initially high level of viable
chondrocytes in the grafts declines rapidly during
the first 2 years. By 6 years, only about 15% of the
cells remained viable, and the grafts had resorbed
significantly. Clinical results with use of allograft car-
tilage have shown that these grafts are unpredictable
and shrink over the long term. 72 Therefore, when allo-
graft cartilage has been used for reconstruction of
anatomic structures that require detail in the curvi-
linear features, like the ear, shrinkage and replacement
of the grafted cartilage by connective tissue have
resulted in poor long-term outcomes. Xenogeneic car-
tilage fares even worse than allografts according to
Gibson and Davis.74 Slightly better results with allo-
geneic cartilage have been reported with the use of
osteochondral allografts for orthopedic indications.80,8'
This may be due to the placement of the grafts in
reconstruction of diarthrodial joints, where the car-
tilage is not directly exposed to the vascular environ-
ment of the host.
With the evolution of tissue engineering, a central
issue involves the transplantation of isolated allogeneic
or xenogeneic chondrocytes and their potential for
eliciting an immune response. Removal of the cells
from their surrounding extracellular matrix may
expose major histocompatibility complex antigens
on the surface of the chondrocyte. 82 Tiku et al83 have
demonstrated that rabbit chondrocytes express la
antigens (class II) on their cell membranes and that
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Dr.Mustafa D.
627
chondrocytes themselves can function as antigen-
presenting cells. Lance84 has demonstrated that chon-
drocytes isolated from the ends of the long bones from
rat pups can stimulate an allogeneic immune response
in a mixed lymphocyte-chondrocyte reaction com-
parable to a mixed lymphocyte reaction in the same
rat strains. Studies in our laboratory by Mukerji85 have
confirmed the potential for allogeneic chondrocytes
to stimulate a mixed lymphocyte-chondrocyte reac-
tion in vitro. In studies in which cartilage grafts were
placed into host animals and challenged with skin
grafts, the animals rejected the skin in a fashion similar
to second-set skin rejection.75,76 Moskalewski et al86
showed that isolated chondrocytes elicited host leuko-
cyte invasion into the injection site in muscles, whereas
intact cartilage fragments stimulated only a benign
response from the host. In conclusion, chondrocytes
can stimulate a vigorous immune response, but the
relatively small number of cells and the extracellular
matrix of whole cartilage allografts probably slow the
rejection process. Nonetheless, allogeneic and xeno-
geneic sources are not preferred either for cartilage
grafts or to obtain cells to engineer cartilage at the
present time.
Preservation Techniques
The topic of preservation and banking of cartilage is
intimately associated with the use of allograft mate-
rial, fresh as well as devitalized. Chondrocytes can
survive for prolonged periods after somatic death,
possibly because of their low metabolic and oxygen
requirements. On the one hand, preservation tech-
niques have been employed to preserve the integrity
of the chondrocytes and the cartilage matrix. On the
other hand, many methods have been used to decrease
the antigenicity of the cartilage grafts primarily through
the destruction of the cellular elements.
Refrigeration is the simplest form of cartilage
preservation. Studies by Brent87 and others have shown
that banking of autologous cartilage tissue can be
achieved by moist refrigeration at 3°C to 5°C for as
long as 7 days. Refrigeration has little practical clini-
cal utility but demonstrates that chondrocytes within
cartilage are resistant to dying by merely cooling them
for prolonged periods. These results may have
significant implications for storage of chondrocytes
for engineering of cartilage.
The most prevalent technique for cartilage storage
is cryopreservation. Some chondrocytes are able to
survive freezing at -20°C, however, even without use
of cryopreservation solutions. Multiple freeze-thaw
cycles are necessary to completely eliminate viable
chondrocytes. 88 If viable chondrocytes in the cartilage
are preferred, as with osteochondral allografts, preser-
vation solutions such as glycerol or dimethyl sulfox-
ide can be employed to prevent disruption of the cell
628 I • GENERAL PRINCIPLES
membranes and subsequent death of the chondro-
cytes.80,89 These cryopreservcd allografts do not fare
any better than fresh allografts over the long term.
Other reported means for preservation of cartilage
grafts are lyophilization (freeze-drying), irradiation,
and thimerosal (Merthiolate) treatment. Lyophiliza-
tion is effective for completely eliminating the cellu-
lar elements of cartilage grafts and permits long-term
storage of cartilage matrix.90 There appears to be no
clinical advantage for use of lyophilization to preserve
cartilage grafts. With minor exception, the use of
thimerosal and irradiation can result in mineraliza-
tion of the graft.91*95
Another serious concern for use of cartilage from
allogeneic or xenogeneic sources is the potential for
disease transmission, particularly those diseases caused
by viruses. Tomford96 has extensively reviewed the
potential for disease transmission through transplan-
tation of musculoskeletal allografts. Although there are
no reported human cases of viral transmission asso-
ciated with the use of cartilage allografts, there are doc-
umented cases of patients receiving frozen bone grafts
from donors who harbored the human immuno-
deficiency virus and hepatitis C.97'99 Because cartilage
is encased in an avascular matrix and chondrocytes
lack a CD4 receptor, it is unlikely that human immun-
odeficiency virus can be transmitted by cartilage
grafts.100 However, the grafts could be contaminated
with blood at harvest, which could raise the risk of
infection. Other forms of preservation and steriliza-
tion, such as high-dose gamma irradiation and chem-
ical fixatives, have not been effective in totally
eliminating human immunodeficiency virus.101-102
There is a risk for transmission of zoonotic viruses from
xenogeneic tissue, but no reports have been docu-
mented in the literature from cartilage transplants. In
conclusion, the poor long-term results from use of allo-
geneic cartilage grafts have precluded more study into
preserving these tissues. Unless other options are not
available, clinicians are advised against using cartilage
allografts or xenografts.
CARTILAGE INJURY AND HEALING
The encapsulation of cells within a dense extracellu-
lar matrix that has no vascular network directly affects
the innate ability of cartilage to heal after injury or
grafting.2,3 Injury or lesions to ear or nasal cartilage
can stimulate the perichondrium to proliferate, and
the accompanying invasion of blood to the site can
facilitate scar formation. With the exception of the tem-
poromandibular joint, cartilage in the cranium does
not bear significant loads, and scar formation may be
satisfactory for filling contour deficits. The placement
of cartilage grafts to fill or to enhance contour deficien-
cies does not specifically require cartilage to cartilage
healing for successful clinical outcomes. Nonetheless,
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Dr.Mustafa D.
the grafts should be adequately incorporated into
the defect site to provide long-term stability for the
intended purpose.
Cartilage healing in articulating joints is critical to
long-term function. Lesions in the joints that pene-
trate through the subchondral bone can repair to some
degree by forming a layer of fibrocartilage, presum-
ably from the invading progenitor cells brought by the
blood.103 Partial lesions to the joint surface, however,
are isolated from repair by having no direct source for
cellular invasion or blood supply.2 Only recently have
Reindel et al104 demonstrated in vitro that chondro-
cytes can "bud" from the cut surfaces of cartilage and
proliferate along the interface of cartilage slices to form
a bond. This phenomenon may not occur in sufficient
numbers to permit healing of superficial lesions clin-
ically. Current clinical strategies to repair lesions in
articular joints employ microfracture or drilling
through to the subchondral bone to permit blood and
cell invasion; mosaicplasty, in which cartilage plugs are
harvested from uninvolved sites and transferred to the
defect in a mosaic pattern (also with blood invading
in between the plugs); and cellular therapy with cul-
tured autologous chondrocytes.9'103,105,106 Each method
has demonstrated relief of clinical symptoms, but the
tissue formed bears little resemblance to hyaline joint
cartilage.
Peretti et al88,107 studied the capacity of chondro-
cytes seeded onto dead cartilage matrix to bond the
pieces together. The chondrocytes formed matrix, and
the binding strength was tested in tension. These results
demonstrated that isolated chondrocytes were capable
of forming new matrix with favorable binding strength.
To study the healing capability of cartilage engineered
with fibrin polymer, Silverman108 performed experi-
ments analyzing the interaction between the engineered
cartilage and native cartilage in vivo (Fig. 23-6). A
polymer-chondrocyte mixture was sandwiched
between two disks, 6 mm in diameter, of fresh swine
articular cartilage and implanted into a subcutaneous
pocket on the backs of nude mice. Histologic and elec-
tron microscopic evaluation of the experimental con-
structs revealed a layer of neocartilage between the two
cartilage disks (see Fig. 23-6).The neocartilage appeared
to fill all irregularities along the cartilage disk surface
without any gaps. Safranin O and toluidine blue stain-
ing indicated the presence of glycosaminoglycans and
collagen, respectively. The mechanical properties of the
bonded experimental constructs, as calculated from
stress-strain curves, differed significantly from those
of the control samples. Failure was observed to occur
in all cases at the interface between the neocartilage
and the native cartilage. This study demonstrated that
tissue-engineered cartilage produced by use of a fibrin-
based polymer permitted adherence to adjacent car-
tilage and could withstand forces significantiy greater
than those cartilage samples adherent only by fibrin
image.

23 • REPAIR. GRAFTINC, AND ENGINEERING OF CARTHAGE 629

- r - -
~ —

w •
-. C? ••'

i
• 4
4

«Neo Nat
m

FIGURE 2 3 - 6 . Photomicro- r
graph showing tissue-engineered
cartilage (Neo) bonded to native
cartilage (Nat). (Toluidine blue, % .
x200.)

glue. Subsequent work in our laboratory has explored
the adherence of neocartilage to bone and synthetic
materials such as ePTFE.
TISSUE ENGINEERING
OF CARTILAGE
Harvesting of autologous cartilage grafts inevitably
causes donor site morbidity, and the graft material is
frequently inappropriate for reconstruction of the
defect. One possible solution for providing quality
cartilage graft tissue could be to engineer new carti-
lage to meet the requirements for the repair. By
definition, tissue engineering is the combination of cells
with a biocompatible polymer resulting in the forma-
tion of functional tissue units (Fig. 23-7). As such, the
material properties of synthetic or natural compounds
can be manipulated to allow the delivery of an aggre-
gate of dissociated cells into a host in a manner that
will result in the formation of new tissue.109,110
Cartilage is a favorable tissue to engineer because
of its simple structure and avascular nature.

Seed polymer
Dissociate cells and scaffold with cells

s/\
multiply in culture
Small Cartilage Biopsy

Implantation of construct
to form new tissue
FIGURE 2 3 - 7 . Concept of tissue engineering in which cells can be obtained by biopsy, grown in culture, seeded onto
a polymer scaffold, and implanted into a defect to generate new tissue.

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
image...
630 I • GENERAL PRINCIPLES
Theoretically, a small sample of normal chondrocytes
could be obtained by enzymatic digestion from unin-
volved cartilage tissues of an individual. These isolated
cells could then be grown in vitro to multiply to some
desired number. After a sufficient quantity of cells is
obtained, the cells could be combined or composited
with a polymer and transplanted into the defect site
to restore normal function (see Fig. 23-7). Cells pos-
sessing chondrogenic potential have been derived from
bone marrow and human lipoaspirates. The use of alter-
native cell sources and tissue engineering technology
could avoid many of the potential problems associ-
ated with other forms of treatment by minimizing
donor site morbidity and reducing the use of alloplastic
materials. To achieve the desired result, however, one
must consider both the properties of the tissue native
to the site and the properties of the polymer being used
to generate or to regenerate the cartilage repair tissue.
After several years of experimentation on tissue engi-
neering in our laboratory and by others, many lessons
have been learned in tissue engineering of cartilage.
Cells and Cell Sources
The primary obstacle to engineering of cartilage is
acquiring the appropriate numbers of chondrogenic
cells to generate the cartilage tissue. It is clear that the
type of cells, the number of cells, and the milieu into
which they are placed are critical elements for successful
cartilage tissue engineering. The seeding density of cells
capable of chondrogenesis in or onto a polymer
carrier is a critical ingredient for successful engineer-
ing of cartilage.
The simple structure of cartilage, which is gener-
ally composed of only one differentiated cell type, allows
relatively pure populations of chondrocytes to be iso-
lated from the cartilage matrix by use of commercially
available enzymes. Thus, small numbers of chondro-
cytes can be obtained by digestion of small amounts
of cartilage, and the cell number is expanded in culture
for subsequent autologous reimplantation. However,
it has consistently been observed in several species that
when chondrocytes are removed from their extra-
cellular matrix and grown in monolayer culture, they
become phenotypically unstable as evidenced by
flattening, spreading, and transforming into "dedif-
ferentiated" cells characteristic of fibroblasts.111"115
Benya et aIIM have demonstrated that collagen type II
synthesis declines steadily in articular chondrocytes
cultured in monolayer and essentially ceases by the fifth
subculture passage. Others have shown that chondro-
cytes grown in low-density monolayer culture begin
slowing the production of their characteristic large
aggregating proteoglycans and begin producing pre-
dominantly small nonaggregatingproteoglycans." 6,117
Thus, it is clear that growing chondrocytes in mono-
layer culture to achieve large numbers of cells may not
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Dr.Mustafa D.
permit the production of high-quality cartilage matrix.
Other means for culturing chondrocytes, such as sus-
pension culture or high-density monolayer culture,
may prevent dedifferentiation of the cells and sustain
a chondrocyte phenotype but are less effective in
expanding the numbers of cells.118"123 For various
reasons, the harvest of cartilage to acquire chondro-
cytes for generating new cartilage may not be the pre-
ferred method to obtain cells.
The use of other mesenchymal cells with chon-
drogenic potential may permit the generation of car-
tilage, given the correct polymer and appropriate
conditions. For example, Mizuno and Glowacki123 have
demonstrated that human dermal fibroblasts seeded
onto collagen type I sponges containing demineral-
ized bone matrix and grown in culture can be
stimulated to produce a cartilage-like tissue including
collagen type II. Caplan and Bruder29 have published
extensively on the use of bone marrow-derived mes-
enchymal stem cells to generate various muscu-
loskeletal tissues including cartilage when these cells
are given the appropriate signals. Lorenz et al31 have
described the chondrogenic potential of cells derived
from lipoaspirates when the appropriate culture con-
ditions were presented in vitro. These results demon-
strate that cells from different sources can be used to
engineer cartilage, possibly eliminating the need to
collect chondrocytes directly from cartilage that could,
in essence, cause unwarranted morbidity to fragile
tissues. However, in vivo studies on cartilage genera-
tion and repair with use of some of these cell types
have been equivocal, and none has reached clinical
application.124
One option that has not been exploited is use of
chondrocytes from allogeneic or xenogeneic sources
for engineering of cartilage. Whereas the use of allo-
geneic and xenogeneic cartilage en bloc has not
enjoyed favorable results clinically, isolated chondro-
cytes from these sources may perform satisfactorily
under the appropriate conditions. As reviewed before,
the central issue involving the transplantation of allo-
geneic or xenogeneic chondrocytes is their potential
to elicit an immune response once the extracellular
matrix is removed and major histocompatibility
complex antigens are exposed.83 Therefore, means to
stifle the immune response are necessary if allogeneic
or xenogeneic chondrocytes are used to engineer car-
tilage. It may be possible to develop scaffolds that will
permit the formation of new extracellular matrix while
simultaneously preventing immune rejection of the
isolated chondrocytes.
Scaffolds
The other critical element for engineering of cartilage
is finding suitable scaffold materials that permit or
accelerate the formation of new extracellular matrix.
TeWttf^Sd'iee image...
23 • REPAIR, GRAFTING, AND ENGINEERING OF CARTIU\CE
Use of polymers, both natural and synthetic, that
undergo controllable bulk erosion or resorption can
be favorable for engineering of cartilage tissues in vitro
or in vivo. For example, polymers that degrade at a
rate proportional to which cartilaginous extracellular
matrix is being deposited into the intercellular spaces
could be employed to generate cartilage in situ. When
properly orchestrated, cartilage with its characteristic
microarchitecture can be generated by the chondro-
cyte's intrinsic "programming" and facilitated by the
polymer's engineering.125 Several scaffolds, both natural
and synthetic, have been tested in animal models for
engineering of cartilage. Whereas many favorable poly-
mers are hydrogels, some are open lattice structures
with large pores into which cartilage matrix is permitted
to form.
NATURALORBIOLOGICSCAFFOLDS. Many scaffolds
for engineering of cartilage can be derived from
natural biologic scaffolds. For example, collagen is the
most prevalent structural biomolecule in the extra-
cellular matrix of cartilage, making it a logical choice
for a tissue engineering scaffold. Collagen sponges,
often made from animal tissues such as type I colla-
gen from bovine tendon, have many desirable prop-
erties as a biologic scaffold for cartilage, including
porosity, biodegradability, and biocompatibility. Col-
lagen scaffolds can be made from a si ngle collagen type
or composites of two or more types and can be chem-
ically modified to enhance certain characteristics,such
as pore size and biochemical attributes, that promote
cartilage formation.123,126"128 Open lattice collagen scaf-
folds, some of which also include glycosaminoglycans,
have been synthesized to generate new cartilage matrix
and show favorable results with regard to chondrocyte
adherence and the ability to maintain cells with a chon-
drocyte phenotype. 127,128 Despite their appeal as a bio-
logic material to make a tissue engineering scaffold,
these scaffolds can cause a foreign body reaction, result-
ing in a thin fibrous capsule surrounding the collagen
sponge implants when they are placed subcuta-
neously.129 Such reactions may interfere with the inte-
gration of new cartilage formed in the scaffold with
the surrounding native cartilage in the recipient site.
Other natural materials have been tested for scaf-
folds with some success. Hyaluronan is one of the major
constituents of undifferentiated mesenchyme in the
developing embryo and is believed to play a significant
role in the physical microenvironment affecting chon-
drocyte function.'30"132 Hyaluronan can be formulated
into many different chemical and physical entities that
provide a favorable environment for cartilage gener-
ation, allowing both synthesis of matrix components
and differentiation of the progenitor cells.133,134 Like
collagen, it has been formulated into sponge-like car-
riers and has been shown to support proliferation
of mesenchymal progenitor cells and differentiation
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Dr.Mustafa D.
631
into chondrocytes. A study by Solchoga et al135 showed
encouraging results in vivo in the treatment of an osteo-
chondral defect in a rabbit knee model with use of
hyaluronan-based polymer.
The inability to deliver chondrocytes through min-
imally invasive techniques with use of fibrous or open
lattice polymers stimulated investigations into other
types of polymer carriers, such as hydrogels. Biologic
hydrogels, such as fibrin glue and alginate, have proved
to be extremely useful for providing a hospitable, three-
dimensional support matrix for the immobilization
of cells.I36"139 Hydrogels are gelatinous colloids produced
by mixing a soluble polymer in water and adding a
cross-linking agent to gel the mixture into a stable,
three-dimensional structure. By existing in an initial
liquid phase, these polymers can be employed as
injectable delivery vehicles and subsequently poly-
merized in situ. The combined high water content and
elasticity of polymer hydrogels lead to many tissue-
like properties of these materials, making them ideal
candidates for tissue engineering matrices. By sus-
pension in a highly porous gelatinous matrix, chon-
drocytes can maintain their differentiated function and
are capable of producing large quantities of extra-
cellular matrix macromolecules.140,141
Our laboratory has reported on the use of sodium
alginate, a polysaccharide extracted from brown
seaweed algae that forms a hydrogel in the presence
of calcium ions, as a delivery vehicle for isolated chon-
drocytes to generate cartilage in situ.136,137 Although
successful, only "islets" of cartilage formed rather than
contiguous cartilage matrix throughout; thus, the
quality of the cartilage was indeterminate. Subsequent
studies in our laboratory have focused on use of fibrin
glue polymer as a hydrogel scaffold for engineering
of cartilage. Fibrin, which can be obtained from autol-
ogous blood products and is favorably biocompati-
ble, can be formulated as an injectable vehicle with
degradation controlled by agents like aprotinin that
slow fibrinolysis.139,142 Silverman et al139 investigated
the possibility of using a fibrin glue polymer to
produce injectable tissue-engineered cartilage but
reported that a significant reduction in volume (>60%)
occurred after implantation of swine articular chon-
drocytes into nude mice. To avoid this volume reduc-
tion of the scaffold, probably intrinsic to the use of
fibrin glue, Peretti et al143 added devitalized cartilage
matrix chips to prevent volume reduction and to
enhance the mechanical properties of the potential
reparative tissue. Biomechanical analyses of compos-
ite constructs showed higher modulus and lower
hydraulic permeability values in these experimental
samples with respect to the other groups.144,145 These
studies demonstrated that the balance between absorp-
tion of polymer scaffold and production of cartilagi-
nous matrix is key for controlling volume of
chondrocyte-fibrin glue constructs. Whereas many
image...
632 I • GENERAL PRINCIPLES
early studies used juvenile bovine articular chondro-
cytes, current research is focusing on auricular and
costal chondrocytes and their ability to synthesize a
matrix that maintains the implant volume in the sub-
cutaneous environment,
146
SYNTHETIC SCAFFOLDS. Advances in material sci-
ences and chemical engineering have now enabled the
production of biocompatible as well as biodegradable
materials that may provide favorable qualities for engi-
neering of cartilage. Many early investigations for engi-
neering of cartilage from synthetic polymers employed
poly(ct-hydroxy esters) because the Food and Drug
Administration had already approved them for human
use, primarily for suture material.109,147*150 Kim et al147
have demonstrated that implants of polyglycolic acid
and articular cartilage cells designed into specific shapes
can retain these shapes during in vivo incubation in
nude mice (Fig. 23-8). Employing synthetic rather than
naturally occurring polymers could offer many prac-
tical advantages. A significant body of practical knowl-
edge has emerged for manipulating synthetic polymers.
Chemical synthesis of polymers could allow the precise
engineering of matrix configuration to permit optimal
cell survival, proliferation, and subsequent tissue for-
mation. The physical properties of synthetic matrices
can also be altered to obtain desired characteristics of
the engineered cartilage. For example, the configura-
tion of the synthetic matrix could be manipulated to
vary the surface area available for cell attachment as
well as to optimize the exposure of the attached cells
to nutrients. Similarly, the chemical environment sur-
rounding a synthetic polymer might be affected in a
controlled fashion as the polymer biodegrades. With
a growing understanding of cell biology, it may be
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Dr.Mustafa D.
possible to attach ligands, such as cell adhesion pep-
tides, to the polymer backbone to promote or to foster
optimal cellular interactions. The potential also exists
for binding or incorporating growth factors and
hormones that could be continuously released in a
controlled fashion to provide signals promoting
chondrocyte differentiation and cartilage growth. The
ability to add multiple side chains to the polymer struc-
ture could allow a wide array of substances to be
deployed for defined purposes. Finally, chemically syn-
thesized polymers can be consistently and reliably pro-
duced with strict quality control, unlike the variable
quality of naturally occurring polymers.
Investigators have sought alternative synthetic
gels in which the chemical parameters can be carefully
controlled because biologic hydrogels, like fibrin
glue and alginate, are highly variable. Sims150 initially
demonstrated the capacity to generate cartilage
with a nonpolymerized form of poly(ethylene oxide),
a linear polyether with repeating molecular units of
(-CH 2 CH 2 0-) n .Poly(ethylene oxide) molecules can be
cross-linked by adding a photosensitive initiator to the
end groups that can form cross-links between mole-
cules with activation by ultraviolet light. In situ polym-
erization can permit such hydrogels to be sculpted
into desired shapes in defect sites.151,152 For example,
Elisseeff et al153,154 demonstrated that chondrocyte-
poly(ethylene oxide) constructs could be injected
subcutaneously, molded to the desired shape, and then
polymerized transdermally with ultraviolet light.
Other synthetic hydrogels have also been used to gen-
erate cartilage. Ashiku and others have investigated
the use of pluronics, a thermosensitive copolymer gel
made from combinations ofpoly(ethylene oxide) and
poly(propylene oxide), to encapsulate chondrocytes
• . * • ' -
FIGURE 2 3 - 8 . Specimens of
cartilage engineered into specific
shapes determined by the design
of the polyglycolic acid polymer
scaffold. (From Kim WS, Vacanti
JP, Cima L, et al: Cartilage engi-
neered in predetermined shapes
J employing cell transplantation
on synthetic biodegradable poly-
mers. Plast Reconstr Surg 1994;
94:233-237.)
I W t ^ a e c i W image...
23 • REPAIR, GRAFTING, AND ENGINEERING OF CARTILACE
for injection to generate cartilage.155"157 Polyvinyl
alcohol) is another photo-cross-linkable hydrogel
with desirable chemistry that allows easy modification
of the macromer backbone and has a long history in
medical applications.158,159 These polymers and gela-
tion processes can be designed to provide easy place-
ment (through photo-cross-linking chemistry), to
provide mechanical and structural stability with de-
sirable transport properties during the regeneration
process (through chemical modifications and pho-
tografting), and to allow the formation of complex
shapes with suitable adhesion for treatment of cran-
iofacial and joint defects. Rational design of synthetic
materials could optimize the immunoprotective
capacity of the photopolymerizable gels through
modifications of the network structure and chemistry.
INERT NON-RESORBABLE MATERIALS. Cao et al160
demonstrated proof of principle for engineering of car-
tilage into desired shapes on a resorbable endoskele-
tal scaffold by forming a human auricle in nude mice
with use of articular chondrocytes and an internal
biodegradable polyglycolic acid/poly-L-lactic acid scaf-
fold. These polyglycolic acid-based scaffolds, however,
elicit vigorous foreign body reactions in immune com-
petent animals. To avoid the inflammatory response
to polyglycolic acid-type scaffolds, Arevalo-Silva et al15'
investigated the use of nonbiodegradable endoskele-
tal scaffolds made from high-density polyethylene,
soft acrylic, polymethyl methacrylate, extrapurificd
Silastic, and conventional Silastic. They concluded that
use of a permanent biocompatible endoskeleton
demonstrated success in limiting the inflammatory
response to the scaffold, especially the high-density
polyethylene, acrylic, and extrapurified Silastic. Despite
their success of use of these materials for endoskele-
tal support, the biomechanical properties of neocar-
tilage were never evaluated.
Studies in our laboratory examined the mechani-
cal contribution of perichondrium to ear cartilage.
Intact perichondrium prevented fracture of ear carti-
lage in destructive testing. These studies demonstrate
that a perichondria! layer is important to confer flexi-
bility to engineered cartilage tissue intended for cran-
iofacial reconstruction. Compositing or bonding of
engineered cartilage to nondegradable membranes to
simulate the perichondrial layer could prevent frac-
tures in the neocartilage.161
To simulate a perichondrial layer, expanded poly-
tetrafluoroethylene (ePTFE) was tested as a structural
component for supporting the engineered cartilage.
ePTFE is a biocompatible material that has been used
successfully in a multitude of biomedical and clinical
applications. 162 One advantage of this material is its
microporous structure that allows biointegration
for soft tissue fixation as well as overall mechanical
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Dr.Mustafa D.
633
integrity.163 The results from the gross mechanical
testing (Fig. 23-9) on engineered cartilage-ePTFEcom-
posites demonstrated that ePTFE membrane matched
the needs of a pseudoperichondrium for engineered
cartilage. ePTFE membrane is firm enough to sustain
the tension placed on the surface of the engineered
cartilage-ePTFE composite. The adhesive character of
fibrin polymer allowed the fibrin glue-chondrocyte
composite to combine with ePTFE membrane com-
pactly at the outset of the experiment. Subsequently,
the chondrocytes permeated the micropores of ePTFE
membrane and produced neocartilaginous matrix,
forming a tight bond between ePTFE membrane and
engineered cartilage (Color Plate 23-3). This integra-
tion of cartilage and ePTFE membrane formed a flexible
cartilage framework with a pseudoperichondrium.
When the polymer is placed on both surfaces of the
composite, the ePTFE membrane can maintain the
flexibility of tissue-engineered cartilage. Thus, recre-
ating a pseudoperichondrial layer similar in structure
and position to the native perichondrium could
provide the necessary flexibility for making suitable
tissue-engineered cartilage for craniofacial repair.161
Other natural and synthetic materials could serve
to enhance the mechanical function of engineered
cartilage.
Other Considerations for
Engineering of Cartilage
Engineering of cartilage relies heavily on the cells to
produce extracellular matrix products and on the scaf-
fold material selected. There are other considerations
for generating cartilage as well. If cartilage tissue is to
be generated entirely in vitro, the culture conditions
play a significant role in seeding the polymers and the
composition of the final cartilage matrix. In addition,
growth factors have been shown to have a significant
effect on the proliferation of cells and chondrogenic
differentiation. These growth factors can be added
to cell culture or incorporated into the cell-polymer
scaffolds.
SUMMARY
The use of autologous sources of cartilage for graft-
ing will continue to provide the best clinical results in
the foreseeable future. Results with use of allogeneic
cartilage have been disappointing, and it is unlikely
that new approaches will be able to improve outcomes.
Furthermore, the potential for disease transmission
from allogeneic cartilage has curtailed its use, except
in extreme situations. Tissue-engineered cartilage
could have widespread application in the future if
several obstacles are overcome. For example, causing
morbidity by harvesting cartilage to obtain small
 image...

I
I

COLOR PLATE 2 3 - 1 . Photomicrographs of samples of hyaline, elastic, and fibrocartilage from swine. Articular
hyaline cartilage (A) shows cells in lacunae embedded in a homogeneous extracellular matrix; staining with safranin O
(B) demonstrates the rich proteoglycan production by the cells. The superficial layer of articular cartilage can be noted
to the right of specimen B showing the tangential layer of cells. The specimen in C is a section of elastic ear cartilage;
the perichondrium is shown on the surface of the cartilage on the left. The cells and lacunae appear to be oriented
perpendicular to the surface of the cartilage. Specimen D is ear cartilage stained with Verhoeff elastin stain; the dis-
tribution of elastin fibers is shown in black. Fibrocartilage from the meniscus is shown in E and F. The chondrocytes in
the meniscus can be noted in lacunae surrounded by a halo of extracellular matrix in E. A meniscus specimen stained
with trichrome (F) demonstrates the predominance of type I collagen fibers in fibrocartilage.

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
image

COLOR PLATE 2 3 - 2 . Specimen of rib cartilage demon-

strates groups of cells arranged into chondrons and
surrounded by pericellular matrix rich in collagen and
proteoglycans. (Hematoxylin and eosin, x200.)

COLOR PLATE 2 3 - 3 . Photomicrograph of engineered cartilage bonded tightly

to ePTFE membrane as evidenced by cells and new matrix penetrating the ePTFE.

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Dr.Mustafa D.
Vt&*)ttf(9el(fltf image..

634 • GENERAL PRINCIPLES

{IZW)

Bending Torsion

* • • " * * * * * *

— : J

2 ,
'Jem if
E >£*....*L..i.
u*n;
02W)

icm
Jmsliii!
FIGURE 2 3 - 9 . Expanded polytetrafluoroethylene (ePTFE) placed on the surfaces of engineered cartilage and used
as a pseudoperichondrium shown in the schematic drawing and after 12 weeks of growth in vivo in a mouse. The new
cartilage with this pseudoperichondrium has the ability to resist fracture when it is bent or placed under torsion.

numbers of chondrocytes is not a favorable option to
engineer small amounts of cartilage. The reliability of
engineered cartilage has not been demonstrated, even
in animal models. Investigations into multipotent mes-
enchymal stem cells or other modified cell type may
expand the potential for engineering of cartilage. Once
cartilage can be consistently engineered with the ap-
propriate matrix and mechanical properties, many
cartilage structures will be amenable to grafting and
repair.

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
image...
23 • REPAIR, GRAFTING, AND ENGINEERING OF CARTILAGE
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*»***> ttf^eldW image...
638 I • GENERAL PRINCIPLES
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image...
CHAPTER
24
•
Repair and Grafting of Bone
BABAK J. MEHRARA, MD • JOSEPH C. MCCARTHY, MD
ANATOMY AND HISTOCHEMISTRY OF BONE
Components of Bone
BONE FRACTURE REPAIR
Primary Bone Repair
Secondary (Callus) Bone Repair
Variables Influencing Bone Repair
MOLECULAR MECHANISMS OF FRACTURE REPAIR
Bone Morphogenetic Proteins
Transforming Growth Factor-P
Fibroblast Growth Factors
Platelet-Derived Growth Factors
DISTRACTION OSTEOGENESIS
History
Histology
Variables Affecting Osteogenesis
BONE CRAFTING
History
Autogenous Bone Grafting
Variables Affecting Free Bone Graft Survival
Vascularized Bone Transfers
The regulation of bone formation during embryo-
genesis, its subsequent remodeling during growth and
development, and the regenerative potential of bone
have been topics of intense research and special inter-
est to the surgeon. The quest for a complete under-
standing of these mechanisms is an important one
because this knowledge may lead to improved clini-
cal methods of bone repair. The goal of this chapter
is to provide a summary of the mechanisms under-
lying bone development and repair. In addition, a
review of the available bone substitutes and the
surgical techniques to replace bone deficiencies is
presented.
ANATOMY AND HISTOCHEMISTRY
OF BONE
Bone is a complex organ system that provides struc-
tural support for the human body while also serving
an important protective function for the internal
organs. The combination of these two functions is best
exemplified in the craniofacial skeleton; the calvaria
protects the underlying brain, and the facial skeleton
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CLINICAL USES OF BONE TRANSFERS
Tibia
Ilium
Greater Trochanter and Olecranon
Rib
Fibula
Scapula
Metatarsus
Calvaria
ALLOGENEIC BONE CRAFTS
History
Processing and Preservation
Risk of Disease Transmission
Immunogenicity
Incorporation of Allograft Bone
Formulations of Allogeneic Bone Grafts
XENOGENEIC BONE CRAFTS
BONE SUBSTITUTES
Calcium Sulfates
Calcium Phosphates
Methyl Methacrylate
provides the scaffold on which the soft tissues and
muscles of facial expression arc built.
The human skeleton is composed of two embry-
ologically distinct bone types. Endochondral bone is
formed by the ossification of a cartilaginous interme-
diate and is found in the tubular long bones of the
appendicular skeleton. In contrast, membranous bone
is derived from direct ossification of mesenchymal pre-
cursors and is found in the flat bones of the axial and
craniofacial skeleton. Each bone type has a cortical and
cancellous component (fig. 24-1). The cortical or the
smooth, strong outer surface of the bone component
provides structural integrity. This osseous tissue is
lamellar in structure (i.e., bone is deposited in organ-
ized layers in the direction of maximal stress) and con-
tains osteocytes within lacunae. Lacunae surround
haversian canals containing nutrient vessels that
anastomose with vessels within the bone marrow and
periosteum (through Volkmann canals). The lacunae
surrounding each haversian canal are the basic unit of
bone and are known as osteons or haversian systems.
The external surface of cortical bone is covered
by the periosteum, a sturdy two-layered cellular
639
640 I • GENERAL PRINCIPLES

COMPACT/CORTICAL BONE
SPONGY/CANCELLOUS
BONE
. . • • ; . . • * • ...••.•.•».•.-;•;••••;:
• " • • • . • - ;.•.•*••"••'•*-.;
FIGURE 2 4 - 1 . Diagrammatic representation of axial
compact cortical bone microarchitecture. (Modified from
Cutting CB, McCarthy JC, Knize DM: Repair and grafting
of bone. In McCarthy JC, ed: Plastic Surgery, vol 1.
Philadelphia, WB Saunders. 1990:583-629.)
membrane with important roles in fracture repair and
angiogenesis. The outer layer is fibrous in nature and
contains flat cells that resemble fibrocytes. The inner
(cambium) layer contains bone cell precursors that
appear as large, round cells with abundant cytoplasm
(Fig. 24-2). The internal surface of cortical bone is
covered by a fibrous sheet known as the endosteum.
This structure is also thought to contribute to bone
formation during fracture repair; however, the exact
nature of this contribution remains unknown.
The cavity within the cortical bone contains the
bone marrow and cancellous bone and is a rich source
of hematologic and osteoblastic precursors. Cancel-
lous bone provides internal support for the cortical
bone and bone marrow elements by acting as an inter-
HAVERSIAN
CANAL nal strut, thus augmenting axial loadi ng strength. Can-
cellous bone is made up of trabecular bone of varying
TRABeCULAE thickness with the thickest portions containing mature
osteons (Fig. 24-3).
VOLKMANN'S
CANAL
Components of Bone
INORGANIC COMPONENT
Mature lamellar bone is composed of approximately
VOLKMANN'S 93% solid material and 7% water.1 The solid compo-
CANAL nent can be further divided into inorganic and organic
components. The inorganic component constitutes
most of the total bone volume by weight (approximately
70%) and consists primarily of calcium phosphate
(hydroxyapatite) with the chemical composition of
Ca,0(PO4)6(OH)2. These mineral crystals are deposited
along interwoven collagen fibers and form rod-shaped
bone crystals measuring 20 nm in length and 2.5 to
7.5 nm in width. Bone crystals are surrounded by a
thin layer of water, known as the hydration shell, allow-
ing free exchange of ions with the crystalline surface.
The large quantities of calcium, phosphate, and mag-
nesium in bone act as a reservoir for these ions and
through the action of local and systemic factors main-
tain their homeostasis.
ORGANIC COMPONENT
The organic component of bone is composed of bone
cells and extracellular matrix. Three principal bone
cell types are identified during bone formation and
remodeling—osteoblasts, osteocytes, and osteoclasts
(Table 24-1).

h
: -

¥
i '• '' r* > ' • - i - ^--* "

J • 1_ / » * ' \

FIGURE 2 4 - 2 . Low-power {A, magnification xlOO) and high-power [B, magnification x200) views of an adult rat
mandible 56 days after a partial osteotomy of the mandibular angle and stained for BMP-2/4 with polyclonal rabbit
antibodies conjugated to diaminobenzidine. P, periosteum.

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Dr.Mustafa D.
 TABLE 24-1 • BONE CELLS

Differentiation
Cell Type Morphology Location Function Source Precursor Cell Product

Osteoblast Rounded, basophilic cells External surfaces of Produce bone matrix Periosteum Preosteoblast Osteocyte
Stain strongly for alkaline bone in areas of Endosteum ?Bone lining cells
phosphatase active remodeling Bone marrow
and bone formation ?Others
Bone surfaces in
fractures
Osteocyte Stellate cells with thin Embedded in lacunae Exact function Osteoblasts that Osteoblasts Terminally
cytoplasmic processes unknown become embedded differentiated
Potential functions: in osteoid cell
Mechanosensory
Mineral homeostasis
Bone resorption
Osteoclast Large, multinuclear cells Endosteal and Bone resorption Bone marrow Hematopoietic None
with ruffled border periosteal surfaces Spleen stem cell
Stain positive for tartrate- of bone in areas of ?Lung, peritoneum,
resistant acid active remodeling peripheral blood
phosphatase On fractured bone
surfaces

en
4S

- .„

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Dr.Mustafa D.
image...

642 I • GENERAL PRINCIPLES

,- Osteoblast
Lacunae

Calcified
Uncalcified
osteon osteon

{:$f}>-Canaticuli
'4

m^^3g&& TBone
^ 9 e 5 ^j.D- Haversian
canal with
G.A. de Stefano, M.D.
marrow its vessels
B
FIGURE 2 4 - 3 . A, Cross section of compact bone as seen by microradiography. Note that the osteons are oriented
in the longitudinal axis of the long bone. The dark masses represent recent decalcified osteons. The light masses rep-
resent older calcified osteons. B, A single osteon of the haversian system. (From Cutting CB, McCarthy JG, Knize DM:
Repair and grafting of bone. In McCarthy JG, ed: Plastic Surgery, vol 1. Philadelphia, WB Saunders, 1990:583-629.)

Osteoblosts during bone development and repair is not entirely

HISTOLOGY AND FUNCTION. Osteoblasts are
plump, rounded, basophilic cells localized on the exter-
nal surfaces of bone and in the areas of active bone
formation and remodeling (Figs. 24-4 and 24-5). These
metabolically active mesenchymal cells have a large
endoplasmic reticulum (responsible for the basophilia)
and are the principal cell involved in bone formation
by producing bone matrix. The source of osteoblasts
clear, although surrounding periosteum, endosteum,
and bone marrow appear to be important. Terminal
differentiation of osteoblasts results in the formation
of osteoid (unmineralized bone matrix) and eventual
surrounding of the cell within mature bone, thus
forming an osteocyte within a lacuna. Dedifferentia-
tion of osteocytes into osteoblasts during fracture
repair has been proposed but has been intensely
debated.

FIGURE 2 4 - 4 . Cross section

of an adult rat mandible (magni-
fication x200) 28 days after a
partial osteotomy of the man-
dibular angle and stained for
BMP-2/4 with polyclonal rabbit
antibodies conjugated to diami-
nobenzidine. Note large, active,
positively stained osteoblasts
(OB) at the bone margins.

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Dr.Mustafa D.
image...

24 4- REPAIR AND CRAFTINC OF BONE 643

* t w ••
«'
^
¥
** ^N. \ Bone c g g c ^
# *
A*
OB

FIGURE 2 4 - 5 . A High-power magnification (x200) of an adult rat mandible 7 days after a partial osteotomy of the
mandibular angle and stained for BMP-2/4 with polyclonal rabbit antibodies conjugated to diaminobenzidine. Note
osteoblasts (OB) lining bone edge. B, High-power magnification (x400) of an adult rat mandible 1A days after osteotomy
stained for BMP-2/4. C, High-power magnification of human mandible sections stained with hematoxylin and eosin.
Note large, active osteoblasts at bone margin. (Courtesy of Drs. Clarkson and Huvos, Department of Pathology, Memo-
rial Sloan-Kettering Cancer Center.)

The regulation of osteoblast differentiation and
function has been extensively investigated. Despite this
research, however, significantly less is known about
osteoblast differentiation than about osteoclast dif-
ferentiation. These studies have been hampered, in
part, by the facts that osteoblast precursors are less
well defined than osteoclast precursors and that
osteoblastic gene expression patterns are, with the
addition of a few specialized genes, similar to those
of fibroblasts. Thus, although some gene products
are up-regulated in osteoblastic cells (e.g., bone sialo-
protein) compared with fibroblasts, only one protein
has been found to be osteoblast specific (osteocalcin).2
These findings complicate the differentiation of
osteoblast precursors from fibroblasts and fibroblast
precursors, thus impeding cellular investigative
studies.
Research has demonstrated that the bone marrow
stroma contains a small number of multipotential mes-
enchymal cells ( < 1 % of total) and that exposure of
these cells to various environmental stimuli can elicit
differentiation into various mature cell types, includ-
ing osteoprogenitors, chondroblasts, adipocytes, and
myoblasts.2,3 The existence of these multipotential cells
is supported by studies demonstrating that clonally
derived, immortalized cell lines (e.g., with the SV40
large T antigen or spontaneous immortalization)
maintain the ability to differentiate into multiple
differentiated cell types in vitro. Whether these cells
are true stem cells (i.e., maintain unlimited ability to

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Dr.Mustafa D.
644 I • GENERAL PRINCIPLES
repopulate their population) remains unknown;
however, it is clear that multipotential cells with at
least a limited ability to propagate (8 to 10 cell divi-
sions/ exist 1
Functional assays of osteoblast differentiation have
defined at least four maturational stages in osteoblast
development: the preosteoblast, mature osteoblast,
osteocyte, and bone lining cells.3"3
Prcosteoblasts are the immediate precursor to
osteoblasts and are derived from, among other sources,
pluriputential mesenchymal cells within the bone
marrow and the cambium layer of the periosteum.
These cells resemble mature osteoblasts histologically
and ultrastructurally and are localized approximately
one or two ceil layers away from osteoblasts lining
bone- forming surfaces. Similar to mature osteoblasts,
these cells also stain positively for alkaline phosphatase
and produce some bone matrix proteins; however,
unlike mature osteoblasts, preosteoblasts have not
acquired other differentiated characteristics and main-
tain a limited ability to divide. Some authors have
hypothesized that spindle-shaped cells close to the pre-
osteoblast layer and localized farther away from bone-
forming surfaces represent osteoprogenitor cells (i.e.,
undifferentiated mesenchymal cells).5 These cells do
not produce bone matrix proteins but may be iden-
tified by their histologic characteristics in combina-
tion with monoclonal antibodies.
Osteoblasts are post-proliferative cells lining the
bone matrix at sites of active matrix production. These
cells stain strongly for alkaline phosphatase, a mole-
cule with important roles in mineralization and bone
formation. Osteoblasts produce large amounts of
bone matrix proteins (collagen I, bone sialoprotein,
osteopontin, osteocalcin; see later) as well as hormone
receptors (most notably parathyroid hormone recep-
tor), cytokines, and growth factors.3 Ten percent to
20% of mature osteoblasts become incorporated into
bone matrix and form osteocytes (see later).6,7 These
cells are also post-proliferative and are, essentially,
metabolically inactive. The existence of osteocytic
osteoblasts, a transitional cell type with limited ability
to dedifferentiate into mature osteoblasts, has also been
proposed. 8 ' 10
Bone lining cells are flat, thin, elongated cells lining
the bone surfaces of resting adult skeleton.3"5 These
cells are found in areas that are not undergoing active
remodeling or bone synthesis and, like mature
osteoblasts, are post-proliferative. Bone lining cells are
thought to represent an inactive form of osteoblasts
(i.e., not actively producing bone matrix). Although
it has been proposed that bone lining cells may form
active osteoblasts in response to environmental stimuli,
this possibility has not been directly demonstrated.
Two gene products, core-binding factor al and
Indian hedgehog, have been identified that either
directly or indirectly control osteoblast differentiation.
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Dr.Mustafa D.
In addition, a large number of cytokines and secreted
growth factors have been implicated in this process,
including members of the transforming growth factor
(TGF) (i superfamily, fibroblast growth factors,
insulin-like growth factors, and platelet-derived growth
factors (see later).
Core-Binding Factor al. Core-binding factor al
(Cbfal), a transcription factor, is the earliest and most
specific marker of osteoblast differentiation and rep-
resents the mammalian homologue of the DrosophHa
transcription factor Runt. 1 'Numerous lines of evidence
support a critical role for this molecule in osteoblast
differentiation and function and have shown that the
functions of this molecule are not redundant with other
proteins. For example, Cbfal has been shown to bind
to osteoblast-specitic cfs-acting elements in the pro-
moter of most genes expressed by osteoblasts.12'1,1 In
addition, expression of Cbfal during development and
repair is highlv specific to osteoblasts and is regulated
by osteogenic growth factors (e.g., bone morphogenetic
growth factors).13 Ectopic expression of Cbfal in
nonosteoblastic cells, such as fibroblasts, promotes
osteoblast differentiation with resultant expression of
osteoblast-specific gene products such as osteocalcin.I3
Cbfal knockout mice (animals in which Cbfal gene
is deleted) demonstrate a cartilaginous skeleton
without any evidence of bone formation.15,16 Finally,
Cbfal function is dominant and likely to be evolu-
tionarily preserved in humans because heterozygote
(Cbfa 1 +/~) mice demonstrate hypoplastic clavicles and
abnormal cranial suture development, findings similar
to those in cleidocranial dysplasia, and clinical cases
of cleidocranial dysplasia have been linked to muta-
tions within the human CBFA1 gene.'6"'8
The regulation of Cbfal appears to be complex and
has not, as yet, been deciphered in vivo. Thus, although
bone morphogenetic proteins can induce the expres-
sion of Cbfal in vitro, this expression is delayed and
implies an indirect rather than a direct mechanism of
action.2,13
Indian Hedgehog. Indian hedgehog (IHH) is a
secreted growth factor expressed in the developing
skeleton and has also been implicated in the regula-
tion of osteoblast and chondrocyte differentiation. The
finding that IHH-deficient mice have disorganized
growth plates and absence of osteoblasts within endo-
chondral bone supports this conclusion.19 The mech-
anism of action of IHH is complex, however, because
seemingly normal osteoblasts are observed in mem-
branous bones of IHH-deficient mice.19 In addition,
failure of osteoblast differentiation within endochon-
dral bones does not appear to be related to chondro-
cyte differentiation because selective interference
with IHH biologic function within chondrocytes of
transgenic mice was not associated with the absence
of osteoblasts within endochondral bone. 20 Thus,
image...

24 • REPAIR AND GRAFTING OF BONE 645

although IHH appears to play an important role in
osteoblast differentiation, the exact nature of this role
is not completely understood.
Osteocytes
HISTOLOGY AND FUNCTION. Osteocytes are the
most abundant cell type in adult human bone, repre-
senting nearly 10 times the number of osteoblasts.
Osteocytes are derived from osteoblasts, and although
the mechanisms of osteocyte differentiation remain
unknown, it is thought that these events are initiated
when osteoblasts become embedded within osteoid
(unmineralized bone matrix) during the process of
active bone formation. Osteocyte differentiation is a
gradual process and is associated with decreased meta-
bolic activity, loss of intracellular organelles, and loss
of cellular division. 3 Mature osteocytes (Fig. 24-6) are
stellate cells whose cell body is embedded within
lacunae. Thin cytoplasmic processes extending from
the osteocyte cell bodies within the bone canalicular
system link the embedded cells with haversian canals,
thus enabling cellular transport of nutrients and waste
products. In addition, the canalicular system provides
a mechanism of cellular interconnection through gap
junctions between embedded osteocytes, osteoblasts,
osteoblast precursors within bone marrow and perios-
teum, and osteoclasts.
The exact function of osteocytes within bone
remains unknown, but their location within bone and
the cellular interconnections through the canalicular
system suggest several potential roles. For example,
the large number of cellular interconnections within
the osteocyte and the surrounding cells suggests
that these cells may play a role in transmitting
mechanical loads, thus functioning as mechanosen-
sory elements within bone. Furthermore, the large
number of osteocytes within lacunae may play a role
in extracellular matrix mineral homeostasis by increas-
ing the bone mineral surface area that is exposed to
extracellular fluid and cellular activity.
Osteocytes as Mechanosensory Cells. Mechanical
loading can alter the geometry and mass of bone. This
concept, first proposed by Wolfe in 1892, has become
known as Wolfe's law. The concerted action of
osteoblasts, osteocytes, and osteoclasts during skele-
tal growth is referred to as modeling; the term remod-
eling is applied to changes in osseous tissues resulting
from mechanical loading or trauma during adult life.
The mechanisms by which mechanical loading and
osseous remodeling are coupled remain unknown, and
although osteoblastic bone synthesis and osteoclastic
resorption are the final common pathway in thi.>
process, it appears that direct communication between
these cells does not occur and may not be necessary.
Studies have implicated the osteocyte as a critical com-
ponent of this process. Evidence for this hypothesis
can be derived from anatomic considerations because
osteocytes appear to form a syncytium with sur-
rounding cells through their canalicular systems, thus
providing a communication link between the mechan-
ical stimuli and effector cells. In addition, mechani-
cal loading of bone has been shown to alter osteocyte
gene expression and cellular activity, with resultant
increases in the activation of glucose-6-phosphate
dehydrogenase production of signaling molecules
such as prostaglandins and nitrous oxide, secretion
of osteoclast inhibitors such as osteoprotegerin,

TT:
• -* :
• *• f

m&ftfr * >& *.

FIGURE 2 4 - 6 . A, Cross section of an adult rat mandible (magnification xlOO) 56 days after a partial osteotomy of
the mandibular angle and stained for BMP-2/4 with polyclonal rabbit antibodies conjugated to diaminobenzidine. Note
osteocytes (OS) within lacunae of mature lamellar bone. B, High-power view of human mandible stained with hema-
toxylin and eosin demonstrating osteoblasts (OB), osteocytes (OS), and osteoclasts (OC). (Courtesy of Drs. Clarkson
and Huvos, Department of Pathology, Memorial Sloan-Kettering Cancer Center.)

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Dr.Mustafa D.
646 I • GENERAL PRINCIPLES
and changes in the production of extracellular matrix
molecules implicated in the regulation of bone
turnover (e.g., osteopontin).21"26 These changes result
from shear forces, which cause displacement of extra-
cellular fluid within the lacunar and canalicular
systems.27
Programmed cell death (apoptosis) may represent
an alternative method by which osteocytes regulate
bone remodeling.25 Osteocyte apoptosis can be induced
by a number of stimuli associated with bone resorp-
tion, including either decreased or excessive mechan-
ical loading, radiation, advanced age, and withdrawal
of ovarian hormones. 28,29 In contrast, mechanical
loading of osteocytes with physiologic levels of stress
is associated with inhibition of osteocyte apoptosis,
thus preventing bone resorption.30*34 Dodd and
Raleigh35 have proposed that osteocyte apoptosis
caused by decreased mechanical loading is due to stag-
nation of extracellular fluid with resultant cellular
hypoxia. According to this hypothesis, mechanical
loading prevents this process by promoting extracel-
lular fluid flow. In addition, Tomkinson et al28,36 have
shown that the loss of estrogen antioxidant effect may
exacerbate the cellular effects of hypoxia and may
represent one mechanism by which postmenopausal
osteopenia occurs.
Osteocytic Osteolysis. A potential role for osteo-
cytes in bone resorption has been hypothesized.25,37
Support for this hypothesis has largely been indirect
and based on the histologic observation of varying
lacunar size and the finding that osteocytes are capable
of producing degradative enzymes (e.g., collagenase,
acid phosphatase, aminopeptidase). The validity of this
hypothesis has been strongly questioned because
changes in lacunar size and shape may be a histologic
artifact and degradative enzymes are produced in only
minute amounts. 38,39 It has been suggested that osteo-
cytes are capable of localized bone resorption within
the lacunar and canalicular systems to maintain their
patency and potentially regulate mineral composition
within the extracellular fluid.40 Whether this process
is systemically regulated by parathyroid hormone,
vitamin D 3 , or calcitonin remains unknown.
*
Osteoclasts
HISTOLOGY AND FUNCTION. Osteoclasts are large
multinuclear cells responsible for bone resorption, a
process necessary for bone growth, tooth eruption,
fracture repair, and calcium homeostasis (Fig. 24-7).
Osteoclasts are found on the endosteal and periosteal
surfaces of bone in areas of active bone remodeling
and resorption and are characterized by multiple
nuclei, ruffled cell border abutting bone surfaces, pos-
itive staining for tartrate-resistant acid phosphatase,
and expression of calcitonin receptors.41 Osteoclasts
are derived from hematopoietic stem cells, as
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Dr.Mustafa D.
demonstrated by experiments using chick-quail
chimeras and bone marrow transplantation in
ostcopetrotic mice.42,43 Hematopoietic stems cells can
differentiate through common pathways to form
osteoclasts, macrophages, or dendritic cells, depend-
ing on environmental stimuli (see later). Clinically,
overactivity of osteoclasts leads to increased bone
resorption and osteoporosis; decreased osteoclastic
function leads to osteopetrosis. In contrast, increased
activity of osteoblasts results in osteosclerosis.
Bone resorption results from a complex series of
events known as the bone resorption cycle. This cycle
is characterized by a number of cellular events includ-
ing osteoclast migration, attachment, membrane polar-
ization, dissolution of crystalline hydroxyapatite,
degradation of organic matrix, removal of debris, and
cellular inactivation or death.
The exact mechanisms regulating migration of
osteoclasts remain unknown; however, secreted growth
factors released at the site of injury or bone remod-
eling appear to play an important role. Once present,
osteoclasts form a sealing zone, a specific membrane
domain with the bone matrix, resulting in a tight seal
that separates the area to be resorbed from the sur-
rounding extracellular fluid. Sealing zone attachment
may be mediated by integrins and cadherins because
monoclonal antibodies against cCyP3 or cadherins have
been shown to block bone resorption in vivo and in
vitro.44"46 Once sealing zone formation has been com-
pleted, the osteoclast cell membrane becomes polar-
ized such that the area adjacent to the resorbing bone
surface forms the ruffled border; the cell membrane
directly opposing the ruffled border forms the func-
tional secretory domain (also known as the apical
domain). The ruffled border is essentially a complex
absorbing organ that resorbs crystalline hydroxyap-
atite and degrades organic matrix products through
the secretion of intracellular acidic vesicles and
proteolytic enzymes.47,48 The membrane surface area
involved in bone resorption is increased effectively by
finger-like projections of the ruffled border into the
resorption lacunae. Degradation products are removed
by endocytosis at the ruffled border followed by
transcytotic vesicular transport and exocytosis into
the extracellular space by the functional secretory
domain. 49,50 Tartrate-resistant acid phosphatase, a
widely used marker of osteoclasts, is highly expressed
in transport vesicles and appears to play an impor-
tant role in collagen degradation through oxygen
radical generation. 51
OSTEOCLAST DIFFERENTIATION. Osteoclast differ-
entiation is a complicated cellular process that has been
intensely studied. Osteoclasts belong to the monocyte-
macrophage lineage and can be formed from
hematopoietic and embryonic stem cells.52"58 Osteo-
clast precursors can be found in a number of tissues
image...

24 • REPAIR AND GRAFTING OF BONE 647

?sn
Vfl
• «

FIGURE 2 4 - 7 . ,4, High-power view of an adult rat mandible 7 days after a partial osteotomy of the mandibular angle.
The tissues have been stained for BMP-7 with polyclonal rabbit antibodies conjugated to diaminobenzidine. Note large.
multinucleated, positively stained osteoclasts (OC). B, High-power view of human mandible stained with hematoxylin
and eosin demonstrating osteoclasts at bone edges. C, High-power view of human mandible stained with hematoxylin
and eosin demonstrating multinucleated osteoclastic giant cell (OC). (Courtesy of Drs. Clarkson and Huvos, Depart-
ment of Pathology, Memorial Sloan-Kettering Cancer Center.)

indudinglx>nemarrow,spleen,lung,peritoneum,and deficient mice can reverse their osteopetrotic pheno-

peripheral blood.52'58"60
Numerous molecules have been implicated in the
regulation of osteoclast differentiation. Macrophage
colony-stimulating factor (M-CSF), a factor produced
ubiquitously by mesenchymal cells (e.g., fibroblasts,
stromal cells), appears to play a critical role in osteo-
clast differentiation.61 This hypothesis is supported by
the finding that mice deficient in functional M-CSF
(op/opmutant mice) have an osteopetrotic phenotype
with few mature osteoclasts.62,63 In addition, blockade
of M-CSF activity with neutralizing antibodies in vivo
or in vitro inhibits osteoclast differentiation.2,64 The
effects of M-CSF appear to be mediated by a survival
and proliferation effect on osteoclast precursors
because restoration of cellular proliferation in M-CSF-
type.65 There appears to be some redundancy in the
regulation of osteoclast differentiation by M-CSF,
however, because mice lacking functional M-CSF
(op/op mutants) exhibit spontaneous resolution of
osteopetrosis in adulthood. 66
A recently identified molecule termed osteoclast dif-
ferentiation factor (ODF), also known as osteoprote-
gerin ligand (OPGL), also appears to play a critical
role in osteoclast differentiation.2,67 ODF/OPGL is a
member of the tumor necrosis factor family of growth
factors and is produced by stromal cells, including
osteoblasts. Production of ODF/OPGL is controlled
by a number of molecules known to regulate bone
resorption, including lCt,25-dihydroxyvitamin D 3 ,
dexamethasone, interleukin-1, prostaglandin E2> and

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648 l • GENERAL PRINCIPLES
parathyroid hormone. An important role for
ODF/OPGL in osteoclast development and differen-
tiation is implicated by the finding that in the pres-
ence of M-CSF- ODIVOPGL i* the only molecule
required to generate mature osieoclasts from stem
cells.67 In addition, systemic administration of
ODF/OPGL has been shown to increase bone resorp-
tion, whereas ODF/OPGL deficient mice lack osteo-
clasts and demonstrate severe osteopetrosis.*8,60
Osteohistogenesis inhibitory factor (OCIF), also
known as osieoprotegerin (OPG), is a soluble recep-
tor that is produced by stromal cells and binds
ODF/OPGL wiih hi^h affinity and specificity, result-
ing in inacrivation of ODF. Thus. OCIF/OPG inhibits
ostcoc last differentiation by a specific blockade of ODF
activity."•'"'n*'2 Further support for an inhibitory action
of OCIF/OPG on osteoclast differentiation can be
derived from the finding that OCIF/OPG knockout
mice display an osteoporotic phenotype because of
an increase in the number of osteoclasts.71,73
Numerous transcription factors have been shown
to regulate osteoclast development and differentiation.
PU. 1, the earliest known regulator of osteoclast devel-
opment, is a transcription factor expressed by B-Iym-
phoid and myeloid hematopoietic cells and appears to
be essential for osteoclast formation. This is supported
by the finding that mice deficient in PU.l lack both
macrophages and osteoclasts, thus implicating this mol-
ecule in the regulation of a common precursor cell.74
In addition, PU. 1 is thought to regulate osteoclast dif-
ferentiation through effects on c-/ms, the active recep-
tor for M-CSF.75 Similar studies have implicated c-fos*
a transcription factor and nuclear oncogene, in the reg-
ulation of osteoclast differentiation. Thus, knockout
mice deficient for c-fos also display an osteopetrotic
phenotype because of a complete absence of osteo-
clasts. However, unlike in PU. 1 mice, macrophage devel-
opment occurs normally, a finding implicating c-fos
as a downstream regulator of osteoclast differentia-
tion from macrophage-osteoclast precursor cells.76
EXTRACELLULAR MATRIX
The extracellular matrix of bone is a highly special-
ized structure that contains a large number of
proteins including collagens, noncollagenous phos-
phoproteins, and proteoglycans (Table 24-2). Most of
these proteins are not exclusive to bone and are
expressed in other tissues. However, the combination
and proportion of these molecules result in a calci'
fied tissue capable of regeneration and remodeling.
Type I collagen is composed of two al chains and one
a2 chain.77 This trilaminar protein is the most abun-
dant protein in bone, accounting for more than 90%
of the organic matrix of bone. Type I collagen is
expressed by both mature and immature osteoblasts,
and its expression increases before that of any other
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Dr.Mustafa D.
matrix molecule."* The important role of type I col-
lagen as the primary scaffold of bone is highlighted
by the finding that patients with osteogenesis imper-
fecta, a disease with variable type I collagen deficits,
have smaller, less perfect, mineralized crystals and
resultant weak, brittle bones.79"82
The exact mechanism by which the bone type I col-
lagen scaffold becomes mineralized has been a subject
of considerable research. It has long been postulated
that phosphoproteins in the bone matrix serve as nucle-
ation sites of mineralization.83,84 It appears that this
hypothesis is an oversimplification, however, because
other studies have demonstrated that the lack of
inhibitors of mineralization in bone may also con-
tribute to deposition of calcium phosphate molecules
in the bone extracellular matrix.85"87 This conclusion
is based on the finding that type I collagen and, more
recently, elastin and fibronectin elicit spontaneous pre-
cipitation of calcium phosphate. In addition, deletion
of matrix Gla protein, a mineral-binding protein found
in blood vessels and cartilage but not in bone, results
in massive tissue calcification in affected mice.88 Thus,
bone extracellular matrix mineralization may be the
end result of a complex, coordinated interaction
between activators and inhibitors of mineralization.
At least seven different noncollagenous phospho-
proteins have been identified in bone. Most are
expressed in other tissue types; however, some (e.g.,
osteocalcin, bone sialoprotein) are more specific for
bone. 77,89 When mineralization is studied in vitro, the
expression of these molecules follows a typical pattern:
type I collagen, alkaline phosphatase, osteonectin, and
osteopontin expression occurs before mineralization;
bone sialoprotein expression is concurrent; and osteo-
calcin expression occurs after completion of bone
deposition.90,91
Although the exact role of noncollagenous extra-
cellular matrix in bone is unknown, several conclu-
sions can be drawn. For example, alkaline phosphatase
is thought to play a role in migration, adhesion, and
differentiation of osteoprogenitor cells.92 In addition,
alkaline phosphatase appears to be an important reg-
ulator of bone extracellular matrix mineralization
because mutations of alkaline phosphatase in humans
lead to hypophosphatemia and defects in skeletal min-
eralization.93,94 Osteonectin, a secreted phosphorylated
glycoprotein, has calcium- and type I collagen-binding
properties and is thought to have important functions
in the regulation of calcium turnover, bone remodel-
ing, and initiation of mineralization. 78 Osteopontin
also has calcium-binding properties; however, it does
not appear to regulate mineralization because osteo-
pontin-deficient mice do not have mineralization
defects.95 Instead, the major osseous tissue defects in
osteopontin knockout mice appear to be alterations
in osteoclast activation and extracellular matrix
remodeling. 96 Bone sialoprotein is structurally similar
TABLE 2 4 - 2 • EXTRACELLULAR MATRIX MOLECULES IN BONE

Present in Phenotype of Knockout

Nonosseous Animals or Deficiency
Molecule Protein Structure Cell Source Tissues Function in Humans

Collagen type I Trilaminar protein Many Yes Primary scaffold of bone Osteogenesis imperfecta in
consisting of 2 al Mature and immature 90% of matrix humans
chains and 1 ct2 chain osteoblasts in bone
Alkaline Metalloenzyme Mature and immature Yes Enzyme Hypophosphatemia and defects
phosphatase osteoblasts Regulator of extracellular in skeletal mineralization in
Different isoforms expressed matrix mineralization knockout mice
by cardiac and hepatic cells Regulator of cellular
migration, adhesion, and
differentiation
Osteopontin Phosphorylated Osteoblasts/osteoclasts Yes Osteoclast activation and Alterations in extracellular
glycoprotein Tumor cells (e.g., breast) extracellular matrix matrix remodeling in
remodeling knockout mice
Anchors osteoclasts to
mineralized matrix
Osteonectin Glycoprotein Osteoblasts Yes Binds calcium and collagen Unknown
Endothelial cells, type I
megakaryocytes Regulator of mineralization
Bone sialoprotein Phosphorylated Almost exclusively produced No Exact function unknown Unknown
glycoprotein by skeletal cells (osteoblasts, Regulator of cellular
osteocytes, hypertrophic adhesion
chondrocytes)
Osteocalcin Vitamin K-dependent Osteoblasts No Regulator of bone turnover Osteopetrosis in knockout mice
y-carboxyglutamic Odontoblasts Regulator of osteoclast
acid-containing protein Hypertrophic chondrocytes migration
Binds hydroxyapatite
Biglycan Proteoglycan Mature and immature Yes Exact function unknown Osteoporosis and small, thin,
osteoblasts Regulates apatite formation short limbs in knockout mice
Nonosseous cells

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650 I • GENERAL PRINCIPLES

to osteopontin, but in contrast to osteopontin, it BONE FRACTURE REPAIR

is expressed almost exclusively in skeletal cells
(osteoblasts, osteocytes, hypertrophic chondrocytes).97
The exact function of bone sialoprotein remains
elusive because different studies have had conflicting
results. Finally, osteocalcin (also known as bone Gla
protein) is a vitamin K-dependent protein expressed
only by mature, post-mitotic osteoblasts.3,98 This mol-
ecule has high affinity for calcium and other mineral
ions and appears to play an important role in the reg-
ulation of bone turnover because osteocalcin-deficient
mice have an osteoporotic phenotype.99"'01
Proteoglycans are also found abundantly in bone
extracellular matrix and are thought to contribute to
matrix organization. Biglycan is the most abundantly
expressed proteoglycan in bone and appears to act as
both a promoter (low concentrations) and an inhibitor
(high concentrations) of apatite.100 The in vivo actions
of this molecule are likely to be complex because bigly-
can-deficient mice display an osteoporotic phenotype
with small, short, thin bones. 102
The interaction between the various components
of bone is extremely complex and tightly regulated.
The elucidation of these mechanisms holds great clin-
ical promise because it may identify methods that could
augment or accelerate bone repair. The complexity of
this system has proved that deciphering these mech-
anisms requires ingenuity because traditional methods
of experimentation (i.e., knockout and transgenic
models) have not been entirely successful.
Fracture repair or healing is a complex series of bio-
logic events designed to repairand regenerate damaged
bone. The ability of bone to regenerate completely
without intervening scar formation is a critical feature
of this specialized organ because it enables the resump-
tion of normal activities. The biomechanics of long
bone fractures have been well described. In general,
bone is most resistant to fracture when it is exposed
to compressive forces, weakest when it is exposed to
shear forces, and intermediate in tensile strength. 1
When excessive compressive forces are applied to bone,
particularly tubular bones, fractures tend to occur
along planes exposed to the highest shear stresses—
typically at a 45-degree angle to the load direction. In
contrast, when bone is exposed to bending forces,
mechanical failure occurs initially on the tensile
surface and is subsequently propagated to the com-
pressed surface. Propagation into the compressed
portion of bone leads to failure along the planes of
maximum shear (i.e., 45 degrees), thus resulting in
comminution. Torsional forces usually result in spiral
fractures because failure occurs as the transverse
stresses are propagated as shear forces that rotate
around the bone at 45-degree angles to its long axis.
Two types of bone repair are noted, referred to as
primary and secondary (callus) repair (Fig. 24-8).
Primary bone repair occurs under two circumstances:
healing of small bone defects (e.g., pin tracks) and,

Non-displaced
Fracture Segments

Marrow
space

Nutrient Artery
Periosteum Re-established
Hematoma Woven Bone R e m o d e I e d Bone

A
Displaced
Fracture Segments

- * -

1
Remodeled Bone
Woven Bone
Hypertrophic Chondrocytes
Hematoma
B
FIGURE 2 4 - 8 . Schematic representation of primary and secondary (callus) bone repair. A, Primary bone repair:
nondisplaced bone fragments heal without cartilaginous intermediate. B, Secondary (callus) bone repair: displaced (or
unstable) bone segments heal with cartilaginous intermediate.

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image...

24 • REPAIR AND CRAFTING OF BONE 65

more commonly, when fractured or osteotomized bone

segments are rigidly fixed and closely apposed by com-
pression plating. Healing in primary repair proceeds
by direct deposition of woven bone in a process similar
to membranous ossification during development. In
contrast, secondary or callus bone repair proceeds .1 ^ ^
by a cartilaginous intermediate similar to endochon-
dral ossification. This type of repair is observed in
fractures of tubular long bones that have not been
rigidly fixed.
A
Primary Bone Repair
Primary bone repair is often observed in the treat-
ment of craniofacial fractures. The use of plates and
screws for reduction and fixation of fractures was first
reported by the German surgeon Hansmann in 1886.103 €3te
However, these devices were not widely used until the
late 1960s when the Swiss Association for the Study
of Internal Fixation (ASIF) developed and dissemi-
nated the principles of stable fixation and axial com- mmm •w*

pression in long bone fractures. These principles are

based on the concept that bone healing occurs under B
axial compression and fails under tension (Fig. 24-9).
The ASIF studies addressed the main drawbacks of
early rigid fixation devices, namely, mechanically
weak plates, lack of adequate fixation and reduction,
and shearing motions, thereby decreasing the incidence •?p.o;c

of infection and nonunion. In addition, rigid fixation

of fractures was shown to improve rehabilitation by
enabling early loading of the fractured bone segments.
The principles of meticulous reduction, axial com-
pression, rigid fixation, and early rehabilitation have
since been applied to the craniofacial skeleton. These
advances have had dramatic results in the treatment
of elective craniofacial osteotomies and fractures by
reducing the incidence of malunion, nonunion, and
prolonged immobilization. For example, the use of
compression plating in mandibular fractures has
significantly simplified the treatment of complex
fractures (e.g., comminuted fractures or edentulous
mandibles) and has, for the most part, obviated the
need for intermaxillary fixation.
The primary drawback to the use of compression
plating and rigid fixation is the wide undermining of
the periosteum required for accurate device placement.
This dissection interferes with a primary source of
blood supply (i.e., periosteal) to the fractured bone
segments. In addition, removal of the periosteum
decreases the pool of preosteoblasts in the cambium
layer. These factors are likely to be responsible for the
increased time necessary for complete osseous repair
with use of compression plates compared with sec-
ondary bone healing. Other disadvantages of internal
fixation are potential foreign body infections, contour
deformities, palpable plates, weakening of bones due
to pin placement, and osteoporosis surrounding the
plates.
0M*+
FIGURE 2 4 - 9 . The compression mode of miniplate fix-
ation. A, A four-hole plate. Note that the inner holes are
eccentrically shaped so that as the screws are tightened,
the head falls into the wider portion and compresses the
bone margins (B). C, Completed view of the skeletal fix-
ation. (From Cutting CB, McCarthy JC, Knize DM: Repair
and grafting of bone. In McCarthy JC, ed: Plastic Surgery,
vol 1. Philadelphia, WB Saunders, 1990:583-629.)
The finding of an external callus with compression
plating indicates lack of rigid fixation with the result-
ant excessive motion leading to varying amounts of
endochondral bone formation. In long bone fractures,
hardware removal is advocated to prevent excessive
bone resorption because compression plates absorb
the majority of stress exerted on the bone. This does
not seem to be a major concern in the treatment of
craniofacial fractures, although plate removal for
contour defects or the patient's discomfort is occa-
sionally required.
Primary bone healing is associated with a mild
inflammatory reaction in the soft tissues and marrow
spaces. In addition, minimal or no hematoma for-
mation is observed. Bone healing in primary repair
is initiated with the formation of active osteoclasts
at the junction of the live and necrotic skeletal seg-

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652 I • GENERAL PRINCIPLES
ments. Osteoclasts resorb the bone matrix by forming
cutting cones that cross the fractured bone segments
along empty haversian canals.IW New osteons are laid
down immediately behind the cutting cone and cross
the fractured area accompanied by new blood vessels.
New bone is laid down as immature woven bone and
is remodeled during a period or months to lamellar
bone with complete repair of the fractured bone
segments.
The periosteum plays a critical role in primary frac-
ture repair by providing osteoprogenitor cells and
uncommitted mesenchymal cells in a process similar
to embryonic inlramembranous ossification. It is gen-
erally thought that under normal circumstances,
intramembranous ossification resulting from periosteal
stimulation can lead to successful repair of defects up
to half the diameter of the bone.104 This response is
limited, however, by numerous factors, including
wound contamination, severity of injury, and quality
of the surrounding soft tissues. In addition, it has been
shown that small degrees of motion at the fracture site
can augment periosteum-generated intramembra-
nous ossification, whereas excessively rigid fixation has
a negative effect.
Failure to reduce fractures accurately or to bring
the fractured bone segments into close contact can
prevent bone healing and result in a fibrous union. In
these instances, a critical distance exists beyond which
bone healing cannot proceed. This distance is vari-
able and depends on the particular bone, its soft tissue
envelope, and the nature of injury. Fibrous healing of
bone defects is thought to result from several factors,
including fibrous tissue ingrowth at a rate faster than
bone deposition and diminished blood supply.
Evidence for the first hypothesis can be derived from
numerous clinical and experimental studies demon-
strating successful bone repair in bone gaps covered
with membranes designed to prevent fibrous tissue
ingrowth (e.g., polytetrafluoroethylene).105"111 These
studies have demonstrated that prevention of fibrous
tissue ingrowth can promote osseous repair of bone
defects that would ordinarily heal by fibrous union in
the absence of the barrier.
Secondary (Callus) Bone Repair
Secondary or callus bone repair can be divided into
three overlapping phases (inflammatory, reparative,
and remodeling) on the basis of histologic criteria (Fig.
24-10). lI2 This division simplifies description of frac-
ture healing; however, it is somewhat arbitrary because
fracture repair proceeds as a cascade of reparatory
events.
The inflammatory phase of fracture healing com-
mences immediately after bone injury and functions
to provide temporary immobilization of the fractured
bone segments by splinting due to pain and removal
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of necrotic debris. This phase is characterized by
vasodilatation and hyperemia due to release of local
factors (e.g., histamines, prostaglandins, cytokines);
hematoma formation; vasoconstriction and vascular
clotting; and invasion by neutrophils, basophils, and
macrophages. Hematoma formation results in the
organization of a fibrin network, providing tempo-
rary immobilization as well as a pathway for cellular
migration. Differentiation of tissue macrophages leads
to the removal of necrotic debris and sets the stage
for the reparative process. The inflammatory phase
typically peaks after 48 hours and is decreased signif-
icantly by approximately 1 week after injury.
The reparative phase of fracture healing is activated
within the first few days of injury and initiates the
process of bone repair. This phase typically lasts weeks
to months and is associated with the development of
the primary fracture callus and its gradual conversion
to bone. The primary callus consists of cartilage,
minimal amounts of woven bone, fibrous tissue,
osteoid (unmineralized bone matrix), and newly
formed blood vessels. The cellular components of the
primary callus are thought to be derived from marrow
elements and periosteum and result from differentia-
tion of pluripotential mesenchymal cells to form chon-
droblasts, osteoblasts, fibroblasts, and so on. Once the
fractured bone segments are united by the primary
callus, the callus matures and forms a structure known
as the hard callus (also known as bridging callus).
Failure of the primary callus to unite the fractured bone
segments, as may occur with segmental bone loss, is
detrimental because it may result in resorption of the
callus. The hard callus becomes progressively more ossi-
fied through a variable mixture of endochondral and
membranous ossification, depending on local oxygen
tension. 113 Endochondral ossification is the predom-
inant method of bone formation in most instances
because cellular growth and differentiation outstrip
the developing blood supply.
Remodeling of newly formed woven bone into
mature lamellar bone characterizes the remodeling
phase of fracture healing. This process may remain
active for prolonged periods and depends on the nature
of and host response to injury. Remodeling is influ-
enced primarily by mechanical loading of the fractured
bone segments and continues until optimum regen-
eration is reached. This phase corresponds clinically
with resolution of pain and resumption of normal
activities. The bone remains susceptible to injury,
however, until replacement of all woven bone elements
is complete.
Variables Influencing Bone Repair
Fracture repair is influenced by a number of variables,
including blood supply, immobilization, and age of
the patient.
image...

24 • REPAIR AND GRAFTING OF BONE 653

Fracture
•- hematoma
Necrotic
bone edge PMN

Inflammation

Primitive *'*'#X » Nutrient artery

A mesenchymal cells disrupted

Callus
Hypertrophic
chondrocytes

Wefts
. F7epa/r

Newly -•-^.^l.^'-- -
formed blood "' — Periosteum
B vessel

Repair

FIGURE 2 4 - 1 0. Schematic diagram of callus frac-

ture repair in endochondral bone. A, Early stages of
fracture repair characterized by hematoma formation,
inflammatory cell migration and differentiation (poly-
morphonuclear neutrophil [PMN|), and scattered
primitive mesenchymal cells. B, As healing progresses,
a callus is formed between the bone edges, and hyper-
trophic chondrocytes can be seen. In addition, newly Remodeled
formed blood vessels sprout from the nutrient artery N* "• \ \ \ \
bone
."*•.•» o*
and local blood vessels. C, Primitive woven bone has
bridged the fractured bone segment. D, Woven bone
is remodeled into lamellar bone. D

BLOOD SUPPLY The metaphyseal system, in contrast, represents

The blood supply to the long bones in the noninjured
adult is through three separate systems with signifi-
cant overlap and anastomoses."4""6 The medullary
system is the primary blood supply to the diaphysis
and is derived from the nutrient artery (Fig. 24-1.1).
the dominant blood supply to the cancellous bone of
the proximal and distal metaphysis. Blood vessels in
the periosteal system penetrate and supply the outer
third of the cortex and are particularly significant in
areas of fascial or tendinous attachment. Epiphyseal
vessels represent an additional source ofnutrients with

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654 I • GENERAL PRINCIPLES

Articular
cartilage
^i"1**
End-arterial
J" terminals
Q / H ^ T lALhWffff \
a.
Metaphyseal arteries ULf / Venous sinusoids and
and terminals of the OVA '1/1 ITW'T V
^metaphyseal veins
medullary arterial \ .
system /^ 1
/, 1 !\V\
V
AI
9 ' * \\

\ \A/ 1
/ f

Principal nutrient
artery and vein
a.
1 jjf O^ J
'1 '
m Medullary
sinusoids

Periosteal capillaries
in continuity with 1 «I\F 1 Interfascicular veins and
cortical capillaries capillaries in muscle
! i

1 i\ i Central venous
* 1 il channel
; l
• i
i : /
JIT Large emissary vein
FIGURE 2 4 - 1 1 . The three sources of
blood supply to the long bone are illustrated.
The nutrient artery provides the principal
v. II
is
\ \ \

\
source of blood supply to the marrow cavity
and the inner cortex. The diaphyseal
periosteal vessels supply the outer cortex of
v. the diaphysis. The metaphyseal-epiphyseal
If j periosteal vessels penetrate the cortex ofthe
NKV Transverse

J \ epiphyseal bone in the adult and anastomose with the

00 nutrient artery, providing adequate supply
rTWMBHI" Y ^ venous channel to the marrow cavity and inner cortex in cases
'"TZ-v. of disruption of the nutrient artery. (From
v.« V. Brookes M: The Blood Supply to Bone.
London, Butterworths. 1971.)

significant overlap with metaphyseal vessels in skele-
tally immature animals and humans. The venous
supply (efferent system) closely parallels the arterial
supply (afferent system). Anastomoses between affer-
ent and efferent systems occur through marrow sinu-
soids or arterioles within the haversian systems. Thus,
mature bone lacks the capillary beds typically found
in soft tissues.117 The primary direction of flow of
blood and interstitial fluid in bone is centrifugal and
occurs from the endosteum to the periosteum along
a pressure gradient similar to capillary pressures.' l8,119
The blood supply of membranous bone is similar to
that of endochondral bone with contributions from
medullary, periosteal, and endosteal blood vessels.
During the early stages of fracture or bone repair,
the vessels of the periosteal callus serve as the most
significant source of blood supply (Fig. 24-12), prob-
ably because the metaphyseal and medullary systems
are often severely damaged by the traumatic incident,
whereas the fibrous nature and extensive network of
periosteal vessels provide some degree of protection.
The surrounding soft tissues also serve as an impor-
tant source of blood supply to the damaged bone
during fracture repair.119"121 This finding is supported
by the fact that canine tibial fractures exhibit signifi-
cantly increased blood flow and demonstrate improved
osseous regeneration when they are covered by muscle
flaps compared with coverage by skin flaps.122 This phe-
nomenon probably represents a potential mechanism
by which osseous repair during fracture healing or
distraction osteogenesis ofthe craniofacial skeleton is
significantly faster and technically easier than long
bone distraction.
A correlation between angiogenesis and bone for-
mation has long been suspected.123 This hypothesis
is supported by the findings that osteocyte survival
requires proximity to nutrient vessels (<0.1 mm) and
that the quality of the vascular bed with subsequent
bone graft revascularization is a critical determinant
of osteocyte survival.124 Furthermore, the rate of bone
deposition during fracture repair is closely correlated
with the vascular surface area, and inhibition of

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image...
FIGURE 2 4 - 1 2 . Microangiogram showing the devel-
opment of anastomoses between the nutrient artery and
the diaphyseal periosteal vessels in response to fracture.
{Reprinted with permission from Rhinelander FW: The
normal microcirculation of diaphyseal cortex and its
response to fracture. An Instructional Course Lecture of
the American Academy of Orthopedic Surgeons. J Bone
Joint Surg Am 1968;50:784.)
angiogenesis prevents capillary invasion and trabec-
ular bone formation within developing mouse epi-
physeal growth plates and in hypertrophic
chondrocytes in vitro.125 The negative effects of irra-
diation (osteoradionecrosis and impaired osseous
repair), as well as studies demonstrating augmenta-
tion of fracture repair in these situations with use of
angiogenic cytokines, also support the hypothesis that
successful osteogenesis is dependent on angiogenesis.
Finally, numerous studies have demonstrated an
increased blood flow to fractured bone segments and
an increased rate of nonunion in poorly vascularized
bones (e.g., scaphoid).
Although the exact mechanisms by which angio-
genesis is regulated during fracture repair and bone
development remain unknown, it is clear that angio-
genic cytokines play an important role (Table 24-3).
This concept was first proposed in 1963 by Trueta116
and has since been confirmed by histologic and molec-
ular studies. Direct-acting angiogenic cytokines vas-
cular endothelial growth factor (VEGF) and fibroblast
growth factor 2 (FGF-2) have been strongly implicated
in this process and appear to be central players in a
cascade of events that ultimately result in new vessel
ingrowth. However, it is likely that a complex interplay
between inflammatory cytokines, indirect- and direct-
acting angiogenic factors, angiogenesis inhibitory
factors, degradative enzymes, and local environmental
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24 • REPAIR AND GRAFTING OF BONE 655
cues ultimately regulates new vessel ingrowth during
fracture healing and bone development.
VEGF is a dimeric heparin-binding glycoprotein
that is a critical modulator of vasculogenesis (the
formation of primitive embryonic vasculature) and
angiogenesis (formation of new blood vessels from pre-
existing ones). 126 VEGF is highly expressed in tissues
rich in newly formed blood vessels (e.g 0 placenta) and
is the most potent endothelial cell mitogen. Deletion
of VEGF from the mouse genome is a uniformly lethal
mutation resulting from a poorly developed vascular
system. The major physiologic actions of VEGF include
increased vascular permeability, increased expression
and activity of degradative enzymes that enable vas-
cular sprouting, and up-regulation of regulatory mol-
ecules critical for inflammatory and endothelial cell
adhesion and migration. ,27 ' l29 In addition, the biologic
actions of VEGF are synergistic with other direct- and
indirect-acting angiogenic cytokines. VEGF intracel-
lular signaling is initiated by two cell surface tyrosine
kinase receptors, VEGF-R1 (also known as Fit-1) and
VEGF-R2 (also known as KDR or Flk-1).129
Support for the hypothesis that VEGF plays an
important role in the regulation of bone formation
can be derived from the finding that inhibition of VEGF
biologic activity by use of a soluble VEGF receptor
(i.e., capable of binding VEGF but not activating intra-
cellular signaling pathways) in developing mice sig-
nificantly inhibits blood vessel invasion and trabecular
bone formation. The treated mice demonstrated an
expanded hypertrophic chondrocyte zone, a finding
supporting the hypothesis that VEGF-mediated cap-
illary ingrowth is a critical signal regulating growth
plate development, cartilage remodeling, and trabec-
ular bone formation. Similarly, Carlevar et al130 have
demonstrated that hypertrophic chondrocytes, similar
to those found in developing bone or during endo-
chondral fracture repair, produce VEGF in significant
quantities and exhibit defects in ossification when
treated with anti-VEGF antibodies. These findings,
together with the observation that these cells express
high-affinity membrane-bound receptors for VEGF,
led the authors to conclude that VEGF is a critical reg-
ulator of hypertrophic chondrocyte ossification during
endochondral bone formation or fracture repair and
that at least some of these actions may be through
autocrine mechanisms.
The role of VEGF during membranous ossification
is less clear. In a rat model of mandibular fracture
repair, Saadeh et al131,132 have demonstrated that VEGF
mRNA and protein expression is up-regulated during
osseous regeneration and that this cytokine is highly
expressed in active osteoblasts, osteoclasts, and mes-
enchymal cells localized to the fractured bone seg-
ments. On the basis of these findings, therefore, it is
likely that VEGF plays a critical role in the healing
of membranous bone fractures by regulating
TABLE 24-3 • GROWTH FACTORS AND ANGIOGENESIS

Growth Regulation of
Factor Structure Angiogenesis Function Role in Fracture Healing Expression Receptor

BMP Single large propeptide Indirect
molecule
Cleavage enables
dimerization
Member of the TCF-p
superfamily
Conserved series of 7
cysteine residues at
carboxyl terminal
At least 15 known isoforms
TCF-p Propeptide Indirect
Cleavage necessary for
activation
At least 3 different
isoforms
Mitogen and Expressed by mesenchymal cells Patterning genes and Serine-
regulator of chemoattractant for early in fracture repair transcription factors threonine
angiogenesis osteoblasts and Also expressed by osteoblasts (e.g..Cbfa1) kinase
mesenchymal cells and osteoclasts receptors
Apoptosis Exogenous BMPs can heal
Patterning critical-sized defects
Ectopic bone formation
?Accelerate fracture repair
?Actions synergistic with TCF-p
Chemoattractant and Produced by osteoblasts Patterning genes and Serine-
regulator of mitogen for osteoblast mesenchymal cells, osteoclasts transcription factors threonine
angiogenesis precursors and Increases callus formation and Mechanical strain kinase
osteoblasts volume receptors
Inhibits osteoblast Subperiosteal injection promotes
differentiation both chondrogenesis and
Regulates expression of membranous ossification
other growth factors Exogenous TGF-p may heal some
important in critical-sized defects
angiogenesis and
osteogenesis
Increases matrix synthesis

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FGF-2 Heparin-binding Direct Angiogenesis Increases angiogenesis in fracture Inflammatory cells and Tyrosine
glycoprotein regulator of Regulator of bone site acute inflammation kinase
At least 9 different angiogenesis development and Increased expression during Patterning genes and receptors
isoforms skeletal patterning fracture repair transcription factors
Can regulate osteoblast Exogenous FGF-2 can increase
differentiation and mechanical strength of fractures
proliferation (actual ?Accelerates fracture repair or
effect is dose promotes healing of critical-
dependent) sized defects

VEGF Dimeric glycoprotein Direct Increases vascular Increased expression during Microenvironment (e.g.. Tyrosine
regulator of permeability fracture repair pH, hypoxia, lactic kinase
angiogenesis Increases vascular Expressed by osteoblasts, acid concentration) receptors
sprouting osteoclasts, and mesenchymal Growth factors (e.g.,
Increases endothelial cell cells TCF-p, FGF, BMP, IGF)
migration, proliferation, Increases blood vessel ingrowth Inflammatory cytokines
adhesion during fracture repair (e.g., PCE2)

PDGF Dimeric, disulfide-bonded Indirect Promotes chemotaxis of Released by degranulating Inflammation and injury Tyrosine
polypeptide chain regulator of osteoblasts and platelets and acts to increase Mechanical strain kinase
a and p subunits determine angiogenesis inflammatory mediators osteoblast chemotaxis, and TCF-p (decreased receptors
isoform (AA, AB) Decreases cellular possibly proliferation expression)
differentiation Expressed by osteoblasts,
Increases collagen macrophages, and mature/
synthesis immature chondrocytes during
Increases collagen fracture repair
degradation and turnover Promotes synthesis of angiogenic
May promote osteoblast molecules (e.g., VEGF)
proliferation Promotes matrix deposition and
turnover

BMP, bone morphogenetic protein; FGF-2, fibroblast growth factor 2; PDGF, platelet-derived growth factor; TGF-p, transforming growth factor beta; VEGF, vascular endothelial growth factor.

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658 I • GENERAL PRINCIPLES
angiogenesis and revascularization of the fractured
bone segments.
The mechanism and the cells responsible for the
regulation of VEGF expression during fracture repair
have been the subject of intense debate. Evidence has
implicated osteoblasts and hypertrophic chondrocytes
in this process. In a set of experiments, it was demon-
strated that isolated osteoblast-enriched cell cultures
and osteoblast-like cells produce moderate amounts
of VEGF in vitro.131"134 In these experiments, VEGF
production was sharply and rapidly up-regulated,
however, when cell cultures were stimulated with
growth factors that are abundantly found within the
healing fracture environment, including FGF-2, TGF-
P (p 1, [32, and p3), and platelet-derived growth factors
(PDGF-BB). Similar results have been demonstrated
with insulin-like growth factors, prostaglandin E u and
vitamin D3.135'136 Increase in VEGF production by
osteoblasts in these experiments was in general due
to mRNA up-regulation without significant effects on
mRNA stability or changes in protein synthesis.
Tissue hypoxia, secondary to vascular disruption
and vasoconstriction, has also been hypothesized to
contribute to angiogenesis and subsequent bone for-
mation during fracture repair. The finding that active
bone growth in the metaphyseal border of the epi-
physeal plate and during fracture repair occurs under
conditions of relative tissue hypoxia supports this
hypothesis.137,138 VEGF is probably a critical regulator
of angiogenesis secondary to hypoxia. This hypothe-
sis is based on the finding that hypoxia is the most
potent inducer of VEGF production in a number of
cell lines including osteoblasts.133,134 In addition, the
expression of this molecule by osteoblast-enriched
cultures and osteoblast-like cells is precisely regulated
by oxygen tension in vitro. Up-regulation of VEGF
expression by osteoblasts secondary to hypoxic stim-
ulation occurs through transcriptional activation and
is not due to alterations in mRNA stability or protein
translation. In addition, VEGF stimulation occurs pri-
marily through a heme-containing hypoxia response
mechanism similar to the erythropoietin gene.
Transient (not continuous or chronic) hypoxia
is the critical factor in the regulation of VEGF and
osteogenesis during fracture repair. It has been pos-
tulated that chronic hypoxia diminishes oxygen gra-
dients encountered by cells within the fracture zone. I39
Alterations in oxygen gradients may thus result in
decreased production of angiogenic stimuli, dimin-
ished neovascularization, and impairment of fracture
repair.
Vasoconstriction and vascular disruption produce
an acidic fracture microenvironment with elevated levels
of lactate secondary to anaerobic metabolism.140*143
Spector et al144 investigated the relative contribution
of alterations in pH and lactate concentration on
the production of VEGF by osteoblasts exposed to
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hypoxic and normoxic culture conditions. These
studies demonstrated that pH and lactate concentra-
tion independently regulate osteoblast VEGF protein
production. However, contrary to teleologic expecta-
tions, acidic pH as well as elevated lactate concentra-
tions independently caused significant decreases in
VEGF production, under both normoxic and hypoxic
conditions. This decrease was primarily transcrip-
tionally regulated. Furthermore, the effects of increas-
ing acidity and elevated lactate appeared to be additive.
Based on the fact that decreased pH is stimulatory to
osteoclastic bone resorption, the authors speculated
that acidic pH down-regulated VEGF production and
osteogenesis in areas where osteoblastic bone resorp-
tion is necessary before active bone deposition.' 45 In
addition, the negative consequences of sustained
hypoxia on fracture repair may be, at least in part,
due to increasing concentrations of the products of
anaerobic metabolism (i.e., increased lactate and
hydrogen ion).
FGF-2 is a potent angiogenic modulator that has
also been implicated in the regulation of angiogene-
sis during fracture repair and bone development. FGF-
2 is a highly conserved heparin-binding growth factor
that, similar to VEGF, is a powerful stimulator of
endothelial cell migration, proliferation, and new vessel
formation during injury and development.146,147 In fact,
it is likely that FGF-2 biologic activity is closely asso-
ciated with VEGF because, in vitro, VEGF-induced
angiogenesis is dependent on FGF-2. In addition, FGF-
2-mediated angiogenesis in vivo is dependent on VEGF,
and VEGF expression is regulated by FGF-2 in numer-
ous cell lines, including osteoblasts.132,148,149 These
findings, coupled with the facts that FGF-2 is produced
by osteoblasts, is present in large quantities in bone
extracellular matrix, and is localized in expression to
proliferating chondrocytes of the epiphyseal growth
plate and osteoblasts and endothelial cells lining newly
formed blood vessels within the distraction regener-
ate of rat mandibles, suggest that this cytokine is an
important regulator of angiogenesis during osseous
regeneration.150'152 Further support for this hypothe-
sis can also be derived from experiments demonstrating
enhanced bone graft incorporation in irradiated and
nonirradiated tissues.153'154
IMMOBILIZATION
Mechanical stabilization, an important principle in
fracture treatment, enables new vessel ingrowth,
osteoid deposition, and mineralization. Stabilization
must be differentiated from absolute immobilization,
however; absolute immobilization may cause distur-
bances in bone healing by promoting bone resorption
due to stress protection and inhibition of callus for-
mation. 155 In fact, controlled axial loading and micro-
motion have been shown to accelerate fracture repair.156
VtM>!tf(Selcrt# image...
Thus, the use of less rigid fixation devices, such as tita-
nium or perhaps resorbable materials, may be asso-
ciated with decreased cortical bone resorption due to
stress protection, increased bone callus volume, and
accelerated osteogenesis.157,158
ACE
It is commonly known that children heal fractures of
membranous and endochondral bones more rapidly
than adults do. This concept has been clearly demon-
strated and quantified in bone regeneration during
distraction osteogenesis.' 59 ' 163 Although the exact
mechanisms responsible for differential fracture
healing rates are not known, they are probably not
related to inherent cellular differences because
osteoblasts derived from trabecular bone of young and
old patients show similar metabolic characteristics.164
It is possible that these differences may be related to
the presence of a proportionately larger pool of undif-
ferentiated mesenchymal cells capable of more rapid
cellular differentiation and osteoblast formation. 163
This concept is supported by the findings of Green-
wald et al,165,166 who demonstrated that the dura mater
of immature rats has a significantly greater popula-
tion of osteoblasts compared with adult rats and that
osteoblasts derived from younger animals differenti-
ated more rapidly.
MOLECULAR M EC HAN I SMS OF
FRACTURE REPAIR
Fracture repair involves a complex series of coordi-
nated events that in many ways represent a recapitu-
lation of embryonic bone development. A precise
symphony of molecular signals is thought to trigger
mesenchymal cell migration, proliferation, and dif-
ferentiation leading to callus formation and bone repair
(Table 24-4). Although the histologic and ultrastruc-
tural characteristics of fracture repair have been well
characterized, the exact sequence of molecular events
responsible for these events remains unknown. These
studies have been hampered by the fact that success-
ful osseous regeneration involves an intricate inter-
action between regulatory proteins, local cytokines,
inflammatory molecules, extracellular matrix mole-
cules, and systemic hormones. Thus, analysis of an
isolated growth factor or even a series of growth factor
molecules solves only a small portion of this complex
puzzle. Nevertheless, these studies are instructive and
have identified a number of important regulators of
bone repair: bone morphogenetic proteins, TGF-P
growth factors, fibroblast growth factors, insulin-like
growth factors, and platelet-derived growth factors.
In addition, these studies have identified critical
nuclear regulatory proteins such as core-binding
factor al and Indian hedgehog (see earlier).
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Dr.Mustafa D.
24 • REPAIR AND GRAFTING OF BONE 659
Bone Morphogenetic Proteins
Bone morphogenetic proteins (BMPs) are secreted
growth factors that are members of the TGF-p super-
family. BMPs were discovered when Urist and col-
leagues showed that implantation of demineralized
bone matrix in submuscular or subcutaneous pockets
of rodents induced ectopic bone formation.167,168 This
process has been termed osteoinduction. Histologic
and ultrastructural analysis of bone development in
the ectopic pockets revealed a process that mimicked
embryonic bone development and endochondral frac-
ture repair with the appearance of a cartilage scaffold,
subsequent replacement by bone, and hematopoietic
bone marrow formation.169"171 Isolation of protein fac-
tions responsible for migration and differentiation of
pluripotential mesenchymal cells led to the discovery
of the BMPs. To date, 15 different isoforms of BMP
have been identified. These isoforms are further
divided into three subfamilies on the basis of amino
acid sequence homology: the BMP-2/BMP-4 family
(92% sequence identity); the BMP-3 family (BMP-3
is the sole member with 4 3 % to 49% sequence iden-
tity with other subsets); and the BMP-5/BMP-6/BMP-
7/BMP-8 family (-89% sequence identity). BMP-1,
a procollagen C proteinase, is not related to the
other BMP families and does not have osteoinductive
properties.172
BMPs are synthesized as large precursor molecules
consisting of a signal peptide, a pro-domain, and a
carboxyl region of 100 to 125 amino acids.172 A dis-
tinguishing feature of the BMPs is a highly conserved
series of seven cysteine residues in the carboxyl ter-
minal of the molecule. These residues are critical for
correct folding and dimerization of the molecule
through intramolecular and intermolecular cysteine
and disulfide bond formation. 173 Cleavage of the pro-
domain enables dimerization and is a prerequisite for
osteoinduction. Although only homodimeric forms
(i.e., identical BMP subtypes) of BMP have been
demonstrated in vivo, the potential for heterodimerk
BMP molecules has been demonstrated in vitro and
implicated in vivo by the finding that multiple mRNA
subtypes have been co-localized during embryo-
genesis and fracture repair.
The process by which BMPs are assembled,
processed, and secreted remains unclear. Studies
suggest that dimerization and proteolytic cleavage
between the pro-domain and mature domain precede
secretion.174,175 Thus, in contrast to TGF-P 1, a closely
related molecule in the TGF-p superfamily that is
secreted as an inactive molecule, BMPs are thought to
be secreted in active form. In addition, although BMPs
are likely to be bound by extracellular proteins such
as follistatin, the existence of molecules homologous
to latent TGF-P binding protein (see later) has not been
demonstrated.176,177
en
o
o

TABLE 24-4 • GROWTH FACTORS AND FRACTURE REPAIR

Ectopic Segmental Combination Effective

Bone Defect with Other in Lower Effective in
Molecule Formation Healing Effect on Fractures Growth Factors Vertebrates Primates Potential Clinical Use

BMPs Yes Endochondral ++++ Increase callus Synergistic with TGF-p Yes Yes Spinal fusion
Membranous 1111 volume Alveolar bone deficiency
Increase mechanical Segmental defects
strength Augment bone graft
?lncrease rate of healing
healing Dental implants
TCF-p No Endochondral ++ Increases callus size Synergistic with BMP Yes No (limited Role alone unclear
Membranous -H- Increases mechanical Increases FCF-2 study)
strength expression
Increases VECF
expression
FCFS No Endochondral +/- Increase callus and Increase VEGF Yes Yes (limited Potential for augmenting
Membranous +/- bone volume expression study) angiogenesis in
Increase mechanical ?Synergistic with TCF-p compromised wounds
strength
PDCF No Endochondral - Increases callus Increases VEGF Yes No Unknown
Membranous - volume Synergistic with TGF-p
Increases mechanical for chemotaxis
strength

t-, very active; +/-, minimally active; -, no activity.

BMPs, bone morphogenctic proteins; FGFs, fibroblast growth factors; PDGF, platelet-derived growth factor; TGF-p, transforming growth factor beta.

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Dr.Mustafa D.
l^ttf'aeltfWimage...
Intracellular signal transduction by the BMPs is ini-
tiated by binding of the cell surface serine-threonine
kinase receptors BMP receptor IA (BMP-RIA), BMP
receptor IB (BMP-RIB), and BMP receptor II (BMP-
RII). 177 In addition, BMPs bind activin receptors with
high affinity. Binding of BMP-RII by dimeric BMP
molecules leads to association with and phosphory-
lation of the glycine-serine domain of BMP-RIA or
BMP-RIB, thus forming an active receptor-ligand
complex. Activated receptor-ligand complexes initi-
ate phosphorylation of intracellular molecules (Smads)
that mediate the complex actions of BMPs by enter-
ing the cell nucleus and activating the transcriptional
machinery for early bone morphogenetic response
genes.
BMPs have numerous effects on skeletogenesis and
fracture repair. In general, BMPs promote mitogene-
sis and chemotaxis of osteoblasts and undifferentiated
osteoblast precursors. 178 BMPs can cause differentia-
tion of many cell types into cartilage and bone
phenotype (e.g., expression of osteocalcin, increased
alkaline phosphatase production) and regulate cellu-
lar differentiation, apoptosis, and patterning. The cel-
lular differentiation state is important in this process
because mature cells (even osteoblasts) either do not
respond to BMP stimulation or do so in only a limited
fashion.179"182 Thus, the osteoinductive actions of
BMPs are primarily noted in immature or pluripo-
tential cells.
Although different BMP subtypes tend to have
similar qualitative osteoinductive effects, quantitative
differences in osteoblastic response have been demon-
strated. For example, comparison of chick periosteal
cells stimulated with similar concentrations of BMPs
2, 3, 4, 5, 6, and 7 revealed that BMP-2 and BMP-4
increased DNA synthesis nearly twice as much as BMP-
5 or BMP-6 did, whereas BMP-7 had only a minimal
effect and BMP-3 had no effect.183 Differences in
osteogenic potential have also been demonstrated
among different isoforms; however, these findings have
been somewhat inconsistent and conflicting. These dif-
ferences are less apparent and likely to be less relevant
when pharmacologic doses of BMPs are used.
EXPRESSION OF BMPS DURING
FRACTURE REPAIR
The expression of BMPs during endochondral bone
fracture repair has been studied in a number of animal
models. The earliest demonstration of BMPs during
bone repair was performed with use of a partially puri-
fied anti-BMP antibody in a rabbit model of mandibu-
lar fracture repair.184 These studies demonstrated the
presence of BMP in the mesenchymal cells as early as
3 days after fracture. Two weeks after fracture, in addi-
tion to mesenchymal cell staining, strongly stained
osteoblasts were noted to line the bone tissue. BMP
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Dr.Mustafa D.
24 • REPAIR AND GRAFTING OF BONE 661
staining decreased on days 21 and 30 after fracture
and corresponded to a decrease in the number of
mesenchymal cells within the healing fracture. More
specific polyclonal antibodies have been used to study
the expression of BMP-7 and BMP-2/4 in a rat model
of mandibular fracture repair.185 This study demon-
strated that shortly after osteotomy, BMP-7 expres-
sion is prominent within the newly formed fracture
callus, localizing primarily to osteoblasts and osteo-
clasts along the osteotomy edges, mesenchymal cells
within the callus itself, and periosteal cells near the
osteotomy site. Mature osteocytes, in contrast, failed
to demonstrate significant BMP-7 staining. As frac-
ture healing continued, the population of cells that
stained positively for BMP-7 decreased at each suc-
cessive time point such that by 8 weeks after opera-
tion, BMP-7 immunostaining was minimal.
In contrast to BMP-7, the expression of BMP-2/4
was less prominent within the early fracture callus 1
week after osteotomy. There appeared to be fewer
spindle-shaped mesenchymal cells and early
osteoblasts staining positively for BMP-2/4 compared
with BMP-7. Similar to the pattern noted with BMP-
7, however, the cells that stained most intensely at this
time point were osteoblasts and osteoclasts abutting
the osteotomy edges as well as periosteal cells adja-
cent to the osteotomy site. As was the case for BMP-
7, osteocytes failed to demonstrate positive staining
for BMP-2/4 at any of the time points examined. These
findings support the hypothesis that BMPs are criti-
cal regulators of mesenchymal cell migration, prolif-
eration, and differentiation. In addition, differential
expression of BMP molecules in the early phases of
fracture repair implies iso form-specific regulation of
these functions.
The patterns of BMP expression have also been
intensely investigated during long bone fracture repair.
This process is interesting because it includes not only
membranous ossification (i.e., primary repair) but also
ossification of a cartilaginous intermediate (i.e., endo-
chondral). Thus, the expression of BMPs can be studied
in both processes. During the early phases of mem-
branous-type fracture repair of long bones, BMP
(BMPs 2, 4, and 7) protein expression is localized to
the thickened cambium layer of the periosteum and
osteoblasts near the fractured bone segments and coin-
cides closely with that of BMP-RII. 186188 This staining
decreases as the woven bone is remodeled into lamel-
lar bone. These findings led the authors to conclude
that fracture repair stimulates a periosteal reaction and
induces the synthesis of BMPs by immature periosteal
cells. As the process of primary (i.e., membranous)
bone repair continues, cellular differentiation ensues
and results in decreased BMP expression.
During endochondral-type fracture repair in long
bones, the expression of BMP-2/4 and BMP-7 is
minimal within the fracture hematoma. As the
image...
662 • GENERAL PRINCIPLES
hematoma subsequently begins to organize, an increas-
ing number of primitive mesenchymal cells staining
positively for BMP-2/4 and BMP-7 are noted in the
fracture gap. Chondrogenesis becomes evident approx-
imately 1 week after fracture and is associated with
intense staining of proliferating chondroid precursor
cells and immature chondrocytes. Moderate staining
is also present in local osteoblasts and early hyper-
trophic chondrocytes. By day 14 after fracture,
immunostaining for BMP-2/4 remains strongest in
proliferating chondrocytes and, to a lesser degree, in
undifferentiated mesenchymal cells and osteoblasts.
In contrast, staining for BMP-7 in proliferating chon-
drocytes disappears. As the newly formed woven bone
is replaced by lamellar bone, the intensity of staining
decreases dramatically in osteoblasts, returning to base-
line levels after the completion of remodeling. Thus,
primitive cells within the fracture callus may initially
be responsible for BMP production, and these growth
factors—acting through autocrine or paracrine mech-
anisms—may cause cellular differentiation and ulti-
mately bone formation. This conclusion is supported
by the finding that BMP-4 mRNA is produced primarily
by less differentiated osteoprogenitor cells in the pro-
liferating periosteum and medullary cavity as well as
by muscle cells near the fracture site and not by dif-
ferentiated osteoblasts, mature osteocytes, or hyper-
trophic chondrocytes. 189
EXOGENOUS BMPS AND
FRACTURE REPAIR
The finding that BMPs are capable of inducing bone
formation in ectopic pockets spawned interest in the
use of these molecules to augment bone repair.
Recombinant forms of human BMP-2 (rhBMP-2),
human BMP-4 (rhBMP-4), and human BMP-7
(rhBMP-7, also known as osteogenic protein 1 [OP-
l ]) have been developed and used in a variety of exper-
imental models. In addition, recombinant and partially
purified mixtures of BMPs have been used in a
number of difficult clinical situations to improve bone
formation in clinical trials.190"194 Many studies have
evaluated the ability of BMPs to promote healing in
critical-sized defects (defects that ordinarily would not
heal). In rats, rabbits, dogs, sheep, goats, and monkeys,
the implantation of rhBMP-2, rhBMP-7, or partially
purified BMP fractions has been shown to promote
osseous bone repair in endochondral and membra-
nous bone defects.195"214 In addition, the use of aden-
oviral vectors and gene therapeutic approaches with
BMPs have shown promise in augmenting bone
formation.215-221
The majority of experimental studies with recom-
binant BMPs have been performed in endochondral
bone segmental defects and spinal fusion. These
studies have shown that in a variety of animals,
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Dr.Mustafa D.
including nonhuman primates, the delivery of BMPs
with various carrier molecules can promote the healing
of large bone defects.204' *WIW«M*M» BMPs can induce
significant increases in bone formation and promote
complete repair with excellent mechanical strength.
In contrast, control defects usually heal with only a
fibrous union. The doses of recombinant protein have
ranged from as little as 10ug to 15 mg (depending on
animal model and carrier protein used), and most
studies have demonstrated a dose-dependent increase
in bone regeneration. In general, it appears that 40 to
50|ig of rhBMP-2 is the lower limit of clinically effec-
tive doses.228 The dose range for rhBMP-7 (OP-1)
appears to be similar.
Although it is clear that BMPs can induce bone
repair in segmental bone loss, it is less clear whether
these molecules can accelerate or enhance fracture
repair without bone loss. Cook224 injected BMP-7 with
a bovine type 1 collagen carrier directly into fresh tibial
fractures in rabbits and demonstrated that fracture
repair was accelerated as a result of greater and earlier
new bone formation. In contrast, Bax et al223 found
no improvement or acceleration when rhBMP-2 with
a bovine type I collagen carrier was injected into stable
fractures of rabbit tibia. However, similar treatment
of unstable fractures resulted in acceleration of cor-
tical union and an increase in the size of the fracture
callus. Thus, BMPs may have a role in the treatment
of some fractures; however, this role requires addi-
tional investigation.
The use of BMPs to promote bone healing in cal-
varial defects has also been studied. In 1982, Takagi
and Urist250 demonstrated that 8-mm skull defects in
rats healed after the application of purified bovine
BMP. Healing occurred by outgrowth of bone from
the trephine rim and also as a consequence of prolif-
eration and differentiation of perivascular mes-
enchymal cells (pericytes) of the dura mater into
osteoblasts forming chondroid and woven bone. Other
investigators have demonstrated similar findings in
adult canine and adult rabbit cranial defects.251'253 In
addition, exposure of the spinal cord or the meninges
to BMPs does not induce ectopic bone formation
and is not associated with histologic or neurologic
abnormalities. 244
Another potential clinical use of BMPs is in the treat-
ment of alveolar bone deficiency and dental implants.
Cochran et al254 demonstrated that rhBMP-2 could
significantly augment bone regeneration around
endosseous implants in a critical-sized defect of the
canine mandible with either a collagen or a poly-L-
lactide/glycolide carrier. Covering the bone defect with
a nonresorbable barrier enhanced bone regeneration
with rhBMP-2. In a follow-up study, the authors
demonstrated a significant increase in bone to implant
contact compared with control subjects.255 A signifi-
cant vertical bone gain was demonstrated when
image...
rhBMP-2 was delivered to nonhuman primate
mandibular defects before placement of titanium
osseointegrated implants.256 In a clinical study of extrac-
tion socket healing and osseointegrated implant place-
ment, Becker et al 25 ' compared rhBMP-2 with
xenogeneic bovine bone graft, demineralized freeze-
dried bone, and autogenous cancellous bone graft. The
authors demonstrated that treatment with rhBMP-2
resulted in the formation of woven and lamellar bone
resulting in a bone implant interface, whereas xeno-
geneic bone graft and demineralized bone graft both
resulted in a less desirable connective tissue interface.
Defects treated with autogenous cancellous bone graft
also demonstrated bone healing; however, this was
judged to be less favorable than in defects treated with
rhBMP-2 because some connective tissue was also
noted at the implant interface. Not all studies have been
favorable, however. A study demonstrated that treat-
ment of surgically formed class III alveolar defects in
dogs with rhBMP-2 and a collagen sponge carrier
resulted in only limited augmentation. 258 The addition
of hydroxyapatite to the BMP-collagen sponge mixture
resulted in significant increases in vertical bone gain;
however, the bone was not of high quality (i.e., sparse
bone trabeculae with hydroxyapatite particles and
limited contact).
The treatment of segmental defects of the mandible
with BMPs has also been evaluated. Toriumi et al259
demonstrated that 3-cm full-thickness (critical-sized)
defects of canine mandibles undergo excellent bone
regeneration with treatment by reconstruction plates
and rhBMP-2 delivered in a poly-L-lactide/polygly-
colide carrier. In contrast, control animals demon-
strated no bone formation. Long-term follow-up of
the BMP-treated animals (30 months) demonstrated
only minimal loss of height but an increase in the area
of new bone. All animals underwent successful hard-
ware removal after 10 weeks and resumed a normal
diet by 9 months. Terheyden et al260 used a different
approach to mandibular reconstruction by prefabri-
cating a vascularized bone graft in the latissimus dorsi
of miniature pigs after injection of rhBMP-7. Segmental
defects of the mandible were treated with microvas-
cular free flap reconstruction using the prefabricated
vascularized bone grafts with excellent radiologic and
histologic outcomes. In addition, when prefabricated
flaps were compared with directly applied BMP-7, the
authors found a significant increase in bone mineral
content and mandibular bone regeneration in the
prefabricated flap.
Several studies have evaluated the effects of com-
bining BMPs with other osteoinductive molecules.
Ripamonti et al234 demonstrated that low doses of TGF-
p (0.5,1.5, or 5 p,g) synergize with OP-1 in the induc-
tion of extraskeletal bone formation in baboons with
an optimum ratio of TGF-p to BMP-2 of 1:20. This
finding was confirmed by other investigators who
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24 • REPAIR AND GRAFTING OF BONE 663
demonstrated that the combination of TGF-P 1 and
BMP-2 (120 jig of TGF-p and 12 mg of BMP-2) accel-
erated the bridging of 1.5-cm mid-radial segmental
defects in rabbits compared with BMP-2 alone.232 In
addition, newly formed bone in animals treated with
the combination of TGF-P and BMP-2 was more
mature (i.e., lamellar) than with BMP-2 alone. Another
study, however, failed to demonstrate significant
synergy between rhBMP-2 and TGF-P 1 when the
authors compared the effects of BMP-2 alone (1.5 or
15mg) with BMP-2 plus lOng of TGF-pl on bone
regeneration in a diaphyseal nonunion model in the
canine radius.225 This finding may be due to the fact
that the authors used a very low dose of TGF-p (nearly
500-fold less than Ripamonti et al and 12,000-fold less
than Sun et al).
The use of BMPs with autologous bone marrow
cells has also been investigated. These studies have, in
general, demonstrated enhancement of osteogenesis
compared with BMP alone. For example, Lane et al,206
using a rat femoral segmental bone defect, demon-
strated that the combination of rhBMP-2 with bone
marrow cells resulted in union in 100% of animals 6
weeks postoperatively. This was a significant improve-
ment over the group treated with rhBMP-2 alone, in
which only 80% of animals formed a stable union even
when observed as long as 12 weeks. Takagi and Urist23
demonstrated that treatment of rat midshaft femoral
nonunions with BMP alone induced bone formation
but rarely union, whereas the addition of bone marrow
cells to BMP resulted in bone formation and success-
ful union. The additive effect of bone marrow cells
and BMPs is also observed in the treatment of cal-
varial bone defects.261
A number of carrier molecules have been used to
deliver BMPs, including absorbable collagen sponges,
various mixtures of poly-L-lactide/glycolide, hydro-
xyapatite, hydrogels, porous tricalcium phosphate,
and calcium carbonate (coral). Only a few studies have
compared these materials directly, often with con-
flicting results. In general, the carrier molecules have
all been shown to augment bone repair and to promote
osteogenesis in segmental defects of endochondral and
membranous bone. Later studies have evaluated the
role of gene therapeutic delivery of BMPs and have
demonstrated promising results.215"221
Transforming Growth Factor-p
TGF-P growth factors have also been strongly impli-
cated in the regulation of osteogenesis. To date, three
mammalian isoforms of TGF-P have been identified
(Pi, P2, P3) and shown to have protean effects on
cellular mitogenesis, angiogenesis, wound healing, cel-
lular proliferation, immunologic reactions, epithelial-
mesenchymal interactions, and skeletogenesis.l83,262"264
All three isoforms have similar actions and functional
664 I • GENERAL PRINCIPLES
overlap, but subtle differences in cellular binding and
regulation have been demonstrated. The effects of TGF-
P1 on bone development and repair have been the most
closely studied. These studies have demonstrated that
TGF-(3l is a potent chemoattractant for osteoblasts
and stimulates the proliferation of osteoblast precur-
sors."65 In addition, TGF-P is produced by isolated
osteoblasts in vitro and is expressed by osteocytes,
osteoblasts, and osteoblast precursors during fracture
repair and distraction osteogenesis.183,263,266"270
Most cells secrete TGF-pl as an inactive precursor
covalently associated with a pro-region derived
from its precursor molecule (latency-associated
peptide).266,271 Furthermore, this complex is usually
associated with a second protein molecule known as
the latent TGF-pl binding protein.262*264 Association
of TGF-pl with these molecules is thought to play an
important role in the storage and regulation of TGF-
Pl activity.264,272
A significant body of literature supports the
hypothesis that TGF-pl plays an important role
in osteogenesis and that increased TGF-P 1 expres-
sion at a fracture site may accelerate fracture
healing.'83-263'267-269-273'274 For example, increased TGF-
Pl expression may augment the migration of
osteoblasts and osteoblast precursors to the fracture
site. This conclusion is supported by in vitro studies
demonstrating potent chemotactic activity on fetal
calvarial osteoblasts, clonal osteoblast-like cells, and
embryonic mesenchymal stem cells.270,275"278 In addi-
tion, TGF-Pl-mediated osteoblast migration may be
augmented by transcriptional activation of other
cytokines important in the regulation of osteoblast
chemotaxis.'83'272'276-279
In addition to potent effects on osteoblast migra-
tion, TGF-Pl is an important regulator of osteoblast
proliferation and differentiation. In general, at phys-
iologic doses, TGF-Ps stimulate osteoblast mitogene-
sis and proliferation, augment bone matrix synthesis,
and inhibit osteoblast differentiation.265 For example,
TGF-pl is a potent mitogen for osteoblast-enriched
cultures and fetal rat calvaria in vitro; the in vivo
delivery of recombinant TGF-pl protein to femurs of
young rats results in mesenchymal proliferation and
osteoblast formation.266'272,280 In addition, TGF-pl
gene therapy of osteoblasts in vitro modulates the
expression of extracellular matrix products. 281
Numerous studies have evaluated the effect of exoge-
nously delivered TGF-p on fracture repair. In fractured
long bones, serial injections (4 to 40 ng every other
day for 40 days) or continuous infusion of TGF-P (1
to 10 jig/day for 6 weeks) in rabbit and rat tibias is asso-
ciated with a dose-dependent increase in callus volume
and increased mechanical strength compared with con-
trols.267,282,283 Daily subperiosteal injection of TGF-pl
or TGF-P2 into newborn rat femurs is associated with
intramembranous ossification and chondrogenesis. 274
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After cessation of injections, endochondral ossifica-
tion is noted within the newly formed cartilaginous
matrix. Adsorption of TGF-pl on ceramic coated
implants also appears to enhance mechanical fixation
and bone growth on the implant, thus improving
mechanical strength.284 Delivery of TGF-P 1 with use
of tricaldum phosphate and amylopectin has also been
shown to augment bone union and mechanical
strength in rabbit tibial segmental defects; however,
this effect was not significant, a finding probably related
to the facts that more than 80% of TGF-P 1 was released
within 24 hours and that the model used was not a
critical-sized defect.285 Finally, the combination of rel-
atively large doses of TGF-Pl (750 Ltg) and deminer-
alized bone matrix as a single application has been
shown to be effective in a sheep tibial defect model.286
Exogenous TGF-P has also been shown to augment
osseous repair in membranous bones. For example,
Hong et al287 demonstrated that rabbit skull defects
treated with TGF-p 1 (0.1 jig) delivered in a biodegrad-
able hydrogel carrier significantly increased bone
regeneration. Using this carrier, the authors demon-
strated gradual release of TGF-P 1 as the hydrogel
degraded. Delivery of TGF-P 1 in solution had no effect
regardless of the dose used. Arnaud et al288 showed
that delivery of TGF-pl in fibrin glue and coral gran-
ules to rabbit skull defects was significantly more effec-
tive than delivery of the growth factor by methyl
cellulose and fibrin glue. Moxham et al286 demonstrated
that the delivery of large doses of TGF-pl (750 Lig) as
a single application in combination with demineral-
ized bone matrix resulted in complete bridging of
critical-sized calvaria! defects in rabbits. In contrast,
animals treated with demineralized bone matrix alone
healed with a fibrous scar. Similar results were observed
with lower doses of TGF-pl (0.4 to 5|ig) in rabbit
skull defects.273
Exogenous application of TGF- P1 may also be effec-
tive in the treatment of critical-sized defects of the
mandible. Delivery of TGF-Pl (250(Jg) and dem-
ineralized bone matrix demonstrated significant bone
formation and increased mechanical strength.289 Zellin
et al290 also demonstrated significant, dose-dependent
(0.1 to 20 (Ig) bone formation in a 5-mm critical-sized
defect of the rat mandible regardless of the carrier used
(methyl cellulose, porous calcium carbonate, poly-L-
lactide/coglycolide beads). Bone bridging was not com-
plete, however, and may have been related to a short
follow-up period (24 days). Treatment of rabbit cal-
varial defects with 5 to 10|Xg of TGF-Pl in the same
study, however, resulted in complete healing after 28
days, a finding implying differential TGF-pl biologic
activity according to the site and animal model used.
Not all experiments have demonstrated a utility for
exogenous TGF-P 1 in the treatment of segmental
defects. For example, Bosch et al291 evaluated the effects
of a single application of TGF-pl (2, 5, lOjlg) to
image...
critical-sized calvarial defects in rats and demonstrated
that although the higher doses of TGF-pl stimulated
statistically significant increases in bone formation,
they did not promote clinically relevant osteogenesis.
Ripamonti et al292 also found little therapeutic effect
in baboon calvarial defects treated with a single appli-
cation of a large dose of TGF-pl (5,30,100 mg) deliv-
ered with a collagenous bone matrix carrier. Smaller
doses were also ineffective in a dog radial diaphysis
nonunion model (10 ng) and in a rabbit tibial dis-
traction osteogenesis model (10 to 40 ng/day).225,29-
Gazit et aP94 have suggested that the effects of exoge-
nous TGF-Pl on osteogenesis may be age related and
demonstrated that systemic delivery of 0.5 to 5 mg/day
of TGF-Pl into old or young mice results in signifi-
cant increases in trabecular bone volume, bone for-
mation, mineral apposition rate, and fracture healing
only in old animals. The authors hypothesize that this
effect may be due to diminishing endogenous TGF-
P1 levels in old mice, resulting in decreased osteogenic
marrow osteoprogenitor cells.294 Thus, unlike for
BMPs, the clinical utility of TGF-ps remains unclear.
Fibroblast Growth Factors
Fibroblast growth factors (FGFs) are a family of evo-
lutionarily conserved, structurally related peptides
characterized by their high affinity for heparin. To date,
nine isoforms of FGF have been identified in
mammals. 295 These molecules have been implicated in
the regulation of skeletal patterning, neural differen-
tiation, angiogenesis, and wound repair.146,295 FGF-l
(acidic FGF) and FGF-2 (basic FGF) are the most
abundant isoforms of FGF with high levels of expres-
sion in a number of tissues. FGF-l is expressed pri-
marily in the brain and retina; FGF-2 is more widely
expressed and has been localized to the brain, adrenal,
liver, blood vessels, inflammatory cells, bone, and bone
matrix.279'296'298 FGF-l and FGF-2 have a sequence
homology of approximately 55% and are thought to
have similar three-dimensional structures.299 The other
members of the FGF family are primarily expressed
during embryonic development and oncogenesis.
An interesting feature of FGF-l and FGF-2 is the
lack of a signal peptide in the mature molecule.295 The
expression of this molecule is thought to be required
for uptake of the peptide by the endoplasmic reticu-
lum and packaging for cellular secretion. Thus, the
mechanisms by which FGFs are secreted into the extra-
cellular matrix remain unclear and may be mediated
by cellular disruption during injury or by an as yet
undescribed cellular transport mechanism.300'302
FGFs transmit their intracellular signals by binding
cell surface tyrosine kinase receptors. Receptor-ligand
interaction leads to receptor dimerization and acti-
vation of intrinsic tyrosine kinase activity. Ligand-
receptor interaction is further modulated by
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Dr.Mustafa D.
24 • REPAIR AND GRAFTING OF BONE 665
interactions with membrane-bound or matrix-
associated heparin-like proteoglycans.303 At least four
families of FGF receptors (FGF-R1, FGF-R2, FGF-R3,
FGF-R4) have been identified. Ligand specificity and
binding affinity are mediated by alternative splicing
of the Hgand-binding domain. 304 Although FGF-R1
and FGF-R2 have similar ligand-binding properties
with equal affinity for FGF-l and FGF-2, the distri-
bution of these receptors is spatially distinct during
development and has led some authors to hypothe-
size that functional specificity is based on differential
expression. * FGF receptors have been the topic of
intense research in recent years because of the iden-
tification of mutated, constitutively active FGF recep-
tor isoforms in familial craniosynostosis.309"313
In general, FGFs are mitogenic for mesoderm- and
neuroectoderm-derived cells.314 Likewise, FGF stimu-
lation of isolated osteoblast-enriched cultures in vitro
causes cellular proliferation but inhibits cellular dif-
ferentiation, as evidenced by decreased expression of
alkaline phosphatase, collagen type I, and osteocal-
cin.279,315-321 In addition, short pulse treatments with
FGF-2 are associated with increased collagen deposi-
tion, an effect that appears to be mediated by an increase
in the number of osteoblastic cells and possibly alter-
ations in collagenases and their inhibitors.315,322,323
FGF-2 is thought to be an important regulator of
bone development because disruption of the FGF-2
gene is associated with decreased bone mass and bone
formation.324 During development, FGF-2 expression
has been localized to osteoblasts as well as to the upper
hypertrophic zones of the growth plate, a finding
implying a potential role in chondrocyte maturation
during bone growth and possibly during endochon-
dral fracture repair.319,325330 Additional support for this
hypothesis has been derived from experiments demon-
strating epiphyseal plate ossification after continuous
infusion of FGF-2.331 Finally, FGF-2 is thought to reg-
ulate the expression of patterning genes during limb
development and cranial bone formation.332'335
FGFs also play an important role in fracture repair
and are expressed during the early phases of mem-
branous and endochondral fracture repair. This expres-
sion is limited primarily to the granulation tissue and
fracture hematoma and is thought to result from release
of FGF from injured cells and infiltrating inflamma-
tory cells (primarily macrophages).336,337 As fracture
healing progresses, FGF-2 expression is localized to
mesenchymal cells, osteoblasts, and immature or
maturing chondrocytes. 336 In addition, FGF-2 is
expressed by the expanded cambial layer of the perios-
teum and is spatially and temporally associated with
a rapid increase in the number of spindle-shaped mes-
enchymal cells.338
Numerous studies have investigated the potential
of FGF-2 to accelerate or to augment fracture repair.
Although most of these studies have been conducted
666 I • GENERAL PRINCIPLES
in rodents and rabbits, it is clear that FGF-2 can accel-
erate fracture repair and promote closure of critical-
sized defects in endochondral bones. For example, in
a rabbit fibula fracture model treated with a single dose
of FGF-2 (dose ranging from 20 to 200 |ag) delivered
during surgery, it was demonstrated that fibula frac-
tures treated with FGF-2 had a significant increase in
callus size, bone volume, and osteoblastic activity com-
pared with controls." 9 Increased bone formation and
callus size were dose dependent and translated to his-
tologically successful bone repair in all animals treated
with FGF-2 versus similar healing in only 60% of
controls. FGF-2 treatment was also associated with
significant increases in mechanical strength. Similar
findings were reported in a canine tibial osteotomy
model, in a baboon fibula osteotomy model, and in
normal and streptozotocin-induced diabetes rat fibular
osteotomy models. 340 ' 3,n In addition, FGF-2 delivered
by atelocollagen minipellets or a single injection pro-
moted significant increases in bone and collagen for-
mation.34,1,345 Recombinant FGF-2 has been shown to
accelerate bone consolidation in a rabbit model of tibial
distraction osteogenesis.346 It has been hypothesized
that FGF-2-mediated osteoblast and fibroblast prolif-
eration promotes collagen synthesis within the frac-
ture callus, thus leading to enhanced fracture repair
and mechanical stability.347
The effects of FGF-2 on membranous bone regen-
eration have also been studied. Eppley et al154 used a
mandibular defect model to analyze the effectiveness
of FGF-2 administered continuously during 14 days
on cortical bone graft incorporation and demonstrated
that although FGF-2 treatment increased angiogene-
sis, it did not accelerate fracture healing. Schliephake
et al348 did not find significant differences in mandibu-
lar bone regeneration in segmental defects in minip-
igs treated with polylactic acid tubes with or without
a single dose of recombinant FGF-2. In a follow-up
study, Eppley et al153 demonstrated that improved
angiogenesis associated with FGF-2 treatment may have
clinical utility in compromised clinical situations; pre-
treatment with FGF-2 of irradiated rabbit mandibles
2 weeks before corticocancellous bone grafting sig-
nificantly improved new vessel ingrowth, bone graft
incorporation, and osseous repair. No significant dif-
ference in bone graft incorporation or vessel counts
was noted in the irradiated mandibles treated with FGF-
2 at the time of bone grafting.
Several studies have investigated the effects of
FGF-2 on cranial bone regeneration. Blanquaert
et al349 investigated the use of heparan-like molecules,
carboxymethyl benzylamide sulfonated dextrans
(CMDBS), on rat cranial critical-sized defect regen-
eration because these compounds are known to poten-
tiate FGF activity. This study demonstrated a
dose-dependent increase in bone defect closure after
a single application of CMDBS in a collagen vehicle.
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Other studies, however, have failed to demonstrate
significant improvements in bone formation with a
single application of FGF-2. In contrast, continuous
delivery of FGF by use of osmotic pumps or gelatin
hydrogels was associated with significant increases
in cranial bone regeneration in rat and primate
models.35"*352 In a study using a recombinant,
replication-deficient FGF-2 adenovirus, Greenwald et
al353 demonstrated increased cranial bone formation
after injection of the virus into the dura mater. Thus,
it appears that FGF-2 has the potential to augment
bone repair in clinical use; however, improved osseous
regeneration is likely to be dependent on continuous
delivery of the growth factor.
Platelet-Derived Growth Factors
Platelet-derived growth factors (PDGFs) are a group
of growth factors thought to have important roles
in the regulation of inflammatory reactions, cellular
proliferation, and chemotaxis. PDGFs are dimeric
molecules consisting of disulfide-bonded A and B
polypeptide chains and exist as either homodimeric
(PDGF-AA or PDGF-BB) or heterodimeric (PDGF-
AB) forms. PDGF-AB and PDGF-BB are the pre-
dominant circulating isoforms of PDGF; in normal
unstimulated osteoblasts, PDGF-AA is the primary
isoform.354 The various forms of PDGF (AA, BB, or
AB) exert their biologic effects by dimerization of struc-
turally related cell surface tyrosine kinase receptors as
a result of receptor binding to each subunit of the PDGF
molecule. Differential specificity for the A or B
polypeptide chain (the a receptor is capable of binding
either the A or B polypeptide chain, whereas the P recep-
tor binds only the B polypeptide chain) is responsible
for activation of various PDGF receptors by PDGF
dimers. PDGF-AA activates only the act receptor;
PDGF-AB activates either the aa or ap receptor; and
PDGF-BB activates the a a , a p , or pp receptors. Recep-
tor dimerization results in autophosphorylation and
the initiation of intracellular signaling. Thus, varia-
tions in PDGF dimerization, as well as differential
expression of PDGF tyrosine kinase receptors, add a
layer of complexity and contribute to the regulation
of PDGF biologic activity.
PDGFs are initially released by degranulating
platelets in the fracture hematoma, where they are
thought to play a role in the regulation of cellular
inflammatory reaction, chemotaxis, cellular prolifer-
ation, and angiogenesis. In the early phases of fracture
repair, PDGF-A subunit is more abundant than PDGF-
B; thus, the majority of PDGF found within the early
fracture microenvironment is PDGF-AA.355 As frac-
ture healing continues, PDGF expression is noted
in macrophages that infiltrate the traumatized bone
and callus as well as in early and mature hypertrophic
chondrocytes. 338
 image...
The primary effects of PDGF on osteoblasts include
chemotaxis, increased proliferation, and decreased
cellular differentiation.355065 In addition, PDGFs reg-
ulate bone collagen balance by increasing collagenase
production, thereby increasing collagen degradation
while at the same time increasing collagen synthe-
sis.366,367 In addition, it appears that mechanical strain-
induced proliferation of osteoblastic cells in vitro is
mediated, at least in part, by PDGF.361 PDGFs also inter-
act with other growth factors that play a role in the
regulation of bone formation. For example, treatment
of osteoblastic cells with PDGF-BB decreases steady-
state insulin-like growth factor 2 mRNA expression.368
In contrast, exposure of osteoblasts to TGF-P results
in a decrease in PDGF a receptor mRNA expression
and significantly decreased PDGF-AA binding.369 The
combination of TGF-P and PDGF-BB strongly stim-
ulates proliferation and chemotaxis of osteoblastic
cells.283
The effects of PDGF on bone healing, fracture repair,
and bone density have also been studied in vivo in a
limited number of studies. For example, systemic
administration of PDGF-BB in rodents prevents bone
loss and increases vertebral body compressive strength
and femoral shaft torsional stiffness in ovariectomized
rats. In a pilot study with a limited number of animals,
the injection of 80 |im of PDGF by a collagen carrier
into a unilateral tibial osteotomy model in rabbits
resulted in a subjective increase in callus density and
volume and a significant increase in mechanical
strength compared with vehicle controls.371 Although
A B
FIGURE 24-1 3. Three-dimensional computed tomographic scan of distracted human mandible. A, Predistraction
view shows hypoplasia of the body and lower aspect of the ramus. B, Postdistraction view shows bone generation in
the deficient areas. Note the pin holes. The new bone is robust.
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24 • REPAIR AND GRAFTING OF BONE 667
these results are intriguing, further studies with larger
experimental groups are necessary to confirm these
conclusions because other studies have not demon-
strated significant increases in bone ingrowth.372
DISTRACTION OSTEOGENESIS
The use of inductive surgery such as distraction osteo-
genesis to generate bone is becoming the preferred
method for treatment of a variety of craniofacial and
endochondral bone deficits (Fig. 24-13). This technique
relies on the endogenous cellular machinery of the host
to orchestrate bone formation and remodeling and
offers a number of advantages over traditional means
of treatment of skeletal deficiencies. For example, bone
formed by these techniques is, in general, of better
quality and is less susceptible to relapse. This may be
attributed in part to the accompanying changes in the
soft tissue envelope, thus enabling its expansion to
accommodate the newly formed bone.
History
Distraction osteogenesis is the generation of viable
bone by the gradual separation of osteotomized bone
edges. The roots of distraction osteogenesis can be
traced to the late 19th century when the treatment of
shortened limbs by osteotomy followed by acute
lengthening and bone grafting was first described.373
During the ensuing decades, enthusiasm for these pro-
cedures waxed and waned as clinical needs resulting
image...

668 I • GENERAL PRINCIPLES

from World War II injuries and the polio epidemic osteogenesis has been a major focus of clinical cran-
were offset by the requirement for multiple operative iofacial research and has led to improved treatment
procedures, a significant incidence of complications, modalities for difficult clinical situations.
and the need for subsequent bone grafting.374"379
In a fortuitous observation, Ilizarov, a Russian ortho-
pedic surgeon, noted the spontaneous generation of Histology
bone when an external fixator designed to compress
Osteogenesis in both endochondral and membranous
bone ends was accidentally distracted at a slow rate.380
bone distraction occurs primarily through membra-
This observation led to a series of experiments with
nous ossification with no evidence of a cartilaginous
use of the canine tibia and hundreds of clinical cases
intermediate.380-382-388-394-396 Although the appearance of
in which Ilizarov identified the biomechanical factors
a cartilaginous intermediate has been noted in several
responsible for bone formation in distraction osteo-
studies, the absence of type II collagen matrix and the
genesis and established guidelines that result in the pro-
consistent demonstration of bone formation by mem-
duction of viable bone in a majority of cases.381"383
branous ossification in most experimental and clini-
Ilizarov hypothesized that slow controlled separation
cal studies suggest that these isolated reports are
of osteotomized bone results in the "tension stress
probably secondary to other variables, most notably
effect" leading to metabolic activation, angiogenesis,
unstable fixation. 386 ' 388 - 394,395 - 397 ' 398 During the early
and new bone formation. Through carefully designed
phases of distraction, a marked angiogenic response
experiments, Ilizarov demonstrated that bone forma-
occurs in association with the appearance of primi-
tion resulting from distraction osteogenesis is multi-
tive mesenchymal cells and the synthesis of collagen
factorial and dependent on patient-specific variables
I matrix in the distraction zone. As distraction pro-
(i.e., age, osteotomy site, regional blood supply) and
ceeds, tapered fibroblast-like cells produce a network
mechanical factors (i.e., pin rigidity, device stability).
leading to the formation of a fibrovascular bridge with
Furthermore, these experiments demonstrated that a
increasingly dense collagen fibrils organized in the
delay period after osteotomy and before the start of
direction of distraction (Fig. 24-14).386'388-389'394'395'399
distraction (termed the latency period) and the rate
Active, mature osteoblasts and mineral deposition can
and frequency of distraction significantly affect bone
be appreciated 10 to 14 days after the onset of dis-
formation during distraction osteogenesis. In the last
traction, beginning at the margins of cut bone sur-
20 years, the validity of these guidelines has been con-
faces and adjacent to newly formed vascular channels
firmed by numerous clinical and experimental studies,
and extending to the central avascular fibrous inter-
and distraction osteogenesis has become the standard
zone. 383,386,388,400
limb-lengthening procedure.380,384-386 Collagen bundles progressively min-
eralize into early bone spicules extending from the
Distraction osteogenesis has more recently been
edges of corticotomy toward the central fibrous inter-
applied to the craniofacial skeleton. Snyder et al387 are
zone, forming a structure known as the primary min-
credited with the first experimental study to use dis-
eralization front. Bone spicules are surrounded by
traction bone lengthening in the craniofacial skele-
thin-walled vascular sinusoids that extend to but do
ton. In this study, the authors demonstrated that a
not cross the fibrous interzone.386,388-389,401 Progressive
surgically created crossbite in a dog mandible (result-
calcification of the primary mineralization front
ing from a 1.5-cm bone resection) could be corrected
results in the closure of the distraction gap, and remod-
by an external distraction device with movements of
eling of newly formed bone continues with eventual
1 mm/day for 2 weeks. McCarthy et al388,389 expanded
formation of normal lamellar bone and marrow ele-
on these findings by conducting a large number of
ments. The overall histologic pattern of bone forma-
experiments on the canine mandible and demonstrated
tion in distraction osteogenesis is similar to the growth
that distraction osteogenesis can be produced in the
plates at the zone of Ranvier.160
membranous bones of immature and mature animals.
The use of intraoral devices was first reported in a
limited study by Michieli and Miotti390,391 and later cor-
roborated in a larger study by McCarthy et al392 using Variables Affecting Osteogenesis
canine mandibles. ACE
393
McCarthy et al were the first to report a clinical The negative effects of aging on fracture healing and
series of craniofacial distraction for the correction of distraction osteogenesis have been well described (see
mandibular hypoplasia. Since this report, mandibu- earlier). In clinical practice, fractures heal most rapidly
lar distraction osteogenesis has become the treatment in infants; healing rates decrease steadily until skele-
of choice for moderate to severe mandibular hypopla- tal maturity, reaching a plateau thereafter.I5S The
sia. In addition, distraction osteogenesis has been increased fracture healing rate in infants and children
successfully applied to other craniofacial structures translates to a distraction-healing index (a measure
including the calvaria, midface, zygoma, orbit, and ofregenerate bone ossification rate) that is nearly twice
hard palate. The continuing evolution of distraction that of adults.161,380 This finding is supported by the

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Dr.Mustafa D.
 image...
SITE OF CORTICOTOMY
FIGURE 24-1 4. Schematic of
the stages of bone tormation
during distraction osteogenesis:
1, zone of fibrous tissue; 2, zone
of extending bone formation; 3,
zone of bone remodeling; 4, zone
of mature bone. (From Karp NS,
McCarthyJC.SchreiberJS.etal:
Membranous bone lengthening:
a serial histological study. Ann
PlastSurg 1992;29:2-7.)
fact that bone formation and bone mineral deposi-
tion in children undergoing distraction osteogenesis
occur at a significantly accelerated rate (385p.m/day)
compared with adolescents (300p.m/day) and adult
patients (213|im/day).380 This finding highlights the
explosive bone growth noted during distraction osteo-
genesis; bone formation during this process occurs at
rates that parallel bone formation in human fetal
femurs (400|xm/day) and is nearly eight times faster
than bone formation at the fastest growing epiphy-
seal bone plate.402 Such age-related differences in bone
formation have led some investigators to recommend
variable distraction protocols according to the patient's
age.385 However, although the maximal rates of osteo-
genesis in older animals may be decreased relative to
younger animals, bone lengthening by distraction
osteogenesis is a viable option even after skeletal matu-
rity has been reached.
BLOOD SUPPLY
Factors influencing blood supply to distracted bone
segments are known to have significant effects on
osteogenesis.161,381,382,386,403 These findings are not sur-
prising given the fact that osteocyte survival requires
proximity of less than 0.1 mm to nutrient vessels.124
Osteogenesis during distraction, similar to fracture
repair in general, is dependent on angiogenesis. Sur-
gical technique can significantly alter the blood supply
to distracted bone segments and may contribute to
variability in the outcomes of experimental and clin-
ical distraction osteogenesis.403,404 These changes are
most prominent in long bones because their blood
supply is less vigorous than that of the bones of the
craniofacial skeleton. For example, disruption of the
medullary nutrient artery or the overlying periosteum
in long bones significantly decreases total and corti-
cal blood flow and is associated with significant reduc-
tion in bending moment, rigidity, and fracture energy
of the regenerate bone in endochondral distraction
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24 • REPAIR AND GRAFTING OF BONE 669
1
SITE OF CORTICOTOMY
osteogenesis.120'12M60a6I-38,-383'38M0,'4°3'404 In fact, in long
bones, even minor disruption of the periosteum
results in significantly decreased rates of osteogenesis
and postoperative mechanical strength, whereas its
excessive dissection is associated with significantly
decreased callus volumes and an increased incidence
of postoperative fractures.161-38'-383,405,406 Although the
effects of periosteal dissection in distraction osteoge-
nesis of the craniofacial skeleton have not been svs-
tematically investigated, most studies suggest a less
critical role for this variable than in long bone dis-
traction. The increased tolerance to surgical dissec-
tion and widespread periosteal undermining is likely
to be related to the robust vascularity of the cranio-
facial soft tissue envelope and the overlying facial mus-
culature. In turn, the ability to perform wide periosteal
elevation in craniofacial distraction provides the
surgeon with unlimited therapeutic options.
LATENCY PERIOD
Most experimental evidence suggests that optimal
osteogenesis is obtained when distraction is delayed 5
to 7 days after osteotomy. This time interval is termed
the latency period. In general, shorter latency periods
tend to generate smaller callus volumes and result
in inadequate osteogenesis, whereas longer periods
(i.e., > 14 days) are associated with premature consol-
idation.382,386,398,405 Histologic studies have demon-
strated that callus volume and capillary ingrowth are
increased with a short delay before the initiation of
distraction.407"409 Several factors may account for the
impaired osteogenesis resulting from immediate dis-
traction protocols. For example, disruption of the frac-
ture hematoma, as may occur with immediate
distraction, is associated with a 26% decrease in callus
cross-sectional area and results in significantly
decreased mechanical strength.406 In addition, an
immediate distraction gap may inhibit the prolifera-
tion of osteogenic precursors because in bones of the
670 I • GENERAL PRINCIPLES
axial and appendicular skeleton, a critical distance exists
beyond which bone union does not occur.410 Finally,
immediate distraction may disrupt btidding capillar-
ies, thus impairing angiogenesis. In contrast, a delay
before distraction may allow growth and differentia-
tion of blood vessels that, once formed, may better with-
stand distraction forces.409-4"""3
The significance of the latency period has been
debated to some extent.however, because some studies
comparing immediatedistraction with latency periods
of 7, 14, and 21 days have failed to demonstrate sig-
nificant differences between immediate and delayed
distraction.* MU This apparent discrepancy is proba-
bly related to differences in other factors that may alter
the osteogenic response with distraction (e.g., the age
of the experimental animals, surgical techniques, site
of osteotomy).
RATE AND FREQUENCY OF DISTRACTION
Numerous studies have investigated the effects of
varying the rate and frequency (rhythm) of distrac-
tion on regenerate bone formation. Although ideal dis-
traction rates and frequencies depend on multiple
factors, in general, optimal endochondral bone for-
mation in large animal models occurs at a rate of
approximately 1.0 mm/day.382 In a series of 400 canine
tibial lengthening experiments comparing distraction
rates of 0.5, 1.0, and 2.0 mm/day, Ilizarov382 demon-
strated that distraction at the lowest rate was frequently
complicated by premature consolidation, whereas dis-
traction at a rate of 2.0 mm/day often resulted in inad-
equate bone formation and fibrous union. In contrast,
distraction at a rate of 1.0 mm/day consistently
resulted in spontaneous osteogenesis with excellent
bone stock in virtually all cases.
Optimal distraction rates for craniofacial bones have
not been systematically studied; however, rates ranging
from 1.0 to 2.0 mm/day have been reported to result
in adequate osteogenesis with mandibular distraction
in a number of models.387'388'394'398'414-4'6 Rates in excess
of 2.0 mm/day should probably be avoided because
they have been associated with fibrous union in the
mature canine mandible.417 Optimal distraction rates
for other craniofacial bones appear to be similar to
those of mandibular distraction osteogenesis; success-
ful osteogenesis is associated with rates of 0.5 to
2.0 mm/day in midface advancement, orbital distrac-
tion, and cranial remodeling.418"421
Dividing daily distraction distances into multiple,
uniform, regularly paced intervals can significantly
enhance osteogenesis and distraction rates. This
concept was first demonstrated by Ilizarov, who com-
pared the rate of osteogenesis in canine tibias distracted
a total of 1.0 mm/day in 60 even increments (by use
of a motorized autodistractor), in 4 even increments,
or once daily. Ilizarov demonstrated a significant
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augmentation of bone formation with increasing fre-
quency of distraction (i.e., 60 even increments > 4 times
daily > once per day) .m In fact, distraction with motor-
ized devices was so much more efficacious that exper-
imental animals often had premature consolidation of
the osteotomy segments even when distraction was per-
formed at accelerated rates (1.5 to 2.0 mm/day). More
recently, Aronson and Shen380 have demonstrated that
a regular pattern of distraction is critical to this process
beca use random patterns, even those resulting in move-
ments of 1.0 mm/day, result in fibrous union.
In addition to enhanced osteogenesis, frac-
tionated distraction protocols are associated with
significantly less soft tissue injury and enhanced
angiogenesis.161'381"383 For example, canine tibias dis-
tracted once daily are noted to have significant focal
homogenization of muscle, periosteum, fascia, nerves,
skin, and blood vessels and have only a few newly
formed vessels.382'400 In contrast, fractionation of the
distraction distance into four even increments is asso-
ciated with significantly decreased soft tissue damage
and enhanced angiogenesis, whereas distraction with
the autodistractor (i.e., 60 even increments per day)
results in essentially normal soft tissue structures with
histologic patterns reminiscent of growth during
embryonic and fetal life and massive increases in
capillary formation with multiple anastomoses. The
current recommendation for endochondral bone dis-
traction is a rate of 1 mm/day. There is more variabil-
ity in rates of distraction for membranous bone;
however, most authors use a rate of 1 to 2 mm/day
either performed once daily or divided into two equal
advancements.
DEVICE STABILITY
Stable fixation of osteotomized bone segments is a crit-
ical factor in distraction osteogenesis.159,381,382'399 Com-
parison of canine tibial osteotomies distracted with
devices that had varying degrees of stability revealed
significantly enhanced osteogenesis with secure fixa-
tion and nonunion with pseudarthrosis formation with
unstable devices.382 Even slightly decreased stability was
deleterious and resulted in a significant increase in time
required for full remodeling.
Many devices have been designed for mandibular
and craniofacial distraction with varying rates of
success. In general, device stability in craniofacial
distraction osteogenesis does not appear to be as
critical as in long bone distraction; however, gross
instability is not well tolerated and must be avoided.
In mandibular distraction osteogenesis, stability is gen-
erally established with use of one- or two-pin devices
(one or two pins in each distracted segment). Although
adequate osteogenesis has been reported with each
device type, decreased stability associated with two-
pin devices may be responsible for the appearance of
T^kWyelePWimaqe...
cartilaginous intermediates in some studies that use
these devices.398
Several mechanisms are thought to contribute to
the effects of device stability on distraction osteogen-
esis. AdequaLe fixation of bone segments is thought
to prevent repetitive localized trauma to regenerate,
resulting in enhanced angiogenesis and subsequent
osteogenesis.381,382 Thus, enhanced blood flow result-
ing from stable fixation is particularly important with
significant soft tissue trauma and in anatomic areas
with marginal blood supply.422 In addition, limiting
excessive motion at the osteotomy site permits earlier
weight bearing and resumption of daily activities, thus
increasing transmission of loads to the regenerate.
Micromotion has been shown to enhance bone
formation and to decrease bone resorption in a
number of clinical and experimental models of frac-
ture repair and may have a similar role in distraction
osteogenesis.1,422'427
BONE GRAFTING
History
The history of bone grafting can be traced to van
Meekren,428 who in 1668 reported the use of canine
calvarial bone to repair a cranial defect in a Russian
soldier. Pressure from the church, however, forced van
Meekren to remove the xenograft. In the years that fol-
lowed, bone grafting was performed and taught anec-
dotally. Scientific interest in bone grafting was fueled
by Oilier,429 who published his experiments with bone
grafting and emphasized the importance of the perios-
teum in osseous regeneration. Oilier hypothesized that
both periosteum and bone graft must be viable for
success. Using these techniques, Macewen430 reported
the successful reconstruction of an extensive humeral
defect in a child with iliac crest allografts. Macewen
later demonstrated the repair of a mandibular defect
with autogenous rib grafts.
Barth431 challenged Ollier's conclusions about the
need for viability of the periosteum and bone graft
by demonstrating that most cells in bone grafts are
necrotic shordy after transplantation. He suggested that
osseous regeneration after bone grafting occurs by
gradual resorption and replacement of the necrotic
bone graft by surrounding host bone, a process he
termed creeping substitution.
In a series of experimental studies, Axhausen432
demonstrated that cells within the periosteum of
grafted bone remain viable and are capable of induc-
ing osteogenesis. Phemister 433 published his observa-
tions in a large series of experimental studies and
demonstrated that both endosteum and periosteum
remain viable during bone grafting in animals. In addi-
tion, he showed that both sources contribute to osteo-
genesis and that bone grafts cut into small pieces
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24 • REPAIR AND GRAFTING OF BONE 671
generated more callus and resulted in more rapid
fusion. These findings led him to conclude that cellu-
lar survival in bone grafts is dependent on diffusion
from surrounding tissue.
Gallie and Robertson 434 followed up the work of
Phemister and demonstrated the importance of the
periosteum at the recipient site in revascularization.
In addition, they found that cancellous bone graft sur-
vival was superior to cortical grafts. The authors con-
cluded that improved bone graft survival in cancellous
bone grafts was due to increased porosity of the graft,
thereby increasing the surface area and facilitating
osteoblast survival through diffusion.
Mowlem435,436 is credited with popularizing the use
of cancellous bone grafting in a wide variety of clini-
cal scenarios. He thought that the surgeon should max-
imize bone graft survival as a means of delivering viable
osteoblasts. He concluded that the surgeon "should be
directed to the creation of circumstances under which
maximum cellular survival is insured under conditions
which will make the subsequent activity of the cells
most effective. No longer is the bone graft that inor-
ganic bridge which is to be completely resorbed and
slowly replaced. Instead it is only the scaffold to carry
these cells which can rapidly envelop it with new bone
and incorporate it in the new repair." These conclu-
sions remain valid today.
Studies have demonstrated that in addition to pro-
viding scaffold and cellular products, autogenous
bone grafts are a potential source of growth factors
capable of inducing bone formation and cellular dif-
ferentiation. Thus, substances such as bone morpho-
genetic proteins are capable of inducing differentiation
of undifferentiated mesenchymal cells into osteoblasts
and promote osteogenesis. In addition, other growth
factors expressed in high concentrations in bone, such
as fibroblast growth factor, TGF-(3, and insulin-like
growth factor, are also transferred in bone grafts and
are likely to play an important role in revasculariza-
tion and osteogenesis.
Autogenous Bone Crafting
Bone grafts are used in a variety of clinical situations
and can be divided into two broad categories: treat-
ment of bone gaps (inlay bone grafting) and bone pro-
jection (onlay bone grafting). Cortical grafts are useful
in situations requiring immediate mechanical strength.
These grafts can survive with or without complete
revascularization or resorption and are primarily used
by plastic surgeons in the treatment of bone volume
deficiency (e.g., mandibular augmentation). Cancel-
lous grafts, in contrast, have no mechanical strength
and therefore require additional support to bridge bone
defects. Cancellous grafts are used primarily for the
treatment of bone gaps and in general revascularize
quickly, resorb completely, and stimulate significant
image...
672 I • GENERAL PRINCIPLES
new bone formation. The terms bone slurry and bone
paste are usually used to describe morselized cortical
or corticocancellous bone grafts combined with blood
or other compounds (e.g., demineralized bone matrix,
collagen). These grafts revascularize quickly, have no
mechanical strength, and are used in the treatment of
non-stress-bearing areas. A number of sources are avail-
able for autogenous bone graft, and the particular graft
chosen depends on the reconstructive needs at hand
(Table 2-1-5).
Autogenous bone graft healing is thought to occur
by a mechanism similar to fracture repair. Although
the timing of repair, degree of bone graft resorption,
and neovascularization differ according to the type of
graft used (cortical versus cancellous) and the recipi-
ent site, the basic histologic processes are in general
similar. Induction of host-graft cells occurs shortlyafter
bone grafting and is followed by the invasion of inflam-
matory cells during the next 4 to 5 days. Polymor-
phonuclear cells debride devitalized tissue and precede
vascular ingrowth. Neovascularization occurs at a vari-
able rate, depending on the vascularity of the recipi-
ent bed, the type of graft used, and the graft size.
Resorption of necrotic bone and bone matrix occurs
by activation of osteoclasts. During bone grafting of
endochondral bones, soft callus formation results from
chondroblast differentiation and chondroid matrix
deposition. Hard callus formation follows after resorp-
tion and calcification of the chondroid matrix. In con-
trast, bone grafting of membranous bones results from
woven bone formation by osteoblasts, and the process
is associated with minimal cartilage formation. During
the remodeling phase of graft repair, immature woven
bone is replaced by lamellar bone.
The repair of cortical bone grafts is initiated by
osteoclastic activation and bone resorption. Vascular
invasion is dependent on this process and begins toward
the end of the first postoperative week.437"139 Complete
revascularization is delayed until approximately 1 to
2 months and is dependent on graft size and recipient
site. Osteoclastic resorption is followed by osteoblas-
tic activation and bone deposition. Simultaneous
resorption and deposition continue until residual areas
of necrotic bone graft are sealed off by new bone, thus
preventing further resorption. Sequestered necrotic
bone, as well as active resorption of cortical bone graft,
weakens the mechanical strength of the graft and is
responsible for fatigue fractures.438 Prolonged healing
periods (1 to 2 years) during which immature woven
bone is replaced by strong lamellar bone may be nec-
essary for maximal increases in bone strength.
Cancellous bone graft healing, in contrast to cor-
tical bone, is initiated by the activation of osteoblasts
derived from the graft and the surrounding tissues,
leading to osteoid deposition. New osteoid deposition
correlates with increased mechanical strength of the
graft. Thus, although cancellous bone grafts have little
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mechanical strength initially, the mechanical proper-
ties of these grafts improve with progressive ossifica-
tion. In addition, in contrast to cortical bone grafts,
necrotic cancellous bone grafts are usually completely
resorbed with little or no evidence of sequestered bone.
Vascular invasion of cancellous bone grafts occurs
rapidly and is facilitated by the interstices of cancel-
lous bone. New vessel ingrowth is not dependent on
osteoclastic resorption and is usually complete by
approximately 2 weeks postoperatively.
Variables Affecting Free Bone
Graft Survival
MECHANICAL STRESS
Mechanical stress is an important regulator of bone
graft survival. Deforming forces tend to cause bone
deposition and hypertrophy. In contrast, limited stress
leads to bone resorption. Bone grafts used to treat bone
gaps (e.g., defects in the mandible or long bones) are
referred to as inlay grafts. These grafts are subjected
to mechanical stress and have a tendency to survive
and remodel into strong lamellar bones. In contrast,
bone grafts used to augment bone volume (onlay grafts)
for the restoration of contour deficiencies are subjected
to limited stress and therefore undergo various degrees
of resorption and remodeling.440,441
SKELETAL FIXATION
Stabilization of fractured bone segments is a critical
regulator of bone healing. In like fashion, stabiliza-
tion of bone grafts has been shown to augment bone
graft survival. Improved bone graft survival may be
related to multiple factors, including transmission of
mechanical stress from the surrounding tissues as well
as more rapid and complete revascularization. Phillips
and Rahn442 first demonstrated this concept when they
compared cortical bone graft survival with and without
lag screw fixation. The authors demonstrated that
fixation significantly increased the survival of both
endochondral (rib) and membranous (calvarial) bone-
derived cortical onlay grafts on the mandible of sheep.
Philips and Rahn443 subsequently demonstrated that
rigid fixation increases revascularization of cortical
bone grafts derived from membranous bones but
decreases revascularization of endochondral bone-
derived cortical grafts 2 weeks postoperatively. The
authors suggested that improved bone graft survival
with rigid skeletal fixation may be related to biome-
chanical and structural factors rather than to revas-
cularization. The results and the conclusions of this
study are somewhat questionable, however, because
differences in revascularization of membranous bone-
derived cortical grafts were not statistically significant.
LaTrenta et al440 evaluated the effects of wire and
plate fixation on endochondral and membranous bone
TABLE 2 4 - 5 4- SOURCES OF BONE GRAFTS

Embryonic Type of Pedicle

Bone Origin Blood Supply Bone Pedicle Length Size Uses Disadvantages Advantages

Tibia Endochondral Nonvascularized Cortical Tibioperoneal Variable Variable Nasal bone Contour irregularity Thick cortex
(usually) Cancellous Trunk grafting Pain
Vascularized Pathologic fractures
(case reports) Minimal soft tissue
coverage
Ilium Endochondral Nonvascularized Cortical DCIA/V 4-6 cm 4 x 11 cm All-purpose Contour irregularity Large amounts of
Vascularized Cancellous Periosteal bone cancellous Pain cancellous bone
blood Skin paddle bone Hernia (if harvested available
supply Mandible with soft tissues) Excellent bone stock
reconstruction Skin paddle can be suitable for
(vascularized) bulky osseointegrated
Nasal dorsum Vascularized flap implants
grafting cannot be Contour irregularities
osteotomized minimal for
Lateral femoral cancellous grafts or
nerve injury unicortical bone
Intra-abdominal harvest
organ injury
Greater Endochondral Nonvascularized Cortical — 1-2 cm cortical Small cortical Pathologic fractures Large amounts of
trochanter Cancellous bone grafts Pain cancellous bone
6-8 mL packed Cancellous graft graft available
cancellous if ilium not
bone available
Olecranon Endochondral Nonvascularized Cortical — 3-4 cm cortical Nasal bone Pain Long, durable cortical
Cancellous 1-2mL grafting Contour bone
cancellous irregularities
Rib Endochondral Nonvascularized Cortical Intercostal Variable 8-9 cm long, Nonvascularized Pain Large amounts of
Vascularized vessels (short if 2 cm wide rib for calvarial Possible cortical bone with
IMA/V intercostal May harvest reconstruction pneumothorax appropriate contour
Perforators or IMA/V, multiple ribs Vascularized rib Poor blood supply for calvarial
from long if with serratus has limited in vascularized reconstruction
TDA/V TDA/V) muscle uses (i.e., if no bone Bone is malleable and
other options No osteotomies useful in calvarial
available for possible with reconstruction
anterior vascularized bone
mandible No skin paddle
reconstruction)
Continued

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TABLE 24-5 • SOURCES OF BONE CRAFTS—cont'd

Embryonic Type of Pedicle

Bone Origin Blood Supply Bone Pedicle Length Size Uses Disadvantages Advantages

Fibula Endochondral Nonvascularized Cortical Peroneal Variable; Up to 25 cm Usually first Donor site scar Can be osteotomized
Vascularized artery and depends bone choice for most and pain safely
vein on length Skin paddle reconstructions Skin paddle may be Large amount of
of bone requiring unreliable cortical bone
required vascularized Skin paddle firmly Minimal functional loss
bone attached to the Skin paddle is
bone usually thin and
Floating toe pliable
Potential
neurovascular
injury
Potential lower
extremity ischemia
Scapula Endochondral Vascularized Cortical Circumflex 6-8 cm 3 cm wide. Composite tissue Widened scar Can provide large
scapular 11 cm long reconstruction Pain amounts of soft
artery Skin paddle requiring bone Bone stock limited tissue and bone
Latissimus and targe and usually not composite
dorsi muscle amounts of soft appropriate for Bone and soft tissue on
Rib/serratus tissue osseointegrated separate pedicles,
anterior Secondary choice implants therefore have large
muscle for mandibular Minimal ability to degree of freedom
reconstruction perform May harvest together
osteotomies with vascularized rib

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Radius Endochondral Nonvascularized Cortical Radial 12-18cm 1.5 cm wide, Composite tissue Potential ischemic Soft pliable skin cover
Vascularized Cancellous artery 5 cm long reconstruction complications in Long vascular pedicle
Skin paddle requiring bone the hand
and small Requires partial
volume of disinsertionofthe
pliable skin flexor muscles
Secondary choice Donor site scar
for mandibular Pathologic fractures
reconstruction Small amount of
Vascularized bone bone available
for small Minimal ability to
nonunions perform
Cortical bone osteotomies
grafting in the
hand/wrist
Metatarsus Endochondral Vascularized Cortical Digital 2-3 cm Whole or Thumb Short vascular Excellent neurologic
(first or vessels portion of a reconstruction pedicle recovery potential
second toe Donor site scarring One-stage repair of
toe) May be bulky for complicated hand
thumb anomalies
reconstruction Minimal donor site
(first toe) morbidity
Calvaria Membranous Nonvascularized Cortical Deep — Variable; may Caivarial Contour irregularity Good contour for
(usually) temporal harvest large reconstruction if in situ technique caivarial
Vascularized artery and amounts if Facial bone used reconstruction
vein craniotomy grafting Potential brain Readily accessible in
(periosteal performed Zygomatic injury, dural tear, facial bone grafting
perforators) reconstruction bleeding Contour irregularities
{vascularized Vascularized bone and scar hidden by
flap) has limited blood hair
supply Membranous bone has
decreased resorption
compared with
endochondral bone
for onlay bone
grafting

DCiA/V, deep circumflex iliac artery/vein; IMA/V, internal mammary artery/vein; TDA/V, thoracodorsal artery/vein.

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676 I • GENERAL PRINCIPLES
onlay and inlay graft survival in dogs. The authors
demonstrated that rigid skeletal fixation improved bone
graft survival (both weight and volume) in both mem-
branous and endochondral cortical bone inlay and
onlay grafts. In addition, bone grafts with rigid skele-
tal fixation went on to form bone union, whereas those
with wire fixation demonstrated only a fibrous union.
Lin et al444 evaluated the effect of skeletal fixation
on the survival of membranous and endochondral cor-
tical onlay bone grafts applied to areas of low motion
(snout) and high motion (femur) in a rabbit model.
The authors demonstrated that rigid fixation signifi-
cantly improved graft survival in areas of high motion,
whereas no difference in graft volume retention was
noted in areas of low motion. Rigid fixation appeared
to alter graft resorption in the early period after graft-
ing. In addition, membranous bone-derived grafts,
either fixed or unfixed, retained their volume to a
greater extent than did endochondral bone grafts.
In a clinical study, Jackson et al445 evaluated cranial
bone graft survival in nasal reconstruction in 363
patients during a 14-year period in mostly young
patients. The authors demonstrated excellent bone graft
survival and attributed this to the use of rigid
interosseous stabilization.
EMBRYONIC ORIGIN
In 1951, Peer446 noted that cortical bone grafts obtained
from endochondral bones (tibia, rib, iliac crest) and
transplanted either orthotopically or heterotopically
were replaced primarily by fibrous tissue. In contrast,
he found that bone grafts derived from membranous
bone (vomer, nasal bones, septum) maintained their
original dimensions and were not replaced by fibrous
tissue. Peer hypothesized that bones that have marked
regenerative potential from the periosteum (i.e., rib)
do not survive as well as bones that have limited regen-
erative potential. He concluded that bone cells from
different bone sources (membranous versus endo-
chondral) are differentiated such that cells obtained
from grafts of bones with limited regenerative poten-
tial are "endowed with a tenacious ability to retain their
calcified matrix regardless of their contact with bone,
whereas the cells in bone grafts with regenerative powers
do not appear to have this ability unless the graft was
in contact with living bone."446
Thompson and Casson447 confirmed the findings
of Peer using an onlay model of canine mandibular
augmentation. The authors demonstrated that
membranous bone-derived cortical bone grafts had
significantly improved survival compared with endo-
chondral grafts. LaTrenta et al441 also demonstrated
similar findings in an onlay and an inlay canine model.
Smith and Abramson 448 demonstrated that in rabbits,
subperiosteal or subcutaneous implantation ofbicor-
tical endochondral bone grafts (iliac crest) led to nearly
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complete resorption, whereas similar treatment of
membranous bone grafts (parietal calvaria) was asso-
ciated with minimal resorption. Zins and Whitaker449
compared endochondral and membranous cortical
bone grafts in primates and found that similar to the
findings in rabbits, membranous bone grafts have
improved survival. The authors hypothesized that
improved survival of membranous bone grafts may
be related to earlier revascularization and suggested
that reconstruction of osseous defects in the cranio-
facial skeleton should be performed with cranial bone
grafts whenever possible. Kuziak et al450 agreed with
Zins and Whitaker and showed that membranous bone
onlay grafts revascularize faster than endochondral
grafts.
Sullivan and Szwajkun451,452 questioned the finding
that membranous bone grafts revascularize more
rapidly than endochondral bone grafts when they
demonstrated that revascularization is accelerated in
endochondral bone in the rat. Lin et al,453 Chen and
Shih,454 and Pinholt et al455 found that revasculariza-
tion is dependent on the cancellous component of the
bone graft. Thus, no differences in revascularization
rates were noted in cortical bone regardless of its embry-
ologic origin if the volume of the cancellous compo-
nent was controlled.
Dado456 compared corticocancellous endochondral
bone grafts with cortical membranous bone grafts and
bone paste derived from each type in an onlay graft
model and found that endochondral bone-derived
grafts underwent significant resorption whereas
membranous bones did not. Interestingly, bone paste
derived from either source failed to survive to a meas-
urable extent. This finding, together with the finding
that differences in revascularization are unrelated to
the embryologic origin of the graft, provided evidence
for the hypothesis that inherent cellular or embryologic
differences are probably not responsible for the resorp-
tion of endochondral bone-derived grafts. To this end,
Hardesty and Marsh 457 suggested that improved sur-
vival of membranous grafts is due to architectural dif-
ferences, specifically the three-dimensional osseous
structure and cortical-cancellous ratio, and not the
embryologic origin or revascularization (Fig. 24-15).
They suggested that cranial bone grafts are more resist-
ant to resorption because of the thicker cortical plates»
smaller intercortical cancellous network, and stronger
cortical struts. Ozaki and Buchman 458 tested this
hypothesis in a rabbit subperiosteal cranial onlay model
by comparing cortical bone obtained from endo-
chondral (iliac) or membranous (lateral mandible)
origins with cancellous endochondral bone grafts. Graft
volume and bone architecture were then assessed by
micro-computed tomographic scanning and bone
histomorphometry. They authors found that after 16
weeks, cortical membranous bone grafts retained 56%
± 16.8%, cortical endochondral bone grafts 52.1% ±
image...
FIGURE 2 4 - 1 5 . Hardesty and
Marsh hypothesis for improved sur- CORTICAL
vival of membranous bone-derived
cortical bone grafts. Differences in
thickness of the cortical plates and
diploe lead to improved survival of
membranous bone grafts after
resorption of the cancellous inter-
cortical bone. {From Hardesty RA,
Marsh JL: Craniofacial onlay bone
grafting: a prospective evaluation
of graft morphology, orientation, and
embryonic origin. Plast Reconstr CORTICAL
Surg I990;85:5.)
76.6%, and cancellous endochondral bone grafts 2.1 %
± 4.1% of their original volumes. The differences
between cortical membranous and cortical endo-
chondral bone grafts were not statistically significant.
In a follow-up study, Buchman and Ozaki459 found no
significant differences in the ultrastructure (bone
volume fraction, bone surface area to bone volume,
trabecular number, and anisotropy) of endochondral
and membranous cortical bone grafts.
PERIOSTEUM
Peer446 demonstrated that onlay bone grafts harvested
with their periosteum intact have improved survival.
Vainio460 found that preservation of periosteum
improved inlay bone graft survival. Thompson and
Casson447 compared grafts with and without perios-
teum and grafts placed with their cortex facing the bone
or soft tissues and demonstrated that preservation of
periosteum improved survival by approximately 10%.
In addition, the authors noted periosteal hypertrophy
and osteocyte proliferation resulting in improved peri-
pheral bone growth in grafts with periosteum. Thomp-
son and Casson theorized that the periosteum played
an important role in revascularization and emphasized
the importance of blood supply in graft survival.
Knize461 studied the role of periosteum in onlay
bone graft (iliac crest) survival on the nasal bones of
rabbits and demonstrated severe volume loss when
the periosteum was removed. In contrast, grafts in
which periosteum was preserved demonstrated
improved survival, especially when periosteum was
placed in contact with the soft tissues. Like Thomp-
son and Casson, Knize theorized that periosteal
preservation improved revascularization of the graft,
thus enabling survival of the outer cortical bone, par-
ticularly in bone devoid of medullary blood supply.
In addition, Knize thought that periosteum may be a
source of osteogenic cells.
Burstein and Ariyan462 used tetracycline fluorescence
incident photometry, a new technique described by
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24 • REPAIR AND CRAFTING OF BONE 677
ENDOCHONDRAL ORIGIN
CANCELLOUS
MEMBRANOUS ORIGIN
DIPLOE
the authors, to quantitate new bone formation in canine
rib grafts with or without periosteum. Periosteal
preservation significantly increased new bone forma-
tion in both cortical and trabecular bone. In a follow-
up study, the authors demonstrated that grafts
transplanted with an intact periosteum remain cellu-
lar with little osteoclastic bone deposition. In addi-
tion, the cortical bone contains numerous osteoblasts
actively depositing bone along the haversian canals,
trabecular bone spaces, and endosteal lining. High-
magnification views of the periosteum demonstrated
three distinct layers: the inner cambial layer, the
middle layer of "osteogenic reserve cells " and an outer
vascular network of arterioles and venules. Rib grafts
transplanted without the periosteum were largely
acellular with minimal cortical osteogenesis, loss of
cortical cellularity, and osteoclastic bone resorption.
Quantification of new bone formation by tetracycline
fluorescence incident photometry revealed a 26% and
29% decrease in the cortical and trabecular compart-
ments, respectively. Microfil studies demonstrated vas-
cular channels running parallel to the cortical bone
surface only in grafts harvested with periosteum. The
authors speculated that the outer vascular network may
be responsible for early graft revascularization through
the process of inosculation.
GRAFT ORIENTATION
Numerous studies have evaluated the effect of graft
orientation with respect to the periosteal and cortical
bone surfaces on graft survival. In general, graft
survival is improved when the periosteal surface of
the graft is directed toward the soft tissues and the
cancellous surface is placed in contact with the host
bone.447,457,461,463 Most researchers think that improved
survival is related to earlier revascularization.
RECIPIENT BED
The recipient bed is an important determinant of bone
graft survival. This effect is probably a multifactorial
678 I • GENERAL PRINCIPLES
regulator and may be related to vascularity and
mechanical stress. Various regions of the craniofacial
skeleton are thought to be resorptive (i.e., promote bone
graft resorption), whereas others are thought to be
depository/ 6,1 Enlow464 hypothesized that these changes
result from continual remodeling by bone deposition
onto the periosteal surfaces in depository areas and
periosteal resorption in resorptive areas. Zins et al46J
evaluated cortical endochondral bone graft survival
in depository (nasal snout and mandibular body) and
resorptive (buccal surface of the mandible) areas of
the craniofacial skeleton of immature rabbit. The
authors demonstrated that after 3 months, bone grafts
to periosteal depository regions (snout and mandibu-
lar body) maintained significantly more volume than
did those placed in periosteal resorptive areas.
LaTrenta et al440 compared the survival of cortical
onlay bone grafts with wire fixation or rigid skeletal
fixation and placed in depository (mandible) or
resorptive (maxilla) regions of the canine craniofacial
skeleton. Using multivariate analysis, the authors
demonstrated that embryologic origin (membranous
bone) and fixation (rigid skeletal fixation) were equally
important in bone graft survival. The recipient site,
however, was not a significant determinant, even as
long as 4 months postoperatively. The authors con-
cluded that onlay bone graft survival in mature
animals, in contrast to growing animals, is little
changed by graft placement at resorptive or deposi-
tory recipient sites.
Bone graft revascularization has been hypothesized
to be an important determinant of graft survival.
Kusiak et al450 used microangiographic techniques to
study the rate of vascularization of membranous and
endochondral cortical onlay bone grafts in adult New
Zealand White rabbits and demonstrated that mem-
branous bone grafts revascularize more rapidly and
completely than endochondral bone grafts. In addi-
tion, the authors showed that the dense cortical sur-
faces of the membranous bone grafts did not act as a
physical barrier to new vessel ingrowth. The authors
correlated this more rapid revascularization with
improved survival of membranous bone grafts and
suggested that locally produced humoral or diffusible
factors were responsible for accelerated membranous
bone revascularization. In addition, although they did
not demonstrate a direct cause-and-effect relationship,
the authors thought that enhanced survival of mem-
branous bone grafts, similar to other tissues, was related
to prompt vascularization.
In a study using mature New Zealand White rabbits,
LaTrenta et al441 evaluated onlay bone graft survival
under nonexpanded and expanded skin and demon-
strated significantly improved bone graft survival in
onlay bone grafts placed under expanded skin 2 weeks
after expander removal, compared with immediate
bone graft placement or placement under nonexpanded
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skin. The authors suggested that the improved vascu-
larity of the capsule and expanded skin allowed more
rapid revascularization of onlay bone grafts, thus
leading to improved survival.
An important determinant of bone graft revascu-
larization is the vascularity of the recipient bed.
Support for this hypothesis can be derived from the
fact that bone grafts heal poorly in irradiated tissues,
in which the microcirculation is damaged, as well as
from the finding that bone graft healing can be
improved by implementing techniques designed to
augment the vascularity of radiation-damaged tissues
(e.g., hyperbaric oxygen and the use of microvascular
bone transfers).465'467 For example, Lukash et al468
studied bone graft healing in irradiated tissues of a
rabbit model and demonstrated that rib grafts placed
in irradiated chest wall defects had minimal revascu-
larization, underwent significant resorption, and
healed with fibrous union. In contrast, rib grafts
wrapped with healthy (i.e., nonirradiated) latissimus
dorsi muscles revascularized rapidly, maintained bone
volume, and healed with bone union. The authors con-
cluded that the vascularity of the recipient bed is an
important regulator of bone graft revascularization and
survival.
Eppley et al154 studied the effect of exogenously
applied basic FGF-2 on endochondral bone-derived
cortical bone graft healing in rabbit mandibular
defects and demonstrated marked increase in new vessel
ingrowth lOand 14 days postoperatively. The authors,
however, failed to demonstrate significant differences
between FGF-2-treated bone grafts and controls. In
a follow-up study, Eppley et al153 evaluated the effects
of continuous FGF-2 administration on bone graft
healing in an irradiated bed of a rabbit mandibular
defect model. The authors demonstrated that in all
control animals (i.e., non-FGF-2 treated), bone grafts
underwent necrosis, sequestration, and failure to heal
to the recipient osseous margins. In contrast, in recip-
ient sites treated with FGF-2 before bone grafting,
nearly 50% of animals demonstrated bone healing and
active bone formation at the cortical margins adjacent
to the recipient sites. Furthermore, FGF-2 pretreatment
animals demonstrated significant increases in new
vessel ingrowth compared with controls. The authors
concluded that improved vascularity at the recipient
bed secondary to FGF-2 pretreatment led to improved
bone graft survival.
Although it is clear that a well-vascularized recip-
ient bed is a critical component to successful bone
grafting, it is not entirely clear whether bone graft revas-
cularization necessarily improves long-term graft
survival. A study by Fisher and Wood469 comparing
revascularization of cortical bone grafts (iliac) covered
with skin or muscle flaps in Yorkshire pigs is an example
of this disparity. Using radioactive microsphere
injections, the authors demonstrated that 4 weeks
image...
postoperatively, blood flow to bone grafts covered by
musculocutaneous flaps (0.22mL/g/min) was nearly
half that of unoperated bone segments and was sig-
nificantly greater than that of bone grafts placed
beneath skin flaps (0.001 mL/g/min). In addition, bone
grafts placed beneath muscle flaps demonstrated less
marrow necrosis, the presence of active osteoblasts and
osteoclasts along bone trabeculae, live osteocytes
within lacunae, vascular channels, and proliferating
fibrous tissue. In contrast, analysis of bone beneath
cutaneous flaps demonstrated necrotic marrow with
empty lacunae. Increased blood flow, however, did not
correlate with increased bone graft survival and
mechanical strength. In fact, the cortex of bone
beneath muscle flaps was soft and could be easily cut,
whereas bones beneath cutaneous flaps were sclerotic
and hard. The authors concluded that these differences
were due to vessel ingrowth with subsequent bone
resorption and fibrous tissue proliferation in bone
grafts covered by muscle flaps. It is possible, however,
that revascularization of bone grafts placed beneath
muscle flaps augmented cellular survival and led to
increased bone resorption due to the heterotopic place-
ment and absence of strain of these grafts.
Using an immature rabbit model, Ermis and Poole 122
studied the survival of iliac crest onlay bone grafts
placed in subcutaneous or submuscular pockets. They
showed that after 4 months, submuscular graft place-
ment in resorptive areas (buccal surface of the
mandible) or heterotopic placement (i.e., not in
contact with bone) was associated with statistically
increased graft resorption compared with subcuta-
neous placement. In contrast, no significant differences
were noted in grafts covered with muscle or skin flaps
and placed in depository areas. The authors attributed
increased submuscular bone graft resorption to
"movement imparted to the graft which impairs vas-
cularization or in some other way leads to greater
resorption"
Vascularized Bone Transfers
HISTORY
Early attempts at vascularized bone transfers involved
cranial bone transferred with periosteal or cutaneous
pedicles. Huntington 470 reported the first successful
vascularized fibula transfer in a series of clinical cases
with large tibial bone defects. He emphasized the supe-
riority of vascularized bone transfer by demonstrat-
ing excellent bone repair in situations in which bone
healing would otherwise be unexpected. Transfer of
bone with its intrinsic blood supply maintains the via-
bility of bone cells and bone matrix, thus avoiding the
need for creeping substitution as in nonvascularized
grafts.
The use of vascularized bone transfers was also an
important advance in the treatment of segmental bone
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24 • REPAIR AND GRAFTING OF BONE 679
loss in the craniofacial skeleton resulting from cancer
ablation or trauma. Blair"'71 reported the successful
transfer of a vascularized osteocutaneous composite
flap for the reconstruction of a large mandibular defect
after tumor resection. Blair and others noted the
marked superiority of primary repair associated with
vascularized transfers compared with free bone grafts,
especially after radiation therapy.
The introduction of microsurgical techniques has
vastly expanded the surgical options in bone recon-
struction. Ostrup and Fredrickson472 were the first to
describe the microvascular transfer of a rib by trans-
planting the canine ninth rib to a mandibular defect
in the same animal using the posterior intercostal artery
and vein. Control animals underwent rib grafting
without microvascular anastomosis. Evaluation at 8
weeks postoperatively revealed successful bone healing
with no evidence of bone resorption in the experi-
mental animals (with microvascular anastomosis),
whereas control animals had significant resorption and
failed to demonstrate bone healing. After microvas-
cular transfer, the rib marrow and periosteum were
found to be viable with only patchy osteocyte loss,
whereas grafted bone appeared to be completely
necrotic with loss of nearly all osteocytes. Thus, the
authors demonstrated that microvascular transfer of
bone flaps can, in contrast to free bone grafting, main-
tain viability of the majority of bone-producing cells,
leading to more rapid and complete bone union. In
this setting, the healing of vascularized bone segments
can be thought of as segmental bone repair without
the need for creeping substitution.
Taylor et al473 were the first group to report the clin-
ical use of free vascularized bone transfer and described
a contralateral fibula flap for the treatment of exten-
sive lower extremity bone loss. Buncke et al474 reported
the first clinical case involving an osteocutaneous
flap reconstruction of a tibial defect by use of vascu-
larized rib. These studies demonstrated the superior-
ity of vascularized bone flaps for the treatment of
bone defects longer than 6 cm. Since these prelimi-
nary reports, the successful use of vascularized bone
flaps has been reported by a number of groups for
the treatment of traumatic lower extremity bone
defects, osteomyelitis, postablative defects, avascular
necrosis of the hip, and congenital pseudarthrosis of
the tibia.
BLOOD SUPPLY OF VASCULARIZED
BONE GRAFTS
A number of studies have attempted to identify the
critical blood supply of vascularized bone transfers.
The early studies with vascularized rib transfers em-
phasized the use of the posterior intercostal artery
because this vessel was thought to give rise to the endos-
teal blood supply (nutrient vessel) of the rib.426,472,475
680 I • GENERAL PRINCIPLES
Ariyan"176,477 reported the use of vascularized rib
transfers based only on the periosteal blood supply
through the internal mammary artery and demon-
strated excellent clinical outcomes in a limited number
of patients. He speculated that collateral circulation
was able to maintain the viability of the deeper
portions of the bone. Berggren et aI47MW compared
vascularized rib transfers with intact medullary and
periosteal blood supplies (posterior grafts) to grafts
with only periosteal blood supply (posterolateral
grafts) in dogs using a mandibular defect model. The
authors found that although osteocytes and osteoblasts
can survive transplantation in both circumstances, sur-
vival of bone cells and marrow contents is not as com-
plete in bone grafts with only periosteal blood supply.
In a follow-up study, Berggren et al480 re-evaluated
osteocyte survival after transfer of rib grafts to sub-
cutaneous tissues and found minimal differences in
viability of grafts transferred with or without an intact
medullary blood supply. In addition, the authors
demonstrated that elimination of the medullary blood
supply did not alter cortical blood flow, a finding that
led them to conclude that collateral circulation from
a dual blood supply to cortical bone can maintain vas-
cularized bone transfers, therefore eliminating the need
for more complicated tissue harvest.481
ADVANTAGES OF VASCULARIZED
BONE GRAFTS
Puckett et al482 compared nonvascularized fibular
bone grafts with vascularized rib transfers or vascu-
larized periosteum in a 4-cm non-stress-bearing
fibular bone defect in a dog model. Animals treated
with vascularized periosteum did not demonstrate sig-
nificant bone healing. In contrast, animals from both
nonvascularized and vascularized groups demon-
strated excellent new bone formation with a stress tol-
erance of 68.5% of normal bone in nonvascularized
grafts and 90.5% in vascularized transfers. The lack
of significant differences in stress tolerance together
with the finding that both vascularized and nonvas-
cularized transfers had similar nonunion rates led the
authors to conclude that vascularized bone transfers
are best suited for situations in which traditional graft-
ing techniques would be unsuccessful.
Long bone defects, extensive scarring, and a history
of irradiation or infection of recipient beds represent
common problems in reconstructive surgery and are
the most frequent indications for vascularized bone
transfer. In these settings, revascularization of the bone
graft is delayed with resultant bone graft necrosis,
resorption, and nonunion. Vascularized bone trans-
fers avoid the need for revascularization from the
surrounding tissues and maintain viability of the
bone cells and bone matrix. In addition, vascularized
bones are transferred with healthy soft tissue, thereby
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Dr.Mustafa D.
improving the blood supply of the recipient bed.These
factors lead to improved vascularity surrounding the
bone defect and significantly improve the odds of suc-
cessful bone repair.475'477
Increased Strength and More
Rapid Healing
Vascularized bone grafts have significantly higher bio-
mechanical properties than nonvascularized grafts.
This phenomenon was described by Moore et al,483 who
demonstrated that vascularized bone transfers were
more than 234% stronger than conventional grafts in
a canine model. In addition, vascularized transfers were
nearly 500% more resistant to energy absorption (a
property they termed bone toughness) and had an
elastic modulus that was 263% greater. Thus, vascu-
larized bone transfers have increased strength com-
pared with traditional bone grafts and should be
considered when more rapid healing is desired.
Maintenance of Growth Potential
Numerous studies have shown that vascularized bone
grafts maintain the potential for growth in immature
animals. For example, Nettelblad et al484 demon-
strated that in the axial skeleton, microvascular trans-
fer of bone together with its epiphyseal plate results
in nearly normal growth compared with nonvascu-
larized epiphyseal grafts. Using an immature canine
model, Antonyshyn et al485 have demonstrated that
vascularized onlay bone grafts maintain potential
for growth, albeit somewhat less than undisturbed
bone does.
•
CLINICAL USES OF BONE
TRANSFERS
Tibia
Mention of tibia transfer is made only as a historical
note. The tibia was used during World War I and several
years thereafter as a source of cortical and cancellous
bone grafts. Bone is harvested from the anteromedial
surface of the tibia by a curvilinear incision parallel
to the tibial crest (Fig. 24-16). Grafts are harvested by
a chisel or gouge together with the overlying perios-
teum. Small bone graft harvests are well tolerated.
However, harvesting of corticocancellous grafts may
produce contour irregularities, pain, and pathologic
fractures and as such is not recommended.
Ilium
NONVASCULARIZED GRAFTS
The ilium is an excellent source of cortical and can-
cellous bone grafts because it is easily accessible, leaves
no significant contour deformity, and can provide an
abundant amount of bone. The primary criticism of
image...

24 • REPAIR AND GRAFTING OF BONE 68

this donor site is postoperative pain due to muscle

spasm.

Nonvoscularized Iliac Bone Croft Harvest

A B
FIGURE 2 4 - 1 6 . Tibial bone grafts. A, Incision for
removal of the graft. B, Removal of the graft with an
osteotome. (From Cutting CB, McCarthy JG, Knize DM:
Repair and grafting of bone. In McCarthy JG, ed: Plastic
Surgery, vol 1. Philadelphia, WB Saunders, 1990:583-
629.)
in Adults
Cortical and cancellous grafts are best harvested from
the thickest portion of the bone, measuring between
1.3 and 1.7 cm, between the anterior superior iliac spine
and the tubercle of the crest (Fig. 24-17). An incision
is made with the skin retracted superiorly such that
when retraction is released, the incision lies below the
iliac crest, is thus inconspicuous, and does not overlie
the bone prominence (Fig. 24-18). In the adult, the
incision is carried down through the superficial fascia,
the tensor fascia lata muscle and tendon, and the perios-
teum. The periosteum is reflected with a periosteal ele-
vator, exposing the crest and the inner and outer tables
as necessary. It is important not to disturb the tendi-
nous attachments to the anterior superior iliac spine
because these attachments play an important role in
the stabilization of the knee and hip joints. To harvest
cancellous bone graft, the cortical bone is split with
an osteotome directed parallel to the bone (Fig. 24-
19). In addition, perpendicular osteotomies can be
made at the medial and lateral extents of the cortical
split osteotomies to limit extension of the fracture line
and to maintain the integrity of the anterior superior
iliac spine. Cancellous bone grafts may be harvested
with a large curet or alternatively as a wedge. The inner
and outer cortical tables are reapproximated to elim-
inate dead space, and the closure of the periosteum
and soft tissues is performed with heavy sutures. In
addition, cortical bone can be harvested from the inner

A B C
FIGURE 2 4 - 1 7 . Removal of bone from the ilium. A, The periosteum has been incised and is being raised by an ele-
vator. B, Resection of bone from the crest. C, Resection of bone from the inner table. (From Cutting CB, McCarthy JG,
Knize DM: Repair and grafting of bone. In McCarthy JG, ed: Plastic Surgery, vol 1. Philadelphia, WB Saunders, 1990:583-
629.1

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image...
682 I • GENERAL PRINCIPLES
FIGURE 2 4 - 1 8 . Exposure of the crest of the ilium for
bone graft. A, The patient's hip is elevated by a sandbag
to make the iliac crest prominent. The assistant presses
a gauze pad against the skin just below the crest of the
ilium and retracts the skin over the crest. The skin inci-
sion lies lateral to the crest of the ilium. (From Cutting
CB, McCarthy JG, Knize DM: Repair and grafting of bone.
In McCarthy JC, ed: Plastic Surgery, vol 1. Philadelphia,
WB Saunders, 1990:583-629.)
table as needed. This technique does not leave a visible
contour deformity and is, in general, well tolerated if
postoperative ambulation is started early.
Robertson and Baron486 described a technique by
which large amounts of cancellous bone graft can be
harvested by sectioning the ilium below the crest and
reflecting the bone to allow access to the cancellous
bone. Bone graft is harvested as described before, and
the bone cap is replaced in its original position, thus
preserving the origin of the abdominal muscles.
A number of trephine devices have become avail-
able to harvest cancellous bone grafts with minimal
incisions and tissue dissection. The devices are well
tolerated and can yield large amounts of cancellous
bone grafts. Care should be taken to avoid disturbance
of the anterior superior iliac spine as well as peritoneal
perforation with disruption of the inner cortex.
For cortical bone grafts, a similar exposure is per-
formed and the periosteum is reflected. The desired
bone graft size is marked on the bone and harvested
with an osteotome or sagittal saw. If unicortical bone
is desired, the inner cortex is used preferentially
because elevation of the periosteum is easier over the
smooth surface compared with the lateral surface,
which has numerous grooves for the insertion of gluteal
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muscles. The inner cortex is delineated by elevating
the periosteum away from the origin of the iliac muscle,
thus exposing a portion of the iliac fossa. A section of
the inner cortex is harvested by making a vertical cut
in the inner cortex and crest and separating the bone
from the outer cortex. Care must be taken to avoid
injury to the overlying iliac muscle to prevent peri-
toneal perforation. In addition, resection of the ante-
rior superior iliac spine should be avoided if at all
possible to prevent contour deformity and potential
gait abnormalities.
In general, less postoperative pain and easier ambu-
lation are associated with unicortical (i.e., inner table)
bone graft harvests than with full-thickness grafts.
Increased discomfort at the donor site is likely due to
more extensive muscle and periosteal stripping asso-
ciated with full-thickness harvests. Postoperative pain
in full-thickness bone graft harvests maybe alleviated
by limited dissection and careful reapproximation of
the periosteum, gluteal muscles, and tensor fascia lata.
The lateral femoral cutaneous nerve must be pro*
tected during iliac cortical or cancellous bone graft
harvest because damage to this nerve can produce
paresthesia, hypoesthesia, and even dysesthesia in the
region of the outer thigh. The nerve follows a retroperi-
toneal course across the deep surface of the iliac muscle
and leaves the pelvis by a variable route. The most
common route is deep to the attachment of the
inguinal ligament to the anterior superior iliac spine;
however, it may pass through the ligament or across
the spine.487
The removal of large segments of the ilium, failure
to repair the fascial attachments to the ilium, or dis-
ruption of the inguinal ligament may result in hernia
formation. In addition, hematoma formation may
complicate iliac bone graft harvests, particularly if a
large dead space remains between the bone and the
detached muscle. Gelfoam soaked with thrombin or
bone wax maybe used to stop bleeding from bone sur-
faces. In addition, repair of the separated muscle to
the remaining bone and the possible use of closed
suction drains may prevent small fluid and blood
collections.
Nonvascu/orized Iliac Bone Croft Hon/est
in Children
APPLIED ANATOMY. At birth, the iliac crest is com-
posed of a thick cartilage cap that later ossifies to form
the rim and superior portions of the ala. By the age of
9 years, the cap has significantly decreased in size and
measures approximately 1 cm.488 Toward the end of
puberty, ossification centers appear and lead to com-
plete ossification of the cartilage by the age of 20 to 25
years. In children, as in adults, the region of the ante-
rior superior iliac spine should not be disturbed because
this area is an important attachment of ligament and
muscle support of the lower extremity.
image...

24 • REPAIR AND GRAFTING OF BONE 683

FIGURE 2 4 - 1 9 . A technique for removal of cancellous bone from the ilium. A, Incision of
the periosteum after exposure of the crest. B, Separation of the cortex with an osteotome.
C, Cross section showing lines of separation of the inner and outer cortex from the cancel-
lous bone. D, Exposure of cancellous bone. E, Cross section showing exposure. F, Reunion
of the inner and outer cortex by stainless steel wire suture. (After Tessier; see also Wolfe
SA, Kawamoto HK: Taking the iliac-bone graft. J Bone Joint Surg 1978;60:411.) C, Blocks
and lamellae of cancellous bone obtained. (From Cutting CB, McCarthy JC, Knize DM: Repair
and grafting of bone. In McCarthy JC, ed: Plastic Surgery, vol 1. Philadelphia, WB Saunders,
1990:583-629.)

TECHNIQUE. The pelvis is rotated 30 to 40 degrees
away from the surgeon by use of a roll. The skin is
prepared away from the anterior superior iliac spine,
exposing the anterior half of the iliac crest. Care should
be taken to avoid use of instruments that have been
used in a nonsterile area (e.g., during alveolar bone
grafting). The skin is retracted medially and superi-
orly, and a skin incision is made approximately 2 cm
posterior to the anterior superior iliac spine. Skin
retraction ensures that the incision does not lie directly
over the bone prominence and is hidden in the under-
wear line. The wound is extended through the super-
ficial fascia and the fascia lata and the muscle below
by electrocautery. The bone is exposed approximately
2 cm below the curve of the crest, and subperiosteal
dissection is performed. The overlying cartilage cap
is split while care is taken to avoid the disruption of
the attachment of the periosteum to the epiphyseal
line. Corticocancellous grafts can be harvested with a
curved osteotome starting at a point at least 1.5 cm
posterior to the anterior superior iliac spine.488 Can-
cellous bone grafts may be obtained by splitting the
bone with an osteotome and harvesting the bone with
a large curet or gouge.
The wound is closed carefully in layers with repair
of the fascia lata, muscle, Scarpa fascia, and skin. Repair
of the fascia lata and reapproximation of the bone cor-
tices aid in hemostasis and can prevent contour defor-
mities. A closed suction drain may be used for 24 hours;
however, this is not usually necessary if hemostasis is

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684 I • GENERAL PRINCIPLES

obtained. The proper closure of the fascia lata and the
tensor fascia lata muscle is the most critical portion
of this operation because inappropriate repair may
lead to prolonged pain, bleeding, and abnormal gait.
VASCULARIZED ILIAC B O N E TRANSFER
The ilium can be used as a source of vase ularized bone.
The flap may be harvested as an osteocutaneous flap
based on the deep circumflex iliac artery (DCIA) or
as an osseous flap (posterior iliac crest) based on the
superior gluteal artery (Fig. 24-20,).
The groin-iliac crest DCIA flap can yield a rela-
tively large segment of bone—as large as 4 cm wide
and 11 cm long with a skin paddle measuring 8 cm
wide and 14 cm long.489 This flap, although a second-
ary choice, is most useful in hemimandibular recon-
struction but can also be used for lower extremity
reconstruction. Reconstruction of long bones is limited
because of the curvature of the bone. The primary
advantages of this flap include the maintenance of an
endosteal and periosteal circulation, low donor site
morbidity, and relatively long vascular pedicle (4 to
6 cm). The disadvantages include a difficult dissec-
tion, curvature of the bone, bulky soft tissue, and
hypoesthesia of the lateral thigh due to sacrifice of the
lateral femoral cutaneous nerve. In addition, gait
abnormalities and abdominal herniation may occur
if the tensor fascia lata and the fascia lata muscle are
not closed appropriately. The use of alloplastic mate-
rial for closure of the fascial defects may be associated
with infection. Finally, harvest of a skin paddle often
requires augmentation of the vascular supply by a vein
graft from a branch of the DCIA to the superior cir-
cumflex artery.
The posterior iliac crest flap is indicated as a poten-
tial bone source for segmental bone loss resulting from
irradiation, trauma, or tumor resection. In addition,
this flap has been used in the treatment of diaphyseal
pseudarthrosis.400 Similar to the groin-iliac crest DCIA
flap, this bone flap has an excellent blood supply with
an acceptable donor site. The disadvantages of the flap
include the lack of a cutaneous paddle, difficult dis-
section, and limited bone supply (approximately 5 to
6 cm long, 4 to 5 cm wide, and 2cm thick).
Greater Trochanter and Olecranon
The greater trochanter and olecranon are usually sec-
ondary choices as cortical and cancellous bone donor
sites. Cortical bone from the olecranon has been used
for nasal reconstruction as an alternative to cranial bone
grafts.491 In addition, the olecranon can provide a
limited supply (approximately 2 to 3 mL) of cancel-
lous bone graft.492 An incision is made over the prox-
imal end of the olecranon process and extended down
through the periosteum. After subperiosteal dissection,
an appropriate section of bone can then be removed
with an osteotome or powered sagittal saw. Cancel-
lous bone graft can be harvested with a curet.
Bone from the greater trochanter can be harvested
through a 3- to 4-cm vertical incision directly over the
bone. The fascia lata and tendon are divided and the
periosteum is elevated. An osteotome can be used to

Ascending
branches

Internal oblique m.

External -V-—Transversus
J
oblique m abdominis m,

Deep circumflex
iliac a, & v.

FIGURE 2 4 - 2 0 . The deep circumflex artery vascularized bone flap. Vascularized bone based on the deep circum-
flex iliac artery and vein (DCIA/DCIV) is harvested and can be taken with an overlying skin paddle.

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TtJWt^aeleMtf image...
harvest a 1- to 2-cm section of unicortical bone. A
large volume of cancellous bone (approximately 6 mL
of packed bone graft) can be harvested with a curet.
Cancellous bone grafts from the greater trochanter may
be used as a secondary source of autogenous bone graft
when more bone graft is required than is available from
the iliac crest or, alternatively, in patients who have
had previous iliac crest bone graft harvests.493
Bone harvests from these areas are usually well tol-
erated with limited postoperative morbidity. Ambu-
lation after greater trochanter bone graft harvest is said
to be less painful than after bone graft harvest from
the iliac crest.
Rib
NONVASCULARIZED RIB GRAFTS
Rib grafts were initially used as full-thickness grafts
for mandible and cranial reconstruction.430 This donor
site fell into disfavor, however, because revasculariza-
tion was possible only through the cut ends of the
bone, resulting in necrosis and eventual resorption or
infection. Splitting of the rib increases the surface area
of cortical bone available for reconstruction and
improves vascular ingrowth by exposing the cancel-
lous border of the bone to the soft tissues of the recip-
ient site.494 Thus, nonvascularized rib grafts can
provide a large supply of cortical bone with accept-
able donor site deformity. In addition, the rib can
regenerate repeatedly and provide a continual source
of autogenous cortical bone.
Surgical Technique
An incision placed directly over the anterior portion
of the seventh rib can yield moderate amounts of cor-
tical bone as a single rib. Alternatively, the posterolat-
eral thoracoplasty approach over the seventh rib can
be used to harvest a large amount of bone because this
exposure enables dissection of three or four ribs of
longer length. Alternating ribs should be removed, and
each rib bed should be closed separately with a
running suture to prevent segmental collapse and to
promote bone regeneration.494 Chest wall deformities
can result from multiple rib harvests.
The posterior thoracoplasty incision is performed
with the patient in the lateral decubitus position (Fig.
24-21). The incision is made parallel to the seventh rib
from the posterior to the anterior axillary line. The
dissection is carried down through the latissimus dorsi
muscle, and the fibers of the serratus anterior are sep-
arated. By elevation of the scapula, a fascial plane is
entered, allowing exposure of the second to tenth ribs.
Alternating ribs can be harvested in a subperiosteal
plane. Care must be taken to avoid pleural perforation.
If pleural perforation does occur, it may be repaired
with an absorbable suture after the introduction of a
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24 • REPAIR AND GRAFTING OF BONE 685
red rubber catheter placed under water seal in con-
junction with positive-pressure ventilation to inflate
the lungs fully.
After the rib is harvested, the periosteum should
be closed with a running suture to allow rib regener-
ation. The harvested rib is split longitudinally with a
large scalpel blade. The split graft can then be shaped
and contoured to fit the defect. At the time of fixation
(wire or plates and screws), it is important that the
rib graft is placed in the defect under compressive forces
(Fig. 24-22).
VASCULARIZED RIB CRAFTS
Vascularized rib grafts can be based on a nutrient
(endosteal) or periosteal pedicle. The original descrip-
tion of vascularized rib grafts discussed the use of the
posterior rib segment containing both the endosteal
and periosteal blood supply.472,473,475 This pattern of
blood flow was thought to provide the most reliable
blood flow to the bone segment and thus to optimize
osteoblast survival. However, this vascular pedicle is
short and extremely difficult to dissect because the
nutrient vessels of the rib take off from the posterior
intercostal vein and artery and enter the bone j ust distal
to the costovertebral junction. In addition, separate
repositioning of the patient is usually required for
donor and recipient site dissections. These short-
comings led to experiments with vascularized rib trans-
fers based only on a periosteal blood supply. The
posterolateral-lateral rib periosteal flap, intercostal flap,
and anterior rib periosteal flaps have been well
described.476'477'495"497
The posterolateral-lateral rib periosteal flap is based
on the posterior intercostal artery and vein. The vessels
supply the interosseous segment of the rib through
multiple periosteal and musculoperiosteal perfora-
tors.495"497 The inner cortex of the bone is perfused
through collateral vessels. In general, the 10th or 11th
rib is selected, and an overlying intercostal flap (8 to
10 cm wide and 5 to 20 cm long) is harvested. The
primary advantages of the posterolateral-lateral rib flap
include a well-vascularized bone segment (2 to 15 cm
in length), technically simple dissection, adequate
pedicle length potential for a cutaneous paddle,
primary closure of the donor site, limited bulk, and
lack of need for unique repositioning of the patient.
The advantages are offset by the morbidity of a tho-
racotomy, the relatively small volume of bone harvested,
and the difficulty in contouring.
The anterior periosteal flap is based on the inter-
nal mammary artery and vein. In general, the fourth
or fifth rib is selected and can provide an osseous
segment approximately 8 to 9 cm in length with a
musculocutaneous paddle measuring 10 cm wide and
20 cm in length.476,477 The length of the osseous segment
is limited medially by the costal cartilage and laterally
686 I • GENERAL PRINCIPLES
f/S/h
by the midclavicular watershed area. The advantage of
the flap is that the dissection is performed with the
patient in the supine position; thus, no repositioning
is required, and both donor and recipient sites can be
dissected simultaneously. In addition, the dissection
is relatively simple. The disadvantages of this flap are
similar to those of the posterior rib flap: a relatively
short bone segment, a small volume of bone, the need
for a thoracotomy, and the difficulty of contouring the
rib segment.
Fibula
The fibula has become the donor site of choice for long
bone free flaps. In addition, the versatility of this
flap has made it the primary source of bone for
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FIGURE 2 4 - 2 1 . A and B, Removal
of full length of rib by the subperiosteal
technique. The Doyen elevator is used
to free the periosteum of the rib bed.
C Closing the periosteal bed with a
running chromic catgut suture. D and
f. Technique of splitting the rib with a
No. 10 knife blade. (From Cutting CB,
McCarthy JG, Knize DM: Repair and
grafting of bone. In McCarthy JG, ed:
Plastic Surgery, vol 1. Philadelphia, WB
Saunders, 1990:583-629.)
mandibular reconstruction.497,498 The flap is based on
the peroneal artery and vein, which provide both an
endosteal and periosteal blood supply (Fig. 24-23).
Using this pedicle, one can obtain up to 28 cm of vas-
cularized cortical bone. The advantages of this flap
i nclude an excellent blood supply, large volume of bone
(ideal for long bone defects), minimal donor site mor-
bidity, relative ease of contouring, potential for simul-
taneous donor and recipient site dissection, and
reliable skin paddle. In addition, the excellent blood
supply, as well as the muscle cuff associated with trans-
fer, leads to rapid graft union in uncomplicated repairs
and improves the chance of success in compromised
recipient beds (i.e., irradiation, scarring, infection). The
disadvantages of the free fibula flap include a relatively
difficult and lengthy dissection, potential injury to the
image...

24 • REPAIR AND CRAFTING OF BONE 687

FIGURE 2 4 - 2 2 . The use of split rib grafts for cranial contour deformities. A, Split rib grafts contoured to fit
snugly against the skull during reconstruction of a cranial defect. B, Scalp flap placed back in position, restoring cranial
contour.

Popliteal
a. &v.

Deep peroneal n.,

anterior tibial a. & v.
Extensor digitorum
Anterior & extensor hallucis
tibial a. & v. Posterior
tibialis m.
Flexor
Posterior digitorum Peroneus brevis
tibial a. & v. longus m. longus m.

Peroneal
a.&v.

Fibular
flap

Fibula with skin

paddle
Posterior
tibial a. & v.(
tibial n.

Peroneal a. & v.

Gastrocnemius m. Flexor hallucis

longus m.

FIGURE 2 4 - 2 3 . The fibula free flap. Vascularized fibula is based on the peroneal artery and vein pedicle and can
be raised with or without an overlying skin paddle.

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688 I • GENERAL PRINCIPLES
peroneal and tibial nerves, poor donor scar, relatively
short pedicle length (if the full length of bone is
required), and insufficient blood flow to the epiph-
ysis. Thus, if bone growth is desired, additional time
is required to dissect and anastomose the anterior or
posterior branches of the anterior tibial artery because
this is the primary vascular supply of the proximal fibula
epiphysis. In addition, attachment of the skin paddle
to the bone by a thin intermuscular septum compli-
cates the dissection because of potential injury to the
perforators and limits mobility of the skin paddle in
relation to the bone.
Scapula
The scapula may also be used as a source of vascu-
larized bone. The transfer may be as composite skin
and osseous segment of the lateral portion of the
scapula as a free flap based on the musculoperiosteal
branches of the circumflex scapular vessels. The
medial osseous segment may also be harvested as a
composite flap with the scapular flap; however, the
blood supply of this segment is thought to be less reli-
able than that of the lateral segment. As an island flap,
the scapular spine can be harvested based on the muscle
attachments to the trapezius, which is supplied pri-
marily through the transverse cervical artery. This flap
has been used to reconstruct small mandibular
defects.499'500
The scapular flap is useful in composite tissue recon-
struction requiring thin cortical bone and soft tissue
contour, such as in maxillary and orbital floor recon-
struction. Scapular flaps are a secondary choice for
mandibular reconstruction. A cortical segment meas-
uring approximately 3 cm wide, 11 cm long, and 1 to
3 cm thick can be obtained in association with the over-
lying skin and fascia. In addition, the latissimus dorsi
and serratus anterior as well as a portion of rib can
be included in the same vascular pedicle.
The primary advantage of the scapular osteocuta-
neous flap is the potential for variable amounts of soft
tissue and osseous transplantation based on a single
long pedicle. The disadvantages of the flap include a
moderately difficult dissection in the triangular space
and the potential for a widened scar.
Metatarsus
Vascularized transfer of the composite first or second
toe is useful in reconstruction of the thumb in cases
of thumb amputation or congenital absence. This
flap is useful because it is relatively easy to harvest, can
become reinnervated, has intact joint function, and
can continue to grow if it is harvested with an intact
epiphysis.501 Reinnervation of the composite flap is
excellent with two-point discrimination of 5 to
10 mm. The use of the free metatarsus in mandibular
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ramus reconstruction in a case of congenital ankylo-
sis of the temporomandibular joint has also been
reported.502,503
Calvaria
NONVASCULARIZED AUTOGRAFTS
The average thickness of the adult calvarial bone is
7 mm; however, there is significant variability (3 to
12 mm). In a study by Pensler and McCarthy,504 the
authors evaluated the thickness of 200 adult calvaria
based on different sites and demonstrated little dif-
ference between the left and right sides of the cranial
vault. In addition, the authors demonstrated that on
average, the thickest portion of bone is localized in the
parietal area posterior to the coronal suture.
In clinical practice, split calvarial grafts (in situ)
are not used in infants and young children because
the calvarial bone is extremely thin, often with no
diploic space, thus increasing the risk of brain injury.
Multiple methods have been described to harvest cal-
varial grafts. The two most common methods split
the bone through the diploe, thus separating the inner
and outer cortices.505 By splitting of the calvaria, the
outer cortex is used as the graft; the inner cortex
remains intact to provide a protective covering of the
brain.
If relatively small graft sizes are needed, the in situ
technique can be used. In this technique, a burr is used
to produce a trough around the proposed graft (Fig.
24-24). The graft is harvested by use of a curved
osteotome placed within the diploic space. The edges
of the graft site are burred down to avoid excessive
step-off and to improve the resulting cranial contour.
Care must be taken to avoid full-thickness bone
removal, especially in the center of the graft; this can
cause inadvertent dural tears and intracranial injury.
In addition, the harvest should be performed slowly,
with sharp osteotomes placed alternately from the sides
of the graft to avoid fracturing the bone graft. Finally,
the area of the sagittal sinus should be avoided to
prevent inadvertent venous sinus hemorrhage, which
can be extremely difficult to control.
When larger sections of bone graft are required, it
is often easier and safer to perform a formal craniotomy,
remove a full-thickness segment, and split the bone
on a back table with a mechanical saw or osteotome
(Fig. 24-25). After separation, the inner cortex is used
to cover the donor area; the outer cortex is used as a
graft.
VASCULARIZED CALVARIAL TRANSFER
(TEMPOROPARIETAL FLAP)
In 1890, Muellar506 reported the first osteocutaneous
flap incorporating the outer table of the calvaria toge-
ther with the overlying skin and scalp. Composite flaps
VeWK^adtfW image...

24 • REPAIR AND GRAFTING OF BONE 689

FIGURE 2 4 - 2 4 . The technique of in situ harvesting of split calvarial bone graft. The graft is marked and a trough is
drilled around the periphery of the bone, exposing the diploe. The graft is then removed by separating the outer table
from the inner table by use of an osteotome. (From McCarthy JG, Zide BM: The spectrum of calvanal bone grafting:
introduction of the vascularized calvarial bone flap. Plast Reconstr Surg 1984;74:10.)

were later used for mandibular reconstruction. 50
Conley508 and Strieker et al509 separately reported cal-
varial osteomuscular flaps; van der Meulen510 reported
a full-thickness calvarial bone flap based on the tem-
poralis muscle. McCarthy and Zide505 used the galea,
periosteum, and deep temporal fascia as a pedicle to
FIGURE 2 4 - 2 5 . Splitting a full-thickness calvarial bone
graft after removal by neurosurgical technique. The bone
is split with a sagittal saw applied directly to the diploic
space around the edges of the bone. Curved osteotomes
are used to complete the separation of the inner and outer
tables. This technique enables harvesting of large pieces
of calvanal bone graft. (From Cutting CB, McCarthy JG,
Knize DM: Repair and grafting of bone. In McCarthy JG,
ed: Plastic Surgery, vol 1. Philadelphia, WB Saunders,
1990:583-629.)
transfer the outer table of the parietal bone to recon-
struct the zygoma.
Anatomy
The inner table of the calvaria is perfused predomi-
nantly by perforators from the middle meningeal
system (Fig. 24-26). In contrast, the outer table is per-
fused by perforating vessels from the periosteum. The
blood supply of the periosteum is derived from a rich
anastomotic network above the galea. The vascular
pattern is irregular in organization without a true axial
orientation. 5 " The superficial temporal artery, a
branch of the external carotid artery, contributes an
axial vessel to the galea in the region of the frontal
parietal calvaria and can be used as a vascular pedicle
for vascularized calvarial bone transfer. With these tech-
niques, a flap containing an osseous segment meas-
uring 5 to 6 cm in width and 7 to 8 cm in length can
be harvested.
The advantages of vascularized calvarial bone
grafts include minimal donor site morbidity, camou-
flaged scar, accessibility through the same incision used
for craniofacial reconstruction, and long-lasting
contour (bone) restoration, particularly in compro-
mised recipient beds. In addition, vascularized calvarial
grafts maintain some growth potential when they are
transferred in immature animals.512 The disadvantage
of vascularized calvarial flaps are similar to those
of free calvarial grafts, including the potential for

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Dr.Mustafa D.
690 • GENERAL PRINCIPLES
Perforators from
Superficial Temporal Artery
Middle
Meningeal A.
FIGURE 2 4 - 2 6 . The blood supply of the calvaria. The
inner table of the calvaria is primarily supplied by
the middle meningeal artery. The deep temporal vessels
under the temporalis muscle provide the blood supply
to the temporal bone. The principal blood supply of
the outer table of the calvaria is through a network
of vessels within the periosteum that are, in turn, sup-
plied by an anastomotic network of vessels above the
galea and SMAS, including the superficial temporal, pos-
terior auricular, supraorbital, and supratrochlear arter-
ies. (From Cutting CB, McCarthy JG. Berenstein A: The
blood supply of the upper craniofacial skeleton: the search
for composite calvarial bone flaps. Plast Reconstr Surg
1984;74:603.)
A B
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Dr.Mustafa D.
intracranial injury, dural tears, contour irregularities,
and bone fracture.
Temporoparietal Flap Technique
After a bicoronal incision is made, the scalp skin is
elevated in a suhfollicular plane above the superficial
musculoaponeurotic system (SMAS) and the galea to
preserve the superficial temporal artery. The scalp ele-
vation continues to expose the temporalis muscle, tem-
poral crest, coronal suture, and superficial temporal
artery. By use of a template, the calvarial donor site is
marked, and the overlying galea and periosteum are
incised approximately 5 mm away from the proposed
bone edge. Similar to a split calvarial graft, a burr is
used to create a trough around the bone flap, and the
outer cortex is elevated carefully with a curved
osteotome. Full-thickness bone may be harvested by
a formal craniotomy. It is helpful to suture the over-
lying periosteum and galea to the bone with drill holes
placed in the periphery of the flap. The flap can then
be mobilized based on the superficial temporal artery
(Fig. 24-27). A Doppler probe may be useful in iden-
tifying the artery.
If only the outer cortex is harvested, the donor defect
may be managed by burring the margins of the outer
table defect. For full-thickness harvests, split calvaria
may be harvested from another region and used to cover
the donor defect. The donor bone flap can be con-
toured by an air-driven burr to place partial-thickness
FIGURE 24-27. A The outer table of the
parietal bone is harvested with a curved
osteotome after a trough is created around
the periphery of the bone flap. The blood
supply of the bone flap is maintained by
preserving the periosteal blood vessels in
continuity with the superficial temporal
artery system within the galea-SMAS and
the deep temporal fascia. B, Sutures passed
between the overlying galea, periosteum,
and calvaria are helpful in keeping the
periosteum attached to the bone and pre-
serving the blood supply. (From McCarthy
JC, Cutting CB, Shaw WW: Vascularized cal-
varial flaps. Clin Plast Surg 1987; 14:43.)
Tewttf<aeicr«f image...
FIGURE 2 4 - 2 8 . The arc of rotation of the bone flap
for augmentation of the zygomatic complex and the lateral
orbital wall. (From McCarthy JC, Cutting CB, Shaw WW:
Vascularized calvarial flaps. Clin Plast Surg 1987; 14:43.)
longitudinal bone cuts in the cortical bone. Zygomatic
and lateral orbital wall complex augmentation maybe
obtained by placing the vascularized calvarial bone flap
in the midfacial regions (Fig. 24-28). This procedure
is particularly useful in the reconstruction of the
zygomatic complex deficiency in Treacher Collins
syndrome.
ALLOGENEIC BONE GRAFTS
History
Allogeneic bone grafting refers to the use of bone har-
vested from non-genetically related individuals. The
history of allogeneic bone grafting can be traced to
Macewen,430 who reported the use of morselized cor-
ticocancellous bone grafts harvested from children
undergoing tibial osteotomies to treat a patient with
a bone gap resulting from debridement of an infected
humeral fracture. The patient was noted to have excel-
lent function even 30 years postoperatively. In the early
20th century, allograft bone was used sporadically to
promote spinal fusion and to treat fracture nonunions;
amputated limbs served as the primary donor tissue.513
Allograft bone was in limited supply, however, because
specimens could be maintained only for a short
period at 4°C. The development of electric freezers in
the 1940s and the report that deep-frozen bone allo-
grafts were less immunogenic led to improved storage
of bone grafts and contributed to an increase in their
use.513 At that time, the chief source of bone graft mate-
rial was femoral heads obtained from living donors
with hip fractures. Small bone banks maintained by
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24 • REPAIR AND CRAFTING OF BONE 691
orthopedic surgeons managed harvested bone. In the
1950s, during the midst of the Korean conflict, the
United States Navy developed the Navy Tissue Bank
as a means of anticipating possible military need for
stored human tissues. However, the military use never
materialized and the stored tissues were made avail-
able for civilian use, leading to an increase in bone
allograft use for postablation reconstructive surgery,
revision of joint replacement, and complicated
fractures.514*518 Allografts have been used sparingly in
craniofacial surgery because of unpredictable rates of
resorption and bone formation.
Processing and Preservation
Modern processing of allograft bone is designed to
produce a sterile, acellular implant that is biocompat-
ible and osteoconductive. Removal of cells and tissue
debris is a critical step in the process because it decreases
the immunogenicity of the graft and reduces the inci-
dence of disease transmission. These steps, however,
lead to the inactivation of osteoinductive factors in cor-
ticocancellous allografts.
Processing of allograft bone includes an optional
low-dose irradiation (<20 kGy) that destroys surface
bacteria, physical debridement, ultrasonic or pulsatile
water washes, an ethanol wash, an antibiotic soak, and
finally a terminal sterilization step. Various methods
of sterilization have been used, including ethylene oxide
and irradiation. The use of ethylene oxide has been
largely abandoned owing to an inflammatory residue
and decreased osteoinduction.519,520 Irradiation in
moderate doses (<20 kGy) is effective for eradicating
bacteria and only minimally changes the mechanical
properties of the graft. Larger doses (minimum of
30 kGy) are needed to neutralize significant viral loads
and can significantly diminish the mechanical strength
of the allograft.521,522
The most common methods of preservation are
deep-freezing (-70°C) and freeze-drying. Deep-
freezing minimally changes the mechanical properties
of the graft.523 In contrast, freeze-drying significantly
changes the material properties of the graft and leads
to decreased torsional and bending strengths. These
changes are attributed to damage to the bone matrix
resulting from microcracks along collagen fibers
and are significantly worse in combination with
irradiation.522,524
Risk of Disease Transmission
In July 1997, the United States Food and Drug Admin-
istration (FDA) released industry standards to estab-
lish rules for donor screening.525 These rules include
an extensive donor screening including social and
medical history and serologic testing. History alone is
692 I • GENERAL PRINCIPLES
thought to eliminate 90% of inappropriate donors;
advances in antibody and DNA technology have led
to significant improvement in virus detection.
The primary pathogens of concern are the human
immunodeficiency virus (HIV), hepatitis B virus, and
hepatitis C virus. The risk of HIV transmission is
thought to be extremely low (1 in 1.6 million) because
of the extensive screening as well as the acellular nature
of the grafts.526 Newer tests, including polymerase chain
reaction analysis, will likely decrease the rates of disease
transmission even further; however, their routine use
remains prohibitive because of high costs. Removal of
blood and blood products from allografts decreases
the chances of HIV transmission to virtually zero. In
fact, the three cases in which HIV transmission was
documented after allograft implantation occurred
when fresh frozen grafts harvested from a single
infected donor were used in a manner that retained
the donor's blood and bone marrow. In contrast, 38
patients treated with freeze-dried or reamed allograft
bone from the same donor did not seroconvert.522
Immunogenicity
The immune response to allograft bone implants is
predominandy a cell-mediated response to cell surface
major histocompatibility antigens, although humoral
responses have also been noted.522,527"530 The extracel-
lular matrix and inorganic components of allograft
bone are not antigenic. Nucleated bone marrow cells
are the most antigenic cells in allograft bone implants.
Thus, the removal of these cells as well as other viable
cells significantly reduces the immunogenicity of allo-
graft bone grafts. Fresh allografts are the most potent
immunologic challenge to the host. Fresh frozen allo-
grafts also sensitize T lymphocytes; however, they do
not elicit a humoral response. Freeze-dried cortical
and corticocancellous allograft bone implants531,532 are
the least immunogenic and elicit only a minimal
humoral or cellular immune response.
Allograft rejection, unlike in solid organ trans-
plantation, is often difficult to identify because no
serum markers have been identified and histologic
examination is cumbersome. Rejection is usually
inferred from resorption or premature mechanical dys-
function. Chronic rejection results in sequestration of
the bone implant in a fibrous capsule, thus prevent-
ing further implant resorption and remodeling. These
factors are thought to be responsible for the lack of
complete repair and late skeletal breakdown, particu-
larly when massive amounts of allograft bone are used.
Incorporation of Allograft Bone
The phases of repair after allograft bone implantation
are similar to fracture repair and include an inflam-
matory response and variable revascularization,
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Dr.Mustafa D.
resorption, bone formation, and remodeling. Allo-
geneic cortical bone grafts processed by modern
methods contain few if any intact cells and are asso-
ciated with a limited inflammatory response that
usually subsides within a few days after surgery. Vas-
cular invasion of the allograft is variable and depend-
ent on the size and density of the implant, the resultant
immune response, and the type of bone used (corti-
cal versus cancellous versus demineralized).
Cancellous bone chips are incorporated more
quickly than cortical grafts because they are more
quickly revascularizcd and remodeled. Remodeling is
variable, however, and areas of sequestered necrotic
bone can be demonstrated even on long-term follow-
up. Massive cortical allografts are penetrated by host
vessels and substituted by new bone more slowly
and to a variable degree.533 This lack of remodeling,
together with sequestered necrotic bone that is inca-
pable of repair, is thought to account for the variable
rates of fatigue fractures (16% to 50%) resulting from
cyclical loading.533"536 Thus, in most instances, allograft
cortical bone used in reconstruction of weight-bearing
bones remains significantly weaker than autografts
for a considerable time after surgery.523 On long-
term follow-up (more than 10 years), most cortical
allografts retain unremodeled necrotic bone, but most
go on to resemble autografts biomechanically and
structurally."2
Two physical factors determine the incidence and
rate of union between host bone and allograft bone:
the stability of fixation and the contact between host
and graft bone. In general, the interface between host
and graft bone heals with an osseous union regardless
of the implant type (i.e., fresh or frozen, cortical or
cancellous), provided stable fixation is performed with
compression plates and the bone fronts are in intimate
contact.537,538 Deviation in either variable results in
fibrous union.
Formulations of Allogeneic
Bone Crafts
MORSELIZED CORTICAL AND
CORTICOCANCELLOUS ALLOGENEIC
BONE CRAFTS
Morselized allogeneic bone grafts are available from a
number of commercial sources and are used as bone
graft substitutes and bone graft extenders (Table 24-
6). These grafts have minimal mechanical strength
(mostly resistance to compression) and are only osteo-
inductive. Bone chips of variable size (0.5 to 1.0 cm)
are available and are most frequendy supplied as freeze-
dried bone. When they are used in ideal conditions
(i.e., well-vascularized host bed, intimate bone contact,
stability, lack of infection or colonization), morsel-
ized bone grafts are replaced nearly completely by
TABLE 2 4 - 6 4- BONE SUBSTITUTES

Bone Mechanical
Substitute Formulations Uses Strength Osteoinductive Osteoinductive Resorption Comments

Allogeneic Corticocancellous Mechanical support Yes Yes (limited) No Slowly Contraindicated in

Bone grafts Fill defects infected or poorly
Buttress constructs vascularized tissues
Morselized Bone graft extender No Yes No Moderate Contraindicated in
freeze-dried infected or poorly
cancellous vascularized tissues
grafts
Demineralized Bone graft extender No Yes Yes Rapid Contraindicated in
bone matrix In conjunction with other infected or poorly
bone substitutes vascularized tissues
Calcium OsteoSet Experimental No Yes No Slowly
Sulfates

Calcium Phosphates
Coralline HA Pro Osteon 200 Periodontal augmentation Yes (block Yes No Slowly
implants HA (granules or and prosthetics (FDA form)
blocks) approved)
Pro Osteon 500 Repair metaphyseal Yes Yes No Very slowly
defects (FDA approved)
Bone derived OsteoCraf/N Maxillary augmentation Yes (depending Yes No Slowly
BioOss Tooth socket repair on formulation)
Preparation for
osseointegrated implants
Craniofacial augmentation
Spinal fusion
Laboratory- OsteoCraf/LD Dental applications NO Yes No Slowly
produced OsteoCraf/D Yes Yes No Slowly
HA ceramic (if at all)
Tricalcium Collagraft (paste Acute long bone fractures No Yes No Slowly
phosphate or sheet) (FDA approved)
Traumatic bone defects
(FDA approved)
Spine surgery
(experimental)
Continued

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Dr.Mustafa D.
TABLE 2 4 - 6 • BONE SUBSTITUTES—cont'd

Bone Mechanical
Substitute Formulations Uses Strength Osteoinductive Osteoinductive Resorption Comments

Calcium BoneSource Craniofacial reconstruction, Minimal Limited No Slowly Isothermic reaction

Phosphate neurosurgical burr holes, Sets in 20-25 minutes
Cements craniotomy cuts, Final set 4-6 hours
craniofacial defects If reconstituted with
<25cm2 (FDA approved) NaPhos, set time is
6-7 minutes
Need dry field
Norian Adjunct for fracture Minimal No No Rapidly Injectable
stabilization and 15-minute setup
treatment of low-impact, Cure for 24 hours
unstable metaphyseal
distal radial fractures
(FDA approved 1998,
not indicated in primary
treatment of comminuted
fractures, diaphyseal
fractures}
Augment bone contour in
craniofacial skeleton
(FDA approved 1998)
Cranioplasty with surface
area <25 cm2
Apatitic calcium Craniofacial applications, Minimal No No Rapidly Enothermic reaction
phosphate dental applications (FDA Long set times
bone substitute approved) [>\ hour)
(a-BSM) Orthopedic applications Hardens after 20
(experimental)
minutes

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fl&WWadtfWimage...
osteoconduction and are rarely complicated by infec-
tions.539 A history of infection or active infection is con-
sidered a contraindication to their use.
CORTICOCANCELLOUS ALLOGRAFTS
Corticocancellous allografts are full-thickness grafts
ranging in size from short ring-like structures to the
entire diaphysis preserved as deep-frozen or freeze-
dried grafts. Massive grafts inclusive of cortical-
cancellous bone and articular cartilage have also been
reported.485,539'543 The grafts are osteoconductive to a
limited degree and are used to fill defects, to buttress
constructs, and to provide structural support. Resorp-
tion and remodeling are variable and never complete.
A number of studies have demonstrated acceptable
functional outcomes in orthopedic reconstructions
with excellent results in 50% to 80% of patients. The
primary complications noted were infections (5%
to 17%), fractures (16% to 20%), and nonunion
( 1 1 0 / o ) i 485,539.M3
DEMINERALIZED BONE GRAFTS
Demineralized bone grafts are chemically treated,
freeze-dried, allogeneic grafts used alone, as auto-
genous bone graft extenders, or in conjunction with
other bone substitutes to augment osseous repair.
The grafts revascularize quickly but offer no struc-
tural support; they are quickly resorbed. Unlike other
types of allograft bone, demineralized bone grafts are
both osteoconductive and osteoinductive. The poten-
tial for these processes with demineralized bone
grafts, however, varies with the processing method
used in their production. Bone induction by dem-
ineralized bone grafts occurs by the endochondral
pathway and is critically dependent on the process-
ing methods used. For example, the use of hydrochlo-
ric acid (0.5 to 0.6 M) or a combination of formic
acid and citric acid for demineralization retains
osteoinductive potential. Other agents, such as acetic
acid, nitric acid, nitrous acid, and alcohol, significantiy
impair or abolish osteoinduction by demineralized
bone grafts.167'544'545
Grafton* is a commercially available freeze-dried
demineralized bone graft available as flexible sheets
(Grafton Flex) or putty (mixed with a glycerol carrier).
The material has been used in a number of clinical and
experimental studies in both membranous and endo-
chondral bones.543,546'554 Shermak et al546 demonstrated
that the use of either flexible sheets or putty leads to
healing of 15-mm critical-sized defects in New Zealand
White rabbits. Neigel and Ruzicka549 evaluated the use
of Grafton in orbital reconstruction and reported a
satisfactory to excellent result in all patients with no
'Osieotech, Eatontown, New Jersey.
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Dr.Mustafa D.
24 • REPAIR AND GRAFTING OF BONE 695
complications related to the use of demineralized bone
alone. The authors concluded that demineralized
bone grafts are safe to use in orbital reconstruction
and may eliminate the need for a second donor site to
harvest bone graft.
The use of Grafton in dentoalveolar reconstruction
has also been reported. Levine et al554 reported a pre-
liminary study of seven patients who underwent
placement of dental implants and noted bone forma-
tion in five patients. Callan et alS52 studied the use of
Grafton Flex and Grafton Putty to fill extraction sockets.
The authors performed biopsies of the alveolar ridges
at the time of permanent implant placement and
demonstrated extensive new bone formation and
minimal residual bone graft matrix after an average of
5 months of follow-up. They concluded that this mate-
rial is useful in dentoalveolar reconstruction.
XENOGENEIC BONE GRAFTS
Xenogeneic bone grafts are generally ineffective as bone
graft material because of a profound immune reac-
tion. This reaction prevents bone graft revasculariza-
tion and incorporation, resulting in a sequestrum that
has minimal load bearing and repair capacity. These
properties make the use of these grafts inadvisable, par-
ticularly because other osteoconductive treatment alter-
natives exist. Some authors have referred to the use of
acellular, deproteinized bovine bone hydroxyapatite as
xenogeneic bone grafts; however, these products are
more accurately described as implants because they
are biocompatible and elicit minimal or no immune
reaction.
BONE SUBSTITUTES
The shortcomings of autogenous bone grafting, includ-
ing limited donor supply, need for a second operative
site, increased operative time, and associated comor-
bidities (postoperative pain, nerve damage, infection,
and bleeding), have led to attempts to develop bone
graft substitutes. The ideal bone graft substitute, one
that is inexpensive, biocompatible, radiolucent, resist-
ant to infection, strong, and replaced by host bone,
remains elusive. A number of promising materials have
been identified, and future research combining tissue
engineering principles and bone graft substitutes may
offer an alternative to autogenous bone grafting (see
Table 24-6).
Calcium Sulfates
The use of bone substitutes to fill bone defects or to
augment fracture repair can be traced to the use of
gypsum, also known as plaster of Paris, in the late 19th
century. The hemihydrate form of calcium sulfate is
made by an exothermic reaction resulting from mixing
696 I • GENERAL PRINCIPLES
gypsum and water. The internal use of gypsum as a
bone filler was reported in 1892 by Dreesman,555 who
described a slurry of plaster of Paris and 5% phenol
to treat bone gaps resulting from trauma or
osteomyelitis. The report was ignored, however, until
1925, when Kaufman reported satisfactory results in
a patient treated with plaster or Paris/5% phenol for
bone loss resulting from osteomyelitis.556,557 Petrova also
reported satisfactory results after treatment of surgi-
cally created, noninfected bone cavities in dogs with
antibiotic-impregnated plaster of Paris.556 In the years
to follow, plaster of Paris was used sparingly in extrem-
ity reconstruction and only briefly in craniofacial recon-
struction during the Vietnam conflict.558
The primary advantages of calcium sulfate bone sub-
stitutes include ease of handling, resorption by osteo-
clasts, and attachment and deposition of osteoid by
osteoblasts.559 However, the use of these compounds
as bone substitutes has been largely abandoned because
of unpredictable and rapid biodegradation, lack of
complete biocompatibility, and potential toxicity. The
shortcomings result from random crystallization
leading to randomly sized and shaped crystals with
variable solubility, mechanical properties, and poros-
ity. Newer forms of calcium sulfate bone substitutes
(e.g., OsteoSet*) have become available and offer a
highly controlled microenvironment to produce reg-
ularly sized crystals with slower, more predictable sol-
ubility and resorption. These materiab are
osteoconductive, biocompatible, and slowly re&orbed
in vivo (30 to 60 days). Early animal experiments with
OsteoSet have been promising.556
Calcium Phosphates
Calcium phosphate-based bone substitutes have sup-
planted calcium sulfates because they more closely
resemble the inorganic matrix of bone, resorb less
slowly, and are biocompatible. The implants are avail-
able in ceramic or nonceramic forms. Ceramic implants
are derived from the exoskeleton of naturally occur-
ring corals or synthesized in the laboratory and are
supplied as blocks or granules that are shaped for use.
Ceramic implants tend to be brittle and difficult to
contour.560,561 Nonceramic calcium phosphate-based
bone substitutes (also known as calcium phosphate
cements) are supplied as powders that are reconsti-
tuted before use and can be injected with syringes or
molded to fit irregular defects.
CERAMIC HYDROXYAPATITE IMPLANTS
Coralline Hydroxyapatite Implants
Chiroff et al562 made the observation that the exoskele-
ton of corals, a marine invertebrate, is similar in struc-
ture to both cortical and cancellous bone. This
'Wright Bio-Orthopedics, Arlington, Tennessee.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
observation, together with the knowledge that bone
formation requires a physical structure that can be
invaded by new blood vessels and to which osteoblasts
can adhere, led to analysis of a variety of coral species
to identify the most suitable sources of bone implants.
The analysis centered on the pore diameter (ideally
between 100 and 500 (im) and the interconnections
between the pores because these factors are critical to
bone ingrowth.503"565
The exoskeleton of corals belonging to the genus
Porites was found to be structurally similar to cortical
bone with a void volume of 66% with parallel inter-
connections that are 230 Jim in diameter with inter-
connections measuring 190 \im in diameter. Similarly,
the exoskeleton of corals in the genus Goniopora was
noted to be similar to cancellous bone with parallel
longitudinal pores approximately 600 |xm in diameter
and interconnecting pores of 220 to 260 UMn. These
species are converted to usable implants after the coral
animal is removed in a chemical reaction and a
hydrothermic exchange process (known as replamine-
form processing) converts the coral calcium carbon-
ate exoskeleton to hydroxyapatite (calcium phosphate).
Implants derived from Porites and Goniopora coral
species are available commercially as Pro Osteon 200
HA and Pro Osteon 500. Pro Osteon 200 is supplied
as granules or blocks and is FDA approved for orthog-
nathic surgery, periodontal augmentation, and pros-
thetics. Pro Osteon 500 is FDA approved for the repair
of metaphyseal defects.
Bone-Derived Hydroxyapatite Ceramics
A number of bone-derived hydroxyapatite ceramics
are commercially available, including OsteoGraf/N*
(bovine bone from U.S. sources) and Bio-Oss1 (bovine
bone from European sources). Recent outbreaks of
bovine spongiform encephalopathy and new variants
of Creutzfeldt-Jakob disease do not appear to pose a
potential hazard with regard to bovine-derived hydrox-
yapatite ceramics on the basis of theoretical and exper-
imental data.566
Bio-Oss and, to a lesser degree, OsteoGraf/N have
been used extensively in maxillary augmentation, tooth
socket repair, and preparation for osseointegrated
implants. Bio-Oss, either alone or in combination with
locally harvested autogenous bone or as graft mate-
rial with guided tissue regeneration, resulted in most
cases in successful maxillary sinus augmentation and
implant osseointegration.567'573 In these studies, Bio-
Oss implants were well tolerated, osteoconductive,
slowly resorbed, and replaced by host bone, and newly
formed bone was maintained as long as 5 years
postoperatively.567 Successful use of Bio-Oss in the
treatment of experimental models and clinical
cases of periodontal osseous defects has also been
'Cera Med, Lakewood, Colorado.
'Osteohealth, Shirley, New York.
l^WW'aelcri^ image...
reported.574"579 Bio-Oss has been used sparingly in other
craniofacial applications and has only recently been
reported in cranial bone augmentation and in the
treatment of crilical-sized defects overlying the frontal
sinus.580'583 Only a few preliminary reports have eval-
uated the use of this implant material in extremity
reconstruction and spinal fusion.539,58*4 In general, the
results of these applications have been less promising
than in dentoalveolar reconstruction.
OsteoGraf/N has also been used either alone or in
conjunction with guided bone regeneration, auto-
genous bone grafts, and demineralized allogeneic
bone in dentoalveolar reconstruction and maxillary
sinus augmentation.541,542,585-588 The results of these
applications, although less conclusive than those of Bio-
Oss, demonstrate that OsteoGraf is biocompatible,
resorbable, and osteoconductive.
Laboratory-Produced Hydroxyapatite
Ceramics
Laboratory-produced ceramic calcium phosphate-
based bone substitutes have been commercially
available since the 1970s.589 These hydroxyapatite
formulations are fabricated under conditions of high
pressure and temperature with formation of sintered,
crystalline, ceramic hydroxyapatite. CeraMed markets
two formulations of laboratory-produced particulate
ceramic hydroxyapatite: OsteoGraf/LD (low density)
and OsteoGraf/D (dense). OsteoGraf/LD is micro-
porous and resorbable; OsteoGraf/D is nonporous
and marketed as a nonresorbable permanent implant.
These formulations, similar to bovine bone-derived
OsteoGraf/N, have been used in dental applications
(i.e., preservation of alveolar ridge contour, periodontal
augmentation, periodontal defects).
Tricalcium Phosphate
Tricalcium phosphate porous implants are calcium
phosphate ceramics that have greater solubility than
hydroxyapatite implants and as such are resorbed more
rapidly. These compounds have a porous structure
(36% porosi ty with pores ranging from 100 to 300 (am),
are britde, and have a low impact resistance and low
compressive strengths. Biodegradation is rapid but
irregular and inadequate for complete osseous
ingrowth, making tricalcium phosphate alone a poor
bone graft substitute.590 Resorption of tricalcium
phosphate leads to the development of calcium phos-
phate-rich microenvironments that are thought to
enhance osseointegration of the implant at the bone-
implant interface through limited osteoconduction.590
Because of its rapid resorption, tricalcium phos-
phate alone has limited application in craniofacial
reconstruction and has been used primarily as a bone
graft expander. Collagraft* is a combination of bovine
'Zimmcr, Warsaw, Indiana.
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Dr.Mustafa D.
24 • REPAIR AND CRAFTING OF BONE 697
type I collagen, tricalcium phosphate, and hydroxya-
patite and is supplied as a paste or sheets. The manu-
facturer recommends mixing with autogenous bone
marrow before use. Type I collagen in this formula-
tion is thought to promote mineral deposition by
binding mineral, noncollagenous matrix proteins,
and circulating and local growth factors. In addition,
collagen is thought to provide a template for vascular
ingrowth.
Collagraft is FDA approved as a bone substitute in
the treatment of acute long bone fractures and trau-
matic osseous defects. This material has been shown
to be more effective than mineral alone when it is used
in the treatment of an experimental model of long bone
defects.591 In addition, mixed with autogenous bone
marrow, Collagraft was as effective as autogenous can-
cellous bone graft for the treatment of acute extrem-
ity fractures in a multicenter trial.592 The use of
Collagraft in spine surgery has also been reported.593
Immune reactivity to xenogeneic collagen does not
appear to be a significant problem. These antibodies
did not cross-react with human type I collagen and
did not appear to alter the function of the graft.594
In Vivo Properties of Calcium Phosphate
Ceramics
Ceramic hydroxyapatite implants have a high com-
pressive strength but are relatively weak with regard
to tensile strength and stress-bearing capacity.595 This
property is likely due to the porosity of the implant.
Block forms of calcium phosphate ceramics have been
used primarily as interpositional grafts in craniofacial
reconstruction. Because of the low stress-bearing
capacity of this material, however, its use in load-
bearing areas of the craniofacial skeleton should be
avoided.
Porous ceramic hydroxyapatite implants are readily
invaded by fibrovascular tissue, slowly resorbed, and
partially converted to mature lamellar bone.596 The
pores in hydroxyapatite implants are initially filled with
hematoma. The clot is resorbed within 3 weeks of
implantation and is followed by fibrovascular ingrowth.
The rate of fibrovascular ingrowth (approximately 2
to 3 mm/day) is minimally affected by implant pore
size, pore volume, or location of the implant, as long
as the recipient bed has a healthy vascular supply.595
Thus, hydroxyapatite implants with a pore diameter
of 500 p;m have not been shown to have consistently
more rapid fibrovascular ingrowth than those with 200-
u\m pores. Fibrovascular invasion of ceramic hydrox-
yapatite implants is thought to have an antimicrobial
effect and to impart a resistance to infection.597,598
However, anecdotal reports of long-term infections
question this conclusion (J.G. McCarthy and Court B.
Cutting, personal communication, 2001).
Multinucleated, osteoclast-like cells resorb the
surface of the implant; however, remodeling of the
deeper portions of the implant occurs slowly owing
TeWttf'aelcrKf image...
698 I • GENERAL PRINCIPLES
to the insoluble, inert structure of crystalline hydrox-
yapatite.560 Resorption is also likely to be related to
mechanical loading of the implant, which is thought
to be responsible for the more rapid resorption of
hydroxyapatite blocks observed in use for reconstruc-
tion of cortical bone defects (10% to 20% resorption
per year) compared with cancellous bone defects (2%
to 5% per year). Implant dissolution (a chemical reac-
tion related to the solubility of the implant matrix),
surface area to volume ratio, and local microenviron-
ment (e.g., temperature, acidity) are variables con-
tributing to implant resorption.
Implants must be rigidly stabilized and closely
abutting viable host bone for osteoconduction to occur
(<1 mm gap).1199,600 This concept is referred to as the
triad of osteoconduction (i.e., stability, viability, prox-
imity). Bone formation at the bone-implant interface
occurs through a process resembling membranous ossi-
fication and results in osseointegration.595 The final
amount ofbone formation is variable and is influenced
by the mechanical loads exerted on the implant.560,601,602
This effect is thought to be an expression of Wolfe's
law.595
Numerous studies have shown that regenerated
bone formed in ceramic hydroxyapatite implants
remodels over time.601,603 This process is dependent on
mechanical loading and leads to an increase in the
volume of regenerated bone from approximately 14%
at 1 month to 56% by 12 months in load-bearing dia-
physeal defects. Increases in bone volume are associ-
ated with improved bending and compressive strengths
reaching approximately 50% of normal cortical bone.601
In contrast, even though the compressive strength of
ceramic implants in nonloaded metaphyseal defects
of the tibia increased significantiy, the volume frac-
tion of bone decreased by 50% from 1 month to
1 year.
Several clinical and experimental studies have eval-
uated the use of ceramic hydroxyapatite implants in
craniofacial reconstruction. In general, these studies
can be grouped as craniofacial augmentation, recon-
struction of osseous defects, and growth factor
delivery.
A number of experimental models have been used
to study hydroxyapatite implant materials for cranio-
facial augmentation. Holmes and Roser604 compared
porous hydroxyapatite blocks with autogenous bone
graft for alveolar ridge restoration in a dog model. The
authors demonstrated that hydroxyapatite implants
were osseointegrated (91% covered with bone
ingrowth) and that the newly formed bone was mature
and vascularized. In addition, the implants were not
associated with a significant inflammatory response
and maintained their contour throughout the post-
operative period. In contrast, autogenous bone grafts
resorbed over time. Histologic analysis after 18 months
demonstrated that the implant materials were com-
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Dr.Mustafa D.
posed of 43% hydroxyapatite matrix, 45% new bone,
and 11.7% soft tissues. The authors concluded that
porous hydroxyapatite blocks are a useful bone graft
substitute; however, these grafts are difficult to contour
and may result in ulceration with denture use.
In a similar study, Holmes and Hagler605 augmented
the buccal contour of the mandible in dogs using
porous hydroxyapatite blocks or two-layered split rib
autografts. Animals were observed for 4 years postop-
eratively. Rib grafts were found to resorb increasingly
with time with eventual loss of contour and augmen-
tation. In contrast, hydroxyapatite implants remained
intact, maintained their contour, and in all but one
implant became osseointegrated. The composition of
the implant specimen was noted to be 35% hydrox-
yapatite matrix, 2 1 % bone, and 34% soft tissues. The
authors concluded that porous hydroxyapatite blocks
are an excellent alternative for craniofacial augmen-
tation because the material is capable of long-term
contour maintenance.
el Deeb and Roszkowski606 studied the use of non-
porous hydroxyapatite granules as an extracranial and
extranasal augmentation material in dogs. The authors
demonstrated that although the granules became
stable within 6 weeks, the final contour was difficult
to predict because of loss of height and settling of the
material in the subperiosteal pocket. In a follow-up
study, the authors 607 compared hydroxyapatite gran-
ules with nonporous hydroxyapatite blocks for
extracranial augmentation in rhesus monkeys. Similar
to the previous study, the authors demonstrated that
hydroxyapatite granules became stable within 3 to 4
weeks; however, loss of contour and height resulted
from settling of the material. Hydroxyapatite blocks
maintained their contour throughout the study period
(as long as 12 months postoperatively). Neither mate-
rial was associated with an inflammatory response or
bone resorption. Although both hydroxyapatite gran-
ules and hydroxyapatite blocks were surrounded by
a fibrous capsule, osseointegration did not occur. In
addition, approximately 25% of the block specimens
demonstrated mobility. The authors concluded that
in extracranial augmentation, nonporous hydroxyap-
atite granules are more stable than hydroxyapatite
blocks; however, block implants maintain a better
contour.
In an effort to compare dense blocks of hydroxy-
apatite with porous hydroxyapatite implants, el Deeb
et al608,609 studied zygomatic and mandibular aug-
mentation in rhesus monkeys. The authors demon-
strated that whereas dense implants were completely
encapsulated by fibrous tissue without evidence ofbone
growth, porous implants were attached to the under-
lying bone cortex with bone ingrowth. The authors
hypothesized that the porous implants promoted
earlier fibrous ingrowth with resultant stabilization and
osseointegration.
image...
The use of hydroxyapatite implants has also been
reported in a number of clinical studies. Kent et al610
conducted a 4-year prospective clinical trial of partic-
ulate hydroxyapatite to augment deficient alveolar
ridges. The hydroxyapatite granules were used either
alone or in combination with autogenous cancellous
bone and implanted subperiosteally by syringe injec-
tion. The authors found an improved alveolar ridge
height and width with minimal resorption or loss of
height. Hydroxyapatite implants supported permanent
denture placement and improved denture fit. The
authors thought that hydroxyapatite granules are
potentially useful in alveolar ridge augmentation, either
alone or as a bone graft expander, and require further
clinical investigation.
Waite and Matukas 61 ' used hydroxyapatite granules
mixed with microfibrillar collagen and blood to
augment and correct symmetry of zygomatic bones
in 11 patients after Le Fort I osteotomy. The authors
reported a stable augmentation (4 to 9 mm) that main-
tained the desired contour without evidence of migra-
tion, infection, or pain in the follow-up period (6 to
22 months). Similarly, Byrd and Hobar612 reported on
their experience with porous hydroxyapatite granules
(Interpore 200 mixed with Avitene and blood) for aug-
mentation of the craniofacial skeleton in 43 patients
with congenital, aesthetic, and post-traumatic defor-
mities. The longest follow-up was 5 years. The authors
reported a low complication rate with no evidence of
infections, resorption, migration, or loss of contour.
Only two patients required minor revision surgery. His-
tologic analysis of biopsy specimens obtained post-
operatively revealed fibrous encapsulation without
bone ingrowth. Byrd and Hobar stressed careful sub-
periosteal dissection of the pocket to produce the
desired contour and to minimize implant settling.
Kwon et al613 were among the first to report the use
of solid cones of hydroxyapatite ceramic for implan-
tation in fresh extraction pockets. The authors evalu-
ated 70 implants in 10 patients during a follow-up
period of 12 to 24 months and found that approxi-
mately 53% of implants became exposed and 27%
required removal. No statistical differences were noted
in alveolar ridge preservation. The authors concluded
that hydroxyapatite ceramic implants should not be
used for repair of extraction sockets.
el Deeb et al614 reported the use of porous hydrox-
yapatite blocks and granules in augmentation of 20
mandibular and maxillary alveolar ridges in 28 patients
with a follow-up period of 2 years. Patients were eval-
uated by clinical and radiographic examination and
by questionnaires. The authors reported a high level
of improvement (95% for hydroxyapatite granules and
88% for hydroxyapatite blocks) in prosthodontic
reconstruction. Satisfaction rating with denture fit was
82% in patients treated with granules and only 55%
in patients treated with blocks. The authors concluded
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24 • REPAIR AND CRAFTING OF BONE 699
that hydroxyapatite granules are useful in alveolar ridge
augmentation, whereas hydroxyapatite blocks are
associated with complications (e.g., dehiscence) and
should be used selectively. These findings were con-
firmed in a follow-up study in which the authors eval-
uated 39 patients during a 5- to 7-year period.615
The use of hydroxyapatite in reconstruction of bone
defects in membranous and endochondral bones has
also been reported. Horswell and el Deeb616 compared
nonporous hydroxyapatite granules with autogenous
bone grafts in the repair of surgically created alveolar
defects in adult rhesus monkeys. Hydroxyapatite gran-
ules stabilized by 2 months and demonstrated healing
and dehiscence rates comparable to those of autoge-
nous bone grafts. The repaired alveolar processes were
noted to be similar in bulk and contour in both groups,
and osseous ingrowth was demonstrated in 66% of
animals treated with hydroxyapatite granules. The
authors concluded that hydroxyapatite granules are
an acceptable alternative to bone grafts in the treat-
ment of alveolar clefts if tooth eruption and ortho-
dontic movement are not necessary.
Ripamonti 6 ' 7 reported the use of porous hydrox-
yapatite (Interpore 500) for calvarial reconstruction
in baboons. Histologic and histomorphometric analy-
sis of sections harvested after 3,6, and 9 months revealed
substantial bone ingrowth in hydroxyapatite implants.
Bone ingrowth in the implants was significantly greater
than that noted in defects treated with autogenous bone
grafts. By 9 months, the entire hydroxyapatite implant
was penetrated by new bone; however, the extent of
bone ingrowth did not correlate with the site of sur-
gical implantation. In fact, although most implants
demonstrated extensive bone deposition within the
center of the implant, numerous nonunions were
observed at the hydroxyapatite-calvarial interface.
Ripamonti et al618,619 have also described the use of
hydroxyapatite as a delivery vehicle for osteogenin. In
one study, osteogenin was delivered into rods of non-
resorbable or resorbable hydroxyapatite (porosity of
600|im) and implanted into intramuscular pockets
in adult baboons. Bone differentiation was noted in
nonresorbable implants treated with or without
osteogenin.618 In contrast, resorbable implants failed
to elicit osteogenesis even when admixed with
osteogenin. The authors concluded that nonresorbable
hydroxyapatite may have some osteoinductive prop-
erties and that these properties may be spontaneous
adsorption of endogenous osteogenin on the surface
of nonresorbable hydroxyapatite.
In a follow-up study, Ripamonti et al620 treated cal-
varial defects with resorbable and nonresorbable
hydroxyapatite implants treated with or without
osteogenin. Histomorphometric analysis revealed
improved osteogenesis in osteogenin-treated nonre-
sorbable and resorbable hydroxyapatite implants
compared with controls. Overall, however, resorbable
700 I • GENERAL PRINCIPLES
implants demonstrated significantly less osteogenesis
than nonresorbable implants did. The authors con-
cluded that nonresorbable porous hydroxy apatite is
a potential delivery system for osteogenin and that
the concurrent use of osteoinductive growth factors
with hydroxyapatite implants may improve osseous
regeneration.
In a preliminary report, Ono et al621 discussed the
use of porous hydroxyapatite implants for the recon-
struction of large, complex cranial defects. The authors
avoided potentially difficult implant contouring by
use of preoperative full-scale models. Initial analysis
of these patients revealed satisfactory cranial contour
with no evidence of infection or postoperative
complication.
Wolford et al622 reported the use of coralline porous
hydroxyapatite as a bone graft substitute in orthog-
nathic surgery. In a prospective study, 92 consecutive
patients were treated with a total of 355 block implants
to the mandible, maxilla, and midface. Of note, 200
implants were positioned directly adjacent to the max-
illary sinus. The authors reported a minimal compli-
cation rate, with exposure of the implant listed as the
most common. Histologic analysis of nine patients
revealed bone and soft tissue ingrowth into the
implant.
Rosen623 described 46 patients treated with
blocks of porous hydroxyapatite (Interpore 200) after
orthognathic surgery. After a follow-up period of
6 to 20 months (average, 9.3 months), a low compli-
cation rate (4%) was attributed to the use of the
implant, and osseous integration was confirmed in all
but two patients. The authors concluded that porous
hydroxyapatite is a feasible bone graft substitute for
interpositional defects in orthognathic surgery.
In a follow-up study, Rosen and McFarland624
obtained biopsy specimens from 11 patients previ-
ously treated with blocks of porous hydroxyapatite
implanted into osteotomy gaps after elective facial
osteotomies. Hydroxyapatite implants were rapidly
invaded by fibrovascular tissue, and bone ingrowth
was observed in 21 of 24 biopsy specimens. The finding
that bone ingrowth was dependent on close, stable
contact with host bone confirmed the conclusions of
Donath et al.600
Cottrel and Wolford625 reported a long-term eval-
uation of 471 coralline hydroxyapatite implants placed
during orthognathic surgery in 111 patients. The
average follow-up was 7.2 years (range, 5.0 to 10.3
years). Ninety six percent of implants were placed
through an intraoral approach. All implants were rigidly
fixed. Two hundred and eighty-nine implants were
placed in direct communication with the maxillary
sinus. A total of 23 implants (4.9%) were removed.
Seven (14%) midpalatal implants used for palatal
expansion required removal. The use of porous
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hydroxyapatite implants for alveolar cleft grafting was
associated with a 100% failure rate. These findings led
the authors to conclude that porous hydroxyapatite
implants are useful for facial augmentation and orthog-
nathic surgery but not for alveolar cleft grafting. In
addition, adequate soft tissue coverage in the nasal floor
and palate is a critical determinant of success in mid-
palatal implants.
Rosen626 and Johnson et al627 have reported on the
salvage of infected hydroxyapatite implants by local
debridement and antibiotic therapy. The authors
attributed the favorable response of hydroxyapatite to
soft tissue ingrowth and resultant vascularization.
However, the limited number of patients (a total of
three in both reports) makes it difficult to draw defin-
itive conclusions about the ability of hydroxyapatite
to resist infection.
CALCIUM PHOSPHATE CEMENTS
The need for a moldable calcium phosphate-based bone
substitute led to the development of the calcium phos-
phate cements. Calcium phosphate cements are easier
to handle because they can be shaped to fit irregular
defects. These products are various formulations of
laboratory-produced calcium phosphate compounds
and are supplied as powders that are reconstituted in
the operating room with a liquid (water, saline, or
sodium phosphate). Three calcium phosphate bone
cements currently marketed are BoneSource,* Norian
Skeletal Repair System/Craniofacial Repair System
(SRS/CRS),* and apatitic calcium phosphate bone sub-
stitute.*
BoneSource
BoneSource was the first reported calcium phosphate
cement.628 It is based on a formulation of tetracalcium
phosphate and dicalcium phosphate dihydrate and is
mixed with water in a ratio of 4:1 just before use. The
reaction is isothermic and occurs at physiologic pH.
This formulation becomes a dense paste that can be
shaped intraoperatively and sets to pure hydroxyap-
atite in 20 to 25 minutes with a final set time of approx-
imately 4 to 6 hours.629 Reconstitution with 0.25 M
sodium phosphate significantly accelerates setting
time (6 to 7 minutes) by decreasing the reaction pH.
The presence of blood or fluid in the operative site can
impede the reaction and thus significantly increase the
time necessary for final set. Thus, a "dry" operative field
is essential for BoneSource use. The compressive
strength of BoneSource after final setting is 50 MPa
"Leibinger Inc., a division of Stryker/Howmcdica, Kalamazoo, Michigan.
T
Noriart Corporation, Cupertino, California.
'ct-BSM, Etex Corporation; marketed by Lorenz in the United States as
Embark and by Merck as Biobon in Europe.
TfcWR^aeldWimage...
with a diametral strength of 8 MPa. The average pore
diameter of BoneSource is 2 to 5 nm, allowing passage
of ionic materials and dyes but not tissue cells or bac-
teria.630
Since its initial description, BoneSource has been
used in a number of craniofacial reconstructive pro-
cedures and has been shown to be biocompatible, non-
mutagenic, slowly resorptive, and partially replaced
by bone."28 BoneSource is FDA approved for repair of
neurosurgical burr holes, contiguous craniotomy cuts,
and other cranial defects with a surface area no larger
than 25 cm2. In addition, BoneSource is approved for
augmentation or restoration of bone contour in the
craniofacial skeleton, including the fronto-orbital,
malar, and mental areas. The use of BoneSource in
sinus obliteration has been reported but is not FDA
approved.631 In addition, the use of BoneSource in
stress-bearing areas (i.e., segmental mandibular recon-
struction) is not advised.
BoneSource is initially invaded by fibrovascular
tissue and is slowly replaced by bone. Osseointegra-
tion of the implant and surrounding bone occurs at
the interface with native bone. In a feline model of
frontal sinus obliteration, approximately 65% of Bone-
Source implants were converted to normal bone by 18
months.632 According to the manufacturer, however,
the extent to which BoneSource is converted to bone
clinically is dependent on a combination of the volume
of implant used, the age and sex of the recipient and
the recipient's general metabolic health, and the
anatomic site of implantation.631
In a relatively large clinical trial, 103 patients were
observed for 2 to 6 years after repair of cranial defects.
Implant volume was judged to be stable at 24 months.631
The overall surgical infection rate was 5.8%, and 2.9%
of patients required implant removal. In this study,
approximately 60% of implants were in contact with
the paranasal sinuses or mastoid air cells. The implants
did not have a higher incidence of infection than clean
sites. This finding was corroborated in a feline model
of frontal sinus obliteration.632
Burstein et al633 reported their experience with 61
patients who underwent secondary craniofacial recon-
struction for contour defects (partial- or full-thick-
ness cranial defects) with BoneSource during a 3-year
period (20-month mean follow-up). In approximately
one third of the patients, 1 g of cephalosporin was added
per 10 g of BoneSource as a means of slow release of
the antibiotic during hydrolyzation of the cement.634
Eleven percent of patients experienced postoperative
complications, most commonly seromas. No adverse
effects on skull growth were noted in the study period.
This finding is corroborated by Lykins et al,635 who
examined the effects of BoneSource reconstruction on
growing feline skulls, and by Gosain,636 who reported
no changes in skull growth after correction of
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24 • REPAIR AND CRAFTINC OF BONE 701
temporal hollowing in a 4'/2-year-old boy with use of
hydroxyapatite bone cement.
Kveton et al637 described the use of BoneSource for
lateral skull base reconstruction in 15 patients with a
maximal follow-up of 24 months. The authors reported
a 75% success rate in restoration of cranial bone in-
tegrity. Suboccipital cranioplasty was least successful
as a result of complete resorption of the bone cement
in three of eight patients. Two patients developed
aseptic meningitis. Exposure to cerebrospinal fluid did
not alter the stability of the cement. In addition, the
authors believed that the careful application of Bone-
Source to mastoid air cells significantly attenuated the
possibility of cerebrospinal fluid rhinorrhea. This con-
clusion was also supported by Friedman et al.631
The use of BoneSource in dentoalveolar recon-
struction has also been reported. Bifano et al638 eval-
uated the potential of BoneSource to augment
edentulous canine mandibles and reported excellent
results with no loss of implanted material. The implants
were partially replaced by bone. Unfortunately, no long-
term data on infection rates were reported.
In a preliminary study, Lew et al639 used hydroxy-
apatite cement to support implants placed in extrac-
tion sockets immediately after tooth extraction. After
3 months, bone contact was variable, and a consider-
able loss of the bone cement was noted. This loss was
attributed to "washout" of the cement before com-
plete setting. All of these cited studies lack adequate
long-term follow-up.
Norton SRS/CRS (Carbonated Calcium
Phosphate Cement)
Norian SRS and Norian CRS are supplied as a
powder (monocalcium sulfate, monohydrate, alpha-
tricalcium phosphate, calcium carbonate) and a solu-
tion of sodium phosphate that are mixed together
before use.640 The cement is implanted at room tem-
perature during a 5-minute interval (implant period),
when the cement is injectable. After injection, the
cement remains moldable for approximately 2 minutes
at physiologic temperature with a final set time of appro-
ximately 10 minutes. After final set, Norian SRS/CRS
continues to cure for approximately 24 hours and
becomes pure carbonated microporous, polycrys-
talline apatite with a maximum compressive strength
of approximately 50 MPa and a tensile strength of 2.1
MPa. These figures can be contrasted with the com-
pressive (1.9 MPa) and tensile (2.42 MPa) properties
of cancellous bone.641 The average pore diameter of
Norian SRS/CRS is approximately 30 nm.642
Norian SRS was FDA approved in 1998 as an adjunct
for fracture stabilization in the treatment of low-
impact, unstable, metaphyseal distal radius fractures
and when early mobilization (cast for 2 weeks, then
removable splint for 2 to 4 weeks) is indicated. The
702 I • GENERAL PRINCIPLES
purpose of Norian in these situations is to fill the voids
between bone fragments of a reduced fracture. Norian
SRS is not indicated in the primary treatment of com-
minuted fractures, in the presence of active or suspected
infection, in diaphyseal fractures, or as a substitute for
external fixation.
Norian SRS has been shown to be clinically useful
in the treatment of distal radius fractures and femoral
neck fractures by increasing initial stiffness and failure
strengths of the fractures.643'650 Norian SRS has been
shown to augment screw fixation in osteopenic bone
and significantly increase the in vitro pull-out
strength.651,652 The use of Norian SRS in distal radius
fractures has been shown to decrease the immobiliza-
tion time (from 5 weeks to 2 weeks), to decrease pain,
to improve range of motion, and to improve grip
strength.643,645,64^!^ most common complication was
loss of reduction (29%). Infection was uncommon
(< 1 %) and did not require implant removal. Care must
be exercised in the use of Norian in distal radius
fractures to avoid intra-articular injection because the
long-term effect of this compound on joint surfaces
is unknown.
Norian CRS was FDA approved in May 1998 for
restoration or augmentation of bone contours in the
craniofacial skeleton, including the fronto-orbital,
malar, and mental areas. In addition, Norian CRS is
approved for cranioplasty procedures with a surface
area of less than 25 cm2. Human trials are currently
under way to evaluate the use of this compound in
frontal sinus reconstruction.
Kirschner et al653 have demonstrated that Norian
CRS may be used as a carrier material for gene therapy
vectors. In this study, the authors showed that aden-
oviral vectors containing the bacterial lacZ gene may
be incorporated into Norian CRS bone cement to
provide sustained local gene delivery. Although in vitro
gene expression was noted as long as 30 days after incor-
poration of the adenovirus into the bone cement, in
vivo expression was evaluated only 5 days after implan-
tation. Thus, longer term studies and evaluation with
functional genes need to be performed.
Similar to BoneSource, Norian SRS/CRS is bio-
compatible with no significant evidence of cytotoxi-
city, systemic toxicity, mutagenicity, sensitization, or
acute intracutaneous reactivity. In addition, chronic
toxicity reactions have not been reported in long-term
animal studies (as long as 4.5 years in canines). Norian
SRS and Norian CRS are invaded by blood vessels and
are fully resorbable and replaced with bone in a process
resembling bone remodeling.654 It has not, as yet, been
definitively proved that Norian is osteoconductive.
Embarkla-BSM
Apatitic calcium phosphate bone substitute is a crys-
talline calcium phosphate apatite cement. Embark cur-
rently has marketing clearance in the United States for
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
craniofacial applications and dental and periodontal
applications. An orthopedic clinical trial is under way.
Embark is approved for craniofacial, dental, and
orthopedic applications in Europe and Canada.
Similar to BoneSource and Norian, Embark is sup-
plied as a powdered blend of amorphous and crys-
talline calcium phosphate that is rehydrated with saline
in the operating room.655The reaction is endothermic,
occurs at neutral pH, and results in a compound with
a long working time (i.e., no setting even after 1 hour at
room temperature). Embark hardens within 20 minutes
at physiologic temperature and can be prepared to
harden at a variety of compressive strengths (ranging
between 5 and 40 MPa). In contrast to BoneSource,
Embark is fully resorbable when set with approximately
2% residual implant after 4 weeks and less than 1% by
26 weeks in a canine femoral slot model.656 Embark is
reported to be osteoconductive and is replaced by fully
remodeled bone after 12 weeks.655 However, further
research is required to confirm the findings of these
animal experiments, and long-term clinical studies are
needed for proper evaluation.
Methyl Methacrylate
Methyl methacrylate is a hydrophilic acrylic resin used
in plastic surgery for the repair of cranial defects and
craniofacial contouring.657"659 The use of this material
in chest wall reconstruction with synthetic mesh has
also been reported.660 Acrylic compounds have been
used extensively in orthopedic surgery as a bone cement
for joint prostheses and as spacers for bone gaps in the
extremities.
Methyl methacrylate is supplied as a powdered
mixture of methyl methacrylate polymer, methyl
methacrylate-styrene copolymer, and benzoyl perox-
ide monomer that is mixed intraoperatively (cold
curing) to form a thick paste. Antibiotics can be added
to the powder, leading to slow release.540 An exother-
mic reaction, generating temperatures as high as
85°C, follows during approximately 8 to 10 minutes
and leads to the formation of a rigid, durable, semi-
translucent, and radiolucent polymer. The mixing and
initial curing of the polymer must be performed on
the back table, and tissue should be irrigated copi-
ously during the polymerization process to avoid tissue
injury.
Methyl methacrylate has numerous advantages
including low costs, custom intraoperative fabrication
with molding to fit irregular defects, ability to contour
after final set, lack of significant biodegradation, and
low thermal conductivity. In addition, once implanted,
methyl methacrylate implants are surrounded by a
fibrous capsule and are well tolerated. The disadvan-
tages of methyl methacrylate include high cure
temperatures, high bacterial adhesion property, and
pungent allergenic fumes when it is mixed.661,662 Methyl
T-ek^s^adtfW image...
methacrylate is susceptible to infection and is not indi-
cated in the repair of contaminated or infected areas.
T h e use of methyl methacrylate in pediatric craniofa-
cial reconstruction has been complicated by thinning
of the overlying skin, leading to implant exposure and
extrusion. 657
Lorenz Surgical markets a variant of methyl
methacrylate as a substance referred to as hard tissue
replacement. This c o m p o u n d is a composite of poly-
methyl methacrylate and polyhydroxyethyl methacry-
late and is available as a custom-fabricated, preformed
(heat cured) implant based on three-dimensional
reconstructions from computed tomographic scans.
This c o m p o u n d is extremely strong and has inter-
connected porosity that enables fibrovascular invasion
and limited osseointegration at the implant-bone inter-
face. This c o m p o u n d has been used in large, full-thick-
ness calvarial a n d orbital reconstructions and is
primarily indicated when autologous material is not
available or is otherwise contraindicated. 657,663
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image...
CHAPTER
25 •
Repair and Grafting of
Peripheral Nerve
SALEH M. SHENAQ, MD, FACS •
HISTORICAL BACKGROUND
MORPHOLOGY AND PHYSIOLOGY OF PERIPHERAL
NERVE
PERIPHERAL NERVE INJURY AND REGENERATION
CLASSIFICATION OF NERVE INJURY
CLINICAL EVALUATION
ELECTRODIAGNOSIS
Electromyography
Electroneuronography
Nerve Conduction Studies
Somatosensory Evoked Potentials
IMAGING STUDIES
SURGICAL TREATMENT OPTIONS
Principles of Nerve Repair
Peripheral nerve injuries manifest themselves in
myriad forms from acute penetrating trauma to
chronic compression neuropathies, obstetric birth
trauma, and iatrogenic injury. A careful analysis of pre-
senting history and clinical examination findings can
unveil the salient anatomic and pathologic aspects of
the injury and thereby direct management.
The fundamental grounding in the morphology and
physiology of nerve injury and regeneration provided
by Seddon and Sunderland still carries practical sig-
nificance for the modern peripheral nerve surgeon.1"3
Concomitantly, the gains in understanding and appli-
cation of microneurosurgery by Millesi and others are
brought to bear in every case encountered. 4 However,
new technologies, creative new application of tradi-
tional principles, and a deeper, keener understanding
of the molecular mechanisms of nerve injury and repair
are heralding an oncoming revolution in the field. The
prominent natural historian Stephen Jay Gould has
postulated that the general process of evolution is not
simply a gradual accretion of minute change but rather
an equilibrium punctuated by sudden, violent accel-
erations in development. 5 We may very well be at the
cusp of a similar dramatic change in how we perceive
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
JOHN Y. S. KIM, MD
End-to-Side Neurorrnaphy
Nerve Grafting
Vascularized Nerve Grafts
Allografts
Nerve Conduits
OUTCOME OF PERIPHERAL NERVE REPAIR
Upper Extremity
Lower Extremity
Brachial Plexus Reconstruction
Facial Nerve
Cavernous Nerve Reconstruction After Radical
Retropubic Prostatectomy
The Effect of Irradiation
POSTOPERATIVE CARE AND REHABILITATION
new technologies and principles and apply them to
peripheral nerve injury.
HISTORICAL BACKGROUND
Although there are early references to the repair of
severed nerves (Paulus Aegineta, 7th century; Roger
of Parma and William of Saliceto, 13th century), the
rapid evolution of surgical understanding and treat-
ment of nerve injury has been a phenomenon of
the last 2 centuries. These advances in clinical man-
agement have been predicated on more precise
investigations of the pathophysiology of injured
and rehabilitated nerves. For instance, in the late 18th
century, Galvani drew on developments in microscope
optics and careful animal experiments to demonstrate
the important relationships among nerves, muscle con-
traction, and electrical stimuli. Bell and Purkinje
further elucidated the intimate connection between
spinal roots and the axons of peripheral nerves. Waller
made his seminal discovery of the postinjury degen-
eration of the axon in 1850. Paralleling these basic
science discoveries were such clinical developments as
Paget's successful primary suture repair of a transected
719
TeWttf'aeldWimage...
720 I • GENERAL PRINCIPLES
median nerve (1847) and Vulpian's experimentation
with nerve grafts (1810).6"9
Silas Weir Mitchell drew on the unfortunate
circumstance of Civil War trauma to provide detailed
clinical observations of peripheral nerve injury and
causalgia in 1872. Similarly, and perhaps in response
to the mass of nerve injuries in World War I, the clin-
ical study and application of nerve grafting techniques
intensified in the early part of the 20th century with
Mayo-Robson (1917), Delangeniere (1924), and
Bunnell (1927).3,8 At this time, Wyeth and Taylor (1917,
1920) were claiming favorable results with primary
nerve repair.3,8
World War II afforded Seddon and others the oppor-
tunity to investigate a broad spectrum of peripheral
nerve injury, with associated attempts at primary repair
and grafting. St. Clair Strange10 reported on the first
vascularized nerve pedicle for reconstruction of a large
nerve defect in 1947. However, disappointing clinical
outcomes discouraged widespread acceptance of nerve
reconstruction for decades to come.
The introduction of microsurgery challenged the
idea that successful nerve reconstruction was implau-
sible. Millesi was one of the first to advocate a tension-
free repair, and his refinement of grafting techniques
brought about a renaissance in peripheral nerve
surgery that has carried its momentum into the new
century.4
MORPHOLOGY AND PHYSIOLOGY
OF PERIPHERAL NERVE
An appreciation of the anatomy and physiology of the
peripheral nervous system is fundamental to our assess-
ment and repair of these lesions. Fundamental to func-
tional nerve repair is a comprehensive knowledge of
the gross anatomy and microanatomy of peripheral
nerves, their relationship to neurons and supportive
connective tissue, and their sensory and motor end
organs in relation to their biochemical and biome-
chanical properties.
Peripheral nerve is derived embryologically from
the ectodermal layer. During the third to fourth weeks
of embryonic life, neural crest cells form in the neu-
roectoderm and migrate into mesoderm. There they
will give rise to dorsal root ganglia, Schwann cells, and
other neuroblastic cells. As the spinal cord develops,
axons of motor neurons based in the basal plate (what
will become the ventral horn) start sending out
processes to the mesodermally derived muscle. Dorsal
root ganglia start sending out processes in bidirectional
fashion to the rudimentary dorsal horn and to the
periphery. Biochemical ontogeny studies with trans-
genic mice have shown that Schwann cell-derived
signals, such as a variant of Sonic hedgehog, are respon-
sible for induction of connective tissue sheath devel-
opment. 11 Schwann cells start myelination of these
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Dr.Mustafa D.
axons in the fourth month of fetal life, but some motor
axons do not begin this process until the first postna-
tal year.12,12"
The peripheral nerve is composed of sensory,
motor, and sympathetic fibers. These fibers are extended
processes of nerve cell bodies located in the dorsal root
ganglion, lamina XI of the anterior motor horn,
and sympathetic ganglia (Fig. 25-1). The nerve fibers
themselves are composed of axons—processes extend-
ing from the cell body through which conduction of
electrical impulses occurs. An axon may progress thou-
sands of multiples of its originating cell body length
and compose more than 90% of the total cytoplasmic
volume of the nerve.
Axons can be either myelinated or unmyelinated
and are supported by Schwann cells. In the myelinated
axon, Schwann cells generate myelin over an inter-
node. The region between myelinated axonal segments
or Schwann cell processes is an unmyelinated section,
the node of Ranvier. An intricate interplay of adhe-
sion molecules and sodium ion channels at these nodes
results in saltatory conduction, accelerating the rate
at which electrical impulses travel the length of the
axon.13
Moreover, the degree of myelination also has an
impact on the conduction velocity of the nerve. In
general, the larger myelinated fibers correspond to
higher conduction velocity. An unmyelinated motor
or sensory nerve may be 0.2 to 1.5 Lim in diameter with
a conduction velocity of 0.4 to 2.0 m/s. A large myeli-
nated nerve may be 12 to 20|im in diameter with a
conduction velocity several orders of magnitude
higher—72 to 120 m/s.14
Axoplasm contains a complex network of micro-
tubules and neurofilaments that are important not
only for structural integrity but also for axonal trans-
port.15"17 Anterograde transport allows both membrane
and axoplasmic structural elements to be ferried to
areas in need of repair or synthesis. Retrograde trans-
port allows constituent byproducts and certain neu-
ronotrophic factors such as nerve growth factor to be
relayed back to the cell body for processing.18"20
Each individual nerve fiber is surrounded by
endoneurium, and within the endoneurial space lies
a dense network of capillaries (Fig. 25-2A) The capil-
lary endothelial cells form a blood-nerve barrier—not
unlike the well-characterized blood-brain barrier—
allowing diffusion and active transport of critical pro-
teins and signaling chemicals.21
A group of nerve fibers may form a nerve fascicle
when they conglomerate and are surrounded by a mul-
tilamellar collagenous sheath known as the per-
ineurium. 22 Blood vessels also lie between the different
lamellae of the perineurium separated from endo-
neurial capillaries by this thin fibrous membrane.
The perineurium maintains a high pressure inside
the nerve fascicles; this same pressure explains the
image...

25 • REPAIR AND GRAFTING OF PERIPHERAL NERVE 721

FIGURE 2 5 - 1 . The pathway from spinal

cord to the various sensory end organs
through the dorsal rootganglion. A, Spindle
cell-mediated sensations of muscle stretch
and tension. B, Free nociception nerve
endings. C, Pacinian corpuscle for high-
frequency vibrations and moving t o u c h -
often found in the deep dermis. Note the
bipolar nature of the dorsal root ganglion.
The motor end plate is the critical juncture
where acetylcholine is released to activate
muscle sarcoplasmic reticulum and thereby
initiate muscle contraction (D).

phenomenon of "mushrooming" of nerve fibers on
perineural transection. The perineurium also main-
tains a diffusion barrier around the nerve fascicle and
functions as the main tensile load-carrying connec-
tive tissue component of peripheral nerve.7,23,24
A loose connective tissue layer known as the
epineurium surrounds groups of fascicles and thereby
defines a nerve trunk. Fascicles can be arranged in a
variety of patterns; however, three general layouts
predominate (Fig. 25-2B):
1. A monofascicular pattern is composed of one
large fascicle without interfascicular epineurium.
2. An oligofascicular pattern consists of a small
number of large fascicles. Fascicle size and
minimal nonfascicular tissue allow greater flex-
ibility during repair.
3. A polyfascicular pattern is composed of many
small fascicles of varying size.
Because individual fascicles may need to be isolated
before alignment, a large amount of nonfascicular
tissue or a large number of fascicles or small fascicle
size can intensify the difficulty of repair.25
The topographic anatomy of peripheral nerves has
a variable degree of fascicular mingling with redun-
dant branching that may be rationalized teleologically
by the protective advantage afforded if partial nerve
injury occurs. Moreover, the patterns of intraneural
topography can abruptly change over short distances
of nerve (Fig. 25-2Cand D). From a practical stand-
point, the altered fascicular arrangements of nerve as
they traverse in a proximal to distal direction should
be noted. The interconnections between fascicles
appear to lessen in the distal aspect of the extremity,
and interfascicular dissection is clinically feasible.8 Fas-
cicular patterns of motor and sensory branching in
peripheral nerves are essential in such contexts as
brachial plexus reconstruction, in which accurate

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Dr.Mustafa D.
722 I • GENERAL PRINCIPLES

Vasa nervorum

Endoneurium
Perineurium
Epineurium

&k
•• *. •• JLAR
v ..

mp*.\
I

m* .,; —"c-iCUlAR

u*V
FIGURE 2 5 - 2 . A, The layers of the normal
. 1 * * nerve fiber including myelin-ensheathed axon,
endoneurium, perineurium, and epineurium.
The Schwann cell nuclei and vasa nervorum can
B also be seen relative to the constituent layers.
B, Patterns of intraneural structure: monofas-
cicular, oligofascicular, polyfascicular. (From
Lundborg G: Nerve trunk. In Lundborg G, ed:
Nerve Injury and Repair. Edinburgh, Churchill
Livingstone, 1988:42-56.) C, Changes in fasci-
cular topography over a 3-cm segment of the
musculocutaneous nerve. (From Sunderland S:
Nerve and Nerve Injuries, 2nd ed. New York,
Churchill Livingstone, 1978.) D, Cross section
of fascicular pattern at 2-mm intervals of the
radial nerve. Note the abrupt changes in fas-
cicular topography over short segments. (From
A -* 2 mm *• B Aon 8 Sunderland S: Nerve and Nerve Injuries, 2nd
ed. New York, Churchill Livingstone, 1978.)

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Dr.Mustafa D.
T*W)W<aa<I1W image...
25 • REPAIR AND CRAFTING OF PERIPHERAL NERVE
coaptation of fascicular patterns can ameliorate prob-
lems of deranged cortical somatotopy.
The vascular supply to nerves is a complex arrange-
ment of epineurial, perineuria!, and endoneurial
plexuses along with an extrinsic paraneurial network
of vessels.26,27 This rich vascularity provides a measure
of resistance against ischemic insult at a specific
injury locus. However, more global neuropathy can
occur if the inflow to the vasa nervorum is violated,
as in the instance of thrombosis of a proximal
artery.28
More subtle regulatory pathways of axonal metab-
olism may be present in the nervi nervorum, termi-
nal free nerve endings derived from the constituent
connective tissue layers of nerves. This intrinsic affer-
ent system has the capacity to release neuropeptides
implicated in regional vasoactive responses. 29
Extrinsic influences on axons also occur by Schwann
cell interactions. .Vxon caliber itself may be modulated
by Schwann cell-mediated actions leading to alter-
ations in neurofilament phenotypic expression.
Phosphorylation of filaments seems to play a role in
determining density of these neurofilaments and
hence the caliber of myelinated axons.30,31
The endpoint of somatic motor neurons is the
motor end plate. Ultrastructural studies reveal the pres-
ence of a synaptic cleft from which neurotransmitters
like acetylcholine are released to activate the border-
ing muscle cell and evoke the cascade of muscle action
potential (see Fig. 25-2). The injurious effect of axon
transection leads to acetylcholine receptors cropping
up at extrasynaptic sites with concomitant generation
of disordered fibrillation potentials approximately 3
weeks after denervation. 32
Somatic sensory receptors are divided into multi-
ple classification schemes. Essentially there are
Fibroblast
Schwann cell
Leukocyte
FIGURE 2 5 - 3 . A representative
sample of the complex of nerve
growth factors and other cytokines
that modulate interactions among
the nerves, Schwann cells, and
inflammatory cells. CNTF, ciliary neu-
rotrophic factor; GDNF, glial cell
line-derived neurotrophic factor;
IFN-Y, interferon-y; IGF, insulin-like
growth factor; IL, interleukin; NCAM,
neural cell adhesion molecule; NGF,
nerve growth factor; TGF-p, trans-
forming growth factor-p. Proximal
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Dr.Mustafa D.
723
mechanoreceptors, nocireceptors, and thermorecep-
tors with differing fiber thicknesses indicative of their
conduction velocities. In addition, receptors can
demonstrate a slow or rapid adaptive response. For
instance, in glabrous skin, Meissner corpuscles are fast
adapting, whereas Merkel cell receptors are slow adapt-
ing.33 Often, even putatively, pure motor nerves will
have substantive afferent myelinated components.
Neurotrophic growth factors certainly enhance
neurotropism, that is, the guidance of the direction of
growth cone regeneration that can be induced by end
organs or the distal cellular and structural components
of Schwann cell and matrix and conduit, and these
same mediators appear to work in concert to exert their
neurotrophic effect. Both sensory and motor end
organs secrete a complex of neurotrophic factors in
varying fractions with varying temporal relations (Fig.
25-3). Nerve growth factor, brain-derived neurotrophic
factor, neurotrophins, ciliary neurotrophic factor,
platelet-derived growth factor, and glial cell line-
derived neurotrophic factor are all involved in main-
taining the integrity of axonal projections and may
factor in target organ specificity. For instance, glial cell
line-derived neurotrophic factor mRNA is seen in
skeletal muscle, and evidence suggests that it is trans-
ported in retrograde fashion to motor neurons.
Axotomy-induced changes in motor neurons are
attenuated by overexpression of glial cell line-derived
neurotrophic factor in a dose-dependent manner. 34
PERIPHERAL NERVE INJURY AND
REGENERATION
Regardless of the etiology, classic changes associated
with nerve injury follow a similar pattern. By focus-
ing on the pathophysiologic aspects of the injury,
\
— 1 «•» fcj
IL-1 NGF
IL-2 GDNF
IL-6 CNTF
TGF-p IFN-y
IGF NCAM
&&A
Distal
724 I • GENERAL PRINCIPLES
surgical strategy can be extrapolated without great
difficulty.
At a molecular biologic level, axotomies induce a
cascade of changes in the proximal and distal axon,
the cell body, and the surrounding Schwann cells and
recruited inflammatory cells. Many of these changes
are mediated by neurotrophic factors and other gen-
eralized cytokines (see Fig. 25-3).
Axonal injury leads to axoplasmic leakage and
increased membrane permeability with eventual col-
lapse and edema formation (Fig. 25-4). The standard
release of cytokines leads to leukocyte recruitment with
clearance of cellular and axonal debris. Monocytes in
turn secrete interleukin-1, interleukin-2, interleukin-6,
transforming growth factor- (i, and interferon-y, which
act through autocrine and paracrine pathways on both
inflammatory cells and native Schwann cells (see Fig.
25-3).35"38 This process occurs at the site of injury but
may also occur at the cell body. In fact, the severity of
injury at the axonal level may induce apoptotic events
within the neuron. 39
The axons distal to the lesion start to undergo
degenerative changes pursuant to the loss of axoplas-
mic continuity with the cell body, a process better
known as wallerian degeneration. The direction of
axonal loss is from distal to proximal, and the
axolemma and myelin sheath degradation stimulates
the activation and proliferation of Schwann cells, which
act in concert with macrophages to scavenge the
byproducts of axonal loss. If the endoneurium remains
intact, the Schwann cells will generally arrange them-
selves spatially to form a cellular conduit across the
axotomy site and form the histologic structure known
as the band of Bungner. The process of generating this
scaffolding of cells and matrix is mediated by up-
regulation of cell adhesion molecules such as neural
cell adhesion molecule and cytokines such as nerve
growth factor.40"42
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Dr.Mustafa D.
The axon proximal to the lesion will degenerate in
retrograde fashion with an immediate activation of
axonal growth factors, leading to formation of fresh
neuronal growth cones within hours (Fig. 25-5 and
Color Plate 25-1). The attempted program of regen-
eration follows a target organ-sensitive complex of
tropic signals in conjunction with the physical plat-
form laid down by Schwann cells (see Fig. 25-3). The
success of this process is a function of the degree and
anatomic location of injury as well as of the magni-
tude and appropriateness of neuronal and Schwann
cell response. In experimental models, 20% to 40% of
axotomies of the sensory axons result in dorsal root
ganglion apoptosis.43,44 Thus, survival of the cell body
is one parameter of regeneration and a measure of
lesion severity.
Centrally, microglial and astroglial cells will
undergo changes in conjunction with the transgan-
glionic changes of sensory ganglia. The profile of adap-
tation favors axonal growth with down-regulation of
factors related to synaptic transmission.45,46 Higher
order processing at the cortical levels also impinges
on the injury and regeneration cycle. For instance,
after transection and repair of sensory nerves in imma-
ture primates, there is a noted lack of topographic
order in the regenerating extremity nerve. Yet the
somatosensory cortex has a high degree of order in
its somatotopic representation, suggesting that reor-
ganization of sensory topography at the cortical level
can compensate—to a degree—for the relative chaos
in topography at the peripheral nerve level. The
corollary to this premise is that sensory re-education
may be more facile in the developing brains of the
young. 47 This relation of age to pliability of cortical-
peripheral sensory networks may explain, in part, find-
ings by Onne 48 and others that perceptual recovery
after sensory nerve repair is significantly enhanced in
children relative to adults.
FIGURE 2 5 - 4 . Electron micrograph of acute
degenerative changes in a large myelinated axon
as seen in wallerian degeneration. There is loss of
axonal integrity and secondary dissolution of
compact myelin (arrow). A normal thickly myeli-
nated axon is seen on the left. (Electron micro-
graph courtesy of Dr. Hanno Vogel, Texas Children's
Hospital, Houston.)
T%Wttf<8fl<rw image...
25 • REPAIR AND GRAFTING OF PERIPHERAL NERVE
FIGURE 2 5 - 5 . Electron micrograph of a regen-
erating unit of small axons (arrow] shows the char-
acteristic tendency to fill the residual basal lamina
tube after disappearance of the myelinated fiber.
(Electron micrograph courtesy of Dr. Hanno Vogel,
Texas Children's Hospital, Houston.)
CLASSIFICATION OF
NERVE INJURY
The longevity of the Seddon (1943) and Sunderland
(1951) classification systems stems from their useful-
ness. Their elegant schemas accurately predict the prog-
nosis of nerve injury and can therefore direct
appropriate management (Fig. 25-6). 3,49
Seddon developed a simple scheme to classify
peripheral nerve injury into the following cohorts:
Neurapraxia: a temporary conduction block with
axonal continuity. This mildest form of injury most
commonly stems from modest compression or
traction.
Axonotmesis: loss of axonal continuity with
surrounding connective tissue sheath components
intact. Functionally, this mode of injury results in
wallerian degeneration. Regeneration, however,
occurs from the intact proximal nerve, proceeding
as limited by axonal transport and regrowth of
approximately 1 mm/day. The regenerating nerve
front may be clinically detectable as an advancing
Tinel sign.
Neurotmesis: loss of axonal continuity as well as
complete disruption of the surrounding connective
tissue sheath. The injury to axon and Schwann cells
elicits a potent inflammatory response with the
subsequent likelihood of neuroma formation.
Sunderland's classification is based on the anatomic
layers of the nerve. Sunderland first-degree injury
denotes axonal continuity with a conduction defect,
correlating with Seddon s neurapraxia. Second-degree
injury implies axonal disruption and corresponds to
Seddon's axonotmesis. Neurotmesis comprises Sun-
derland third- through fifth-degree injuries. Sunder-
land third-degree injury implies a severance of the
endoneurium and axonal disruption. Sunderland
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725
fourth-degree injury implies the summed result of
axonal, endoneurial, and pcrineurial disruption, and
fifth-degree injury is complete transection of the nerve
including the critical epineurial layer. Mackinnon has
modified the Sunderland scheme to include a sixth-
degree injury, a multilevel injury with a combination
of any of these lesions along a single segment of nerve.
In neurapraxia or Sunderland first-degree lesions,
the nerve is maintained in continuity, and there is no
wallerian degeneration; spontaneous recovery can vary
from days to months. Second-degree nerve injury is
termed axonotmesis and, like neurapraxic injury, does
not require surgical intervention for functional re-
covery to occur. However, a mild histopathologic
wallerian degeneration occurs distal to the injury
site. Proximal to the site of injury, axonal regeneration
will progress through an intact endoneurium and
perineurium. Second-degree injury is limited to the
axon, so nerve conduction is not disrupted even with
incipient neuroma formation. Recovery is nearly
complete but may require more than 3 months and
can be followed by an advancing Tinel sign.
Of all types of nerve injury, third-degree injuries
have the greatest variability in the level of functional
restoration. Two properties of this type of nerve injury
play important roles in determining level of recovery:
the status of the Schwann cell basement membrane
and the location of the insult along the course of the
nerve. Violation of the Schwann cell basement mem-
brane predisposes the nerve to neuroma formation
with concomitant disruption of axonal regrowth. The
location of the injury also affects recovery. A distal
extremity injury has a greater likelihood of maximal
recovery. Proximally, motor and sensory nerves are
closely juxtaposed within a single fascicle.25 Disrup-
tion of this fascicle will lead to incorrect alignment of
these fibers with their respective end-organ destina-
tions. Increasing nerve specialization occurs distally
726 I • GENERAL PRINCIPLES
Sunderland Seddon
1 The pathophysiologic process of a fourth-degree
_<r^i-ih=g> Neurapraxia
n zz3z
> Axonotmesis
> Neurotmesis
FIGURE 25-6. Classification scheme of Seddon and Sun-
derland. Sunderland's first degree corresponds to
Seddon's neurapraxia—violation of myelin sheath integrity
while axonal continuity is maintained. Sunderland's
second degree reflects violation of the axolemma and loss
of axonal continuity and corresponds to Seddon's
axonotmesis. Sunderland's third degree denotes loss of
endoneurial continuity. Sunderland's fourth degree implies
perineurial violation, and Sunderland's fifth degree is
epineurial violation. Seddon's neurotmesis corresponds
to Sunderland's third through fifth degrees. Mackinnon's
modification, a sixth degree of nerve injury, is defined as
multiple types of these lesions at various loci along the
same nerve.
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in an extremity. As the nerve trunk progresses distally,
each fascicle is increasingly composed solely of either
motor or sensory nerve fibers. Thus, a similar degree
of injury located distally in the extremity may have a
greater likelihood of matching sensory and motor
fibers to the correct end organ.
injury follows a more exacerbated course of third-
degree injury. Derangement of perineurial conduits
complicates the regeneration of fascicular architecture.
Surgical management is almost always necessary.
Complete transection of all layers of the nerve
including the outer epineurium is defined as Sunder-
land fifth-degree injury, and the cascade of inflam-
matory events—wallerian degeneration, leukocyte
and Schwann cell activation, and eventual neuroma
formation—is the most severe. Third- through
fifth-degree injuries correlate with Seddon's
neurotmesis.
Finally, sixth-degree nerve injury implies injury at
multiple anatomic sites along a single segment of nerve
and is often termed neuroma-in-continuity. A nerve
may have various degrees of injury along its course,
depending on a variety of factors, including proxim-
ity to the primary injury.8 The importance of recog-
nizing a neuroma-in-continuity is evident in brachial
plexus surgery: fascicles with advanced third- to fifth-
degree injury will need to be identified intraopera-
tively by inspection and electrophysiologic measures
and ultimately nerve grafted, whereas portions of the
nerve with less severe injury can undergo internal neu-
rolysis without grafting.8,9
CLINICAL EVALUATION
A truism in medicine is that clinical history is the prima
facie evidence of injury or a pathologic process.
Trauma is a common context of peripheral nerve injury.
An investigation of admissions at a level I trauma center
found that 2.4% of all admissions presented with
peripheral nerve injury; 54% of these required oper-
ative intervention. 50 For penetrating trauma, the
weapon, trajectory, and possible ballistics all contribute
to determining the character—and possible progno-
sis—of the peripheral nerve insult. Similarly, traction
and compression injuries may elicit alternative algo-
rithms of treatment.
On physical examination, pain is the most common
indicator of injury; however, its absence is not uncom-
mon by virtue of the patient's concomitant injuries.
Such signs as bruising or swelling in the anatomic dis-
tribution of a suspected impaired nerve are as vital
clues as frank lacerations.
Sensibility is a complex measure of morphologi-
cally differing perceptive receptors. Diminished sen-
sation is often first manifested by decreased ability to
perceive a stimulus. More specifically, the threshold at
image...
25 • REPAIR AND CRAFTING OF PERIPHERAL NERVE
which a stimulus is perceived clearly is altered—-the
actual number of nerve fibers has not changed, but
their sensitivity has been diminished. In compression
injuries, this change in threshold of perception can
progress to frank loss of nerve fibers secondary to the
pathophysiologic response in axoplasmic metabolism
mentioned earlier. Loss of nerve fibers heralds a
decrease in innervation density- The common test
modality of static and dynamic two-point discrimi-
nation measures this very phenomenon; and in the
setting of acute penetrating trauma where the loss of
nerve fibers is at issue, a test of innervation density is
indicated. Detection of early compression neuropathy
may require more subtle threshold tests, however, such
as vibratory sense.51 Normal values of two-point dis-
crimination vary by anatomic location: at the pulp of
the fingertip, static values are 2 to 6 mm, and moving
two-point discrimination is 2 to 3 mm. The pulp of
the great toe has normal values of 8.5 ± 2.2 mm and
8.1 ± 2.4 mm. 52 Vibratory threshold testing is usually
performed with a 256-Hz tuning fork, applying either
the double prong or single end to the pulp and com-
paring this with the contralateral equivalent.
Results of sensory recovery can be expressed by a
grading system originally devised by Highet and
Sanders with a modification made by Mackinnon and
Dellon (Table 25-1).8,53 Purely objective measures of
sensory nerve injury are limited to electrodiagnostic
testing, Moberg's Ninhydrin test, and O'Rain's wrinkle
test. In Moberg's test,54 amino acid-containing sweat
is marked by the applied Ninhydrin; denervated areas
will generally not produce basal sweat and hence will
not chemically react with the Ninhydrin. Similarly,
O'Rain 55 noted that a denervated finger will not
wrinkle when it is placed for a prolonged period in
water.
Motor testing relies on anatomic correspondence
of nerve to muscle. In injury or rehabilitative settings,
the loss or gain of motor function can be assessed
in semiquantitative fashion by use of the British
Medical Research Council (MRC) grading system
TABLE 25-1 • GRADING OF SENSORY
RECOVERY
50 No recovery
51 Deep cutaneous sensation
52 Superficial cutaneous sensation
S2+ Hyperresponse of S2
53 Pain and touch sensation with loss of
hyperresponse; two-point discrimination >15mm
S3+ Good localization; two-point discrimination
7-15mm
54 Complete recovery; two-point discrimination
2-6 mm
Modified from Mackinnon S, Dellon A: Surgery of the Peripheral Nerve.
New York, Thiemc, 1988.
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727
TABLE 2 5 - 2 • GRADING OF MOTOR
RECOVERY BY ASSESSMENT OF
MUSCLE FUNCTION: BRITISH
MEDICAL RESEARCH COUNCIL
GRADING SYSTEM
MO No contraction
Ml Palpable contraction
M2 Active joint motion—but not against gravity
M3 Active joint motion against gravity
M4 Full range of active motion against gravity-
subnormal strength
M5 Full range of active motion—normal strength
Modified from Barnes R: Traction injuries of the brachial plexus in adults.
J Bone Joint Surg Br 1949;31:10-36.
(Table 25-2).* Force transducing measurements have
shown that M3 correlates to 17% to 42% of con-
tralateral normal strength values and M4 correlates to
a range of 66% to 79% of normal. 57
The pattern of nerve regeneration after injury
and repair can often be gauged by an advancing Tinel
sign. The regenerating front of nerve fibers will elicit
a distinct tingling sensation on tapping, and Tinel
noted that the presence of such a progressing sign
corresponded to improved prognosis. 58 Small myeli-
nated and unmyelinated fibers appear to regenerate
faster, resulting in a more rapid return of pain and
temperature sensation first. Sudomotor function as
manifested by sweating returns concurrently. In
terms of perceptive sensation, low-frequency vibra-
tory sense precedes higher frequency vibratory sense
recovery, and if necessary, this can be monitored
clinically.
ELECTRODIAGNOS1S
Electrodiagnostic tests such as nerve conduction
studies, electromyography, electroneuronography, and
somatosensory evoked potentials can be a valued
adjunct to clinical examination in determining the site,
type, and severity of peripheral nerve injury. This in
turn allows greater accuracy in delineating the prog-
nosis and appropriate management. Furthermore,
these tests help evaluate the recovery of nerve func-
tion after peripheral nerve injury and after surgical
repair (Table 25-3).
Electromyography
Electromyography evaluates nerve function by study-
ing the neurophysiologic responses of muscles sup-
plied by a specific nerve during rest and activity
through insertion of a needle electrode into these
muscles. At rest, normal muscle does not display spon-
taneous electrical activity. Peripheral nerve injury leads
728 • GENERAL PRINCIPLES

TABLE 25-3 • ELECTRODIAGNOSTIC TESTS IN PERIPHERAL NERVE INJURY

Pathophysiologic Findings

Normal Axonotmesis or
Methodology Findings Neurapraxia Neurotmesis

Electromyography Measures muscle action Normal muscle Absent muscle Absent muscle response
potentials to motor response response Fibrillations present at
nerve stimulation Fibrillations 2-4 weeks
absent
Nerve conduction Measures nerve Normal action Reduced motor Absent motor and
study conduction velocities potentials and sensory sensory action
Normal latency action potential potential
Prolonged latency Latency absent
Somatosensory Measures cortical Normal cortical Decreased Markedly decreased
evoked potentials response to distal response conduction conduction (>50%)
sensory stimulation Increased latency Increased latency
(>10%)
Electroneuronography Measures facial muscle Equal bilaterally Reduced Reduced amplitude
response to stimulus amplitude (>90% degeneration)

to the appearance of different kinds of spontaneous
activity in different stages of evolution of the injury.
During voluntary contraction, firing of motor units
generates recordable motor unit action potentials.
Changes in the durations, amplitude, number of
phases, and firing properties of these potentials occur
in different stages of peripheral nerve injury and nerve
recovery.
With neurapraxia, changes in recruitment of motor
unit action potentials occur immediately after injury.
In a complete lesion (conduction block), there will be
no motor unit action potentials with attempted con-
traction. In partial lesions, there will be a reduced
number of motor unit action potentials but firing more
rapidly than normal. Because no axonal loss occurs
in neurapraxia, there will be no axonal sprouting and
no changes in motor unit action potential morphol-
ogy at any time after injury.
With axonal nerve injury, denervation is indicated
by the appearance of spontaneous activity (fibrilla-
tion and positive sharp waves) 1 to 2 weeks after distal
and 3 to 4 weeks after proximal peripheral nerve injury.
Understanding this time frame is diagnostically crucial
so that severity is not underestimated when a study is
performed early after peripheral nerve injury and so
that development of increased fibrillation potentials
over time is not misread as a worsening of the periph-
eral nerve injury.59*61
Reinnervation occurs through axonal regeneration
and axonal sprouting. Axonal regeneration leads to the
appearance of small polyphasic unstable motor unit
action potentials (nascent potentials) as the earliest evi-
dence of reinnervation, which usually precedes the
onset of clinical motor recovery. Axonal sprouting will
be manifested by morphologic changes in the existing
motor units. Amplitude will increase, duration will
become prolonged, and the percentage of the polypha-
sic units will increase as the motor unit territory
increases. This process is practically noted 3 weeks after
the injury.62 Evidence of reinnervation at 2 to 4 months
in a previously completely denervated muscle near the
site of the lesion indicates that axonal regeneration has
occurred and some degree of spontaneous recovery is
expected.63,64
Furthermore, electromyography helps define the site
of peripheral nerve injury, which is usually between
the branches to the most distal normal muscles and
the most proximal denervated muscle. Electromyog-
raphy is crucial for localization of brachial plexus
injuries (a full discussion of which is beyond the scope
of this chapter). Denervation of paraspinal muscles is
a sign of motor nerve root and not plexus injury.
Sampling of muscles supplied by different cords and
trunk levels of the plexus (latissimus dorsi, infra-
spinatus, rhomboid, serratus anterior) is needed for
localization of such injuries.
Electroneuronography
A variant of electromyography, electroneuronography
records facial muscle potentials after stimulation of
the facial nerve. Serial electroneuronography readings
are performed in the setting of Bell facial nerve palsy,
and more than 90% degeneration within 2 weeks of
injury had a poor prognosis for recovery (with the
corollary that surgical intervention in these candidates
achieved superior outcome). Conversely, patients with
less than 90% degeneration at 2 weeks spontaneously
returned to House-Brackman grade I or grade II by
7 months. 65

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25 •
Nerve Conduction Studies
To determine conduction velocity of a motor nerve, a
recording electrode is placed on a muscle supplied by
that nerve. The nerve is stimulated at two different sites
sequentially, and the resulting muscle contraction
(compound muscle action potential) is recorded each
time. The distance between these points divided by
the time the impulse needed to travel between them
produces the conduction velocity in meters/seconds.
Measurement of conduction velocity of the sensory
nerves follows the same principles except that the
recording electrode is not placed on a muscle but on
the nerve itself. Sensory action potentials are much
smaller than compound muscle action potentials and
are easily affected by noise. Normal nerve conduction
velocity is 40 to 50 m/s in the legs, 50 to 60 m/s in the
arms. Lower values are used for infants and low body
temperature.
Nerve conduction study plays an important role in
identifying the type and age of peripheral nerve injury
and provides an objective tool for assessment of nerve
recovery spontaneously and after repair. In neu-
rapraxia, compound muscle action potential ampli-
tude remains normal with distal stimulation and drops
or disappears (depending on the severity) with stim-
ulation proximal to the lesion. By use of inching tech-
nique, one can localize the site of the conduction block
precisely. This finding is observed immediately after
the injury. Concomitant conduction slowing is often
demonstrated across the lesion as well. In axonal injury,
the compound muscle action potential amplitude
elicited with distal (as well as proximal) stimulation
starts falling detectably a week after the injury because
of wallerian degeneration. 66 Axonal injuries, however,
cannot be differentiated from neurapraxic ones in the
first week after injury and before wallerian degener-
ation has occurred, a matter that should be borne in
the mind of the referring surgeon.
Compound muscle action potential amplitude
reflects the number of the surviving axons (until col-
lateral sprouting has occurred, then compound muscle
action potential amplitude will be falsely high, leading
to underestimation of the degree of axonal loss). There-
fore, compound muscle action potential amplitude
provides some guide to the prognosis. In facial nerve
lesions, it has been demonstrated that patients with
compound muscle action potential amplitude of 30%
or more of the other side have an excellent outcome,
those with 10% to 30% have good but partial recov-
ery, and those with less than 10% have poor outcome. 67
Comparison of sides is useful to overcome the wide
variation in normative values among individuals.
Sensory nerve conduction studies are also helpful in
localization of peripheral nerve injury. Preserved
sensory nerve action potentials in spite of clinical
sensory impairment in the corresponding dermatomes
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REPAIR AND GRAFTING of PERIPHERAL NERVE 729
are typical of preganglionic lesions such as nerve root
avulsions.68,69 Sensory nerve action potentials are typ-
ically lost or reduced in postganglionic lesions such
as plexus injury.
Somatosensory Evoked Potentials
Somatosensory evoked potential testing involves
recording of the contralateral cerebral cortex responses
to peripheral sensory nerve stimulation by use of skin
surface electrodes. Somatosensory evoked potential
testing is particularly useful to assess proximal (mainly
preganglionic) lesions such as brachial plexus injuries,
for which the utility of nerve conduction studies is
limited anatomically and technically.
IMAGING STUDIES
A number of imaging modalities have found utility
in preoperative evaluation of peripheral nerve injury.
Indirectly, plain radiographs can demonstrate injury
suggestive of potential peripheral nerve injury (e.g.,
elevated hemidiaphragm for phrenic nerve insult, mid^
humeral fractures for radial nerve injury). Classically,
computed tomographic myelography has been helpful
in examining the brachial plexus subset of peripheral
nerve injuries. Computed tomographic myelograms
with 1- to 3-mm slices have a predictive accuracy of
85% compared with 52% for magnetic resonance
imaging.70 The presence of meningocele and the loss
of spiral nerve roots intradurally are highly sugges-
tive of spinal root avulsion (Fig. 25-7).
Magnetic resonance imaging is more effective in
detailing soft tissue and more peripheral lesions.
Indeed, a modified form termed short Tl inversion
recovery shows high correlation with electromyo-
graphic findings of denervated muscle and may detect
injury significantly earlier than electromyography
does.71,72 In the acute setting, this imaging modality
maybe useful in differentiating neurapraxic from neu-
rotmetic injury at an earlier stage than with traditional
electromyography, allowing more expedient inter-
vention in neurotmetic injury.
Another rapidly developing field within magnetic
resonance technology is magnetic resonance neurog-
raphy. Higher resolution scans of peripheral nerves
are being performed with exquisite fascicular detail
and delineation of injury states.73,74
SURGICAL TREATMENT OPTIONS
When a neurologic deficit is associated with trauma,
the two main decision-making avenues depend on
whether the injury is open or closed. If the injury is
open and the mechanism of injury is one of sharp pen-
etrating trauma to the nerve, immediate exploration
is warranted with either primary repair or repair with
730 I • GENERAL PRINCIPLES

FIGURE 2 5 - 7 . A, Magnetic resonance imaging. Coronal section of brachial plexus shows a telltale protruding meningo-
cele (circled area). B, Computed tomographic myelogram. Dye is extravasating through the meningocele between the
sixth and seventh cervical vertebrae (arrow).

a short nerve graft. If, however, the mechanism is one
of traction, blunt trauma, or open injury with a blast
effect, it is acceptable to allow demarcation of con-
tused nerve followed by delayed exploration and
repair as necessary. The question of when to operate
in the setting of peripheral nerve injury is admittedly
problematic. Certainly the mechanism of injury is an
important prognostic determinant. For example,
precise terminal differentiation between viable and
nonviable fascicles may take 8 to 10 weeks for low-
velocity gunshot wounds or 12 to 16 weeks for high-
velocity gunshot or traction injuries.25,75,76
In this regard, serial clinical examinations can be
used to follow the trajectory of the injury—whether
it improves (suggesting neurapraxia or possible
axonotmesis) or remains static or degenerates (sug-
gesting a severe axonotmesis or neurotmesis). In addi-
tion, electromyography at the 3- to 4-week interval
may be helpful in defining the nature of the nerve
response to injury by the denervation patterns in the
affected muscle. On occasion, magnetic resonance
imaging and its variants can also help define aspects
of the injury. If any of these examinations or studies
reveals a progressive denervation pattern or an
anatomic lesion suggestive of neurotmesis or severe
axonotmesis, operative exploration is warranted. In
the case of neurapraxia or mild axonotmesis, close
observation and supportive care are sufficient.
The presence of conduction across a lesion or
neuroma implies a good prognosis without the need
for aggressive intervention (possibly external neurol-
ysis). The absence of such conduction suggests a neu-
rotmetic lesion that requires neurolysis and grafting.
If the injury sustained involves spinal root avulsion
(by radiographic imaging or absent somatosensory
evoked potentials), a neurotization procedure must be
performed whereby grafts are taken to transfer fasci-
cles from proximate donor nerves to the distal portion
of the injured nerve (with neuroma presumably
resected).9,77
If the injury is chronic and end-organ denervation
has evolved to frank atrophy, end organs will not be
available despite potential regeneration across a nerve
graft. However, exploration and neurolysis may still
achieve some amelioration of pain symptoms. Muscle
transplantation in conjunction with nerve grafts may

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25 • REPAIR AND GRAFTING OF PERIPHERAL NERVE
allow restoration of local motor function distal to the
site of chronic injury.
Principles of Nerve Repair
Once the decision to explore the operative field has
been made, the affected nerves are identified and iso-
lated. In the extremities, tourniquet control is helpful
in this regard. With subacute injury, a neuroma-in-
continuity will often be encountered. The dissection
is initiated in normal-appearing nerve through a lon-
gitudinal incision along normal epineurium. As the
neuroma is approached, the scar zone is evaluated
under high loupe magnification (4.5x or better).
Release of the fibrosed epineurium may result in freeing
of soft, pliable fascicles. If deeper scar encasing the
fascicles is noted, internal neurolysis may be neces-
sary. Depending on the severity of the neuroma for-
mation, all or part of the bridging fascicles may need
to be resected and the ensuing defect grafted. Intra-
operative electrodiagnosis may assist in differentiat-
ing viable, conducting fascicles from nonfunctional
ones.
A central dogma of peripheral nerve surgery is a
tension-free coaptation of nerve to nerve or nerve to
graft. Tension will invariably lead to an increased
fibrotic reaction and deranged attempts of regenera-
tion at the repair site.1,78 An adjunct to the direct
mechanical harm that tension causes on nerve regen-
eration is the secondary effect of ischemia. Nerve elon-
gation can result in injury from rupture simply from
ischemic damage. Whereas the peripheral nerve is less
susceptible to ischemic damage than muscle is, as little
as 8% elongation of a nerve segment may result in
decreased blood flow to a nerve, and in fact an elon-
gation of between 10% and 15% may occlude all blood
flow to the nerve. Total ischemic time of more than 8
hours will lead to axonal loss and eventual necrosis.79'80
However, the determination between an acceptable
and unacceptable degree of tension is still largely
dependent on intraoperative judgment and not merely
a calculus of gap length to type of repair.81 Tempo-
rizing measures to reduce tension at the repair site
(extensive mobilization of nerve and extremity posi-
tioning) are controversial because they may hamper
the longer processes of regeneration. Extensive dis-
section may devascularize nerve segments; bringing
the extremity to neutral position several weeks after
surgery may still induce noxious traction injury on
regenerating axons.81*83
For relatively clean transections of nerves in which
significant retraction has not occurred, primary repair
is a viable option. If debridement of nerve ends results
in a nerve gap of more than 2.0 to 2.5 cm, nerve graft-
ing needs to be considered.84 This is true in either acute
or secondary repair situations. On occasion, a con-
taminated surgical wound may prohibit immediate
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Dr.Mustafa D.
731
coaptation of nerves. Alternatively, in a crush injury
situation, the precise demarcation between injured and
uninjured nerve may not be known. In these contexts,
delayed repair of nerves is justified, and the nerves
may be tagged at the initial debridement to facilitate
discovery at an early secondary exploration. Some
advocate placement of several epineurial sutures at
primary surgery to prevent progressive retraction;
however, this does not preclude the potential need
for excision of incipient neuroma at early secondary
exploration. 85
Coaptation is commonly performed with 8-0 to
10-0 monofilament in epineurial or fascicular fashion
(Fig. 25-8). Guide sutures are typically placed at 180
degrees, and the intervening distances are bisected in
serial fashion starting with the posterior surface. The
number of sutures placed depends on the caliber of
nerves (or fascicles), with care taken to avoid tension
and to prevent egress of fascicular contents without
introducing excess foreign body. For smaller fascicles,
a single suture may be sufficient to coapt the ends
adequately.
Tsuge86 has described the use of anchoring funic-
ular sutures to minimize gap defects in coaptation (Fig.
25-9). Jabaley85 has further emphasized the possible
use of epineurial splint sutures placed at a distance 1.5
to 2 times the nerve diameter from the defect to dis-
tribute tension symmetrically. These epineurial splint
sutures do not obviate the principle of tension-free
coaptation but simply distribute tension uniformly on
the cross-sectional area of repair.
Although epineurial sutures have historically been
considered adequate, fascicular sutures should be
considered when intraoperative identification of
fascicular arrangements by electrophysiologic or
immunohistochemicai methods is possible.87'88 Acetyl-
cholinesterase may be used to selectively target motor
axons for intraoperative identification. Problems with
prolonged immunohistochemicai processing times
have been ameliorated by more rapid techniques (2
hours) that are congruent with identification and repair
in a single stage.89 In addition, carbonic anhydrase is
available to stain sensory nerves selectively.90 The evo-
lution of frozen section techniques has improved so
that qualitative assessments of the adequacy of resected
nerve stumps can be delivered by frozen section if the
gross appearance is equivocal.91
The polemic debate over epineurial versus fascic-
ular repair has not been clearly resolved. Prospective
clinical trials are rare; one that examined nerves
repaired by epineurial or fascicular technique found
no significant difference in outcome. 92 In the paucity
of comparative data, many opt for the theoretical
advantage of fascicular repair when a specific and iden-
tifiable topography of motor and sensory fascicles
exists. Using modern intraoperative electrophysi-
ologic testing, one group succeeded in identifying
732 I • GENERAL PRINCIPLES

A. Epineurial repair

B. Fascicular repair

FIGURE 2 5 - 8 . Epineurial (A) versus fascicular (B)

microsuture repair.

sensory and motor fascicles in acute and chronic low

est
FIGURE 2 5 - 9 . Tsuge method of funicular anchoring
suture. (From Tsuge K, Ikuta Y, Sakaue M: A new tech-
nique for nerve suture: the anchoring funicular suture.
Plast Reconstr Surg 1975;56:497.)
median and ulnar nerve injuries with 92% accuracy;
this was followed by fascicular repair, with 78% report-
ing M4 or M5 recovery.96
Another dimension to nerve repair, especially in
chronic peripheral nerve injury secondary to traction
or compression, is neurolysis. External neurolysis—
the release of scarred epineurium affixed to extrinsic
structures, such as an overlying ligament or sur-
rounding soft tissue—can often be employed during
exploration. Internal neurolysis—the release of fasci-
cles encased in scarred internal epineurium—has
been cautiously advocated by some as a preamble to
fascicular repair in chronic injury or with evidence of
severe interfascicular constriction or specific motor
fiber loss and atrophy.83,96,97 Any manipulation of inter-
fascicular anatomy has been demonstrated to result in
fibrosis, and the caveat to any internal neurolysis is a
careful consideration of risk-to-benefit ratios.98
With the advent of new biotechnologies, alterna-
tives to basic suture repair currentiy under evaluation
include lasers and fibrin adhesives. Experimental
studies with carbon dioxide, neodymium:yttrium-
aluminum-garnet, and argon lasers have shown his-
tologic and electrophysiologic evidence of superior
nerve regeneration and coaptation strength compared
with suture repair.99"104 Although the application of
lasers to nerve coaptation showed some promise

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25 •
initially, enthusiasm has diminished as problems with
tensile strength and excessive thermal effects have been
demonstrated. 105
The most serious challenge to simple suture repair
of nerve is the use of fibrin glue and similar adhesives
to achieve nerve coaptation. Although there is con-
troversy about the efficacy of fibrin glue, some studies
purport that tensile strength and gross measures of
regeneration do not seem to be decreased by this tech-
nique.98,105'106 By allowance of molecular diffusion and
ablation of escape growth cones, experimental studies
suggest possible advantages to adhesive use.106,10'
Narakas103 performed clinical studies of fibrin glue in
brachial plexus injuries and found a 30% decrease in
operative time with slightly superior functional
outcome relative to traditional suture-based coapta-
tion. As with any evolving technology, there is a learn-
ing curve associated with fibrin glue use, and the
product is relatively expensive in its current market
incarnation.
End-to-Side Neurorrhaphy
The basic concept of end-to-side neurorrhaphy is that
a distal nerve can be coapted end to side to an adja-
cent, intact nerve with regeneration occurring from
the healthy nerve to the distal degenerating nerve.108,105
The hope is to provide an alternative to standard nerve
grafting when the proximal nerve stump is not avail-
able. Concerns about the origin of the regenerating
axons and effect on donor end-organ innervation have
been raised with the technique. Indeed, there appears
to be a transient loss of donor end-organ innervation
as axons from the intact nerve siphon off into the distal
injured nerve; however, there is rapid compensation
within the donor nerve that prevents frank donor
muscle atrophy." 0
Permutations of the end-to-side neurorrhaphy
include experimental models of side-to-side neuror-
rhaphy and the use of the epineurium of an intact
nerve as a bridge for defects.111,112 In the latter study,
sectioned proximal motor nerves were coapted to the
epineurium of an adjacent nerve, and at some dis-
tance away, the distal end of the sectioned nerve was
coapted to the epineurium of the same intact adja-
cent nerve—in effect creating a double end-to-side
neurorrhaphy of not just the distal cut nerve but the
proximal portion as well. The authors found that in
this manner, proximal nerve axons regenerated along
the epineurium of the intact adjacent nerve, using it
as a bridge to cross into the distal end of the sectioned
nerve. Functional endpoints suggested equivalency
with a control with standard autograft across the same
size defect. However, when nerve grafts were inter-
posed between donor and recipient nerves in a lower
limb experimental end-to-side model, functional aug-
mentation of gait could not be demonstrated. 113 These
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REPAIR AND CRAFTING OF PERIPHERAL NERVE 733
creative approaches to traditional problems of nerve
defects continue to be proffered for more complete
clinical trial evaluation.
Nerve Grafting
Nerve grafting is the sine qua non method of achiev-
ing tensionless coaptation. Autogenous nerve graft
sources include the sural nerve, medial and lateral ante-
brachial cutaneous nerve, sensory branches of C4, great
auricular nerve, terminal posterior interosseous nerve,
and lateral femoral cutaneous nerve. The grafts are laid
in relaxed fashion between the prepared ends of the
recipient and donor nerves, and epineurial sutures
effect tensionless coaptation. All these autogenous
donor nerves will undergo wallerian degeneration but
retain the critical connective tissue scaffold for ingrow-
ing growth cone axons.114 The vascularization of
donor grafts occurs by angiogenesis abetted by sur-
rounding Schwann cells and presumed action of the
complement of growth factors like basic fibroblast
growth factor and nerve growth factor.
Sural nerves typically give 30 to 40 cm of donor
graft with minimal long-term residual morbidity.
Medial and lateral antebrachial cutaneous nerves
allow 10 cm of donor graft and are useful for repair
of median and ulnar nerve defects.114 The lateral ante-
brachial cutaneous nerve has anterior and posterior
divisions that may provide valuable sensory capacity
to the distal forearm and hand, especially in the context
of median and ulnar nerve defects. However, if it needs
to be taken, the distal sensory area of the lateral ante-
brachial cutaneous nerve overlaps with the superfi-
cial sensory radial nerve.115 Conversely, this redundant
innervation has also been noted as a justification for
use of the superficial sensory radial nerve.116 The
sensory branch of C4 and great auricular nerve can
also be useful donors when primary brachial plexus
reconstruction is considered. These sensory nerves can
often be harvested by virtue of their proximity during
the initial exploration of the proximal brachial plexus
in the neck.9 For distal digital nerve grafts, the termi-
nal posterior interosseus nerve is commonly used.117
More proximal nerve grafts in the hand may require
grafts of larger diameter, such as the sural or ante-
brachial cutaneous nerves.118 Cross-sectional area,
typical length, number of axons, donor deficit, and
potential applications of select donor nerves are pre-
sented in Table 25-4. 9 ' ll6 ' I,8 - ,2 °
Vascularized Nerve Grafts
Vascularized nerve grafts are nerve grafts with identi-
fiable vascular pedicles (Table 25-5). Often based on
the sural and ulnar nerves, these specialized grafts have
been advocated for certain extreme grafting situations:
poorly vascularized beds, massive skin defects, and
734 I • GENERAL PRINCIPLES

TABLE 25-4 • SELECT DONOR NERVE CRAFTS

Cross- Typical
sectional Length Number of Potential
Donor Nerve Graft Area (mm 2 ) (cm) Fascicles Donor Deficit Applications

Sural 2.5-3.0 30-40 8-10 Lateral lower leg Brachial plexus,

extremity nerve
defects, cavernous
nerve reconstruction
Lateral antebrachial 1.0-1.5 10-15 4-6 Lateral forearm Extremity nerve defects
cutaneous
Medial antebrachial 0.5-1.0 10-15 2-4 Medial forearm Extremity nerve defects
cutaneous
Great auricular nerve 0.5 3-5 1-2 Upper neck, ear Brachial plexus
Sensory branch C4 0.5 3-5 1-2 Upper neck, ear Brachial plexus
Anterior interosseous 0.5 3-5 2-4 Volar forearm Digital nerve
Posterior interosseous 0.5 3-5 1-2 Distal wrist capsule Digital nerve
Superficial peroneal 1.0-3.0 25-40 2 Lateral aspect of Extremity nerve defects
lower leg
Superficial radial 1.0-2.0 10-15 2-12 Dorsal radial aspect Extremity nerve defects
sensory of distal forearm
and hand
Posterior cutaneous 1.5-3.0 1-7 3-11 Posterior thigh Extremity nerve defects
femoral
Lateral femoral 1.5-3.0 2-8 2-9 Lateral aspect of Extremity nerve defects
cutaneous • thigh

extensive gaps.'21,122 In a long-term study of vascular-
ized nerve grafts to the upper extremity, calculated nerve
regrowth was found to be in excess of 1.5 mm/day,
suggesting possible superior regenerate e capacity as
well.123 Breidenbach12,1 surveyed the potential choices
for vascularized nerve grafts and suggested a classifi-
cation of vascularized nerve grafts based on the blood
supply: no dominant pedicle, one dominant pedicle,
and multiple dominant pedicles.
The caveat is that not all nerves have a suitable vas-
cular pedicle for transfer. Anatomic studies have noted
a variable incidence of suitable pedicles from the super-
ficial radial nerve (100% of nerves with suitable pedi-
cles) to the lateral antebrachial cutaneous nerve (30%
of nerves with suitable pedicles).
TABLE 25-5 • VASCULARIZED NERVE GRAFTS
WITH ASSOCIATED BLOOD
SUPPLY124
The technique of vascularized nerve graft harvest
entails meticulous dissection of the pedicle in prox-
imity to the nerve with preservation of a 2- to 3-mm
cuff of fascia. A skin island can be taken for moni-
toring purposes, and reconstructions are typically
splinted for 3 to 4 weeks postoperatively.125 It may be
desirable to obtain multiple cable strands of vascu-
larized nerve graft to better conform to the diameter
of nerves composing the defect; this can be accom-
plished by incising the epineurium longitudinally fol-
lowed by nerve transection transversely (Fig. 25-10).
ixxx^cr BB 1 CC

Vascularized
Nerve Graft Blood Supply

Sural Superficial sural

Saphenous Saphenous
Anterior tibial Anterior tibial
Ulnar Superior ulnar collateral FIGURE 25-1 0. Vascularized nerve graft. The graft is
Superficial radial Radial cabled while vascularity to the nerve is maintained. (From
Superficial peroneal Superficial peroneal Breidenbach WC, Terzis JK: The blood supply of vascu-
larized nerve grafts. J Reconstr Microsurg 1986;3:43.)

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25 •
Allografts
Allografts have been examined closely as alternatives
to autografts by incorporation of new immunosup-
pressive regimens such as FK506 and monoclonal anti-
body therapy, reduction of the antigenicity of allografts
by rendering them less cellular, and use of nascent
tissue engineering techniques to enhance regenera-
tive potential.126"130 A clinical trial of seven patients
whose reconstructive need for nerve grafts exceeded
available autogenous supply showed that with finite
immunosuppression (12 to 26 months), six of the
patients had some sensory recovery and varying
motor recovery. One patient rejected the allografts
despite therapy. The immunosuppression may allow
the allograft to act as a viable tissue conduit until nerve
regeneration has proceeded to the point at which such
cellular and matrix bridging is no longer necessary—
and at this point, immunosuppression can be stopped
without untoward effects on graft patency or func-
tional recovery.131 The systemic hazards of immuno-
suppression are thus limited to a finite duration. Other
evolving techniques of local immunologic control,
such as use of monoclonal antibodies to CD4 to
pretreat donor antigen, hold the promise of poten-
tially avoiding systemic immunosuppression alto-
gether.125 In select patients with a paucity of donor
grafts relative to a significant anatomic requirement,
allograft nerve transplantation may be of some
utility.
Nerve Conduits
The morbidity of autogenous graft harvest stems from
the loss of sensory nerve and the surgical procedure
itself. Alternatives to autogenous nerve grafts include
vein grafts; other autogenous nerve conduits, such as
amnion tubes; alloplastic conduits, such as silicone and
polyglycolic tubes; and tissue-engineered constructs
that incorporate matrix, scaffold, and cytokine
components.
Vein grafts have the theoretical advantage of being
autogenous, but again they bring a requisite donor site
morbidity. Whereas the results of grafting of defects 3
cm or less are equal to the results of traditional nerve
grafts, longer gaps are not as reliably covered by vein
grafts.132'133
Amnion tubes are another source of allograft mate-
rial, and proof of concept studies have shown that sig-
nificant nerve regeneration can occur in smaller (1 cm)
nerve gaps.134,135 Alternatively, de-epithelialized amnion
has been formulated as a matrix sheet to line nerve
conduits. 136
Early experimental models focused on silicone as
a nerve conduit. 137 Of special interest was the pres-
ence of nerve growth factor and other regenerative
cytokines found within the tube matrix during the
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REPAIR AND GRAFTING OF PERIPHERAL NERVE 735
process of regrowth.13* The advantage of using sili-
cone tubes is to establish a preformed space between
proximal and distal ends; neurotrophic and neu-
rotropic processes allow native regeneration without
the confounding factor of degenerating donor graft
fascicular architecture or infiltrating fibrosis. This
hypothesis was tested in a prospective randomized
clinical trial of small gaps (3 to 4 m m ) treated with
conduit versus primary repair. Early follow-up sug-
gests essentially equivalent results between the cohorts,
with improved touch sensation in the tubulization
group.
Biodegradable material such as extracellular matrix
constituents (collagen, laminin, fibronectin) and
synthetic variants (polylactic acid, polyglycolic acid,
biodegradable polyurethanes and phosphazenes)
have been used in the manufacture of experimental
nerve conduits. I40"U2 An early comparison of collagen-
polyglycolic acid tubes with standard nerve autografts
showed functional equivalence, with the nerve auto-
grafts demonstrating larger axonal diameters. 143 A
decade later, the first randomized prospective clinical
trial of biodegradable nerve conduits in digital nerve,
reconstruction concluded that for large nerve gaps (8
mm or more), polyglycolic acid conduits resulted in
superior moving two-point discrimination versus
autogenous nerve graft; for smaller nerve gaps (4 mm
or less), nerve conduit reconstruction gave superior
moving two-point discrimination versus primary
repair.144
With such promising clinical trials and a plethora
of experimental models awaiting clinical trials, the evo-
lution of these biodegradable nerve conduits will cer-
tainly accelerate. Relevant parameters for optimizing
these systems will include texture, charge, porosity, and
antigenicity of the conduit material; use of soluble neu-
rotrophic and neurotropic factors to be incorporated
into the conduit and to augment regeneration of
growth cones; and possible seeding and architectural
support of Schwann cells and matrix.140,145
OUTCOME OF PERIPHERAL
NERVE REPAIR
Upper Extremity
DIGITAL NERVE
Numerous studies have demonstrated the benefit of
digital nerve repair by grafting or primary neuror-
rhaphy.93,146"152 Sensory recovery is usually S3+or better
in more than two thirds of patients. In one multicen-
ter review of 172 epineurial repairs, prognostic factors
favoring better outcome included younger age and
sharp versus crush injuries. Gender, anatomic loca-
tion of injury (ulnar or radial side; digit), and—sur-
prisingly—interval from injury to repair did not elicit
statistically significant differences.152
736 I • GENERAL PRINCIPLES
MEDIAN NERVE
Motor recovery after microsurgical median nerve
repair is, on the whole, good; 77% to 90% of repairs
achieve M4 or M5 at follow-up.93,96,150 Sensory recov-
ery is less impressive with a wide variation in results;
S3+ and S4 recovery is seen in 46% to 78% of
repairs.93,96,150 The same pattern of prognostic predic-
tors as in digital nerve injury is seen in median nerve
injury. For one, children appear to do remarkably better
(Tajima153 reported a 90% S3+ or S4 sensory recov-
ery) . With simple epineurial neurorrhaphy, Hudson154
noted a mean return of motor power to 4.5 on the
MRC scale and a mean static two-point discrimina-
tion of 5 mm. In addition, low median injuries and
repairs done earlier tend to do better.8,155
For high median nerve injuries, an option is
transfer of the radial sensory nerve, the dorsal cuta-
neous branch of the ulnar nerve, or the ulnar digital
nerve to third web space to the radial digital nerve of
the index finger and the ulnar digital nerve of the
thumb to restore critical hand sensibility. For motor
function in these lesions, ulnar motor branches
to the flexor carpi ulnaris'or expendable motor
median branches can be transferred to the pronator
teres.156
ULNAR NERVE
Ulnar nerve repair, whether by primary neurorrha-
phy or graft techniques, seems to result in universally
poorer motor and sensory recovery compared with
median nerve repair. In most series, approximately half
of repairs result in M4 or M5 recovery.93,150,157 Sensory
recovery was 44% to 60% S3+ or S4.93,150 Results of
delayed secondary repair were similar.158,159 These
nerve repair results are not as good as those noted in
most series of median nerve repair when level of injury
is taken into account. Age again is a significant prog-
nostic factor; in fact, primary epineurial repair of prox-
imal injury—normally antithetical to intrinsic hand
recovery in adults—resulted in satisfactory recovery
of intrinsic hand function in children.160 Strickland15'
noted that whereas distal repair is superior to proxi-
mal repair, delays of up to 6 months did not seem to
impair recovery versus immediate repair. He further
cautioned that a decrease of pinch and grip strength
between 20% and 50% is to be expected irrespective
of the method of repair.
Simple repair or nerve grafting is occasionally dif-
ficult because of long-distance gaps between the site
of nerve injury and the target end organ or because
crush injury has effaced margins of viability. Nerve
transfers have been advocated in cases of irreparable
ulnar and median nerve lesions to restore protective
sensibility to the hand.161 The investigators transferred
ulnar digital nerves of the index and ring finger to
affected denervated areas and noted a 72% rate of
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Dr.Mustafa D.
sensory recovery to the S3+ or S4 level on long-term
follow-up (mean, 78 months).
RADIAL NERVE
Although selected studies report up to 76% M4 recov-
ery in the pre-microsurgery era, a meta-analysis of
radial nerve graft repairs from 1972 to 1990 shows that
66% obtained M4 or M5 recovery.162 Age, nerve gap,
and delay all factored prominently in the pattern of
results. Distal lesions recovered better after grafting than
proximal repairs did. Interfascicular grafting of the
radial nerve resulted in 44% M4 functional recovery;
however, the spectrum of prognostic factors was
somewhat different—earlier grafting (<6 months)
showed superior outcome, but age and length of graft
did not figure prominently.'63 Conclusions on repair
of the radial sensory branch are limited by the small
number of patients enrolled in studies; however, 42%
of those in Frykman's meta-analysis showed evidence
of S3+ or S4 sensory recovery after grafting.162
Lower Extremity
The lower extremity fares worse than the upper
extremity in terms of recovery after peripheral nerve
repair. In sciatic nerve injury, the largest series of lower
extremity peripheral nerve repairs concluded that per-
oneal nerve repair carried a poorer outcome than tibial
nerve repair, with only 36% significant recovery.164
Another study demonstrated modest functional return
with graft repair of sciatic or peroneal defects; ankle
dorsiflexion strength returned to an average of 11%
of that of contralateral normal controls.165
Brachial Plexus Reconstruction
Intraplexus nerve transfer has demonstrated improved
functional outcome in both obstetric and adult brachial
plexus injuries.166"168 Once healthy proximal nerve has
been identified, nerve grafts are used to perform trans-
fers to proximal anterior and posterior divisions of
trunks or to terminal nerves such as the supraspina-
tus (Color Plate 25-2). Terzis167 has noted the general
trend of improved neurotization with increased axon
number and specificity of target; regression analyses
of another series of nerve transfers suggested an inverse
relationship between the length of graft and functional
outcome.169
For C5-6 lesions, employing this strategy in obstet-
ric brachial plexus primary reconstruction yielded
an improvement in deltoid and biceps function. For
C5-7 lesions, triceps also improved significantly,
and in complete C5-T1 injury, moderate gains were
obtained in hand function as well (Table 25-6).
For severe avulsions of the upper or, less commonly,
the lower trunk, nerve transfer from intercostals,
image...

25 • REPAIR AND CRAFTING OF PERIPHERAL NERVE 737

TABLE 25-6 • COMPARISON OF PREOPERATIVE Microvascular muscle transplantation with rein-

AND POSTOPERATIVE nervation by ipsilateral facial nerve or by contralateral
FUNCTION BY INJURY* cross-nerve grafts is now a part of the reconstructive
surgeon's armamentarium for facial nerve injury.180The
Percentage of Patients with lack of suitable donor nerve for free muscle transfer
• M 4 o r 1v!5 Function often necessitates the use of cross-facial nerve graft-
ing in a preliminary stage, followed by coaptation of
Injury Profile Preoperative Postoperative
regenerated nerve to donor muscle nerve at a later
C5-6 * time. No donor morbidity results with division of
Deltoid 1% 26% the contralateral donor buccal branches, and the
Biceps 5% 45% majority (86% in one series) report satisfactory return
C5-7 of symmetry and nearly natural animation.182,183
Deltoid 0% 18%
Biceps 10% 35%
Triceps 20% 57% Cavernous Nerve Reconstruction
C5-T1 After Radical Retropubic
Deltoid 0% 7% Prostatectomy
Biceps 0% 15%
Triceps 796 29% The cavernous nerves are derived from parasympa-
Hand 1% 17% thetic fibers from S2 to S4 and from sympathetic fibers
from Tl 1 to L2.184 These fibers then form an autonomic
"The proportion of patients with M4 or M5 function before and after primary plexus innervating the corpora cavernosa. During
brachial plexus reconstruction is compared by level of manifest injury.168 radical retropubic prostatectomy, the distal portion of
the cavernous nerves may be sacrificed to ensure ade-
quate oncologic resection. These nerves are largely
accessory, phrenic, and contralateral C7 can be con- responsible for erectile and sexual function. The loss
sidered. Experiences vary, but intercostal and intra- of even one neurovascular bundle may result in impo-
plexus nerve transfers have been found to be superior tence, and the loss of both bundles will inexorably
to contralateral C7 nerve transfers.167,168 prevent spontaneous erection.185,186
Experimental models demonstrated a 50% return
Facial Nerve of stimulated erections after interpositional nerve graft-
ing across the cavernous nerve defect.187 On the basis
In general, immediate neurorrhaphy or nerve of these results, early clinical studies have been initi-
grafting of facial nerve injury yields excellent to ated with interposition sural nerve grafts to bridge cav-
superb results in more than 50% of patients.170,171 ernous nerve defects in both unilateral and bilateral
Hypoglossal-facial nerve crossover is less effective but resections.185,187,188 The technique involves grafting
can generate good to excellent results in 42% to 6 1 % across a 5- to 6.5-cm defect (Color Plate 25-3). The
of patients. 172,173 Prognostic parameters of poor location of the distal plexus is facilitated by use of the
outcome after repair and grafting of the facial nerve
in the setting of oncologic ablation include duration
of injury, presence of preoperative palsy, and age older
than 60 years.174 A scale of facial muscle function after
TABLE 25-7 • SCALE OF FACIAL MUSCLE
reconstruction is presented in Table 25-7.
FUNCTION AFTER
Elimination of tongue atrophy and improved facial RECONSTRUCTION175
muscle function have been reported with use of inter-
position nerve graft between donor hypoglossal nerve Grade Results Definition of Recovery
fascicles and recipient facial nerve.176 Use of the con-
tralateral facial nerve as a donor and grafting in cross- l Superb Excellent with minimal mass
facial fashion have been successful in providing movement
reinnervation to ipsilateral facial muscles or to func- II Excellent Mass movement; can close eyes,
tional muscle transplants. 171,177 While waiting for smile
III Good Tone and symmetry without
axonal growth across the graft, a hypoglossal nerve or ability to smile and close eyes
motor branch to the masseter transfer may be useful simultaneously
to prevent denervation atrophy of mimetic muscles IV Fair Incomplete eyelid closure or very
before definitive contralateral facial nerve transfer. weak mouth movement
Avoidance of end-organ muscle atrophy pending V Poor Symmetry only, tone intact, no
movement
cross-facial graft repair has improved functional
VI Failure Flaccid, tone lost
outcome.' 78,179

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Dr.Mustafa D.
TeWR^aadW image...
738 I • GENERAL PRINCIPLES
CaverMap, an electrical stimulation system that local-
izes the distal end of the cavernous nerve.189 Prelimi-
nary reports show that sural nerve grafting across
bilateral cavernous nerve defects results in 33% to 50%
return of sexually useful erectile function (overall,
>75% return of erectile function).184,188 Maximal
return of function begins at 14 to 18 months.184
The Effect of Irradiation
Grafting in the setting of oncologic resection (e.g., after
facial nerve resection in head and neck cancer or after
cavernous nerve sacrifice in prostatectomy) is often
fraught with the potential of postoperative irradia-
tion. Experimental studies in a posterior tibial nerve
graft model have shown that although there is a
decreased number of axons in the distal irradiated
nerve segments, no functional disability is noted rel-
ative to the nonirradiated cohort.190,191 Clinical corre-
lates of these experimental studies are few; however,
studies have generally shown that irradiation does not
impair functional outcome after peripheral nerve graft-
ing.174,192 A larger retrospective analysis investigating
facial nerve grafting found that the median time to
optimal function was slightly longer in the irradiated
patients; however, the overall House-Brackman grade
was no different between irradiated and nonirradi-
ated patients. Whether irradiation occurred in the
immediate postoperative period (<6 weeks) or later
(>6 weeks) did not factor in overall best functional
recovery.174
POSTOPERATIVE CARE AND
REHABILITATION
Primary nerve repairs are at slightly higher risk for
mobilization-induced injury and are generally immo-
bilized for 3 weeks. Nerve graft repairs may generally
begin some passive motion exercises at 2 weeks. Elec-
tromyography and nerve conduction tests can be per-
formed at 3- to 6-month intervals to chart the progress
of regenerating nerve. A Tinel sign may be present at
the leading edge of regeneration through a graft. If
there is a lack of electrophysiologic or clinical evidence
of nerve regeneration or if severe pain accompanies
partial return of function (suggesting neuroma for-
mation), re-exploration may need to be considered—
generally after 6 months. 23
When a mixed function nerve has been repaired
with graft, attention must be focused on re-
educating sensory and motor cortical maps. Integra-
tion of the novel sensory inputs into an adapting
cortical map is critical to full functional recovery.142
Repetitive, active exercise and tactile discrimination
are features of a rehabilitation program geared to this
awareness. A prospective clinical trial based on this
premise showed that aggressive pursuit of tactile
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Dr.Mustafa D.
stimulation after digital nerve repair resulted in 68.8%
of the treatment group's achieving S3+ or S4 sensi-
bility versus only 36% of those who did not undergo
a formal sensory re-education program.193
CONCLUSION AND
FUTURE DIRECTIONS
The central quest in peripheral nerve repair is to opti-
mize the regeneration of nerve so that function can
return. This perforce requires the integration of sound
surgical planning and precise timing and execution
with the use of suitable graft or donor nerves. The
vista of peripheral nerve surgery presented in this
chapter suggests that in most models of injury, this
paradigm of action allows decent return of function.
What are the evolving concepts in peripheral nerve
repair and grafting then?
Nerve Conduits
Ongoing clinical trials are testing the premise that
conduits of varying composition are as efficacious
as standard autogenous nerve grafts in repair situa-
tions. The purported advantages of conduits include
simplification of surgical repair by obviation of the
need for donor graft harvest; manufacturable supply,
so they are not subject to the finite resources of
autogenous material; prevention of scar in growth;
and, potentially, sequestration of neurotropic and
neurotrophic factors for more active and precise
regeneration.194
Incorporated into the nerve conduit scheme is the
increasing awareness of sundry growth factors and
cytokines involved in regeneration. By incorporation
of these factors into the conduit construct itself, con-
duits may actively augment regenerative rates. More
sophisticated constructs are being used in animal
studies—for example, conduits with electromagnetic
and biomolecule chcmotactic gradients.195 Alterna-
tively, evolving analysis of end-to-side neurorrhaphies
has shown that—in principle—nerve can regenerate
unimpeded in healthy nerve trunks through an
epineurial window.196
Gene Therapy and Tissue Engineering
A corollary to the development of nerve conduits is
the possible manipulation of the supporting connec-
tive tissue matrices and Schwann cells.197 Knowing that
nerve growth factor and brain-derived neurotrophic
factor secretion from Schwann cells can promote
growth cone regeneration, constructs are being
designed to constitutively express these genes in
Schwann cells by retroviral transfer and then trans-
plantation of these cells into conduits specially designed
to retain Schwann cells in an artificial lamellar
sheath.145,198 Animal models of peripheral nerve injury
after axotomy have demonstrated the potential utility
image...
25 • REPAIR AND GRAFTING OF PERIPHERAL NERVE
of treatment with adenovirus encoding brain-derived
neurotrophic factor in facilitating recovery. 199
The permutations of conduit and matrix and cells
and growth factors are legion, and as with multimodal
therapy in other diseases, optimal nerve regeneration
may require a chimeric technology. O n e tissue-
engineered nerve graft construct composed of cultured
Schwann cells and basal lamina derived from muscle
was used in a rat sciatic nerve model. 2 0 0 Added to this
was an osmotic insulin-like growth factor 1 p u m p that
was used to bathe the graft with cytokine in the attempt
to enhance functional regeneration. Although the
ambitious addition of the cytokine to the tissue-
engineered graft did not a u g m e n t nerve regrowth in
this specific m o d e l , clearly such sophisticated medleys
of construct and technology will continue to be devel-
oped with increasing relevance and success.
Moreover, these approaches need not be limited to
nerves and their supporting connective tissue elements;
modification of end organs such as muscle to fortify
against denervation atrophy is also an active inves-
tigative topic. 201 Whether gene therapeutics can effec-
tively alter the clinical milieu of degenerating muscle
by cytokine transfection or muscle cell transplanta-
tion remains to be seen.
Nerve Connections
T h e m e t h o d by which nerves and grafts are coupled
may change with emerging clinical data on the effi-
cacy of fibrin glue a n d like substances. Novel ways of
joining nerves—end to side, side to side—need to be
further evaluated not only to delineate the precise
mechanism by which they support regeneration b u t
also to compare t h e m in prospective clinical trials with
preexisting techniques.
Technologic Enhancement of Nerve
and Muscle
Another evolving vista in postoperative care in nerve
repair is the transposition of microtechnology to the
peripheral nerve surgical field. Proof of concept
studies have demonstrated the feasibility of implant-
ing microelectrodes into muscle undergoing dener-
vation changes while nerve regeneration occurs. 202 As
microtechnology and perhaps even nanotechnology
develop, the stimulation of both end-organ and nerve
regeneration m a y be enhanced by bioartificial electric
stimulation systems. Moreover, from the perspective
of the regenerating nerve proper, the advent of nan-
otechnology has yielded new theoretical vistas—for
instance, the creation of carbon nanotubes that repli-
cate conducting axons a n d m a y potentially act as sub-
strates for regenerating nerves. 203
T h e coda to repair and grafting of peripheral nerves
is that reconstructive surgeons will have the o p p o r t u -
nity to define and direct the o n c o m i n g technology.
By doing so, we will take our clinical mission into
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Dr.Mustafa D.
739
intersecting realms of science and innovate a keener,
more relevant form of medicine.
Acknowledgments
The authors would like to thank Aziz Shaibani, MD, FACP, of
the Nerve and Muscle Center of Texas for his contribution,
with special thanks to Lydia Bebczukfor her editorial work on
this chapter.
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imental alternative for vascularized nerve grafts over short gaps.
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135. Mohammed J, Shenaq J, Rabinovsky E, Shenaq S: Modulation
of peripheral nerve regeneration: a tissue-engineering
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1 -centimeter nerve gap. Plast Reconstr Surg 2000; 105:660-666.
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tional repair of median and ulnar nerves in the human forearm:
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140. Furnish EJ, Schmidt CE: Tissue engineering of the peripheral
nervous system. In Patrick CW, Mikos AG, Mclntire LV, eds:
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1998:514-535.
141. Hudson TW, Evans GR, Schmidt CE: Engineering strategies
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142. Lundborg G: A 25-year perspective of peripheral nerve surgery:
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143. Rosen JM, Padilla JA, Nguyen KD: Artificial nerve graft using
collagen as an extracellular matrix for nerve repair compared
with sutured autograft in a rat model. Ann Plast Surg
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144. Weber RA, Breidenbach WC, Brown RE, et al: A randomized
prospective study of polyglycolic acid conduits for digital nerve
reconstruction in humans. Plast Reconstr Surg 2000; 106:1036-
1045.
145. Patrick CW Jr, Assistant Professor and Director of Research,
Dept. of Plastic Surgery, M.D. Anderson Cancer Center,
Houston, Texas. Personal communication, 2002.
146. Uuncke HJ: Digital nerve repairs. Surg Clin North Am
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147. Poppen NK, McCarroll HR Jr, Doyle JR, Nicbauer JJ: Recov-
ery of sensibility after suture of digital nerves. J Hand Surg
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148. Young L, Wray RC, Weeks PM: A randomized prospective com-
parison of fascicular and epincural digital nerve repairs. Plast
Reconstr Surg 1981;68:89-93.
149. Sullivan DJ: Results of digital neurorrhaphy in adults. J Hand
Surg Br 1985;10:41-44.
150. Mailander P, Berger A.SchallerE, Ruhe K: Results of primary
nerve repair to the upper extremity. Microsurgery 1989; 10:147-
150.
151. Wang WZ, Crain GM, Baylis W: Outcome of digital nerve
injuries in adults. J Hand Surg Am 1996;21:138-143.
152. Weinzweig N, Chin G, Polley J, et al: Recovery of sensibility
after digital neurorrhaphy: a clinical investigation of prognostic
factors. Ann Plast Surg 2000;44:610-617.
153. Tajima T, Imai H: Results of median nerve repair in children.
Microsurgery 1989;10:145-146.
154. Hudson DA, Bolitho DG,Hodgetts K: Primarycpineural repair
of the median nerve in children. J Hand Surg Br 1997;22:54-56.
155. Lundborg G: A 25-year perspective of peripheral nerve surgery:
evolving neuroscientific concepts and clinical significance. J
Hand Surg Am 2000;25:391-414.
156. Mackinnon SE, Novak CB: Nerve transfers: new options for
reconstruction following nerve injury. Hand Clin 1999;15:643-
666, ix.
157. Strickland JW, Idler RS, DelSignore JL: Ulnar nerve repair.
In Gelberman R, ed: Operative Nerve Repair and Recon-
struction. Philadelphia, JB Lippincott, 1991:425-436.
158. Vastamki M, Kallio PK, Solonen KA: The results of secondary
microsurgical repair of ulnar nerve injury. J Hand Surg Br
1993;18:323-326.
159. Barrios C, Amillo S, de Pablos J, Canadell J: Secondary repair
of ulnar nerve injury. 44 cases followed for 2 years. Acta Orthop
Scand 1990;61:46-49.
160. Bolitho DG, Boustred M, Hudson DA, et al: Primary epincural
repair of the ulnar nerve in children. J Hand Surg Am
1999;24:16-20.
161. Ozkan T, Ozer K, Gulgonen A: Restoration of sensibility in
irreparable ulnar and median nerve lesions with use of sensory
nerve transfer: long-term follow-up of 20 cases. J Hand Surg
Am 2001;26:44-51.
image...
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162. Frykman G, Gramyk K: Results of nerve grafting. In Gelber-
man R, ed: Operative Nerve Repair and Reconstruction.
Philadelphia, JB Lippincott, 1991:553-567.
163. Nunley JA, Saies AD, Sandow MJ: Results of interfascicular
nerve grafting for radial nerve lesions. Microsurgery 1996;
17:431-437.
164. Kline DG, Kim D, Midha R, et al: Management and results of
sciatic nerve injuries: a 24-year experience. J Neurosurg
1988;89:13-23.
165. Trumble T, Vanderhooft E: Nerve grafting for lower-
extremity injuries. J Pediatr Orthop 1994; 14:161 -165.
166. Narakas AO, Hentz VR: Nerve grafts. Clinical experiences. Ann
Chir Main 1988;8:302-311.
167. Terzis JK, Papakonstantinou KC: The surgical treatment of
brachial plexus injuries in adults. Plast Rcconstr Surg
2000;106:1097-1122.
168. Shenaq SM: Obstetrical brachial plexus palsy: a twelve-year
experience with 1012 cases. American Society for Recon-
structive Microsurgery, Hawaii, January 12-20,1999.
169. Samii M, Carvalho GA, Nikkhah G,et al: Surgical reconstruction
of the musculocutaneous nerve in traumatic brachial plexus
injuries. J Neurosurg 1997;87:881-886.
170. May M: Management of cranial nerves I through VII follow-
ing skull base surgery. Otolaryngol Head Neck Surg
1980;88:560-575.
171. May M: Perspectives in facial reanimation. In May M, ed: The
Facial Nerve, 2nd ed. New York, Thieme, 2000:551-570.
172. Luxford WM, Brackmann DE: Facial nerve substitution: a
review of sixty-six cases. Am J Otol 1985;suppl:55-57.
173. Pensak ML, Jackson GG, Glasscock ME, et al: Facial reanima-
tion with the XII-VH anastomosis: analysis of the functional
and psychological results. Otolaryngol Head Neck Surg
1986;94:305-310.
174. Brown PD, Eshleman JS, Foote RL, et al: An analysis of facial
nerve function in irradiated and unirradiated facial nerve grafts.
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175. May M: The Facial Nerve. New York, Thieme, 1986:318.
176. May M, Sobol SM, Mcster SJ: Hypoglossal-facial nerve inter-
positional-jump graft for facial reanimation without tongue
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177. Scaramella LF: Cross-face facial nerve anastomosis: historical
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178. Endo T, Hata J, Nakayama Y: Variations on the "baby-sitter"
procedure for reconstruction of facial paralysis. J Reconstr
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179. Yoleri h, Songur E, Mavioglu H: Cross-facial nerve grafting as
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evaluation. Ann Plast Surg 2001;46:301-307.
180. Harii K, Ohmori K, Torii S: Free gracilis muscle transplanta-
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181. Harii K: Microneurovascular free muscle transplantation for
reanimation of facial paralysis. Clin Plast Surg 1979;6:361-375.
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184. Kim ED, Nath R, Kadmon D, et al: Bilateral nerve graft during
radical retropubic prostatectomy: 1-year followup. J Urol
2001;165(pt 1):1950-1956.
185. WalshPC,EpsteinJI.LoweFC:Potencyfollowingradicalprosta-
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186. Quinlan DM, Epstein JI, Carter BS, et al: Sexual function fol-
lowing radical prostatectomy: influence of preservation of neu-
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restore erectile function in dencrvated rats. J Urol 1991; 145:380-
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tectomy: The MD Anderson Experience. American Society of
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189. Canto EI, Nath RK.Slawin KM: Cavermap-assisted sural nerve
interposition graft during radical prostatectomy. Urol Clin
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190. Brandt K, Evans GR, Ang KK, et al: Postoperative irradiation:
are there long-term effects on nerve regeneration? J Rcconstr
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ation: theeffectsof postoperative radiation. Plast ReconstrSurg
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192. McGuirt WF, Welling DB, McCabe BF: Facial nerve function
following irradiated cable grafts. Laryngoscope 1989:99:27-
34.
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early tactile stimulation after digital nerve repair. Clin Orthop
2001;384:169-175.
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RP, Langer R, Vacanti J, eds: Principles of Tissue Engineering,
2nd ed. San Diego, Academic Press, 2000:785-798.
195. Yukscl E: Division of Plastic Surgery, Baylor College of Med-
icine, Houston, Texas. Personal communication, 2002-
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1 decreases muscle atrophy following denervation. Micro-
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image.

COLOR PLATE 25-1. Axonal sprouting seen in cross

section (hematoxylin and eosin stain). Regenerating axons
are seen in association with Schwann cell proliferation,
resulting in the discrete bundles of regenerating units
(arrows) in a background of reactive fibrosis (asterisk).
(Photomicrograph courtesy of Dr. Hanno Vogel, Texas Chil-
dren's Hospital, Houston.)

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Dr.Mustafa D.
image...

COLOR PLATE 2 5 - 2 . Primary brachial plexus reconstruction. Note sural nerve inter-
position graft across resected neuroma defect.

Puboprostatic Urethra
ligament Urogenital
diaphragm
Sural n. graft

Neurovascular
bundle (preserved)

Rectum
Levator ani m.

Dorsal vein Bladder

complex
C O L O R PLATE 2 5 - 3 . Sural nerve grafting of cavernous nerve defects after radical prostatectomy.

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Dr.Mustafa D.
image...

CHAPTER

26 •
Alloplastic Materials
TANYA A. ATAGI, MD • V. LEROY YOUNG, MD, FACS

HISTORY SUTURES
History
APPLICATIONS AND ADVANTAGES
Forms, Formulations, and Properties
REGULATORY APPROVAL
PATHOLOGY AND COMPLICATIONS
SAFETY TESTING AND STANDARDS General
OPERATIVE TECHNIQUES Infection
Toxicity
METALS Carcinogenicity
History Hypersensitivity Reactions
Forms, Formulations, and Properties Implant-Related Complications
CERAMICS AND GLASSES EXPLANTATION, RETRIEVAL, AND TESTINC
History
Forms, Formulations, and Properties ECONOMICS
POLYMERS FUTURE
General Tissue Engineering and Regeneration
Thermoplastics New Materials and Technology
Elastomers
Thermosets

HISTORY surgeons for use in a variety of closures. In 1902, Meyer7

used silver wires to close large hernias; Robb, in 1907,
For centuries, surgeons have artfully adapted the use
used silver wires to close abdominal fascia. Cushing
of foreign materials in the quest to repair bodily injury.
employed silver ligature clips to control difficult-to-
Early evidence of these materials applications exists in
access hemorrhage during resection of cerebral tumors
archeological archives. Metals, gold in particular, are
in 1911. Possibly the earliest documented implant study
found in skulls retrieved from ancient excavation sites,
can be attributed to Levert,9 who in 1829 tested a
such as a gold hammered plate used to reconstruct the
number of metal ligatures. Experimentally, among
frontal bone defect of a Neolithic Peruvian chieftain.1
silver, gold, lead, and platinum, he found platinum to
In the 1500s, gold plates aided in the repair of cleft
be the least irritating in dogs. The earliest ventures
palates.2 Alloplastic applications are also found in
meeting with any success, however, appear subsequent
ancient orthopedic injuries as bone healing was pro-
to the introduction of aseptic technique by Lister in
moted through stabilization and strengthening of frac-
the late 1800s.10
tures. For example, more than 500 years ago, the Aztecs
of Central America were thought to employ wood as The greatest modern strides in material formula-
intramedullary bone splints. 3 Hansmann, 4 in 1886, was tions and product development emerged in response
credited by some with the first use of "preferably to World War II and the subsequent demands of
unhardened nickel-plated sheet steel" for internal postwar industry. The growth of the aerospace indus-
fixation. try further supported rapid expansion in the variety
and availability of biomaterials. 11 Despite seemingly
An alloplastic material is defined as "an inert
enthusiastic exploitation of foreign implant mate-
foreign body used for implantation into tissue."5
rials, alloplast use was met with healthy skepticism even
Although the first documented use of an alloplastic
late in the 1940s. The following statement, made during
material is difficult to corroborate, Gluck used ivory
an address by Gallie,12 is a fitting example:
clamps as early as 1888;Jassinowsky,in 1889, exploited
the qualities of silk that are still appreciated today to It would seem particularly important that when the ingen-
repair vessels.6 Silver found favor among a number of ious surgeon feels the urge to add some new foreign body
745

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Dr.Mustafa D.
746 I • GENERAL PRINCIPLES
to our armamentarium he should pause to see whether he
can not then and there figure out the physiological proce-
dure by which his bright idea, if it really is a good one, will
surely be replaced.
APPLICATIONS AND ADVANTAGES
Applications for alloplastic materials are myriad:
replacement, augmentation, fixation, reinforcement,
and substitution. Potential applications continue to
expand with the development of new materials and
increasingly sophisticated integration of biomaterials
into tissue with the ultimate goal of creating artificial
organs.
There are several functional uses of implants (Table
26-1). 10 Alloplastic implants also offer several advan-
tages over autologous tissue (Table 26-2). Unfortu-
nately, the disadvantages are numerous as well. The
alloplastic nature of the biomaterials makes them
susceptible to the usual host of potential biologic and
physiologic problems: infection, immunogenicity,
mechanical failure over time, potential difficulty in
removal of a well-incorporated device, and morbid-
ity of a second operative procedure should the implant
require removal.
In some instances, resorbable biomaterials are an
option to permanently implanted devices. Absorbable
materials also offer several advantages over perma-
nently implanted devices (Table 26-3). 13 Resorbable
materials must meet additional criteria; they must
provide initial load-bearing support needed for the
patient to be functional, continue to provide support
during the healing process, meet the biocompatibiiity
criteria of the parent product, and produce inert degra-
dation products.
A number of diverse criteria affect the use of
implants and influence the selection of implant
TABLE 26-1 • BASIC FUNCTIONAL USES OF
IMPLANTS*
To replace a damaged, diseased, or worn part of the
anatomy, including, for example, total joint
replacements'
To simulate a congenitally absent part of the anatomy,
as with a mammary or facial prosthesis'
To aid in the healing process of a tissue, including
orthopedic fracture plates, temporary grafts used in
the treatment of burns, and surgical adhesives
To correct some deformity produced congenitally,
traumatically, or pathologically, with examples of
spinal plates and hydrocephalus tubes
To rectify the mode of operation of an organ, a
category principally including heart pacemakers but
also eyelid and penile implants
*As outlined by Williams.10
'The term prosthesis is used to describe these implant contexts.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
TABLE 2 6 - 2 • ADVANTAGES OF ALLOPLASTIC
IMPLANTS OVER
AUTOLOGOUS TISSUE
Avoidance of donor site morbidity
Unlimited supply
Avoidance of additional operative time and resources
required for graft harvest
Potential to customize prostheses
Potential to enhance performance relative to
autologous tissue (e.g., strength of steel over callus
alone in fracture splinting)
Tighter control over resorption if resorption is desired
materials. The advancement of medical technology,
increases in regulatory and economic restrictions, and
other additional issues—such as interference with radi-
ographic or magnetic imaging, product-related prob-
lems (e.g., quality assurances, manufacturing processes,
cost controls, sterilization techniques), and potential
medicolegal matters—must be considered. Scales1,1
developed an oft-published table of implant criteria.
The authors think it is important to elaborate on this
information and also include patient- and surgeon-
directed issues as well as manufacturing and regula-
tory criteria for implants (Table 26-4).
REGULATORY APPROVAL
The Food and Drug Administration (FDA) is the
primary regulatory agency of medical devices in the
United States. The Center for Devices and Radiologi-
cal Health (CDRH) is one branch of six overseen by
the agency. The CDRH, in turn, oversees the Office of
Device Evaluation, which is charged with the onerous
task of ensuring the safety and efficacy of myriad
implantable and nonimplantable medical devices. In
1976, the FDA established test guidelines for devices.
However, proof of safety and efficacy is not the respon-
sibility of the FDA; it remains the burden of the man-
ufacturer to develop and conduct tests sufficient to
TABLE 2 6 - 3 • ADVANTAGES OF ABSORBABLE
MATERIALS' 3
Avoid a second surgical procedure to remove the
device
Mitigate adverse local reactions compared with devices
left in place
Minimize chronic local tissue irritation or corrosion
Eliminate potential sources of growth disturbances,
when applicable
Eliminate palpability problems
Resume normal loading and remodeling without stress
shielding
Alleviate imaging artifacts
H&Wttf'SatfW image...
TABLE 2 6 - 4 • IMPLANT CRITERIA
Biocompatible
Immunologically inert
Noninflammatory, nonallergenic
Nontoxic
Noncarcinogenic
Unobtrusive
Nonpalpable
Nonpainful
Radiolucent
MRI compatible
Low interference with metal detectors (e.g., airport)
Low interference with electromagnetic and electronic
devices (e.g., microwaves)
Convenient
Easy to transport
Easy to handle (operatively)
Adjustable, removable, repositionable
Reliable
Withstand physiologic fluid environment
Withstand immune and inflammatory response
Withstand internal or external stresses and trauma
(bending, puncture, tension, compression, shear,
abrasion)
Withstand shipping, handling, storage
Withstand or control degradation over time
Withstand temperature variations
Withstand self-degradation
Adaptable for anatomic variants
Anatomic and realistic
Manufacturable
Sterilizable
Reproducible
Consistent product
Predictable host integration and response
Affordable
Meets regulatory criteria
convince the FDA jury of the integrity, safety, and
efficacy of a new product. "Caveat emptor has never
been—and never will be—the philosophy at the FDA"
(David Kessler, Chairman of the FDA, June 18,1992).15
Medical devices are categorized into one of three
classes, depending on degree of complexity, invasive-
ness, and a number of other criteria. A Class 1 device
exposes patients to little or no risk (e.g., those that are
not implanted and have only temporary contact with
the body, such as a tongue blade or surgical marker)
and can be approved for marketing with only general
controls in place. A Class 2 device exposes patients to
intermediate risk (e.g., those implanted for brief
periods but designed to be removed, such as an intra-
venous cannula) and may be approved with regula-
tions that encompass quality assurance and good
manufacturing processes, among other criteria. Class
3 devices are the most carefully regulated because they
are deemed to expose patients to significant risk (e.g.,
those designed for permanent implantation). For
implantable devices or life support-related equipment,
more stringent criteria must be met before market
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
26 • ALLOPLASTIC MATERIALS 747
release. Products shown to be sufficiently similar to
existing approved devices might be issued approval
for marketing on the basis of substantial equivalence.
A device that does not meet such criteria must be sub-
mitted under a Premarket Approval Application or
Premarket Development Protocol and undergo the
scrutiny of an assigned task force that must be con-
vinced by the manufacturer of device safety and effec-
tiveness. In vitro and in vivo studies and mechanical,
chemical, and toxicity studies, as well as clinical data
demonstrating device safety and efficacy, may be
required. Clinical trials for premarket testing are con-
ducted under the regulation of the FDA's Investiga-
tional Device Exemption. Product and package labeling
must also comply with FDA guidelines before approval.
After market approval of any product, the manu-
facturer must register with the FDA. Postmarket sur-
veillance controls must be met; these include the Quality
Systems and Medical Device Reporting regulations. The
Quality Systems control, a quality assurance check,
covers diverse entities, such as quality management and
organization, device design, manufacturing facilities,
equipment, purchase and handling of components,
production and process controls, packaging and label-
ing controls, device evaluation, distribution, installa-
tion, complaint handling, servicing, and records. As
the manufacturing process itself is under the purview
of the FDA, Good Manufacturing Practice must be out-
lined, strictly followed, and validated with Quality
Assurance testing. Outlined specifications must be
strictly satisfied. For example, the assurance of clean-
liness (freedom from contamination of materials) and
the ability to trace each lot must be guaranteed. The
Good Manufacturing Practice provides detailed pro-
cedural guidelines in 18 areas as varied as designing
products and processes, training employees, acquir-
ing adequate facilities, distributing devices, packaging
devices, and servicing devices. The Medical Device
Reporting regulation is an important mechanism for
reporting adverse events (www.fda.gov/cdrh/devadvke).
Government mandate is destined to play an increas-
ingly significant role not only in the use of alloplastic
materials and bioimplants but also in the regulation
of informed consent. The chair of the Institute of
Medicine review of the safety of silicone breast
implants issued the following caveat:
The committee believes... that more consistent and higher
quality informed consent is possible and, among its recom-
mendations, urges the development and testing of model
processes and systems for ensuring fully informed consent
for future recipients of silicone breast implants. A success-
ful system may be applicable to other implantable devices
in the future.16
Similar discussion continued during the premar-
ket approval process for saline-filled breast implants.
748 I * GENERAL PRINCIPLES
At issue is the relative culpability of the manufac-
turer for disclosing information including study
results, of the surgeon for interpreting and trans-
ferring data and revealing potential complications,
and of patients for ultimately understanding this
information and its physical and psychological health
implications. Despite intense ongoing deliberations
regarding the role and culpability of each party—the
FDA, the manufacturer, the surgeon, and the patient—
in the informed consent process, definite conclusions
remain to be established.
SAFETY TESTING AND
STANDARDS
Although implantable materials must adhere to an
expansive array of criteria, the most basic requirements
of any alloplastic material are twofold: first, the mate-
rial must not elicit an adverse response once it is inside
the body—it must be biocompatible; and second, the
material must possess the necessary functional char-
acteristics.17 The critical importance of safety testing
and the role of regulatory monitoring call to mind
the topic of silicone breast implants. Angell,15 then
editor of the New England Journal of Medicine, refer-
encing evidence in regard to the purported dangers
of silicone, stated, "Strict adherence to scientific
procedures—in particular, the requirement for
evidence—saves such people (and us) from them-
selves." One difficulty of proving both safety and
efficacy of an implant lies with the challenge of estab-
lishing an acceptable model of the physiologic and
mechanical conditions to be tested. That is to say, it
is challenging to duplicate the conditions of use (i.e.,
the physiology and mechanics of the human body)
for rigorous testing of the proposed implantable
device. Acute toxicity evaluation, in vivo toxicity tests,
inflammatory response tests, bacterial contamination
measurements, cell-mediated response tests, interac-
tion of degradation products with tissue studies, and
carcinogenicity tests are common constituents of the
basic battery of studies recommended by the FDA
Medical Device Agency.
The American Society for Testing and Materials,
established in 1898, is one of the largest voluntary stan-
dards development organizations in the world. It is
a not-for-profit organization that provides a forum
for the development and publication of voluntary
consensus standards for materials, products, systems,
and services. The organization also develops standard
test methods, specifications, practices, guides,
classifications, and terminology in 130 areas covering
topics such as metals, plastics, textiles, petroleum,
energy, the environment, consumer products, medical
services and devices, computerized systems, and many
others. Information about a variety of implantable
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
medical devices, including breast implants, is avail-
able (www,astm.org).
The study of materials generates a precise termi-
nology, as with any science, to describe material
properties. A brief introduction to this terminology
will facilitate the understanding of mechanical prop-
erties and wear test results of materials. Four types of
stresses are of primary importance in evaluating
materials. The first two are sufficiently similar to be
considered together, namely, tensile and compressive
stresses. Shear stress and torsion are the remaining two.
An object experiences one or more forces when a
load is applied. An object under tension experiences
forces that pull individual layers of atoms apart. These
forces are measured as stress or force applied per unit
of cross-sectional area.
Tensile stress = force/cross-sectional area
Similarly, as compressive forces directly oppose
tensile forces, compressive stress is then also defined
in terms of a force per cross-sectional area.
Compressive stress = force/cross-sectional area
An object under tension experiences forces dis-
tancing individual atoms; the material therefore
undergoes extension, whether on a microscopic or
macroscopic level. Strain is defined as the measure
of this extension or elongation under the action of
stress. The total elongation of an object relates to the
multiple of the individual lengthening between layers
of atoms and the number of layers of atoms in the length
of the object. Consequently, the greater the original
length of the object undergoing tensile forces, the
greater the potential elongation. Strain is therefore
expressed as the amount of extension per unit length.
As units of length describe both numerator and
denominator, multiplication of the resultant fraction
by 100 yields a result in percentage strain.
Tensile strain = elongation/length 0
Conversely, compressive strain describes the amount
of shortening per unit of original length, that is to say,
these forces shorten the object along the line of action
of the force.
Compressive strain = shortening/length,,
Shear strain describes tangential forces, or the rel-
ative lateral displacement of two contiguous surfaces.
Theoretically, a tangential force acts on one of two sur-
faces of a mass in which the remaining surface is fixed.
The stress acting on the object is shear stress. Shear
stress is the applied tangential force divided by the cross-
sectional area of the top surface. The object will shear
if there is a lateral displacement of the upper surface
relative to the lower surface. On a molecular level, unlike
tensile or compressive stresses—wherein forces act on
individual molecules along the same axis of force
image...
joining them—an externally applied shear force acts
at right angles to the line of force joining the atoms.
Shear strain defines the angle through which the object
is sheared.
Shear strain = displacement of surface/thickness
of mass = t a n 0
Torsion is a more complex relative of shear. Torsion
or coupled forces produce a twisting action around
the longitudinal axis of an object and are related direcdy
to the shear stress on the material. The twist angle is
proportional to the shear strain.
Bending force describes the circumstance in which
tensile, compressive, and shear stresses are all present.
Some portion of the structure, namely, the convex
surface, will experience tensile strain, while compres-
sive strain will be produced on the concave surface.
The act of bending also generates shear stresses on
some aspect of the structure as forces necessarily act
perpendicular to the original orientation to generate
the bending movement.
Quantifying and outlining the independent forces
acting on an object or, more specifically, on an implant
provide useful information. Of course, integration of
these data further elucidates material and implant per-
formance expectations. Understanding a stress-strain
curve or load-deformation curve enhances apprecia-
tion of a material's characteristics. For example, plot-
ting a load versus deformation curve will describe the
strength and stiffness of an implant. A typical load-
deformation curve demonstrates several strength
characteristics (Fig. 26-1). The elastic portion of the
curve describes the range offeree that can be applied
and still allow an object to return to its original shape
without permanent deformation once the force is
NDN-ELASTIC REGION
x x
' DEFDRMATIDN
FIGURE 2 6 - 1 . Load-deformation curve typical of ductile
materials. (From Holmes RE: Alloplastic implants. In
McCarthy JC, ed: Plastic Surgery. Philadelphia, WB Saun-
ders, 1990:698.)
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
26 • ALLOPLASTIC MATERIALS 749
BRITTLE METALS AND CERAMICS
DUCTILE METALS
POLYMER
STRAIN
FIGURE 2 6 - 2 . Stress-strain curves for four types of
materials. (From Holmes RE: Alloplastic implants. In
McCarthy JC, ed: Plastic Surgery. Philadelphia. WB Saun-
ders, 1990:698.)
removed. After the yield point on the curve is exceeded,
the sample will enter the nonelastic or plastic portion
of the curve; without failing, the structure will con-
tinue to deform plastically and lack the capacity
to return to its original configuration. Continuation
along the nonelastic or plastic portion of the load-
deformation curve by application of additional
force will eventually lead to the points of ultimate
strength and ultimate failure. In summary, the load-
deformation curve plots several key measures of an
object's strength: the ultimate strength of an implant;
the potential deformation it can sustain before failure;
the energy stored before failure (i.e., the area under
the curve); and the stiffness, or elastic modulus, of the
curve as indicated by the slope of the curve within the
elastic region.
A stress-strain curve displays characteristics similar
to a load-deformation curve but describes mechani-
cal properties in terms of force per unit area, thus
eliminating factors attributable to the shape and con-
tour of the object. Thus, the stress-strain curve more
specifically describes the strength characteristics of a
material.18 A material can be classified as brittle, ductile,
or rubbery, depending on characteristics demon-
strated on the stress-strain curve. Brittle materials, such
as ceramics, deform very little before failure. This is
indicated by the absence of a plastic region on the stress-
strain curve (Fig. 26-2). Ductile materials (e.g., mal-
leable metals) potentially deform significantly before
failure. Rubbery materials, such as some polymers and
rubber, can undergo extensive deformation before
failure and, in fact, store energy in the form of defor-
mation. These elastic materials maintain the potential
to return to their original configuration over a large
elastic region on the curve.
Toughness defines the amount of energy required
to induce fracture formation or failure. The area under
the stress-strain curve quantifies the amount of energy.
750 I • GENERAL PRINCIPLES
Toughness measures both the amount of stress a mate-
rial can withstand and the amount of deformation it
will tolerate before breaking. For example, a material
such as a ductile metal that can undergo high stresses
with considerable plastic deformation is considered
tougher than a material like ceramic (which will resist
high stress but has no capacity for deformation) or
rubber (which has a high capacity for deformation
but can withstand only relatively low stress).
Impact tests, whereby a pendulum hammer exert-
ing a known quantity of energy strikes a material spec-
imen, measure material toughness. The rebound
height of the pendulum after impact is noted. Tough-
ness testing is particularly useful for brittle materials,
for which impact-loading conditions are far more likely
to affect product or material performance because of
crack formation and propagation. If brittle materials
are tested only under slow or static loading conditions,
small amounts of plastic deformation may mask
the failure potential more likely under impact loading
conditions.
Fracture stress refers to the point of applied stress
at which plastic deformation ceases and fracture
occurs. Ultimate tensile strength is the fracture stress
of a material under tensile force.
Hardness refers to the measure of resistance a mate-
rial has to abrasion, indentation, and other forms of
applied compressive stress. Hardness is considered
somewhat difficult to define, and a number of differ-
ent modalities are used to characterize material hard-
ness. A relative measure of hardness can be made by
use of the Mohs scale, in which a series of standard
materials are arranged in order of increasing hardness,
with talc as number 1 and diamond as number 10. A
material of higher number or hardness will scratch any
material of a lower number.
Plasticity refers microscopically to a shift in the
relative position of neighboring atoms without
TABLE 26-5 • MECHANICAL PROPERTIES OF SKIN, FASCIA, TENDON, CORTICAL BONE, AND
IMPD\NT MATERIALS
Material Tensile Strength (MPa)
Skin 6-14
Fascia 12-14
Tendon 59-69
Cortical bone 140
Cold 130
Polymethyl methacrylate 55-85
(PMIVIA, bone cement)
Silicone 2.4-7
Stainless steel (316L)
Annealed 550
Cold worked 960-1000
Titanium alloy (6AI-4V) 896-1020
Modified from Holmes RE: Alloplastic implants. In McCarthy JG, ed: Plastic Surgery, vol 1. Philadelphia, WB Saunders, 1990:698.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
producing a change in the overall strain within the
material or exceeding the intermolecular bond energy
such that these bonds break and the material cracks
or fractures. Permanent deformation occurs without
material failure.
Ductility describes the quantitative reduction of
cross-sectional area or change in length of an object
when tension is applied. Materials considered ductile
generally range from 60% to 90%.
Ductility = change in cross-sectional area at
fracture site/original cross-sectional area x 100%
or
Ductility = change in length/original length x 100%
The phenomenon of fatigue refers to cumulative
effects of deformational stresses applied repetitively.
An example is the cyclic loading and unloading
stresses of ambulation on a hip prosthesis. Materials
may ultimately fail at stresses significantly lower than
those of a statically applied force under conditions of
fatigue (Table 26-5).
In addition to fatigue and failure due to deforma-
tional forces, the degradation or weakening of mate-
rials, and therefore devices, can also occur secondary
to wear. Surface wear or the loss of material results
primarily from two mechanisms, adhesive wear and
abrasive wear. Adhesive wear occurs when material ele-
ments on opposing surfaces come into contact and
then fuse. Subsequently, due to relative motion, these
fused elements are broken apart either at the original
surface of fusion or along another plane. This repet-
itive fusion and rupture results in the transfer of mate-
rial from one surface to another or in the release of
particulate matter or wear debris. Abrasive wear
describes the phenomenon of fracture or release of
particles from one or more material surfaces due to
continual abrasive contact between the two surfaces.
Elongation (%) Compressive Strength (MPa)
1 10-140
14-17
8-9
1 130
45 130
2-7 75-144
100-700
50
9-22
12-15
VtJWttf^eldW image...
Wear testing of implantable devices is important
for a number of reasons. Release of wear debris can
expose different implant surfaces to modified prop-
erties and increase the area of surface exposed. These
changes in the original implant can result in unpre-
dictable physiologic reactions in addition to acceler-
ating material degradation. Wear debris can also
accumulate within local tissue or be transported sys-
temically. Either result may detrimentally activate
host defense mechanisms. Released wear particles can
further accelerate the wear processes of the shedding
device. Wear can, of course, result in device malfunc-
tion or failure.
In considering metallic implants, corrosion is
important to both design parameters and biocom-
patibility. Corrosive wear refers to the dissolution of
metal as metallic ions in an electrolytic solution. Body
fluids act as the necessary conducting medium in
concert with a metallic implant to create the requisite
environment for corrosion to occur. Pitting corrosion,
crevice corrosion, stress corrosion cracking and cor-
rosion fatigue, fretting corrosion, intergranular cor-
rosion, and galvanic corrosion are forms of local
corrosion that can lead to implanted metallic device
failure.19 Protective films on metal surfaces can control
passivity (a term referring to the conditions that exist
on a metal surface) and greatly lower corrosion rates.19
OPERATIVE TECHNIQUES
There are several generalized guidelines for the safe
application of implant materials (Table 26-6). 20 Pro-
phylactic antibiotic use is strongly supported, as is the
timing of administration of antibiotics. It is recom-
mended that the first dose be administered before
surgery because there is a 15- to 60-minute delay of
cephalosporins and other antibiotics in reaching ade-
quate bone levels. Additional intraoperative doses every
4 hours are also recommended. However, a single dose
TABLE 2 6 - 6 • GENERAL GUIDELINES FOR
IMPLANT PLACEMENT20
Shape the implant to avoid sharp corners and edges.
Bury the implant as deeply as possible under the skin
and subcutaneous tissue.
Avoid tension in the adjacent tissues or tension against
the overlying cutaneous coverage.
Place the incision line as far from the implant as
possible.
Handle the implant with instruments to avoid soiling it
with glove powder, lint, or fingerprints during and
subsequent to the preparation period.
Use the proper stiffness of material; it should be as soft
as is consistent with the application.
Do not use any hard material for soft tissue
replacement.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
26 • ALLOPLASTIC MATERIALS 751
of prophylactic antibiotic may be sufficient, especially
since the need for restraint in antibiotic use has grown
in proportion to the growing threat of antibiotic-
resistant organisms. 21
METALS
History
Metals such as gold and iron are found in remains
excavated from ancient civilizations. Gold, silver, iron,
and copper were some of the early metals used to fab-
ricate implants. The majority of early devices formally
studied were implanted as fracture plates and ligatures.
Although Bell,22 in 1804, discovered galvanic corro-
sion in body fluids from the steel-pointed silver pins
used for wound closure, other early surgeons claimed
the type of metal employed was irrelevant, aside from
the specific property required for use, such as strength
or malleability. Before the initiation of aseptic tech-
niques, the inevitable problems with infection made
formal evaluation of implanted materials impossible.
However, biocompatibility ultimately proved sig-
nificant; in fact, of all factors related to successful
implantation, biocompatibility is the most critical.
Iron, chromium, cobalt, nickel, tantalum, molyb-
denum, titanium, silver, and tungsten are the primary
elemental metals used in the formulation of most alloys
in production today. Most metallic implants presently
in use are made of alloys, a composite of two or more
metals that produces the desired physical properties.
Manufacturing techniques are often as important as
composition in the production of metal alloys and their
products.
A summary is provided of metals and alloys com-
monly used, including some of their applications,
advantages, and disadvantages. The three most com-
monly used are two alloys, stainless steel and cobalt-
chromium alloy, and the elemental metal titanium.
Forms, Formulations,
and Properties
Stainless steel is a popular prosthetic device material
(Table 26-7) manufactured as one of four main classes
(series 100, 200, 300, 400). The most common for-
mulation applied to medical implants is 316L, which
is an iron-based alloy composed of iron (60%),
chromium (17% to 20%), nickel (12% to 17%),
molybdenum (2% to 4%), and manganese (2%). It
was initially popular for implantation because of its
resistance to corrosion, at the expense of mechanical
strength. Compared with newer materials, however,
stainless steel is more corrosive than titanium or cobalt-
chromium alloys. Stainless steel (316L), cobalt-
chromium, and titanium-based alloys all resist
corrosion by formation of a thin oxide layer on the
752 I • GENERAL PRINCIPLES

TABLE 26-7 • COMPOSITION OF STAINLESS Alterations in manufacturing techniques have

STEEL ALLOY (WROUGHT, improved the strength and fatigue resistance charac-
ASTM--F55) teristics of cobalt-chromium alloys, which are less
ductile than iron- or titanium-based alloys and have
Element Weight (%) the highest moduli of elasticity among orthopedic
implants. Given their good wear and corrosion resist-
Chromium 17-20 ance, these alloys may be considered superior to tita-
Nickel 12-17 nium in some instances. Several common formulations
Molybdenum 2-4
are manufactured in either cast or wrought forms. In
Carbon 0.03 max
Manganese 2.00 max cast products, the major metal is cobalt, followed by
Phosphorus 0.03 max chromium, molybdenum, and nickel. In the wrought
Sulfur 0.03 max form, the molybdenum is replaced by tungsten."
Silicon 0.75 max Common applications of cobalt-chromium alloys
Nitrogen 0.10 max
include replacement of load-bearing joints; porous
Copper 0.50 max
Iron Balance forms are used as plates that allow bone ingrowth.
Tantalum is a stable elemental metal and aptly fulfills
From Holmes RE: Alloplaslic implants. In McCarthy JG.ed: Plastic Surgery. the requirements of inertness and biocompatibility. It
Philadelphia, WB Saunders, 1990:698. is comparable to glass in its ability to resist electro-
chemical degradation. 23 Unfortunately, it is quite
ductile with only medium-range strength properties.
material's surface. Even though titanium and cobalt- It has been used in cranial reconstruction in the form
chromium alloys do not corrode when they are of plates and as mesh for the repair of orbital floor
implanted, metal ions can slowly diffuse through the defects as well as in surgical staples.11
oxide layer and accumulate in local tissue. Applica- Nickel-titanium alloy (nitinol)" is known for its
tions of stainless steel implants include skeletal fixation, shape memory properties. It also exhibits good cor-
electrical leads, and encasements for generators.11 rosion resistance. Studies have found that nickel-
Titanium is perhaps the most popular metal used titanium alloy showed no cytotoxic, allergic, or
today. Titanium itself is a highly inert, corrosion- genotoxic activity. Applications include orthodontic
resistant, ductile metal with a variety of applications. tooth alignment and osteosynthesis staples.
Joint replacement and fracture fixation devices, encase- Platinum is a rare, high-density metal to which
ments for generators, cardiac valve components, and iridium is often added as a hardening agent. Platinum
maxillofacial and dental implants are some of the end is exceptionally inert, corrosion resistant, and relatively
products. 11 ductile—characteristics often exploited for implantable
The titanium alloy aluminum-vanadium (T1-6AI- electrodes.' 1 Platinum-cobalt magnets have also been
4V) is remarkably biocompatible, light, strong, and implanted in paralyzed eyelids to effect lid closure.
corrosion and fatigue resistant (Table 26-8). In its Historically, platinum and platinum-iridium alloys had
modulus of elasticity and measure of material stiff- been used in several intraocular lens designs. However,
ness, it is closer to bone than many of the other alloys these iridocapsular intraocular lenses induced erosive
and would theoretically apply a more even stress load problems attributed to a relatively high aqueous
at the implant-bone interface. weight of the metal-polymethyl methacrylate lenses
and were discontinued.24
Gold and silver, like platinum, are relatively high in
TABLE 26-8 • COMPOSITION OFTI density and cost. Gold, more than silver, is relatively
(ASTM-F67) AND TI-6AL-4V resistant to environmental degradation, and both
ALLOY (ASTM-F136) demonstrate relatively high conductivity, with silver
being the highest of all metals. Eyelid weights used for
PureTi TJ-6AI-4V seventh nerve palsies capitalize on the relative high
Element (weight %) (weight %) density of gold. As is true with platinum, gold and silver
are soft and ductile, which limits their usefulness in
Iron 0.05 max 0.25 max situations requiring mechanical strength.
Carbon 0.10 max 0.08 max
Oxygen 0.45 max 0.13 max
Aluminum — 5.5-6.5
Vanadium — 3.5-4.5
CERAMICS AND GLASSES
Titanium Balance Balance History
From Holmes RE: Alloplaslic implants. In McCarthy JG,cd: Plastic Surgery. Ceramics are among the oldest manufactured mate-
Philadelphia, WB Saunders, 1990:698. rials. In materials terminology, the word ceramic refers

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Dr.Mustafa D.
*&WRj { afltfW image...
to all nonmetallic and inorganic materials, a some-
what broader term than the popular reference to the
ancient art of silicate ceramics—pottery, stoneware,
and porcelain.25 Nevertheless, the common denomi-
nator is referred to as sintering, the high-temperature
fusion of the crystalline components of the native
material. Ceramics are typically brittle at room tem-
perature, characteristically lack plasticity, possess low
tensile and compressive strength, and resist deforma-
tion up to the breaking point of the material. However,
this resistance to deformation and relative compres-
sive strength make ceramics an attractive option for
many types of implants. Only a few biomaterials are
described from the vast number of ceramic materials
available: oxide ceramics, glass ceramics, glasses con-
taining calcium phosphate, ceramics of calcium phos-
phate salts, and certain modified carbons.
Alloplastic materials classified as ceramics have
found extensive use as bone substitutes (Fig. 26-3). In
the 1920s, attempts were made to develop materials
that could be used as temporary bone substitutes to
stimulate or at least to permit adjacent bone ingrowth
as the material itself was gradually resorbed.26,27 Osteo-
conduction, osteoinduction, and osteogenesis refer to
three types of bone dynamics interaction. Facilitating
the bone repair response on a scaffold exemplifies
osteoconductivity, which means the material promotes
the distribution of a bone healing response through-
out a defined volume and allows bone growth from
an osseous bed. Materials with osteoconductive prop-
erties include mineralized or demineralized bone, type
I collagen, hydroxyapatite and tricalcium phosphate
ceramics, titanium and cobalt-chrome alloys, and
others. Osteoconductivity does not depend on whether
a material is degradable but does relate to a number
of structural and material properties that influence
FIGURE 2 6 - 3 . Transmitted light
micrograph of a glass ceramic
implant in a rat tibia after 1 month,
showing bone bonded to the implant.
B, bone; BG, bulk implant; CaP,
calcium phosphate; O, osteocytes;
S, silica-rich layer. (From Hench LL,
Clark AE: Adhesion to bone. In
Williams DF, ed: Biocompatibility
of Orthopedic Implants, vol II.
Boca Raton, Fla, CRC Press, 1982.
© CRC Press, Boca Raton, Florida,
www.crcpress.com. Reproduced
with permission.)
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26 • ALLOPLASTIC MATERIALS 753
cell attachment, migration, differentiation, and vas-
cular ingrowth. Important structural properties
include porosity, pore size, connectivity between
pores, and surface roughness. Important material
properties are likely to include surface charge, surface
free energy, protein-binding affinity, degradation rate,
concentration of local degradation products, and par-
ticle size of degradation products. 28 Presently the target
of significant research focus, osteoinductivity refers
to the capacity of a substance to induce differentia-
tion of pluripotent cells into osteoblasts with subse-
quent bone formation. Osteogenesis refers to bone
formation by living cells.29"31
Forms, Formulations,
and Properties
Compressive load strength and resistance to wear and
deformation make ceramics an attractive option as a
bone substitute. Ceramics can be classified by struc-
ture and manufacturing process as glasses, oxide
ceramics, special ceramics, and carbons. They can also
be characterized on the basis of biologic characteris-
tics (Table 26-9). 32
CALCIUM PHOSPHATE CERAMICS
A principal attraction of calcium phosphate ceramics
is their bioactivity. Bioactivity is defined by Williams 33
as "a material which induces specific biological activ-
ity." For bone substitutes—and implant materials in
general—bioactivity is the characteristic that allows
bonds to form with living tissues.29,34"36 The two prin-
cipal types of calcium phosphates are hydroxyapatite
and tricalcium phosphate. Both are capable of bonding
strongly with host bone.
BG
BG
754 I • GENERAL PRINCIPLES

FIGURE 26-4. Microporous hy-

droxyapatite containing intercon-
nected macropores after 30 weeks
on top of rat calvarial bone. Note
that the ingrowth of bone extends
through the width of the implant
(magnification x4). (From Holmes
RE: Alloplastic implants. In McCarthy
JG, ed: Plastic Surgery. Philadelphia,
WB Saunders, 1990:698.)

Hydroxyapatite occurs naturally as a phosphate
complex of calcium Ca 5 (P0 4 )GH. It is an inorganic,
porous, stable mineral compound with minimal
absorption (Fig. 26-4). Not only is it mined as the prin-
cipal source of the phosphate ion, but it is also the
chief structural element of vertebrate bone. Hydrox-
yapatite makes up 90% of inorganic bone matrix. The
raw mineral form is neither sufficiently pure nor con-
sistent for medical use; therefore, synthetic equivalents
have been produced and marketed in a number of
different forms.26 In addition, one source of biologic
hydroxyapatite can be obtained by treating bovine bone
to eliminate all cellular components. A variety of
studies have shown outstanding biocompatibility. The
primary role of hydroxyapatite in composite grafts is
to enhance osteoconduction. It is not osteoinductive
or osteoconductive when it is used alone.37
The slow resorption rate of hydroxyapatite is both
its advantage and disadvantage. Hydroxyapatite is pro-
duced in dense and porous forms and also as granules
or block structures. Particulate porous hydroxyapatite
in conjunction with autogenous particulate marrow
and cancellous bone has been used clinically in bone
reconstruction. 38
Coral has been studied as a potential source for bone
substitute. Perhaps as a foretelling of future marine
lifeapplications,Hamilton39in 1881 soaked sea sponges
in dilute carbolic acid to treat open infected wounds
and to provide scaffolding for capillary ingrowth.
The natural mineral skeletons of scleractinian coral
(genus Goniopora) manifest macroscopic architecture
similar to human cancellous bone.'10 This material
was introduced in 1988 under the trade name
Biocoral with applications reported in a number of
surgical specialties.26
Coralline hydroxyapatite is a synthetic bone sub-
stitute that mimics porous coral structure but is pro-
duced by the replamineform process (Fig. 26-5). The
replamineform manufacturing technique uses a
hydrothermal exchange method to produce ceramic
replicas of coral structures. The coralline architecture
remains unaltered du ring the chemical conversion from
calcium carbonate to hydroxyapatite, and the result-
ant hydroxyapatite is devoid of any organic matter.26

TABLE 2 6 - 9 • CLASSIFICATION OF SYNTHETIC BIOMATERIALS 32 ' 123

Materia! Interaction Between Implant and Host Biodynamics

Bone cement, metal Distance osteogenesis Biotolerant

Carbon materials Distance osteogenesis Bioinert
Oxide ceramics Contact osteogenesis Bioinert
Tetracalcium phosphate ceramic Contact osteogenesis Bioactive
Tricalcium phosphate ceramic Bonding osteogenesis Bioactive
Bioglasses Bonding osteogenesis Bioactive
Hydroxyapatite ceramic Bonding osteogenesis Bioactive
Calcium carbonate Bonding osteogenesis Bioactive

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Dr.Mustafa D.
VtSWttf'SelClWimage...

26 • ALLOPLASTIC MATERIALS 755

bioactive glass) and Ceravital (a bioactive glass-

ceramic). Bioglass, Ceravital, and sintered hydroxya-
patite, a specially heat-processed hydroxyapatite, are
thought to bond to bone through a calcium phosphate
surface layer; a common layer of chemical apatite forms
on the surface of the bioactive ceramic, and biologic
apatite develops from the bone. Yamamuro49"52 devel-
oped a bioactive glass-ceramic-containing crystalline
apatite and wollastonite, a calcium silicate mineral.
This composite, called A/W, which exhibits high
mechanical strength and a strong chemical bonding
with bone, has been applied clinically in spinal fusion.
Bioactive glass demonstrates the added benefit of
promoting soft tissue ingrowth, a characteristic that
FIGURE 2 6 - 5 . A scanning electron micrograph of the has particular application in treatment of periodon-
porous structure of coralline hydroxyapatite. The porous
structure is similar to that of cancellous bone. (From Cornell tal defects (Fig. 26-6). Bioactive glasses are also used
CH: Osteoconductive materials and their role as substi- as ossicular replacements in the middle ear and as
tutes for autogenous bone grafts. Orthop Clin North Am bioactive surface coatings. 53
1999;30:591.)
Glass ionomer cements have been used primarily
in dentistry and considered for use as bone cements
because of their proven osteogenic features.
Tricalcium phosphate [Ca 3 (P0 4 ) 2 ] is a synthetic, A porous carbon has been evaluated, historically,
generally porous calcium phosphate with the distinc- for potential bone ingrowth5,1 and as a coating for
tion of relatively rapid resorption. In contradistinc- porous titanium.
tion to hydroxyapatite, tricalcium phosphate resorbs The crystalline structure of oxide ceramics is dic-
within days to weeks and alone has not been success- tated by the distribution of metal ions within the inter-
ful as a bone substitute. Klein'" and LeGeros42 capi- stices of a closely packed array of oxygen ions. Alumina
talized on the differential resorption rates of tricalcium
phosphate and hydroxyapatite by combining the two-43
Hydroxyapatite provided the necessary scaffolding; tri-
calcium phosphate provided the minerals to sustain
osteoblasts. Tricalcium phosphate is well tolerated, and
both porous and dense forms have demonstrated
chemical bonding to bone.
Although calcium sulfate is not a ceramic, it is
included here because it has been reported in appli-
cations similar to those of ceramics. Heated gypsum
forms the hemihydrate of calcium sulfate (CaO.,S),
more commonly known as plaster of Paris. In 1892,
Dreesmann 44 from Trendelenburg's clinic reported
packing bone defects with a mixture of calcium sulfate
and phenol. Most modern reports involving calcium
sulfate are limited to small series and individual
reports, although Peltier45,46 reported successfully
packing bone defects with calcium sulfate pellets after
curettage of unicameral bone cysts. Moreover,
Coetzee47 described good results with excision and
calcium sulfate packing after mastoid infections and
cholesteatomas. Nevertheless, plaster of Paris has not
found widespread use in implant applications.
Glass ceramics are based on silica, Si0 2 . Hench 48
performed initial studies of calcium phosphate-
silicate glasses and demonstrated a strong adherent FIGURE 2 6 - 6 . A, Augmentation of the anterior maxil-
mechanical interface. Gross et al48a further elucidated lary envelope with hydroxyapatite. B, Panoramic radi-
ograph showing ridge augmentation with alveolar ridge
the mechanism of bond formation between bioactive graft and core vent implants 1 year postoperatively. (From
glasses and bone. This work subsequently led to the Valauri AJ: Maxillofacial prosthetics. In McCarthy JG, ed:
development and clinical application of Bioglass (a Plastic Surgery. Philadelphia, WB Saunders, 1990:3497.)

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Dr.Mustafa D.
756 I • GENERAL PRINCIPLES
or corundum is the primary example of an oxide
ceramic. Corundum is used to produce the colorless,
scratch-resistant glass of watches, and ruby and
sapphire are also related chemically. AI2O3 is the basic
unit of alumina, with each aluminum ion being sur-
rounded by six oxygen ions. Formulations of alumina
in various combinations with silica and magnesium
and calcium oxides, as an aluminum oxide, and as
calcium aluminate have been produced and tested with
some success as ceramic implants. Porous constructs
designed to facilitate tissue ingrowth demonstrated
bonding to some extent with all of these formulations.26
POLYMERS
General
Synthetic polymers can be classified into three cate-
gories on the basis of characteristic properties: ther-
moplastics; thermosets, discussed later in this chapter;
and rubbers and elastomers. Selection of the appro-
priate biopolymer naturally depends on the desired
physical, mechanical, chemical, and occasionally
thermal properties. Several parameters to consider
include tensile strength, modulus and elongation,
fatigue strength, impact resistance, abrasion and wear
resistance, viscoelastic properties such as creep resist-
ance, swelling, gas permeability, and hardness. The
properties of polymers are based on their structural
and chemical features. For example, tensile strength
can be increased by several mechanisms. Increasing
interchain attraction between purely hydrocarbon
polymers can form a more regular structure by packing
chains more closely; this can be accomplished by alter-
ing manufacturing conditions or changing produc-
tion techniques. Increasing cross-links and changing
or adding polar side chains can also affect chemical
and mechanical properties. Drawing or stretching a
polymer past its yield point will orient polymer chains
in a single direction and increase the material's
strength. In general, polymers of very low molecular
weight are liquids, and their viscosity increases as chain
length increases.
The technique of copolymerization of two or more
monomers can yield a material that possesses desir-
able characteristics from each monomer. For example,
blending a hard and brittle polystyrene with a rubbery
polybutadiene will produce a material with less tensile
strength but improved toughness than either mate-
rial has independendy.55 Adding low-molecular-weight
plasticizers can increase material flexibility by sepa-
rating a relatively rigid polymer chain through solvent
action.56
Thermoplastics
Thermoplastics are made of linear or branched
polymer chains and make up the largest variety of
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Dr.Mustafa D.
implant polymers. Because these polymers are not
cross-linked, they can, for the most part, undergo
reversible melt-solid transformation on heating. This
allows relatively easy processing or reprocessing. Ther-
moplastics usually exhibit moderate to high tensile
properties with moderate elongation, and they undergo
plastic deformation at high strains.57 Their structure
is highly variable, depending on the molecular
organization and structure of the polymer chains.
Thermoplastics may be amorphous (polystyrene),
semicrystalline (low-density polyethylene), or highly
crystalline (high-density polyethylene). Commonly
used bio-thermoplastics include polytetrafluoroeth-
ylene (typically referred to as Gore-Tex), polyesters
such as polyethylene terephthalate (Dacron),
poly(lactic acid), and poly(glycolic acid).
Polytetrafluoroethylene (PTFE) is a highly inert and
biocompatible material made up of an ethylene
monomer backbone with four covalently bound
fluorine molecules. Gaseous tetrafluoroethylene is
polymerized under high temperature and pressure to
manufacture Teflon. The polymer that composes
Gore-Tex is constructed by interconnecting PTFE fibrils
between solid PTFE nodes to form a grid pattern. The
resultant material is pliable and durable, and it allows
some tissue ingrowth with little inflammatory reac-
tion and minimal encapsulation. The product is avail-
able in sheet and mesh form, in blocks that can be
custom carved, as preformed implants, in strips, in
tubular strands, and as suture. Gore-Tex has been used
for abdominal fascial reconstruction; for chest wall
reconstruction58; as a soft tissue filler for nasolabial and
glabellar creases; and for lip, nasal, chin, mandible, and
malar augmentation (Fig. 26-7).59'60
Propiast is no longer marketed but is worth mention
because it was met with great enthusiasm when it was
introduced and used in a variety of applications. A few
years later, it was removed from the American market
by the FDA in 1990. Propiast I was available as a highly
porous, somewhat spongy, black Teflon-carbon
composite. Propiast II was a more rigid white
FIGURE 2 6 - 7 . GORE Subcutaneous Augmentation
Material (CORE SAM.) is a permanent yet revisable
implant material made of biocompatible, microporous
expanded PTFE that supports rapid tissue incorporation.
This material is available in preformed configurations as
well as in sheets and blocks. (Photograph courtesy of W.L.
Gore & Associates, Inc.)
 image...
Teflon-alumina composite.59 Proplast was marketed for
use in a variety of contexts, including correction of
chin, zygomatic, orbital rim, maxillary, mandibular,
skull, and rib cage deformities.61 Proplast products were
taken off the market after reports of biomechanical
failure, intense inflammation, infection, and extrusion
related to temporomandibular joint prostheses.59
Polymethyl methacrylate (PMMA) is a biocom-
patible, inert, rigid, high-molecular-weight polymer.
In its most common form, a liquid monomeric methyl
methacrylate is combined with powdered methyl
methacrylate polymer granules at the time of appli-
cation in surgery. This generates a compound that
maintains a moldable consistency during the 10-minute
polymerization process. The material then sets and
hardens in the final form. The advantage of the com-
pounding process is that the implant can be produced
before a surgical procedure or tailored to fill a defect
intraoperatively. A disadvantage of the material is the
resultant exothermic reaction that generates temper-
atures in excess of tissue tolerance, which may poten-
tially result in bone necrosis and soft tissue burns.
Local and systemic allergic reactions have also been
attributed to the unbound monomer. 59
Although many early uses of PMMA-related sur-
gical appliances ultimately proved unfruitful, PMMA
today is nearly synonymous with bone cement, and it
is still widely used as a bone substitute. In an injectable
form, PMMA microbeads are used as a soft tissue filler
for deep creases and scars.
PMMA combined with polyhydroxyethyl methacry-
late (HTR, Hard Tissue Replacement*) is produced by
combining PMMA beads with liquefied hydroxyethyl
methacrylate, which is then coated with calcium
hydroxide.62 Despite its porosity, HTR is highly resist-
ant to compressive forces. Reports suggest biocom-
patibility, although some evidence suggests that
nonresorbable HTR hinders normal healing.31 Poten-
tial applications include chin and malar augmentation
and craniomaxillofacial reconstruction.
Polyamide was one of the first commercially avail-
able nylon compounds manufactured in the 1930s.
When it is used as an implant, the material initially
elicits a foreign body reaction that is later replaced by
fibrous tissue as the material is resorbed. 63 Polyamide
has been used as a mesh onlay for repair or augmen-
tation of the chin, maxilla,and nasal dorsum. However,
because polyamide is resorbable, it is questionable as
a permanent implant. 59
NONRESORBABLE POLYESTER
Polyethylene terephthalate (Dacron) is a flexible,
nonabsorbable aromatic polyester that is suitable for
"HTR Sciences, U.S. Surgical Corporation, Norwalk, Connecticut.
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Dr.Mustafa D.
26 • ALLOPLASTIC MATERIALS 757
applications demanding tensile strength and stability.
Primarily used as suture and in arterial prostheses,
Dacron is also available as a mesh sometimes employed
for abdominal and chest wall reconstruction as well
as for chin and nasal augmentation.59,6,1
RESORBABLE POLYESTERS
Polyglycolide and poly-L-lactic acid are aliphatic com-
pounds that undergo hydrolytic degradation. During
the course of several months, these polyesters are
resorbable at physiologic pH. Polyglycolide and poly-
L-lactic acid have been used for body wall reconstruc-
tion and internal fracture and osteotomy fixation. Both
are available as mesh sheets and as rods, miniplates,
and screws for internal fixation. Polyglycolide scaf-
folding has been seeded with cultured chondrocytes
and periosteal cells for tissue engineering of both
cartilage and bone, respectively.65
Polyolefins
Polyethylene is an inert, highly biocompatible mate-
rial available with different biochemical properties
based on the density of the specific formulation. Very-
low-density to ultrahigh-molecular-weight poly-
ethylenes are available; chemical resistance, tensile
strength, and hardness tend to increase with increas-
ing density.
A high-density polyethylene product, MEDPOR, is
a stable implant that is well tolerated by local tissue.
This high-density polyethylene nonabsorbable mate-
rial is nonantigenic, nonallergenic, and easy to implant.
The material is somewhat flexible, and its porosity
allows rapid tissue ingrowth. Although there have
been reports of implant exposure and low-grade
infection,66"71 several of the complications occurred
either in problem areas with thin or atrophic soft tissue
coverage or extensive scarring 67 or in patients with risk
factors such as smoking, drug abuse, or prior surgery.70
MEDPOR products have been popular and used suc-
cessfully for the last decade.66,67,70'71 Block and sheet
forms are available, as are numerous preformed prod-
ucts for auricular and facial reconstruction. High-
density polyethylene has also been used for vertebral
body replacement as part of a composite prosthesis72
and to prevent recurrent tethering of the spinal cord
(Figs. 26-8 and 26-9).
Polypropylene is closely related to polyethylene. A
single substitution of one methyl group for a hydro-
gen atom in each polyethylene monomer gives rise to
polypropylene. Like polyethylene, polypropylene is
highly inert. The molecular structure is that of a loosely
woven, high-density polymer; it is available as a woven
mesh under the trade names Marlex1 and Prolene*
'Bard Cardiosurgery, Billerica, Massachusetts.
'Kthicon, Inc., Somervillc, New Jersey.
image...

758 • GENERAL PRINCIPLES

FIGURE 2 6 - 8 . MEDPOR Biomaterial facial implants. A, Single-piece chin implants (may be cut in half for
easier insertion). B, Extended chin implants with a separate alignment tab (round and square styles with dif-
ferent sizes for projection). C, Square version of extended RZ chin. D, RZ Mandibular Matrix System to augment
the entire mandible. (Photographs courtesy of Porex Surgical Products Group, © 2002.)

(Fig. 26-10). The material is easy to suture, has good
tensile strength, and exhibits early fibrous tissue
ingrowth that facilitates fixation and incorporation."
The mesh is frequently used to repair abdominal fascial
defects,73,74 and it can be applied alone57,75,76 or as a
methyl methacrylate composite in chest wall recon-
struction.77"79 Polypropylene is also available as suture.
Elastomers
In general, elastomers are highly elastic, impact resist-
ant, and highly gas permeable. As a result, elastomers
are well suited for cardiovascular and soft tissue appli-
cations. Elastomeric compounds are either amorphous
or linear. Most, including rubber, are amorphous with
low cross-link density. They have low to moderate
modulus and tensile properties with high reversible
elongations (100% to 1000%). The linear polyurethane
elastomers are linear block copolymers that consist of
polyether (soft) amorphous segments and urethane-
containing (hard) glassy or crystalline segments. The
soft segments through which the hard domains are
dispersed form an amorphous matrix; the hard
domains act as physical cross-links and also as rein-
forcing filler. These formulations result in materials
of relatively high modulus and exceptionally good
long-term stability under sustained cyclic loading.
Silicones are a large family of organic polymers with
a repeating backbone of alternating silicon and oxygen
atoms. Organic groups attach directly to the silicon
atom through silicon-carbon bonds to produce poly-
dimethylsiloxane (PDMS). In a process called cross-
linking or curing, chains of PDMS can be linked
together to form a polymer network as a chemical reac-
tion occurs between a silicon-vinyl group on one chain
and a hydrogen atom bonded to silicon on another
chain. Depending on the polymer length, silicone can
exist in either liquid or solid form. Silicone fluids and
oils have their molecules arranged in linear chains,
with viscosity dependent on chain length. These
straight chains mayrange from fewer than 10 to many
thousand silicon-oxygen units. For silicone gels,
molecules are cross-linked to branch into a semiliq-
uid three-dimensional polymer network. More branch-
ing produces thicker gels. This network is swollen with
PDMS fluid to produce a sticky, cohesive mass. To

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Dr.Mustafa D.
image...
FIGURE 2 6 - 9 . MEDPOR Biomaterial customized
implants. A, Implant manufactured to fit custom cranial
defect from model. B, Custom implants can be used to
repair orbital and zygomatic defects secondary to complex
orbital fractures. [A, Courtesy of Robert D. Wallace, MD.
Memphis, TN, and Porex Surgical Products Croup. ©2002.
Reproduced by permission.)
produce silicone elastomers, long-chain PDMS fluid
is joined for side bonding, and elastomer is much more
densely cross-linked than gel. Special forms of amor-
phous silica are added and tightly bound into the
polymer to give elastomer its strength and extensibil-
ity. Crystalline forms of silica are never used in the
manufacture of silicones with medical applications.
Silicone gel and elastomer are composed of the
PDMS polymer, a cross-linker, and a catalyst. Cross-
linkers are shorter chained polymers. The catalyst is
typically either platinum or tin. Silicones are ideal for
medical uses because of their unique combination of
material properties, especially the fact that silicone is
biologically inert. The hydrophobicity of PDMS means
that cells cannot attach themselves to implants, and
chemicals and enzymes cannot gain sufficient contact
to affect the material. In addition, PDMS remains stable
at all temperatures and is highly permeable to gases,
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Dr.Mustafa D.
26 • ALLOPLASTIC MATERIALS 759
transparent, and flexible. It also has low rigidity and
low wettability. Medical applications of silicones are
numerous. Fluids are used to coat needles, sutures,
syringes, and implanted devices as well as to lubricate
instruments. Gels are made into sheeting and used to
fill some breast and testicular implants. Elastomer is
the material of tubing, catheters, drains, and shunts;
it also comes in block forms for carving and as pre-
formed implants with a wide variety of applications
(calf, gluteal, and pectoral implants; testicular and
penile implants; and chin, cheek, ear, maxilla, nasal
dorsum, or orbital floor implants).
Silicone elastomer can be compounded in two
forms, the standard heat-temperature vulcanized
(HTV) form and a room-temperature vulcanized
(RTV) form. The advantage of heat vulcanization is
that the byproduct of the vulcanizing agent is ther-
mally eliminated during the curing stage. RTV silicone
is useful in instances in which the application of heat
is inadvisable or inappropriate, for example, in the
encapsulation of heat-sensitive components. RTV
silicones are available as single- or double-component
agents. One-component RTV silicone is hydrolyzed by
water, requires time to cure, and produces acetic acid
as a byproduct. Two-component RTV silicone requires
a catalyzing agent and a specific nontoxic agent (as in
medical-grade implantable silicones).
The ubiquity of devices made from or coated with
silicone for innumerable applications demonstrates the
success and popularity of silicone as an implant mate-
rial. Temperature stability, high resistance to chemi-
cal and environmental insults, and minimal reactivity
have contributed to the wide acceptance of silicone as
an implant material since its successful placement as
All iji%
)!ii\ (!
FIGURE 2 6 - 1 0 . Prolene polypropylene mesh system
for hernia repair with onlay patch and connector. (Pho-
tograph courtesy of Ethicon, a Johnson St Johnson
company.)
760 1 • GENERAL PRINCIPLES
a urethral implant in the 1950s. It is still considered
the "gold standard" to which other implant materials
are held and has, thus far, weathered a battery of
biologic, chemical, mechanical, and political testing.
Polyurethanes were originally developed in
Germany in the early 1900s as adhesives, foams, and
surface coatings, with further development after World
War II as elastomers and flexible foams.80,81 This group
of polymers consists of a diisocyanate and an alcohol.
Its porous structure has been exploited as a way to
lower capsular contracture rates in polyurethane
foam-covered breast implants. 82 These implants
generated a significant foreign body giant cell reac-
tion with subsequent tissue ingrowth and adhesion.59
Unfortunately, the potentially adverse effects of a break-
down product of polyurethane, toluene diamine,
prompted an FDA request for a voluntary delay of
production and sales of these devices. As such,
polyurethane implantable devices are not presently
available.
Natural rubber (polyisoprene) is perhaps the most
familiar of elastomers. The polymerized isoprene
monomer contains bulky methyl side groups that result
in a helical coil structure. This configuration confers
the highly elastic property characteristic of rubber. The
use of sulfur atoms in a process called vulcanization
results in sufficient cross-linking to produce a soft
rubber with its familiar characteristics. However,
processed rubber is generally not useful for implan-
tation because of toxicity problems. Purified forms of
natural rubber are somewhat better tolerated and have
been explored as a potential implant material although
not presently used as such. Lackluster pursuit of rubber
in implant applications may be due, in part, to the
performance and acceptance of silcone.
Thermosets
Thermosets demonstrate stronger intermolecular
attractions and are, in fact, linked by primary cova-
lent bonds, in contrast to thermoplastics, which are
generally long-chain molecules maintained by weaker
van der Waals attractions. Because of their highly cross-
linked polymer chains, thermosets have inherently
stronger intermolecular bonds that yield a harder and
stronger substance. Thermosets are usually chemically
inert and possess high modulus and tensile proper-
ties with negligible elongation; therefore, most are char-
acteristically strong but brittle. Because of extensive
cross-linking, thermosets characteristically maintain
their solid state and therefore do not undergo solid-
melt transformation on heating. Consequently, ther-
mosets cannot be melted, reprocessed, or dissolved by
use of solvents. Temperature increases generally, result
in thermal degradation.
Thermosets are not extensively employed as implant
materials but are occasionally used for component
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Dr.Mustafa D.
encapsulation. Some common types of thermosetting
resins used in other medical applications are phenol-
formaldehyde (Bakelite), urea-formaldehyde, epoxy
resins, and unsaturated polyester resins. None of these
is used as an implant material in and of itself.
SUTURES
History
The compulsion to close wounds has existed for thou-
sands of years, with perhaps the earliest suggestion of
suture use on an Egyptian scroll dated to 3500 BC.83,84
Hippocrates referred to intestinal suturing in 460 BC,85
and Galen made reference to the application of
"catgut" during tendon repair for gladiators as early
as AD 175 in De Methodo Medendir** Ahmad 89 sug-
gests that the term catgut is not a direct reference to
feline intestines but rather a corruption of the word
kitgut, an early musical instrument called a kit. His-
torically, a plethora of materials has been enlisted to
aid in wound closure; silver, flax, hemp, weeds and
grasses, and human hair and horsehair are among the
most frequently mentioned.87'91 A closure technique
using ants is even documented, whereby pincher ants
were decapitated after biting approximated bowel
edges—the pincers maintained approximation—
hence, the first "stapled" anastomosis.85,92
Suture selection can influence most aspects of
wound healing: rate of healing; strength, before and
after the healing period; resistance to infection; extent
of inflammation at the wound site; and appearance of
the healed wound site.93 In turn, wound factors poten-
tially influence suture selection: rate of healing, stress
and strain of the wound site, growth potential of the
wound, and need for permanent or temporary mechan-
ical support. 93 The ultimate cosmesis of the healed
wound must also be considered.
Forms, Formulations,
and Properties
The suture selections available to surgeons today are
abundant. The increasing sophistication of material
formulations, coatings, and configurations contributes
to greater control over mechanical and physical prop-
erties including strength, elasticity, absorption rates,
and tissue reaction to the suture and its degradation
products. Sutures can be categorized and subcatego-
rized according to whether they are absorbable or non-
absorbable, organic or synthetic, and monofilament
or multifilament (twisted or braided).
Although suture material itself appears to have little
impact on the incidence of infection and other post-
operative wound complications such as dehiscence
and hernia,94"96 studies suggest a potential increase in
infections with multifilament suture resulting from
image...

26 • AuoPLftSTic MATERIALS 761

the braiding or twisting interstices.96,97 Multifilament
suture is also apparently susceptible to failure by shear
forces, especially in the braided configuration. 96 Com-
paratively, monofilament suture can be damaged and
weakened by crushing forceps and other instruments.
Wounds regain strength at varying rates,98,99 and dif-
ferential healing rates depend on tissue type.100 Con-
sequently, a wide variety of sutures with different
absorption rates are available. Surgeons must select the
suture most appropriate for the specific wound con-
ditions, the strength of the tissue, and the tissue type.
Tissue that experiences inherently high stresses and
urinary and biliary tract wounds that are susceptible
to stone formation from a suture nidus 96 require
prudent suture selection (Tables 26-10 and 26-11).
NONABSORBABLE SUTURES
Silk has long been a mainstay in the surgeon's suture
armamentarium. Its handling and tying characteris-
tics are favored by many; however, tissue reaction to
silk can be vigorous and chronic, with degrading silk
fragments acting as nidi for granuloma formation.
The resorptive characteristics of silk are variable and
largely unpredictable.
Nylon is better tolerated histologically than silk is.
It is rapidly encapsulated, and tensile strength is main-
tained for a longer time than with silk.
Polypropylene suture is considered inert and main-
tains tensile strength for several years. Although inju-
dicious handling of the suture filament can result in
weakening, the long-term stability of the suture and
in situ performance characteristics for long-lasting
strength with minimal tissue reaction make it an attrac-
tive choice.101
Like polypropylene sutures, polyester sutures main-
tain tensile strength over time. Polyethylene tereph-
thalate (Dacron) is an aromatic polyester suitable for
closures that require tensile strength and stability.
Tissue responses to sutures of this type are generally
mild; however, a number of chemical variations and
coatings are available to improve the handling prop-
erties of polyester sutures. For example, Teflon can
greatly increase cellular response to the presence of
the suture because it contains particulates. In contrast,
polybutilate, which is used to coat Ethibond, elicits
only mild cellular reaction.
Stainless steel suture is assuredly nonabsorbable and
is eventually encapsulated by collagen. Advantages of
stainless steel are that it is inert and generates almost
no tissue reaction. In addition, stainless steel is stable
and possesses high tensile strength. Disadvantages of
this suture material include the difficulty of handling
it and tying knots. Furthermore, there is a risk of punc-
ture wounds in the surgeon or operating room staff.
ABSORBABLE SUTURES
Polyglycolic acid and poly-L-lactic acid are aliphatic
compounds that undergo degradation by hydrolysis
and therefore are resorbed during the course of several
months. Polyamide is a nylon compound that is also
resorbed over time.
PATHOLOGY AND
COMPLICATIONS
General
Some have postulated that no implanted artificial
material can be considered totally inert in the body.36,102
The body's response to the implantation of biomate-
rials is myriad. Greco 6 outlined six broad categories
of potential host responses to an implant ranging from
inflammation and extracellular matrix to integrins and
adhesion molecules. Hench and Wilson 36 presented
four major categories of host responses to an implant
(Table 26-12). 57 ' ,03a04

TABLE 26-10 • ABSORBABLE SUTURES'2"

Break Stren gth (MPa)

Trade Elongation to
Material Name Filament Absorption* Straight Pull Knot Pull Break (%)

Catgut (protein) Chromic Monofilament -90 days 310-380 110-210 15-35

Polyesters
Poly-p-dioxanone PDS Monofilament 90 days-6 mo 450-560 240-340 30-38
Polyglycolic acid Dexon 5 Braided 90 days 760-920 310-590 18-25
Polyglycolide-co-lactide Vicryl Braided 40-70 days 580-910 300-400 18-25
Glycolide-caprolactone Monocry! Monofilament 90-120 days
Polyglycolide-co- Maxon Monofilament 90-120 days 310-380 110-210 15-35
trimethylene
carbonate

•Time depends on diameter and material.

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Dr.Mustafa D.
762 • GENERAL PRINCIPLES

TABLE 26-11 • NONABSORBABLE SUTURES59'84-93-124

Break Strength (MPa)

Trade Elongation to
Material Name Filament Straight Pull Knot Pull Break (%)

Cotton Twisted monofilament 280-390 160-320 3-6

Silk Surgical silk Braided 370-570 240-290 9-31
Dermal Twisted
Virgin silk Twisted
Polyesters
Polyethylene Eacron Monofilament 510-1060 300-390 8-42
terephthalate Ticron Braided 300-390
Mersilene
Ethibond
Ethiflex
Polydek
Tevdek
Mirafil
Polybutester Novafil Monofilament 480-550 290-370 29-38
Polyamides
Nylon Surgilon Braided 460-710 300-330 17-65
Dermalon Monofilament
Nurolon Braided
Ethilon Monofilament
Supramid Sheath/core
Polyolefins
Polypropylene Prolene Monofilament
Surgilene Monofilament 410-460 280-320 24-62
Polytetrafluoroethylene Gore-Tex Monofilament
(PTFE)
Stainless steel Flexon Monofilament/twisted
stainless monofilament
steel
Surgical
stainless
steel

In the evaluation of implant- and material-related

TABLE 26-12 • FOUR MAJOR CATEGORIES
OF HOST RESPONSES TO AN
IMPLANT36
The material releases some toxic compounds, leading
to the death of surrounding tissue.57''03-10*
The material is nontoxic but is gradually resorbed and
replaced by the surrounding tissue that is under
repair.
The material is nontoxic and biologically inactive but
cannot be degraded by the host, which reacts by
encapsulation. (Several metallic and plastic
biomaterials belong to this category.)
The material is nontoxic but highly interactive with the
surrounding tissues in forming chemical bonds with
it, which stabilize the implant. (Dense hydroxyapatite
ceramics, bioactive glasses, bioactive glass-ceramics,
and bioactive composites are examples of this
category of biomaterials.)
complications, it is important to distinguish compli-
cations that are directly attributable to the product
versus complications that are related to surgical tech-
nique or host response. Accuracy in reporting these
complications is critical in the evaluation of the safety
and efficacy of a device. The controversy generated in
regard to silicone gel breast implants is a compelling
example of the importance of this delineation.
Infection
Numerous factors contribute to implant infections, not
the least of which involves predisposing host factors.
Perturbations in the host defense mechanisms in
the vicinity of implanted foreign bodies have been
frequently suggested although not experimentally
confirmed.
The presence of a foreign body markedly increases
the pathogenic potential of organisms of low

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Dr.Mustafa D.
TtJWK^eltfW image...
virulence, such as Staphylococcus epidermidis.105
Patients infected with these organisms in connection
with a biomaterial implant may be considered by some
to be immunocompromised. An argument in favor of
local defect in the host defense against staphylococ-
cal foreign body infection was obtained by studies per-
formed with experimentally infected animals. Studies
have shown that a "subinfective" bacterial inoculum
for a particular kind of experimental wound is
sufficient to cause severe clinical infection in the pres-
ence of foreign materials such as sutures, hemostats,
soil, devitalized and crushed muscle tissue, gelatin, and
oxidized cellulose. Particularly impressive were the dif-
ferences obtained for minimally infective doses for
Staphylococcus aureus; in the presence of silk sutures,
as few as 100 colony-forming units produced a chronic
infection, whereas 107 organisms were not clinically
infectious in the absence of foreign material.106 Other
experiments have shown that bacteria, either grown
in vitro as adherent biofilms or recovered from
infected prosthetic devices, are less susceptible to
antimicrobials. 107
Although the American Cardiology Society has out-
lined recommendations in the prophylactic adminis-
tration of antibiotics in valvular heart disease and
artificial heart valves during potentially infective
events, the overall use of prophylaxis during instances
of potential seeding is controversial. Infections in
distant areas of the body can cause sepsis in a pros-
thetic joint through hematogenous or lymphatic
seeding. Common causes include dental, respiratory,
dermal, and urinary infections. The frequency of this
phenomenon and the effects of prophylactic anti-
biotics remain unknown. 21
Urinary catheters, central spinal fluid shunts,
central venous lines, bone cement, PMMA microbeads,
and sutures coated or impregnated with antibiotics
have been found to reduce the risk of infection around
these implanted devices. Urinary tract infections asso-
ciated with indwelling bladder catheters are among
the most common hospital-acquired infections. The
use of catheters coated with silver alloy can significantly
reduce the risk of these infections compared with stan-
dard catheters. m Randomized prospective clinical trials
have also found that antibiotic-impregnated cere-
brospinal fluid shunts significantly decrease the risk
of shunt infections.109 In addition, the number of blood
stream infections (which typically lead to longer hos-
pital stays) can be significantly reduced through the
use of antibiotic-impregnated central venous catheters.
Although these types of catheters are more expensive
than standard varieties, they result in overall cost
savings by decreasing morbidity rates.110
Antibiotic-impregnated bone cement has been
shown to significantly lower the reinfection rate after
replacement of infected total joint prostheses. Simi-
larly, antibiotic-impregnated PMMA microbeads and
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Dr.Mustafa D.
26 • ALLOPLASTIC MATERIALS 763
spacers have been found useful in treatment of bone
and joint infections.111,112 Early studies suggest that
sutures coated with antibiotics may be beneficial in
decreasing wound infections.113
Toxicity
Toxicity refers to the detrimental migration of a sub-
stance from some material into surrounding tissue.
Both the type and dose of the leachable substance will
determine the degree of toxicity. Toxicity testing can
encompass numerous biologic studies and chemical
tests that in combination establish a toxicity profile.
This profile identifies a dose-response correlation. In
implantable biomaterials, a dose-response relationship
may be difficult to establish; if so, tests might be
conducted solely to determine whether biologically
extractable ingredients are present. Numerous test pro-
tocols have been established for the testing of bioma-
terials and are available through resources such as the
United States Pharmacopeia and the American Society
for Testing and Materials. Common types of tests
include the direct examination of materials, for
example, acute reaction of intramuscular implanta-
tion, subcutaneous implantation, hemolysis, and cell
culture testing. Indirect studies of extractable ingre-
dients may include examination of systemic toxicity,
intracutaneous irritation testing, tissue culture testing,
isolated organ testing, and long-term animal implan-
tation studies. Practical and financial parameters will
ultimately influence the array of chemical and bio-
logic studies selected to determine the toxicity and
safetyofabioimplant. 103 ' 104 ' 114
Carcinogenicity
The cause-and-effect relationship between implanted
devices and tumor development in humans remains
controversial. There are numerous reports of several
cancer types that appear to have developed in relation-
ship to a variety of different implants in humans.115"'17
These reports, in addition to tumorigenesis demon-
strated in laboratory animals, sustain understandable
vigilance in the medical and scientific communities.
Material-induced tumors, primarily sarcomas, have
been produced in test animals by nearly all solid mate-
rials tested. One term applied to this observation is
solid-state carcinogenesis. The initial recognition of
this phenomenon has been historically attributed to
Turner, 115 Brand, n6 and Lawrence" 7 (Table 26-13).The
studies of Oppenheimer et al118 found that presarco-
matous changes occurred when the material was in
place for about 6 months, although tumors may not
appear until much later.
A number of theories have been presented that
include potentiation by chemical leachables, biode-
gradation products, physical contact between the

764 I • GENERAL PRINCIPLES
TABLE 26-13 • ELEMENTS OF SOLID-STATE
CARCINOGENESIS"5-117
The composition of the material appears to be of little
importance (unless it contains leachable carcinogens)
because a wide variety of materials elicit a similar
response.
A continuous, impermeable surface is important
because perforations, weaves, or powders tend to
reduce or abolish tumorigenicity.
The implant must be of a minimum ("critical") size.
The implant must remain in situ for a minimum time.
material and surrounding tissues, facilitation of mat-
uration for existing preneoplastic cells, and a combi-
nation of two or more of these scenarios.117
The relevance of tumorigenesis due to implant
materials in humans remains to be proved, however.
Despite direct cause-and-effect relationships seen in
some studies in laboratory animals, the evidence of
such relationships in humans is less apparent.
Hypersensitivity Reactions
Potential hypersensitivity reactions to biomaterials are
difficult to predict and to evaluate. The diagnosis of
a hypersensitivity reaction to an implanted material
may be a problem as well. These difficulties are miti-
gated, however, by the observation that hyper-
sensitivity reactions to biomaterials appear to be
uncommon. Because the mechanism of producing an
immune response typically necessitates intracellular
processing by macrophages and subsequent presen-
tation within the immune system, many bioimplants
and biomaterials are not candidates for immunologic
processing. They are too large or they are not
biodegradable and as such are not processed through
the immune system. However, degradation or break-
down products resulting from wear, corrosion, disso-
lution, or leaching from an implanted material may
cause immunogenicity.
In type I hypersensitivity reactions, the physiologic
response results from immunoglobulin E interaction
with an antigen. Such responses to biomaterials are
of little practical concern. There have been reports of
type I reactions in individuals working with chromium
salts and perhaps nickel salts, but these incidents were
not associated with implanted materials.
Type II hypersensitivity reactions to biomaterials
have also not been reported. Biomaterials containing
pharmaceuticals or those that produce corrosion or
degradation products might act as potential antigens
by adhering to platelet, mast cell, or basophil cell mem-
branes (and thus triggering the release of vasoactive
substances). However, such reactions have not been
observed.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
•
Type III hypersensitivity reactions require the
simultaneous presence and persistence of antibody and
antigen as a complex of a particular size. Although
many biomaterials are potential candidates for elicit-
ing such a reaction, this phenomenon either has not
been demonstrated or has not been detected in
biomaterials.
A type IV or cell-mediated delayed hypersensitiv-
ity reaction is more commonly associated with bio-
materials. Individuals may develop contact sensitivity
to biomaterials components, and type IV reactions can
be identified in pathology specimens harvested from
deep tissue surrounding an implant. Systemic symp-
toms may not be detected, but local tissue reactions
may result in a palpable increase in tissue mass
associated with the implant.1
Implant-Related Complications
EXPOSURE OR EXTRUSION. The risk of implant
extrusion and exposure can be limited by abiding by
the operative principles previously outlined. Avoidance
of tension on incision closure, use of a"no-touch" tech-
nique to minimize introduction of glove powder or
other foreign materials into an implant pocket, and
implantation of a truly benign device are some of
the techniques for successful, long-term implant
placement.
DEVICE FAILURE. Device failure can be minimized
by appropriate use of the device within the parame-
ters and indications for use outlined by the manufac-
turer. Establishing and maintaining a registry of
implants, along with good surgical technique and edu-
cation of the patient, can go far in promoting the
longevity of an implantable device.
PROMINENCE, VISIBILITY, AND PALPABILITY. The
prominence, visibility,and palpability of an implanted
material or device can be minimized by good surgical
technique to some extent. However, surface texturing,
material hardness, surface contouring, and other
design parameters can be useful in camouflaging an
implant.
EXPLANATION, RETRIEVAL,
AND TESTING
Evaluation of removed materials and devices con-
tributes immensely to the study and improvement of
implantable products. As mentioned earlier, a princi-
pal problem with premarket device testing is the
difficulty of replicating the clinical scenario; accord-
ingly, the abundance of information obtained from
an explanted device is invaluable. Numerous authors
advocate establishing an organized implant retrieval
and evaluation system.56,120,121 The prudence of sys-
tematic retrieval and testing becomes increasingly
TtM'ttf'aeltfW image...
evident as materials and devices become more
complex. Increased complexity makes it even more
difficult to simulate the physiologic environment in
which a device operates. Furthermore, as the patient-
consumer becomes more sophisticated, the demands
on the product rise. Favorably, device testing and
retrieval may further promote product improvement;
lamentably, the medicolegal concerns regarding the
product will likely escalate. A proactive approach on
the part of both manufacturers and surgeons is imper-
ative. The sequelae following the use of silicone
gel-filled breast implants (despite a lack of evidence
incriminating silicone) should suffice as an example
of the magnitude of the issue. As Angell15 concluded,
In the absence of structured requirements for risk assess-
ment before 1992, much of the literature on aspects of
silicone breast implants is anecdotal, lacking in appropri-
ate controls, or otherwise of little value in establishing
risk. This report stands as strong evidence of the need
for thorough and systematic assessment of medical devices
prior to their utilization and for continuing assessment
after widespread utilization to discover any rare complica-
tions that premarketing studies of feasible size might not
demonstrate.
Given the adverse economic effects of the silicone
gel breast implant controversy, manufacturers are more
inclined to establish and to maintain national registries
in spite of the cost. It remains debatable as to where
and with whom the responsibility of maintaining a
registry lies. Logistics are such that academic institu-
tions may necessarily share the retrieval and analysis
responsibilities while individual surgeons and their
patients become partners in culpability with the man-
ufacturers. Several large implant retrieval programs
have been established within the United States.56 Most
focus on orthopedic implants, but several are devoted
to cardiovascular and neurologic implants.
Cook122 recommends taking a systematic approach
to post-implant evaluation. A team with intimate
knowledge of the clinical applications of the device
and specialized post-retrieval testing should be assem-
bled. Ideally, the team might consist of a physician and
an engineer. In addition, sufficient staff should be avail-
able to classify and store the devices, and appropriate
laboratory resources for pathologic, microbiologic, bio-
chemical, metallurgical, and mechanical testing should
be available. Procurement of the device from the
surgeon is a critical step in the process. In addition to
securing the device itself, collection of associated spec-
imens and documentation of vital clinical data con-
tribute immeasurably to device evaluation. Clinical
forms compatible with the American Society for
Testing and Materials standards have been developed
for orthopedic devices. These forms plus those used
for premarket clinical studies can serve as starting points
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Dr.Mustafa D.
26 • AUTOPLASTIC MATERIALS 765
for the eventual development of device- and applica-
tion-specific data collection. Important clinical data
include history, patient demographics, initial and
current diagnoses, indications for implantation and
explantation, and any unusual events. The surgeon's
presence in the operating room is necessary for pho-
tographs, accurate documentation of intraoperative
findings pertinent to the device, collection of tissue
and fluid samples and culture specimens, and device
procurement. Cook122 details a number of potentially
applicable tests to be considered for device, tissue, and
fluid samples.
ECONOMICS
Outcomes studies have proliferated as the practice of
medicine concedes to the realities and importance of
the impact of business practices and economics on
care of patients. Outcomes analyses will continue to
multiply as new protocols, techniques, and technolo-
gies arise to compete with traditional methodologies
and practice and as economic pressures continue to
intensify. Pertinent examples of such evaluations in
plastic surgery include cost comparisons between
autologous tissue transfer and implant reconstruction
and immediate versus delayed reconstruction after
mastectomy. There is little doubt that these types of
analyses will influence the use of implant materials
and define their role in reconstruction by elucidating
the fiscal advantages and disadvantages of the proce-
dures involving their use.
FUTURE
Tissue Engineering
and Regeneration
The burgeoning interest in tissue engineering is
exemplified by the growth in coverage of this topic since
the last edition of Plastic Surgery.The previously limited
discussion of the topic in the preceding edition con-
trasts with the expansion into an entire chapter
devoted to tissue engineering in this edition. Tissue
engineering from the level of matrix replacement to
the potential for whole organ replacement with
artificial organs brings the promise of the next revo-
lution for the future of plastic surgery and perhaps
much of surgery. A comprehensive discussion can be
found in other chapters.
New Materials and Technology
Numerous approaches to resolving the host versus
implant saga are under investigation. One is the devel-
opment of new biomaterials with surface characteris-
tics improved by reducing adsorption of the most active
host proteins that promote bacterial adhesion. Three

766 I • GENERAL PRINCIPLES
strategies currently under investigation include the
alteration of surface physicochemical properties, appli-
cation of modified surface coatings, and employment
of protein coatings to prevent bacterial adhesion. 21
Fluid-phase agents that interfere with microbial adhe-
sion or enhance the phagocytic host defenses may also
improve surface properties. Improved antibiotics
aimed at microbial tolerance are yet another tactic. It
may be necessary to perform detailed analyses of each
biomaterial, including examination of the composi-
tion of adsorbed host proteins and cell populations
and delineation of which proteins promote bacterial
attachment and colonization. 107 Gene therapy, nan-
otechnology, less invasive surgical techniques, and
numerous other technologic advances demonstrate
almost limitless possibilities in expanding the b o u n d -
aries of repair, remodeling, replacement, and aug-
mentation of the h u m a n body.
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69. Romano JJ, Iliff NT, Manson PN: Use of Medpor porous
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71. Niechajev I: Porous polyethylene implants for nasal recon-
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81. Baatich C, DePalma D: Materials used in breast implants:
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image...
CHAPTER
27
•
Prostheses in Plastic Surgery
ARIAN MOWLAVI, M D •
• MICHAEL W. NEUMEISTER, MD, FRCSC, FACS
• ROBERT C. RUSSELL, MD, FRACS, FACS
FACIAL PROSTHETICS
Retention
Osseointegration
Impressions
Prosthetic Materials
Color
Ear
Nose
Orbit
Ocular
Summary of Facial Prostheses
The word prosthesis originates from the Greek noun
prostithenai, meaning "the act of adding to" or "put in
addition." The first mention of prostheses in Greek
mythology involved the tale of the Trojan War. During
this war, Apollo's oracle at Delphi prophesied that Troy
could be seized only if the prosthesis of Pelops was
brought back to Troy. Indeed, the Achaeans recovered
the prosthesis and took it to Troy, and the Trojans were
defeated. Pelops had ruled as a king—his name is emu-
lated by a peninsula, the Peloponnese—and had been
an avid promoter of the Olympic games. Pelops rose
to power despite punishment of his father, Tantalus,
into the Underworld. Pelops had been dismembered
by Tantalus, who in his attempt to test the wisdom of
the gods had served his son as a meal to immortal
Olympian guests. Although Hermes saved Pelops' life
by collecting his dismembered pieces and reheating
them in a cauldron, he could not salvage Pelops' shoul-
der because it had already been eaten by the goddess
Demeter. Thus, an ivory shoulder prosthesis was
created that would later become a critical determinant
of the Trojan War.1
Various ancient civilizations detail references to
prostheses that were developed to treat war injuries.
An ancient sacred poem from India, the Rig-Veda
The images for this chapter were obtained from Juan R. Garcia, Assistant Pro-
fessor, Facial Prosthetics Clinic of the Department of Art as Applied to Med-
icine, Johns Hopkins University, and Aesthetic Concerns Prosthetics Inc.
(www.Livingskin.com).
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DlMITRIOS DANiKAS, M D
UPPER EXTREMITY PROSTHETICS
Objectives
Prosthetic Types
Digital Prostheses
Thumb Prostheses
Partial Hand Prostheses
Complete Hand Prostheses
Summary of Upper Extremity Prostheses
(3500-1800 BC), recounts the story of a warrior, Queen
Vishpla, who was fitted with an iron prosthesis after
losing a leg in war so she could return to battle. The
Egyptian Herodotus (424 BC) mentioned Hegistratus
of Elis, who was condemned to death by the Spartans.
Hegistratus escaped from his ankle shackles by ampu-
tating his own foot and using a wooden replacement
to escape by foot. A Roman prosthesis from the Samite
Wars (300 BC) was discovered in Capau, Italy, in 1858.
It was constructed of a wooden core, with a bronze
shim and leather straps. Three centuries later, Pliny
the Elder (AD 23-79) wrote of Marcus Sergius, a Roman
general who sustained a right arm amputation while
leading his legion against Carthage in the Second Punic
War (218-210 BC).An iron hand was fashioned to hold
his shield so that he could fight again.2 Finally, the
emperor Justinian II, referred to as the Rhinotmetus,
one with an amputated nose, suffered a rhinectomy
in AD 695 during a revolt against him. During this
era, disfigured men were not allowed to become
emperors; it was speculated, then, that Justinian II
managed to recover his throne in AD 705 by wearing
an artificial golden nose.3
The term plastic is derived from the Greek word
plastikos, meaning"to mold"or"to contour the shape."
Reconstructive efforts in plastic surgery are a con-
tinuum of procedures from a minor local rearrange-
ment of tissue to the most complex multistaged,
sequential use of regional or distant composite tissue
to restore function, contour, or appearance of some
769
770 I • GENERAL PRINCIPLES
part of the body. The amputation or ablation of com-
posite tissues may therefore require the reconstruc-
tion to incorporate skin, subcutaneous tissue, muscle,
cartilage, or bone. The ears, nose, and eyelids are exam-
ples of highly specialized composite tissues that chal-
lenge even the most experienced reconstructive
surgeons in their efforts to restore these organs if they
are removed through trauma or cancer resection. Sim-
ilarly, the upper extremity, with its intricate functions
employing intrinsic and extrinsic muscles, sensibility,
and appearance, offers a formidable reconstructive
challenge to restoration of function and appearance
after amputation.
Reconstruction of these complex, composite body
parts by use of autologous structures alone requires
the manipulation, shaping, and transfer of living tissue.
The benefit of autologous reconstruction is that it
replaces the lost body part with the patient's own tissue,
which is pliable, permanent, and not rejected. The dis-
advantage, however, is that there is always a certain
degree of donor site morbidity and scarring with autol-
ogous reconstruction. Infection, hematomas, tissue
resorption, or poor vascularity may have an adverse
impact on the final outcome. Autologous reconstruc-
tion entails multiple surgeries and requires the patient's
dedicated compliance.
Prosthetic replacement, on the other hand, offers
another option for restoration of the amputated part
and a viable alternative in selected cases to autolo-
gous reconstruction. Prostheses can be used to replace
eyes, ears, noses, and even entire facial units to restore
an aesthetic appearance. Prosthetic limbs can restore
form and function. The indications for prosthetic use
must be individualized to each patient's needs, which
are dictated by the patient's personal goals for recon-
struction. Small defects are typically amenable to local
reconstruction, whereas larger defects require either
distant tissue transfer or prosthetic reconstruction.4
A young child may benefit more from autologous
reconstruction for microtia, whereas an elderly patient
may be best suited for a prosthesis. It is essential for
the plastic surgeon to maintain a working alliance with
the prosthetist, who can aid in the therapeutic plan.5
The decision to choose a prosthesis, therefore, depends
on a number of factors including the patient's age,
size and complexity of the defect, desired function,
existing comorbidities, and availability of donor sites.
It is essential for the patient and the surgeon to
communicate their respective expectations before
undertaking prosthetic or autologous tissue recon-
struction. The expectations of a young patient with
the acquired loss of a body part may be quite differ-
ent from those of an elderly patient who has recently
undergone tumor ablation (Fig. 27-1). Each patient's
needs and expectations are unique to that individual.
The patient's overall satisfaction and acceptance of
a prosthesis depend on a number of intrinsic and
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
FIGURE 2 7 - 1 . Autogenous tissue reconstruction has
donor site morbidity and may be difficult to mold
accurately in some patients. (Courtesy of the Facial Pros-
thetics Clinic, Johns Hopkins University, Baltimore, Md.)
extrinsic factors. The extrinsic factors, such as age, sex,
body image, psychological stability, systemic medical
illness, life expectancy, social awareness, and occupa-
tional issues, may directly affect the success and use
of a prosthesis. Intrinsic factors that affect the patient's
satisfaction with a prosthesis are properties that relate
to comfort, functionality, ease of care, and aesthetic
contour. These factors undoubtedly influence the
patient's expectations before a prosthesis is ordered
as well as the long-term use of a device. A psycholog-
ical assessment is therefore prudent before construc-
tion of a prosthesis to define the patient's expectations
and to estimate the long-term use.
Coping strategies used by individuals to adapt to
a significant medical crisis including the loss of a body
part have been summarized by Moos and Tsu.6 The
major coping progressions that Moos and Tsu describe
include denying or minimizing the seriousness of a
crisis, seeking relevant information, requesting reas-
surance and emotional support, learning specific
illness-related procedures, setting limited concrete
goals, and rehearsing alternative outcomes. Perhaps
the most important psychological factor in the suc-
cessful adjustment of accepting a prosthesis involves
the patient's social and emotional support systems.
Close friends, family, therapists, physicians, and sur-
geons may provide positive support. For a patient
facing major disfigurement, this support is a critical
factor to be able to cope with the fear of rejection.7
FACIAL PROSTHETICS
The fabrication of a facial prosthesis demands an under-
standing of three-dimensional, multilaminated, spe-
cialized structures, such as the nose, eyes, and ears. The
T^WWfcfltfW image...
topography, support structures, and surface of the face
provide guidance for construction of a facial pros-
thesis. Radiography, especially magnetic resonance
imaging and spiral computed tomographic scan
imaging, now allow three-dimensional evaluation of
facial anatomy in precise detail. 8 The advent of three-
dimensional computed tomographic image format-
ting has allowed visualization of even more intricate
detail, and it is an invaluable tool in attempting to
assemble a working three-dimensional prosthesis. 9
Retention
A patient's ability to use a prosthesis successfully
depends not only on its appearance but also on its ability
to be securely fixed to the body. Maxillofacial pros-
theses can be retained by adhesives, mechanical attach-
ments, anatomic landmarks with retentive contours,
and osseointegration.
A number of adhesives can be used to secure a pros-
thesis to the underlying skin, including pastes, liquids,
sprays, and double-coated tapes (Fig. 27-2). The choice
of adhesive depends not only on the type of prosthe-
sis and the material used to make it but also on the
contour and condition of the tissues where the pros-
thesis will be placed. Acrylic resins, such as Pros-Aide,
are mixed with water to create a rubber-like substance,
often referred to as a latex adhesive. Rubber, vinyl
acetate, vinyl chloride, and styrene are incorporated
into this adhesive. Surfactant is used on one surface as
a wetting adhesive to create a strong bond between the
prosthesis and the skin. Two separate layers of adhe-
sive are applied to the prosthesis and allowed to dry
serially during 1 to 10 minutes before the prosthesis
is placed into its host bed. The application of this adhe-
sive is not labor-intensive, and removal requires only
a cloth moistened with rubbing alcohol. Epithane-3
adhesive is an emulsion of acrylic polymer in water.
It is applied as a watery liquid that becomes transpar-
ent on drying. Silicone adhesives (Hollister Medical
FIGURE 2 7 - 2 . Adhesives used to
secure the prosthesis to the body part.
(Courtesy of the Facial Prosthetics
Clinic, Johns Hopkins University,
Baltimore, Md.)
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Dr.Mustafa D.
27 • PROSTHESES IN PLASTIC SURGERY 771
Adhesive, Secure Medical Adhesive, and Dow Corning
355 Medical Adhesive) are dissolved in a solvent that
evaporates after application, leaving a tacky surface.
Silicone adhesives such as the Bard appliance adhesive
have the advantage of withstanding the effects of sun-
light, ozone, and prolonged contact with skin oils and
chemicals. The disadvantages of the silicone adhesives
are their poor tensile strength and a tendency to build
up over time. Silicone and acrylic resin adhesives can be
used in combination to overcome some of the limita-
tions posed by use of each separately. Rubber latex adhe-
sives are formed by dissolving reclaimed rubber with
naphtha, which forms a sticky cement. The main dis-
advantage is that they are opaque after drying and may
be visible through the thin margins in the prosthesis.
Pressure-sensitive tapes consisting of a backing strip
of cloth, paper, film, foil, or laminate coated with an
adhesive can also be used to adhere a prosthesis. These
tapes are applied by finger pressure. Tapes like 3M Bi-
Face Tape use adhesives on both sides and are applied
to both the prosthesis and the skin after removal of
the sealant cover slip. The tape can be difficult to
manipulate because of its sticky nature, and its use
should be avoided in patients with poor manual
dexterity. The tensile strength of the tape is less than
that of most liquid paste adhesives and can be reduced
even further if either surface is contaminated before
application.
The selection of the appropriate adhesive system
should consider the tensile strength requirements and
biocompatibility of the adhesives to both the pros-
thesis and the skin. The tensile strength of acrylic resin
adhesives is stronger than that of the rubber, silicone,
or tape adhesives. Skin compatibility can often be
assessed with a locally applied patch test. Rubber-based
adhesives are more likely to promote skin irritation.
In contrast, tape and acrylic resin adhesives are usually
well tolerated by most patients. The use of adhesives
is generally not possible in patients with previously
irradiated skin.10
772 I • GENERAL PRINCIPLES
There are some limitations and long-term prob-
lems associated with use of adhesives to secure a facial
prosthesis. Patients with poor dexterity are clearly at
a disadvantage and may not be able to apply the adhe-
sives correctly or to position the prosthesis. The appli-
cation of the adhesive can be cumbersome, messy> and
time-consuming. Prostheses applied to mobile areas
are often difficult to secure. Some patients develop skin
irritation or allergies to adhesives, necessitating a change
of adhesives or the entire prosthesis. Routine applica-
tion and removal of a prosthesis with repeated adhe-
sive use may, over time, result in external prosthetic
pigment changes. The greater the difficulty and the
more problems encountered in applying and remov-
ing any prosthesis, the less likely a patient is to wear
the prosthesis.
There are other ways to secure a prosthesis without
the use of adhesives. Current methods include mechan-
ical retention by use of eyeglasses, retentive clips,
magnets, and acrylic buttons (Fig. 27-3). In the past,
eyeglasses were routinely used to retain nasal and orbital
prostheses and were intended to prevent lateral
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
FIGURE 2 7 - 3 . An acrylic button
used to attach the prosthesis to
an orbit. (Courtesy of the Facial
Prosthetics Clinic, Johns Hopkins
University, Baltimore, Md.)
movement and to camouflage the prosthesis-facial
interface (Color Plate 27-1). A deficiency of underly-
ing nasal bone remnants and the weight of the pros-
thesis, however, often hindered the use of eyeglasses
as a method to secure a prosthesis to the face. Perma-
nent fixation of a nasal prosthesis to eyeglasses is gen-
erally avoided today so that the patient can remove the
glasses without exposing the underlying defect.
Mechanical retention is outdated today except when
irradiation or the patient's poor dexterity or compli-
ance prevents the use of adhesives.11'13
Another way to retain a prosthesis is to use the
unique anatomic features of a given facial defect,
including the residual skin contours and undermined
bone edges, to secure a custom-made prosthesis
without adhesives. This type of prosthesis is anatom-
ically retained (Fig. 27-4). A properly designed and
fitted prosthesis can use external tissue undercuts to
be held in place without adhesives. Patients with an
anatomically retained prosthesis must be educated
to monitor the condition of the underlying skin to
prevent ulceration from continuous direct external
FIGURE 27-4. An ocular pros-
thesis that is secured by interdigita-
tion with the residual skin creases of
the periorbital region. This uses the
procedure's anatomic undercuts.
(Courtesy of the Facial Prosthetics
Clinic, Johns Hopkins University,
Baltimore, Md.)
image...
compression. Surgical undercuts are maintained with
flexible conformers for 2 to 3 months after surgery
until the shape of the defect is stabilized. The pros-
thetist then makes an exact impression of the final
defect, which is then incorporated into the final design
of the prosthesis. 10
Osseointegration
Titanium metal implants that are anchored into bone
and externalized through the soft tissues and skin or
mucosa are commonly used today to provide contin-
uous and secure implant fixation (Fig. 27-5). There
are three major components to the osseointegrated
system: permanent titanium implants, docking abut-
ments, and the attaching system that is affixed to the
prosthesis."' 14 The first successful osseointegrated
titanium implants were done by Branemark 15 in 1965
to fix a dental prosthesis in an edentulous patient. Since
then, dental prostheses have been successfully held in
thousands of patients by this type of bone-anchoring
device. I6 Numerous investigators have also had success
with use of osseointegration to retain facial and auric-
ular prostheses.17"24 Osseointegration provides a con-
venient and secure attachment mechanism permitting
a single direction of fit that is extremely reliable. The
prosthetist can concentrate efforts on establishing an
aesthetic interface between the edges of the prosthe-
sis and the surrounding skin because it can be ensured
that there will be no shifting or rotation of the pros-
thesis after attachment. Osseointegration eliminates
the need for adhesives.
Titanium remains the implant material of choice
for osseointegration because its surface and mechan-
Auricular: two 4-mm screws
in mastoid region
O
FIGURE 2 7 - 5 . A and B, Titanium implants are anchored to the bone and externalized for docking with the pros-
thesis. (Courtesy of the Facial Prosthetics Clinic, Johns Hopkins University, Baltimore, Md.)
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
27 • PROSTHESES IN PLASTIC SURGERY 773
ical properties in a biologic environment are superior
to those of other metals.25,26 Any metal exposed to air
forms a surface oxide that can incite an inflammatory
reaction and a fibrous capsule.27,28 The degree of capsule
formation varies between individuals but has been
blamed for failed osseointegration. 29 Titanium oxide
is relatively inert, resulting in minimal capsule
formation in most patients. 30
Multiple implants are typically required for secure
prosthetic retention. An auricular prosthesis can be
firmly secured with two or three implants placed
approximately 18 mm from the center of the external
auditory meatus about 15 mm apart. Nasal prostheses
require two or three implants at least 4 mm long that
are connected by a bar, which evenly distributes the
weight of a nasal prosthesis and provides stable, secure
fixation. Three or four implants are typically required
to secure an orbital prosthesis adequately.31
Investigators at the University of Goteborg retro-
spectively reviewed 4636 patients who had osseointe-
gration procedures during a 10- to 20-year follow-up
period. They observed a 95% and 99% osseointegra-
tion retention rate for maxillary and mandibular recon-
struction, respectively, and a 98% success rate in patients
with temporal bone implants. The location of implant
placement in their series appeared to affect the success
rate. Parel and Tjellstrom21 presented a combined
review of their patients who had craniofacial osseoin-
tegration procedures performed in 14 centers in the
United States and Sweden. Successful integration was
achieved in 98.3% of patients in the mastoid region
and in 93.9% of patients in the orbital region, with
more variable outcomes over the midface. Prior
irradiation of the recipient tissue field had the most
at"
B
image...
774 I • GENERAL PRINCIPLES
compromising effect on the overall success rate, which
dropped to 6 1 % in these patients. Jacobsson,18 in a
review of orbital osseointegration, observed a success
rate of 92.1% in nonirradiated fields and 62.7% in Irra-
diated fields. Albrektsson30 reported 389 osseointe-
gration attempts in 174 patients involving various
craniofacial locations. He had an overall success rate
of 98%, with only six patients who had implants that
were not integrated at the time of abutment. Five of
these six patients had been previously irradiated. A
retention rate as low as 46% has been reported after
attempted orbital reconstruction in previously irradi-
ated patients; however, the success rate improved to
88% if preoperative hyperbaric oxygen therapy was
given.
Docking abutments are typically attached 3 to 4
months after the surgical placement of osseointegrated
implants (Fig. 27-6). They are connected to the
osseointegrated implants and act as a dock for the
prosthetic attaching system or fixture. The abutments
permit approximately 1 to 2 mm of space between
them and the skin surface to allow the permanent
fixture to fasten around it. The surgeon is sometimes
limited by the condition of the skin and soft tissue at
the implantation site in attempting to place the
implant docking abutments against thin and immo-
bile tissue. Abutments placed too close to the skin may
result in skin irritation or infection. The skins response
to placement of the docking abutment has been char-
acterized by Holgers et al.32 The skin's response to the
abutment was classified as follows: 0, no irritation; 1,
slight redness; 2, redness and slightly moist tissue; 3,
redness and moist with or without granulation tissue;
and 4, evidence of infection. Surgical intervention was
recommended for patients with a score of 3, who
required revision, and a score of 4, who required
FIGURE 2 7 - 6 . The docking abutments are attached
to the osseointegrated titanium screws. (Courtesy of
the Facial Prosthetics Clinic, Johns Hopkins University,
Baltimore, Md.)
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
removal of the implant. The authors reviewed 136
auricular implants and showed that 91.4% of patients
had a score of 3, whereas only 3.8% had a score of
l.33 A report of 143 percutaneous abutments used for
auricular retention studied periodically during 3.5
years demonstrated symptomatic skin reactions in only
3.5% of patients.34 The skin's response, however, is
related to the patient's individual hygiene in addition
to the intrinsic irritant qualities of the abutments.
Attachment systems using magnets or retention
clips are required to secure the prosthesis to the docking
abutments. Magnets composed of samarium-cobalt
or neodymium-iron-boron alloys measuring 3 mm in
diameter are a preferred prosthesis attachment method
in some areas of the face and provide approximately
500 to 1000 g of retentive force. They are advanta-
geous because they are easy for the patient to use and
permit some give when the prosthesis is minimally
displaced by the action of adjacent muscles. Magnets,
however, are subject to corrosion and a resulting reduc-
tion of the magnetic attractive force over time.12'13 Metal
or plastic retention clips provide more tensile strength
and do not corrode but tend to wear out faster than
magnets. Overall, osseointegration as a method for
prosthesis retention is a major advancement because
it avoids irritating adhesives and is easier to use with
fewer long-term problems than with mechanical
retainers (Color Plate 27-2). Prior irradiation is not a
complete contraindication to the placement of osseoin-
tegrated implants, but the implant retention rate is
less than in nonirradiated areas. Fixtures may remain
intact but should be covered with skin or mucosa.35*38
Implants are typically allowed to remain for 8 to 12
months before loading.37 In contrast, chemotherapy
has not been shown to hinder osseointegration.39'41 In
addition, hyperbaric oxygen therapy has been used
in irradiated patients to improve bone quality before
implant placement.35,42
Children are generally poor candidates for the place-
ment of osseointegrated implants because of their
growing skeleton and poor compliance. Several
upgrade replacements may be required as they grow.
Children are also likely to have poor hygiene and lack
a long-term commitment, which potentially could
exceed 70 years of use. Patients who smoke also have
a higher rate of osseointegration nonunion. 43
Impressions
An exact imprint or impression of the facial defect is
needed to design a facial prosthesis. The accuracy of
this impression will determine the successful appear-
ance and fit of the eventual prosthesis (Fig. 27-7). The
most commonly used material is regular-set alginate,
which is an irreversible hydrocolloid commonly used
to mold dental impressions. The alginate is mixed with
water in a 2:3 ratio and is stirred to a smooth creamy
fl&WW^fltfW image...
FIGURE 2 7 - 7 . Accurate impressions are made to
provide the molds for the prosthesis. (Courtesy of
the Facial Prosthetics Clinic, Johns Hopkins University,
Baltimore, Md.)
consistency to form the impression medium. Several
layers are applied, and each layer is allowed to set for
5 to 10 minutes. Less water is used in subsequent layers
to thicken the alginate, and sheets of cotton are some-
times added to subsequent layers for strength. Thin
layers of plaster gauze are applied as a final layer and
allowed to set for 5 to 10 minutes. Once removed, the
impression can be cast in a variety of materials, such
as dental stone, to produce a facial moulage or cast.44
The moulage provides an exact replica of the facial
contours and the defect and is used to construct
the final prosthesis.
FIGURE 2 7 - 8 . Polyurethane pros-
theses are resistant to abrasions and
solvents and maintain a high tensile
strength. (Courtesy of the Facial Pros-
thetics Clinic, Johns Hopkins Univer-
sity, Baltimore, Md.)
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
27 • PROSTHESES IN PLASTIC SURGERY 775
Prosthetic Materials
The ideal prosthesis should be soft, pliable, and
durable. It should be lightweight, have limited thermal
conductivity, and be precisely matched in color and
texture to the surrounding skin. Modern prostheses
are constructed from methyl methacrylate resins,
polyurethanes, or silicone polymers.
Methyl methacrylate resins have completely replaced
glass eyes because they are more durable and resist
breakage. Methyl methacrylates can be used to con-
struct other external facial prostheses, but their most
common use remains in the field of dentistry. They
are durable and easily molded with good color and
contour match to the surrounding skin. The dis-
advantages of methyl methacrylate resins include a
higher incidence of pressure necrosis and difficulty in
using defect undercuts for adhesion; they have no ability
to give under stress from the adjacent mobile facial
tissue.45
Polyurethanes are constructed from various prepa-
rations of linear polyester-polyether chains reacted with
diisocyanates.46 They are commonly used to construct
facial prostheses but are more difficult to prepare;
precise mixing ratios and avoidance of air exposure
during molding are required to avoid degradation of
the isocyanate. When properly prepared, the
polyurethanes are inert, are resistant to solvents,
maintain high tensile strength, are resistant to abra-
sives, and can be molded in a wide range of flexibili-
ties (Fig. 27-8).
Silicones are constructed from silicone polymers
that are cross-linked by vulcanization with various filler
agents to provide increased strength.47 They can
provide lifelike tissue replacements and are easy to clean.
Prosthetic materials in contact with skin should be
easily wetted. A material that is easily wetted provides
image...

776 l • GENERAL PRINCIPLES

a lubricating layer between the supporting tissues,

reducing friction and the patient's discomfort. Unfor-
tunately, silicone materials lack the capacity for such
wettability."18"50 Consequently, silicone prostheses
are more inclined to cause irritation, abrasion, and
ulceration of the supporting tissues.51

Color
The Munsell color system is the most commonly used
color-matching scheme for the construction of facial
prostheses (Color Plate 27-3). It uses three para-
meters: hue, value, and chroma. Hue denotes the blend
of colors by 10 descriptors: red (K), yellow-red (YR),
yellow (Y), green-yellow (GY), green (G), blue-green
(BG), blue (B), purple-blue (PB), purple (P), and red-
purple (RP). Value characterizes lightness or darkness, FIGURE 2 7 - 9 . A nearly total ear loss in an 80-year-old
ranging from 10 to 1, respectively. A white person's man due to an automobile accident. The elderly are often
inner arm, for example, may be characterized by a hue good candidates for prosthetic ears. {Courtesy of the Facial
Prosthetics Clinic, Johns Hopkins University, Baltimore,
of YR and a value of 7 to 8, whereas African Ameri- Md.)
can skin tones may be assigned values of 2.5 to 5. The
final measure, chroma, designates a scale of dullness
versus brightness. The prosthetist uses a portable
Munsell color meter to match the prosthesis to the morning and removed every night. Contact sports are
patient's skin characteristics. Normal skin, with numer- not advisable because of the potential to dislodge or
ous contour and color irregularities, is not homoge- break the prostheses or bone implants. Even the best
neous in color or texture. The prosthetist must create made prosthesis does not have exactly the same
the best color match considering hue, value, and texture, temperature, or color of the normal skin on
chroma but must also consider the natural skin the other ear, and there may always be a noticeable
texture, which includes wrinkles, folds, pores, and interface between the prosthesis and the underlying
skin appendages.52 skin.
The materials used to construct an ear prosthesis
may be rigid or flexible. Early prostheses made of
Ear methyl methacrylate were rigid and durable. Today,
most ear prostheses are made of flexible silicone whose
Construction of a prosthetic ear is usually reserved
stiffness can be varied by altering the conformation
for older patients with a total or subtotal auricular
defect usually resulting from trauma or tumor abla-
tion (Fig. 27-9). The loss of an ear creates significant
psychological sequelae for the patient but may also be
a functional problem in those who wear eyeglasses (Fig.
27-10). The indications for an auricular prosthesis in
adults include complete or partial loss due to cancer
or trauma, poor-quality local tissue, and salvage after
an unsuccessful autogenous reconstruction; they are
also indicated in patients who are a poor operative
risk (Figs. 27-11 and 27-12).53 Relative indications in
children include patients with congenital loss whose
autogenous reconstruction has failed, severe soft tissue
hypoplasia with or without skeletal hypoplasia, and a
low or unfavorable hairline for autogenous recon-
struction.54 Ear prostheses have several disadvantages.
The underlying skin is susceptible to irritation, and
the patient may be unable to wear the prosthesis for
intermittent periods until the skin heals. Replacement
of the prosthesis may be required every 2 to 5 years FIGURE 2 7 - 1 0 . The ear prosthesis has the appear-
in children, and cost may thus become a significant ance of a normal ear and functions to help stabilize eye-
issue. An ear prosthesis must also be replaced every glasses. (Courtesy of the Facial Prosthetics Clinic, Johns
Hopkins University, Baltimore, Md.)

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
T-ekWaddWimaqe...
FIGURE 2 7 - 1 1 . Partial ear loss in a 72-year-old man
from excision of squamous cell carcinoma. A partial auric-
ular prosthesis can be fitted in patients who are poor
operative candidates. (Courtesy of the Facial Prosthetics
Clinic, Johns Hopkins University, Baltimore, Md.}
elastomer of the mixture.55 Prostheses constructed
with a combination of materials have further improved
the appearance and durability. Polyurethane-lined
silicone prostheses have improved durability and are
held more securely with adhesive bonding.56 Methyl
methacrylate resins have also been incorporated into
FIGURE 2 7 - 1 2 . A complete ear resection in a 70-
year-old man. A flap is used to reconstruct the exposed
cranial base. He has difficulty wearing his eyeglasses
with the current reconstruction. (Courtesy of the Facial
Prosthetics Clinic, Johns Hopkins University, Baltimore, Md.)
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
27 • PROSTHESES IN PLASTIC SuRCf-RY 777
the construction of silicone prostheses to increase
rigidity.57
The site of a prosthetic ear attachment can usually
be determined by matching the position of the ear on
the contralateral normal side. Impressions made of the
contralateral normal ear also provide anatomically
correct detail that can be reproduced in the opposite
prosthetic ear. If the tragus is preserved and in normal
position, it can be used as a reference point; otherwise,
the location of the normal ear in relation to other facial
reference points is used to position the prosthesis.
Several measurements and facial relationships can
be used to position an ear prosthesis correctly. The
posterior protrusion of the ear from the head should
measure 1 to 2 cm from the temporal bone to the helix.
The length of an ear should be approximately twice its
width, which is also equal to the distance from the tail
of the eyebrow to the alar rim of the nose. The length
of the ear is approximately equal to the distance from
the lateral orbital rim to the root of the helix. The
posterior inclination of the ear (i.e., the long axis
angulation) should approximate that of the nose. The
tragus should be positioned slightly posterior to the
temporomandibular joint at the Frankfort line.58
These relationships become even more critical in
patients with bilateral congenital microtia.
Osseointegration is the method of choice for reten-
tion of an auricular prosthesis. It offers superior reten-
tion and is more convenient for the patient.19,22,59,60 Two
or three endosseous implants are typically required to
provide adequate load bearing.61 The holes should be
drilled at least 3 mm deep in adults; but in children,
the bone may be only 1 to 2 mm thick, and careful
drilling is required to avoid dural injury. The mean
thickness of the mastoid cortex is 2.2 mm at 5 years
of age and increases to 3 mm by the age of 12 years.
The thickness of the mastoid is considered sufficient
to hold an implant after the age of 5 years.62 Fixtures
can be 3 or 4 mm, but results are better with the
4-mm-long fixtures.62 After the placement of fixtures,
percutaneous titanium abutments are connected to
the head of the implant fixtures. Various authors have
reported 5-year follow-up success rates greater than
95o/oi9.63-65 W e s t i n 66 r e p 0 r t e d a 3o/0 incidence of sig-
nificant skin reaction in a group of 99 patients with
107 prosthetic ears with a follow-up period ranging
from 1 to 12 years. However, a 40-month follow-up
of 16 prostheses in children revealed a 25% incidence
of skin reactions.17 Granstrom67 observed a low rate of
implant failure and skin reactions in children, virtu-
ally the same as in adults, but children required more
frequent revisions because of new bone formation. The
170 prostheses inserted in children had a 5.8% failure
rate, but revision was required in 22% of these patients
because of appositional temporal bone growth.
Schoen59 placed orbital or auricular endosseous
implants in 26 patients, some of whom were treated
778 I • GENERAL PRINCIPLES

with radiation therapy after surgery. Twelve patients
(31 implants) had implants at the time of tumor resec-
tion, and seven of these patients (20 implants) were
treated with radiation therapy after implant placement.
Fourteen patients (44 implants) received the implants
as a secondary procedure after tumor resection, and
five patients (21 implants) had implants placed after
radiation therapy. Five implants were lost in the
irradiated group, and all implants placed in non-
irradiated tissue were successful. Radiotherapy is not
an absolute contraindication to the use of osseointe-
grated implants, but the complication rate is higher.
Nose
Nasal reconstruction with a prosthesis is indicated
when soft tissue and bone are missing and the defect
is too large for autologous reconstruction or in patients
who are poor surgical candidates. A prosthetic nose
has the potential to restore both aesthetic appearance
and function (Color Plate 27-4). Patients who are can-
didates for a nasal prosthesis should have the condi-
tion of the nasal remnants and the neighboring soft
tissues carefully evaluated. The tissues around the
defect can sometimes be used to secure the prosthe-
sis, and their condition may dictate the method of
retention. It is usually more desirable to reconstruct
the total nose rather than a portion to optimize the
color and contour match. Wide midfacial defects
involving the nose and a portion of the maxilla are
often amenable to reconstruction with a prosthesis.
The prosthesis can be made to reconstruct varying
amounts of supporting tissue and portions of missing
dentition. The patient's age and overall medical con-
dition, the tumor and its prognosis, previous irradi-
ation, recurrence, the patient's preference, and the skill
of the surgeon and prosthetist are all elements that
must be considered in the decision to use a prosthe-
sis or to perform reconstructive surgery (Figs. 27-13
and27-14). 68 ' 69
The surgeon and prosthetist must be aware of
normal facial proportions in designing and con-
structing a facial prosthesis. The nose, for example, is
about twice as long as its height off the face. The dis-
tance between the nasion and anterior nasal spine
determines the length of the nose. The nose is trian-
gular with a base width equal to the intercanthal dis-
tance. The ideal nasal angle for men and women is
approximately 36 degrees. The ideal nasolabial angle
is between 90 and 100 degrees in men and from 95 to
110 degrees in women. Old photographs may help
identity details that are unique to each individual.7"
Flexible polyurethane and silicone elastomers
are the most common materials used to mold nasal
prostheses. Silicone elastomers combined with a
polyurethane liner provide excellent strength and dura-
bility.58,71 Regardless of the material used, the most dif-
ficult part of nasal prosthetic reconstruction is choosing
the method of adherence. Today, osseointegrated
implants are most commonly used to secure a total
nasal prosthesis. Osseointegration provides a more
secure fixation than do adhesives, eyeglasses, or tissue
undercuts around the defect.24 The implants are placed
in the anterior floor of the nose to allow easy access
and hygiene at the nasion. A minimum of three
implants are placed at the nasion, near the anterior
nasal spine, or in the angles at the base of the piriform
aperture. l5 Osseointegration can also be used for large
midfacial defects. The implants may be placed in the
maxillary tuberosity, frontal process of the maxilla,
midzygoma, zygomaticofrontal process, zygomatic
arch, or superior orbital rim.21,72 A period of 4 to 6
months should allow complete osseointegration of the
implants before connection of abutments. 68,70,72
Implants placed in the floor of the nose and in the
premaxillary area have a successful integration in 85%
to 90% of cases.4
Orbit
Elderly patients requiring orbital exenteration for
cancer are excellent candidates for a facial prosthesis.
All patients must be counseled by the surgeon and
prosthetist to establish reasonable expectations.

FIGURE 27-1 3. A 72-year-old man with an ablated squamous cell carcinoma

of his nose and midface. The prosthesis covers the defects and the residual
nose to permit the optimal appearance. Eyeglasses are worn to help camou-
flage the junction between the prosthesis and the skin. (Courtesy of the Facial
Prosthetics Clinic, Johns Hopkins University, Baltimore, Md.)

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
image...

27 • PROSTHESES IN PLASTIC SURGERY 779

FIGURE 27-1 4. A 72-year-old man who has had multiple squamous cell carcinomas resected. He is left with a nearly
total rhinectomy. A nasal prosthesis is designed to blend with the local tissues. (Courtesy of the Facial Prosthetics
Clinic, Johns Hopkins University, Baltimore, Md.)

Surgical preparation of the recipient site is sometimes
necessary to alter the soft tissue contour of the orbital
defect before the prosthesis is fitted and made. Dermal
grafts, local rotation flaps, pedicled regional flaps, and
free flaps have all been employed to "prepare" the site
for a prosthesis (Fig. 27-15).73,74 Prior reconstruction
of the orbit is crucial to accommodate an ocular
prosthesis and to restore equilibrium to the face.75,76
Alternatively, periorbital prostheses have been made to
simulate the eye, eyebrows, cheek, globes, and maxilla.
Prosthetic reconstruction is additionally indicated for
elderly patients at high risk for tumor recurrence and
when autologous reconstruction is not feasible.76
The orbital cavity resembles a four-sided pyramid,
with the optic foramen and orbital rim representing
the apex and base, respectively (Fig. 27-16).77 The
orbital wall contains seven bones, the sphenoid,
frontal, zygomatic, palatine, lacrimal, maxillary, and
ethmoid bones. The normal dimension in an adult
for orbital height is 35 mm, the width is 40 mm, and
the depth is 45 to 50 mm. The inferior border of the
infraorbital rim and the superior border of the audi-
tory canal define the Frankfort horizontal plane of the
face, which is used to position the ocular portion of
an orbital prosthesis.
The soft tissue appendages of each defect are
unique features that must be considered in designing
an orbital prosthesis. These include the eyebrows,
eyelids, and conjunctiva (Fig. 27-17). The eyebrow
should be located at the superior border of the supra -

FICURE 2 7 - 1 5 . A 52-year-old
woman with recurrent ossifying
fibroma and an orbital exenteration
with temporal-parietal flap contour-
ing. The prosthesis is fit and blended
into the defect. (Courtesy of the
Facial Prosthetics Clinic, Johns
Hopkins University, Baltimore, Md.)

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
image...

780 I • GENERAL PRINCIPLES

FIGURE 2 7 - 1 6 . A definitive prosthesis can secondar-

ily fill the void in an orbit. (Courtesy of the Facial Pros-
thetics Clinic, Johns Hopkins University, Baltimore, Md.)

orbital rim with the tail extending laterally to the level

of the uppermost portion of the helical rim. It should
lie at the most anterior position of the orbit. The
eyebrow provides a natural camouflage for the supe-
rior margin of the orbital prosthesis. The lateral and
medial canthi should lie on the same horizontal plane.
The medial canthus should lie on a vertical line through
the alar border of the nose. The palpebral fissure
between the upper and lower eyelids should be an ellip-
tical or "almond-shaped" aperture, which is three times
as wide as it is high. The lids should drape just to the
limbus, overlapping the iris at most by 1 to 2 mm. Folds
should be created within the lids to mimic the supe-
rior and inferior palpebral creases. Two or three rows
of eyelashes should be placed within the lid margins.
Eyeglasses may be used to cover the interface between
the prosthesis and normal skin (Fig. 27-18).24
Osseointegration is performed in two stages. Three
or four bone-anchored fixtures are placed into the supe-
rior or inferior bony orbital rim in the first stage. Skin
penetration and abutment placement are performed
in a second-stage operation 3 to 6 months later.76,78 A
prospective study involving 24 treatment centers
revealed a 100% retention rate in nonirradiated orbits
and a 79% retention rate in irradiated orbits.24 Con-
sequently, some patients must use less desirable
methods of adhesive retention. Nonetheless, some
patients prefer to wear an eye patch because the ocular
FIGURE 27-1 7. The orbital prosthesis can be designed
to reconstruct eyelashes, eyebrows, and eyelids.
(Courtesy of the Facial Prosthetics Clinic, Johns Hopkins
University, Baltimore, Md.)
prosthesis does not move in concert with the normal
eye.79
Ocular
German artisans used glass spheres to produce the first
ocular prostheses. Glass prostheses were less than ideal
because they deteriorated with exposure to lacrimal
fluid, caused eyelid trauma by their roughened contour,
and were brittle and easily broken if dropped or
exposed to extreme heat.
The psychological trauma associated with loss of
an eye is difficult for most patients to overcome. The
functional loss of stereoscopic vision is disconcerting
to all patients, but most, during several months, adjust
to their reduced depth perception. Another problem

FIGURE 2 7 - 1 8 . The series of prosthetic applications. The eyeglasses hide the mild
contour or interface discrepancies between the prosthesis and the skin. (Courtesy of
the Facial Prosthetics Clinic, Johns Hopkins University, Baltimore, Md.)

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
image...
for patients who lose an eye is a significantly limited
field of vision. Patients learn to compensate by actively
turning the head and remaining eye toward the affected
side. Finally, the anophthalmic patient must deal with
the burden of a compromised aesthetic appearance.
Enucleation involves removal of the entire orbital
contents after transection of the extraocular muscles
and optic nerve. The remaining orbital socket under-
goes enlargement secondary to tissue atrophy. The
surgeon and prosthetist must appreciate this fact to
avoid insufficient volume replacement with subsequent
mechanical displacement and asymmetric position-
ing of the ocular prosthesis.76,77 Enophthalmos or a
ptotic appearance of the eye can occur if there is poor
soft tissue or eyelid support. Patients with a congen-
ital anophthalmic socket require expansion of the
socket by serially larger ocular prostheses to stimulate
growth and enlargement.
A new porous coral-derived hydroxyapatite sphere
that becomes incorporated into the orbital cavity has
recently been used as an orbital implant. This pros-
thesis avoids some of the extrusion sequelae seen in
larger nonincorporated implants and can be used in
patients with an eviscerated eye to restore volume loss.
After fibrovascularization of the implant, donor scleral
grafting, muscle insertion, and an ocular prosthetic
peg cap drilled into the implant permit a more natural
mobile replacement eye.80 Dutton 81 reviewed 50
patients with a mean follow-up of 10.4 months and
found the final motility of this type of prosthesis was
superior to that seen with simple spherical methyl
methacrylate implants. There were no cases of migra-
tion or extrusion. Huang et al82 reported their expe-
rience of 73 patients with a mean follow-up period of
13.5 months. There were no complications such as
orbital infection, implant extrusion, or implant migra-
tion, and motility of the socket and fornices was excel-
lent. Most patients were also satisfied cosmetically with
the motility of the prosthesis. Hydroxyapatite implants
provided an excellent cosmetic reconstruction without
the complications of infection and extrusion seen in
implants made of polymethylmethacrylate or silicone
in both series of patients.81,82
Summary of Facial Prostheses
The ideal facial prosthesis should be easy to apply, fit
comfortably, blend imperceptibly with the surround-
ing facial skin, and restore an aesthetic appearance close
to normal.83 Modern face prostheses developed during
the last 5 years look and feel more realistic than earlier
designed models because of the introduction of sili-
cone materials and the use of osseointegration as a
reliable retention method.84,85 Adhesive retention pros-
theses may need to be replaced annually, whereas those
held by osseointegration usually last for 2 to 3 years,
reducing the long-term cost. It has been estimated that
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Dr.Mustafa D.
27 • PROSTHESES IN PLASTIC SURGERY 78
the break-even point for the two methods occurs at
approximately 5 years. The average cost of a cranio-
facial prosthesis held by osseointegrated implants
during 10 to 20 years is estimated at $ 17,500 to $26,200.
This appears to be a more cost-effective method than
the use of an adhesive retention prosthesis, which is
estimated to be $21,000 to $39,200 during the same
period.86
Patients need to be well informed of the surgical
and social commitment necessary to fit and wear a
facial prosthesis. They should also be advised that
several staged surgical procedures may be required,
especially when osseointegration is used as the method
for retention. The life span of a given prosthesis may
be several years, depending on prosthetic handling,
the method of retention, environmental exposures, and
the patient's hygiene. Despite these constraints,
osseointegrated prosthetic implant systems have
proved highly successful. The Food and Drug
Administration approved the osseointegration system
as a viable method for prosthetic reconstruction in
1995 after a 30-month prospective study of 115
patients treated at 24 centers around the country.
There were 452 craniofacial implants in this study
placed in a variety of defects with an extraordinary
overall success of nearly 99% demonstrated.24
UPPER EXTREMITY PROSTHETICS
Technology has revolutionized upper extremity pros-
thesis design and construction during the last 20 years,
yet bioengineers have failed to design a prosthesis that
can completely replace a missing hand. The prosthetic
hand made for Luke Skywalker after he suffered a light
saber amputation at the hands of Darth Vader in the
Star Wars episode "The Empire Strikes Back" today is
still a fantasy. This is unfortunate for the 12,000 patients
who annually sustain a partial or complete upper
extremity amputation, Ninety percent of amputations
are the result of a traumatic injury, which occurs most
often in men between the ages of 20 and 40 years.87
These amputees must deal with disfigurement and the
loss of function.88 Loss of function is most devastat-
ing in those patients who lose both hands, an unfor-
tunate and rare occurrence in less than 1% of all
amputation accidents. In contrast, when one hand is
preserved, patients can perform most activities of daily
living with the unaffected hand. Psychological evalu-
ation and therapy are critical for patients who have
lost a limb. A patient's mental well-being after suffer-
ing an amputation is dictated by his or her values and
social support network.
Objectives
Upper extremity prostheses fall into two broad cate-
gories, active and passive. An active prosthesis can be
782 I • GENERAL PRINCIPLES

used to perform a desired task, such as grip, grasp, or

pinch. Passive prostheses provide an aesthetic repli-
cation of the missing digit or limb but have little or
no function. Most patients prefer a functional (active)
prosthesis to assist in their activities of daily living.
There are some patients, however, who are self-
conscious and prefer a more lifelike prosthesis despite
limited function.89 Passive prosthesis advocates have
argued that the unnatural movements of a functional
prosthesis may draw more attention to the amputa-
tion.90 Patients must therefore weigh the advantages
of a beautifully molded passive prosthesis over a func-
tional prosthesis that may be less aesthetic. The goals
and expectations of the patient should be determined
before any attempt at prosthesis fabrication or limb
FIGURE 2 7 - 2 0 . A well-fit prosthesis custom made for
reconstruction is undertaken.91 appropriate length, appearance, and function. (Courtesy
Many authors advocate prosthetic fitting in the early of Aesthetic Concerns Prosthetics Inc., Middletown, NY.)
postoperative period.92 The vascularity of the stump
and remaining limb is usually good, and wound healing
problems are uncommon. The prosthetist can usually transmetacarpal, hand, or below-elbow amputations.
visit the patient even before discharge from the hos- Active opening hook and myoelectric prostheses can
pital, although definitive fitting is usually delayed until be used bypatients with above-elbow amputations but
the stump swelling has resolved and the amputation are more difficult to fit, require a tighter shoulder
has acquired its final shape. An upper extremity pros- harness for functioning hook prosthesis, and are more
thesis is easier to fit and use if elbow function is present difficult for the patient to learn to use. A passive pros-
and 10 to 14cm of proximal forearm length is pre- thesis may therefore be more desirable for aesthetic
served (Figs. 27-19 and 27-20).93 Bone lengthening or reasons in these patients.
soft tissue augmentation may be required for patients
with a short proximal forearm amputation before pros-
thesis fitting and construction. Prosthetic Types
Passive prostheses are best suited for patients with ACTIVE
digital or partial hand amputations (Fig. 27-21). Active prostheses are designed to perform a given
Active prostheses are recommended for patients with mechanical task. In general, functional capabilities are
limited to simple tasks, such as opening and closing

FIGURE 2 7 - 1 9 . Upper extremity prostheses are func-

tionally more useful if elbow flexion is preserved; at least FIGURE 2 7 - 2 1 . A distal finger prosthesis made of
10 to 14 cm of proximal forearm permits appropriate matching color, tone, and skin definition. The prosthesis
fitting. (Courtesy of Aesthetic Concerns Prosthetics Inc., is maintained in place by suction fitting. (Courtesy of
Middletown, NY.) Aesthetic Concerns Prosthetics Inc., Middletown, NY.)

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
fl&WRS'aeitfW image...

27 • PROSTHESES IN PLASTIC SURGERY 783

FIGURE 2 7 - 2 2 . Afunctional upper extremity prosthesis

with an ability to grasp objects. (Courtesy of Aesthetic
Concerns Prosthetics Inc., Middletown, NY.)

hooks that merely hold various objects (Fig. 27-22).

These prostheses will obviously never provide sensi-
bility and fine tactile feedback. The prostheses can be
modular in that several different terminal devices can
be substituted to undertake specific tasks. The most
commonly used terminal device is a simple split-hook
design, which permits grasp and gross object manip-
ulation (Fig. 27-23). One or more passive units, such
as a friction-stabilized wrist rotation joint, are often
incorporated into the prosthesis to improve leverage.
Active prostheses are either body or battery powered.
Body-powered prostheses using a harness on the oppo-
site shoulder do not require an external power supply
and permit some degree of gross sensory feedback.94
Increased sensory feedback is hypothesized to act by
"extended physiologic proprioception," coined by
Simpson.65 He observed that patients quickly learn to
gauge the power and trajectory of the prosthesis as if
it were a natural extension of the limb, similar to strik-
ing a golf ball with a club. The more proximal joints •*»^,-j«fiMLij A hat-»-.*•*> . -
therefore have a pivotal role in sending peripheral feed-
FIGURE 2 7 - 2 3 . The split-hook design prosthesis
back eventually to the muscles that control the harness permits grasp of larger objects. (Courtesy of Aesthetic
system. Concerns Prosthetics Inc., Middletown, NY.)
Active shoulder-powered prostheses motor the
terminal device through a cable system attached to a
harness running across the opposite shoulder (Fig. 27- and practice to use the shoulder-powered terminal
24). Motion is transferred by shrugging the shoulder device effectively. Lightweight prostheses have been
through the cable attached to the terminal device. The developed that allow independent elbow and termi-
jaws of the terminal hook are held together by a rubber nal device control with a specialized cable system.96
band and pulled open by the cable when the opposite The coordination of movements necessary to open and
shoulder is moved. As the shoulder is relaxed, the close the terminal hook must be learned because these
rubber band closes the jaws, permitting prehensile grip. movements are not intuitive.
Effective transfer of the cable-generated force requires Wrist-powered active prostheses are used in patients
control of every joint crossed by the cable to prevent with distal carpal or proximal transmetacarpal ampu-
buckling. Patients with preserved elbow function tations with preserved wrist function. Typically,
must actively fix the elbow into a static position before patients should be able to close their prosthetic fingers
activating the cables that transfer force to the distal by flexing the wrist.97 Flexing the fingers with the wrist
opening hook. This sequence can create confusion for extended is not desirable because it does not permit
the patient because every motion at the elbow must the patient to pick up objects from a tabletop. The
be preceded by disengaging the distal hook before grip vector is positioned in the direction of the thumb
another can be performed.95 Patients must be trained and index-middle finger to permit the grasping of small

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
784 I • GENERAL PRINCIPLES
FIGURE 2 7 - 2 4 . Prosthesis opening and closing is
provided by shoulder shrugging. (Courtesy of Aesthetic
Concerns Prosthetics Inc., Middletown, NY.)
and large objects. Advances in materials and con-
struction are continually improving the function of
these prostheses. Some experimental hand prostheses
now include movable metacarpophalangeal and prox-
imal and distal interphalangeal joints in all four digits
as well as a multipositional passive thumb. 98
Battery-powered myoelectric prostheses are acti-
vated by myoelectric impulses generated from con-
traction of stump muscles. Myoelectric prostheses use
cutaneous sensors to detect the action potentials of
remnant stump muscles that are processed by a micro-
computer and magnified to activate an electric motor
inside the prosthesis.99,100 The terminal device is there-
fore controlled by signals that are generated from elec-
trodes placed on the surface of extensor and flexor
muscles of the stump.101*103 For example, antagonistic
muscle potentials, such as those detected from the
biceps and triceps, can be used to provide the oppos-
ing actions of opening and closing a terminal device.I04
Prostheses are typically designed to mimic the opening
and closing of a hand as well as to provide some degree
of pronation and supination to enhance maneu-
verability.105"106 More complex devices have been
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Dr.Mustafa D.
developed that offer independent finger movements,
but these more complicated internal mechanisms are
all too susceptible to malfunction.101'107 Independent
finger motion requires separate sensors, a more
complex signaling pathway, and independent motors
for each digit. The complexity of these prototype pros-
theses is now problematic, and they are as yet still exper-
imental and not up ro Luke Skywalker's standard*.
Myoelectric prostheses currently require frequent
electrical and mechanical adjustments. The amputee
often needs to live at or near a metropolitan center
that services these prostheses. Alternatively, frequent
long trips to the service center may be required, which
can adversely affect the patient's use of a myoelectric
prosthesis. Computer hardware and software have
been developed that permit automated tuning of these
prostheses at home.108 Computer-literate patients may
benefit from this technology and subsequently be more
inclined to wear the prosthesis. Silcox109 studied 44
patients with myoelectric devices and found that half
of them did not use their prostheses after 5 years. The
main reason the patients stopped using the prosthe-
sis was the lack of sensory feedback.107 Other reasons
cited included the inability of myoelectric prostheses
to function in moist environments, the need for con-
tinual refitting in children and some adults, and the
temperamental nature of these intricate prostheses.
Finally, incidental factors included old age, low socioe-
conomic status, and psychological illnesses.107,110,111
It is difficult for patients to control their grip
strength when using a myoelectric prosthesis because
sensory and proprioceptive feedback is limited. Pres-
sure sensors on the gripping surfaces of the terminal
device produce an electrical signal that is transmit-
ted to the proximal stump skin surface. Both mechan-
ical and electrical stimulation of the stump skin
surface have been used with limited success.110
Mechanical stimulation is transmitted to the patient
by variable frequency tapping on the skin surface,
whereas electrical stimulation delivers a pulsed
electrical shock. Mechanical stimulation systems are
limited by the fact that no more than five different
stimulus patterns can be perceived by patients.112 Elec-
trical stimulation systems can sometimes interfere with
outgoing electrical signals controlling the terminal
device,112 Finally, feedback mechanisms of myoelec-
tric prostheses are currently limited by the technol-
ogy of pressure sensors. One obstacle to accurate
pressure detection results from coverage of the sensor
by a thick vinyl glove (Figs. 27-25 and 27-26). The
differential stretch of the vinyl covering during flexion
and extension of the terminal device as well as ongoing
change in the elastic properties of the glove con-
tinually alters the pressure readings detected by the
sensors.113 Many centers are attempting to create
biofeedback systems that will allow the patient to gauge
grip strength more accurately.71,112*119 Techniques are
Tt&*>«^6d'T# image...
FIGURE 2 7 - 2 5 . Myoelectric prostheses
use continuous sensors to detect arm muscle
movements resulting in flexion of the thumb
and fingers. (Courtesy of Aesthetic Concerns
Prosthetics Inc., Middletown, NY.)
being developed that will allow direct feedback stim-
ulation of the peripheral nerve stumps instead of the
skin surface. Prostheses designed to provide both pres-
sure and friction sensors are intended to offer a more
sensitive gauge of grip strength and to prevent objects
from slipping through the artificial fingers.120
Efferent Limitations
Other investigators have developed a myoelectric
hand that attempts to mimic digital motion, incor-
porating variable compliance around joints in the hope
of transferring a more gentle force when delicate
objects are grasped.117 In addition, independent
•
\
•'»*w..
FIGURE 2 7 - 2 6 . The myoelectric hand is covered with
a thick vinyl glove. Differential stretch of the vinyl for exten-
sion and flexion alters pressure reading detected by the
sensors. (Courtesy of Aesthetic Concerns Prosthetics Inc.,
Middletown, NY.)
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
27 • PROSTHESES IN PLASTIC SURCERY 785
multifinger control has been demonstrated in an exper-
imental model using pneumatic sensors placed
between the prosthetic socket and superficial extrin-
sic tendons associated with individual finger flexion.121
Prototype robotic hands have been fabricated with five
fingers and individually driven joints.122,123
Battery-powered prostheses have several note-
worthy limitations. They are slow and cannot be used
for quick repetitive motions. Prototype pneumatic
systems have been designed in an effort to deliver
higher frequency action to the terminal device. To date*
experimental prostheses with hydraulic systems are
not practical because of the human hazards involved
in use of highly pressurized fluids. It is also difficult
for the amputee to precisely control the amplitude of
force generated, which potentially could be made to
exceed that of a normal hand. Finally, all prostheses
lack sensibility and the normal sensory feedback loop
that enables us to regulate the force generated by our
hands. Pressure and pain receptors tell us how hard
or softly we are gripping an object. This lack of sensory
feedback forces patients to consciously monitor each
action of their prosthesis, usually visually, to gauge
the amplitude of force produced. A conscious effort
is additionally required to trigger a prosthetic task
because the prosthetic movement desired is not
intrinsic to the muscles initiating the myoelectric
impulse.
Externally powered prostheses with a vinyl hand
are more aesthetic than a split hook but less lifelike
than a passive silicone prosthesis. The mechanical parts
used in the battery-powered prostheses make them
heavy and difficult to fit and wear. Battery-powered
prostheses are more expensive to construct and main-
tain than are shoulder harness or passive prostheses,
creating financial constraints for many patients.1124
PASSIVE
Passive prostheses are designed to mimic the appear-
ance of the amputated part.125 A properly fitted aes-
thetic prosthesis, however, may offer an assist function
for some hand activities. These prostheses can act as
a post to stabilize objects for grasp by the remaining
786 I • GENERAL PRINCIPLES
fingers or the other hand. The advantages of a passive
prosthesis include that they are lightweight, have a life-
like texture and appearance, are easily cleaned, and are
easy to apply (usually with an adhesive). They are most
useful for patients with digital or partial hand ampu-
tations. These prostheses are lifelike reproductions of
the missing part primarily designed to restore the cos-
metic appearance or wholeness of the hand or finger.
They are more commonly worn by women and are
often used for work or social functions when the
patients hands will be most visible (see Fig. 27-21).
Passive prostheses today are usually made of silicone
elastomers that are not durable enough to be used for
manual labor or factory work,126 Specialized passive
prostheses of wood, metal, plastic, or other materials
have been made to assist individual patients in the per-
formance of specific tasks, such as grasping a tool or
handle. These passive prostheses are custom made on
an individual basis and are not made for aesthetic
reasons. The disadvantages include daily application
for some patients, staining, discoloration by environ-
mental factors such as newsprint, and fading and dis-
coloration of the prosthesis with time due to chemical
and sunlight exposure. Passive silicone digital pros-
theses are fitted and fabricated at specialized centers
and require the patient to travel some distances for
service or replacement.127
Digital Prostheses
Approximately 200,000 patients a year require treat-
ment by a physician for finger amputations.128 A prop-
erly fitted digital prosthesis can provide aesthetic
symmetry and in some cases functional oppo-
sition.89,129 Digital prostheses are constructed from a
silicone base with inlaid acrylic nails. The finger stump
should be allowed to heal with resolution of edema
before prosthesis fitting is undertaken.129,130 Neuroma
or an open wound precludes the use of a prosthesis.
The finger remnant stump should measure at least
1.5 cm in length to permit proper prosthesis retention.89
The remnant stump may occasionally require surgi-
cal revision to ensure reliable fixation. A passive pres-
sure prosthesis may help pad a tender digital stump
or provide protective warmth in patients with cold
intolerance.131 A truncated prosthesis is preferred for
distal digital amputations to permit unrestricted
movement of the normal proximal joints.92
The patient's initial enthusiasm for a digital pros-
thesis may fade over time. Many patients will wear a
passive digital prosthesis for a number of months and
then discontinue use. Others will use the prosthesis
for social events only. Satisfaction of patients and use
reported in a number of series range from 63% to
97o/0>i27,i3M36 T h e s e stuc iies were conducted in sepa-
rate centers, however, with different sample sizes
and follow-up periods, and most of them do not
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Dr.Mustafa D.
distinguish use between single- and multiple-digit
amputees.127 Hooper's retrospective study133 of 178
patients fitted with 281 digital prostheses found that
49 patients (28%) never or only occasionally used their
prostheses, whereas 42 patients (24%) used them more
than 4 hours per day. Stump problems were reported
by 110 patients (62%); these interfered with prosthe-
sis use in 37 patients (21%). Manual workers were less
likely to use these prostheses. Factors associated with
a low utilization rate were male gender, stump prob-
lems, and distal amputation level. Ring finger pros-
theses were less likely to be used; small finger prostheses
were more likely to be used. Women more commonly
requested and received a second set of prostheses. A
national safety study127 of 65 patients who had a digital
prosthesis for more than 5 years demonstrated that
63% of patients with single-digit amputations and 81%
of patients with multiple-digit amputations used their
prostheses; 94% of patients believed that prostheses
were of "great value in providing psychological support
for post-traumatic rehabilitation," and 86% stated that
overall, "prostheses made a positive difference to their
rehabilitation"
Lundborg et al137 introduced osseointegration
as a viable method for prosthesis retention instead
of traditional adhesive methods. His patients had
stable retention, minimal skin breakdown, and useful
functional and cosmetic results.
Thumb Prostheses
The natural anatomic position of the thumb is in a
plane offset 90 degrees from the other digits. This posi-
tion permits the specific hand functions of pinch, grasp,
and prehension, which require opposition of one or
more digits to the thumb. Thumb prostheses have been
designed to lengthen the thumb and to provide a stable
post for pinch and grasp functions when finger motion
is preserved. Passive thumb prostheses may be diffi-
cult to hold in place, depending on their design and
the amount of proximal stump length retained.
Approximately 1.5 cm of proximal phalanx stump is
necessary to secure a cosmetic thumb prosthesis. These
prostheses are made of Silastic or silicone to match
the appearance of the opposite thumb and except for
minimal pinch and grip are not meant to be func-
tional. A passive prosthetic thumb is difficult to wear
if the proximal thumb stump is shorter than 1.5 cm.
Osseointegration has permitted successful retention
of cosmetic prostheses at more proximal amputation
levels.138 Thumb prostheses held by osseointegrated
techniques are also more stable and can be used for
limited pinch and grasp function. A functioning
thumb prosthesis can be secured with a glove or wrist
band and used to improve hand function by provid-
ing an opposable post with limited or no motion. These
prostheses were typically made for manual laborers
image...
and fashioned to accommodate a specific job activity.
The need for thumb prostheses is less common today
because superior results can be achieved in most
patients by autogenous reconstruction with second-
or great-toe microvascular transplantation.139
Partial Hand Prostheses
Partial hand prostheses have been fabricated to recon-
struct the missing digits of patients with partial hand
amputations through the palm. The objective of these
prostheses is to replace the lost portion of the palm
and digits for aesthetic reasons.140 The prosthesis is
typically designed as a glove to match the appearance
of the contralateral natural hand. Unaffected digits are
brought through the glove and remain functional. This
has the disadvantage of covering a large area of the
remaining normal palmar and dorsal hand surface,
reducing sensibility and increasing stump perspira-
tion. Newer gloves are being made of biosynthetic
materials to reduce internal friction and heat pro-
duction in the underlying partial hand.14' Some
patients are satisfied with passive partial hand pros-
theses, believing they provide psychological support
and enhanced self-image.68 These prostheses are aes-
thetically pleasing but are today infrequently made.
Patients usually prefer to undergo surgical interven-
tions, such as pollicization or microsurgical free tissue
transfers, to restore missing tissue.142
Complete Hand Prostheses
Complete passive hand prostheses are made for patients
with wrist disarticulations or distal radial amputations.
These hand prostheses provide a lifelike appearance
for social functions. Passive hand prostheses must be
statically positioned by the opposite hand and can be
used to hold light objects such as a glass or a pencil
but are not truly functional. Many patients find these
prostheses of psychological benefit but use them only
for special occasions.127 Today, myoelectric prostheses
can be made that closely resemble the appearance of
the opposite normal hand as well as the surface skin.
Many patients choose active myoelectric prostheses
over the passive prostheses to regain more mobility
and function (see Figs. 27-25 and 27-26).
There is some controversy in fitting prostheses for
children with congenital amputations of the upper
extremity. Some investigators prefer the application
of prostheses, such as a plastic mitten or paddle, as
early as 6 months of age so that the child can develop
skills of crawling, balancing, and grasping with an assist
hand.22 Early fitting helps prevent substitution pat-
terns of pinch and grasp. The sensory stimulation
gained at the stump-prosthesis interface will also
develop visual feedback.143 Children can be fitted with
a shoulder-driven active prosthesis with a hook device
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Dr.Mustafa D.
27 • PROSTHESES IN PLASTIC SURGERY 787
terminal. Children from 3 to 6 years old can then be
fitted with a myoelectric prosthesis.144 Interestingly,
one study of 11 children with supportive parents fitted
with myoelectric prostheses at an average age of 20.6
months related a 73% satisfaction rate.144 Unfortu-
nately, most children with unilateral congenital defects
are noncompliant and find it difficult to wear the pros-
thesis. Most of these children seem to be happy and
can interact with their environment without many
hurdles. A prosthesis at this early age may, in fact,
impede the child's ambitious nature. It is essential
to provide counseling to the parents, who are the
critical factor in determining the child's acceptance
of and compliance with a prosthesis.145 The parents
must provide continuous encouragement and allocate
a substantial number of hours a week helping the child
learn to use the prosthetic device.146
Summary of Upper
Extremity Prostheses
Many surgical options are available to the hand
surgeon to help patients restore upper extremity
function and appearance after amputation. There are
circumstances, however, that either preclude further
surgical intervention or preferentially mandate the use
of a prosthesis. The goals and limitations of autoge-
nous reconstruction or prosthesis use must be thor-
oughly understood by the surgeon, prosthetist, and
patient. Many amputees can now benefit from advances
in technology that have improved the appearance and
function of prostheses. Each prosthesis, however, has
specific characteristics with its own intrinsic limita-
tions. Passive prostheses can be designed with a life-
like and aesthetically pleasing appearance but have little
or no function. Active hook-type prostheses restore
certain "grasp" functions to aid in the patient's activ-
ities of daily living but are less aesthetically pleasing.
Newer myoelectric prostheses are functional and aes-
thetic, but their use is limited by higher maintenance
requirements. The success of any prosthesis, however,
depends on the patient's compliance, emotional adjust-
ment, and personal expectations. The patient's socio-
economic status, employment, and responsibility in
society and at home play important roles in the use of
any prosthetic device. As with anything in life, if a device
is cumbersome, nonfunctional, and time-consuming
to use or to maintain, the patient's long-term use
would decrease and eventually cease. Upper extremity
surgeons must have an understanding of the various
options to better educate and guide amputees in their
decision in choosing the type, function, and suitabil-
ity of a prosthesis.
Above-elbow amputees still do not have a sound
device that will effectively control multiple distal joint
functions, including elbow and wrist motion, while
still allowing manipulation of a terminal device,
788 I • GENERAL PRINCIPLES
Moreover, at present, there are no devices available for
proximal shoulder-level amputees.H7 Multilevel control
is limited by signal-to-noise ratios inherent in attempt-
ing to detect individual myoelectric triggers from
several muscles by distant implanted skin electrodes.148
Attempts to simplify signal recognition have included
use of a single contracting and relaxing muscle to
initiate both closing and opening of a terminal device
based on contraction amplitude instead of trying to
detect separate antagonistic muscle groups.149 The
development of more complex microprocessors and
technology will eventually permit more innovative
pattern recognition and creation of the multifunctional
prosthesis like theone used by Luke Skywalker.115,147,150
One of the concerns of prosthesis users is the imbal-
ance of stresses at the interface of the residual limb
and prosthetic socket. Stress imbalances create
increased morbidity related to skin breakdown with
the requirement of frequent soft tissue revision sur-
geries.73,128 Such revision is necessary to avoid further
breakdown and subsequent infection with ultimate
further proximal amputation. Instruments have been
developed to permit the accurate measurement of the
stresses at the interface of a residual limb and pros-
thetic socket, referred to as stump-socket finite element
models.151 The field of computer-aided design and
computer-aided manufacture may allow not only the
capture of a detailed and accurate image and dynam-
ics of the body part being mimicked but also the capa-
bilities of actually prefabricating the prosthesis.152"154
The lack of neurosensory feedback remains a con-
stant obstacle, constraining wearers to visual input for
directing the action of their prostheses. Motor sound
and transmission of pressure and vibrations may be
helpful.107 Experimental work is under way with sur-
gically implanted telemetry systems, in which electrodes
are implanted directly into muscles and nerves to
provide multilevel and potentially two-way commu-
nication with the body."2 Osseointegration may permit
transmission of pressure and vibrations from the pros-
thesis to the endosteal nerves and sensory organs of
the extremity. This type of sensory perception has been
termed osseoperception.107,138 Identification of differ-
ent textures, such as glass, metal, wood, and paper, may
be possible without vision by the use of condenser
microphones. Sense substitution may prove useful
for generation of artificial sensibility in prostheses in
the future.155 Development of a sensory system pro-
viding feedback in combination with advanced and
improved grip functions will significantly increase the
utility level of hand prostheses.107,156,157
REFERENCES
1. Flaum E: The Encyclopedia of Mythology, Gods, Heroes and
Legends of the Greeks and Romans. Philadelphia, Running
Press Books Publishers, 1993.
Bin kilometrelik bir yolculuk ilk adimla baslar.
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image...

COLOR PLATE 2 7 - 1 . Eyeglasses can be used to cam-

ouflage the prosthesis. This is a 64-year-old woman with
an orbital prosthesis. The prosthesis is held on with adhe-
sives and magnetic techniques. (Courtesy of the Facial
Prosthetics Clinic, Johns Hopkins University, Baltimore,
Md.)

COLOR PLATE 2 7 - 3 . The Munseil color system uses

COLOR PLATE 2 7 - 2 . An ear prosthesis is maintained hue, value, and chroma to accurately match skin tones.
in place with the osseointegrated technique. (Courtesy of (Courtesy of the Facial Prosthetics Clinic, Johns Hopkins
the Facial Prosthetics Clinic, Johns Hopkins University, University, Baltimore, Md.)
Baltimore, Md.)

COLOR PLATE 2 7 - 4 . A 72-year-

old woman with partial resection of
her nose secondary to squamous cell
carcinoma excision. The nasal pros-
thesis usually blends with local tissues.
(Courtesy of the Facial Prosthetics
Clinic, Johns Hopkins University, Bal-
timore, Md.)

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Dr.Mustafa D.
image...
CHAPTER
28
•
Exfoliative Disorders
ROBERT C. CARTOTTO, MD, FRCS(C) •
TOXIC EPIDERMAL NECROLYSIS
Definitions and Classification
Epidemiology
Pathogenesis and Histopathology
Clinical Presentation
Differential Diagnosis
Treatment Principles
Prognosis and Outcome
Plastic surgeons will encounter a variety of skin dis-
orders apart from cancerous conditions and trauma
for which extensive and difficult wound care is neces-
sary. These diseases will often be diagnosed by other
health practitioners, and the plastic surgeon is con-
sulted for the wound care problems that follow. A
knowledge of exfoliative disorders is helpful because
they are often treated along with thermal injuries or
as part of a wound care multidisciplinary approach.
Although this chapter does not cover all dermatologic
exfoliative disorders, there are discussions (with an
emphasis on surgical treatments) of selected condi-
tions that are more likely to be encountered by plastic
surgeons.
TOXIC EPIDERMAL NECROLYSIS
In 1956, Lyell1 reported his observations of four
patients who developed an acute, febrile, and toxic
illness characterized by epidermal necrosis, which pro-
ceeded to eventual detachment and slough of large
sheets of epidermis. Lyell named this syndrome toxic
epidermal necrolysis (TEN). TEN is the most exten-
sive form of a group of exfoliative disorders of the skin
that include erythema multiforme and Stevens-
Johnson syndrome, both of which are characterized
by detachment of the epidermis from the dermis.2"5
Historically, TEN was treated by dermatologists.
However, plastic surgeons, especially those who rou-
tinely deal with patients who have sustained extensive
skin loss from large burn injuries, are now frequently
involved in the care of patients with TEN. As early as
1978, it was recognized that burn units provide exper-
tise in the care of critically ill patients with large areas
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Dr.Mustafa D.
JOEL S. FISH, MD, MSC, FRCS(C)
EPIDERMOLYSIS BULLOSA
Clinical Presentation
Pathophysiology
Investigations
Treatment Principles
of skin loss and are ideally suited to care of patients
with TEN.6"9 The authors' regional adult burn center
began to admit patients with TEN in 1995. To date,
the center has treated 40 patients with TEN, which
represents one of the largest single-institution expe-
riences with this disease entity in North America. The
burn center originally became involved in the care of
these patients because of the expertise of the nurses
in dealing with large open wounds. Since then, a com-
plete burn team approach to patients with TEN has
evolved, which includes standardized wound man-
agement, aggressive critical care support, nutrition,
rehabilitation therapy, family and social support, and
prevention. It is firmly believed that TEN is best
managed in a burn care facility led by surgeons who
routinely deal with patients with large cutaneous burns.
This chapter provides the reader with a complete review
of the current concepts on TEN as well as an indi-
vidualized approach to the care of patients with this
complex and challenging disease.
Definitions and Classification
Since LyeH's original description of the syndrome, sub-
stantial controversy and debate have surrounded the
definition of TEN and the classification of the other
severe related exfoliative diseases of the skin, such as
erythema multiforme and Stevens-Johnson syndrome.
A concise and clinically relevant classification system
is essential because overlapping terminology and poor
nomenclature plague the majority of published reports
on TEN and the related disorders. This has arisen, in
no small part, from the similarities between TEN and
several of the related exfoliative skin disorders.
793
age...

794 I • GENERAL PRINCIPLES

Erythema multiforme is a cutaneous hypersensi-
tivity reaction usually associated with an infection, such
as recurrent herpes simplex or Mycoplasma pneumo-
niae infection.l0,li Erythema multiforme is subclassified
as minor or major. Erythema multiforme minor is
characterized by the appearance of dusky, erythema-
tous "target" or "iris" lesions, sometimes with blisters
or bullae, symmetrically distributed on the extensor
surfaces of the limbs and on the palms and soles.10,11
Erythema multiforme major features a similar picture,
but mucosal surfaces, usually the mouth, are involved
with erosions as well.11
Stevens-Johnson syndrome (SJS) was originally
described in two children who presented with an aggres-
sive disseminated cutaneous eruption, severe stomatitis,
and conjunctivitis.12 As a result of the apparent
similarity with erythema multiforme major, SJS was
thought to be a variant of it. However, SJS is distinct
from erythema multiforme major and should be
classified separately. Erythema multiforme major is
caused by an infection, features characteristic target-
like lesions in a symmetric acrai distribution, and has
low morbidity and no associated mortality. SJS is drug
induced, features more widespread and central areas
of skin involvement with epidermal detachment, and
has high morbidity and occasional mortality.13
TEN, like SJS, features mucosal involvement and
is a severe drug-induced exfoliative disorder of the skin.
Currently, SJS and TEN are considered to be variants
of the same drug-induced process and probably exist
on a spectrum, with TEN being the more severe form
of the same process.4'13*15 The current consensus is that
the diagnosis of SJS is given to patients with mucosal
involvement, widespread purpuric macules, and epi-
dermal detachment involving less than 10% of the total
body surface area. SJS-TEN overlap applies to patients
with mucosal involvement, widespread purpuric
macules, and epidermal detachment involving between
10% and 30% of the total body surface area. The diag-
nosis of TEN is applied to those patients with wide-
spread purpuric macules, mucosal involvement, and
epidermal detachment involving more than 30% of
the total body surface area (Table 28-l)/ , u , , 3 J 6
Epidemiology
Patients with SJS, SJS-TEN, and TEN are relatively rare.
The incidence of SJS ranges from 1.2 to 6 patients per
million per year.4 The incidence of TEN is estimated
to range from 0.4 to 1.9 patients per million per
year.17*2' However, it is recognized that TEN is proba-
bly an underreported disease entity. SJS and TEN have
been observed worldwide in all human populations.13
Whereas SJS is considered to be a drug-induced reac-
tion, a causative drug is found in only about 50% of
those patients with the disease.4 This probably reflects
erroneous diagnosis of SJS as erythema multiforme
major. In TEN, a causative drug is identified in approx-
imately 80% of patients, and less than 5% have no
associated drug use.22,23
The drugs most commonly implicated in SJS and
TEN are the sulfonamides (co-trimoxazole), the
anticonvulsants (phenobarbital, phenytoin, carba-
mazepine), some antibiotics (aminopenicillins,
quinolones, cephalosporins), nonsteroidal anti-
inflammatory drugs, and allopurinol.24 However, many
other drugs have been associated with the onset of SJS
and TEN, including common antipyretics such as acet-
aminophen and acetylsalicylic acid.14 Although no
reliable test exists to prove the association between a

TABLE 28-1 • TOXIC EPIDERMAL NECROLYSIS AND RELATED EXFOLIATIVE DISEASES

OFTHESKIN 4 ' ,,J5

Erythema Multiforme

Minor Major SJS SJS-TEN Overlap TEN

Etiology Infection Infection Drug induced Drug induced Drug induced

Mucosal No Yes (usually Yes (usually >2 sites) Yes (usually >2 sites) Yes (usually £2 sites)
involvement oral)
Skin lesions Iris or target lesions Irregular dusky Irregular dusky Extensive purpuric
with dusky purpuric macules purpuric macules macules
erythematous center Central distribution Central distribution Central and acral
Acral, symmetric Atypical targets Atypical targets distribution
distribution Confluence of lesions Confluence of lesions Rapid confluence to
Lesions may blister Lesions may blister Lesions may blister diffuse erythema
Epidermal None <10%TBSA 10%-30%TBSA >30% TBSA
detachment
Mortality 0% <5% 30%

SJS, Stevens-Johnson syndrome; TBSA, total body surface area; TEN, toxic epidermal necrolysis.

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image...
specific drug and the onset of TEN,14,25 the lympho-
cyte toxicity assay (LTA) shows promise. The LTA is
based on the concept ti lat reactive metabolites of certain
drugs are implicated in TEN.' 6 The LTA exposes the
patient's lymphocytes in vitro to a drug in the pres-
ence of a metabolizing system. Cytotoxic effect is used
as evidence of increased .sensitivity to newly formed
toxic metabolites from the drug, 2 ' ' The LTA has been
used to confirm sensitivity to anticonvulsants in a
patient with TEN treated at the authors* facility who
had been receiving both anticonvulsants and
cephalosporins. 30 The LTA has the potential to test not
only the patient but also first-degree relatives of the
patient for the likelihood of a similar adverse drug reac-
tion. Hence, the LTA offers enormous possibilities in
prevention of the disease in patients and their fami-
lies. However, at present, implication of a drug in the
pathogenesis of SJS or TEN relies on obtaining a careful
history of the patient's drug use with the recognition
that most instances of TEN arise within 1 to 3 weeks
of starting the causative drug.13,31'32 Nonetheless, TEN
may develop with use of a drug outside of this range.
For example, SJS and TEN have been significandy asso-
ciated with up to 8 weeks of use of phenytoin, phe-
nobarbital, and carbamazepine. 33 Some medical
conditions may be associated with an increased risk
of TEN. These include systemic lupus erythematosus, 19
recent bone marrow transplantation, 34,35 and the
acquired immunodeficiency syndrome.36"3 TEN is
more common in the elderly, but this may only reflect
greater use of medications in this group. 3,10
Pathogenesis and Histopathology
Whereas the exact pathogenesis of SJS and TEN
remains unknown, evidence has accumulated to
suggest that the patients who develop SJS or TEN have
aberrant metabolism of the culprit drug and altered
detoxification of reactive drug metabolites. This
has been most extensively studied in patients who
developed TEN from sulfonamides or anticonvul-
sants.26,40"44 It is believed that reactive drug metabo-
lites then induce a cell-mediated cytotoxic immune
response against the epidermis.45"48 CD8 + T lympho-
cytes and macrophages appear within the epidermis45'48
and are believed to mediate this autoimmune response.
Cytokines such as tumor necrosis factor (which has
been found in TEN blister fluid) probably contribute
to epidermal cell injury as well.4,13 Apoptosis, which is
essentially an activation of a genetic program that leads
to cell death, appears to be the final common pathway
of keratinocyte death in TEN and SJS-TEN overlap.49
The keratinocyte apoptosis in TEN appears to be acti-
vated by an interaction between the death receptor Fas
(CD95), normally found on keratinocytes, and active Fas
ligand (FasL or CD95L), abnormally produced by ker-
atinocytes in patients with TEN.50 This is a particularly
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28 • EXFOLIATIVE DISORDERS 79b
exciting finding because the Fas-Fasl. interaction can
be blocked by antibodies found in intravenous immune
globulin,50 leading to a potential therapeutic inter-
vention for TEN.50
In early SJS and TEN, patchy necrosis of ker-
atinocytes is seen at the dermal-epidermal junction.
Later, the necrosis extends throughout the epidermis,
and detachment of the epidermis from the dermis
is noted. The underlying dermis is essentially normal
with only sparse dermal infiltrate of helper T
lymphocytes.10,13
Clinical Presentation
The cutaneous manifestations of TEN are typically pre-
ceded by a 2- to 3-day prodrome of what appears to
be influenza or an upper respiratory tract infection.
Patients initially have fever and malaise, and they expe-
rience pharyngitis or conjunctivitis. The skin may
become pruritic. After this prodrome, dusky erythe-
matous macules appear on the skin, usually on the
trunk and face initially and then spreading to the
extremities. These macules maybe target-like but more
often are irregular and ill-defined. Blisters or bullae
may appear within these macules. Within 3 or 4 days
(but occasionally within hours) of the onset of these
skin lesions, confluence of the macules into diffuse
erythema develops, large bullae appear, and extensive
sheets of epidermis begin to detach (Fig. 28-1), leaving
raw areas of glistening bright red dermis exposed (Fig.
28-2). The Nikolsky sign, although nonspecific, is
present in the spectrum of SJS and TEN. This sign
refers to the immediate detachment of the epidermis
with lateral digital pressure on the skin in the areas
where confluent erythema is present. Mucosal involve-
ment is usually advanced by this stage and involves
blistering, slough, and erosion of mucosal surfaces.
The lips and oral pharynx are most commonly
involved, followed by the conjunctiva, genital mucosa,
and anorectal mucosa. Mucosal sloughing may also
involve the esophagus, the remainder of the gastroin-
testinal tract, and the tracheobronchial surfaces.51,52
Involvement of the lips and oropharynx can be
particularly aggressive with severe pain, dysphagia,
odynophagia, and bleeding. The lips typically become
crusted. Similarly, ocular involvement is also usually
severe (Fig. 28-3). Pseudomembranous conjunctival
erosions may result in the formation of synechiae
between the lids or between the conjunctiva and the
eyelids.8,32
Laboratory abnormalities on presentation may
include anemia, neutropenia, thrombocytopenia, and
abnormal indices of renal and hepatic functions.32 As
a consequence of extensive areas of skin loss, the patient
may develop problems related to fluid loss, hypo-
thermia, and invasive infection. Prerenal azotemia,
urosepsis, bronchopneumonia, and sepsis commonly
796 I • GENERAL PRINCIPLES
FIGURE 2 8 - 1 . Toxic epidermal necrolysis. Coalescence
of macules with early blister formation (arm), with further
progression to sheet-like epidermal detachment
(chest).
occur.' • ' T h e most common infective organisms
appear to be Staphylococcus aureus, Pseudomonas
species, and Acinetobacter species.I3,25,57 Mortality is
most commonly the result of sepsis and multiple organ
failure.9'53'55-59
FIGURE 2 8 - 2 . Complete epidermal detachment and
slough.
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FIGURE 2 8 - 3 . Severe oral mucocutaneous involvement
and conjunctivitis.
Assuming the patient survives and the dermis is
not secondarily injured by desiccation, infection, or
mechanical trauma (e.g., pressure), re-epithelialization
proceeds within a few days and is complete within 3
weeks.8,13 Mucosal surfaces may remain eroded and
crusted for several more weeks.
Survivors of TEN may experience a number of
significant complications and permanent sequelae. As
long as the epidermis regenerates within 2 to 3 weeks,
the risk of cutaneous scarring is minimal.60 However,
in areas where delayed healing occurs (e.g., due to pres-
sure, repetitive shear, or infection), hypertrophic scars
may arise. Hyperpigmentation or mixed irregular pig-
mentation is common in healed areas. Nail deformi-
ties, phimosis, and vaginal synechia have also been
reported.3,13,61 Ocular sequelae may be severe and can
include entropion, ectropion, inverted eyelashes,
corneal erosions or scarring, photophobia, visual
impairment, and even blindness.13,62 Some patients
experience chronic tearing (due to tear duct obstruc-
tion from scar); others develop a chronic dry eye
"Sjogren-like" syndrome24,62 with punctate keratitis.
Long-term pulmonary dysfunction, even in patients
who did not receive mechanical ventilation, has been
reported.63
Differential Diagnosis
Although the diagnosis of SJS-TEN is usually clear, a
biopsy should be performed to confirm the diagno-
sis.10,13,64 Important exfoliative disease entities to be
distinguished from TEN include staphylococcal scalded
skin syndrome, pemphigus, pemphigoid, scarlet fever,
acute exanthematous pustulosis, toxic shock syn-
drome, and unrecognized scald injuries in comatose
patients.4,10,13 Staphylococcal scalded skin syndrome
is probably the most common condition to mas-
querade as TEN. It is of interest that LyelPs 1956
image...
description of TEN probably included a patient with
staphylococcal scalded skin syndrome.1,13,64 Staphylo-
coccal scalded skin syndrome usually occurs in chil-
dren and never has target lesions, and oropharyngeal
involvement is uncommon. A biopsy easily differen-
tiates the intraepidermal split within the granular layer
in staphylococcal scalded skin syndrome from the
dermal-epidermal split in TEN.64
Treatment Principles
GENERAL
Burn units are ideally suited to the care of patients
with large areas of skin loss. Thus, whereas patients
with erythema multiforme or SJS may not qualify, those
with more severe SJS-TEN overlap or TEN should be
referred to a burn center.6*9,53,57,58 Familiarity with the
care of large open wounds, nursing expertise, and
aggressive critical care are important advantages that
a burn treatment facility can offer to a patient with
TEN. Early referral to a burn center (i.e., within 3 to
7 days of onset of skin slough) has been found to reduce
mortality and hospital length of stay in patients with
TEN.9,55'58,65
ABCs
In a prospective study of pulmonary complications in
SJS-TEN overlap and TEN patients, significant involve-
ment of the respiratory system at presentation was
noted in 24% of patients.66 Patients may be at risk for
acute upper airway obstruction from excessive secre-
tions, bleeding, or edema.66,67 Alternatively, the patient
may present with severe dyspnea or hypoxemia from
bronchopulmonary desquamation, established bron-
chopneumonia, or evolving acute respiratory distress
syndrome.2,66 Therefore, careful consideration should
be given to the need for intubation and mechanical
ventilatory support. This must be counterbalanced with
the recognition of the potential risk for ventilator-
associated pneumonia in this group of patients.
Intubation of these patients maybe extremely difficult
because of mucosal sloughing, swelling, and bleeding
in the upper airway. Intubation should be done by a
physician experienced in dealing with the difficult
airway. The airway is best secured with ties around
the neck or by wiring the endotracheal tube to the
dentition. Adhesive tape should not be used because
it will not securely stick to the skin and may peel off
facial and neck epidermis. If the endotracheal tube is
wired, wire cutters must be immediately available at
the bedside. It is recommended that TEN patients who
are intubated undergo immediate fiberoptic bron-
choscopy. This is done to assess the state of the tra-
cheobronchial mucosa and to obtain bronchoalveolar
lavage specimens for immediate Gram stain and then
culture and sensitivity testing. Bronchial mucosal
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28 • EXFOLIATIVE DISORDERS 797
detachment identified at early fiberoptic bronchoscopy
appears to indicate a poor prognosis.66
Although patients with TEN do not experience the
massive fluid shifts that would occur in a patient with
comparable second-degree burns, early attention must
also be given to fluid and hemodynamic support.
Peripheral intravenous access is preferred to avoid the
infective risks associated with central access. However,
the difficulty in finding and then securing a periph-
eral intravenous site in a patient with widespread exfo-
liation often necessitates a central line. Crystalloid fluid
replacement maybe necessary to reverse dehydration
from inadequate oral intake due to severe stomatitis
or from insensible fluid losses from open wounds.
Some patients may present with established sepsis and
may require more aggressive fluid and vasopressor
support56 and invasive monitoring.
WOUND CARE
Dermal protection is the primary goal in the care
of the wounds that result from exfoliation of the
epidermis and is exactly analogous to the care of
a superficial partial-thickness burn. Unimpeded re-
epithelialization will occur as long as this goal is
achieved. Desiccation, shear, pressure, and infection
must be avoided. An early surgical approach is advo-
cated in which the sloughing sheets of epidermis are
removed, the raw dermal wounds are cleaned and irri-
gated, and the wound is covered with a temporary
biologic or biosynthetic dressing.8,9,53,55"58 Areas not
involved with slough or imminent slough are left intact
until such time as confluent epidermal detachment
develops. During wound irrigation and debridement,
caustic detergents should be avoided. Tap water from
a hydrotherapy shower cart combined with chlorhex-
idine soap or, occasionally, bacitracin solution may be
used. The choice of temporary skin substitute varies
among institutions. In a multicenter survey of burn
units that treat TEN patients,55 Biobrane* was the most
commonly used skin substitute, followed by porcine •
xenograft and cadaveric allograft.
Application of a skin substitute to the raw dermis
provides protection, minimizes fluid electrolyte and
heat loss from the wound, reduces exogenous bacte-
rial invasion of the wound, reduces pain, and facili-
tates movement of the underlying parts. Regardless of
the choice of substitutes, the key principle is meticu-
lous removal of the epidermis, irrigation and clean-
ing of the wound, and fixation of the substitute with
sutures or staples. The substitute of choice is Bio-
brane.68,69 Biobrane is preferable because it is inert,
relatively inexpensive, available off the shelf, and
transparent, which allows inspection of the wound
through the material (Fig. 28-4). Involved skin areas
*Dow B. Hickam, Inc., Sugarland, Texas.
798 I • GENERAL PRINCIPLES
FIGURE 28-4. Application of artificial skin substitute
to raw dermal surface.
that have not yet begun to slough are treated with a
nonadherent tulle gauze layer, covered with gauzes
soaked in a topical antimicrobial solution, changed
twice a day. Effective antimicrobial solutions include
silver nitrate,2,3,70 chlorhexidine gluconate solution,3
and polymyxin-bacitracin.71 Topical 5% mafenide
acetate (Sulfamylon) and topical silver sulfadiazine
cream (SSD) have been used,55 but the unknown risk
of sulfonamide cross-reactivity in a TEN patient
makes the use of silver sulfadiazine cream a less suit-
able choice. A 5% mafenide acetate solution is pre-
ferred because it is clear and colorless and because of
its broad-spectrum coverage abilities.
A second important goal of wound care in these
patients is the separation of opposed mucosal surfaces.
Erosion and subsequent fibrous synechia formation
can lead to adhesions and strictures between surfaces
that should normally be mobile relative to each other.
Examples of this include the vaginal labia, the exter-
nal urethral meatus, and the conjunctivae. Daily per-
ineal care with lubrication and frequent change of
nonadherent materials (e.g., tulle gauze, Telfa) between
the vaginal labia should be considered. A Foley catheter
usually maintains patency of the urethral tract. Con-
junctival care is discussed in the later section on ocular
care.
Other important principles of wound care include
daily inspection and documentation of the skin
involvement with use of a burn diagram, frequent
turning and position changes, and use of specialty
pressure-reduction airbeds.
DRUG WITHDRAWAL AND THE ISSUE OF
CORTICOSTEROIDS
When the drug causing SJS or TEN is known, it should
be immediately withdrawn. Evidence from a retro-
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spective study involving ] 13 patients with SJS or TEN
suggests that prognosis is improved by earlier with-
drawal of the causative drug.72
The issue of corticosteroid therapy remains highly
controversial. Use of corticosteroids has been recom-
mended early in the course of the disease73,74 in an
effort to reverse inflammation and progression to skin
sloughing. However, the effectiveness of this strategy
has never been demonstrated in a clinical trial. TEN
has developed in patients already receiving cortico-
steroids for other diseases,75 suggesting that cortico-
steroids do not prevent or limit progression of TEN.
A multicenter survey of TEN treated in U.S. burn
centers found that treatment with steroids before
admission did not improve survival.55 Retrospective
data involving patients with SJS and TEN treated in
burn centers revealed that survival rates were
significantly lower in patients who received high-dose
corticosteroids.9,70 Although all of the evidence is
retrospective, steroids do not appear to improve
prognosis in SJS and TEN and may actually worsen
morbidity and mortality. Hence, their use is not rec-
ommended, especially in patients who have significant
skin slough (SJS-TEN overlap and TEN). A careful
drug use history should be obtained and the suspected
inciting drugs should be immediately withdrawn. This
may require substitution with an alternative drug, for
example, when an anticonvulsant is implicated. If
corticosteroids were started before admission, these
should be stopped or rapidly tapered during 48 to 72
hours.
GENERAL CARE ISSUES
Attention should be given to the fluid and electrolyte
balance because there maybe ongoing fluid losses from
the wounds or evaporative losses when heated spe-
cialty airbeds are used. Aggressive pulmonary toilet,
chest physiotherapy, and occasionally therapeutic
fiberoptic bronchoscopy are essential for the removal
of secretions and plugs of sloughed tracheobronchial
mucosa. Oral care and hygiene are difficult and neces-
sitate meticulous nursing care. Topical viscous lido-
caine may alleviate some of the pain associated with
severe stomatitis. Whereas skin substitutes may dimin-
ish some of the pain from the wounds, aggressive pain
control with parenteral opioid analgesics is usually
required. As with patients with major burn injuries,
the ambient temperature should be raised to 30°C to
32°C to reduce heat loss and hypermetabolism. Pro-
phylaxis against deep venous thrombosis and gastric
stress ulcers should be instituted.
Enteral nutrition is a mainstay of treatment and
should be initiated as early as possible with a small
orogastric or nasogastric feeding tube. Radiologic
advancement of the feeding tube into the small bowel
ltJWttf'SelcrKf image...
is ideal and may promote better tolerance of the
feeding. Use of endoscopy to advance the feeding tube
may not be advisable owing to the risks of perforat-
ing involved mucosal surfaces of the esophagus or gas-
trointestinal tract. Calorie and protein requirements
may be initially calculated as for a burn of similar
extent, but the estimated requirements should be
adjusted on the basis of measured resting energy
expenditure derived from a metabolic cart. Parenteral
nutrition has been associated with increased mortal-
ity in TEN55 and should be avoided whenever possi-
ble. A rehabilitation therapist should be involved early
in the patient's care to reduce the risks of stiffness,
weakness, and impaired mobility that frequently
develop during this illness.76
Patients should be carefully monitored for evidence
of infection. This usually includes regular documen-
tation of temperature and leukocyte count and fre-
quent microbiologic screening of the skin, urine,
sputum, central lines, and blood for bacteria and
fungus. Use of systemic prophylactic antibiotics is con-
traindicated, and antibiotics should be used only for
documented infections and sepsis. Central line sites
should be inspected daily, and central lines should be
rotated to fresh sites every 3 to 5 days. A switch to
peripheral intravenous access should be considered as
soon as it is feasible.
OCULAR CARE
An ophthalmologist should be consulted early and
should observe the patient daily.8 Antibiotic eye drops
and lubricants are usually instilled every 2 hours, and
synechiae must be carefully broken down with a glass
rod on a daily basis.77
NOVEL PHARMACOLOGIC THERAPIES
At present, there are no definitive pharmacologic inter-
ventions that halt or reverse SJS or TEN. However, a
number of novel approaches have been described. The
use of any of these agents must be carefully consid-
ered and approached with caution; none has been
evaluated in prospective randomized studies.
In small uncontrolled series, plasmapheresis78,79 and
cyclophosphamide 46 have been reported to have
beneficial results in halting disease progression.
Cyclosporine has anti-inflammatory and anti-
apoptotic properties and theoretically might be of use
in SJS and TEN.80 A number of reports have described
favorable results in TEN patients treated with
cyclosporine.81"87 In an unblinded series of 11 TEN
patients treated with cessation of steroids and
cyclosporine compared with historical controls
who had been treated with cyclophosphamide and
varying doses of corticosteroids, therapy with
cyclosporine was associated with faster arrest of disease
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28 • EXFOLIATIVE DISORDERS 799
and re-epithelialization and improved survival. 88
However, in the absence of a randomized prospective
trial comparing cyclosporine with placebo that is not
confounded by the use of corticosteroids, use of
cyclosporine cannot be recommended, especially in
view of its immunosuppressive effects in TEN patients,
in whom there is a moderate to high risk of death from
septic complications.
An interesting potential therapy is intravenous
immune globulin (IVIG). Since the report of Viard et
al,50 which described rapid reversal of TEN in 10
patients by blocking Fas-FasL-mediated apoptosis with
IVIG, a number of reports and a small series have
emerged seeming to confirm that IVIG successfully
slows or halts TEN progression.89"92 The authors'
initial experience with IVIG in patients with TEN was
similarly favorable.30 However, in a retrospective study
involving 16 TEN patients treated with IVIG and 16
TEN patients who did not receive IVIG, it was found
that use of IVIG did not result in any reduction in
length of stay, duration of mechanical ventilation,
severity of multiple organ failure, or mortality rate,
although there was a statistically insignificant trend
toward less severe wound progression in the IVIG-
treated patients. 93 Similarly, a study from the Loyola
University Burn Center that compared 23 TEN patients
treated with IVIG with 20 historical control patients
found no improvement in hospital length of stay or
survival with the use of IVIG.94 Thus, although IVIG
appears to be a promising therapy, its value must
be assessed in a randomized double-blinded pro-
spective trial against placebo. Current practice includes
initiation of IVIG therapy immediately on admission
in a dosage of approximately 0.7 g/kg per day for 4
days.
Prognosis and Outcome
The mortality rate for SJS is less than 5%.4,23,25 The
reported mortality rate for TEN is much more vari-
able because this depends on the population of
patients studied. For example, TEN patients treated
at burn centers may represent the more severe end
of the disease spectrum. The mortality rate from
TEN reported in the larger series of patients (i.e., more
than 30 patients) ranges from 4% to 83% 23,25,56 - 58 ;
however, the majority of these studies reported a mor-
tality rate between 30% and 44%.23,25,56,57 Factors that
appear to worsen the prognosis are advanced age,
extent of epidermal detachment, and serum urea level.25
The multicenter review of TEN treated at U.S. burn
centers identified that increased mortality was also
associated with an elevated score of the Acute Physi-
ology and Chronic Health Evaluation (APACHE II)
and parenteral nutrition before transfer to a burn
center.
800 I • GENERAL PRINCIPLES

EPIDERMOLYSIS BULLOSA

Epidermolysis bullosa is a group of inherited bullous

disorders characterized by massive blistering of the
skin developing in response to mechanical trauma.9S
Historically, epidermolysis bullosa subtypes have been
classified according to morphologic features of the skin
and the zone of the basement membrane that is
involved. Three primary forms are seen; epidermoly-
sis bullosa simplex (intraepidermal skin separation),
recessive dystrophic epidermolysis bullosa (skin sep-
aration in lamina lucida or central basement mem-
brane zone), and recessive junctional epidermolysis
bullosa (sub-lamina densa basement membrane
zone separation). A new category termed hemidesmo-
somal epidermolysis bullosa, which produces blis-
tering at the hemidesmosomal level in the most
superior aspect of the basement membrane zone, is FIGURE 2 8 - 5 . Typical trauma blister presenting in a
also documented.96101 newborn. Biopsy is essential for diagnosis.
Epidermolysis bullosa simplex is usually associ-
ated with little or no extracutaneous involvement,
whereas the more severe hemidesmosomal, junc-
tional, and dystrophic forms of epidermolysis bullosa undetected until adulthood or occasionally remain
may produce significant multiorgan system involve- undiagnosed.
ment. This rare genetic disorder affects all ethnic and
racial groups. Estimates indicate that as many as Clinical Presentation
100,000 Americans suffer from some form of epi-
dermolysis bullosa. According to a National Epi- The hallmark of these conditions is the formation of
dermolysis Bullosa Registry report, 50 instances of large, fluid-filled blisters that develop in response to
epidermolysis bullosa occur per 1 million live births. minor trauma. Some infants may have large blisters at
Of these, approximately 92% are epidermolysis bullosa birth (Fig. 28-5). Others start shortly after birth. Minor
simplex, 5% are dystrophic epidermolysis bullosa, degrees of chafing of the skin, rubbing, or even
1% arc junctional epidermolysis bullosa, and 2% are increased room temperature may cause blisters to form.
unclassified.96" The blister formation tends to be in anatomic areas of
high wear and tear over the joints and on weight-
Infancy is an especially difficult time for patients bearing surfaces.
with epidermolysis bullosa. Generalized blistering
In the severe forms, the blistering process is fol-
caused by any subtype may be complicated by infec-
lowed by repeated cyclic scarring and healing result-
tion, sepsis, and death. Severe forms of epidermolysis
ing in severe contractures and deformity (Fig. 28-6).
bullosa increase the mortality risk during infancy.
It is in this process that plastic surgeons often become
Patients with junctional epidermolysis bullosa have the
involved to help maintain functional hands and
highest risk during infancy, with an estimated mor-
feet, particularly the fingers and toes. The mouth
tality rate of 87% during the first year of life, and have
and esophagus scarring that results from minor
been cared for in burn units because of the large body
trauma of daily use also leads to feeding and
surface area involved.102,103
swallowing difficulties resulting from the contracture
In patients with epidermolysis bullosa who survive and constriction rings. Severe malnutrition often
childhood, the most common cause of death is results from an inability to handle solid foods
metastatic squamous cell carcinoma. This skin cancer (Fig. 28-7).
occurs specifically in patients with recessively inher-
Healing is of course delayed, and open areas that
ited epidermolysis bullosa (recessive dystrophic epi-
are of long standing can become colonized and sec-
dermolysis bullosa), who most commonly are aged 15
ondarily infected.'02-'06
to 35 years. In contrast, dominantly inherited epider-
molysis bullosa simplex and dystrophic epidermoly-
sis bullosa and milder forms of junctional epidermolysis EPIDERMOLYSIS BULLOSA SUBTYPES
bullosa may not affect a patient's life expectancy AND CLINICAL CHARACTERISTICS
adversely. Onset of epidermolysis bullosa is at birth or Epidermolysis bullosa simplex is characterized by
shortly after. The exception occurs in mild instances intraepidermal blistering with relatively mild internal
of epidermolysis bullosa simplex, which may remain involvement. Lesions typically heal without scarring.

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 image...
FIGURE 2 8 - 6 . Patient with dystrophic epi-
dermolysis bullosa with characteristic syndactyly
and contractures.
B affected by erosions, resulting in strictures. Some
FIGURE 2 8 - 7 . A, Infant with palatal erosion from bottle-
feeding, an indication of mucosal involvement in the gas-
trointestinal tract. B, Oral involvement of lips and tongue
further aggravates the nutritional deficiencies that accom-
pany epidermolysis bullosa.
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28 • EXFOLIATIVE DISORDERS 801
Most commonly, these diseases are dominantly
inherited.
Mild epidermolysis bullosa simplex, or the Weber-
Cockayne subtype, is the most common form. Blisters
are usually precipitated by a known traumatic event.
They can be mild to severe and most frequently occur
on the palms and soles (Fig. 28-8). Hyperhidrosis can
accompany this disorder.
Severe epidermolysis bullosa simplex is usually
characterized by a generalized onset of blisters at or
shortly after birth. Hands, feet, and extremities are the
most common sites of involvement. Hyperkeratosis
and erosions of the hands and feet are common
(Fig. 28-9).
Junctional epidermolysis bullosa may be lethal
or nonlethal. Lethal junctional epidermolysis bullosa
is characterized by generalized blistering at birth
and arises from an absence or a severe defect in ex-
pression of the anchoring filament glycoprotein
laminin 5.106-108 Patients with lethal forms of junc-
tional epidermolysis bullosa show characteristic
involvement around the mouth, eyes, and nares,
often accompanied by significant hypertrophic
granulation tissue. Multisystemic involvement of
the corneal, conjunctival, tracheobronchial, oral,
pharyngeal, esophageal, rectal, and genitourinary
mucosa is present. Patients usually do not survive past
infancy.
Patients with nonlethal junctional epidermolysis
bullosa manifesting generalized blistering who survive
infancy and clinically improve with age have junctional
epidermolysis bullosa mitis.109 Scalp, nail, and tooth
abnormalities may increasingly become apparent as
the patients age. Erosions and hypertrophic granula-
tion tissue can be present. Mucous membranes are often
patients with junctional epidermolysis bullosa mitis
can present with blistering localized to the intertrigi-
nous regions.
802 I • GENERAL PRINCIPLES
^pr
Dystrophic epidermolysis bullosa is a group of
diseases caused by defects of anchoring fibrils.109,110
Blisters heal followed by dystrophic scarring.
Formation of milia (1- to 4-mm white papules)
results as a consequence of damage to hair follicles.
Dominantly inherited dystrophic epidermolysis
bullosa is characterized by the onset of disease usually
at birth or during infancy, with generalized blistering
as a common presentation. With increasing age, an
evolution to localized blistering is present as well as
changes in the nails.
Recessively inherited dystrophic epidermolysis
bullosa ranges from mild to severe in presenta-
tion.102,103,110"112 A mild form often involves acral areas
and nails (Fig. 28-10) but shows little mucosal involve-
ment. The severe form usually shows generalized
blistering at birth and subsequent extensive dys-
^Bi^^ *t
W I
^^r^ "•
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FIGURE 28-8. Mild involvement of epider-
molysis bullosa simplex, with blistering confined
to the feet only.
trophic scarring that is most prominent on the acral
surfaces (see Fig. 28-6). This is the form of the disease
that may present to the plastic surgeon for pseu-
dosyndactyly (mitten hand deformity) of the hands
and feet (see Fig. 28- 12A).102,103,110 Flexion contractures
of the extremities are increasingly common with
age. Nails and teeth are also affected. Involvement
of internal mucosa can result in esophageal strictures
and webs, urethral and anal stenosis, phimosis, and
corneal scarring.111,113,114 Malabsorption commonly
results in a mixed anemia from a lack of iron absorp-
tion, and overall malnutrition may cause failure to
thrive.104,110 Patients with severe recessive dystrophic
epidermolysis bullosa who survive to childhood are
at significant risk for development of aggressive
squamous cell carcinoma in areas of chronic erosions
(Fig. 28-11).
i
FIGURE 2 8 - 9 . Hyperkeratosis is commonly
seen in the milder forms of epidermolysis bullosa
simplex.
image...

28 • EXFOLIATIVE DISORDERS 803

MF*

w
•
r
* 1

T- *

FIGURE 2 8 - 1 0 . A and B, Patient with dys-

trophic epidermolysis bullosa diagnosed in ^^d
adulthood after an orthopedic trauma admis-
sion to the hospital with acral involvement and
limited blistering to the feet and hands, clini-
cally present only during times of stress. B

FIGURE 28-1 1. Squamous cell carcinoma in severely

involved terminal digits had been ignored until excessive
keratinization was clinically evident. Open healing blistered
areas more commonly form granulation tissue and not
keratin because the keratinocytes are absent.

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804 I • GENERAL PRINCIPLES
TABLE 28-2 • EPIDERMOLYSIS BULLOSA SUBTYPES1 i a , n W 1 9
Morphologic Type Gross Pathology
Epidermolysis bullosa Skin separation is at the mid
simplex basal cell
Junctional epidermolysis Blistering in the lamina lucida
bullosa and variable hemidesmosomal
abnormalities
Dystrophic epidermolysis Skin cleavage at the subMamina
bullosa lucida
Pathophysiology
The pathologic process is localized to the basement
membrane zone of the skin and other surfaces lined
by stratified squamous epithelial tissues. The under-
lying common mechanism is that defects in the
anchoring system of the epithelial tissues allow detach-
ment with trauma (Table 28-2).,1W15"119
Investigations
Skin biopsy is essential for the diagnosis; the speci-
men is sent for electron microscopy and im-
munofluorescent microscopy. Electron microscopy
is the standard for determining the level of blis-
tering. Immunomapping with antibodies can dis-
tinguish the different types of epidermolysis bullosa.
If surgery is being contemplated, a nutritional eval-
uation is useful to aid in prediction of wound
healing.104 The patient should be evaluated by estab-
lishing the range of motion of limbs and digits to
monitor contractures and effectiveness of physical
therapy.
Treatment Principles
The complete medical treatment of patients with epi-
dermolysis bullosa involves many specialties. There are
specific concerns of the respiratory, gastrointestinal,
and urogenital systems that are vital to the overall treat-
ment of patients with epidermolysis bullosa.118 The
manifestations of the disease resulting in wound care
problems and physical deformities would be treated
by a plastic surgeon.
Optimizing wound healing in patients with epi-
dermolysis bullosa involves controlling all of the
factors that potentially delay wound healing, includ-
ing foreign bodies, bacteria, nutritional deficiencies,
tissue anoxia, and mechanical trauma. Extensive areas
of denuded skin represent loss of the stratum corneum
barrier to microbial penetration. Accumulation of
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Molecular Pathology
Mutations of the genes coding for keratins 5
and 14
Mutations in genes coding for laminin 5 subunits,
collagen XVII, 6 integrin, and 4 integrin have
been demonstrated
Mutations of the gene coding for type VII collagen
serum and moisture on the surface enhances the growth
of bacteria.
Extensive cutaneous injury is associated with
marked alterations in both hemodynamic and meta-
bolic responses, requiring increased calorie and protein
intake for recovery. The development of nutritional
deficiencies inhibits successful wound healing and the
body's return to a normal hemodynamic and meta-
bolic profile.
The nutritional well-being of patients with epi-
dermolysis bullosa should be dealt with before any
surgical intervention is considered.103,104,118 Compli-
cations include oral blistering, abnormal esophageal
motility, strictures, dysphagia, diarrhea, malabsorp-
tion, and dental problems. A nutritional assessment
taking these factors into account is essential for replen-
ishing the malnourished patient and improving wound
healing.119
Prevention of infection is the preferred strategy.
With extensive areas of crusting and skin loss, a strict
wound care regimen should be followed. Such a
regimen entails regular whirlpool therapy followed by
application of topical antibiotics. The wound should
be covered with semiocclusive nonadherent dressings.
Adhesive tape should not be applied directly to the
skin. Self-adhering gauze or tape is a better choice for
keeping dressings in place. Many adult patients will
explore the use of multiple wound care products and
often develop their own strategies to deal with recur-
rent areas of breakdown. Extensive areas of skin loss,
particularly common in children who cannot avoid
the mechanical trauma, might require admission to a
burn unit.
Squamous cell carcinoma often arises in chronic
cutaneous lesions in patients with epidermolysis
bullosa because of recurrent breakdown and repair;
peak incidence begins to increase dramatically in the
second and third decades of life. 10 Squamous cell car-
cinoma often occurs at multiple primary sites, which
is especially true for patients with recessive dystrophic
epidermolysis bullosa. The distribution of cutaneous
image...

28 • EXFOLIATIVE DISORDERS 805

squamous cell carcinoma in patients with recessive dys-
trophic epidermolysis bullosa is different and involves
any area of nonhealing. Careful surveillance of non-
healing areas is important.
Chronic blepharitis can result in cicatricial ectro-
pion and exposure keratitis.l M Moisture chambers and
ocular lubricants are used commonly for management.
This disorder has also been treated with full-thickness
skin grafting to the upper eyelid; however, complete
correction is difficult to obtain because the oculofa-
cial region will still continue to break down, and
repeated scarring will often result in recurrence of the
ectropion.
Potential future therapies include protein and gene
therapies.120"122 Protein therapy involves applying the
missing or defective protein, which is produced in vitro
by recombinant methods, directly to blistered skin.
Protein therapy may be most useful in epidermolysis
bullosa subtypes involving a defect or deficiency in
laminin 5 because this protein does not require
complex processing or transmembrane cellular anchor-
age. In gene therapy, the goal is to deliver genes tar-
geted to restore normal protein production.
SURGICAL CARE
Surgical restoration of the hand involves treatment of
the mitten deformity of the hand.I02 Repeated episodes
of blistering and scarring eventually result in fusion
of the web spaces. As a result, fine manipulative skills
and digital prehension are lost. Surgical procedures
can correct this deformity, but the rate of recurrence
is high. The dominant hand has earlier recurrence.
Recurrence appears to be delayed by the prolonged
use of splinting in the interphalangeal spaces at night.
The preferred method of release involves restoring the
thumb opposition and separating the precision-based
radial digits for fine motor skills. The surgical release
involves fixation of grafts to the surgically formed clefts.
Flaps have generally not been used because of the poor
skin component.
Invasive aggressive squamous cell carcinoma is a
particularly troubling complication of recessive dys-
trophic epidermolysis bullosa. When it is detected, exci-
sion of the carcinoma is indicated. Both Mohs and
non-Mohs surgical approaches have been used. Skin
graft harvesting can be difficult because of the total
skin involvement in many patients. Split-thickness
grafts should be harvested with a hand-held knife as
opposed to electric or mechanical dermatomes, which
have been reported to cause full-thickness wounds.
Donor sites usually heal rapidly if they can be kept
free of infection. Full-thickness grafts can be harvested
from areas of intact skin with excellent healing of the
donor site, but the thinning process of the full-thick-
ness graft must be done with care because the epider-
mal layer will naturally fracture if it is overhandled.,02,103
A technique has been described in which the full-
thickness graft is obtained by trying to cleave the dermis
in situ with a large scalpel blade to minimize tissue
handling.
The anesthetic care of patients with epidermolysis
bullosa requires a presurgical consultation and is also
beyond the scope of this chapter.123 Consultation of
an anesthesiologist experienced in the care of patients
with epidermolysis bullosa is optimal.
USE OF SKIN EQUIVALENTS
It is safe to say that any new wound healing product
that has been produced has been used in this condi-
tion. An Internet review reveals that the epidermoly-
sis bullosa Web sites with interactive areas post
numerous substances that have been tried with varying
success. The literature includes reports of different
products that are used to heal both open recurring
wounds and donor sites for grafting procedures. None
is known to be superior. Integra artificial skin has been
tried, but the chronic nature of these wounds increases
the rates of infection and loss of the dermal matrix
while vascular ingrowth is awaited. Dermal replace-
ment analogues and epithelial cell culture techniques
have been used to treat patients with epidermolysis
bullosa. Apligraf* is a human allograft of fibroblasts
and keratinocytes.124 Whereas the short-term effects
of Apligraf have been studied carefully, the long-term
effects and the persistence of grafts remain in ques-
tion (Fig. 28-12). Apligraf may represent an effective
short-term therapy for chronic nonhealing wounds in
epidermolysis bullosa, but claims that Apligraf offers
a long-term cure for epidermolysis bullosa remain
unsubstantiated. This is not surprising given that
Apligraf does not vascularize to the wound bed and
the persistence of allografted cells is only temporary.
It is hoped that in the future, tissue engineering will
produce a product with characteristics that allow
epithelial anchoring and a possible effective means of
maintaining skin integrity for these patients.
'Organogenesis, Inc., Canton, Massachusetts.

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806 I • GENERAL PRINCIPLES

*"~

C D
FIGURE 2 8 - 1 2 . A, Classic mitten hand deformity with absent phalanges requires surgical release to restore func-
tion. B, Intraoperatively, the epidermal "casting" due to minimal trauma of preparing the limb is common. It is for this
reason that handling is gentle and the tourniquet cannot be used. C, Apligraf used to cover index and middle fingers
as donor sites that were judged to be poor for graft harvest. D, EpitheNalization eventually occurred after weeks of
dressings. It was the authors' impression that the Apligraf provided a biologic dressing, allowing native epithelializa-
tion to occur. {Photograph courtesy of Dr. R. Zuker, Toronto, Canada.)

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Dermatol 1996;134:710-714.
50. Viard I, Wehrti P, Bullani R, et al: Inhibition of toxic epider-
mal necrolysis by blockade of CD95 with human intravenous
immunoglobulin. Science 1998;282:490-493.
51 Choisdow O, Delchier JC, Chaumette MT, et al: Intestinal
involvement in drug-induced toxic epidermal necrolysis.
Lancet 1991;337:928.
52 Tismit JF, Mion G, Rouyer N, et al: Bronchopulmonary dis-
tress associated with toxic epidermal necrolysis. Intensive Care
Med 1992;18:42-44.
53. Yarbrough DR: Experience with toxic epidermal necrolysis
treated in a burn center. J Burn Care Rehabil 1996;17:30-33.
54. Khoo AK, Foo CL: Toxic epidermal necrolysis in a burns centre:
a 6-year review. Burns 1996;22:275-278.
55. Palmieri TL, Greenhalgh DG, Saffie JR, et al: A multicentcr
review of toxic epidermal necrolysis treated in U.S. burn centers
at the end of the twentieth century. J Burn Care Rehabil
2002;23:87-96.
56. Murphy JT, Purdue GF, Hunt JL: Toxic epidermal necrolysis.
J Burn Care Rehabil 1997;18:417-420.
808 • GENERAL PRINCIPLES
57. Schulz JT, Sheridan RL, Ryan CM, et a!: A 10 year experience
with toxic epidermal necrolysis. J Burn Care Rehabil
2000;21:199-204.
58. McGec T, Munster A: Toxic epidermal necrolysis syndrome:
mortality rate reduced with early referral to a regional burn
center. Plast ReconstrSurg 1998;102:1018-1022.
59. Wong KC, Kennedy PJ, Lee S: Clinical manifestations and
outcomes in 17 cases of Stevens-Johnson syndrome and toxic
epidermal necrolysis. Australas J Dermatol 1999;40:131-
134.
60. Deitch EA, Wheelan TM, Rose MP, et al: Hypertrophic burn
scars: analysis of variables. J Trauma 1983;23:895-898.
61. Meneux E, Wolkenstein P, Haddad B, et al: Vulvovaginal involve-
ment in toxic epidermal necrolysis: a retrospective study of 40
cases. Obstet Gynecol 1998;91:283-287.
62. de Felice GP, Caroli R, Autelitano A: Long-term complications
of toxic epidermal necrolysis (Lyell's disease). Clinical and
histopathologic study. Ophthalmologica 1987;195:1-6.
63. Mclvor RA, Zaidi J, Peters WJ, et al: Acute and chronic respi-
ratory complications of toxic epidermal necrolysis. J Burn Care
Rehabil 1996;17:237-240.
64. Feder HM, Hoss DM: Toxic epidermal necrolysis (letter]. N
Engl J Med 1996:334:922.
65. Smoot EC: Treatment issues in the care of patients with toxic
epidermal necrolysis. Burns 1999;25:439-442.
66. Lebargy F, Wolkenstein P, Gisselbrecht M, et al: Pulmonary
complications in toxic epidermal necrolysis: a prospective clin-
ical study. Intensive Care Med 1997;23:1237-1244.
67. Whale D, Bestc D, Conley SF: Laryngeal involvement in toxic
epidermal necrolysis. Otolaryngol Head NeckSurgl992;6:796-
799.
68. Kucan JO: Use of Biobrane in the treatment of toxic epider-
mal necrolysis. J Burn Care Rehabil 1995;16:324-328.
69. Sowder LL: Biobrane wound dressing used in the treatment
of toxic epidermal necrolysis: a case report. J Burn Care Rehabil
1990;11:237-239.
70. Halcbian PH, Corder VJ, Madden MR, et al: Improved burn
center survival of patients with toxic epidermal necrolysis
managed without corticosteroids. Ann Surg 1986;204:503-511.
71. Prendville JS, Hebert AA, Greenwald MJ, et al: Management
of Stevens-Johnson syndrome and toxic epidermal necrolysis
in children. J Pediatr 1987;115:881-887.
72. Garcia-Doval I, LeCieach L, Bocquet H, et al: Toxic epidermal
necrolysis and Stevens-Johnson syndrome: does early with-
drawal of causative drugs decrease risk of death? Arch Der-
matol 2000;136:323-327.
73. Sherertz EF, Jegasothy BV, Lazarus GS: Phenytoin hypersen-
sitivity presenting with toxic epidermal necrolysis and severe
hepatitis. Report of a patient treated with corticosteroid"pulse
therapy." J Am Acad Dermatol 1985;12:178-181.
74. Fine J: Management of acquired bullous skin diseases. N Engl
J Med 1995;133:1475-1484.
75. Rzany B, Schmitt H, Schopf E: Toxic epidermal necrolysis in
patients receiving corticosteroids. Acta Derm Venereol
1991;71:171-172.
76. McDonald K, Johnson B, Prasad JK, et al: Rehabilitative con-
siderations for patients with severe Stevens-Johnson syndrome
or toxic epidermal necrolysis. J Burn Care Rehabil 1989; 10:167-
171.
77. Power W, Ghoraishi M, Merayo-Lioves J, et al: Analysis of the
acute ocular manifestations of erythema multiforme/Stcvens-
Johnson syndrome/toxic epidermal necrolysis disease spec-
trum. Ophthalmology 1995;102:1669-1676.
78. Yamada HtTakamori K, Yaguchi H, et al: A study of the efficacy
of plasmapheresis for drug-induced toxic epidermal necroly-
sis. TherAphcr 1998;2:153-156.
79. Egan CA, Grant WJ, Morris SE, et al: Plasmapheresis as an
adjunct treatment to toxic epidermal necrolysis. J Am Acad
Dermatol 1999;40:458-461.
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80. Paquet P, Pierard GE: Would cyclosporin A be beneficial to
mitigate drug-induced toxic epidermal necrolysis? Dermatol-
ogy 1999;198:198-202,
81. Renfro L, Grant-Kels JM, Daman LA: Drug-induced toxic epi-
dermal necrolysis treated with cyclosporin A. Int J Dermatol
1989;28:441-444.
82. Hewitt J, Ormerod AD: Toxic epidermal necrolysis treated with
cyclosporin A. Clin Exp Dermatol 1992;17:264-265.
83. Szepietowski J, Wasik F, Szybejko-Machaj G, et al: Toxic
epidermal necrolysis treated with cyclosporin A: a report
of three cases. J Eur Acad Dermatol Venereol 1997;9:169-
172.
84. Zaki Y, Patel S, Reed R, et al: Toxic epidermal necrolysis asso-
ciated with severe hypocalcemia and treated with cyclosporin
A. Br J Dermatol 1995;133:329-347.
85. Jarrett P, Rademaker M, Havill J, Pullon H: Toxic epidermal
necrolysis treated with cyclosporin A and granulocyte colony
stimulating factor. Clin Exp Dermatol 1997;22:146-147.
86. Jarrett P, Ha T, Snow J: Toxic epidermal necrolysis and
cyclosporin A. Clin Exp Dermatol 1997;22:254.
87. Sullivan JR, Watson A: Lamotrigine-induced toxic epidermal
necrolysis treated with intravenous cyclosporin A: a discus-
sion of pathogenesis and immunosuppressive management.
Australas J Dermatol 1996;37:208-212.
88. Arevalo JM, Lorente JA, Gonzalez-Herrada C, et al: Treatment
of toxic epidermal necrolysis with cyclosporin A. J Trauma
2000;48:473-477.
89. Phan TG, Wong RC, Crotty K, et al: Toxic epidermal necroly-
sis in acquired immunodeficiency syndrome treated with
intravenous gammaglobulin. Australas J Dermatol 1999;40:
153-155.
90. Stella M, Cassano P, Bollero D, et al: Toxic epidermal necrol-
ysis treated with intravenoushigh dose immunoglobulins: our
experience. Dermatology 2001;203:45-49.
91. Paquet P, Jacob E, Damas P: Treatment of drug-induced toxic
epidermal necrolysis with intravenous human immunoglob-
ulins. Burns 2001;27:652-655.
92. Peck MD: Treatment of toxic epidermal necrolysis syndrome
with intravenous immunoglobulin (IVIG) and silver-impreg-
nated gauze dressings [abstract). J Burn Care Rehabil
2000;21:S174.
93. Shortt R, Gomez M, Mittman N, Cartotto RC: IVIG does not
improve outcome in toxic epidermal necrolysis [abstract]. J
Burn Care Rehabil 2003;24:S88.
94. Brown KM, Silver GM, Haler ZM, et al: Toxic epidermal necrol-
ysis syndrome: does IgG make a difference? J Burn Care Rehabil
2003;24:S87.
95. Fine JD, Bauer EA, Briggaman RA, et al: Revised clinical and
laboratory criteria for subtypes of inherited epidermolysis
bullosa. A consensus report by the Subcommittee on Diag-
nosis and Classification of the National Epidermolysis Bullosa
Registry. J Am Acad Dermatol 1991 ;24:119-135.
96. Fine JD, Bauer EA, McGuire J, Moshell A, eds: Epidermolysis
Bullosa: Clinical, Epidemiologic, and Laboratory Advances and
the Findings of the National Epidermolysis Bullosa Registry.
Baltimore, Md, Johns Hopkins University Press, 1999.
97. Fine JD, Eady RA, Bauer EA, et al: Revised classification system
for inherited epidermolysis bullosa: report of the Second Inter-
national Consensus Meeting on diagnosis and classification
of epidermolysis bullosa. J Am Acad Dermatol 2000;42:1051-
1066.
98. Fine JD, McGrath J, Eady RA: Inherited epidermolysis bullosa
comes into the new millennium: a revised classification system
based on current knowledge of pathogenetic mechanisms and
the clinical, laboratory, and epidemiologic findings of large,
well-defined patient cohorts. J Am Acad Dermatol 2000;43(pt
1):135-137.
99. Lin AN, Carter DM: Epidermolysis bullosa. Annu Rev Med
1993;44:189-199.
TWttf'BStfWimage...
100. Uitto J, Eady R, Fine JD, et al: The DEBRA International
Visioning/Consensus Meeting on Epidermolysis Bullosa:
summary and recommendations. J Invest Dermatol 2000;
114:734-737.
101. McGrath 1A, Eady RA: Molecular basis of blistering skin dis-
eases. Hosp Med 1998;59:28-32.
102. Terrill PJ, Mayou BJ, Pemberton J: Experience in the surgical
management of the hand in dystrophic epidermolysis bullosa.
Br I Plast Surg 1992;45:435-442.
103. Terrill PJ, Mayou BJ, McKee PH, Eady RA: The surgical man-
agement of dystrophic epidermolysis bullosa (excluding the
hand). Br J Plast Surg 1992;45:426-434.
104. Allman S, Haynes L, MacKinnon P, Atherton DJ: Nutrition in
dystrophic epidermolysis bullosa. Pediatr Dermatol 1992;9:
231-238.
105. Ciccarelli AO, Rothaus KO, Carter DM, Lin AN: Plastic and
reconstructive surgery in epidermolysis bullosa: clinical expe-
rience with 110 procedures in 25 patients. Ann Plast Surg
1995;35:254-261.
106. Ryan MC, Christiano AM, Engvall E, et al: The functions of
laminins: lessons from in vivo studies. Matrix Biol 1996; 15:369-
381.
107. Cameli N, Picardo M, Pisani A, et al: Characterization of
the nail matrix basement membrane zone: an immunohis-
tochemical study of normal nails and of the nails in Herlitz
junctional epidermolysis bullosa. Br J Dermatol 1996; 134:182-
184.
108. Marinkovich MP: Update on inherited bullous dermatoses.
Dermatol Clin 1999; 17:473-485, vii.
109. Marinkovich MP, Meneguzzi G, Burgcson RE, et al:
Prenatal diagnosis of Herlitz junctional epidermolysis
bullosa by amniocentesis. Prenat Diagn 1995;15:1027-
1034.
110. McGrath JA, Ishida-Yamamoto A, Tidman MJ, et al: Epider-
molysis bullosa simplex (Dowling-Meara). A clinicopatho-
logical review. Br J Dermatol 1992;126:421-430.
111. Tong L, Hodgkins PR, Denyer J, et al: The eye in epidermoly-
sis bullosa. Br J Ophthalmol 1999;83:323-326,
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28 • EXFOLIATIVE DISORDERS 809
112. HeagertyAH,EadyRA,KcnnedyAR,etal:Rapidprenataldiag-
nosis of epidermolysis bullosa fetalis using GB3 monoclonal
antibody. Br J Dermatol 1987;117:271-275.
113. McGrath JA, Schoficld OM, Mayou BJ, et al: Epidermolysis
bullosa complicated by squamous cell carcinoma: report of
10 cases. J Cutan Pathol 1992;19:116-123.
114. Wright JT, Fine JD, Johnson L: Hereditary epidermolysis bullosa:
oral manifestations and dental management. Pediatr Dent
1993;15:242-248.
115. Marinkovich MP, Herron, GS, Khavari, PA: Hereditary epi-
dermolysis bullosa. In Freedberg IM, Eisen AZ, Wolff K, et al,
eds: Fitzpatrick's Dermatology in General Medicine, 5th ed.
New York, McGraw-Hill, 1999:690-702.
116. Pulkkinen L, Uitto J: Mutation analysis and molecular genet-
ics of epidermolysis bullosa. Matrix Biol 1999;18:29-42.
117. Tabas M, Gibbons S, Bauer EA: The mechanobullous diseases.
Dermatol Clin 1987;5:123-136.
118. Uitto J, Pulkkinen L, McLean WH: Epidermolysis bullosa: a
spectrum of clinical phenotypes explained by molecular het-
erogeneity. Mol Med Today 1997;3:457-465.
119. Schober-Florcs C: Epidermolysis bullosa: a nursing perspec-
tive. Dermatol Nurs 1999;11:243-248,253-256.
120. Bauer EA, Herron GS, Marinkovich MP, et al: Gene therapy
for a lethal genetic blistering disease: a status report. Trans Am
Clin Climatol Assoc 1999;110:86-92.
121. Vailly J, Gagnoux-Palacios L, DelPAmbra E, et al: Corrective
gene transfer of keratinocytes from patients with junctional
epidermolysis bullosa restores assembly of hemidesmosomes
in reconstructed epithelia. GeneTher 1998;5:1322-1332.
122. Seitz CS, Giudice GJ, Balding SD, et al: BP180 gene delivery in
junctional epidermolysis bullosa. Gene Ther 1999;6:42-47.
123. Ames WA, Mayou BJ, Williams KN, Williams K: Anaesthetic
management of epidermolysis bullosa. Br J Anaesth
1999;82:746-751.
124. Falabella AF, Valencia IC, Eaglstein WH, Schachner LA:
Tissue-engineered skin (Apligraf) in the healing of patients
with epidermolysis bullosa wounds. Arch Dermatol
2000;136:1225-1230.
image...
CHAPTER
29 •
Burn and Electrical Injury
DAVID M. YOUNC, MD, FACS
HISTORY OF TREATMENT
EPIDEMIOLOGY
PATHOPHYSIOLOGY
Fluid Resuscitation
NUTRITION
BURN WOUND HEALING, DRESSINGS, AND SURCICAl
INTERVENTIONS
Wound Care
Topical Dressings
Surgical Procedures
Wound Coverage
REHABILITATION
Pain Control
HISTORY OF TREATMENT
In considering the history of the treatment of burn
injuries, one might quote Adam MacDougall, who in
1819 stated that "it would equally exceed the bounds
of convenience and utility to particularize all the reme-
dies that have been recommended in the treatment of
accidents of this kind."
The writings on this subject reflect that burn care
evolved slowly as a rational treatment process (Table
29-1). Pack and Davis (1930) described the treatments
of the ancients, such as the salve of Paracelsus con-
taining the fat of old wild hogs, wasted angle worms,
and moss "from the skull of a person hung." Paulus
Aeginata advocated light herbs mixed with vinegar to
prevent blisters and bull's gall dissolved with water.
Pigeons' dung, burned and mixed with oil, was also
recommended. The British, at the Battle of Cr£cy in
1346, were the first to use gunpowder, and this devel-
opment gave rise to many medical problems includ-
ing those associated with the treatment of burns. The
stimulus of the war experience initiated new and exper-
imental types of treatment. In 1596, Clowes wrote a
treatise on gunpowder burns. He did not differentiate
the depth of burns but rather described multiple types
of treatment on different parts of the body. He
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COMPLICATIONS
Infection
Gastrointestinal Ulcers
Heterotopic Ossification
Hypertrophic Scar
RECONSTRUCTION
SPECIAL INJURIES
Electrical Injury
Tar
Smoke Inhalation
suggested oily dressings containing many drugs, did
not open the blisters, and was an advocate of bleed-
ing. Fabricius Hildanus (1610), who wrote De Com-
bustionibus, was the first to classify burns into three
categories and also showed pictorially the early suc-
cessful surgical release of hand contractures. Pare*
(1634) clearly described the differences between
second-degree and third-degree burns, early excision
of the burn wound, and those burns that frequently
developed contractures."One must be careful if burns
affect the palpebres or the legs or the fingers or the
throat or the axilla or the joint of the knee or of the
arm for these joints should not stick together."
Richard Wiseman in 1676 wrote several "chirurgi-
cal treatises" and discussed splinting to avoid con-
tractures. He advised refrigerants or calefactive
medicaments. Edward Kentish (1797) described pres-
sure dressings as a relief for pain and in his essay on
burns promised to "rescue the healing art from empiri-
cism and to reduce it to established laws." The use of
ice and ice water for analgesia and the prevention of
edema was explained by H. Earle in his essay "The
Means of Lessening the Effects of Fire on the Human
Body" in 1799. Controversies about the best method
to treat the burn wound persist to the present day. Dress-
ings remained popular until Wallace in 1949 advocated
811
812 I • GENERAL PRINCIPLES

TABLE 29-1 • BURN TREATMENT HISTORY Royal Medical Society in which he recognized burn
shock as similar to shock seen with acute peritonitis,
Neanderthal man Extracts of plants and in which he argued against bleeding and purging,
Smith papyrus (1500 BC Cum and goat's milk these practices persisted through the latter part of the
Egyptians) mixed with mother's 19th century. The appreciation by Tappeiner of burn
milk
Strips soaked in oil pathology, however, was a significant event. In 1905,
Chinese (600-500 BC) Extracts of tea leaves Sneve noted the importance of intravenous saline for
Hippocrates (430 BC) Swine's semen, resin, and resuscitation and wrote an article in the Journal of the
bitumen American Medical Association advocating early skin
Oak bark solutions grafting.
Celsus (ancient Rome) Honey and bran
Calen (ancient Rome) Vinegar or wine The understanding of burn pathology took a great
Rhases (9th century) Cold water leap forward when Underhill (1930) studied a group
Pan* (1517-1596) Excision and ointments of patients burned in a theater fire in 1921. He ana-
David Cleghorn (1792) Vinegar and chalk poultice lyzed the content of blister fluid and determined that
Edward Kentish (1797) Pressure dressings
Syme(1827) Wool dressings burn shock was due to fluid loss, not toxins (a popular
Lisfranc(1835) Calcium chloride theory of that time). The Cocoanut Grove fire in Boston
dressings in 1942 resulted in extensive studies by Cope and Moore
Passavant (1858) Saline baths on the diagnosis and treatment of burn shock. For-
Tomasalis(1897) Salt water injections mulas gradually evolved to calculate fluid losses; Evans
in 1952 used burn skin surface area and weight as
From Salisbury RE: Thermal burns. In McCarthy JM, ed: Plastic Surgery. the principal variables. The Brooke formula was a
Philadelphia, WB Saunders, 1990:788.
modification of the Evans formula and used salt,
colloid, and water. Moyer and associates (1965) rec-
ommended only lactated Ringer solution, yielding alert,
exposure treatment for burns of the face, buttock, and oriented patients even when the body surface area burn
perineum. was large. Baxter (1978) modified this recommenda-
Dupuytren (1832), the brilliant French surgeon, tion with the Parkland formula. With these advantages
made multiple contributions to burn research, includ- in the understanding of burn shock and vigorous fluid
ing the documentation of the degree of injury to depth resuscitation, a dramatic improvement in early sur-
and the description of the phases of the postburn vival occurred.
course—irritation, inflammation, suppuration, and The pattern of triage of burn patients changed dra-
exhaustion. In 1823, the Edinburgh Medical Journal matically in the 1960s. The U.S. Army Research Unit
published two papers on postmortem findings in two was initially guided by Pulaski and Artz, who stressed
burn deaths. One patient had a gastric ulcer and another patient care as well as clinical and laboratory burn-
gastric congestion. Multiple lecturers at this time were related research. Critically injured patients, civilian and
describing perforation of the stomach after burn death, military, were referred to the Center, and the concept
and there was increased interest in studying both the of the multidisciplinary burn team evolved. In 1962,
pathology and treatment of thermal injuries. Cotton the Shriners fraternal organization in the United
dressings over burns were first discussed in a Glasgow States began development of three burn centers
medical journal in 1828. Readers were told how to apply affiliated with universities and dedicated specifically
dressings and were cautioned against changing them to the care of burned children.
more than once daily. These centers served as role models that have com-
Sir George Ballingall in 1833 gave one of the best pletely altered burn care around the world. Their superb
descriptions of death from burn sepsis: "sinking in survival statistics made others realize that patients with
a hectic state, exhausted by a profuse discharge of large burns were not automatically doomed but had
matter from an extensive separating surface." James a chance of survival with care in a specialized center.
Sim (1799-1870) advocated pressure dressings for Laboratory and clinical research in burn injury ulti-
burns. In a landmark decision in 1848, the managers mately improved other areas of trauma care. It became
of the Royal Infirmary in Edinburgh designated one ob\ious that the burn patient with multisystem
building for all burn cases, and this became known involvement was the perfect trauma model. The uni-
as the Burn Hospital. In 1875, Joseph Lister recom- versality of the burn problems provided a reason for
mended boric acid and carbolic acid for burn wounds better international cooperation and exchange of
to kill bacteria. In 1881, Tappeiner of Munich studied ideas. In 1960, the first International Congress on
autopsies of burn deaths and recognized the con- Research in Burns was held in Washington, DC. At the
centration of blood, increased hemoglobin concen- second meeting in 1963, the International Society
tration, and decreased blood and water volume. In for Burn Injuries was founded, and it has been con-
spite of a speech by Robert Hornby in 1833 to the ducting meetings every 4 years. The American Burn

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Dr.Mustafa D.
fl&WWaatfW image...
Association was founded in 1968. The society's
membership was unique in that it consisted of all the
members of the burn team, including nonphysicians
(dietitians, physical and occupational therapists, nurses,
and psychologists).1
Plastic surgeons have always been at the forefront
of caring for burn victims because of our interest and
expertise in the treatment of skin injury and our par-
ticular skill in treating cutaneous wounds and scar-
ring. Pioneer plastic surgeon Bradford Cannon
established the use of skin grafting as the preferred
method for treatment of burn wounds rather than
relying on topical treatments. Plastic surgeons have
since evolved from a position of a wound care spe-
cialist to directing the entire team caring for the burn
patient. A substantial number of burn units registered
by the American Burn Association are directed by
plastic surgeons. The interest of plastic surgeons in burn
care and their contributions to it are substantial. It is
therefore imperative that plastic surgeons have a
working knowledge of all the fundamental aspects of
burn treatment rather than only of reconstruction.
Plastic surgeons often manage the long-term recon-
struction of severely scarred burn patients, and this
experience offers us unique insights into the early, acute
treatment of these patients. This global perspective
about the outcome and quality of life for survivors of
an often devastating injury affords us a special posi-
tion in this field.
Treatment of burn victims has evolved during the
past 50 years into a well-defined and organized sub-
specialty of surgery. Observing victims in mass casu-
alty situations and later in specialized burn units,
clinicians realized that most burn patients respond to
injury in a predictable and uniform fashion. The ability
to assess treatment outcomes in a relatively objective
manner has led to a rapid advancement of practical
knowledge. Few practitioners debate the need for fluid
resuscitation of patients with large surface area burns
to prevent hypotension and renal failure, but the
optimum amount is still questioned. An undisputed
poor outcome (death) results from no resuscitation,
but whether more or less fluid results in better pul-
monary function, less tissue edema, and a "better"
outcome remains controversial. Despite confidence in
our knowledge, comprehensive reviews of the litera-
ture conclude that few undisputed truths about burn
care have actually been proved while many opinions
have been expressed (American Burn Association
Consensus Statement, 2000). The reviewers concluded
that more randomized prospective clinical trials are
needed to determine whether our present therapies do
really influence outcomes (length of hospital stays,
complications, and quality of life of these patients).
Nonetheless, treatment preferences are given in the fol-
lowing and reflect the common practice of most burn
surgeons.
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29 • BURN AND ELECTRICAL INJURY 813
EPIDEMIOLOGY
According to the most recent statistics compiled by
the American Burn Association, approximately 2.2.
million people are burned in the United States every
year; 5500 deaths result from burn injury, and 60,000
people are admitted to the hospital for care. The cost
to treat these patients exceeds $1 billion, and the cost
to society in terms of lost wages, vocational rehabili-
tation, and need for long-term care is staggering.2
It has long been recognized that the best treatment
against a disease is prevention. This is no truer than
for trauma and especially burns. Obtaining precise his-
torical data on the incidence of all burns is difficult
because reporting methods have varied over time.
However, the death rate from thermal injury is fairly
accurate, and according to statistics generated by the
Centers for Disease Control and Prevention, the
number of deaths has steadily decreased since 1975
(Fig. 29-1). The decreased mortality rate probably
reflects both an improved survival rate from injury and
an absolute decrease in the number of injuries. Most
observers attribute the drop in burn injuries to better
methods of prevention, and the American Burn Asso-
ciation has led further efforts to sustain or to enhance
these effects.
Data about morbidity and mortality from burn
injury have been gathered through individual burn
centers for decades and from a national database since
1991.3 Several prognostic factors for survival have been
identified. The best known predictor is still the per-
centage of total body surface area (TBSA) burned (Fig.
29-2).4 It is critical that the total surface area of both
second-degree and third-degree burns be accurately
assessed. The injured area is determined after the
sloughed epidermis is removed and the underlying
tissue examined. Inadequate debridement results in
underestimation of the injury and undertreatment (Fig.
29-3). From the most recent reliable data, the surface
area burn that results in 50% mortality (LA50) remains
relatively constant at 70% to 90% TBSA from the age
of 2 to 40 years. Age is an independent predictor of
NATIONAL FIRE AND FLAME DEATHS
8000 -1
I 6000 - ^ ^ N ^ . ^ ^ ^ ^
;§ 4000 - * • * • •
|2 2000-
0 '1 1 1 ' I ' I • I ' I ' I • I • I '
79 81 83 85 87 89 91 93 95
Year
FIGURE 2 9 - 1 . Decrease in the incidence and number
of deaths from burn injury in recent decades.
814 • GENERAL PRINCIPLES

SAN FRANCISCO GENERAL HOSPITAL Name

MEDICAL CENTER
MRN
ADULT ASSESSMENT SHEET DOB
BURN SERVICE

BURN ESTIMATE AND DIAGRAM: AGE VS AREA

Area Birth-1 yr. 1-4 yrs. 5-9 yrs. 10-14 yrs. 15 yrs. Adult 2° 30 Total donor areas
3
Head
Nock
19
2
17
2
13
2
11
2
9
2
7
2 I
I
Anterior trunk 13 13 13 13 13 13 6
Posterior Irunk 13 13 13 13 13 13
Right buttock 2.5 2.5 2.5 2.5 2.5 2.5
Left buttock 2.5 2.5 2.5 2.5 2.5 2.5
Genitalia 1 1 1 1 I 1
Right upper arm 4 4 4 4 4 4
Lolt upper arm 4 4 4 4 4 4 3
Right lower arm 3 3 3 3 3 3 3
Left lower arm 3 3 3 3 I 3 3
Right hand 2.5 2.5 2.5 2.5 2.5 2.5
25
Left hand
Right thigh
2.5
5.5
2.5
6.5
I "8 2.5
8.5
2.5
9
2.5
9.5
I
Left thigh 5.5 6.5 8 8.5 9 9.5 2
Right leg 5 5 5.5 6 6.5 7
Le'l !oc; 5 5 5.5 6 6.5 7
Right foot 3.5 3.5 3.5 3.5 3.5 3.5
Left foot 3.5 3.5 3.5 3.5 3.5 3.5
Total 19
Date Time Physician signature.
7/94 Medical record copy

FIGURE 2 9 - 2 . An example of the use of a homogram to assess total body surface

area of burn wounds.

survival. For patients younger than 2 years, the LA50
decreases to 60% TBSA; after the age of 50 years, the
LA50 drops steadily to 30% TBSA in patients older than
70 years. The other most consistent factor that deter-
mines survival is the presence of inhalation injury.
Patients with the same size burn were seven times more
likely to die if they also had inhalation injury. Other
reported prognostic factors include obesity, alcohol
abuse, neurologic impairment, and preexisting cardiac,
liver, and lung disease, although the studies that
address these are few.5,6
The American Burn Association established
certification of burn centers, with requisite personnel,
facilities, and significant annual cases to provide ade-
quate clinical experience, in 1989, To date, there are
approximately 80 approved centers around the country.
These centers are equipped to treat large or compli-
cated cases of burn and electrical injury. In addition,

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image...
FIGURE 2 9 - 3 . Extentof injury was underestimated
before debridement of these burn wounds but cor-
rectly assessed after removal of loose, dead skin. A B
they are the preferred environments for treatment of
patients with large and complicated wounds as seen
in some systemic disorders, such as toxic epidermal
necrolysis. Criteria for admission or transfer to burn
centers, delineated by the American Burn Association,
help provide guidelines for treatment (Table 29-2).
Although some people have debated the cost efficiency
of treating burn patients in specialized units,7 it is clear
that the concentration of specialized expertise, facili-
ties, and patients makes sense in the treatment of these
ill patients.8
PATHOPHYSIOLOGY
Thermal injury of the skin results in local tissue destruc-
tion and a systemic response. Much of the treatment
of burns is predicated on the depth (degree) and extent
(percentage TBSA) of the initial injury. Therefore, it
is critical to understand the clinical implications of
accurate evaluation of the injury so that consistent and
timely therapy can be instituted.
Excessively high temperatures cause graded tissue
injury radiating from the point of contact. The in-
creased temperature kills cells in the immediate area
and denatures the surrounding extracellular matrix
proteins (zone of necrosis). Circulation to this area
ceases immediately. The tissue in the surrounding area
continues to be metabolically active for hours after the
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29 • BURN AND ELECTRICAL INJURY 815
TABLE 2 9 - 2 • CRITERIA FOR BURN CENTER
REFERRAL
Partial-thickness burns greater than 10% total body
surface area (TBSA)
Burns that involve the face, hands, feet, genitalia,
perineum, or major joints
Third-degree burns in any age group
Electrical burns, including lightning injury
Chemical burns
Inhalation injury
Burn injury in patients with preexisting medical
disorders that could complicate management,
prolong recovery, or affect mortality
Any patient with burns and concomitant trauma (such
as fractures) in which the burn injury poses the
greatest risk of morbidity or mortality. In such cases,
if the trauma poses the greater immediate risk, the
patient may be initially stabilized in a trauma center
before being transferred to a burn unit. Physician
judgment will be necessary in such situations and
should be in concert with the regional medical control
plan and triage protocols.
Burned children in hospitals without qualified personnel
or equipment for care of children
Burn injury in patients who will require special social,
emotional, or long-term rehabilitative intervention.
American Burn Association Guidelines (2000).
image...

816 • GENERAL PRINCIPLES

Epidermis

First degree

— Second degree

Dermis

Hair — Third degree

follicle

FIGURE 29-4. Illustration of the extent of skin necrosis by the depth of burn.

injury, but eventually circulation ceases and the cells the thermal injury penetrate into the subcutaneous
die (zone of stasis). The depth of tissue destruction or deep tissue.
determines the degree of the burn (Fig. 29-4 and Table Once the injury encompasses more than 10% to
29-3). First-degree burns are limited to the epidermis, 15% TBSA,systemic, physiologic derangements occur.
such as a sunburn. Second-degree burns extend into A cascade of mediators released by the local tissue
but not through the dermis. Third-degree burns result and central nervous system mechanisms cause
in death of the entire thickness of the skin. physiologic changes including increased capillary
The temperature of the heat source and the length hydrostatic pressure, leakage of intravascular fluid
of exposure determine the extent of tissue destruction and proteins into the interstitium, decreased cardiac
(time-temperature curve). Patients burned by higher output, and suppression of the immune system.
temperatures (molten metal, hot grease, or flammable Burns of this magnitude are deemed to be major, and
clothing) have deeper burns than those burned with
hot water. The effect also varies over different types
and parts of the body. The result of heat injury is affected
by variables such as skin thickness. The thicker, TABLE 29-3 • TYPICAL EXAMINATION
glabrous skin of the palms and soles is more resistant FINDINGS IN BURN WOUNDS
to full-thickness injury than is the thinner skin of the
eyelid or dorsum of the hand. Infant skin is also thinner Depth of Burn Symptoms Signs
than adult skin and more likely to sustain full-thick-
ness injury from the same temperature. First degree Pain Erythema, epidermal
slough 1 -4 days later
The depth of any injury is not always obvious ini- Second degree Pain Blisters within 1-6
tially, and observers often disagree. N lany methods have hours, erythema,
been proposed to predict the depth of the injury imme- tenderness, good
diately or soon after injury (ultrasound examination, capillary refill
Third degree ± Pain Insensate, leathery,
intravenous fluorescent probes), but none has been thrombosed vessels,
as reliable as serial examination of the wound over no capillary refill,
time. The final depth of the injury typically becomes ± blisters
obvious 48 to 72 hours after injury. Very rarely does

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image...
Eschar
Eschar
FIGURE 2 9 - 5 . Illustration of burn depth and healing. Rate of epidermal regeneration is more rapid in superficial
second-degree burns (A and B) than in deeper second- or third-degree burns (C and D).
treatment to re-establish homeostasis should be insti-
tuted early to minimize adverse consequences. For
second- and third-degree injuries, the initial physio-
logic response of the patient is largely the same, so it
is not critical to differentiate between the two depths
of burn to guide effective treatment in the first 24 hours.
For long-term prognosis and actual treatment of
the wound, it is critical to distinguish between more
superficial burns (second degree) that heal without
grafts and deeper ones (deep second or third degree)
that require more intensive surgical treatment. Deter-
mination of the actual depth need not be done imme-
diately except in the case of circumferential burns. Most
commonly, the decision to treat a burn by debride-
ment and coverage with grafts in the operating room
is made 48 hours after injury, when the depth of the
injury can be accurately assessed. An exception has been
reported in a few burn centers that practice imme-
diate and total excision of the burn wounds. This
method has the reported advantage of removing all of
the injured tissue early, leading to less systemic
inflammation, lower risk of infection, and faster
recovery.
Extensive burns breach the epithelial barrier over
large areas, and the body loses large quantities of fluid,
proteins, and heat. Re-establishment of the epithelial
barrier is crucial to normalization of the patient's
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29 • BURN AND ELECTRICAL INJURY 817
Regenerating
epidermis
B
Regenerating
epidermis
physiologic state. Every effort is made to optimize the
regrowth of the epidermis. How the skin heals and what
treatment the burn wound requires depend largely on
the depth of the injury. Second-degree burns result in
extensive epidermal loss and variable dermal loss.
Third-degree burns result in complete necrosis of the
skin, epidermis, and dermis.
The skin responds to a second-degree burn by epi-
dermal regeneration through proliferation of ker-
atinocyte stem cells in the "bulge" region of the hair
shaft, located approximately halfway between the root
of the hair and the surface (Fig. 29-5). These cells
migrate from the bulge and continue to proliferate in
the basal cell layer for several generations before dif-
ferentiating and migrating upward into the stratified
epidermis. The time needed to regenerate a complete
barrier depends largely on the distance between
sources of keratinocytes. Injury to the superficial dermis
leaves a large number of residual hair follicles with many
sources of new keratinocytes scattered over the entire
surface. Proliferating keratinocytes need only migrate
the distance between hair follicles to achieve an intact
epithelial barrier. Thus, superficial second-degree
burns and skin graft donor sites heal quickly, typically
resurfacing in 10 to 14 days.
Deeper injury to the skin heals differently. Necro-
sis into the deep dermis or through the entire
818 • GENERAL PRINCIPLES
FIGURE 2 9 - 6 . Example of escharototnies of the forearm (A) and diagram of typical escharotomy
sites (B).
thickness of the skin as seen in deep second- and third-
degree burns leaves few if any hair follicles as sources
of proliferating keratinocytes (see Fig. 29-5). The only
remaining source of keratinocytes is from the edge of
the wound. If the wound is narrow, as in a laceration,
healing can be rapid because the distance the ker-
atinocytes must migrate is small. If the wound is wide,
as is typical of large burns, keratinocytes must migrate
great distances, and the wound may remain open for
months. The risk of infection from these wounds is
extremely high, and death from wound infections is
frequent. The only method to accelerate the regener-
ation of the epithelial barrier is to place proliferative
keratinocytes into the center of the wounds in the form
of skin grafts or cultured epithelium. Even for large
surface area wounds, restoration of the barrier can be
achieved in a few weeks. Typically, areas of second-
degree burns are treated with a topical antibiotic oint-
ment and allowed to heal by epidermal regrowth from
hair follicles, whereas third-degree burns are deT>rided
and closed with skin grafts or cultured keratinocytes.
Full-thickness circumferential burns must be rec-
ognized early to prevent compartment syndrome. The
coagulated collagen of a deep burn has the consistency
of leather (leather is animal skin subjected to a chem-
ical burn) and stretches very little. Tissue edema
typically occurs several hours after injury, and the
burn around an extremity acts like a tourniquet. The
ensuing compartment syndrome can cause necrosis
of the underlying muscles and nerves. Circumferen-
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B
tial chest burns can restrict ventilation, leading to res-
piratory failure. Treatment is urgent, longitudinal inci-
sionsof theburn (escharotomies) to relieve constriction
(Fig. 29-6). Little additional harm results from the pro-
cedure because the full-thickness burned skin requires
debridement and skin grafting anyway.
Abdominal compartment syndrome has been
described in patients after massive fluid resuscitation
with and without burns to the abdominal area. The
extreme tissue edema leads to increased intra-abdom-
inal pressures and venous congestion of the kidneys
and gut. Increased intra-abdominal pressure can limit
thoracic expansion, leading to respiratory failure. Urine
output decreases, and the intra-abdominal organs
become ischemic. Intra-abdominal pressures are meas-
ured through the bladder by use of a Foley catheter
attached to an arterial line monitor. Pressure above
30 mm Hg confirms the diagnosis, and the condition
is treated by decompressive laparotomy. Decompres-
sion of the abdomen reduces the pressure, but the mor-
tality rate is extremely high. 9 Ultrasound-guided
percutaneous drainage of intra-abdominal fluid col-
lections to reduce pressures can successfully treat some
cases of abdominal compartment syndrome. 10
Fluid Resuscitation
Massive injury in general and burns in particular result
in systemic inflammation and leakage of fluid
from the intravascular space into the interstitium.
lJt*y*>ttf<ae!dW image...
Adequate
IV fluids
FIGURE 2 9 - 7 . Adequate fluid
resuscitation to replace interstitial
loss of fluid from the burn injury. Excess
intravenous fluid results in increased
interstitial edema.
Recognition of this response led to a better under-
standing and treatment of burn shock. A large fluid
shift can decrease perfusion to vital organs. Metabolic
acidosis, oliguria, and relative polycythemia result from
inadequate replacement of intravascular volume. The
sympathetic response to burn injury can mask the early
clinical signs of hypovolemic shock and fool the unwary
clinician. Therefore, it is imperative to assess the extent
of the burn early and to initiate adequate fluid replace-
ment before the onset of organ failure.
Fluid replacement is based on the observation that
fluid loss from the vascular space occurs at a constant
rate during the first day after injury. The amount of
replacement fluid is predicted from the extent of burn
and size of the patient, and fluid replacement should
proceed at the same rate as the loss. Fluid adminis-
tered in excess of the leak is excreted by the kidney or
results in increased hydrostatic pressure and extra inter-
stitial edema (Fig. 29-7). All fluid is therefore admin-
istered at a constant rate, and fluid boluses are avoided.
Many formulas can be used (Table 29-4), and the
amount calculated does not vary significantly from one
formula to the next for the average patient. Charles
Baxter proposed the Parkland formula in 1964,11 and
it remains the most widely used. As an example, by the
Parkland formula, a 70-kg patient with a 40% TBSA
burn receives (70 X 40 x 4) = 11,200 mL of lactated
Ringer solution during the first 24 hours after the burn
(approximately 470 mL per hour).
Patients are monitored for an adequate clinical
response to the fluid infusion by measurement of the
hourly urine output. Inadequate urine output calls for
an increase in the rate of fluid infusion. Other param-
eters of fluid volume, such as neurologic function, mean
blood pressure, central venous pressure, and serum base
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29 • BURN AND ELECTRICAL INJURY 819
Excess
IV fluids
Interstitial leak
deficit, are helpful but not always accurate. Use of a
right-sided heart pressure monitor (Swan-Ganz)
during fluid resuscitation does not contribute useful
information unless the patient has cardiac or renal
dysfunction.
It is well established that large amounts of fluid are
required, but many studies question the traditional
endpoint measurements of adequate fluid replacement.
Although the calculated fluid replacement sets a
guideline for the initial rate of fluid replacement, the
physiologic response of the patient dictates whether
the rate is changed during the course of the resusci-
tation. If one uses the standard endpoint of main-
taining a urine output between 0.5 and 1 mL per
kilogram of body weight per hour, studies have shown
that tissue perfusion is often compromised and local
metabolic acidosis may result. Proponents of more
fluid argue that peripheral tissue perfusion is a better
indicator of adequate intravascular volume than is
renal perfusion. Traditional resuscitation volumes
result in inadequate perfusion and further injury to
the burned tissue and deepening of the injury. Oppo-
nents of more fluid argue that increased intravascu-
lar volume results in more interstitial fluid in the lungs
and may increase pulmonary complications. Outcomes
studies have yet to determine the validity of either side
of the issue. At present, the majority of burn surgeons
give enough resuscitation fluid to maintain adequate
blood pressure and urine output and to correct any
base deficits as determined by blood gas measure-
ments. In addition, most clinicians use a rising
hematocrit value as an indication of inadequate fluid
administration.
Significant protein loss occurs with the capillary
leakage in patients with large surface area burns.
image...

820 • GENERAL PRINCIPLES

TABLE 29-4 • RESUSCITATION FORMULAS

Modified
Brooke Brooke Parkland Monafo Evans

Day I

Colloid 0.5mL/kg/% burn None None None 1 mL/kg/% burn

Crystalloid Lactated Ringer Lactated Ringer Lactated Ringer 250 mEq Na, Lactated Ringer
solution, solution, solution, 150mEq lactate, solution,
1.5mUkg/°& 2mL/kg/%burn 4mUkg/% lOOmEqCI, 1 mL/kg/%
burn (adult), 3 mL/kg/% burn titrate to urine burn
burn (child) flow
5 c oD/W 2000 mUm2 None None "Liberal" free 2000 mL/m2
water by mouth
Urine 30-50 mL/hr 30-50mL/hr (adult) 50-70 mL/hr 30-50 ml7hr 30-50 mL7hr
(adult) 1 mL/kg/hr (child) (adult) (adult) (adult)
Rate V2 total in first Same as Brooke V2 total in first Infuse constantly V2 total in first
8hr, Vaotal in 8hr, Vi total in 8hr, •/, total in
next8hr, nextShr, '/« next8hr, '/«
'/« total in next total in next total in next
8hr 8hr 8hr
Calculation Same as Evans Same as Parkland Use total burn Titrate to urine Use burn area
of volume area for all production, not up to a total
sizes of burn burn Of 50% TBSA;
above 50%
TBSA burn,
calculate as
50% burn

Day 2

Colloid 0.25 mL/kg/% 0.3-0.5 mL/kg/% 700-2000mL 0.5 mUkg/% burn

burn burn (adult) as
required to
maintain urine
Crystalloid Lactated Ringer None None — Lactated Ringer
solution, solution,
0.5mLykg/% 0.5 mL/kg/%
burn burn
5% D/W 1500-2000 mL Sufficient to Sufficient to 1500-2000mL
maintain urine maintain urine

From Salisbury RE: Thermal burns. In McCarthy JM, cd: Plastic Surgery. Philadelphia, WB Saunders, 1990:792.

Colloids are commonly used for restoration of intravas-
cular volume and oncotic pressure. To replace intravas-
cular proteins, many resuscitation formulas include
administration ofcoiloid either throughout the period
of fluid replacement or after the first 24 hours. Restora-
tion of intravascular oncotic pressure reduces tissue
edema and overall fluid requirements. Experimental
evidence in large animals suggests that leakage of
albumin is substantial in the first 14 to 16 hours after
injury but then quickly subsides.12 This suggests that
early administration of colloids may not be useful for
minimizing edema. Administration of colloids after
the leakage stops should be more effective in re-estab-
lishing a beneficial oncotic gradient. Despite a com-
pelling theoretical argument, no clear clinical trial has
demonstrated a survival advantage to early or late
colloid administration in burn patients. Initial resus-
citation with colloid solutions decreases the total
amount of fluids administered in the first day but may
be associated with increased pulmonary water content
and complications during the course of treatment.13
Most burn units use colloid replacement in burns of
more than 20% TBSA, and most start administration
24 hours after injury.
Hypertonic solutions have also been used to decrease
the total amount of fluids needed to maintain intravas-
cular volume and to decrease tissue edema. The same
amount of sodium is infused during the same time
period as for the other formulas, only in a higher con-
centration. Thus, the total amount of fluid given is less.
Risks include hypernatremia and altered mental status.
Again, no solid clinical evidence indicates that the use

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image...

29 • BURN AND ELECTRICAL INJURY 821

of hypertonic solution resuscitation improves survival
in burn patients.
NUTRITION
Burn injury can increase the basal metabolic rate 50%
to 100% of the normal resting rate. The main features
include increased glucose production, insulin resist-
ance, lipolysis, and muscle protein catabolism. Without
adequate nutritional support, patients have delayed
wound healing, decreased immune function, and gen-
eralized weight loss. Many formulas predict the nutri-
tional needs of these patients on the basis of lean body
mass and percentage body surface area burned (Table
29-5). Increased intake of both total calories and protein
(1.5 to 3 g of protein per kilogram per day) is needed
to restore the deficit.14 Much like fluid resuscitation,
the exact nutritional requirements are debatable. 15 The
clinical response of the patient remains the best indi-
cation of nutritional repletion during recovery from
the injury. The rapidity of epidermal regeneration
of superficial burns and donor sites and improving
serum nutritional parameters are the best indicators
of adequate nutrition. Measurement of the basal
metabolic rate also guides nutritional replacement
therapy. Measuring weight loss and gain during treat-
ment is not useful because of the large fluid shifts. Even
with adequate nutritional support, most patients lose
muscle mass and weight. Several studies propose the
use ofanabolic steroids or growth hormone to reduce
muscle catabolism and weight loss during the injury
and to enhance weight gain during recovery.16
Enteral feedings through nasogastric or nasoduo-
denal tubes are the preferred method of feeding in many
units. Parenteral nutrition requires additional vascu-
lar access with its concomitant risks. It also lacks the
beneficial effects of gut mucosal stimulation and its
protective effects against bacterial translocation and
stress hemorrhage. Tube feedings also have an advan-
tage over regular oral intake. Patients with large
surface area burns need to consume large amounts of
food to satisfy their nutritional requirements. The rig-
orous schedule of dressing changes, operations, and
rehabilitation sessions interferes with meals. Dimin-
ished appetite from high-dose analgesics also con-
tributes to poor feeding. Adequate nutritional support
is so critical to recovery from burn injury that most
clinicians will place feeding tubes in patients with inad-
equate oral calorie intake despite the risk of aspiration
pneumonia.
BURN WOUND HEALING,
DRESSINGS, AND SURGICAL
INTERVENTIONS
Wound Care
All wounds eventually heal if they are left alone unless
there is infection, lack of blood flow (tissue ischemia),
or inadequate nutritional intake. Meticulous wound
care helps minimize the chance of infection and max-
imize healing. The daily dressing changes in burn
patients permit inspection of the wound to assess the
need for further interventions but, more important,
offer the chance to remove dead tissue that is a nidus

TABLE 2 9 - 5 • PROTOCOLS FOR CALCULATING CALORIE A N D PROTEIN NEEDS

Percentage
Author Age of Burn Calories Protein

Wilmore Adult Any Use nomograms to calculate Adjust nitrogen/total calorie to 1:150
BMR, % change in BMR,
energy requirements
Wilmore All >30 2000-2200 kcal/m2/day 15gnitrogen/m 2 *
Muir Adult Less than 20 35 kcal/kg 1.5g/kg
20-30 40kcal/kg 2.0g/kg
30-40 50 kcal/kg 3.0g/kg
40-50 60 kcal/kg 4.0g/kg
Davies Adult Up to 50* (20 kcal x body wt in kg) + ( I g x b o d y wt in kg) + (3gx burn)
(70kcalx% burn)
Davies Child* Up to 50* (60 kcal x body wt in kg) + (3gxbody wt in kg) + ( l g x burn)
(35 kcal x% burn)
Curreri Adult Any (25 x body wt in kg) + Not calculated
(40 x % burn)

BMR, basal metabolic rate.

* 1 g nitrogen = 6.25 g protein.
*>50% surface injuries are calculated as a 50% injury.
'Up to 12 years of age.
From Salisbury RE: Thermal burns. In McCarthy JM, ed: Plastic Surgery. Philadelphia, WB Saunders, 1990:799.

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822 I • GENERAL PRINCIPLES
for infection. The burn nurse dedicates a large part
of the time to gently scraping off dead skin and pro-
teinaceous debris that have gathered since the last dress-
ing. This leaves a healthy bed for the migration of
keratinocy tes. Typically, the wound is covered between
dressings with a moist, antibacterial covering to min-
imize microbial growth, fluid loss, and painful stimuli
and to maximize skin regeneration. Superficial second-
degree burns heal in a short time with wound treat-
ment only. For deep second-degree or third-degree
burns, the time for healing can be extensive and risks
of infection greater. For these wounds, it is far better
to treat by surgical debridement and coverage with skin
grafts or cultured epidermis. For a deep burn over a
small area or one with a patchy distribution, the time
for healing by secondary intention may be no longer
than the healing of a skin graft. For these wounds, sur-
gical debridement and grafting may not be appropri-
ate. After all, it takes a skin graft 7 to 10 days to stabilize
on a wound and about the same amount of time for
the donor site to heal.
Many ointments serve as good temporary cover-
ings for the wounds between dressing changes. The
simplest is just a petroleum-based antibiotic ointment
such as bacitracin; but for sizable burns, most clini-
cians use some preparation with a stronger bacterici-
dal or bacteriostatic action.
Topical Dressings
Silver sulfadiazine (Silvadene) is the most common
ointment used. It has intermediate wound penetra-
tion and a good antibacterial spectrum. The antibac-
terial activity lasts 8 to 10 hours, and the dressings are
changed twice a day. Silver sulfadiazine causes tran-
sient leukopenia in some patients when it is used on
large open areas. A switch to a different topical agent
for a few days allows the white blood cell count to
recover. Restarting silver sulfadiazine rarely causes
recurrent leukopenia.
Mafenide acetate (Sulfamylon) is also commonly
used and looks similar. It has excellent eschar pene-
tration and bacteriostatic action. Use of mafenide
acetate on full-thickness burns prevents deeper in-
fections. Often used on the ear, it helps against infec-
tion of the cartilage. Systemic absorption of mafenide
acetate, when it is applied to large surface area burns,
produces a metabolic acidosis by inhibition of carbonic
anhydrase. The effect is usually noted after 3 to 5 days.
Use of the compound on open wounds also causes pain
on initial application. The pain subsides after several
minutes, but patients usually do not like it.
Another topical dressing is Dakin solution (0.25%
sodium hypochlorite). This is good for a wet-to-dry
dressing for minor debridement of the wound surface.
It is particularly useful if a skin graft smells or looks
infected.
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Silver nitrate, as a 0.5% solution, is applied as a wet
dressing. It has excellent antibacterial properties but
causes discoloration of the skin and all the surround-
ing clothing and bedding. A newer version marketed
as Acticoat contains gauze material impregnated with
a silver compound. This product does not discolor the
skin as silver nitrate does. The dressing does not have
to be removed. Instead, it is moistened occasionally to
release the active ingredient into the wound.
Agents such as povidone-iodine solution and nitro-
furazone are still used in some burn units but less and
less often. The need to use multiple agents once one
has failed is becoming less common. Burn wound infec-
tions have decreased dramatically during the last 2
decades not from better topical dressings but from a
better understanding of the causes of burn wound
infection. Early tangential debridement and coverage
of the wound with skin have markedly decreased
the opportunity for colonization of the burn eschar.
Despite meticulous wound care, and even under the
most sterile conditions, the patient's own microbial
flora quickly colonizes and then invades the burn
eschar. Only by removing the dead tissue and pro-
viding stable coverage is the risk of wound infection
eliminated.
Surgical Procedures
The coagulated tissue from third-degree burns does
not easily separate from the wound bed until very late,
and the thick layers of dead tissue retard epithelial
regrowth and harbor pathogens. Removal requires
sharp debridement with a knife (tangential). Because
of the intensely painful stimuli and the likelihood of
a large quantity of blood loss from the debridement,
these procedures are typically done in the operating
room.
The main goals of surgical treatment of patients
with deep burns are debridement of the burn and place-
ment of stable permanent skin coverage. Many studies
have demonstrated that early removal of the dead tissue
(1 day to 3 weeks after injury) and aggressive meas-
ures to re-establish the epithelial barrier decrease
wound infections and mortality.17 The dead tissue con-
tinues to incite an inflammatory response, serves as a
growth medium for pathogens, and delays wound
healing. Even after removal of the dead tissue, pathogens
colonize the wound and enter the patient's blood stream
to seed distant sites. Open wounds leak proteins and
fluids and continue to be painful. All these factors con-
tribute to the patient's hyperdynamic and hyperme-
tabolic state. To achieve early debridement and stable
permanent coverage of the wound, the surgeon must
overcome two main obstacles, the extreme physical
insult of the debridement process and the limited source
of replacement skin for permanent coverage of large
surface area burns.
VtJWftf'aeldWimage...
The main limitation to removal of the dead skin in
large burns is severe physiologic disturbance caused
by rapid and copious blood loss as a consequence
of skinning patients over an extensive area. In adults,
blood loss reaches lOOmL for every 1% TBSA of skin
debrided. Although some units practice large (>20%
TBSA) debridement in one procedure, most burn units
limit each operative session to debridement of 10% to
20% TBSA. This keeps blood replacement, fluid
administration, and anesthetic needs to levels that can
be addressed by the operating room team in a timely
fashion. Tangential debridement involves cutting the
skin tissue at the depth of the dermal and subcuta-
neous capillary network. Because of the local inflamma-
tory response in the burn, these capillaries are usually
well dilated by the time of excision. After excision, blood
loss can be torrential, and it is difficult to imagine such
extensive hemorrhage until one participates in such a
procedure. Clinical studies estimate that tangential
debridement of each square centimeter of burn causes
1 mL of blood loss. Thus, in an adult, excision of each
1% TBSA of burn averages lOOmL of bleeding.
Debridement of a 20% TBSA burn results in 2000 mL
or 4 units of whole blood loss. Tourniquet use on
extremities, pressure dressings, electrocautery, hemo-
static agents, avoidance of agents that interfere with
the coagulation, and subcutaneous injection of the burn
with dilute epinephrine all limit blood loss but not
completely. Full-thickness excision of the burn to the
level of muscle fascia with electrocautery limits blood
loss. The loss of such a significant amount of soft tissue
requires skin grafts on muscle fascia and has poor func-
tional and cosmetic results. The best method to control
blood loss is to 1 imit each debridement session to about
10% to 20% TBSA. The patient and the anesthesiolo-
gist better tolerate this amount of blood loss.
Timely coverage of the debrided wounds depends
on available sources of autologous skin. Autologous
split-thickness skin grafts are the "gold standard" for
burn wounds if enough donor sites are available.
Wounds are debrided and covered with skin grafts in
one procedure if blood loss is acceptable. In large area
burns, the patient may undergo skin grafting a few days
after debridement to allow time for the debrided
wounds to stop bleeding and for the patient to recover
from the blood loss. Harvesting of skin grafts, although
less bloody than tangential debridement of the burn,
still results in significant blood loss. Between the time
of excision and the skin grafting procedure, the
wounds are covered with a biologic dressing (pig or
cadaver skin) or a topical wound dressing. Should the
patient need several debridement sessions to remove
all of the burns, debridement can be alternated with
grafting sessions to achieve staged coverage of each
debrided area before going on to the next burned area.
This strategy delays the complete removal of all
burned tissue, leading to some increased risk of burn
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
29 • BURN AND ELECTRICAL INJURY 823
wound infection. An alternative method is to dedicate
the early sessions to debridement of the burns and cov-
erage with a biologic dressing. When all wounds are
debrided, skin grafting is performed. This method
results in the most rapid removal of all necrotic tissue.
With burn wounds of more than 50% TBSA, there are
inadequate donor sites; alternating debridement with
grafting affords time for the donor sites to re-epithe-
lialize before they are harvested again. Donor sites har-
vested a second time can heal slowly, but the alternatives
are limited in these patients with large burns. The use
of cultured autologous epidermis for patients with
more than 50% TBSA burns has helped because it is
a ready and abundant source of autologous epithe-
lium for patients with limited donor sites.18,19
A logical algorithm should be used in skin grafting
of patients with large surface area burns. Most impor-
tant for survival of the patient is to decrease the surface
area of the injury, so in the absence of other restric-
tions, the largest area of burn should be excised and
grafted first, such as the trunk, then the lower extrem-
ity, followed by the upper extremity. Burns to the hands,
neck, and face warrant special consideration, however.
To prevent excessive functional impairment to these
areas after the burn wounds are healed, these areas
should be grafted earlier rather than later. In full-
thickness burns to the hands, neck, and face, delay in
grafting can result in excess scarring and functional
limitations that are difficult to overcome. The scarring
can make the rehabilitation of the patient very prob-
lematic. Thus, deep burns to these areas should be
grafted early so that range of motion and hypertrophic
scar management can be started early.
Wound Coverage
BIOLOGIC DRESSINGS
Biologic dressings have the advantage of being rela-
tively abundant and inexpensive, and they act tem-
porarily like skin. Many biologic dressings have been
sold, and new ones are introduced frequently. Successful
marketing of the product depends largely on the quality
of the sales force behind the product as much as on
any scientific merit. However, the ones that survive the
financial marketplace usually have some advantage
(Table 29-6). This section summarizes some of the com-
monly used materials.
The most widely used biologic dressing remains
fresh or frozen human cadaveric split-thickness skin
both in the United States and throughout the world.
Properly handled, cadaveric skin remains viable and
revascularizes ("takes") when it is placed on a healthy
wound bed. The dermal capillaries of the graft fill with
blood and then develop nutrient flow 2 to 5 days after
grafting by inosculation (Fig. 29-8), just like autolo-
gous split-thickness grafts. The cadaveric skin func-
tions very much like autologous grafts, decreasing fluid
824 I • GENERAL PRINCIPLES

FIGURE 2 9 - 8 . Skin grafts revascularize by

inosculation of recipient vessels to capillaries in the
graft.

loss, lowering local pathogen growth, and decreasing
painful stimuli during dressing changes. The need for
frequent dressing changes decreases, and the overall
effect on the patient's hyperdynamic state is beneficial.
However, just as Medawar described in his Nobel Prize-
winning studies in the 1940s, cadaveric skin under-
goes first-set rejection 1 to 2 weeks after grafting. The
immunosuppression found in massively burned
patients may delay the rejection process some, but even-
tually the grafts develop an abundant inflammatory
cell infiltrate and the epidermis dies and sloughs from
the patient. Loss of the epidermis requires replacement
with another set of cadaveric grafts, or, it is hoped, the
patient is ready for coverage with permanent autolo-
gous tissue. Disease transmission from the donor
to the burn patient remains a theoretical concern.

TABLE 2 9 - 6 • PRODUCTS AVAILABLE AS BIOLOGIC DRESSINGS

Name Material Advantages Disadvantages

Porcine skin Split-thickness pig skin Inexpensive, readily available Does not revascularize
Cadaveric Split-thickness human skin Vascularizes, inexpensive, Occasional shortages
skin antimicrobial activity
Biobrane Collagen-coated netting Readily available, works well Expensive, not for deep burns
in superficial burns
TransCyte Human fibroblast in collagen Live cells Expensive, limited clinical experience
matrix
Integra Bovine collagen and shark Readily available Expensive, vascularizes slowly, no
chondroitin sulfate matrix antimicrobial activity
AlloDerm Acellular human dermis Readily available Expensive, vascularizes slowly, no
epithelial barrier, no antimicrobial
activity

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.

Interestingly, all burn surgeons have observed over
the years that the dermis of the cadaveric graft fre-
quently remains attached to the wound bed and is
eventually incorporated into the wound (see "Dermal
Replacements").
Pig skin and freeze-dried human cadaveric skin do
not have the same properties as fresh or properly pre-
served frozen cadaveric skin. These other skin substi-
tutes do not revascularize and therefore easily detach
from the wound bed during dressing changes. Whether
these materials decrease fluid loss or have antimicro-
bial effects is debated.
Synthetic materials are often used but have other
limitations. Biobrane,TransCyte,Xeroform gauze, and
many other dressing materials can be used to cover the
wounds. If it is applied correctly, the material usually
adheres to the wound bed. Left undisturbed, the dress-
ing limits fluid loss and prevents stimulation of the
wound. Epidermal regeneration is undisturbed
beneath. The dressing falls off once the epithelial layer
completely heals underneath, much like a scab falls off
an open wound once it is healed. These materials work
best on superficial second-degree burn wounds and
skin graft donor sites that heal in 7 to 10 days. Placed
on deeper wounds, the materials adhere poorly and as
foreign material serve as a nidus for infection much
like the burn eschar. These materials have no antimi-
crobial activity and therefore should not be placed on
a contaminated wound. Most of the newly developed
synthetic biologic dressings are used mainly in devel-
oped countries because most of these products are
extremely expensive.
PERMANENT COVERAGE
Autologous split-thickness skin grafts remain the best
material for definitive coverage of the wound, but the
source is limited in patients with large surface area
burns. When available, the extremities, minus the hands
and feet, are the best areas for harvesting of skin grafts.
The trunk is used next, but obtaining the grafts is tech-
nically more challenging because of contour irregu-
larities. The scalp is a great but often underused donor
site. The scalp skin is thick and re-epithelializes rapidly
owing to the density of hair follicles. Regrowth of the
hair is rarely a problem; thus, the donor site is well
camouflaged after healing. Repeated harvesting of skin
graft donor sites multiple times increases the amount
of skin available, but the donor site must heal between
harvest procedures, and these areas typically bleed more
on the second harvest. Most important, the site has
limited potential for recovery as more and more of the
dermis and hair follicles are taken for the graft. Even-
tually, the donor site becomes a full-thickness wound
itself.
The ability to grow and expand human ker-
atinocytes in tissue culture was a major advance in
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Dr.Mustafa D.
29 • BURN AND ELECTRICAL INJURY 825
wound treatment. No longer was an epidermal source
a major limitation for restoration of the epithelial
barrier. In a landmark case in 1984, twin children with
burns over almost their entire bodies were treated with
cultured keratinocytes taken from a small biopsy spec-
imen of undamaged axillary skin. During the course
of their treatment, the keratinocytes were successfully
expanded in tissue culture and used to resurface some
of their wounds. Survival of the patients was directly
attributed to the use of the technique. Now several
major burn centers have laboratory facilities to culture
keratinocytes. Several biotechnology companies offer
the service for a fee. Skin biopsy specimens sent to the
company are expanded in culture and returned to the
patient, usually in 2 to 3 weeks. The sheets of cultured
epidermal autograft (CEA) are placed directly onto a
cleanly d^brided wound bed. The grafts survive well,
and wounds close much faster than without treatment
(Fig. 29-9).
Despite its many advantages, CEA does not address
all of the wound problems facing massively burned
patients. Unlike split-thickness skin, the epithelial cul-
tures contain no dermal matrix tissue (Fig. 29-10). Typ-
ically, the CEA is placed on debrided full-thickness
burns that lack any dermal elements. Because the
dermis provides the elastic quality of the skin, healed
wounds that lack dermis have little give and are stiff.
Covered by CEA, areas around joints and over muscles,
such as the face, have little motion and poor function.
The dermis also provides the foundation for the for-
mation of the basement membrane between the epi-
dermis and dermis. CEA placed directly on muscle or
subcutaneous tissue only gradually forms a basement
membrane, in some cases during 6 months. The base-
ment membrane serves an important attachment func-
tion, and epidermis lacking a well-formed basement
membrane blisters and shears easily. Reopening of a
healed wound is common after application of CEA.
Growth of CEA is slow and expensive. A biopsy spec-
imen must be obtained from the patient, and growth
of the CEA takes several weeks. Several centers have
used cultured epidermal allograft to treat burn wounds
with varying success. Because the donor keratinocytes
are taken from discarded neonatal foreskins from cir-
cumcisions, cultured epidermal allografts can be avail-
able at any time and are much less expensive to produce.
However, the engrafted cells undergo rejection just as
cadaveric skin grafts do. The cells work best as tem-
porary coverage in partial-thickness wounds where a
supply of autologous keratinocytes is available to
replace the allografts after rejection.
Dermal Replacements
Dermal replacements offer better functional results
once they are incorporated in the wound, but engraft-
ment rates have been a problem. Replacement of lost
dermis in deep second-degree or third-degree burns
image..

826 • GENERAL PRINCIPLES

FIGURE 2 9 - 9 . Patient treated with patches of

CEA and split-thickness skin grafts.

during the initial treatment of the wound with these
materials may decrease the need for later reconstruc-
tive surgery. These dermal replacements may prevent
the extensive scarring and associated poor skin elas-
ticity often seen in burns covered with thin skin grafts.
Despite the technical problems with these materials,
the advantage of preventing functional and cosmetic
deformities from scar contractures makes their use
worthwhile in many clinical situations.
The first product available on the market for
dermal matrix was Integra, The matrix is composed
of undenatured bovine collagen and sharkchondroitin
sulfate, a proteoglycan. A thin Silastic sheet, to serve
as a barrier to the air, covers the surface. When it is
placed on a wound, the material is incorporated and
serves as a scaffold for infiltration and growth of fibro-
blasts and capillaries. Engraftment of the material takes
approximately 2 weeks, and any disturbance, such as
excessive movement, fluid accumulation under the
material, or infection, causes loss of the material. Once
the matrix is incorporated, the Silastic membrane is
removed, and the material is covered by epidermis (Fig.
29-11). CEA placed on Integra does not survive, and
no one seems to know the explanation. After the Silas-
tic is removed, the manufacturer recommends use of
a thin split-thickness skin graft to cover the wound to
establish the epidermis. An obvious disadvantage of
this method is the long time from excision of the burn

'
• -
:
-: ' - - . 7

A B
FIGURE 29-1 0. Photomicrograph of CEA (A) and split-thickness skin (B) at the same magnification.

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
image...
FIGURE 2 9 - 1 1 . A, The patient's burn wounds newly excised to fascia were covered with Integra and then with thin
split-thickness skin grafts 3 weeks later. B, Final results 1 year after surgery.
wound to final epithelial coverage. When multiple areas
need skin grafting, this delay may be no more than
waiting for donor sites to re-epithelialize. In addition,
use of only thin split-thickness skin reduces donor site
problems and hastens donor site healing. So far, no
one has demonstrated a survival advantage with the
use of Integra, but many clinicians believe that its use
on extensive full-thickness wounds definitely improves
the final functional results.
AlloDerm is the other commercially available
dermal replacement made from freeze-dried human
dermis obtained from cadaveric split-thickness skin.
Cadaveric dermis was originally used as a research tool
for studying skin in tissue culture; its use in burn
patients resulted from studies done in the late 1980s
by Charles Cuono. He left viable cadaveric skin grafts
on the burn wounds and mechanically stripped the
epidermis off with a microdermabrasion wheel. He
covered the denuded but vascularized dermis with CEA.
The cadaveric dermis was not rejected and became
incorporated into the resultant skin. This technique
produced excellent functional and cosmetic results in
these difficult wounds. 20 In an effort to simplify this
technique and to make it commercially available, the
cells in the cadaveric skin grafts were eliminated, and
the dermal matrix was freeze dried. This product can
be stored on the shelf and is ready for immediate use.
As with Integra, however, the engraftment process for
the matrix is variable, and the matrix does not support
the attachment of CEA well. The main difference
between AlloDerm and the technique originally used
by Cuono is the absence of mesenchymal cells in the
acellular AlloDerm.21 The rapidity of the engraftment
process is likely to depend on the vascularity of the
matrix material as much as the wound bed on which
it is placed. AlloDerm placed over the wound and
covered with a split-thickness skin graft acts as an extra-
cellular dermal matrix. The matrix is incorporated into
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Dr.Mustafa D.
29 • BURN AND ELECTRICAL INJURY 827
the final thickness of the skin. Studies on the long-
term results of wounds treated with AlloDerm are under
way,
To date, most burn centers, including the author's,
do not use dermal replacements for extensive cover-
age of acute burns because of the unpredictable
engraftment rate. Large clinical trials have not demon-
strated a survival advantage with use of any of these
products or presented data to suggest that postinjury
function is improved. Therefore, most surgeons use
dermal replacements for burn scar reconstruction when
supplemental dermis improves functional and cosmetic
outcomes of the grafting procedure and survival of the
patient is not an issue.
REHABILITATION
Rehabilitation of the burn patient starts immediately
after injury. Anticipation and treatment of problems
resulting from the injury and edema prevent many sub-
sequent complications. The rehabilitation therapist
(occupational and physical) evaluates and formulates
a treatment plan and begins functional range of
motion, splinting, edema control, and scar modula-
tion as needed. Hands are a primary concern, espe-
cially deep burns of the dorsal surface. They receive
immediate range of motion and splinting. Although
survival takes precedence in the critically ill patient,
physical and occupational therapy objectives are always
kept in mind. Irrespective of the patient's general con-
dition, injured upper and lower extremities are ele-
vated to allow adequate venous drainage and to reduce
edema. Much of the functional limitations to burned
areas depend on the outcome of skin grafts, the local
tissue healing factors, and the baseline state of the
patient. Nonetheless, the quality and availability of ther-
apists, especially in burn injuries of the upper extrem-
ities, have been shown to influence the outcomes of
828 I • GENERAL PRINCIPLES
surgical interventions. In some circumstances, treat-
ment by good therapists decreases the need for surgi-
cal treatment. Early and proper splinting and stretching
of flexion crease burns, such as the neck, axilla, and
antecubital areas, reduce the extent of scar contrac-
tures and may prevent subsequent functional defor-
mities and the need for reconstruction.
During the recovery phase of the burn injury, reha-
bilitation therapy is even more important, often occu-
pying the majority of the patient's treatment time.
Limitations to activities of daily living, strengthening
and increasing of muscle mass, and even cosmetic
results of burn scars are under the influence of the ther-
apist. The therapists provide pressure garments, ther-
moplastic splints, serial casting, silicone inserts, and
plastic facemasks to decrease hypertrophic scars and
joint contractures.
Pain Control
Severe pain with burns is a major physiologic stress
that can have a negative impact on the patients recov-
ery. A person with burns has exposed functioning nerve
endings. Dressing changes and bedside debridement
often require high doses of opiates and sedatives. The
availability of reversal agents for benzodiazepines
has improved the safety of combining these drugs
with opiates. Close monitoring of respiratory status is
required when consciousness is diminished. Short-
acting agents such as barbiturates (Brevital) and lipid-
solublc agents (Propofol) also require careful
monitoring with use. Ketamine, combined with a seda-
tive like midazolam (Versed), provides pain control
with little respiratory depression.
More emphasis on pain control not only helps the
patient's psychological well-being but may significantly
affect physical outcome as well. Some clinical evidence
and common sense suggest that adequate analgesia may
limit the overall hypermetabolic and catabolic state.
Painful stimuli influence the release of a number of
circulatory factors that affect tissue perfusion, immune
system function, and wound healing. Further research
should help delineate the negative or positive effect of
modulating pain.
Patients without a substance abuse problem before
the injury typically do not develop opiate addiction
even after receiving high doses for prolonged periods,
but physical dependence often occurs after sustained
treatment with opiates. Gradually reducing the doses
of opiates as pain diminishes avoids opiate withdrawal.
Patients with a history of substance abuse present
special problems. Heroin users require much larger
doses of opiates to achieve the same analgesic effects.
Methadone can be used for long-acting pain relief and
to prevent opiate withdrawal. Alcoholic patients risk
alcohol withdrawal and delirium tremens. Benzodi-
azepines prevent discomfort and the potential for
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
progression to life-threatening delirium tremens and
seizure. Skillful pain management can contribute
greatly to wound healing and rehabilitation efforts and
should be given a high priority in the comprehensive
treatment of the burn patient.
COMPLICATIONS
Infection
Patients with large surface area burns are immuno-
suppressed and at increased risk for infections, espe-
cially of the wounds, venous access sites, and lungs.
Small injuries (<10% TBSA) heal rapidly, and infec-
tions are rare. Monitoring at-risk patients for infec-
tion can be a problem because many burn patients have
a fever and altered white blood cell counts without
infections. Injudicious use of antibiotics merely elim-
inates the patient's normal flora and allows resistant
organisms to grow; therefore, prophylactic antibiotics
are rarely used. However, these patients are often fragile,
and delayed treatment of real infections risks severe
episodes of sepsis leading to multisystem organ failure.
Treatment is often initiated empirically before a
specific organism is isolated. Patients with large enough
wounds and with enough time ultimately develop
life-threatening infections that must be treated. Un-
fortunately, treatment of one organism often leads
to colonization by resistant organisms and additional
infections. Bacteria, - such as staphylococci and
pseudomonas, resistant to many antibiotics and fungus
are pathogens commonly found in burn patients late
in the course of treatment. These organisms are more
difficult and risky to treat. Waiting until there is good
clinical evidence of an infection before initiating treat-
ment may delay the infection by resistant organisms.
The majority of burn patients have a low-grade fever
but no source of infection in the first week after injury.
Contamination and then overgrowth of burn wounds
by pathogens causing a systemic picture of sepsis typ-
ically occur 2 to 3 weeks after injury. Early debride-
ment of the necrotic burn tissue and coverage with
skin greatly reduce the incidence and morbidity of burn
wound infections. Patients with large surface area burns
that remain open for long periods still develop wound
infections, have poor healing, and ultimately succumb
to infection. Isolation of the patient in specialized unit
beds along with infection precautions by the health
care workers (handwashing, gloves, and gowns) reduces
the transmission of pathogens from one patient to
another but does not protect patients from their own
pathogens (skin and gastrointestinal tract). A high level
of suspicion for wound infection must be kept when
the patient's condition deteriorates rapidly. Daily
observation of the wounds by trained personnel is crit-
ical even after permanent skin grafts are placed.
Wound cultures, particularly quantitative assessment,
 image...
and biopsies for histologic examination help confirm
the diagnosis and direct therapy. Prompt excision of
infected and necrotic tissue, appropriate topical treat-
ment, and systemic antimicrobial therapy are critical
to survival of the patient.
Because the burn wound is rarely infected initially,
prophylactic use of antibiotics for burns of any size
only selects for more pathogenic organisms to colo-
nize the wound. Rarely, cellulitis of the burn occurs
within a few days of injury, and streptococcal infec-
tion should be suspected and the infection treated with
penicillin. During surgical debridement of the wound,
perioperative antibiotics (such as a first-generation
cephalosporin) to cover common skin pathogens are
administered to treat the transient bacteremia caused
by the excision.
Patients with cutaneous burns have a high incidence
of pulmonary infection even without lung injury from
smoke inhalation. The skin injury increases intersti-
tial fluid in the lung, and the lung is at risk from
pathogens in the blood and the respiratory tree. Chest
radiographic changes, purulent sputum production,
and microbiologic results help determine when and
what to treat. Patients are at risk for pulmonary infec-
tion until the burn wounds are covered. Evidence of a
pulmonary infection should be treated aggressively
with pulmonary toilet and broad-spectrum antibiotics.
A more narrow spectrum antibiotic can be selected
after sputum or pulmonary lavage culture results are
obtained. Mechanical ventilation support may be
needed in cases of severe pulmonary compromise to
augment gas exchange and to decrease the labor of res-
piration for the patient. On occasion, patients develop
adult respiratory distress syndrome marked by wors-
ening hypoxemia, hypercapnia, and lung compliance.
Supportive treatment with supplemental oxygen, pos-
itive end-expiratory pressure, and high-frequency
ventilation is effective in most patients. High-dose
steroids have been used in cases of refractory pul-
monary failure but have not been shown to be effec-
tive. Many patients intubated for more than a month
benefit from a tracheostomy. The use of low-pressure
balloons in modern endotracheal tubes has markedly
decreased the incidence of tracheal erosion and life-
threatening trachea-innominate artery fistulas. Tra-
cheostomies are still useful so patients can be gradually
and safely weaned from prolonged dependence on
mechanical ventilation and to decrease injury to vocal
cords.
Patients with large surface area burns require
venous access for much of their hospitalization for
administration of fluids, antimicrobials, and pain med-
ication and sometimes for arterial pressure monitor-
ing. Peripheral lines are used initially whenever sites
are available. These indwelling catheters can become
seeded with blood-borne pathogens or through the
skin puncture site. The diagnosis is suspected when
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
29 • BURN AND ELECTRICAL INJURY 829
the patient develops fever, leukocytosis, or thrombo-
cytopenia or when organisms are grown from blood
cultures. Septic thrombophlebitis should be suspected
in all burn patients with unexplained infections, and
all sites of prior catheter access are carefully inspected.
Many of these patients require central venous lines at
some point in their treatment because peripheral access
sites are usually limited. Central line-related infections
can cause major morbidity, and constant attention is
given to changing catheters once a line infection is
suspected.
Great emphasis is placed on the isolation and
protection of burn patients from environmental
pathogens. It is worthwhile to place these patients in
protective isolation to limit contact with hospital-based
pathogens, such as multidrug-resistant organisms.
Despite these precautions, most severely injured
patients have one or several bouts of infection through
the course of their treatment. The skin and gut of the
patient harbor pathogens, and no known therapy can
eliminate these sources of infection for long. The best
treatment is to bolster the immune system and re-
establish the barrier function of the gut and skin.
Suspected or proven infections warrant treatment with
systemic antimicrobial medications. Treatment with
an antibiotic usually controls the infections but alters
the patient's microbial flora. Should the patient remain
at risk for infections after the first infection is treated,
a second, more drug resistant infection often occurs.
Should the burn be large enough that the patient
remains at risk for a month or longer, fungal infec-
tions become a serious threat. Treatment with less toxic
fluconazole has greatly increased the therapeutic
options, but many patients still eventually require
amphotericin.
Gastrointestinal Ulcers
Gastrointestinal ulcers, as a result of mucosal ischemia
from the burn injury, were common enough to have
the eponym of Curling's ulcers. Endoscopic examina-
tion of patients with burns of more than 40% TBSA
revealed a large number with mucosal ulcerations. 22
Some lesions were seen as early as 12 hours after injury.
Recognition of the problem and treatment with
prophylactic antacids, H 2 blockers, and early enteral
feedings have greatly decreased the incidence of this
devastating problem. Aggressive nutritional support
has probably helped with ulcer healing and also pre-
vents acalculous cholecystitis.
Heterotopic Ossification
Heterotopic ossification typically occurs in the joints
under the burn injury. Calcium deposition in the soft
tissue around the joints leads to restriction of motion,
pain, and occasionally skin breakdown. Calcium
image..
830 I • CENERAL PRINCIPLES
deposition around the elbow is particularly common
and troublesome. Excision of the deposits, release of the
entrapped ulnar nerve, and closure of soft tissue defects
are done to address these problems. Radiation therapy
has been used to treat ectopic bone formation, espe-
cially when there is loss of motion in the affected joint. 23
Hypertrophic Scar
Hypertrophicscar formation after burn wound healing
is a major problem. Hypertrophic scarring, unstable
epithelium, and poor skin elasticity often occur when
deep wounds are allowed to heal without grafting. Deep
wounds, treated conservatively, tend to develop prob-
lems more frequently than superficial wounds because
the extended period of inflammation elicits a fibrotic
response. Early skin grafting of these deep wounds
shortens the period of healing and inflammation and
avoids some of the later problems of hypertrophic
scarring.
RECONSTRUCTION
Reconstruction of burn scars remains one of the most
challenging aspects of reconstructive plastic surgery.
The debilitating functional problems, cosmetic
A>*
SW K
. ;f,
FIGURE 29-1 2. Patient with hypertrophic burn scars (A) and after treatment three separate times with serial exci-
sion of the scars and primary closure (B).
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
deformities, and frequent lack of autologous tissue to
replace"like with like"demand that therapeutic efforts
be well planned and executed. Haphazard recon-
struction results in improper or inadequate correction
of some problems while more important issues are neg-
lected. Plans for reconstruction begin as soon as the
extent of the injury is determined. Efforts to heal
wounds by either local wound care or excision and
grafting should take into account the ultimate func-
tional and cosmetic effect of the therapy.
Burns of less functionally important areas, such as
the trunk and non-flexion crease parts of the extrem-
ities, require basic wound closure. Even these areas can
often develop debilitating hypertrophic scarring,
unstable epithelium, and pigmentation changes. The
best reconstruction of hypertrophic scars involves
replacement of the burned tissue with uninjured tissue
of the same color, thickness, and texture. If adjacent
skin is available, serial excisions of the scar or tissue
expanders can be used for reconstruction (Fig. 29-12).
If no adjacent tissue is available, use of new skin grafts,
distant flaps, or dermal replacements followed by skin
grafting should be considered.
Burn injuries on the face, hands, and flexion creases
present a greater challenge and require greater atten-
tion. Poor skin quality and especially hypertrophic
B
image...
scarring lead to dramatic deformities. Inadequately
treated burns or severe burns, even with proper treat-
ment, can develop late sequelae. Claw deformities of
the hand, severe flexion crease contractures, and
myriad facial deformities are challenging to correct.
In addition to functional problems, pigmentation and
text lira I changes can lead to severe cosmetic deformity.
Reconstruction for each situation should follow a well-
planned algorithm. Preservation of function is most
important. Burn scars that threaten the airway, oral
continence, protection of the eye, and hand function
should be addressed first. Surgical intervention is often
needed before full scar maturation and softening have
occurred. Less severe problems, such as areas of unsta-
ble epithelium, pigmentation changes, and textural
irregularities, can await treatment until after the scar
matures, typically 6 to 12 months after the wound
closes.
SPECIAL INJURIES
Electrical Injury
The most sinister type of electrical injury results from
high-voltage electrical currents (typically more than
500 volts) passing through the body. The current travels
from the point of contact, through the tissue, and exits
to an electrical sink (ground). Because the current
travels deep to the skin, the extent of the injury is often
underestimated. These injuries result in major tissue
destruction, and treatment requires special expertise.
The current causes necrosis at the entry point in the
skin and along its path through the muscle, nerves,
and bone. An exit point of the current is also often
present. Before tissue necrosis becomes visible, the
physiologic damage to the patient maybe irreversible.
Myonecrosis, with severe myoglobinemia, can cause
acute renal failure if it is not adequately treated by fluid
hydration, diuretics (mannitol), and alkalinization of
the urine. Because the extent of injury cannot be
quantified as in a cutaneous burn, fluid resuscitation
is adjusted to urine output. Liberal amounts of fluid
to achieve higher levels of urine output may have an
advantage for these injuries. Soft tissue damage in the
extremities can precipitate compartment syndrome.
Electrolyte abnormalities and cardiac injury can lead
to fatal arrhythmias. All these parameters must be
addressed early in patients with suspected injury
because the true extent of injury becomes evident only
over time.
Patients must be carefully evaluated for vertebral
injuries; many victims have myotonic contractions or
fall from a height after electrocution. Special attention
should be directed to the neck because occult cervical
fractures can lead to devastating spinal cord injury.
Electrical function of the heart should be assessed by
an initial electrocardiogram and continuous cardiac
rhythm monitoring for the first 24 hours after injury.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
29 • BURN AND ELECTRICAL INJURY 831
Management of deep tissue injury is particularly
important in electrical injuries. Currents through the
scalp can cause partial- or full-thickness necrosis of
the skull and result in a complicated wound. For damage
to the outer cortex of the skull, a temporary option is
debridement and coverage with skin graft on the viable
diploic cavity. For full- thickness skull necrosis, the dead
bone can be covered by vascularized soft tissue with
adjacent scalp flaps or free tissue transfer. The necrotic
bone, if sterile, acts like a bone graft. Current through
the trunk can cause damage to the underlying lung
and abdominal viscera. The current can pass through
the abdominal wall and injure the underlying intes-
tine. Delayed perforation may result and even occur
in another location of the peritoneal cavity because
the intestines are mobile. Therefore, these injuries of
the abdomen warrant early exploration of the wound
to determine whether the peritoneal cavity has been
penetrated. If so, early exploratory celiotomy can
determine whether there is injury of the bowel.
Extremity injuries can result in compartment syn-
drome, and early evaluation with measurement of com-
partment pressures or surgical exploration is often
required. In severe injuries, nerve, bone, and vascular
injury can occur. Limb salvage and reconstruction can
be extremely difficult, and partial or complete loss of
the limb is possible.
If the current does not pass directly through the
patient's body, the nearby arc can produce enough heat
to injure the skin or to ignite clothing. This type of
injury is related solely to the heat, and treatment is no
different from that of other thermal injuries. The tem-
perature can be very high, and third-degree burns
usually result.
Tar
Hot liquid tar splatters or spills can cause severe burns.
The injuries are typically over the exposed skin of the
face and extremities and are deep second degree or
third degree. Once cooled, the tar quickly hardens and
adheres to the skin. Because it is difficult to remove
the tar rapidly and there is no pressing medical need
to do so, it is best to treat the injury as a deep burn
with appropriate fluid resuscitation or preparation
for skin grafting as needed. Organic solvents used
to remove tar may damage the tissue further, so slow
removal with application of silver sulfadiazine or
Neosporin ointment during a 24-hour period works
best. Placing the tar-covered hand in a plastic bag filled
with silver sulfadiazine overnight removes the tar nicely.
Smoke Inhalation
Injury can occur to the airway during a fire or explo-
sion and greatly complicate the cutaneous burn injury.
Thermal injury from the flame or hot gases can damage
TeWttf^elcrKf image...
832 I ••• GENERAL PRINCIPLES
FIGURE 29-1 3. Patient with smoke inhalation injury.
the upper airway (supraglottic). This results in burns
of the lips and oropharynx leading to edema and airway
obstruction. Heat rarely causes subglottic injury.
Rather, toxic substances and particulate matter in
smoke can cause inflammation of the lower airways
and lung parenchyma. The typical adult respiratory
distress syndrome picture of inhalation injury may not
be manifested as altered pulmonary gas exchange and
chest radiographic changes for several hours to days
after injury.
Patients caught in an enclosed, smoke-filled space
are at risk for inhalation injury. They may or may not
have facial burns, erythema of the mucous membranes,
and soot in the airways (Fig. 29-13). Carboxyhemo-
globin levels (carbon monoxide bound to hemoglo-
bin), by blood gas analysis, indicate a significant
exposure to fumes but are not always predictive of
inhalation injury. For instance, the amount of carbon
monoxide produced in a car engine can cause fatal
carbon monoxide poisoning without producing
enough particulate matter to cause chemical pneu-
monitis. Conversely, patients can inhale significant
smoke and have normal carboxyhemoglobin levels
because of the rapid clearance of carbon monoxide
from the blood after administration of oxygen during
transport. Direct laryngoscopy and bronchoscopy
more accurately assess airway injury but can still be
misleading. A nuclear medicine study with tech-
netium Tc 99m uptake in the lung can also be used for
diagnostic purposes.
Because there is no effective treatment of inhala-
tion injury other than supportive care, there is a real
lack of motivation to develop a truly reliable test. The
early accurate diagnosis of the condition has little
therapeutic implication. Pulmonary injury results
in sequestration of fluid in the lungs. When fluid
resuscitation for the visible cutaneous thermal injury
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Dr.Mustafa D.
far exceeds the predicted amount, inhalation injury
should be suspected. Decreasing fluid intake in these
patients may decrease extravasation of fluid in the pul-
monary parenchyma, but the need to maintain
intravascularvolume and tissue perfusion maybe more
important. In significant inhalation injury, fluid
requirements are large, pulmonary capillary leakage
is significant, and impairment of gas exchange is
inevitable. Early endotracheal intubation is important
in patients with upper airway or inhalation injury to
safeguard patency of the airway, to deliver mechani-
cal ventilatory support, and to provide aggressive pul-
monary toilet. To date, we can provide only supportive
care for pulmonary failure from inhalation injury
because no effective therapy has been identified for
prevention or treatment of the damage to the alveoli
by the inhaled toxins.
Hyperbaric oxygen treatment has been used for
acute carbon monoxide poisoning from smoke inhala-
tion. Urgent treatment of patients with neurologic signs
from carbon monoxide exposure has been advocated
to decrease sequelae from hypoxic brain injury. Its use
for patients without neurologic signs is questionable.
Hyperbaric oxygen has not been shown to diminish
lung injury from smoke inhalation. A typical hyper-
baric chamber does not allow access to the patient for
an hour or more during treatment. The safety of placing
a patient with cutaneous burns and inhalation injury
in such conditions has to be weighed against any pos-
sible beneficial effect of the treatment.
REFERENCES
1. Salisbury RE: Thermal burns. In McCarthy JM, ed: Plastic
Surgery. Philadelphia, WB Saunders, 1990:787-789.
2. American Burn Association: Burn Incidence and Treatment in
the US: 2000 Fact Sheet.Availableat: http://www.ameriburn.org/
pub/Publications.htm.
3. Saffle JR, Davis B, Williams P: Recent outcomes in the treat-
ment of burn injury in the United States: a report from the
American Burn Association Patient Registry. J Burn Care Rehabil
1995;16:219-232.
4. Neuwalder JM, Sampson C, Breuing KH, Orgill DP: A review
of computer-aided body surface area determination: SAGE II
and EPRI's 3D Burn Vision. J Burn Care Rehabil 2002;23:55-
59, discussion 54.
5. Muller MJ, Pegg SP, Rule MR: Determinants of death follow-
ing burn injury. Br J Surg 2001;88:583-587.
6. O'Kccfe GE, Hunt JL, Purdue GF: An evaluation of risk factors
for mortality after burn trauma and the identification of gender-
dependent differences in outcomes. J Am Coll Surg
2001;192:153-160.
7. Rees JM, Dimick AR: Burn unit survival strategies in changing
economic times. J Burn Care Rehabil 1994;15:189-190.
8. Guidelines for the operation of burn centers. American Burn
Association and American College of Surgeons. Bull Am Coll
Surg 1995;80:34-41.
9. Ivy ME, Possenti PP, Kepros J, et ah Abdominal compartment
syndrome in patients with burns. J Burn Care Rehabil
1999;20:351-353.
10. Corcos AC, Sherman HF: Percutaneous treatment of second-
ary abdominal compartment syndrome, f Trauma 2001 ;51: 1062-
1064.
image...
11. Rue LVV 3rd, Cioffi WG Jr: Resuscitation of thermally injured
patients. Crit Care Nurs Clin North Am 1991;3:181 -189.
12. Demling RH, Kramer GC, Gunther R, Nerlich M: Effect of non-
protein colloid on postburn edema formation in soft tissues
and lung. Surgery 1984;95:593-602.
13. Goodwin CW, Dorethy J, Lam V, Pruitt BA )r: Randomized trial
of efficacy of crystalloid and colloid resuscitation on hemody-
namic response and lung water following thermal injury. Ann
Surg 1983,197:520-531.
14. Kagan RJ, Matsuda T, Hanumadass M, et al: The effect of burn
wound size on ureagenesis and nitrogen balance. Ann Surg
1982;195:70-74.
15. Adolph M, F.ckart J: Energy requirements of surgically treated,
injured and infected patients [in German]. Infusionstherapie
1990;17:5-16.
16. Demling RH: Comparison of the anabolic effects and compli-
cations of human growth hormone and the testosterone analog,
oxandrolone, after severe burn injury. Burns 1999;25:215-221.
17. Garrison Jl, Thomas F, Cunningham P: Improved large burn
therapy with reduced mortality following an associated septic
challenge by early excision and skin allografting using donor-
specific tolerance. Transplant Proc 1995;27:1416-1418.
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Dr.Mustafa D.
29 • BURN AND ELECTRICAL INJURY 833
18. Gallico GG 3rd, O'Connor NE, Compton GC, et al: Permanent
coverage of large burn wounds with autologous cultured
human epithelium. N Engl J Med 1984;311:448-451.
19. Carsin H, Ainaud P, Le Bever H, et al: Cultured epithelial auto-
grafts in extensive burn coverage of severely traumatized
patients: a five year single-center experience with 30 patients.
Burns 2000;26:379-387.
20. Cuono CB, Langdon R, Birchall N, et al: Composite autolo-
gous-allogeneic skin replacement: development and clinical
application. Plast ReconstrSurg 1987;80:626-637.
21 Langdon RC, Cuono CB, Birchall N, et al: Reconstitution
of structure and cell function in human skin grafts derived
from cryopreserved allogeneic dermis and autologous
cultured keratinocytes. J Invest Dermatol 1988;91:478-
485.
22 McAlhany JC Jr, Czaja AJ, Cathcart RS 3rd, et al: Histochemi-
cal study of gastric mucosubstances after thermal injury: cor-
relation with endoscopic evidence of acute gastroduodenal
disease. I Trauma 1975;15:609-612.
23 Schaeffer MA, Sosncr J: Heterotopic ossification: treatment of
established bone with radiation therapy. Arch Phys Med Rehabil
1995;76:284-286.
image...
CHAPTER
30
•
Radiation Injury
STEPHAN ARIYAN, MD, MBA
HISTORY
ETIOLOGY OF RADIATION
Alpha Particles
Beta Particles
Gamma Rays
X-rays
Rad/Cray
SOURCES OF ENERGY
BIOLOGIC EFFECTS
Systemic Effects of Radiation
Local Effects of Radiation
HISTORY
Soon after Wilhelm Konrad Rontgen discovered in 1895
that a glow from a Crookes tube had the ability to expose
photographic plates, he demonstrated the new dis-
covery to the world by photographing the bones in the
hand of Rudolph Albert von Kolliker in January of 1896.
This discovery ushered in an era of modern medicine
with a diagnostic tool as well as a therapeutic modal-
ity. It was not long after this that the first cases of acute
radiation dermatitis were reported by Daniel, 1 and in
less than a decade, skin cancer from chronic exposure
of the hand of a technician was reported by Frieben.2
Wolbach,3 a Boston pathologist, then described the his-
tologic changes from chronic radiation exposure that
tempered the early enthusiasm for radiation therapy.
Nevertheless, as early as 1909, Budin4 reported two cases
of oral cancer that showed marked regression by the
application of radium.
During the next 3 decades, investigators in this
field began to understand the biologic effects and
consequences of radiation treatment. This resulted in
the improvement of the therapeutic effects by the
establishment of time-dose tables by Paterson 5 and
Parker 6 and divided-dose treatments by Coutard 7 and
Strandqvist. 8 Baclesse9 proposed that the central
portion of the tumor was more resistant to radiation
than the periphery and advocated treatment during
a period of 6 to 10 weeks. Finally, there was fairly
uniform acceptance of Parker's treatment regimen
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
Infections
Osteoradionecrosis
Malignant Transformation
Effects on Wound Healing
TREATMENT
Acute Injury
Surgery After Radiation
Late Ulceration
of radiation in daily divided doses for a period of
5 weeks.10
The further development of supervoltage machines
(to provide penetration of higher doses of radiation
to the tumor while sparing the effects to the skin) led
to the use in Europe and the United States of the com-
bination of surgery with radiation for the management
of advanced cancers.11'14 Although the advantage of
combining the two modalities has never been evalu-
ated by means of a prospective randomized trial, the
many publications on the subject have convinced most
clinicians of the ability of the combination for advanced
cancers. This was initially applied mostly to head and
neck cancers, but in subsequent years, this treatment
modality has been applied to breast cancers, colorec-
tal cancers, and gynecologic cancers. It appears to be
most rewarding in soft tissue sarcomas of extremities,
in which it has been shown that the use of the com-
bination of radiation and chemotherapy can salvage
an extremity with a more conservative surgical
resection.15,16
The various studies comparing treatments with pre-
operative and postoperative radiation have shown no
significant differences in the control rates of the
tumors,16"19 but the complication rates appear to be
greater when the radiation therapy is given before the
surgical resections. Most of these reports showed that
patients who received preoperative radiation therapy
had a higher incidence of wound separation, infections,
and fistulas. It is therefore important to understand
835
836 I • GENERAL PRINCIPLES
the effects of radiation on the suppression of wound
healing.
ETIOLOGY OF RADIATION
In contrast to other types of energy, such as visible
light or heat, that can be seen or felt, the effects of
radiation therapy are due to ionizing packets called
photons. These photons, or packets of high energy, can
penetrate tissues and cause breaks in chemical bonds.
There are several types of these photons or particles
of energy, each with different characteristics.
Alpha Particles
Alpha particles are actually helium nuclei, which are
relatively large and positively charged. Because these
particles have a large mass, none can pass through a
thin sheet of paper, and they can be stopped merely
by the density of 2 to 9 cm of air. Radium and most of
the radioactive isotopes emit alpha particles among
the various energies into the surrounding tissues.
Beta Particles
Beta particles are simply negatively charged particles
of electrons and, as such, have a small mass and travel
at a high speed. They can penetrate up to 1 cm of tissue
but are easily stopped by thin sheets of metal. Because
of this limitation of their penetration, they are often
used therapeutically in thin superficial lesions of the
skin.
Gamma Rays
Gamma rays are uncharged photons of high energy
that travel at the speed of light and have the ability to
penetrate deep layers of tissue. They are a product of
the natural decay of radioactive materials, such as
radium, and are used therapeutically for lesions in
deeper tissue.
X-rays
X-rays have properties identical to those of gamma
rays and differ only in that they are produced artificially
by the bombardment of electrons onto a tungsten
target. The x-rays that are produced can then be filtered
of their weaker energy particles with sheets of various
materials, allowing the higher energy particles then to
be directed toward the tissue targets. For all practical
purposes, gamma rays and x-rays can be thought to
be therapeutically the same.
Rad/Cray
The rad, the most common unit used to measure
therapeutic radiation, is not the energy that leaves the
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
machine but the energy that is absorbed by the tissue.
ft is therefore calculated as the energy of ionizing par-
ticle absorbed per unit mass of tissue- depending on
the type of tissue and the volume of tissue irradiated.
One rad is equivalent to 100 ergs of energy absorbed
per gram of tissue irradiated. A more recently adopted
unit of measurement is a gray (Gy), which is equal to
100 rad. The former measurement of 1 rad is currently
referred to as 1 cGy (centigray).
The concept of energy absorbed by tissue is essen-
tial to the understanding of radiation therapy and its
toleration and consequences. As an example, it is mean-
ingless simply to say that a patient who has been treated
with 6000 cGy to the floor of mouth, 4000 cGy to the
neck, and another 4000 cGy to the chest wall has
received 14,000 cGy. It would be the same as saying
that a five-room house has a temperature of 350°F
because each room is at 70°F. The volume of tissue and
the various locations must be taken into account.
SOURCES OF ENERGY
A variety of sources are available for the clinical appli-
cation of radiation therapy, ranging from naturally
occurring radioactive materials, such as radium, to
manufactured radioactive elements or isotopes, such
as cobalt 60 and iodine 125. The earliest source, radium,
is still sometimes used. However, more recently, iso-
topes such as iridium 192, iodine 125, and cesium 137
(Table 30-1) have been applied as seeds directly in
tissues or in strands of suture material sewn into or
surrounding the tumor.
Because the dose of energy falls off at a rate that is
equal to the square of the distance from the radioac-
tive source, the distance from the source of the radioac-
tive device to the tissue being treated is paramount for
the control and calculation of energy used to treat the
tissue. Brachytherapy is the term used to identify treat-
ment with a very short distance from the radioactive
source to the tissue target. In this treatment modality,
the radioactive sources may be applied either directly
into the tissue by temporary needles or permanent seeds
or adjacent to the tissue by mechanical devices or appli-
ances. The advantage of brachytherapy is that it deliv-
ers a higher dose of radiation energy to the tumor and
TABLE 30-1 • ISOTOPES USED IN
BRACHYTHERAPY
Isotope Half-life Energy
Cold 198 2.7 days 40keV
Iodine 125 60 days 2.8-3.5 keV
Iridium 192 74 days 30-40 keV
Cesium 137 30 years 66keV
Radium 1604 years 18keVto2.2meV
image...

30 • RADIATION INJURY 837

FIGURE 3 0 - 1 . A, Nylon afterloading catheters are placed in the wound after the resection of tumor before the wound
is covered with a well-vascularized flap that can tolerate the high-energy radiation. B, The iridium source is applied
through these tubes later in the patient's room.

less to the surrounding and intervening tissues, which
have a greater falloff because of the distance.
There has recendy been an interest in reintroduc-
ing brachytherapy.20,21 The most commonly used
isotope in brachytherapy has been iridium 192. This
isotope is used as a temporary implant encased in stain-
less steel needles that are placed through small nylon
tubes threaded through the tissues of the patient, who
is under general anesthesia. This method is called after-
loading technique because the iridium needles are
placed into the nylon tubes after the patients have recov-
ered from their general anesthesia and are back in their
room (Fig. 30-1), thus limiting the amount of radia-
tion exposure to all the personnel. In addition, because
the radioactive source can be removed after its thera-
peutic dose has been administered, it does not persist
with the destructive effects of continuous radiation,
as used to be seen with the application of radium seeds,
which had a half-life of 1604 years. More recently,
however, iodine 125 seeds have been embedded in
woven suture material, which is then sutured around
the tumor in various parts of the body, such as the oral
cavity or neck (Fig. 30-2). Because the half-life of this
isotope is only 60 days, these seeds can be sutured
around the tumor and left permanently. With a very
low energy level (0.028 to 0.035 meV), the penetration
extends far enough to cause therapeutic damage to the
cancer in its proximity but not far enough to cause
damage to the nearby tissues, such as the adjacent bone.
There is far less exposure to other personnel, and the
patients do not need to be placed in safety quarantine
rooms.
Teletherapy is the term applied to treatment with
radioactive material that is placed a significant distance
from the tissue target.This is the most common method
of radiation therapy by far. The devices that produce
the radioactivity vary in the amount of energy the
particles generate and hence the degree to which they
penetrate tissue. Orthovoltage machines generate the
radioactive particles with a delivery of energy less than

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Dr.Mustafa D.
838 I • GENERAL PRINCIPLES
a million volts, often in the range of 80 to 400 kilo-
electron volts (keV). Therapeutic x-ray machines are
examples of such devices. Supervottage machines
generate particles whose energy is above a million
electron volts (meV). These higher energy machines
may use a source of cobalt 60 or may generate the
radioactive particle by a particle-acceleration device,
such as the betatron, cyclotron, or linear accelerator.
BIOLOGIC EFFECTS
The total effects of radiation on tissue are not fully
understood. However, damage from ionizing radia-
tion is unlike thermal, mechanical, or chemical injury.
The effect of the ionizing particle as it enters the tissue
is to cause energy damage to structures within the
individual cells. The resultant damage to the cell is
dependent on the relative importance of the damaged
structure to the cell. In the clinical dosage range of
1,000 to 10,000 cGy, the intracellular damage essen-
tially concerns DNA. These effects on the molecular
level are "single hit" events (all or none damage) as
well as "multiple hit" events (cumulative damage).
Most of this damage can be repaired by the cell (par-
ticularly normal cells), and the enzymatic activities
may continue, but the genetic information may be
lost. If that is the case, the cell loses its ability to divide
indefinitely and dies.
The degree of clinical damage is dependent on the
tissue cell types injured. In rapidly dividing cell pop-
ulations, such as lymphocytes, these effects maybe man-
ifested within hours or days. In other tissues, such as
nerves and muscles, in which cells do not normally
reproduce, the effect might not be observed clinically
or microscopically, even though the radiation may have
destroyed the same genetic information, because the
cells usually do not replicate or are very slow to do so.
These tissues are said to be radioresistant.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
FIGURE30-2. Iodine 125 radioactive seeds embed-
ded in woven suture material can be applied to the
resected margins of the tumor bed to cover the entire
field.
These damaging effects are random events. That is
to say that the damage occurs to normal cells as well
as to tumor cells. If we conceive of treatment of a specific
tissue as a room full of balloons being bombarded by
darts, and we fill the room completely with red bal-
loons (tumor cells) and blue balloons (normal cells)
and arm ourselves with a predetermined number of
darts (therapeutic radiation safe dose limit), then we
have an appropriate analogy to radiation therapy. In
the beginning, with each 1000 darts, we are likely to
burst a balloon with each dart thrown into the room,
until we have broken 90% of them. With each subse-
quent 1000 darts, we are less successful at bursting as
many balloons because there are less balloons left in
the room. Our success is based on the chance of destroy-
ing all of the red balloons and still having some blue
balloons left after we have used up all of the limited
number of darts.
The ability of tissues to heal after the radiation injury
depends on the population of the surviving cells. After
that, the efficacy of radiation to treat tumors depends
on the lesser numbers of tumor cells and the slower
turnover rate compared with the surrounding normal
tissue. The surrounding normal cells can then repop-
ulate the area and allow healing to occur, even though
some of their population has been destroyed in the
same fashion as tumor cells, mainly because they are
more numerous and have a rapid turnover rate. If
repopulation did not occur, all therapeutic radiation
of tumors would result in open wounds as the tumors
disappeared.
Systemic Effects of Radiation
In contrast to the effects of radiation given to local
areas, radiation exposure to the whole body is more
devastating. Different tissues in the body have differ-
ent tolerance levels to the radiation (Table 30-2).22
Vemtf<SeldW image..

30 • RADIATION INJURY 839

TABLE 3 0 - 2 • LISTING OF ORGANS IN THEIR involves orthovoltage radiation. Exposure to 5,000 to

ORDER OF SENSITIVITY TO 10,000cGy in a short time will produce local changes
TOTAL BODY IRRADIATION* in the skin and soft tissues that resemble thermal
injury27 but evolve more slowly as the cells react to
Bone mat row the damage. There is itching and edema, and the
Gonads skin becomes erythematous, dry, and tender. The skin
Lungs undergoes necrotic changes within a few days or weeks.
Kidneys
Livof
The early scaling and flaking of the "dry desquama-
Sdlivar> glands tion" stage (Fig. 30-3) give way to the sloughing and
Intestines ulceration of the "wet desquamation." The underly-
Central nervous system ing tissue undergoes ischemic necrosis as a result of
Heart the progressive obliterative endarteritis of the small
Skin and medium-sized vessels.26,28 The tissue may become
secondarily infected (Fig. 30-4) by bacteria, which
"Most scnsitivf to least sensitive."
then cause further necrosis and an often unrelenting
pain.
The hematopoietic system, for example, can be pro- Subacute radiation injury caused by repeated low-
foundly injured with 100 cGy or less. Individuals who dose radiation during a short period leads to thicken-
are exposed to massive radiation, such as that gener- ing and hardening of the tissues into a woody
ated by the atomic bombs or the Chernobyl nuclear induration (Fig. 30-5). The skin becomes thinned out
reactor, develop radiation sickness. This radiation sick- with loss of the rete pegs.29 The examination of skin
ness has three phases: prodromal, latent, and main. reveals that the elastic fibers in the dermis are frag-
The prodromal phase is characterized by symptoms mented, and there is thickening of the vessel walls due
of nausea, vomiting, and diarrhea caused by injury to to deposition of collagen.30,31 The skin appears darker
the mucosa of the gastrointestinal tract. Since the epi- because of hyperpigmentation, and fibrosis of the
thelial cells of the intestines have a rapid turnover rate, dermis and subcutaneous tissue appears. Guelinckx32
these damaged tissues cause the initial symptoms of also demonstrated dehiscence of the endothelial cells,
massive radiation exposure. The dose necessary to cause fibrin deposition, and microthrombi by scanning
these symptoms may vary among individuals but is electron microscopy. Although the irradiated tissue
considered to be in the range of 50 cGy to the total body. may be abundant in the number of vessels present, the
The la ten t phase is the time that it takes for the deple- thickening and fibrosis cause more bleeding when cut
tion of cells that are irreparably damaged by radiation. because the vessels lose their normal ability to con-
This period may last hours to months, depending on tract. Furthermore, the wounds have difficulty fighting
the dose to the body and the tissues that are involved.
In the lung, for example, a single exposure to 700 cGy
causes damage, whereas an exposure of HOOcGy is
lethal.23,24 The latent phase for this manifestation of
radiation injury to the lung may be 1 to 3 months.25
The main phase is manifested as the effects of cell
depletion begin to have clinical significance on the func-
tion of the specific organs or the body as a whole. The
severity of the symptoms depends on the reserves of
immature cells remaining to repopulate the area to pre-
serve or restore function. Severe radiation damage
(20,000 cGy) to the brain or the heart may result in
death within minutes to hours. It is also estimated that
2000 cGy to the whole body will result in fatal enteri-
tis within 2 weeks.26 However, in the absence of such
damage, death from severe exposure usually results
from irreparable bone marrow or intestinal injury.
Damage to the other tissues maybe of secondary impor-
tance in such extensive radiation injuries.

Local Effects of Radiation

Acute radiation injury is usually the result of acci- FIGURE 3 0 - 3 . After radiation to the right breast, the
dental exposure, mostly industrial, and frequently skin reacts with erythema and dry scaling.

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Dr.Mustafa D.
840 I • GENERAL PRINCIPLES

2 3 * J H SFiTM.WMUtA«

FIGURE 3 0 - 5 . After completion of a full course of

%
radiation to the chest, the inflamed tissue healed with
extensive scarring and thickening of the skin.

FIGURE 3 0 - 4 . Wet desquamation of radiated field

with breakdown of skin, serous drainage, and secondary
bacterial contamination.
bacteria and healing because nutrient material and anti-
bodies cannot diffuse readily into the tissue.
Chronic radiation injury has historically occurred
as an occupational hazard among individuals exposed
to repeated low doses of radiation during long periods,
for example, among radiography technicians or den-
tists. It is now also showing up among patients many
years after therapeutic radiation for benign diseases,
such as acne (Fig. 30-6) or tonsillitis. The histologic
changes observed in tissues injured by chronic radia-
tion are the same as for acute and subacute radiation
injury but vary in the intensity and timing of their
evolution. These chronic changes may progress to the

FIGURE 3 0 - 6 . Effects of thinning of the skin many years after radiation to the midface (A) and to the lower face
(B) for acne.

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Dr.Mustafa D.

extent that the cellular changes may ultimately lead to
malignant transformation.
Infections
It has long been recognized that surgery within tissue
that has previously been irradiated is often compli-
cated by a higher incidence of wound complications.33,34
This appears to be particularly true in the head and
neck area because the saliva in the oral cavity is an
abundant reservoir of virulent bacteria with counts
ranging from 107 to 108 organisms per milliliter.35
Ketcham et al36 reported a 60% incidence of compli-
cations among patients who received even a single dose
of 1000 rad before their surgical procedures, compared
with a 10% incidence among control patients who had
not received any radiation.
The infection observed after surgery within the irra-
diated head and neck area is not so much from bacte-
rial invasion from the outside as from the inability of
the irradiated tissue to combat the local bacterial con-
tamination because of its inability to foster an appro-
priate resistance. Surgical procedures in the oral cavity
disrupt the mucous membrane and allow bacteria to
enter the open tissues. The flow of saliva offers a
mechanical defense against the bacterial flora and a
physiologic resistance to the proliferation of bacteria.
The mucous content of saliva is due to the mucin, a
glycoprotein produced by salivary glands that coats and
traps the bacteria. The salivary glands also produce
large amounts of IgA, an immunoglobulin that combats
bacteria by chemotaxis, bacteriolysis, and phagocyto-
sis. However, therapeutic doses of radiation markedly
reduce salivary flow by as much as 90% when all the
major salivary glands are within the radiation field. 37,38
Beumer et al29 have shown that it may take as long as
12 to 18 months for this salivary flow to return to
normal levels.
In a study investigating the effects of surgery within
previously irradiated tissue, Ariyan et al39 demonstrated
that irradiated tissue could not tolerate bacterial
contamination as well as normal tissue. In a study of
rats wounded at varying intervals after a single dose
of 1050cGy (the biologic equivalent of 4000cGy in
divided doses) or 1800 cGy (the biologic equivalent
of 6000 cGy in divided doses), the animals healed
without evidence of infection in 80% to 100% in each
of the groups (Fig. 30-7). However, when the wounds
were then contaminated with an inoculum of 104
Staphylococcus aureus, the animals with previous radi-
ation had infection rates as high as 67% (Fig. 30-8).
Indeed, the incidence of infection in this study
increased significantly with the increasing dose of radi-
ation as well as with the increasing interval from radi-
ation to wounding.
Many factors are believed to have contributed to
these findings, including the local response to the
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Dr.Mustafa D.
30 • RADIATION INJURY 841
bacterial proliferation as well as the systemic response
to infection. In an effort to determine whether circu-
lating antibiotics or other factors could diffuse effec-
tively into the irradiated tissues, additional studies were
undertaken by Cruz et al.40 In this study, the microbi-
ologic assays of the antibiotic levels were found to be
equal in the blood or in the skin in both the irradiated
and the nonirradiated animals at 5 weeks after irradi-
ation, whereas the levels in the skin were found to
decrease to 70% of control levels at 10 weeks and to
40% of control levels at 15 weeks, even though the blood
levels remained normal in all animals in all the groups.
This study confirmed the decreasing perfusion of cir-
culating antibiotics into the irradiated tissue coinci-
dent with the increasing fibrosis of the tissue following
intervals after the irradiation. It appears that although
there may be adequate levels of circulating antibiotics,
the fibrosis and thickening of the walls of these vessels
might not permit ready diffusion out of the vessels
and into the fibrotic tissues of an infected ulcer in an
irradiated field.
Gabka et al41 studied the increased incidence of
infection and impaired healing in irradiated tissue in
1995. The combined effect of radiation (10 to 30 Gy)
on neutrophil function included diminished phago-
cytosis, superoxide function, and Mac-1 expression.
This may provide a cellular mechanism for suscepti-
bility to infection and poor healing in irradiated tissue.
Osteoradionecrosis
Ever since the identification of complications of radi-
ation, the sequela of radiation damage to bone has been
a frustrating challenge for the radiation therapist as
well as for the surgeon. It is important for us to dif-
ferentiate radiation osteitis from osteoradionecrosis.
Radiation osteitis is a demineralization of bone as
a consequence of radiation damage to osteoblasts. This
is a radiographic diagnosis because the overlying skin
and soft tissues are intact and the bone is not exposed.
An evaluation of the bones may reveal demineraliza-
tion (Fig. 30-9), which may be caused by ischemic
necrosis of bone. However, disuse atrophy resulting
from prolonged splinting of a painful extremity may
be another cause of demineralization and must be con-
sidered in the differential diagnosis.
Osteoradionecrosis, on the other hand, is an
osteomyelitis, or infection of bone, that is already man-
ifesting tissue damage as a result of previous radia-
tion. A common site for this is the mandible, which
may have been within the radiation ports for high-
dose radiation to a tumor of the oral cavity. The radi-
ation causes significant mucositis of the lining mucosa
or a radiation dermatitis of the overlyingskin. The radi-
ation causes decreased production of saliva in the oral
cavity and a decreased production of sweat and fatty
acids by the glands of the skin, both of which are
842 • GENERAL PRINCIPLES
100
80
1-
o
40
20
Sham Controls A B A B A
Days 0-42 0 3
Organisms/Gram
• 10 3 or less
0 10 4
10 s or more
FIGURE 3 0 - 7 . Aseptic wounds made within radiated tissue heal with a low incidence of wound infection. (From
Ariyan S, Marfuggi RA, Harder G, et al: An experimental model to determine the effects of adjuvant therapy on
the incidence of postoperative wound infection. I. Evaluating preoperative radiation therapy. Plast Reconstr Surg
1980;65:328.)
essential for the natural defenses against the bacterial
flora in the mouth and on the skin. As a consequence,
the bacterial counts of the oral cavity and the skin are
high. In such an environment, if there is a break in the
skin or in the oral mucosa, the tissue has significant
difficulty in healing, and a chronic ulcer develops. If
this chronic ulcer continues to progress and deepen,
the erosion will eventually reach the bone. Whereas
the bone is usually protected by the periosteum, this
defense is also seriously weakened because of the radi-
ation. The irradiated bone is now susceptible to the
bacterial invasion (Fig. 30-10). This ulcer is the cause
and not the consequence of the infection. Once the
bone is invaded, the infection spreads readily along
the bone because of the reduced resistance of this organ,
and the extent of damage is usually far more than
the size of the ulcer would suggest. Therefore, the true
differential between radiation osteitis and osteora-
dionecrosis is the break in the skin or the lining of the
oral cavity.
In chronic wounds, the possibility of recurrent
tumor or malignant transformation of irradiated
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Dr.Mustafa D.
B A B A B A B A B
7 14 28 42 0-42
Controls
Radiation Dose
A- 1050 rad (4000 rad)
B- 1800 rad (6000 rad)
tissue must also be considered. Whereas a biopsy of
the wound may be prudent in the latter case, such biop-
sies should be performed only after careful consider-
ation in the former case, particularly in the oral cavity.
If the oral mucosa is intact in a previously heavily irra-
diated oral cavity, one should reconsider the value of
any biopsy of the mucosa for a routine follow-up exam-
ination. These areas heal slowly, and secondary bacte-
rial invasion can lead to a persistent ulcer or exposure
of the mandible with subsequent osteoradionecrosis.
Malignant Transformation
Whereas radiation therapy may cure cancers, chronic
or repeated exposure to radiation, either alone or
together with infection, has been shown to have a car-
cinogenic effect in tissues. Radiation administered to
wounds chronically infected with bacteria42,43 or chron-
ically inflamed by sterile foreign body44,45 has been
shown to lead to soft tissue sarcomas in animals.
Soon after the discovery of radium, its improper
use and handling also led to the development of
image...

30 • RADIATION INJURY 843

00 \- r-i r-i r-

Controls A B C A B C A B C A B C A B C A B C

Days 0-42 0 3 7 14 28 42

Organisms/gram Radiation dose

• 10* or less A - 630 rod (2300 rad)

B- 1050 rad (4000 rad)

10* or more C- 1800 rad (6000 rad)

FIGURE 3 0 - 8 . Infection rate increases in wounds within radiated tissue contaminated with 10 S. aureus at various
intervals after radiation. (From Ariyan S, Marfuggi RA, Harder C, et ah An experimental model to determine the effects
of adjuvant therapy on the incidence of postoperative wound infection. I. Evaluating preoperative radiation therapy.
Plast Reconstr Surg 1980:65:328.)

malignant neoplasms, as was seen in the radium watch
dial painters.46"48 These dial painters swallowed the
radium in the fluorescent paint when they dabbed
the brush tips on their tongues. The radium was
absorbed into the gastrointestinal tract and deposited
in bones. The radium in the bones emitted alpha par-
ticles, which repeatedly bombarded the mucosa of the
paranasal sinuses, eventually leading to carcinomas
many years later (Fig. 30-11) ,49 A similar mechanism
of chronic low-dose radiation was found to be the
cause of bronchogenic carcinomas in the uranium
miners of Colorado'17 and the pitchblende miners of
Europe. 50
Chronic low-dose radiation exposure, as to the
hands of dentists and fluoroscopists, may lead to
chronic radiation dermatitis. In subsequent years,
these chronic changes may lead to malignant trans-
formation, most commonly epidermoid carcinomas
(Fig. 30-12). Short-term heavy exposure to radiation,
or acute radiation accidents that lead to burn scars,
or chronic radiation dermatitis may also lead to
malignant transformation in later years, as was seen
in those working on the early stages of atomic energy
development (Fig. 30-13). Extensive studies con-
ducted during 25 years through the joint efforts of
the Atomic Bomb Casualty Commission of the
United States and the Japanese National Institute
of Health have led to the conclusion that there is a
greater incidence of leukemia and thyroid carcinoma
among the bomb survivors.51"55 Subsequent surveys of
cohort studies among these survivors have also
demonstrated a higher incidence of salivary gland
tumors. 56
The potential for malignant transformation of the
soft tissue or bone within the field of therapeutic radi-
ation or accidental exposure is of particular concern.
However, no data substantiate the risk of this devel-
opment. Kilgore and Abbott57 emphasized that malig-
nant transformation should not be considered unless
there is documented histologic evidence of nonma-
lignancy before administration of the radiation.
Cahan et al58 further defined the four criteria that have
to be met before radiation can be considered to
have been responsible for malignant transformation
(Table 30-3).
A thorough review by Krizek and Ariyan59 of the
129 cases of osteogenic sarcoma reported in the liter-
ature by 1970 indicated that the chances of such a trans-
formation are small, for 20 cases followed the ingestion
of radium (dial painters), 35 followed radiation for

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Dr.Mustafa D.
844 I • CENERAL PRINCIPLES
FIGURE 3 0 - 9 . High-dose radiation exposure to the hand (A) in an industrial accident led to radiation damage to the
skin and demineralization (B) of the bones of the hand.
chronic inflammation (possible co-carcinogenic
effect), and another 74 followed the treatment of benign
and malignant neoplasms. The incidence of osteogenic
sarcoma in the normal population is 1 per 100,000,*°
and this rate has been decreasing during the past 30
years at a time when radiation fallout has actually been
increasing.43 Therefore, the risk of malignant trans-
formation must be small indeed compared with the
countless thousands of people exposed to or treated
by radiation every year.
TABLE 3 0 - 3 • CAHAN'S CRITERIA FOR
MALIGNANT
TRANSFORMATION
1. Histologic evidence of nonmalignancy before radiation
2. Reasonable latent period (usually more than 10 years)
3. Occurrence of malignancy within field of radiation
4. Malignancy confirmed by histology
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Effects on Wound Healing
The early investigations of the effects of radiation on
wound healing date to Pohle et al61,62 and Nathanson,63
who reported delayed healing as evidenced by gross
and histologic examination. Dobbs64 demonstrated
that whereas radiation given 1 to 3 weeks before surgery
led to a decrease in the tensile strength of wounds in
rats, radiation given 24 hours after wounding caused
no significant decrease in tensile strength. Stajic and
Milovanovic65 showed that even as long as 4 weeks
after the wounding, the tensile strength of wounds in
irradiated skin still did not approach the strength of
the control group. Archer et al66 studied the effects of
radiation on healing wounds in skin and demonstrated
that the wound's tensile strength is similar to that of
control wounds if the radiation is delayed beyond 7
days after wounding. Fusi and Ariyan67 investigated
the effects of radiation on the rate of wound con-
traction and demonstrated that the contraction of
an open wound progresses normally to healing if the
image...

30 • RADIATION INJURY 845

FIGURE 30-1 0. A, Breakdown of wound over spine after surgery in radiated tissue led to exposure and infection
of the bone. B, Breakdown of tissue overlying radiated jaw led to exposure and infection of the mandible. C, Radi-
ograph of the mandible demonstrates more extensive infection of the bone than is apparent from the skin wound.

radiation to such wounds is delayed beyond 8 days
after wounding.
TREATMENT
The early changes of the skin after radiation are
erythema and dryness. The erythema results from the
early phase of wound healing, in which the injury is
followed by an inflammatory response, increased
capillary permeability, and consequent edema of the
tissues. These changes in the skin are best treated by
bland skin moisturizers.
Patients undergoing radiation therapy to the head
and neck area often complain of the dryness in the
mouth as a result of decreased flow of serous fluid
by the salivary glands. Some mucin production may
continue, leading to a further annoyance of tenacious
mucus in the oral cavity. It is important that these
patients understand the progress of these findings so
that they can appreciate the need for frequent intake
of small amounts of fluid (water or bland juices, such
as apple juice) to keep the mucous membrane moist.
Furthermore, because the mucous membranes have
a rapid turnover rate, they are susceptible to radiation
effects. Significant mucositis and superficial ulceration
in the mouth may make it painful for the patient to
eat. Because of the abundance of mucosa and its rapid
turnover rate, the treated area will soon resurface by
re-epithelialization from adjacent normal mucosa. To
achieve this healing properly, it is essential for the
patient to maintain a high calorie intake, even if only
by means of a liquid diet (milk shakes, eggnogs).

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Dr.Mustafa D.
image..
846 I • GENERAL PRINCIPLES
FIGURE 3 0 - 1 1 . Paranasal sinus tumors in radium watch dial painter (A) with extensive destruction of the bones of
the sinuses (B) by computed tomographic scan.
If there has been an excessive amount of radiation
to the skin, either because of previous irradiation or
because of a high dose of radiation from an industrial
accident, the skin will eventually undergo necrosis and
ulcerate. The wound is unlikely to heal under this
circumstance because of the poor vascularity result-
ing from the fibrosis of the soft tissues and vessels in
the area. Quantitative bacterial counts of infected ulcers
are essential to determine the efficacy of the local treat-
ment. As discussed earlier, irradiated tissue cannot tol-
erate bacterial contamination. Because of the vasculitis
and fibrosis of the tissue, systemic antibiotics will
I L i J ' ^ i , ,
1 . '•*•
~w&^^
1
rtfMJJYiff i^^^^
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
B
provide adequate blood levels, but the antibiotics will
not diffuse well into the previously radiated tissue.
Therefore, topical antibacterials play a prominent role
in the bacterial control of these ulcers, just as in thermal
injuries.
There are several circumstances for which the plastic
surgeon is called on to treat wounds after radiation
therapy. A consultation is sometimes requested before
administration of a full course of radiation to an area
that had previously been treated with radiation. In this
instance, the consultant must anticipate complications
of wound breakdown. A pretreatment consultation is
FICURE 3 0 - 1 2 . An 80-year-old practicing
dentist developed malignant transformation of
the fingers of the nondominant hand that held
dental x-ray films in the mouths of his patient
and were exposed to radiation for much of his
career.
image...
FIGURE 3 0 - 1 3 . Extensive chronic radiation dermatitis in a worker 30 years after a "nuclear explosion" in the
laboratory during the early development of the atomic bomb (A) eventually led to malignant transformation (B) and
destruction of soft tissues and bones of the face 10 years later.
often convened because it is the best circumstance in
which to see the patient. However, more commonly,
the consultation is requested to discuss an accidental
exposure, an untoward response, or late complications.
The approach to these problems varies according to
the nature of the radiation injury and generally falls
into one of three categories: acute injury, planned pre-
operative radiation, or late ulceration.
Acute Injury
Acute radiation injury is usually a result of accidental
exposure, particularly to the hands (Figs. 30-14 and
30-15). An early diagnosis and determination of the
extent of injury are critical. The initial approach to an
injured hand should be the conservative management
of the wound and control of bacterial infection by the
application of topical antibacterial cream. The out-
standing clinical picture is unrelenting pain. The patient
usually needs hospitalization and treatment with
narcotics and sedatives.
The assistance of a radiation therapist and a radi-
ation physicist is mandatory to determine the cir-
cumstances of injury, to estimate the time of exposure,
and to determine the dose to the hands and to the
remainder of the body. Brown et al68*72 have reported
a number of series of patients with these injuries and
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30 • RADIATION INJURY 847
stressed that the conservative approach may be all that
is required with some injuries. Treatment consists of
daily cleansing of the wounds with hydrotherapy and
range-of-motion exercises and skin care.
However, in more severe exposures, the skin breaks
down in the first few weeks. The bacterial infection of
these open wounds sets in motion the cycle of further
ulceration, ischemia, necrosis, and infection. Lanzl et
al73 reported the predictability of this cycle and even
advised early amputation. However, Krizek and Ar iyan59
advocated the management of the wound infection
to gain control of the bacterial flora, then surgical
removal of the injured tissue and proper coverage with
skin grafts or flaps (depending on the degree of damage
to the tissues). For these injuries of the hands, the prin-
ciples of management should be no different from those
for any other injury. Splinting is necessary with the
metacarpophalangeal joints in flexion and the inter-
phalangeal joints in extension to maintain position.
Daily debridement in whirlpool without coverage in
these extensive injuries is completely futile. Once the
erythema disappears and the wound infection appears
to be under control, the involved tissue should be sur-
gically removed and the wound covered at the same
procedure, if possible. There is usually dramatic relief
of pain after the ischemic tissue is removed and the
wound is resurfaced.
image...

848 I • GENERAL PRINCIPLES

FIGURE 3 0 - 1 4 . A right master-handed patient who sustained an industrial radiation accident with exposure of the
hand to 19,500 cGy (A), resulting in radiation necrosis and ulceration of the skin. The wounds over the index and
middle fingers were excised and covered with split-thickness skin grafts. The patient has been observed for 15 years
with good durable healing of the grafts (B), no breakdown of additional skin sites (C), and no radiographic changes in
the bones (D).

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Dr.Mustafa D.
T^WWfcfltfW image...
*i* -
•
FIGURE 3 0 - 1 5 . A patient with an industrial radiation accident with exposure of the left hand to 250,000cCy
(A) had extensive skin and soft tissue damage with exposure of extensor tendons and poor bleeding, requiring cover-
age with a flap (B).
Surgery After Radiation
Therapeutic radiation in combination with surgical
removal of the tumor is a common approach to cancers,
particularly those of the head and neck area. The ration-
ale for combining the two treatment modalities is based
on the biology of tumor growth. The central portion
of the tumor harbors cells that are hypoxic and inac-
tive while still maintaining the malignant potential to
grow and spread. The periphery is composed of more
active dividing cells, at the edges of which are exten-
sions of strings of cells that may not be affected but
are spreading a considerable distance from the tumor.
Surgery is effective in removing the central bulk of the
tumor but may fail in eradicating the microscopic and
submicroscopic (less than 105 cells per gram of tissue)
extension in the periphery (see Chapter 35). Radia-
tion is much less effective in the hypoxic center of the
tumor but can effectively eradicate the microscopic
cells in the vicinity of the tumor's periphery.
These basic principles of tumor biology can lead to
a better understanding of cancer management.
Although no scientific data document these beliefs,
current acceptable practice postulates the following:
1. The volume and extent of tumor resection
necessary for cure are exactly the same after
radiation therapy as before.
2. Although radiation therapy may make an
"inoperable" cancer technically easier to remove,
it does not cure the cancer because of the extent
of the tumor spread.
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Dr.Mustafa D.
30 • RADIATION INJURY 849
*r
B
3. The rate of disappearance of a tumor under-
going radiation therapy has nothing to do with
the ultimate curability of the cancer; anaplastic
tumors that have a rapid turnover rate may shrink
rapidly but may also recur quickly.
The rationale for employing the radiation therapy
before the operation rather than after it is based on
the theory that the spillage of cancer cells during the
procedure is less likely to cause local recurrences if
they are altered by the radiation and cannot divide to
produce clones. Indeed, this was not found to be true
in clinical series of postoperative radiation.17"19 Radi-
ation does diminish the resistance to infection, leading
to more extensive complications if the wounds break
down or become infected. Furthermore, if the radia-
tion is given in the postoperative period, a much higher
dose and more effective course of radiation may be
administered.
Nevertheless, surgery performed in previously irra-
diated fields or surgery for recurrence or persistence
of a tumor after irradiation may result in breakdown
of the wound and infection. In these cases, the wound
should be d£brided, then dressed with topical anti-
bacterial creams that can penetrate an eschar. Once
the bacterial counts are brought to levels below 105
organisms per gram of tissue, the surgical debridement
should be completed (Fig. 30-16) and the area covered
with a well-vascularized flap.74 These vascular flaps can
then provide the nutrient material for proper healing
of the tissues, circulate the prescribed antibiotics, and
image--

850 I • GENERAL PRINCIPLES

FIGURE 3 0 - 1 6 . A laryngectomy performed after a full

course of radiation to the neck resulted in wound infection,
breakdown (A), and exposure of the carotid artery. This
was treated with debridement and coverage with a flap (B).
The pharyngostome was then reconstructed at a second-
stage procedure (C).

permit diffusion of the body's natural defenses of leuko-
cytes and antibodies to the radiation site to fight off
further bacterial invasion.
Late Ulceration
Late ulcerations of irradiated sites are associated with
subsequent injury or break in the skin and bacterial
invasion and proliferation that finally lead to tissue
necrosis. Their distribution is therefore related to the
common sites of tumors that are treated by radiation
combined with surgery. These sites are commonly the
oral cavity, chest wall, and sacrum.
Radiation ulcers that develop subsequent to the
treatment of cancers of the breast, pelvis, or colorec-
tal region are ischemic and cannot be reconstructed
with adjacent tissue that has been in the radiation treat-
ment ports. The principles of therapy are again those
of local wound care, control of infection by topical
antibacterials, resection of the ulcer bed and compro-
mised margins of the wounds, and soft tissue cover-
age (Fig. 30-17). This normally requires a cutaneous

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Dr.Mustafa D.
image...

30 • RADIATION INJURY 851

FIGURE 30-1 7. Achronic radiation ulcer of the parasacral

area after hysterectomy was treated with topical antibacterial
creams to achieve bacterial control of the wound (A). The
entire area of the radiation port was then excised (B), and
the wound was closed with flaps (C).

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Dr.Mustafa D.
852 I • GENERAL PRINCIPLES
flap or musculocutaneous flap (for instance, from glu-
teus maximus muscle or the tensor fascia lata muscle).
If bone is exposed in the wound, as the rib cage may
be a Iter radiation to the chest, the infected and necrotic
b o n e must be resected or it will continue to behave
like a sequestrum. This is also true of the costal carti-
lages that are devascularized after the extensive radi-
ation, exposure, and infection. To describe the extent
of resection required in these cases is difficult, but the
devitalized bone or cartilage must be resected until sub-
stantially viable structures are reached. In cartilage, this
is usually a moistened yellowish cartilage, rather than
a sclerotic grayish white. Most of the irradiated skin
usually needs to be resected within the treatment port,
and ihe area may be resurfaced with a muscle flap or
myoc utaneous flap (such as from the pectoralis major,
latisMinus dorsi, or rectus abdominis muscle). 75
SUMMARY
Radiation therapy has progressed from the early days
of its discovery at the turn of this century to a point
of significance in the treatment of a number of disor-
ders, both malignant and benign. Rontgen's discovery
of the x-ray in 1895 provided medicine with a diag-
nostic tool without which some specialties would not
exist and offered a therapeutic modality that has cured
or alleviated the suffering of innumerable patients.
As with any treatment modality, the significant
advances are tempered by side effects and consequences.
The effects of radiation are long-term, the consequences
are severe, and the effects on wound healing are dis-
couraging. It is important to understand the effects of
radiation energy to be able to appreciate its therapeu-
tic uses as well as to learn how to overcome its side
effects in treating the consequences.
The centennial of the discovery of radiation radioac-
tivity has now passed. During these many decades, the
benefits of radiation have been harnessed, and it is now
possible to manage complications. With a better
understanding of the radiobiology and pathophysiol-
ogy of the effects of radiation and its consequent injury
of tissues, the appropriate surgical principles to prop-
erly manage various conditions can be selected.
The future applications of radiation therapy require
technical advances necessary to control the penetra-
tion of the radioactive materials to selected tissue
depths. With safer techniques to transport and to local-
ize radioactive isotopes, the direct intraoperative appli-
cation to tumors or operative sites after the removal
of tumors may lead to improved cure rates from the
combination of these two treatment modalities.
REFERENCES
1. Daniel J: The x-rays. New Sci 1896;3:562.
2. Frieben EA: Cancroid des rechten Handruckens nach
langdauerner Einwiikung von Rontgenstrahlen. Forstschr
Roentgenstrl902;6:106.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
3. Wolbach SA: The pathological hisro|og\ of chronic x-ray
dermatitis and early x-ray carcinoma. I Med Res 1909;16:
415.
4. Butlin HT: On early diagnosis of cancer of the tongue and on
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19. Vandenbrouck C, Sancho H, LeFur R, et al: Results of a
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20. Son YH, Ariyan S: Intraoperative adjuvant radiotherapy for
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24. Van Dyk J, Keane TJ, Kan S, et al: Radiation pneumonitis fol-
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31. Watson IS: Experimental microvascular anastomoses in radi-
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38. Driezen S, Brown LR, Handler S, et al: Radiation-induced xero-
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39. Ariyan S, Marfuggi RA, Harder G, et al: An experimental model
to determine the effects of adjuvant therapy on the incidence
of postoperative wound infection. I. Evaluating preoperative
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40. Cruz NI, Ariyan S, Miniter P, et al: An experimental model to
determine the level of antibiotics in irradiated tissues. Plast
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41. Gabka CJ, Benjamin P, Mathes SJ, et al: An experimental model
to determine the effect of irradiated tissue on neutrophil func-
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42. Lacassagnc A, Vinzent R: Action des rayons X sur en foyer
infectieux local, provoque chez le lapin par l'injection de
Streptobacillus caviae. CR Soc Biol 1929; 100:247.
43. Lacassagne A, Vinzent R: Sarcomes provoques chez des lapins
par l'irradiation d'absces a Streptobacillus caviae. CR Soc Biol
1929;100:249.
44. Burrows H.Clarkson JR:The roleof inflammation in the induc-
tion of cancer by x-rays. Br J Radiol 1943; 16:381.
45. Lacassagne A: Conditions dans lesqucllcs out ete obtenus, chez
le lapin, des cancers par action des rayons X stir des foyers
inflammatoires. CR Soc Biol 1933;112:562.
46. Hoffman FL: Radium (mesothorium) necrosis. JAMA 1925;
85:961.
47. Martland HS: The occurrence of malignancy in radioactive
persons: a general review of data gathered in the study of the
radium dial painters with special reference to the occurrence
of osteogenic sarcoma and the interrelationship of certain blood
diseases. Am J Cancer 1931;15:2435.
48. Martland HS, Conlon P, Knef JP: Some unrecognized dangers
in the use and handling of radioactive substances: with special
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1925;85:1769.
49. Warren S: Radiation carcinogenesis. Bull N Y Acad Med
1970:46:131.
50. Ludcwig P, Lorenser E: Untersuchungen der Grubenluft in den
Schneebergcr Gruben auf den Gehalt an Radium emanation.
Strahlentherapie 1924; 17:428.
51. Brill AB.TomongerM.Heyssel RM: Leukemia in man follow-
ing exposure to ionizing radiation: a summary of the findings
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52. Finch SC: The study of the atom bomb survivors in Japan. Am
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30 • RADIATION INJURY 853
53. Miller RW: Delayed radiation effects in atom-bomb survivors:
major observations by the Atomic Bomb Casualty Commis-
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in man after exposure to ionizing radiation: a summary of the
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of carcinogenesis in Hiroshima and Nagasaki. Ann N Y Acad
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in atomic bombsurvivors, Hiroshima, Japan. II. Pathologic study
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five cases after x-ray therapy of breast cancer. Radiology
1970:96:593.
61. Pohle EA, Ritchie G: Studies of effect of roentgen rays on healing
of wounds: histological changes in skin wounds in rats follow-
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62. Pohle EA, Ritchie G, Wright CS: Studies of etfect of roentgen
rays on healing of wounds: behavior of skin wounds in rats in
pre- or postoperative irradiation. Radiology 193l;16:445.
63. Nathanson IT: Effect of gamma-ray of radium on wound healing.
Surg Gynecol Obstet 1934;59:62.
64. Dobbs WGH: A statistical study of the effect of roentgen rays
on wound healing. Am J Roentgenol 1939;41:625.
65. Stajic J, Milovanovic A: Radiation and wound healing: evolu-
tion of tensile strength in excised skin wound of irradiated rats.
Strahlentherapie 1970; 139:87.
66. Archer RR, Greenwel EJ, Ware T: Irradiation effect on wound
healing in rats. Radiat Res 1970;41:104.
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contraction. Surg Forum 1983;34:620.
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vocational and atomic exposures: treatment and surgical pre-
vention of chronic lesions. Ann Surg 1949; 130:593.
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group of atomic radiation injuries. Surg Gynecol Obstet
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and neck: seventeen-year follow-up of atomic burns. Ann Surg
1965:162:426.
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Reconstr Surg 1986;77:50.
image...
CHAPTER
31 •
Cold Injuries
Ross I. S. ZBAR, MD, FACS •
MECHANISMS OF HEAT LOSS
TEMPERATURE REGULATION
RISK FACTORS
Increased Heat Loss
Decreased Heat Delivery or Production
HYPOTHERMIA
Symptoms
Treatment
Cold injury occurs when the body is unable to protect
itself adequately from the environment. In the past,
cold injuries were mainly a concern of the military.
Hannibal, on crossing the Alps into Italy in 218 Be,
lost more than half his army and nearly all of his
elephants to the cold. In 1812, Napoleon's troops suf-
fered massive casualties during the winter invasion of
Russia.1 Nearly 130 years later, the German Army made
a similar blunder on the Russian front, resulting in
15,000 cold-related amputations.2 However, at the dawn
of the 21st century, cold injury is no longer a concern
of just the military. Homelessness has raised the specter
of cold injury in the civilian population. In the United
States, nearly 1000 people die each year of cold expo-
sure.3 In addition, with the rise of extreme sports, cold
injury is now more common in the athlete than in the
soldier. In 1996, cold injury was responsible for an
incredibly tragic mountaineering accident on Mount
Everest that claimed the lives of eight experienced
climbers.4
A localized soft tissue injury secondary to freezing
of tissue is known as frostbite. A systemic lowering of
body temperature resulting from cold exposure is
known as hypothermia.
MECHANISMS OF HEAT LOSS
To understand the pathophysiologic process of cold
injury, the multiple mechanisms that cause heat loss
in the human body must be discussed (Fig. 31-1). Fur-
thermore, once these mechanisms of heat loss are
understood, preventive measures can be devised.
In the nude human body, approximately 60% of
heat loss occurs through direct radiation. Radiation is
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
JOHN W. CANADY, MD, MS, FACS, FAAP
FROSTBITE
Degrees of Injury
Pathophysiology
Symptoms
Treatment
ALTITUDE SICKNESS
the transfer of body heat through infrared energy. This
is emanated body heat. If the surrounding environ-
ment is cooler than the body, there is a net loss of heat
as it radiates from the body to the environment. The
head is the largest source for this heat loss by radia-
tion. Prevention includes insulating clothing that
reflects radiated body heat back to the individual.
Evaporation and respiration account for roughly
25% of nude body heat loss. Evaporation involves the
direct absorption of body heat by secreted water from
sweat glands. For each gram of water that evaporates,
0.58 kcal of heat is lost. In addition, during respira-
tion, water secreted from respiratory mucosa absorbs
body heat. In humans at rest, this loss of body
heat through the skin (evaporation) and lungs (respi-
ration) occurs insensibly at a rate of approximately
600 mL/day. This causes a continual heat loss of 12 to
16 kcal/hr. Humans increase their heat loss by sweat-
ing, thereby increasing evaporation and regulating the
core body temperature. Dogs, on the other hand, lose
excess body heat through respiration by panting. It can
be seen how tracheotomy in patients actually increases
the amount of heat loss as a greater volume of air
containing warmed moisture escapes the respiratory
system.
Conduction involves the transfer of heat through
direct contact with another object that is colder. When
a nude body is standing at room temperature, only 3%
of heat loss occurs by this manner.5 However, water is
a more efficient conductor of heat than is air, meaning
that water transfers heat more efficiently from an object
than does air at the same temperature. Therefore, given
the same temperature in the absence of current, com-
plete submersion in water results in more rapid heat
855
856 I • GENERAL PRINCIPLES
Radiation
Evaporation
^;i
Radiation , / / ~"x
*«. •» \ ' y I
^^-^;> * - * I /1 -'\-'
I -'">-- Evaporation
t H Conduction
loss than in air. Increased atmospheric humidity thus
increases heat loss by increasing the efficiency of con-
duction. Wet clothes increase the efficiency of con-
duction and thus increase heat loss from a body.
The transfer of heat by movement of current is
known as convection, which can significantly increase
heat loss in a liquid or gas medium. Whereas exposure
to wet clothing with rapid air current (gas convection)
may increase heat loss by 5-fold, immersion m moving
water (liquid convection) may increase heat loss by
25-fold.6'7 Wind chill index predicts the heat transfer
rate from nude body parts in various combinations of
ambient air temperature and air current speed. In fact,
as skin surface temperature falls from -4.8°C to -7.8°C
(23.4°F to 18.0°F), the risk of frostbite increases from
5% to 95% in people nonadapted to the cold. From
these data, risk curves have been developed that
demonstrate the risk of frostbite to be minor above an
air temperature of 10°C (50°F), regardless of air speed;
but below-25°C (-13°F), there is severe risk of frost-
bite at nearly any air speed.7
TEMPERATURE REGULATION
Temperature regulation is a three-part mechanism of
afferent receptors, efferent receptors, and a regulatory
center.8 . mogenesis requires several weeks. A more rapid heat-
Afferent temperature receptors consist of cold
and warmth receptors within the skin. The density of
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
Respiration
„'1""N
- • Convection
'"* (air currents)
FIGURE 3 1 - 1 . The mechanisms of heat
loss from the nude body include radiation,
conduction, convection, evaporation, and
respiration.
afferent temperature receptors increases in areas with
greater environmental exposure. There are approxi-
mately 10 times greater cold receptors than warmth
receptors in the skin. Thus, the human body is geared
to detect cold much more so than warmth. Deep tem-
perature receptors are also located within the abdom-
inal viscera, spinal cord, and vena cava. Like the skin
temperature receptors, the deep temperature recep-
tors are much more responsive to cold than to warmth.
The temperature center is located in the posterior
hypothalamus and processes the information received
from the afferent system. A temperature set-point is
variable but averages about 37°C (98.6°F). The effer-
ent system is then responsible for maintaining this
temperature set-point.
The efferent system includes both heat-generating
and heat-dissipating mechanisms. The heat-generat-
ing systems involve metabolic rate, muscle machine
(i.e., shiver), and piloerection. A decrease in core tem-
perature causes the release by the hypothalamus of thy-
rotropin-releasing hormone, which is carried by the
hypothalamic portal veins to the anterior pituitary,
where it causes the release of thyroid-stimulating
hormone. Thyroid-stimulating hormone, in turn,
causes the thyroid to increase release of thyroxine, which
increases the rate of cellular metabolism and hence
generates more heat. This process of chemical ther-
generating response is shivering. Shivering increases
image...
the rate of body heat production as high as four or five
times normal. The shivering reflex is regulated by a
primary motor center located in the posterior hypo-
thalamus. Also, the sympathetic system controls the
arrector pili muscles attached to the hair follicles. When
activated, these muscles contract and stand upright,
thereby collecting a column of air to act as insulation.
In addition, the heat-generating system can cause
immediate change in body temperature through vaso-
constriction, thereby shunting heat to the core and
diminishing heat loss through the skin (radiation). This
too is mediated by the sympathetic system.
On the other hand, heat-dissipating mechanisms
include vasodilatation and sweating. Vasodilatation,
mediated by inhibition of the sympathetic centers,
increases the rate of heat loss by bringing large
amounts of blood to the periphery and thereby
increasing radiation of heat. Sweating also increases
heat loss through evaporation.
RISK FACTORS
Certain contributory factors make cold exposure
significantly more dangerous either by increasing
heat loss or by decreasing heat delivery or production
(Table 31-1).
Increased Heat Loss
Factors that increase heat loss by increasing the
efficiency of heat transfer include external environ-
mental factors such as wind and humidity. Clothing
plays a critical role as well. Clothing that traps mois-
ture inside will increase heat loss by allowing an
improved efficiency of heat transfer away from the body.
Ideally, clothing protects a person from the ravages of
wind exposure, thereby decreasing overall heat loss
through convection while preventing a buildup of inter-
nal moisture, which increases the efficiency of heat
transfer and thus promotes heat loss. Decreasing
exposed body surface area also decreases the amount
TABLE 31-1 • RISK FACTORS FOR COLD
INJURY
Increased Heat Loss Decreased Heat Delivery
Environmental Impaired vascular circulation
Increased wind
Cigarettes
Increased humidity Vasoconstrictive drugs
Poor clothing Dysautonomia
Overexertion Prolonged immobilization
Fatigue or apathy Previous cold injury
Alcohol Medical diseases
Anesthetics Atherosclerosis
Diabetes mellitus
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
31 • COLD INJURIES 857
of heat loss. Thus, mittens are better than gloves for
maintaining body temperature. Because nearly 80%
of heat loss can occur from the head and neck, these
regions must be covered at all times.
Overexertion, which increases heat loss through
panting and perspiration, can contribute to cold
injury. It can also lead to fatigue and apathy, which are
well-documented causes of cold injury in the mili-
tary.9,10 Alcohol intoxication plays a significant role in
cold injury in the civilian population.3,5 Not only does
alcohol impair judgment, but it causes vasodilatation,
thereby increasing heat loss as blood flow is rerouted
to the skin.
Vasodilatation is also caused by general and regional
anesthesia, thus increasing heat loss. Receipt of cold
intravenous fluids and blood products increases heat
loss and must be avoided to prevent iatrogenic
hypothermia.
Decreased Heat Delivery
or Production
Impaired vascular circulation can increase the risk
of cold injury as decreased blood flow (and hence
decreased heat delivery) results. Causes include ciga-
rette smoking and vasoconstrictive drugs. These vaso-
constrictive drugs include tricyclic antidepressants,
phenothiazines, antipyretics, and neuromuscular
blocking agents.
Patients paralyzed acutely because of spinal cord
injury risk dysautonomia that can lead to thermoreg-
ulatory problems. This is due to the loss of sympa-
thetic nervous system regulation in this group of
patients.
Prolonged immobilization also decreases circula-
tion and heat delivery, thereby increasing the risk for
cold injury. This is true for both paralyzed patients
and those individuals who remain exposed to a cold
environment and elect to decrease active movement.
Thus, motion of the limbs improves heat production
and blood flow, decreasing the likelihood of cold injury.
Even constricting clothing decreases blood flow to
certain regions of the body and thus decreases heat
delivery. Accordingly, this increases the risk of cold
injury.
Previous cold injury sensitizes an individual to cold
injury, presumably because of decreased baseline
tissue blood flow. In individuals with prior cold injury,
even a minimal repeated exposure can produce tissue
damage.
Certain medical diseases cause a decrease in heat
production. Thyroid disease, adrenal disease, hepatic
disease, and malnutrition can result in impaired ther-
moregulation.3 Atherosclerosis and diabetes mellitus
cause decreased heat delivery through impaired vas-
cular circulation. Thermal burns increase heat loss with
the loss of epidermal coverage.
858 I • GENERAL PRINCIPLES
HYPOTHERMIA
Hypothermia is a decrease in core body temperature
below 35°C (95°F). The severity of hypothermia is
further classified as mild (core temperature between
32.2°C [89.96°F] and 35°C [95°F]), moderate (core
temperature between 28°C [82.4°F) and 32.TC
[89.78°F]), or severe (core temperature <28°C
[82.4°F]).
Core body temperature reflects the largest compo-
nent of body temperature and thus is the most impor-
tant measurement of temperature. Sites that reflect this
temperature are the tympanic membrane, nasophar-
ynx, distal esophagus, and pulmonary artery."
Temperature regulation receives significant prior-
ity during physiologic homeostasis. In fact, even in the
hypovolemic patient, the body will increase muscle
blood flow to increase heat production (i.e., shiver-
ing) if hypothermia is present.5,9,10
Symptoms
Mild hypothermia is characterized by the shiver
response. Central nervous system reactions are slowed,
but the patient is usually conscious. Cardiovascular
changes include tachycardia secondary to cate-
cholamine release from the sympathetic system.
Cardiac output, blood pressure, and renal function are
increased as well because of increased catecholamine
release. As the core temperature decreases, bradycar-
dia follows.
Moderate hypothermia results in decreased cere-
bral blood flow; mental status changes eventually lead
to a stuporous state or total loss of consciousness. Con-
fusion, disorientation, and dysarthria are not uncom-
mon. Cerebral blood flow decreases by 7% per degree
Celsius decrease in core temperature. The shiver
response usually halts. Myocardial irritability devel-
ops with resultant atrial fibrillation. Electrocardiog-
raphy may demonstrate a J wave at the junction of the
QRS complex and ST segment. Cardiac output and
renal functions decrease. Impaired coagulation with
increased bleeding times secondary to reduced clot-
ting factor activity is common. Respiratory drive and
protective airway reflexes decrease.
Severe hypothermia is characterized by ventricular
fibrillation followed by asystole. Muscle tone is
significant for myoclonus. Urine output is minimal.
Treatment
The patient must first be removed from the cold envi-
ronment. This includes placement of the patient in a
warm shelter and removal of wet clothing. Passive exter-
nal warming through the use of blankets is best for
mild hypothermia. In the case of moderate or severe
hypothermia, the patient should be transported to a
care center.
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Dr.Mustafa D.
Once the patient arrives at a medical center, core
temperature must be determined. Specific ther-
mometers are required because clinical thermometers
are not calibrated below 34°C (93.2°F). A hypother-
mia treatment protocol must be instituted." For
moderate or severe hypothermia, this requires elec-
trocardiographic monitoring, urinary output moni-
toring, and central venous pressure determination.
Baseline arterial gas determinations, electrolyte values,
blood glucose concentration, renal function analysis,
complete blood cell count, coagulation studies, and
drug toxicity screens are obtained; any abnormalities
are corrected. When core body temperature is below
30°C (86°F), advanced life support protocols may be
ineffective. If defibrillation fails, rewarming must be
continued.,2 Active warming through the use of radiant
heat (warmed blankets or light sources) or rapid
rewarming through the use of immersion tanks is
required. Other rewarming techniques include intu-
bation with warm airway inhalation, administration
of warm intravenous fluids, and peritoneal dialysis.
Rewarming is best performed in a hospital setting
because rewarming shock or cardiac arrhythmia is a
risk. Patients and health care workers must be prevented
from rubbing injured skin; additional tissue damage
may result.
Rapid rewarming with the immersion tank proto-
col uses a burn Hubbard tank filled with 40°C (104°F)
water. Electrocardiography leads are required because
cardiac arrhythmias are common on rewarming;
however, they tend to self-correct as core temperature
rises. In addition, these arrhythmias tend to be resist-
ant to pharmacologic intervention. In the critically ill
patient with poor cardiac reserve, shiver response,
which demands significant amounts of myocardial
work, may be artificially suppressed through the use
of pharmacologic agents.13 Blood pressure and pulse
are monitored. Urine output is maintained. Warming
is continued until the core temperature reaches 37°C
(98.6°F). Frank and Robson1' as well as Zachary et al14
report excellent results with these techniques.
Rapid rewarming may avoid rewarming shock or
afterdrop, which is a result of shunting of cold blood
to the body's core, with a paradoxical drop in core tem-
perature that follows peripheral vasodilatation and
external rewarming.11,14 An additional advantage of
rapid rewarming over slower rewarming is the
avoidance of acidosis and hypoxemia.
FROSTBITE
Frostbite results from direct tissue injury due to freez-
ing and ice crystal formation. There are certain con-
ditions that can mimic frostbite. Chilblain is a result
of chronic intermittent exposure to high moisture and
low temperature, without actual tissue freezing. This
condition is reversible. Trench foot or immersion foot
image...

31 • COLD INJURIES 859

FIGURE 3 1 - 2 . Blister formation common to second-

degree frostbite of the foot. Note the erythema that
surrounds the blisters.
FIGURE 31 - 3 . Dry eschar that results from demarca-
tion of third- and fourth-degree frostbite of the foot.

is similar to chilblain in that it occurs after wet feet are Pathophysiology

exposed to near-freezing temperatures; however, there
is no actual ice crystal formation.
Degrees of Injury
Frostbite has been categorized into four degrees of
injury.15'18 First-degree injury is heralded by numb-
ness with a central white plaque and surrounding ery-
thema. Edema is common. In general, no tissue is lost.
This has also been referred to as frostnip. Second-degree
injury is characterized by blister formation within the
first 24 hours after injury. These blisters are filled with
clear or milky fluid. The blisters are surrounded by
erythema and edema (Fig. 31-2). Third-degree injury
consists of deeper dermal injury resulting in hemor-
rhagic blisters. These subsequently turn into black
eschars. Fourth-degree injury is full thickness with
tissue loss (Fig. 31-3).
There are three mechanisms of injury: direct, vascu-
lar, and inflammatory (Fig. 31-4).
Direct freezing of tissue leads to the formation of
ice crystals, initially extracellularly and then intracel-
lularly. These crystals compromise cell membrane
integrity and allow intracellular water to be osmoti-
cally drawn out of the cell. Furthermore, freezing leads
to irreversible denaturing of lipid-protein complexes.
If this process is not reversed, cell death is inevitable.
Subsequent vasoconstriction, regulated by cold
receptors in the skin, leads to local tissue hypoxia that
is followed by acidosis. Capillary blood flow becomes
disordered and eventually ceases. This leads to throm-
bosis.This microvascular injury leads to an inflamma-
tory reaction with release of cytokines, thromboxane
A2, prostaglandin F2, and free oxygen radicals and
mobilization of polymorphonuclear leukocytes and
mast cells, all of which intensify local tissue damage.15"20

Tissue injury

I 1
Direct tissue Vasoconstriction Inflammatory
freezing triggered by cold receptors mediators
in the skin

£ 1 f A
Ice crystal Compromise of Denaturing of Acidosis Hypoxia Polymorphonuclear Thromboxane A2
formation cell membranes lipid-proteins leukocytes Prostaglandin F2
Mast cells Oxygen free radicals
Cytokines

FIGURE 31 - 4 . The pathophysiologic mechanism of frostbite is a tripartite event involving direct tissue freezing, vaso-
constriction, and inflammatory mediators.

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
860 I • GENERAL PRINCIPLES
Symptoms
Progressive frostbite is characterized by numbness.
However, during the rewarming process, severe pain
is typical. This pain is throbbing and unrelenting. With
time, ihe throbbing becomes a tingling sensation
(similar 10 an electrical shock; characterized by sensory
loss, told intolerance, and hyperhidrosis.
Blisters filled with clear fluid indicate more
superficial damage; those stained with blood indicate
injury deep 10 the subdermal plexus. Skin that is firm
and solid to loiich corresponds to full-thickness injury,
as opposed to skin that indents when pressed.
Treatment
As for hypothermia, prethaw treatment requires
urgent transport to a care facility. Field rewarming
should not be undertaken if refreezing cannot be pre-
vented. Cycles of freezing and thawing lead to greater
inflammatory mediator release and hence greater
tissue injury in the long run.18,21 The injured part
should be protected with a splint and soft padding to
prevent accidental damage. Rubbing of the body part
suffering from frostbite must be avoided. Elevation
helps decrease edema. Concomitant hypothermia
must be treated. Use of vasoconstrictive agents, such
as cigarettes, must be avoided.
Rapid rewarming decreases further tissue damage
as it halts both direct injury and continued release of
secondary mediators. Submersion of the injured part
in 40°C water for 15 to 30 minutes is ideal. This maneu-
ver stops ice crystal formation and reverses the dele-
terious effects of vasoconstriction.15,22 Use of radiant
heat sources in frostbite can lead to iatrogenic injury
due to uneven thawing and, in unusual cases, second-
ary thermal burn to insensate tissue.
Clear blisters are d^brided because these contain
high concentrations of inflammatory mediators.
Topical application of aloe vera, a strong anti-
prostaglandin agent, every 6 hours is one form of treat-
ment. Dermaide Aloe Cream at 70% concentration is
a good therapeutic choice.15'20 Hemorrhagic blisters
TABLE 3 1 - 2 4- FROSTBITE TREATMENT PROTOCOL
Rewarming protocol: rapid rewarming in water at 40°C
for 15-30 minutes only
Debridement of clear blisters: hemorrhagic blisters are
not debrided because this may cause exposure of
deep structures and run the risk of desiccation and
subsequent necrosis
Elevation and splinting
Application of topical agents containing
antiprostaglandin activity
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
should not be debrided; these represent deeper injury,
and uncovering risks desiccation to underlying struc-
tures.
Pharmacologic intervention includes daily admin-
istration of oral ibuprofen, 12 mg/kg, to provide
antiprostaglandin activity to limit the potential for sec-
ondary mediator damage.15 Liberal use of analgesics
is helpful to counteract the post-thaw throb. Tetanus
toxoid is administered prophylactically; immune glob-
ulin is reserved tor patients who have never been immu-
nized or who are 10 years past the last booster.23
Prophylactic antibiotic administration may indeed be
indicated. Daily hydrotherapy and physical therapy are
mandatory (Table 31-2).
Use of pharmacologic agents that block the cascade
of arachidonic acid by cyclooxygenase strikes a deli-
cate balance. The positive effects include blocking the
inflammatory process that is mediated by throm-
boxane A2. The negative effects include blocking the
generation of prostaglandin l2 and E2 that causes
vasodilatation and increases antiplatelet aggregation
activity.19
Demarcation is the key to long-term treatment of
frostbite. After acute interventions have been under-
taken to decrease the deleterious effects of inflam-
matory mediators, time must pass for clinical
demarcation.24,25 Premature amputation risks sacrifice
of potentially salvageable tissue. Classically, for deep
frostbite injuries, the period for observation has been
1 to 6 months. This allows dry gangrene to declare the
specific regions that must undergo amputation.
However, triple-phase scanning has successfully
been used as a quick and efficient means to delineate
viable tissue. This obviates the need for prolonged
demarcation.26 In patients with little or no blood flow
as indicated by triple-phase scanning, aggressive early
debridement with possible free tissue transfer salvages
additional tissue (Fig. 31-5). Similar findings are
present with early use of magnetic resonance imaging
and magnetic resonance angiography.27
Long-term sequelae of frostbite injury include
hyperhidrosis, pain, decreased sensation, joint stiffness,
hypopigmentation, and risk for further cold injury.
Oral ibuprofen, 12 mg/kg, for antiprostaglandin activity,
unless contraindicated
Analgesics
Prophylactic antibiotics
Tetanus toxoid or immune globulin as indicated
Daily dressing changes and hydrotherapy
image...
Frostbite injury
1 1
Superficial |
1 1
Observation Debridement
FIGURE 3 1 - 5 . Surgical algo-
rithm for the treatment of frost-
bite. New scanning techniques
allow delineation of potentially
viable tissue in deep frostbite,
thus allowing early debridement
and free tissue transfer. Other- 1 ±
wise, standard demarcation can Amputate
take as long as 6 months.
ALTITUDE SICKNESS
As the popularity of extreme adventure sports increases,
physicians must be aware of altitude sickness.
The significance of increased altitude is a reduced
atmospheric pressure and thus a decrease in the partial
pressure of oxygen. This results in a decrease of oxygen
delivery to all organs of the body.
Acute mountain sickness can occur at an elevation
above 7000 feet and is heralded by nausea, insomnia,
headache, palpitation, and mild shortness of breath.
This is not considered a serious illness, nor is it indi-
cative of further medical complications. However,
unfit individuals are indeed more susceptible to this
illness. Symptoms are best corrected through avoid-
ance behavior. This includes a slow ascent. High-
carbohydrate meals and avoidance of dehydration
have also been demonstrated to help.
A much more serious complication of moun-
taineering is high-altitude pulmonary edema. This is
characterized by acute shortness of breath, cough, and
cyanosis. Cerebral edema can accompany high-altitude
pulmonary edema as well. This illness rarely strikes at
an elevation below 9000 feet. The condition is poten-
tially fatal. The pathophysiologic mechanism is poorly
understood, but the pulmonary edema follows a rapid
ascent. Immediate decrease in elevation and adminis-
tration of oxygen can alter the course of this poten-
tially fatal illness. Use of intravenous diuretics (such
as furosemide) to ameliorate alveolar oxygenation is
permissible, but not as a substitute for seeking lower
elevation. Steroids can improve uncomfortable symp-
toms but do not treat the underlying pulmonary edema.
Of concern is that high-altitude pulmonary edema can
strike even the most experienced and physically fit
climber at any time.
Taken 8 to 16 hours before ascent, acetazolamide
(Diamox), 250 mg every 12 hours, has been used for
prevention of acute mountain sickness. The presumed
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
31 • COLD INJURIES 861
Deep
Scanning
I
Salvage status
I Aggressive debridement
Observation Debridement
Flap transfer
mechanism of action for acetazolamide is a shift in the
body's acid-base balance through the inhibition of car-
bonic anhydrase, resulting in a metabolic acidosis. This
presumably stimulates an increase in both depth and
frequency of respiration. Because this medication is a
diuretic, dehydration must be avoided. Although
acetazolamide works well as prophylaxis against acute
mountain sickness, it does nothing for high-altitude
pulmonary edema. 28
Climbers refer to an elevation of 25,000 feet or above
as the death zone. Because of the severe depletion of
oxygen, the body decreases its generation of heat, and
an obligatory hypothermia commences. Cognition and
coordination suffer as the partial pressure of oxygen
in the atmosphere decreases sharply. Although climbers
have ascended to th is altitude without oxygen, this prac-
tice must be severely discouraged.
REFERENCES
1. LarreyDJ:MemoirsofMilitarySurgery,volII.Baltimore,Joseph
Cushing, 1814:156-164.
2. BowenTE, Bellamy RF: Cold injury.In Emergency War Surgery.
Washington, DC, Department of Defense, US Government
Printing Office, 1988.
3. Smith CE, Patel N: Hypothermia in adult trauma patients: anes-
thetic considerations. Am J Anesthcsiol 1996;23:283.
4. Ortncr SB: Life and Death on Mount Everest. Princeton, NJ,
Princeton University Press, 1999.
5. Garry RC: Control of the temperature of the body. Med Sci Law
I969;9:242.
6. Kazenbach TL, Dexter WW: Cold injuries. Postgrad Med
1999;105:72.
7. Danielsson U: Windchill and the risk of tissue freezing. J Appl
Physiol 1996:81:2666.
8. Flackc J W, Flacke WE: Inadvertent hypothermia: frequent, insid-
ious, and often serious. Semin Anesth 1983;2:183.
9. Orr KD, Fainer DC: Cold injuries in Korea during the winter
of 1950-1951. Medicine (Baltimore) 1952;31:177.
10. Whayne TF, DeBakey MF: Cold Injury, Ground Type. Wash-
ington, DC, Office of the Surgeon General, Department of the
Army, 1958.
image...
862 I • GENERAL PRINCIPLES
11. Frank DH, Robson MC: Accidental hypothermia treated without
mortality. Surg Gynecol Obstet 1980;I51:379.
12. Bracker MD: Environmental and thermal injury. Clin Sports
Med 1992;11:419.
13. Rodriguez JL, Weissman C, Damask MC, et al: Physiologic
requirements during rewarming: suppression of the shivering
response. Crit Care Med 1983; 11:490.
14. Zachary L, Kucan JO, Robson MC, Frank DH: Accidental
hypothermia treated with rapid rewarming by immersion. Ann
PlastSurgl982;9:238.
15. McCauley RL, Heggers JP, Robson MC: Frostbite. Postgrad Med
1990;88:67.
16. Reamy BV: Frostbite: review and current concepts. J Am Board
FamPract 1998; 11:34.
17. McCauley RL, Hing DN, Robson MC, Heggers JP: Frostbite
injuries: a rational approach based on the pathophysiology.
J Trauma 1983;23:143.
18. Heggers JP, Robson MC, Manavalen K, et al: Experimental
and clinical observations on frostbite. Ann Emerg Med
1987;16:I056.
19. Ozyazgan I, Tercan M, Melli M, et al: Eicosanoids and inflam-
matory cells in frostbitten tissue: prostacyclin, thromboxane,
polymorphonuclear leukocytes, and mast cells. Plast Reconstr
Surgl998;101:1881.
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Dr.Mustafa D.
20. Zook N, Hussmann J, Brown R, et al: Microcirculatory studies
of frostbite injury. Ann Plast Surg 1998;40:246.
21. Washburn B: Frostbite. N Engl J Med 1962;266:974.
22. Britt LD, Dascombc WH, Rodriguez A: New horizons in man-
agement of hypothermia and frostbite injury. Surg Clin North
Am 1991;71:345.
23. Didlake RH, Kukora JS: Tetanus following frostbite injury.
Contemp Orthop 1985;10:69.
24. Page RE, Robertson GA: Management of the frostbitten hand.
Handl983;15:185.
25. Knize DM, Weatherly-White RCA, Paton BC, Owens JC: Prog-
nostic factors in the management of frostbite. J Trauma 1969;
9:749.
26. GreenwaldD, Cooper B.GottliebL: An algorithm for early aggres-
sive treatment of frostbite with limb salvage directed by triple-
phase scanning. Plast Reconstr Surg 1998;102:1069.
27. Barker JR, Haws M J, Brown RE, et al: Magnetic resonance imaging
of severe frostbite injuries. Ann Plast Surg 1997;38:275.
28. Larson EB, Roach RC( Schoene RB, Hornbein TF: Acute moun-
tain sickness and acetazolamide. JAMA 1982;248:328.
image...
CHAPTER
32
•
Pharmacologic and Mechanical
Management of Wounds
CHRISTOPHER ATTINGER, MD,
• PETER A. BLUME, DPM
DEBRIDEMENT
The Importance of Debridement
Assessing a Wound Before Debridement
Surgical Technique
Necessary Surgical Tools for Debridement
Nonsurgical Tools for Debridement
Debridement of Skin
Debridement of Subcutaneous Tissue
Debridement of Fascia, Tendon, and Muscle
Debridement of Bone
Spread of Infection Along Tissue Planes
The goal in treatment of any type of wound is to
achieve healing in a normal and timely fashion. An
acute wound is a recent wound that has yet to progress
through the sequential stages of wound healing. A
chronic wound is a wound that is arrested in one of
the wound healing stages (usually the inflammatory
stage) and cannot progress further. This chapter dis-
cusses the key local strategies to facilitate normal
wound healing: debridement; current wound dress-
ing regimens; and modern wound healing adjuncts,
such as vacuum-assisted closure therapy, topical
growth factors, cultured skin, and hyperbaric oxygen.
Additional factors critical for wound healing (opti-
mizing blood flow and correction of medical and
nutritional abnormalities) are covered elsewhere.
Debridement is removal of necrotic tissue, foreign
material, and infecting bacteria from an acute or
chronic wound. Necrotic tissue, foreign material, and
bacteria impede the body's attempt to heal by producing
or stimulating the production of proteases, collage-
nases, and elastases that overwhelm the local wound
healing process. In this process, the building blocks
(chemotactants, growth factors, growth receptors,
mitogens) necessary for normal wound healing are
destroyed. This hostile environment is one in which
bacteria can proliferate and further inhibit wound
healing. Bacteria produce their own wound inhibiting
enzymes as well and consume many of the scarce local
resources (oxygen, nutrition, and building blocks) that
are necessary for wound healing.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
FACS • ERWIN J. BUU\N, MD
Approach to the Acute Wound
Approach to the Infected Wound
Approach to Chronic Wounds
MODERN STRATEGIES TO STIMULATE
WOUND HEALING
Wound Dressing
Vacuum-Assisted Closure Therapy
Growth Factors
Skin Substitutes
Hyperbaric Oxygen
Debridement of the acute wound removes damaged
tissue or foreign material that might inhibit sub-
sequent healing. This then enables the wound to go
through the normal healing phases, assuming systemic
and local factors are within normal limits. Aggressive
debridement of a chronic wound converts it to an acute
wound so that it can progress through the normal
phases of wound healing. Concurrently, the systemic
and local factors that led to the chronic wound have
to be identified and corrected.
DEBRIDEMENT
The Importance of Debridement
Infection of a wound site alters the normal healing
process by disrupting and prolonging the inflam-
matory phase1 with subsequent inhibition of the
macrophages1 ability to direct the formation of gran-
ulation tissue and neovascularization. Bacterial status
of a wound can be assessed clinically by quantitative
counts. A well-vascularized wound with a bacterial
count of less than 105 bacteria per gram of tissue should
go on to heal by secondary intention or should
successfully accept a skin graft.2'4 If the bacterial
concentration is higher, local bacterial and wound
proteases overwhelm the graft and prevent it from
adhering to and being revascularized by the underly-
ing bed. Failure of graft survival is frequently observed
in the burn patient, in whom bacterial proliferation
863
864 I • GENERAL PRINCIPLES
is the rule rather than the exception. If the bacterial
infection is allowed to go unchecked, the superficial
infection can become systemic and lead to sepsis.5
Removal of all necrotic and nonviable tissue in burn
wounds is therefore the mainstay of burn therapy 6 and
the basis for the success of early excision and graft-
ing. This aggressive therapy prevents the establishment
of a protease-rich environment that allows bacteria to
proliferate. The application of topical antibiotics,
such as silver sulfadiazine, mafenide acetate, and silver
nitrate, is a useful adjunct to help lower the wound
bacterial count. 7,8 The combination of debridement
to viable tissue and topical antibiotics is currently the
mainstay of successful burn wound coverage.
The lessons of aggressive removal of all necrotic
and nonviable tissue learned in burn surgery can be
applied with equal effectiveness to chronic wounds.
Steed et al9 reviewed the data of platelet-derived growth
factor's effect on the healing of chronic diabetic
wounds and made the seminal observation that
wounds healed more successfully when wound
debridement was performed weekly rather than more
sporadically. They showed that applied platelet-derived
growth factor was far more effective in promoting
wound healing in frequently deT>rided wounds than
in the undisturbed wounds. The most likely reason is
that frequent debridement regularly removes inhibitors
of wound healing (such as proteases, collagenases, and
elastases) and allows growth factors to exert their
positive influence.
The removal of local factors inhibitory to wound
healing may be one of the ways by which vacuum-
assisted closure therapy successfully converts chronic
wounds to healthy healing wounds. 10 The suction
applied by this device to the surface of the wound pre-
vents a buildup of proteases and bacteria and decreases
wound edema. The end result is a decrease in the
bacterial count and rapid formation of healthy
granulation tissue."
Assessing a Wound
Before Debridement
Before considering whether to d£bride a wound, one
has to determine the wound's etiology, the previously
attempted wound therapies, and the patient's medical
condition. A thorough history is taken from the
patient, family and friends, emergency medical tech-
nician, and referring physician to help determine the
wound's cause. The origin (usually traumatic) and age
of the wound are determined. The trauma is further
defined in terms of high impact, low impact, repeti-
tive, temperature related, caustic, radiation induced,
bite, drug abuse, and the like. The patient's tetanus
immunization status is obtained, and the patient is
inoculated if revaccination is indicated. In chronic
wounds, the age of the wound is important because
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
long-standing wounds can be malignant (Marjolin
ulcer). It is important to ask what previous topical
therapy was applied to the wound because certain
topical agents can contribute to the wound's chronic-
ity12 (e.g., caustic agents such as hydrogen peroxide,
10% iodine, Dakin solution).
A careful medical history is obtained with empha-
sis on possible manifestations of atherosclerotic disease
to the heart, nervous system, kidneys, eyes, and lower
extremity. The venous aspect of circulation is likewise
evaluated by noting abnormalities in blood coagula-
bility, liver disease, heart failure, previous venous
thrombi, and pulmonary emboli. Diseases that affect
the neurologic system (e.g., diabetes, paraplegia, spina
bifida, multiple sclerosis) are likewise elucidated. It is
important to establish the presence of autoimmune
disease (e.g., rheumatoid arthritis, pyoderma gan-
grenosum, scleroderma) because the optimal wound
treatment may be medical rather than surgical. In addi-
tion, the medications used to treat autoimmune dis-
eases (i.e., steroids or chemotherapy) are elucidated
because they contribute to poor healing. The
nutritional status is assessed, and a complete list of
medications and drug allergies is obtained.
The wound is assessed carefully by measurement
of its size and depth and then photographed. If cel-
lulitis is present, the border of the erythema is delin-
eated with indelible ink (Fig. 32-1). This permits
immediate bedside assessment of whether subse-
quent antibiotics and debridement are actually effec-
tive in controlling the cellulitis. If the cellulitis has
extended beyond the inked boundary after 4 to 6
hours, either the chosen antibiotics are inadequate or
the wound has not been sufficiently d£brided. It is
important not to confuse cellulitis with dependent
rubor. If erythema present in an extremity disappears
when it is elevated above the level of the heart, the
erythema is due to dependent rubor. With depend-
ent rubor, inflammation is usually absent and the skin
should have visible wrinkling. If the erythema per-
sists despite elevation, the wound has surrounding cel-
lulitis and needs antibiotic treatment with or without
debridement. Dependent rubor is also often seen at
a fresh operative site and should not be confused with
postoperative cellulitis. Again, rapid resolution of the
erythema with elevation and presence of wrinkled skin
at the incision edge indicate dependent rubor rather
than cellulitis.
The depth of the wound is carefully assessed for
bone, tendon, and joint involvement. A metallic probe
(Fig, 32-2) is used to assist in the evaluation of the
depth of the wound. If the probe touches bone, there
is an 85% chance that osteomyelitis13 is present. A radi-
ograph is obtained to assist with the evaluation of
the underlying bone. It can take up to 3 weeks for
osteomyelitis to appear on a radiograph. A magnetic
resonance imaging or nuclear scan is usually
TtSWttf'aeleW image...

32 • PHARMACOLOGIC AND MECHANICAL MANAGEMENT OF WOUNDS 865

FIGURE 3 2 - 1 . A gangrenous foot presents with cellulitis (A). It is initially ctebrided to viable tissue. The
border of the erythema around the wound is delineated with indelible ink (B). The time and date are like-
wise inscribed. Broad-spectrum antibiotics are started. The wound is then checked 4 to 6 hours later. If the
erythema has receded, the debridement performed and antibiotics chosen were appropriate initial treat-
ment. If the erythema has progressed beyond the border, either further debridement is necessary or the
antibiotics need to be changed.

superfluous if the surgeon plans to evaluate the bone
during debridement. However, these studies are useful
when the extent of osteomyelitis in the suspected bone
is unclear or when there is suspicion that other bones
may be involved. If tendon is involved, the infection
is likely to have tracked proximally or distally. One
should check for bogginess proximally and distally
along the suspected tendon sheaths. If the suspicion
is strong that a distal infection has spread proximally,
the proximal areas where the tendon sheaths are readily
accessible should be checked (e.g., dorsal or volar wrist,
extensor retinaculum, tarsal tunnel). Needle aspira-
tion is an easy way to more accurately assess under-
lying purulence.
The blood flow to the area is then evaluated by
palpation or a hand-held Doppler probe (Fig. 32-3). l4
A triphasic Doppler signal indicates normal blood
flow, and a biphasic signal indicates adequate blood
flow; a monophasic signal warrants further investi-
gation. If the quality of flow is questionable, a formal
noninvasive arterial Doppler evaluation has to be per-
formed. If the flow is inadequate, the patient should
be referred to a vascular surgeon who specializes in
distal revascularizations. In the face of undetermined
or inadequate blood flow, debridement should be
delayed until blood flow status has been assessed and
corrected if possible (Fig. 32-4A). However, immedi-
ate debridement is called for regardless of the vascu-
lar status when wet gangrene, ascending cellulitis from
a necrotic wound, or necrotizing fasciitis is present
(Fig. 32-4B and C). Revascularization should follow
as soon as possible thereafter.
Sensation and motor function must also be assessed.
This is important in traumatic wounds because it
allows the surgeon to accurately evaluate the extent
of injury before debridement. A careful nerve exam-
ination is obviously helpful to rule out possible
compartment syndrome. In patients with diabetes or
those with neurologic disorders, the neurologic exam-
ination can help explain whether neuropathy con-
tributed to the wound and, if so, help in mapping out
strategies to prevent recurrences. Lack of protective
sensation can be established when the patient is
unable to feel 10 g of pressure (5.07 Semmes-

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
866 I • GENERAL PRINCIPLES
FIGURE 3 2 - 2 . A metal probe is useful to determine
whether bone is at the base of the wound. If bone is pal-
pated at the base of the wound, there is an 85% chance
that osteomyelitis is present.
Weinstein monofilament; Fig. 32-5). This prevents
patients from sensing damage due to excessive local
pressure (prolonged decubitus position; tight shoes,
clothes, or dressings; biomechanical abnormalities; or
the presence of foreign bodies [ Fig. 32-6]). The repet-
itive trauma of normal ambulation (on average, a
person takes 10,000 steps a day) in neuropathic
patients with biomechanical abnormalities leads to
local ulceration over the area experiencing higher and
prolonged pressures during gait.
Certain specific problems associated with a given
medical condition can also exacerbate pressure prob-
lems and lead to ulceration. For example, diabetic
patients who chronically have high blood glucose levels
develop stiff joints and inflexible tendons because the
excess glucose binds to collagen and renders the joint
or tendon stiff and without elasticity.15 The patient
with uncontrolled diabetes will develop a tight Achilles
tendon and lose his or her ability to dorsiflex the foot
beyond neutral. This puts an excessive and prolonged
amount of pressure during the push-off phase of gait
both at the arch of the midfoot and underneath the
metatarsal heads. The excess pressure at the midfoot
can lead to Charcot collapse of the midfoot; the excess
pressure at the forefoot can lead to metatarsal head
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
FIGURE 3 2 - 3 . A hand-held Doppler probe is essential
in the initial evaluation of any wound when the pulses are
not palpable. If the sound is triphasic, there is normal
blood flow. A biphasic signal suggests sufficient blood flow.
However, monophasic flow warrants a more detailed eval-
uation of the blood supply to the foot. In assessing the
blood supply to the foot, the dorsalis pedis and the pos-
terior tibial arteries are routinely evaluated. The exami-
nation can also evaluate pulses that are not readily
palpable, such as the anterior perforating branch of the
peroneal artery.
ulceration. This problem is further accelerated in the
neuropathic patient who cannot appreciate the effects
of the excessive pressure at the midfoot or forefoot.
Open or percutaneous release of the Achilles tendon16
decreases forefoot pressure in the equinovarus foot
during gait sufficiently to allow the rapid healing of
those plantar forefoot ulcers (Fig. 32-7). Unless cor-
rection of the underlying biomechanical abnormal-
ity is part of the entire treatment plan, debridement
and good wound care may prove to be futile.
Surgical Technique
The most important step in treatment of any wound
is performing adequate debridement to remove all
foreign material and unhealthy or nonviable tissue
until the wound edges and base consist only of normal
 32 • PHARMACOLOGIC AND MECHANICAL MANAGEMENT OF WOUNDS 867

FIGURE 3 2 - 4 . When dry gangrene is present in an ischemic foot, revascularization should precede debridement (A).
The wound is then closely observed because the restored blood supply can convert the dry gangrene into wet gan-
grene. When that occurs, the wound is immediately d£brided. Otherwise, it is preferable to wait 4 to 10 days until the
revascularization has optimized local blood flow around the wound. If wet gangrene is present, the wound is debrided
immediately to normal-looking tissue (B and C). The foot can then be safely revascularized because the distal source
of infection has been debrided.

and healthy tissue. Only excellent atraumatic surgi-
cal technique 17 should be used to avoid damage to the
healthy tissue left behind (Fig. 32-8). The remaining
healthy tissue establishes the necessary surface for suc-
cessful wound healing by ensuring that (1) the wound
FIGURE 3 2 - 5 . The use of a 5.07 Semmes-Weinstein
monofilament (equivalent to lOg of pressure) on the
various neurosomes is a simple way to assess whether
the patient possesses protective sensation. This is espe-
cially important in evaluating the diabetic foot. The lack
of protective sensation accounts for the majority of
diabetic ulcers.
is free from gross infection and (2) there is no dead
or necrotic tissue left behind to inhibit healing.
A useful approach to surgical debridement is to
view a wound much as an oncologic surgeon would
approach a tumor. Reconstructive problems that may
result from adequate debridement should not inhibit
debridement because compromises may jeopardize
subsequent wound healing. The goal is to excise the
wound until only normal soft, well-vascularized tissue
remains. An acute wound has to be trimmed of all
questionably viable tissue and foreign material so that
it can either progress through the normal healing
phases or be ready to be closed safely. A chronic wound
has to be converted by debridement to an acute wound
so that it can proceed through the normal healing
phases or be closed surgically.
Health professionals often limit debridement
because they are uncertain how to deal with the sub-
sequent defect caused by more vigorous debridement.
Thus, it is important to have a physician on the mul-
tidisciplinary wound team who is familiar with modern
wound care techniques (vacuum-assisted closure
therapy, topical growth factor, cultured skin, hyper-
baric oxygen treatments) as well as modern wound
closure techniques (includinglocal flaps, pedicled flaps,
and microsurgical free flaps). More than 90% of

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868 I • GENERAL PRINCIPLES

FIGURE 3 2 - 8 . This is a chronic nonhealing wound on

the thigh of a patient with renal failure, steroid depen-
dency, and diabetes (A). Thorough debridement to healthy
bleeding tissue at the wound edges and base was required
to convert this wound to an acute wound so that it could
go on to heal. The key is to avoid damage to the normal
tissue by use of excellent atraumatic surgical technique.
This meant use of sharp cold dissection rather than dis-
section with cautery (Bj and skin hooks (C) instead of crush-
ing forceps. The result of atraumatic surgical technique
is that the amount of potentially devitalized tissue left
behind after debridement has been minimized (D). Healing
can proceed uniformly throughout the wound without
islands of necrotic and infected tissue to slow the process.

primary closure, or covered with a simple skin graft.

FIGURE 3 2 - 6 . A neuropathic diabetic patient walked
around for 3 days with this screw inside his foot because
he was unable to feel its presence. He came in only because
he noted drainage on his sock and subsequently noted a
small hole in his plantar forefoot.
wounds can be closed without resorting to sophisti-
cated plastic surgery reconstruction techniques, pro-
vided the wound is well vascularized and free of
infection. Therefore, most wounds can be allowed to
heal by secondary intention, closed with delayed
The advent of vacuum-assisted closure therapy has,
in large part, simplified wound care because it rapidly
stimulates the formation of granulation tissue so that
the wound size becomes more manageable. The
wound can then be closed primarily or skin grafted
instead of requiring a microsurgical free flap for
adequate cover.
The extent of debridement can be limited by the
amount of pain the patient feels during the procedure.
The exception is the neuropathic diabetic patient. For
the sensate patient, a regional block with lidocaine
allows the health professional to ddbride aggressively
in the office under most circumstances. Debridement
should be performed in the operating room if the
wound cannot be adequately anesthetized with a
regional block or if the debridement will lead to bleed-
ing that maybe difficult to control. The wound should
be debrided without a tourniquet so that the quality
of bleeding at the freshened wound edges can be
accurately assessed.

FIGURE 3 2 - 7 . This 39-year-old obese diabetic patient had bilateral lateral plantar metatarsal ulcers from equino'
varus deformities due to bilateral tight Achilles tendons. The equinovarus deformity can usually be simply corrected
by lengthening the Achilles tendon. The left Achilles tendon was released, the excessive plantar pressure was relieved,
and the left foot went on to heal in 6 weeks without additional therapy (A). The right Achilles tendon was then released,
and that ulcer healed uneventfully 5 weeks later (B).

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image...

32 • PHARMACOLOGIC AND MECHANICAL MANAGEMENT OF WOUNDS 869

D
FIGURE 32-8. See legend on opposite page.

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Dr.Mustafa D.
870 • GENERAL PRINCIPLES

Necessary Surgical Tools
for Debridement
The basic tools for debridement in an office include
pickups, knife> scissors, and curet (Fig. 32-9). These
should be surgical tools and not "throwaway" suture
removal kits, which are usually dull and cannot grasp
or cut tissue adequately. The resultant extra crushing
or sawing motions that these dull instruments cause
damage the tissue left behind and cause extra pain to
the patient. The pickups should have teeth so that
tissue to be excised can be grasped more easily. A No.
15 blade is used for fine debridement; a No. 10 or 20
blade is used to slice off tissue thin layer by thin layer
(Fig. 32-10) until healthy tissue is reached. It is fre-
quently necessary to change surgical blades because
they dull quickly. Strong sharp scissors (e.g., curved
Mayo scissors) work well to dissect the eschar and
dead tissue from the underlying healthy tissue. Curets
with sharp edges are useful in removing the pro-
teinaceous coagulum that accumulates on top of
both fresh and chronic granulation tissue (Fig. 32-
11). That coagulum contains the proteases that inhibit
healing. Rongeurs are useful for removal of difficult
to reach, indurated soft tissue and for debridement
of bone.
For radical debridement in the operating room,
useful tools are found in the orthopedic trays (Fig.
32-12). A Cobb elevator with its long lever arm and
sharp spoon-size tip is useful for exposure of bone.
McElroy curets (large curets used to ream out the
inside of the femur) are useful in debridement of
chronic granulation tissue, deep cavities, and bone
because their length allows the surgeon to apply con-
siderable pressure to a small defined area. Rongeurs
are useful in biting off indurated soft tissue in narrow
spaces difficult to reach with a knife or scissors.
They are also useful in debridement and biopsy of
bone, although great care has to be taken to avoid
shattering the remaining bone by grabbing too much
in one "bite." Rongeurs should be double action and
include narrow and wide duckbills as well as narrow
and wide straights. An air-driven or electrical sagit-
tal saw is useful to saw off bone slices serially until

FIGURE 3 2 - 9 . The tools of debridement include a pickup with teeth, solid scissors that can cut through tough tissue
easily, and a No. 3 knife handle that carries a No. 10, 11, or 15 blade (A) and a sharp curet that can easily scrape
coagulum or granulation tissue off the wound surface (B).

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image...

32 • PHARMACOLOGIC AND MECHANICAL MANAGEMENT OF WOUNDS 871

FIGURE 32-1 0. Debridement of soft tissue is best done by slicing thin slice after thin slice until healthy tissue is
reached. In A, the proximal dermal veins are still clotted, and there is no bleeding at the skin edge. Thin slices (B) are
removed until normal tissue appears (Cj.

normal cortex and marrow are reached. Cutting
burrs and rasps are likewise useful in the fine debride-
ment of the bone surface to reach the telltale punc-
tate bleeding at the freshened bone surface (Paprika
sign).
When one is through debriding, it is important
to cleanse the wound with a pulsed lavage system
(Fig. 32-13).' 8 The pressure from the pulsating liquid
is effective in getting rid of any loose tissue and super-
ficial bacteria. There is no proven benefit to adding
antibiotics to the saline or water used in the irrigat-
ing solution. However, in lavage of a traumatic wound,
it is important to first tag any important struc-
tures (nerve and tendon ends) with monofilament
suture because those structures tend to swell during
the pulsed lavage and may be difficult to identify
thereafter.
If the wound is going to be closed immediately after
debridement, it is important to ask for a double instru-
ment setup in the operating room to avoid recontam-
inating the newly debrided wound. That is, there should
be two separate sets of instruments, gloves, gowns,
drapes, suction, and Bovie: one for debridement and
one for wound closure. After pulsed lavage, gloves and
gowns are changed, the wound is redraped, and new
suction and Bovie are placed on the field. New instru-
ments are then used to close the wound. The reason-
ing behind this extra setup is that cultures of the
instrument surfaces used in debridement of wounds
show concentrations in excess of 10'1 bacteria.19 Reuse
of the contaminated instruments on the wound that
has just been cleaned adds an unnecessary bacterial
load to the wound before closure that can easily be
avoided with the double setup.

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872 I • GENERAL PRINCIPLES

FIGURE 3 2 - 1 1 . This is a chronic wound covered with a thick layer of proteinaceous material (A). A curet is used to
remove proteinaceous coagulum from the wound surface (B). Underneath should be healthy granulation tissue (Q.
It is critical to do this every time the wound is examined to make sure that only viable tissue is underneath the
coagulum and to stimulate healing. It should be done before topical growth factor is applied to a wound so that the
residual elastase is removed before it can destroy the just-applied growth factor.

FIGURE 3 2 - 1 2 . A setup in the operating room should
include the following orthopedic instruments to perform
a thorough debridement: Cobb elevator, periosteal eleva-
tors, McElroy and angled curets, double-action rongeurs,
chisels, and rasps. In addition, air-driven orelectrical sagit-
tal saws and cutting burrs should be readily available.
FIGURE 3 2 - 1 3 . Placing the ulcerated extremity in a
plastic bowel isolation bag before pulse-evacuating the
wound is an effective way to avoid contaminating the rest
of the operating room field with the spray from the pulse-
evacuation device. A minimum of 3 liters of normal saline
without antibiotics should be used on the wound.

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MMMMmMnage...
32 • PHARMACOLOGIC AND MECHANICAL MANAGEMENT OF WOUNDS
Nonsurgical Tools for Debridement
The time-honored nonsurgical tool for debridement
of tissue is the wet-to-dry saline gauze dressing.20 The
gauze, when dry, is lifted off the wound, and all tissue
adherent to the gauze (alive and dead) is removed with
it. Whereas this technique is effective in debridement
of superficial marginal and necrotic tissue, it can also
slow healing by removal of the underlying healthy new
tissue and neoepitheliurn at the wound's edge. Also,
removal of the gauze is painful to the sensate patient,
and compliance to the dressing-change regimen
quickly becomes a problem. To alleviate the pain, the
gauze is soaked off the wound. However, soaking
the gauze before removal decreases the ability of the
dressing to superficially debride the wound.
Topical preparations containing proteases, papain
derivatives, and collagenases are the medical substi-
tutes for surgical debridement. Topical debridement
agents are not the ideal solution because they work
slowly, can be painful, and are often accompanied by
copious exudates. The health care professional often
has to try various agents to determine which is the least
painful. In addition, these agents may require dilution
with a water-based gel to further diminish the pain.
Overall, they are effective when the amount of tissue
to be removed is minimal and there is a defined end-
point. Although reasonably priced, the agent's true cost
is better reflected in the number of nursing visits
required until the wound is adequately debrided.
Finally, these agents may be most effective in remov-
ing the protein coagulum that forms over granulating
tissue. They should be used carefully in this setting so
that they do not also destroy the necessary growth
factors.
Occlusive dressings do provide a moist atmosphere
for nonviable tissue to liquefy so that it can more easily
be removed. However, unless the wound is very clean,
the occlusive dressing provides an excellent culture
medium for bacteria to proliferate. Bacterial prolifer-
ation can lead to either a deep or surrounding super-
ficial infection. Therefore, although occlusive dressings
are effective in removal of eschar, the co-risk of sub-
sequent infection does not justify the use of occlusive
dressings for debridement.
Biologic debridement agents, such as maggots,
recently rediscovered,21"23 are currently being reintro-
duced in the United States. Maggots, the larvae of the
green blowfly (Phaenicia sericata), digest necrotic tissue
and bacteria. They secrete enzymes to dissolve both
the necrotic tissue and biofilm that surrounds bacte-
ria. The liquefied byproducts are then digested by the
larvae. Thirty larvae consume 1 g of tissue per day. The
larvae have been sterilized with radiation therapy before
being delivered so that they cannot progress to the pupa
stage. The maggots are placed on the wound and
covered with an occlusive dressing, which is changed
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Dr.Mustafa D.
873
every 3 days. Maggots debride the wounds beautifully
because they digest only the necrotic tissue. More
important, they sterilize the wound because they
consume the local bacteria regardless of the bacteria's
resistance to antibiotics. The debridement is painless.
The treatment can be performed on an outpatient
basis.24 Maggots represent an exciting use of an old
technique because they not only painlessly remove
necrotic tissue but also destroy antibiotic-resistant
bacteria (including vancomycin-resistant Enterococcus
and methicillin-resistant Staphylococcus aureus). This
therapy has been shown to work well in infected and
gangrenous wounds, 25,26 with the best results reported
in diabetic wounds.
Debridement of Skin
Debridement of skin consists of removal of nonvi-
able, nonbleeding skin. If the injured skin does not
blanch, is insensate, and has blistered, it is not likely
to be alive. There is no advantage to waiting in the
hope that this skin will suddenly redevelop circula-
tion because it behaves much like the skin in a third-
degree burn. At the edges and under the dead skin,
there is a high concentration of harmful proteases or
bacteria to inhibit subsequent healing. The protracted
course necessary for the dead skin to separate itself
from the underlying tissue may lead to functional loss,
severe scarring, deeper tissue damage, and dissemi-
nated infection.
Therefore, the approach to nonviable skin should
be to remove it as soon as possible. If the border
between live and dead tissue is clearly demarcated, the
skin should be excised along that border. If the border
is not clearly demarcated, one should start at the center
and remove concentric circles of skin until viable tissue
is reached. When excising skin, one should look for
bleeding at the normal skin edge (Fig. 32-14). Clotted
venules at the skin edge reflect a complete interrup-
tion in the local microcirculation and are an excellent
indicator that further excision is necessary. Only when
there is normal arterial bleeding at the edge of
the wound and absence of clotted veins can one be
satisfied that the cutaneous debridement has been
adequate.
In removing the skin, it is important to examine
the subcutaneous tissue. A culture specimen should
be obtained. If the tissue appears viable and not
infected, a biologic dressing or vacuum-assisted closure
therapy can be used as a temporary dressing. If the
tissue is viable but infected, a topical antibiotic such
as silver sulfadiazine8 or moist pure silver sheeting27,28
should be placed on the wound. For Pseudotnonas
infections, 0.25% acetic acid or gentamicin ointment
may be more appropriate. For methicillin-resistant 5.
aureusy mupirocin (Bactroban) is an appropriate
initial topical antibiotic, keeping in mind that
874 I • GENERAL PRINCIPLES

FIGURE 3 2 - 1 4 . This is a diabetic patient who presented with distal gangrene. After revascularization, the foot was
debrided to viable tissue. Note the lack of bleeding along the dorsal skin edge at the time of the initial incision (A).
Removal of the tissue to the metatarsophalangeal level failed to yield bleeding tissue (B). The plantar tissue was seri-
ally removed (C), slice by slice, until a healthy bleeding edge was encountered. The same was done with the dorsal
tissue (D). The metatarsal bones were carefully removed so that there would be sufficient soft tissue envelope to
perform a successful Lisfranc amputation (E).

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image...
32 • PHARMACOLOGIC AND MECHANICAL MANAGEMENT OF WOUNDS
resistance can develop quickly.29 If the tissue is not
viable, deeper debridement is necessary.
Debridement of Subcutaneous
Tissue
Subcutaneous tissue consists of fat, vessels, and nerves.
Because of the decreased concentration of blood
vessels in the subcutaneous fat, bleeding at the tissue's
edge is not always a reliable indicator. Healthy fat is
shiny yellow, soft, and resilient. Dead fat has a gray
pallor to it, is hard, and is nonpliable. Fat should be
debrided until soft, yellow, normal-looking fat is
attained. Undermining should be avoided because it
threatens the viability of the overlying skin. It is impor-
tant to keep the fat in a moist environment after
debridement to prevent desiccation.
Small blood vessels should be coagulated by bipolar
cautery to minimize damage to the surrounding
tissue. If the vessels are larger than 2 to 3 mm, they
should be ligated. Ligaclips are the least reactive
foreign body material to provide hemostasis. If a suture
is to be used, a small-diameter, monofilament suture
should be used to minimize the risk of facilitating
further infection. For example, silk acts like a foreign
body and stimulates a vigorous foreign body reaction;
bacteriostatic polyglycoiic woven suture has multiple
recesses within which bacteria can survive in a semi-
protected state.
Nerves, when viable, have a shiny, white, glisten-
ing appearance. In the subcutaneous tissue, the nerves
are sensory. Intact exposed sensory nerves in a sensate
patient can be painful. The decision has to be made
whether to cut or to preserve them. If the nerve is to
be preserved, it has to be kept moist until it can be
covered with adequate tissue. A skin graft usually does
not provide adequate padding to prevent pain on
contact. Consideration should be given to burying the
nerve underneath other tissue or a flap. If the nerve
is to be excised, longitudinal traction should be used
to allow the nerve to retract within normal tissue when
it is cut at the edge of the wound. Taking the
epineurium and sewing it over the nerve fascicles with
8-0 or 9-0 nylon can minimize subsequent neuroma
formation.
Debridement of Fascia, Tendon,
and Muscle
Healthy fascia has a white, glistening, hard appear-
ance and should be preserved if it looks viable. When
it is dead, the appearance is dull, soft, and stringy
and is in the process of liquefying. The entire necrotic
fascia should be debrided until solid normal-looking
bleeding fascia is reached. Because neurovascular
bundles can be close to overlying fascia, debride-
ment should proceed with caution. The viable fascia
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875
must be kept moist after debridement to avoid
desiccation.
The underlying muscle must be examined as well.
Healthy muscle has a bright red, shiny, and resilient
appearance and contracts when it is grasped with
forceps or touched with cautery. In neuropathic
patients, the muscle may be pale, perhaps yellowish,
and may appear nonviable. It will, however, have some
tone and bleeds when cut. Frankly dead muscle will
be swollen, dull, and grainy when palpated and falls
apart when pinched. If viability of the muscle is ques-
tionable, it is best to err on the side of caution and to
remove only what is not bleeding and appears dead.
Subsequently, the wound should be serially debrided
until only viable muscle remains. There is always a
question whether to remove the entire muscle when
part of it is dead. In general, one should remove only
what is dead because removal of the viable portion of
the muscle involves further dissection that might
compromise blood flow to the surrounding tissues
(i.e., overlying skin).
Tendon debridement is always tricky because sac-
rifice of the tendon leads to loss of function. All
attempts should be made to preserve viable paratenon
surrounding the tendon. The tendon must be kept
moist after debridement, especially if the paratenon
is removed. The tendon should be covered with viable
tissue as soon as the wound is stable (infection free
with adequate blood supply). Otherwise, the tendon
will usually desiccate or become infected and will then
need to be removed. Infected tendon looks dull, soft,
and grainy with parts separating or liquefying (Fig.
32-15). If the tendon is small and part or all of it is
infected, all of the exposed tendon should be removed.
It is important to explore the exposed tendon proxi-
mally and distally with proximal and distal incisions
to ensure that any hidden necrotic tendon is also
FIGURE 3 2 - 1 5 . An infected Achilles tendon in the stages
of liquefaction is shown here. The technique of debride-
ment is to shave it down to viable hard, shiny tendon. It
is then important to make sure it stays moist as it gran-
ulates sufficiently to be skin grafted or is clean enough to
be covered with other tissue.
image...
876 I • GENERAL PRINCIPLES
removed. When the extensor tendons on the dorsum
of the hand or foot become exposed, it is difficult to
preserve them unless they are quickly covered with
healthy tissue. If the tendons remain exposed while
the wound progresses to the point at which it is ready
to be closed, they usually become infected and will
impede further wound healing until they are removed
(Fig. 32-16).
When the tendon has a large diameter (e.g., Achilles
tendon, anterior tibial tendon), only that portion of
the tendon that is necrotic or infected should be
debrided. The hard, shiny tendon underneath is left
intact. Great care should be taken to keep the remain-
ing tendon moist. The Achilles tendon deserves
special mention because it is so large and receives
excellent blood supply from both the posterior tibial
and peroneal arteries. If exposed and healthy, it
should be covered as soon as the wound is stable with
a local, pedicled, or free flap. If part of the tendon
is necrotic, it should be debrided to hard, shiny
tendon (Fig. 32-17). Serial debridement may be nec-
essary. It should be kept moist by use of silver sulfa-
diazine and an occlusive dressing while granulation
tissue forms. The tendon can then be skin grafted.
FIGURE 3 2 - 1 6 . The erythema around this wound persisted despite the patient's receiving systemic antibiotics and
continuous coverage of the wound with silver sulfadiazine (A). The erythema immediately began to resolve once the
soft, stringy, infected extensor tendons were removed (BJ.
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Granulation can be accelerated with vacuum-assisted
closure therapy (first covering the tendon with a petro-
latum mesh gauze) or with the combined use of hyper-
baric oxygen treatments and topical growth factor
(Fig. 32-18).
Debridement of Bone
Debridement of necrotic or dead bone is relatively
straightforward. All soft, nonbleeding bone should be
removed. Useful hand-held tools include the rongeur,
curets, and rasps. Power tools such as the sagittal saw
and the cutting burr are also necessary. The key in
debridement of bone is to remove only what is dead
and infected and leave bleeding bone behind. Care
should be taken not to shatter proximal viable
bone. In this regard, power tools are safer to use
than rongeurs or chisels. The best way to debride
the osteomyelitic smaller long bones (phalanx,
metacarpals, or metatarsals) is to cut slices of bone
serially (Fig. 32-19) until healthy bone is reached. A
cutting burr to remove thin layer after thin layer of
the osteomyelitic cortical bone until only healthy
bleeding bone remains is more tiseful in the larger
image...

32 • PHARMACOLOGIC AND MECHANICAL MANAGEMENT OF WOUNDS 877

FIGURE 3 2 - 1 7 . This Achilles tendon (A) was infected from

just above the calcaneus to the midcalf. The entire area over-
lying the tendon and the posterior exposed portion of the
tendon had to be removed to control the infection (B). The
wound was subsequently covered with a free flap, and
the patient was able to maintain good plantar flexion because
the anterior half of the Achilles had been preserved (C).

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878 I • GENERAL PRINCIPLES

;:
Www"
•m | \ * i fW *C
1 '-vw ., -
1 VJ^'S
m
HSV
|

D E
FIGURE 3 2 - 1 8 . This patient presented with a gangrenous Achilles tendon (A). The necrotic tendon was sharply
debrided to shiny underlying tendon (B). Hyperbaric oxygen and topical growth factor were started, and granulation
tissue began to appear within the first week (C). The tendon was covered with healthy granulation tissue within 3 weeks
(D). The Achilles tendon was then successfully skin grafted and was completely healed 4 weeks later (E).

bones (tibia, fibula, radius, ulna, and skull). Copious
irrigation ensures that the heat generated by the burr
does not damage the healthy bone. In cortical bone,
the process is continued until punctate bleeding is
visualized emanating from the cortical bone (Paprika
sign). This signifies that healthy bone has been reached
(Fig. 32-20). In d^briding cancellous bone, the surgeon
should look for bleeding cortical bone and normal-
appearing marrow. Biomechanical considerations
should not deter the surgeon from d^briding enough
bone to ensure that all osteomyelitis has been eradi-
cated. Preservation of the bone architecture can be
achieved with external fixation until the wound heals.
Current orthopedic techniques, including bone graft-
ing and Ilizarov frames, allow the subsequent repair
of most bone defects. Indeed, the Ilizarov can be used
as an external frame while the wound is being steril-
ized and covered. Bone lengthening can begin once
the wound has been successfully covered.
It is important to obtain culture samples both of
what is considered normal bone proximal to the area
of debridement and of the debrided osteomyelitic
bone. Once the infected bone has been removed and
only bleeding healthy bone is left behind, the wound
is ready to be closed, assuming surrounding soft tissue
is healthy. A subsequent prolonged 6-week course of
antibiotic therapy for osteomyelitis is not only unnec-
essary but also excessive if the infected bone has been
surgically removed. It further jeopardizes the patient
through the complications of prolonged antibiotic
therapy (Clostridium difficile, resistant organisms,
allergic reactions). When only healthy bone remains

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image...

32 • PHARMACOLOGIC AND MECHANICAL MANAGEMENT OF WOUNDS 879

FIGURE 32-1 9. The infected metatarsal bone here is serially cut with a sagittal saw (A) until hard bleeding bone
with normal-appearing cortical and cancellous bone is reached (B).

at the base of the wound, only 1 week of appropriate
antibiotics is necessary after wound closure. The
exception to a 1-week course of antibiotics after
closure is when the surgeon suspects that the bone left
behind may still harbor osteomyelitis (e.g., calcaneus
or tibia). In that instance, a longer course of antibi-
otics is indicated.
Spread of Infection Along
Tissue Planes
When the deeper structures are involved, it is always
important to rule out proximal or distal spread. With
necrotizing fasciitis, the infection spreads along the
fascia and deeper structures. The key is to remove all

A B
FIGURE 3 2 - 2 0 . Infected bone should be debrided back to hard, bleeding cortical and cancellous bone with use
of a cutting burr or rasp (A). The presence of punctate bleeding at the surface of cortical bone indicated viable bone
(Paprika sign) (B).

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880 I • GENERAL PRINCIPLES
questionable tissue, consider use of hyperbaric oxygen
as an adjunct, and repeat debridement every 24 to 48
hours until the wound has stabilized. With necrotic
and purulent ulcers overlying tendon or muscle,
infection can spread along tendon sheaths or fascial
planes. It is important to evaluate any suspected route
along which the infection could spread. For example,
the flexor tendon sheaths, peroneal tendon sheaths,
and extensor tendon sheaths are possible avenues of
spread in any necrotic plantar foot ulcer. Evaluation
of infection within those possible routes includes
feeling for bogginess of the overlying tissue as well as
needle aspiration or direct exploration of the actual
tendon sheath. A small incision in the skin directly
over the tendon sheath followed by gentle spreading
with a straight clamp will reveal whether purulence
is present. It is also useful to milk the suspected area
of spread along the underlying tendon sheath and to
look for purulence emanating at the ulcer site.
Once the spread of infection has been located, it
is best to make an incision directly from the distal
to the most proximal site of spread. All necrotic
paratenon and other tissue are removed. The tendon,
if necrotic, is likewise debrided. Great care is taken to
ensure that the incision and dissection have gone far
enough proximally. The proximal exploration stops
only when the surrounding tissue is normal. This may
require filleting the foot, ankle, and leg all the way up
to the popliteal fossa or the hand, wrist, and arm all
the way to the antecubital fossa. With extensive infec-
tion, debridement is repeated every 12 to 48 hours
until progression of tissue necrosis is stopped and the
infection is under control. This aggressive approach
is often the only chance to save the diffusely infected
limb.
When there is progressive tissue necrosis despite
adequate blood supply, this indicates inadequate
wound debridement or areas of undrained purulence.
The requirement for extensive debridement should
not discourage salvage attempts, as long as a func-
tional limb can be salvaged within a reasonable time.
However, if the debridement is such that the remain-
ing limb will not be functional, an amputation should
be performed. In performing that amputation, one
should try to preserve as much of the limb as possi-
ble. Several staged debridement procedures may be
necessary to achieve a healthy wound so that the
subsequent amputation is as long as possible and
heals successfully.
Approach to the Acute Wound
In the acute wound, management must set the optimal
environment for the phases of wound healing to
proceed without external or internal impairment. The
patient should receive a tetanus inoculation if the
tetanus status is unknown or not up to date (within
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
5 years). After hemostasis is obtained, the wound is
cleaned by removal of foreign bodies and devascu-
larized tissue. The debridement may be performed in
the emergency department if there is a delay (>2
hours) in the availability of the operating room. A
peripheral nerve block can facilitate the emergency
department debridement. The actual cleansing of
the wound is best accomplished with pulsed lavage
using several liters of saline. Specimens of the actual
debrided tissue and loose bone fragments should
be sent for culture because these have been shown to
best correlate with future cultures of osteomyelitis if
it were to develop.30 The wound is then dressed with
saline-soaked cotton gauze while the patient awaits
surgery.
Once the culture samples have been sent, the
patient is prescribed broad-spectrum antibiotics.31
For severe contamination associated with garbage
truck or farm injuries, amidinopenicillins and an
aminoglycoside or a more potent combination of
carbapenems and an aminoglycoside should be
added for better coverage of anaerobic and gram-
negative bacteria. Antibiotics can then be adjusted
for more specific coverage as soon as the initial
wound culture results are available. An infectious
disease consultation is useful for optimal management
of the antibiotic regimen with any contaminated
wound.
In the operating room, the goal of the initial
debridement is to remove all obvious dead skin, sub-
cutaneous tissue, fascia, muscle, and bone while
leaving behind all potentially viable tissue to be re-
evaluated in 12 to 24 hours. If the skin and subcuta-
neous tissue is avulsed, there is an overwhelming
chance that much of it will die if it is tacked back in
place. Therefore, avulsed tissue should be trimmed
until actual bleeding at the skin edge is seen. Culture
samples of the wound are again obtained. The
anatomic damage should be fully evaluated, includ-
ing avulsed nerves and tendons. Cut nerves should
be tagged with a fine monofilamentous suture so that
they do not become lost in the subsequent soft tissue
swelling. The wound should then be cleaned with
pulsed lavage to remove all foreign debris and dressed
in a continuously moist, nonirritating bandage that
keeps exposed tendons, fascia, and bone from desic-
cating. Alternatively, the vacuum-assisted closure
device can be applied directly on the wound to
provide continuous removal of wound discharge and
to reduce edema.32
Serial debridement procedures every 24 to 48
hours are recommended until the wound is ready for
closure. The wound is ready for closure when it con-
tains only viable tissue and is soft, without erythema,
and minimally painful. It has been advocated in the
past that getting the wound ready for reconstruction
within 7 days of injury minimized complications.30,33
image...

32 • PHARMACOLOGIC AND MECHANICAL MANAGEMENT OF WOUNDS 881

In analysis of those wounds, those with closure before
7 days had less scar, had less contracture, and required
fewer secondary procedures. However, with the advent
of vacuum-assisted closure, aggressive debridement
techniques, and good wound management, those
guidelines can often be extended without altering the
outcome.32 The exception is for wounds that have actual
exposed fracture sites. The fracture site should still be
covered with healthy soft tissue within 7 days to min-
imize the risk of subsequent osteomyelitis. The rest of
the wound, however, can be covered at a later date if
the entire wound bed is not ready for closure. The
vacuum-assisted closure device is helpful here in
extending that traditional 1-week critical period for
definite wound closure.
Approach to the Infected Wound
In the infected wound, the optimal environment for
wound healing is impaired by the presence of inva-
sive bacteria (> 105). It is important to know the source
and extent of the infection. A radiograph of the wound
identifies foreign bodies, gas in soft tissue, and bone
damage (Fig. 32-21). If gas is seen within the tissue
planes on the radiograph, gas gangrene is possibly
present and urgent wound management is manda-
tory. This gas is usually a byproduct of anaerobic bac-
teria (usually C. perfringens) that have progressed along
the fascial planes. The wound needs to be debrided
immediately and aggressively to prevent limb loss or
death. The involved compartments of the foot or leg
need to be checked for pressure above 40mmHg. 30
Immediate fasciotomy should be performed with
pressures above 40 mm Hg. For pressures between 30
and 40 mm Hg, monitoring is continued. For pressures
less than 30 mm Hg, one should continue to be vigi-
lant. Hyperbaric oxygen should be considered post-
operatively to help control the anaerobic infection.34
The wound should be re-explored in 24 to 48 hours
if there is any question of residual infection. Ampu-
tation of a limb with gas gangrene should not be auto-
matic because the damage is usually along the fascial
level separating the skin from the underlying muscle
and bone. Aggressive repetitive debridement and
hyperbaric oxygen can often salvage enough of the
limb to preserve a functional extremity.
It is critical to quickly assess whether there is suf-
ficient blood supply to eradicate the infection. Insuf-
ficient blood flow inhibits the body from delivering
the necessary white blood cells, nutrients, oxygen, and

A B
FIGURE 3 2 - 2 1 . This diabetic patient had a massively swollen and erythematous foot that had crepitus when exam-
ined (A). The radiograph revealed subcutaneous gas (B), and the patient was taken to the operating room immediately
for radical debridement. Cas gangrene does not necessarily mandate immediate amputation because the infection ini-
tially involves only the skin, subcutaneous tissue, and fascia. If the patient is operated on in time, the underlying tissue
that survives (underlying muscle and tendon) can eventually be covered with a skin graft or flap.

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
882 I • GENERAL PRINCIPLES
antibiotics to the wound site. Palpable pulses usually
signify sufficient inflow. Otherwise, the arteries should
be assessed by Doppler probe; if the sound is bipha-
sic or triphasic, the flow is probably adequate. However,
if the flow is monophasic or absent, more invasive
testing should be performed. Formal vascular tests of
arterial waveforms, pressure, and transcutaneous
tissue oxygen levels should be obtained. If the flow is
deemed inadequate, an angiogram should be obtained
and the limb should be urgently revascularized. Unless
there is gas gangrene or a rapidly ascending infection,
debridement should be limited to frankly necrotic
tissue until the limb has been adequately revascular-
ized. The reason for initial conservative debridement
is that marginal tissue left behind may survive after
revascularization.
It is important to perform aerobic and anaerobic
culture of the wound as soon as possible by obtaining
a piece of deep, initially unexposed tissue. A swab or
superficial tissue culture specimen is of limited use
because it reflects only surface flora rather than the
actual underlying bacteria responsible for the infec-
tion. If there happens to be access to a quantitative
bacterial culture laboratory, a minimum of 0.3 cm3 of
tissue is necessary for the culture specimen to be
processed. A concentration greater than 105 bacteria
per gram of tissue reflects a significant infection that
will inhibit healing.2,3 One should then debride the
wound as specified before. Broad-spectrum antibiotics
are started pending tissue culture results.
The edge of the erythema around the wound is then
marked with an indelible ink marker and observed
closely. If, subsequently, the redness extends beyond
the drawn margins, either the broad-spectrum antibi-
otic is insufficient or the wound has not been ade-
quately debrided (see Fig. 32-1). The surgeon should
not hesitate to return to the operating room every 12
to 24 hours to debride the wound again if there is sus-
picion that there is undrained purulence or necrotic
tissue inhibiting the resolution of the infection. The
antibiotics are adjusted for maximum efficacy as soon
as the initial culture results are back. The wound is
re-explored to ensure that only healthy viable tissue
remains. Hydrogen peroxide, 1% Dakin solution,
povidone-iodine, and chlorhexidine are bactericidal
and help sterilize the wound. However, these agents
also destroy normal tissue (Fig. 32-22) and should
therefore be used only when there is residual gangrene
or necrotic tissue in the wound.12 If only viable tissue
lies at the base of the wound, topical therapy should
be gentle enough to promote rather than hinder
healing. Appropriate topical antibiotics may be useful
because they can help control the local infection while
minimizing damage to normal tissue. The vacuum-
assisted closure device is an excellent topical dressing,
provided the wound is clean. If there are any exposed
neurovascular structures or internal organs, a
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
FIGURE 3 2 - 2 2 . The use of hydrogen peroxide and other
astringents such as alcohol or 1 % DaKin solution on wound
surfaces should be discouraged because they inhibit
healing and destroy the normal tissue around the wound.
This dehisced below-the-knee amputation was treated
twice a day with a hydrogen peroxide lavage.
petrolatum mesh should be placed between the base
of the wound and the vacuum-assisted closure sponge
to prevent adherence of the sponge to the underlying
structure.
Approach to Chronic Wounds
The difficulty in treatment of chronic wounds lies in
accurately establishing their etiology. This task is com-
plicated by the fact that they are always infected top-
ically and may harbor a deeper infection. Debridement
is not always the first step in treatment. If the wound
is due to vasculitis, the initial treatment is aimed at
control of the vasculitis by pharmaceutical interven-
tion. Fifty percent of these vasculitis patients suffer
from a coagulopathy (e.g., deficiencies in factor
V Leiden or protein C or protein S, hyperhomo-
cystinemia, prothrombin gene mutations) that
contributes to the chronic ulceration. Unless these
deficiencies are corrected, aggressive wound man-
agement (debridement, cultured skin, growth factor,
and hyperbaric) will be futile. If the wound is due to
venous stasis disease, the venous system should be
assessed for venous incompetence or thrombosis and
treated surgically, if appropriate, before wound closure
is attempted. Obviously, the patient with venous
stasis should also be evaluated for coagulopathy, and
if an abnormality is detected, it should likewise be
corrected. If the wound is due to vascular insufficiency,
the affected limb should first be revascularized. If the
wound is due to cancer, a biopsy should be performed
to determine the pathologic process and the extent
of resection required for tumor management. If the
wound is due to irradiation, pretreatment with hyper-
baric oxygen should be considered.35 If the wound is
due to a hematologic abnormality (e.g., clotting
image...
32 • PHARMACOLOGIC AND MECHANICAL MANAGEMENT OF WOUNDS
abnormalities, sickle cell, thrombocytosis, cryoglob-
ulinemia), it should be medically managed until the
patient's condition is optimized.
Once the etiology has been determined and the treat-
ment course set, wound debridement is performed.
The goal is to establish an acute wound devoid of abnor-
mal external and internal factors that delay the normal
progression of wound healing. The chronic wound
surface is d£brided until normal-appearing vascular-
ized tissue is reached. This can be difficult in extensive
chronic venous stasis disease or in radiation wounds.
The amount of resection necessary may require
removal of so much tissue that reconstruction may not
be possible. In those instances, rather than d^briding
until normal tissue is reached, it is preferable to d^bride
to good bleeding scar tissue. This scar tissue, although
indurated and stiff, may develop surface granulation
tissue that can be covered with a skin graft or a flap. If
a flap is the chosen method of reconstruction, the
amount of abnormal tissue removed can be increased
to fit the size of the chosen flap. The larger the selected
flap, the more abnormal tissue can be removed.
MODERN STRATEGIES TO
STIMULATE WOUND HEALING
Once the wound is clean and not infected, wound care
focuses on providing the optimal environment for
healing: moist, clean, and well vascularized. Moist
healing36 has been shown to be far more rapid than
healing under an eschar.37 Minimizing the bacterial
count is likewise critical to healing. 1 Adequate blood
supply brings the necessary nutrients and cells to allow
normal healing to proceed.
The dressing placed on a wound should ensure that
the optimal environment for wound healing is main-
tained. The wound base then can support and promote
successful collagen deposition, angiogenesis, epithe-
lialization, and wound contracture. The result should
be the formation of healthy red granulation tissue:
bright red and finely granular in consistency with
neoepithelialization at the borders. This is in con-
tradistinction to unhealthy granulation tissue, which
can have either a pale, dull appearance with a gross
irregular consistency or an exuberant purplish appear-
ance with boggy, uneven protruding masses of spongy
vascular tissue (Color Plate 32-1). Wet-to-dry dress-
ings, championed in the past and useful on initial
debridement of the wound, impede normal healing
by removing healthy neoepithelium and granulation
tissue every time the cotton dressing is ripped off the
wound.
To assess whether the current conditions for healing
are adequate, it is necessary to measure the size of the
wound on a weekly basis. A reduction in the volume of
the wound of 15% or more per week represents normal
healing.3* One can easily follow wound size weekly by
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
883
measuring the longest vertical axis and then measur-
ing the longest horizontal axis perpendicular to it.
Although this does not account for changes in depth,
the product of the two (length times width) makes
it easy to monitor wound healing progress or lack
thereof. When the healing is occurring at a slower rate,
current wound strategy should be re-evaluated and
adjunctive wound healing modalities should be con-
sidered. These include topical solutions that vary from
vacuum-assisted closure therapy to cultured skin to
topical growth factor. From the systemic side, oxygen
treatments can be added to the topical treatment or
used alone to improve oxygenation around the local
tissue as long as there is adequate vascular inflow to
allow oxygen delivery.
Wound Dressing
The ideal wound dressing regimen after debridement
provides the moist clean milieu discussed before. If
there is any question of local infection,12 topical
antibiotics should be considered as part of the treat-
ment. The presence of gram-negative bacteria strongly
correlates with nonhealing wounds. 39 Quantitative cul-
tures2"4 can aid clinical judgment in assessing whether
the chosen ointment is effectively minimizing the bac-
terial count. Antiseptics should be avoided in clean
wounds because they are not selective in their effect,
with dissolution of both bacteria and the local tissue.40
Antiseptics include iodine, peroxide, hypochlorite,
chlorhexidine, boric acid, alcohol, hexachlorophene,
thimerosal (Merthiolate), gentian violet, and per-
manganate. In addition, antiseptic solutions are not
effective41 in lowering bacterial counts because they
bind to the organic material and thus minimize their
bactericidal effect. Their usefulness (more specifically,
Dakin solution 42 ) has been demonstrated only in dirty
open war wounds, in which they primarily functioned
to dissolve necrotic tissue.
Topical antibiotics are effective in reducing the
number of bacteria to less than 105 per gram of tissue
(Table 32-1). Once that level has been reached, their
further effectiveness is questionable. Silver sulfadiazine
cream is effective in burns and pressure ulcers,8 and
it keeps the wound moist. With Pseudomonas infec-
tion, gentamicin ointment can be applied on the
wound. Both silver sulfadiazine and gentamicin
contain sulfa and should be avoided in patients with
sulfa allergies. An alternative for Pseudomonas infec-
tion is a moist pure silver sheeting43'44 or a dilute acetic
acid solution because Pseudomonas is extremely sen-
sitive to changes in pH.45,46 However, the wound will
desiccate unless it is frequently moistened. Other
topical antibiotic ointments that should be consid-
ered include bacitracin, mupirocin, erythromycin,
and polymyxin B. Against gram-positive bacteria,
mupirocin, bacitracin, and erythromycin have been
884 • GENERAL PRINCIPLES

TABLE 3 2 - 1 • TOPICAL ANTIBIOTICS

Trade Name Generic Name Effective Against Company

Silvadene Silver sulfadiazine Gram-positive, gram-negative, and yeast infections Monarch, Kendall,
1% Marion
Garamycin, Gentamicin Pseudomonas aeruginosa, Aerobacter aerogenes, Clay-Park Labs
Centamar Escherichia coli, Proteus vulgaris, Klebsiella
pneumoniae, streptococci (group A beta-hemolytic,
alpha-hemolytic), and Staphylococcus aureus
(coagulase positive, coagulase negative, and some
penicillinase-producing strains)
Bactrim Bacitracin Gram-positive bacteria Fougera, Major
Bactroban Mupirocin 2% Gram-positive bacteria, MRSA, Staphylococcus aureus. ClaxoSmithKline,
Streptococcus pyogenes. Staphylococcus epidermidis,
and Staphylococcus saprophytics Southwood
Polysporin Polymyxin B and Gram-negative bacteria, Pseudomonas aeruginosa
bacitracin (moderately effective) Warner-Lambert
Neosporin Neomycin, Wide range of antibacterial action for many gram-
bacitracin, positive and gram-negative organisms; Warner-Lambert
polymyxin B Staphylococcus aureus, streptococci including
Streptococcus pneumoniae, Escherichia coli,
Haemophilus influenzae, Klebsiella I Enterobacter
species, Neisseria species, and Pseudomonas
aeruginosa; the product does not provide adequate
coverage against Serratia marcescens
Erythromycin Multiple names Streptococcus pyogenes (group A beta-hemolytic Ortho, Fougera,
streptococci); alpha-hemolytic streptococci (viridans Major
group); Staphylococcus aureus (resistant organisms
may emerge during treatment); Corynebacterium
diphtheriae
lodoflex, Cadexomer iodine MRSA, Pseudomonas, Candida albicans Healthpoint
lodosorb
Silver Sheeting

Acticoat All silver products:

Staphylococcus aureus (MRSA), Enterococcus faecium Smith & Nephew
(vancomycin-resistant Enterococcus), Enterococcus
fecalis, Burkholderia cepacia, Alcaligenes species,
Pseudomonas aeruginosa, Klebsiella pneumoniae,
Pseudomonas species, Acinetobacter species,
Citrobacter koseri
Aquacel Ag ConvaTec
Arglase Medline
Silverlon Argentum Medical

MRSA, methicillin-resistant Staphylococcus aureus.

shown to be effective. For methicillin-resistant 5.
aureus, mupirocin is an appropriate initial topical
antibiotic, keeping in mind that resistance can develop
quickly.47 Polymyxin is effective against most
gram-negative bacteria, moderately effective against
Pseudomonas, and not effective against Proteus. If the
topical antibiotic is placed over a neurovascular
bundle or tendon, it should be covered with an occlu-
sive or semiocclusive dressing to prevent desiccation
of the underlying structure.
Heavily secreting wounds macerate the normal
tissue around the wound.37 The maceration renders
the surrounding tissue more susceptible to injury. To
help control the excess fluid, one can add filler prod-
ucts (gels, powders, beads, granules, or pastes), which
will absorb the excess moisture in the wound (Table
32-2). These absorptive dressings come in two forms:
starch-based copolymers or calcium alginates. The
starch-based absorptive dressings can absorb many
times their weight and form slurry as they absorb more
and more fluid. The slurry can go beyond the con-
fines of the wound to macerate the normal skin. That
is why it is important to monitor the dressing's ability
to absorb the secretions and to schedule dressing
changes so that the risk of maceration is minimized.
Examples include the Bard absorptive dressing,

Bin kilometrelik bir yolculuk ilk adimla baslar.

Dr.Mustafa D.
image...

32 • PHARMACOLOGIC AND MECHANICAL MANAGEMENT OF WOUNDS 885

TABLE 32-2 • DRESSINGS

Absorptive Aquacel ConvaTec Occlusive Tegaderm 3M

dressings Exu-Dry, Smith & Nephew dressings OpSite Smith & Nephew
Primapore ProCyte ProCyte
CombiDERM ConvaTec Transeal DeRoyai
Medipore 3M Polyskin Kendall
Multipad, DeRoyai Suresite Medline
Sofsorb Bioclusive Johnson & Johnson
Tielle Johnson & Johnson Hydrogels Tegagel 3M
CurityAbd, Kendall Amerigel Amerx Health Care
Tel fa max, Biolex Bard Medical
Tendersorb DuoDERM, ConvaTec
Abd SAF-Cel
Bard absorptive Bard Curasol Healthpoint
dressing Nu-Cel Johnson & Johnson
lodoflex Healthpoint Hypergel, Molnlycke Health
Calcium Gentell Gentell Normlgel Care
alginates Algosteril Johnson & Johnson IntraSite, Smith & Nephew
Restore Hollister SoloSite
Hyperion Hyperion Medical Carrasyn Carrington
advanced Laboratories
alginate Restore Hollister
dressing Curafil Kendall
PolyMem Ferris Mfg. Elasto-Cel Southwest Technologies
AlgiCell Dumex Medical Vigilon Bard
AlgiDerm Bard Hydrocolloid Tegasorb 3M
Sorbsan Dow Hickam Comfeel Coloplast
Kalginate DeRoyai DuoDERM ConvaTec
Kaltostat ConvaTec Nu-Derm Johnson & Johnson
Curasorb Kendall RepliCare, Smith & Nephew
AlgiSite Smith & Nephew Cutinova
Dermasorb Bard Restore Hollister
Foam Lyofoam ConvaTec Ultec Kendall
dressings Polyderm DeRoyai Contact Dermanet DeRoyai
PolyMem Ferris Mfg. layers Mepitel Molnlycke Health Care
Mepilex Molnlycke Health Tegapore 3M
Care Wound Multidex DeRoyai
Allevyn Smith & Nephew fillers Mesalt Molnlycke Health Care
Curafoam Kendall Cutinova cavity Beiersdorf-Jobst
Biafine Medix

Dermanet wound contact layer, and Multidex
hydrophilic powder. Calcium alginates, derived from
seaweed, are woven into absorbent dressings. They are
also hemostatic, 48 biodegradable, mildly antibacte-
rial,49 and nonantigenic. Examples include Curasorb,
Dermasorb, Kaltostat, and Sorbsan. In addition, these
absorptive dressings tend to decrease the pain for
reasons that are poorly understood. The drainage will
decrease as the wound granulates in. Vacuum-assisted
closure therapy is an excellent alternative to control
excessive wound drainage while stimulating the for-
mation of granulation tissue.
Once the wound is clean and has granulated in, the
dressing can be greatly simplified. Clinical signs that
the wound is on its way to healing occur when the signs
of inflammation are gone, healthy fine granular red
granulation tissue covers the wound, and neoepithe-
lialization is present along the wound border (Color
Plate 32-1). Resolution of inflammation is indicated
by soft wound edges, presence of skin wrinkles, and
normal skin colors. At this point, any dressing that keeps
the wound surface clean and moist is appropriate. A
wound surface that remains moist epithelializes 30%
faster than a wound surface that is allowed to desic-
cate. An occlusive dressing also promotes angio-
genesis and the more rapid formation of granulation
tissue.53 The quality of a wound that heals under moist
conditions is less fibrotic and scarred than are wounds
that heal under dry conditions. Occlusive dressings help
decrease the pain.54
The type of dressing used may affect the transcu-
taneous voltage that plays a role in wound healing.
Barker55 measured transcutaneous voltages up to
40 mV and noted that the skin surface was always neg-
atively charged compared with the deeper skin layers.
These findings have led researchers and clinicians to

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Dr.Mustafa D.
886 I • GENERAL PRINCIPLES
manipulate that current to stimulate wound healing.
Various forms of electrostimulation (direct current, 56
low-frequency pulsed current," high-voltage pulsed
current, 58 and pulsed electromagnetic fields 59 ) have
been used with varying amounts of success. Occlusive
dressings preserve the voltage gradient across the
wound that is thought to play a role in the rate of epithe-
lial migration.47,60 Dry wounds lead to the loss of the
voltage gradient.
The appropriate dressing should be chosen that
keeps the wound bed moist while ensuring that the
surrounding skin remains dry and avoids maceration
(see Table 32-2). Options 37 include wet-to-wet dress-
ing, film dressing, hydrocolloids, hydrogel dressing,
foams, and the absorptive dressings mentioned before.
Wet-to-wet dressings are the least desirable because
they cannot avoid macerating the surrounding tissue
if the dressing is kept continually wet. If allowed to
dry, they then become a wet-to-dry dressing that slows
epithelialization and leads to tissue loss on removal.
Film dressings are made of polyurethane films that
allow exchange of oxygen, carbon dioxide, and water
vapor.61 The exchange of water vapor prevents fluid
buildup in low-secreting wounds. Examples of film
dressings include Bioclusive, OpSite, Polyskin, and
Tegaderm. Hydrocolloid dressings consist of a water-
impermeable polyurethane film outer covering over a
layer of hydrocolloid. The hydrocolloid is initially
adherent and dissolves as it absorbs the underlying
moisture. Examples of hydrocolloid dressings include
DuoDERM,Tegasorb, and Comfeel. Hydrogels consist
of polymers with high water content (95%) that are
semitransparent and nonadherent. They come in
either a sheet form or gel. They can absorb some fluid
but are best on minimally exudative wounds. Because
they are nonadherent, they need superficial dressing
to keep them in place. Examples of hydrogels include
Biolex wound gel, Hydrogel wound dressing, Elasto-
Gel, Hypergel, Nu-Gel, and Vigilon. Foams are made
of polyurethane and conform nicely to the wound
contour. They are nonadherent and absorb minimal
moisture but enough to avoid maceration. They also
need additional dressing to be kept in place. Examples
include Allevyn cavity dressing, Cutinova, Hydrasorb,
and Lyofoam.
To develop a comfort level with the myriad dress-
ing options, one must become familiar with each dress-
ing category for coverage of a wide array of wounds.
Topical antibiotics should be used judiciously and
should be bacteria specific when appropriate. If antibi-
otics are overused, resistance to the bacteria or skin
allergic reactions may ensue. The simpler the dress-
ing regimen, the better is the patient's compliance.
Moist healing is more rapid and less painful than dry
healing, but the dressing should also be absorptive
enough to avoid maceration of the surrounding tissue.
As long as the wound is healing by 10% to 15% per
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Dr.Mustafa D.
week, the chosen dressing regimen is probably
adequate.
Vacuum-Assisted Closure Therapy
Vacuum-assisted closure therapy consists of placing
an open-cell sponge directly on the wound surface
and covering it with an occlusive film- The sponge is
connected by a tube to a vacuum pump. Subatmos-
pheric pressure is applied to the entire wound surface.
The subatmospheric pressure can be constant or
intermittent with pressures ranging up to 125 mm Hg.
The theory of its effectiveness in wound management
is based on its ability both to reduce the bacterial
colony count and to stimulate the rapid formation
of granulation tissue.10,11 The mechanisms that
cause the vacuum-assisted closure device to stimu-
late the formation of granulation tissue are not fully
understood. Some posit that the induced changes in
the cytoskeleton trigger cell duplication.32,62,63 Con-
stant suction of the wound surface may remove a suf-
ficient concentration of factors inhibiting local wound
healing (proteases such as matrix metalloproteinase
8 and elastases) that the balance of growth factors to
proteases is altered in favor of the growth factors. The
reduction of surrounding edema and resultant
improved blood flow as well as the lower bacterial
count also contribute to the formation of granula-
tion tissue.
The vacuum-assisted closure device can be applied
over any type of tissue: dermis, fat, fascia, tendon,
muscle, blood vessels, bone, and hardware.32 There
are two important prerequisites: that the wound be
clean (i.e., free of necrotic tissue) and that the wound
be well vascularized. To avoid the risk of a deeper infec-
tion, the wound should always be completely debrided
before application of the vacuum-assisted closure
device. Use of the device should also be limited to
well-vascularized wounds. If it is applied to the
ischemic wound, further necrosis may occur at the
wound edges if the wound is not carefully monitored
and lower intermittent pressures are not applied. Pain
can sometimes be a limiting factor to the use of
vacuum-assisted closure therapy, especially when the
sponge is changed. Applying a lower pressure and
placing intervening petrolatum gauze can sometimes
mitigate that pain.
Vacuum-assisted closure therapy works through an
open-cell sponge that is placed directly on the wound
and then covered with an occlusive dressing (Fig. 32-
23). Tubing connects the sponge to an external vacuum
device. Depending on the amount of drainage and the
patient's mobility, the suction pump is either large and
stationary or small and portable (Fig. 32-24). A neg-
ative pressure of 25 to 125 mm Hg is then applied either
intermittently or continuously to the wound sur-
face. All fluid secreted in the wound is immediately
T%W«S(afltfW image...

32 • PHARMACOLOGIC AND MECHANICAL MANAGEMENT OF WOUNDS 887

aspirated into a waste canister. The canister is changed
when it is full. The edema around the wound dimin-
ishes rapidly. Within 4 days, the bacterial count
decreases by a factor of 103 or more, and the granu-
lation forms far more rapidly than in controls." Gran-
ulation tissue forms over any live surface, including
tendon, bone, vascular grafts, heart, and intestine. If
the device is placed over a vessel, bypass graft, intes-
tine, heart, or lung, petrolatum mesh such as Adaptic
should be placed between the structure and the
sponge, and lower suction pressures should be used
(Fig. 32-25). The sponge should be changed every 48
to 72 hours. The sponge can sometimes be difficult to
remove because of the ingrowth of new granulation
tissue. However, it is important to remove any of the
sponge that may have broken off and remained imbed-
ded in the wound bed because it will otherwise remain
as a foreign body. When part of the sponge becomes
imbedded in the granulation tissue, it means that the
vacuum-assisted closure device changes should be per-
formed more frequently (i.e., every 24 to 48 hours).
A smaller caliber open-cell white sponge is available
that breaks up far less often and is useful for shallow
defects.
Vacuum-assisted closure therapy has greatly
simplified wound management. It is currently well
accepted as an excellent initial dressing after wound
debridement because it effectively reduces wound
edema, controls local bacterial growth, and promotes
the formation of granulation. It provides excellent and
safe temporary wound control so that reconstructive
surgery can be electively planned rather than per-
formed emergently. Frequently, the wound contracts
and granulates so rapidly with vacuum-assisted closure
that a simple skin graft is all that is required. The
vacuum-assisted closure can then be used as a bolster
dressing by placing it on top of the skin graft (with
petrolatum or silicone mesh between the two) for the
next 3 to 5 days. This has remarkably increased skin
graft "take" rates, especially in areas where there is dif-
ficulty in stabilizing the skin graft or immobilizing the
recipient site.

- •
• > < . .

-« S 3 £ ' H

i
w*

C D
FIGURE 3 2 - 2 3 . The vacuum-assisted closure device consists of an open-cell sponge that is placed on this sacral
wound (A) until it fills the entire dead space (B). A suction tube is then inserted into the sponge, and the sponge is
covered with an occlusive dressing (C). The other end of the suction tube is inserted into the suction pump (D), and
the pump is turned on. Continued

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Dr.Mustafa D.
T$**>ttf<aelciW image...

888 • GENERAL PRINCIPLES

**• £

G
FIGURE 3 2 - 2 3 , cont'd. The air is aspirated out of the wound, and the sponge becomes hard from the lower pres-
sure created (E). This is the sacral wound after 2 weeks (F), after 2 months (C), and healed (H).

This prolonged vacuum-assisted closure therapy
may also be applied to healthy wounds that have
exposed bone or hardware (Fig. 32-26).32 This approach
is particularly useful around the ankle or rear foot when
an Ilizarov-type frame has been applied to stabilize the
bone. Despite restricted access, vacuum-assisted closure
will shrink the wound sufficiently and promote enough
granulation so that most wounds can be managed with
a skin graft or with a local flap and skin graft (Fig. 32-
27). Vacuum-assisted closure is also useful in
management of pressure ulcers' in nursing home or
high-risk patients who are not candidates for wound
closure with flap coverage.
Growth Factors
Growth factors and their role are discussed and can be
reviewed in Chapter 11. The only growth factor that
has been approved for clinical use is recombinant DNA
platelet-derived growth factor. It has been shown to
accelerate healing and is effective in diabetic foot
ulcers.64 Its effectiveness, however, is directly related

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Dr.Mustafa D.
l W W ' a a t f W image...

32 • PHARMACOLOGIC AND MECHANICAL MANAGEMENT OF WOUNDS 889

W
•

D E F
FIGURE 3 2 - 2 4 . This patient had a dehiscence of her abdominal wound after pelvic surgery for cancer. The wound
was treated on an outpatient basis after initial debridement (A) with vacuum-assisted closure therapy (B). The sponge
was hooked by a tube to a small suction pump (C) that could be hung from a shoulder strap or worn around the belt
(Dj. The wound after 3 weeks of vacuum-assisted closure therapy (E). It healed after 5 weeks (F).

to the cleanliness of the wound9 and to the vascular-
ity of the wound. If elastases are present on the wound
surface, the growth factor will quickly be metabolized
by the elastases and rendered ineffective. Therefore, if
the growth factor is placed on top of a protein coag-
ulum, it will quickly be destroyed and be ineffective
(see Fig. 32-11). If it is placed on a wound with poor
vascular blood supply, the wound will lack the cellu-
lar components of wound healing necessary for the
growth factor to have an effect.
Growth factor should be applied only if the wound
is not healing at the expected rate of 15% per week.39
The growth factor should not be used unless the
wound is clean and has a good blood supply. It should

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Dr.Mustafa D.
890 I • GENERAL PRINCIPLES

FIGURE 3 2 - 2 5 . This patient had his manubrium debrided

after a sternal infection developed after coronary artery
bypass grafting (A). The exposed heart was covered with
petrolatum gauze (B), and the vacuum-assisted closure
therapy was used (C) for the next 3 days until the culture
results were back and the wound was clean.

also be placed on an area where the biomechanical
abnormalities that caused the initial wound have been
corrected. Therefore, if a plantar forefoot wound
occurred because of a tight Achilles tendon, the
Achilles tendon should be lengthened before any deci-
sion is made as to whether growth factor is needed.15,16
Finally, combining hyperbaric oxygen and growth
factor (see Fig. 32-18) sped up healing more than either
adjunct alone in a trial performed on rabbit ears.65
The same result was not noted in aged rabbit ears,
suggesting that the age of the host may affect the
process.66 Clinical human trials are currently under
way to see whether there is added benefit to the com-
bination of hyperbaric oxygen with growth factor.
The growth factor is a clear gel that is applied
as a thin layer on the debrided granulating wound.
It is then covered with a semiocclusive dressing or
saline-soaked gauze. The initial protocol consisted of
placing the growth factor on the wound for the first
12 hours and then replacing it with saline-soaked
sponge gauze the next 12 hours. Current trials under
way suggest that it is equally effective when it is
applied every 24 hours without a hiatus of 12 hours.
In either case, it is important to remove the protein
coagulum on top of the wound every time the growth
factor is applied. The protein coagulum is removed
with a small curet or toothbrush (see Fig. 32-11). If
the pain from debridement is excessive, one can alter-
nate use of the growth factor with an autolytic
ddbrider.
Use of an isolated growth factor to affect the
complex wound healing process is a simplistic
approach given the myriad sequentially produced
growth factors necessary for normal wound healing.
It is probable that applying a wide array of growth
factors within their physiologically appropriate time
in the wound healing cycle will eventually prove to be
far more successful in affecting healing rates. Many
growth factor combinations are currently being worked
on in the laboratory so that the most effective
time-released combinations can be found.
Skin Substitutes
Skin substitutes are useful in converting a hostile, stag-
nant, or nonhealing bed into a healthy wound bed that
will heal. Processed skin grafts such as xenograft
(pigskin)67,68 or allograft (cadaver skin) provide a bio-
logic dressing that promotes wound healing. If the
xenograft or allograft takes, it then demonstrates that

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Dr.Mustafa D.
image...

32 • PHARMACOLOGIC AND MECHANICAL MANAGEMENT OF WOUNDS 891

FIGURE 3 2 - 2 6 . This is a 97-year-old patient's chronically infected tibia (A) that was d6brided down to bleeding bone
with a burr (B). The wound was then treated for 2 weeks with vacuum-assisted closure therapy (C). The wound devel-
oped adequate granulation tissue and was successfully skin grafted (D). Total hospitalization was 3 days.

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Dr.Mustafa D.
image...

892 I • GENERAL PRINCIPLES

FIGURE 3 2 - 2 7 . This heavy diabetic patient had an infected Charcot collapse of her ankle. The infected bone was
resected and the bone reapposed by an llizarov-type frame (A). Vacuum-assisted closure therapy was started, and 1
week later (B), the wound had granulated well enough to be skin grafted (C). She went on to heal while still in the frame
ID).

the wound bed has adequate blood supply to vascu-
larize the graft and is sterile enough to ensure subse-
quent good take of autografts. The xenograft or
allograft can then be successfully replaced by a skin
graft, or the wound can be allowed to heal by second-
ary intention. Living skin equivalents can also be used
to convert the wound bed into a healthy bed. They act
by producing the gamut of growth factors in a physi-
ologic way to stimulate the wound to heal. Again, the
wound bed is then ready to heal by secondary inten-
tion or to support a successful autograft. For skin
substitutes to be effective, the wound bed has to be
adequately vascularized, infection free, and ddbrided
to healthy tissue before the skin substitute is placed on
the wound.
Xenografts are made from porcine skin, and their
success is thought to be due to their underlying
collagen matrix.69,70 The porcine skin is harvested,

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Dr.Mustafa D.
image...
32 • PHARMACOLOGIC AND MECHANICAL MANAGEMENT OF WOUNDS
lyophilized, and frozen in liquid nitrogen. It is then
thawed just before use. It takes like a skin graft during
the next 4 to 6 days. Depending on the immune status
of the patient, rejection will begin anywhere from 9
days to 45 days later. Xenograft can be replaced with
an autologous skin graft at any time after it has ini-
tially taken (Fig. 32-28). Xenograft is an excellent source
of temporary wound coverage if the surgeon is not
sure the actual skin graft will succeed. By adding an
intervening xenograft, the surgeon ensures a much
higher success rate with the subsequent split-thickness
skin graft.
Allograft71 (preserved cadaver skin) can be used in
the same way as xenograft. It likewise is rejected accord-
ing to its antigenicity and the patient's immune status.
The immediate availability of allograft is far more
limited than that of xenografts because the supply
depends on existing skin banks. There is also ever-
present concern for disease transmission when allo-
graft is used. However, both xenografts and allografts
have proved to be extremely useful in the treatment of
burn patients 72 by accelerating healing and minimiz-
ing scarring.
There are engineered skin substitutes that function
in much the same way as xenografts and allografts.
However, because they consist only of collagen, they
become integrated in the underlying wound and do
not stimulate rejection. Integra* artificial skin is com-
posed of an overlying removable silicone film (to
prevent desiccation) with an underlying dermal matrix
of cross-linked bovine collagen and chondroitin
sulfate. The dermal layer functions as a dermal tem-
plate to facilitate the migration of the patient's own
fibroblasts, macrophages, lymphocytes, and endothe-
lial cells. During the ensuing week, a new cell-
populated dermis is formed. Then, the silicone layer
can be removed so that a thin autologous skin graft
(0.004 to 0.006 inch) can be placed on it. AlloDerm t
is an acellular allograft made of cryopreserved cadaver
skin. It consists of a decellularized dermal matrix with
a structurally intact dermis and basement membrane.
The freeze-dried dermis has to be rehydrated with
sterile saline. It is placed on the wound bed and can
immediately be covered with a thin autograft. In a
single trial, it was shown to function almost as well as
a thick skin graft.73 In this instance, however, the quality
of the recipient wound bed has to be equal to one on
which an autograft would be placed. Finally, Biobrane'
consists of a thin Silastic semipermeable membrane
covering a knitted Silastic nylon fabric that is coated
with type I porcine collagen. It is applied to superfi-
cial burns and skin graft donor sites to promote healing.
'Johnson & Johnson Medical, Arlington, Texas.
LifeCcIl Corporation, Branchburg, New Jersey.
Bertek Pharmaceuticals, Morgantown, West Virginia.
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Dr.Mustafa D.
893
Living skin equivalents consist of collagen matri-
ces seeded with living dermal cells that are then cul-
tured to produce a live skin equivalent. Graftskin
(Apligraf*) consists of a bovine collagen matrix seeded
with human dermal fibroblasts and epidermal ker-
atinocytes from neonatal foreskin tissue. They, in turn,
form a living bilayered construct that mimics human
skin. Graftskin effectively stimulates the formation of
granulation tissue and neoepithelialization by acting
as a local producer of the necessary growth factors
and wound healing adjuncts (Fig. 32-29). In about
10% to 15% of patients, it actually appears to behave
much like a normal skin graft, although it is likely
that the final epithelium is from the host. 74 It has been
effective in promoting healing in venous stasis ulcers75
and diabetic foot ulcers.76 Again, for it to be success-
ful, it has to be placed on a clean, healthy wound
surface.
OrCel is also a bilayered product available in
Europe and being tested here in the United States.77
It likewise consists of dermal scaffolding populated
by fibroblasts and an epithelial layer with keratinocytes.
It has been shown to be effective on donor sites for
burn patients, venous stasis ulcers, and diabetic ulcers.
Its mode of effectiveness is thought to be its ability to
locally produce the necessary growth factors for
wound healing. Dermagraft," a polyglycolic mesh infil-
trated by dermal fibroblasts, has been successful in
treating diabetic foot ulcers.78 Again, DermagrafVs
effectiveness is based on its ability to secrete the appro-
priate growth factors and likewise needs to be placed
on a clean, healthy wound surface.
Hyperbaric Oxygen
Oxygen is an essential component of wound healing,
and the rate of healing can be directly linked to the
level of tissue oxygenation. Oxygen is used for protein
synthesis, cell replication, hydroxylation of collagen,
exportation of collagen out of the fibroblast cell,79,80
and neoepithelialization. 81 The strength of the subse-
quent wound repair is related to oxygen concentra-
tion.82,83 Angiogenesis at the wound's edges is driven
by the existing oxygen gradient 84 ; the center of the
wound is oxygen poor, whereas the periphery is
oxygen rich. The resultant oxygen-poor and lactate-
rich gradient drives macrophages to produce angio-
genesis factors until capillary ingrowth is complete.
The periphery of the wound supplies the necessary
oxygen to support the process. Finally, the ability of
leukocytes to resist infection is also oxygen gradient
dependent. 85 Not only does the oxygen concentration
affect the ability of leukocytes to produce free radicals
Organogenesis Inc., Canton, Mass, and Novartis Pharmaceutical Corpo-
ration, East Hanover, New Jersey.
"Smith & Nephew Inc., Largo, Florida.
age...

894 I • GENERAL PRINCIPLES

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A&Wttf'aatfW image...
32 • PHARMACOLOGIC AND MECHANICAL MANAGEMENT OF WOUNDS
and kill bacteria, but it also speeds up the clearance of
bacteria from the wound site.86
Because skin and connective tissue are under the
control of the autonomic system, blood flow and result-
ant oxygen delivery are affected by pain, cold, and
decreased blood volume. 87 Therefore, simple measures
such as controlling pain, keeping the environment
warm, and optimizing blood volume can optimize
oxygen delivery to the wound site. Control of drugs
such as nicotine 88 and p blockers that negatively affect
the autonomic system is critical to optimizing local
blood flow. Patients who are receiving p blockers for
hypertension should be switched to alternative
antihypertensive medications that do not potentiate
a agonists until the wound has healed.89 Because of
the sensitivity of the autonomic system, measuring the
tissue oxygen level around the wound is the most accu-
rate way to assess immediate wound perfusion.90
Indeed, in ischemic limbs, the simplest measures have
been shown to improve tissue oxygenation. Limb
dependency increases the transcutaneous oxygen level
by 22 mm Hg, and adding nasal oxygen can further
increase it by an additional 12 mmHg. 9 1 Supplemen-
tal inspired oxygen has been shown to decrease wound
infection in the surgical patient. 92
Systemic hyperbaric oxygen further increases tissue
oxygenation. The treatment consists of pressurizing
the entire patient in a chamber to pressures greater
than 1 atmosphere and adjusting the surface breath-
ing mixtures to more than 100% oxygen. Each gram
of hemoglobin carries 1.34 mL of bound oxygen,
whereas inhaled air adds only 0.3 mL of oxygen
per 100 mL of blood. This means that someone
with a hemoglobin concentration of 15 g/100 mL
who is breathing normal air carries 20.1 mL of oxygen
(15 x 1.34) by hemoglobin; also, 0.33 mL of dis-
solved oxygen is carried in the surrounding plasma
for a total of 20.4 mL per 100 mL. Hyperbaric
oxygen further increases the amount of dissolved
oxygen so that each additional atmosphere of
pure oxygen adds 2.2 mL of dissolved oxygen per
100 mL of blood (2.2 vol % ) .
Because the capillaries around a chronic wound are
often partially occluded by microthrombi, the passage
FIGURE 3 2 - 2 8 . This is a young healthy patient who
burned his heel in a motorcycle accident (A). The wound
was debrided and covered with xenograft (B). The
xenograft took in the first week and was removed on the
seventh day, revealing a healthy granulating bed under-
neath (C). The bed was successfully skin grafted (D).
Xenograft: is an excellent temporizer if the surgeon is not
sure that an autologous skin graft will succeed. By adding
an intervening xenograft, the surgeon ensures a much
higher success rate with the subsequent split-thickness
skin graft.
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Dr.Mustafa D.
895
of red blood cells is limited. However, plasma can still
flow, and the amount of oxygen it carries therefore
becomes important. 93 Krogh94 has shown that in these
capillaries containing only plasma, the oxygen con-
centration on the arterial side at 2 atmospheres of
oxygen is fourfold that of normal inspired air, whereas
it is twofold that on the venous side. The dissolved
oxygen in the plasma under hyperbaric conditions (2.2
vol %) meets the oxygen extraction rates of skin (i.e.,
the oxygen extraction rate of skin is 2.0 vol % versus
11.0 vol % for the heart, 6.1 vol % for the brain, and
5.0 vol % for muscle). 95 Obviously, for hyperbaric
oxygen treatments to be effective, the circulation to
the wound site has to be patent.
Clinical studies have shown that hyperbaric oxygen
treatments are successful in healing diabetic ulcers96
(randomized nonblinded), preventing diabetic ampu-
tations 97 (randomized double blinded), and healing
venous stasis ulcers98 (controlled blinded). Osteora-
dionecrosis has been treated successfully with hyper-
baric oxygen, especially in the jaw.99,100 Hyperbaric
oxygen treatments are likewise effective in limiting
tissue damage in more extreme medical emergencies:
the treatments minimize tissue necrosis after surgical
release of the fascial compartment of limbs suffering
from compartment syndrome 101 and in patients with
gas gangrene102; they have been used successfully in
reimplantation when there has been a long delay before
reimplantation or there was extensive trauma involv-
ing the reimplanted part103,104; and finally, hyperbaric
oxygen treatments have been successfully used to
salvage failing flaps.105
Selection of patients who might benefit from
hyperbaric oxygen treatment should be strict. The
wound must have failed conservative wound therapy
and is not shrinking by the prerequisite 10% to 15%
per week. The wound must be well vascularized and
adequately debrided. The patient must have a trans-
cutaneous oxygen level at the wound periphery
measuring less than 4 0 m m H g . The patient is
then tested for the affected tissue's response to
increased inspired oxygen. After breathing of 100%
oxygen through a mask, the transcutaneous oxygen
level should increase by at least 10mmHg. Alterna-
tively, if the patient is given a test dive, the trans-
cutaneous oxygen level should increase to above
200mmHg. If the patient fails to respond to these
tests, he or she is unlikely to benefit from hyperbaric
oxygen therapy.
Each treatment lasts for 90 minutes. After treat-
ment, the increased oxygen perfusion persists in
muscle for 1 hour and in the skin and subcutaneous
tissue for up to 4 hours. 106 The need for supplemen-
tal oxygen must be balanced by the risk of oxygen
toxicity. Twice-a-day treatments are used acutely for
extreme conditions (necrotizing fasciitis, ischemic limb
after release of compartment syndrome, radiation
image..

896 • GENERAL PRINCIPLES

FIGURE 3 2 - 2 9 . This patient had a nonhealing Achilles tendon ulcer (A). The wound was dSbrided, and graftskin was
meshed and placed on it (B). At 1 week, the wound had a healthy granulating base (C) that continued to epithelialize
in. The wound shrunk rapidly by 3 weeks, and the base contains only healthy granulation tissue (D).

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image...
32 • PHARMACOLOGIC AND MECHANICAL MANAGEMENT OF WOUNDS
burn, failing flaps). However, for chronic wounds, treat-
ment once a day is sufficient. Adding topical growth
factor61,62 to the wound while hyperbaric oxygen treat-
ments are undergone has been shown in rabbits to
affect the wound more than either treatment alone
(see Fig. 32-18). Current human clinical trials of this
combined treatment are under way. The wound is then
monitored closely, and the hyperbaric treatments can
be stopped when the wound characteristics have
changed to those of an acute wound. Alternative, less
expensive strategies can be used at this point, such as
conservative dressing regimens, topical growth factor,
skin substitutes, or skin grafts.
CONCLUSION
In summary, no w o u n d can heal in an orderly fashion
unless it is clean, healthy, and free of infection.
Debridement is key in achieving this goal provided
(1) the w o u n d is adequately vascularized, (2) appro-
priate antibiotics are prescribed, and (3) all other
medical aspects of the patient have been addressed.
Surgical debridement is the quickest and most effi-
cient way of getting the w o u n d ready for healing. Bio-
surgery with maggots offers a promising alternative.
If the resulting w o u n d bed is healthy, conservative
w o u n d care measures or conventional plastic surgical
techniques can be used.
However, if the subsequent w o u n d bed is thought
to be unable to promote a 10% to 15°bper week wound
shrinkage rate or if vital structures (bone, tendon, neu-
rovascular bundle) are exposed, additional measures
should be used. Vacuum-assisted closure therapy pro-
vides an excellent dressing that stimulates t h e forma-
tion of granulation while decreasing local e d e m a and
keeping the w o u n d clean. It can speed the healing of
a w o u n d by secondary intention or act as an excellent
preparatory agent for subsequent flap surgery or skin
grafting. Other modalities that stimulate the forma-
tion of granulation tissue and speed up w o u n d closure
include skin substitutes, topical growth factor, and
hyperbaric oxygen. Once the w o u n d has been con-
verted so that it starts to heal at 10% to 15% per week,
one can either change to a moist w o u n d dressing
regimen or apply plastic surgical techniques to achieve
closure.
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tic pigs. Nature 1962;193:293.
38. Kantor J, Margolis DJ: A multicentre study of percentage change
in venous leg ulcer area as a prognostic index of healing at 24
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39. Daltrey DC, Rhodes B, Chattwood JG: Investigations into
microbial flora of healing and non-healing decubitus ulcers.
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40. Vilijanto J: Disinfection of surgical wounds without inhibi-
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42. Taylor HD, Austin JH: The solvent action of antiseptics on
necrotic tissue. J Exp Med 1918;27:155.
43. Tredgct EE, Shankowsky HA, Goeneveld A, et al: A matched-
pair, randomized study evaluating the efficacy and safety of
Acticoat silver coated dressing for treatment of burn wounds.
J Burn Care Rehabil 1998:19:531.
44. Yin HQ, Langford R, Burrell RE: Comparative evaluation of
the antimicrobial activity of Acticoat antimicrobial dressing.
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45. Leveen H, Falk G, Boreck B, Diaz C: Chemical acidification of
wounds. An adjunct to healing and the unfavorable action of
alkalinity and ammonia. Ann Surg 1973:178:745.
46. Phillips I, Lobo AZ, Fernandez R, et al: Acetic acid in the treat-
ment of superficial wounds infected with Pseudomonas. Lancet
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47. Vasquez JE, Walker ES, Franzus BW, et al: The epidemiology
of mupirocin resistance among methicillin-rcsistant Staphy-
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48. Kannon GA, Garret AB: Moist wound healing with occlusive
dressing: a clinical review. Dermatol Surg 1995:21:583.
49. Mertz PM, Ovington LG: Wound healing microbiology.
Dermatol Clin 1993;11:739.
50. Hinman CD, Mailbach H: Effect of air exposure and occlu-
sion on experimental human skin wounds. Nature
1962:200:377.
51. Alvarez OM, Hefton JM, Eaglstcin WH: Healing wounds: occlu-
sion or exposure. Infect Surg 1984:3:173.
52. Alvarez OM, Mertz PM, Eaglstcin WH: The effect of occlusive
dressings on collagen synthesis and re-epithelialization in
superficial wounds. J Surg Res 1983:35:142.
53. Linsky CB, Rovee DT, Dow T: Effects of dressings on wound
inflammation and scar tissue. In Hildick-Smith G, ed: The
Surgical Wound. Philadelphia, Lea & Febiger, 1981:191-205.
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54. Freidman SJ, Su WPD: Management of leg ulcers with
hydrocolloid occlusive dressings. Arch Dermatol 1984;120:
1329.
55. Barker AT, Jaffe LF, Vanable JW: The glabrous epidermis of
cavies contains a powerful battery. Am J Physiol 1982;242:
R358.
56. Wolcott LE, Wheeler PC, Hardwicke HM, Rowley BA: Accel-
crated healing of skin ulcers by electrotherapy. South Med J
1969:62:795.
57. Augustinsson LE, Carlsson CA, Holm J, et al: Epidural elec-
trical stimulation in severe limb ischemia. Pain relief, increased
blood flow and a possible limb-saving effect. Ann Surg
1985:202:104.
58. Peters EJ, Lavery LA, Armstrong DG, Fleischli JG: Electric
stimulation as an adjunct to heal diabetic foot ulcers: a ran-
domized clinical trial. Arch Phys Med Rehabil 2001;82:721.
59. Ieran M, Zaffuto S, Bagnacani M, et al: Effect of low frequency
pulsing electromagnetic fields on skin ulcers of venous
origin in humans: a double-blind study. J Orthop Res
1990:8:276.
60. Mertz PM, Davis SC, Oliveira-Gandia M, Eaglstein WH: The
wound environment: implications from research studies for
healing and infection. In Krasner D, Kane D, eds: Chronic
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cations, 1997:57-63.
61. FalangaV:Occlusivewounddressings.Why,when,which?Arch
Dermatol 1988:124:872.
62. Urschel JD, Scott PG, Williams HTG: The effect of mechani-
cal stress on soft and hard tissue repair: a review. Br J Plast
Surg 1988:41:182.
63. Orgill D: Personal communication, December 2000.
64. Steed DL: The Diabetic Study Group: Clinical evaluation
of recombinant human platelet derived growth factor for
treatment of lower extremity diabetic ulcers. J Vase Surg
1995:21:71.
65. Zhao LL, Davidson JD, Wee SC, et al: Effect of hyperbaric oxygen
and growth factors on rabbit ear ischemic ulcers. Arch Surg
1994:129:1043.
66. Bonomo SR, Davidson JD, Tyrone JW, et al: Enhancement of
wound healing by hyperbaric oxygen and transforming growth
factor beta3 in a new chronic wound model in aged rabbits.
Arch Surg 2000:135:1148.
67. Bromberg BE, Song IC, Mohn MP: The use of pigskin as a
temporary biological dressing. Plast Reconstr Surg 1965:36:80.
68. Ersek RA, Lorio J: The most indolent ulcers of the skin treated
with porcine skin graft and silver ions. Surg Gynecol Obstet
1984:158:431.
69. AtnipRG,BurkeJF:Skincoverage.CurrProblSurg 1983;20:624.
70. Tavis MJ, Thornton J, Danet R, et al: Current status of skin
substitutes. Surg Clin North Am 1978:58:1233.
71. Bondoc CC, Butke JF: Clinical experience with viable
frozen human skin and frozen skin bank. Ann Surg 1971;
174:371.
72. Yue-Liang D, Shu-Sung P, Dc-Zhen W, et al: Clinical and
histological observations on the application of intermingled
auto- and porcine-skin heterograft in third degree burns.
Burns 1981:9:381.
73. Wainwright D, Madden M, Luterman A, et al: Clinical evalu-
ation of an acellular allograft dermal matrix in full-thickness
burns. J Burn Care Rehabil 1996; 17:124.
74. Brain A, Purkis P, Coates P, et al: Survival of cultured allogenic
keratinocytes transplanted to the deep dermal bed assessed
with probe specific for Y chromosome. BMJ 1989:298:917.
75. Falanga V, Margolis D, Alvarez O, et al: Rapid healingof venous
ulcers and lack of clinical rejection with an allogeneic cultured
human skin equivalent. Arch Dermatol 1998; 134:293.
76. Vevcs A, Falanga V, Armstrong DG: Graftskin, a human skin
equivalent, is effective in the management of non-infected
neuropathic diabetic foot ulcers. Diabetes Care 2001;24:290.
T W W f c f l t f W image...
32 • PHARMACOLOGIC AND MECHANICAL MANAGEMENT OF WOUNDS
77. BelloYM,FalabellaAF,EaglsteinWH:Tissue-cnginceredskin.
Current status in wound healing. Am J Clin Dermatol
2001;2:305.
78. Gentzkow GD, Prendergast JJ, Iwaski SD, et al: Use of Der-
magraft, a cultured human dermis, to treat diabetic foot ulcers.
Diabetes Care 1996;19:350.
79. Juva K, Prockop DJ, Cooper GW, Lash JW: Hydroxylation of
proline and the intracellular accumulation of a polypeptide
precursor of collagen. Science 1966; 152:92.
80. Hunt TK, Pai MP: The effect of varying ambient oxygen
tensions on wound metabolism and collagen synthesis. Surg
Gynecol Obstet 1972;135:561.
81. Pai MP, Hunt TK: Effect of varying oxygen tension on healing
in open wounds. Surg Gynecol Obstet 1972;135:756.
82. Uitto J, Prockop DJ: Synthesis and secretion of under-
hydroxylated procollagen at various temperatures by cells
subject to temporary anoxia. Biochem Biophys Res Commun
1974;60:414.
83. Shandall A, Lowndes R, Young HL: Colonic anastomotic healing
and oxygen tension. Br J Surg 1985;72:606.
84. Knighton DR, Silver IA, Hunt TK, et al: Regulation of wound-
healingangiogenesis—effect of oxygen gradients and inspired
oxygen concentration. Surgery 1981;90:262.
85. Hohn DC, Mackay RD, Halliday B, et al: The effect of oxygen
tension on the microbicidal function of leukocytes in wounds
and in vitro. Surg Forum 1976;27:18.
86. Knighton DR, Halliday B, Hunt TK: Oxygen as an antibiotic:
a comparison of the effects of inspired oxygen concentration
and antibiotic administration on in vivo bacterial clearance.
Arch Surg 1986:121:191.
87. Chang N, Goodson III WH, Gottrup F, et al: Direct measure-
ment of the wound and tissue oxygen tension in postopera-
tive patients. Ann Surg 1983;197:470.
88. Rees TD, Liverett DM, Guy GL: The effect of cigarette smoking
on skin flap survival in facelift patients. Plast Reconstr Surg
1984;73:911.
89. Hunt TK: Personal communication, September 1998.
90. Jonsson K, Jensen JA, Goodson WH III, et al: Assessment of
perfusion in postoperative patients using tissue oxygen meas-
urements. Br J Surg 1987;74:263.
91. Johnson WC, Grant HI, Baldwin RN, et al: Supplemental
oxygen and dependent positioning as adjunctive measures
to improve forefoot tissue oxygenation. Arch Surg 1988;123:
1227.
92. Lavan F,HuntTK: Oxygen and wound healing. Clin Plast Surg
1990:17:463.
93. Biglow WG: The microcirculation. Can J Surg 1964;7:237.
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899
94. KroghA: The number anddistribution of capillaries in muscle
with calculations of oxygen pressure head necessary for
supplying the tissue. J Physiol 1919;52:409.
95. Van Meter K: Systemic hyperbaric oxygen therapy as an aid in
resolution of selected chronic problem wounds. In Krasner D,
Kane D, eds: Chronic Wound Care, 2nd ed. Wayne, Pa, Health
Management Publications, 1997:260-272.
96. Baroni G, Porro T, Faglia E, et al: Hyperbaric oxygen in
diabetic gangrene treatment. Diabetes Care 1987:19:81.
97. Faglia E, Favales F, Aldeghi A, et al: Adjunctive systemic hyper-
baric oxygen therapy in treatment of severe prevalently
ischemic diabetic foot ulcer;a randomized study. Diabetes Care
1996:19:1338.
98. HammarlundC.SundbergT: Hyperbaric oxygen reducedsize
of chronic leg ulcers: a randomized double blind study. Plast
Reconstr Surg 1996;93:829.
99. Hart GB, Strauss MB: Hyperbaric oxygen in management of
radiation injury. In Schmutz J, ed: Proceedings of the 1st Swiss
Symposium on Hyperbaric Medicine. Basel, Foundation for
Hyperbaric Medicine, 1986:31-35.
100. Marx RE, Johnson RP, Kline SN: Prevention of osteora-
dionecrosis: a randomized prospective clinical trial of
hyperbaric oxygen versus penicillin. J Am Dent Assoc
1988;111:49.
101. Strauss MB, Hargrens AR, Gcrshuni DG, et al: Reduction of
skeletal muscle necrosis using intermittent hyperbaric oxygen •
in a model compartment syndrome. J Bone Joint Surg Am
1983;65:656.
102. Brummelkamp WD, Hogendijk J, Boerema I: Treatment of
anaerobic infections (clostridial myositis) by drenching
the tissues with oxygen under high pressure. Surgery 1961;
49:299.
103. Colignon M, Carlier A, Khuc T, et al: Hyperbaric oxygen
in acute ischemia and crush injuries. In Marroni A, Oriani
G, eds: Proceedings of the 13th annual meeting of the
European Undersea Biomedical Society, Palermo, Italy,
1987.
104. Bao JYS: Hyperbaric oxygen therapy in re-implantation of
several limbs. In Kindwall EP, ed: Proceeding of the 8th Inter-
national Congress on Hyperbaric Medicine, San Pedro, Calif,
1987:182-186.
105. Bower JC.Stauss M B, Hart GB: Clinical experience with hyper-
baric oxygen therapy in the salvage of ischemic skin flaps and
grafts. J Hyperbaric Med 1986;1:141.
106. Cianci P: Adjunctive hyperbaric oxygen therapy in the
treatment of the diabetic foot. J Am Podiatr Med Assoc
1994;84:448.
image...

COLOR PLATE 3 2 - 1 . This is an 8-month-old chronic

wound in a morbidly obese diabetic patient with severe con-
gestive heart failure. Note the dull pale appearance of the
granulation tissue covering the wound (A). After daily
debridement and hyperbaric oxygen, the wound was con-
verted to a healthy wound within 3 weeks. Note the resul-
tant fine, bright red granulation tissue covering the wound
(B). It is now able to successfully accept a skin graft (C).

*\*\

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image...
CHAPTER
33
•
Problem Wounds and
Principles of Closure
SCOTT L HANSEN, MD • STEPHEN J. MATHES, MD, FACS
DEFINITION OF A PROBLEM WOUND
CAUSES OF PROBLEM WOUNDS
Intrinsic Factors
Mechanical (Structural) Factors
Extrinsic Factors
DISEASE STATES ASSOCIATED WITH PROBLEM
WOUNDS
Connective Tissue Diseases
Collagen Disorders
Vasculitis
Pyoderma Gangrenosum
Hidradenitis Suppurativa
Immune Deficiency
Neurologic Disorders
Metabolic Diseases
DEFINITION OF A PROBLEM
WOUND
Wound healing is a complicated process by which mul-
tiple events occur in synchrony to achieve complete
wound closure. Simple wounds are defined as those
wounds that are readily managed by local wound care
with subsequent contraction, direct closure, skin graft,
or local tissue rearrangement. Unlike simple wounds,
complex wounds have excessive depth or size, are in
an unfavorable location, or are limb or life threaten-
ing. Complex wounds usually require tissue that is
distant from the wound site for closure to be achieved.
These wounds are generally closed with regional or
distant flap transposition or by microvascular com-
posite tissue transplantation. A wound that should close
by simple methods (simple wound) but fails to achieve
closure or a wound that recurs (unstable wound) after
a simple or complex wound closure technique (simple
or complex wound) is defined as a problem wound.
Failure of wound healing with simple or complex
wounds or wound recurrence after initial closure can
be related to local or systemic causes or a technical
error at the time of wound closure. When managing
a problem wound, the surgeon must first consider the
cause of the problem wound and the associated disease
state of the patient, then proceed with appropriate
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Organ System Failure
Factitial Wounds
Acne Keloidalis Nuchae
Congenital Abnormalities
MANAGEMENT OF THE PROBLEM WOUND
Clinical Assessment
Timing
Nonoperative Management
Operative Management
Management of Specific Problem Wounds
THE FUTURE OF PROBLEM WOUND MANAGEMENT
Topical Growth Factors
Skin Substitutes and Stem Cell Therapy
Electrical Stimulation
management. Understanding of each facet of the
problem wound is necessary to achieve successful
wound closure.
An analysis of problem wounds demonstrates that
the causes of these wounds are intrinsic, mechanical
(structural), or extrinsic—individually or in combi-
nation. These causes of impaired wound healing are
analyzed as they relate to problem wound management
(Tables 33-1 and 33-2).
CAUSES OF PROBLEM WOUNDS
Intrinsic Factors
Intrinsic factors leading to impaired wound healing
and problem wounds originate from the wound itself,
largely due to vascular insufficiency, although other
intrinsic factors such as impaired cellular function,
infection, malignant disease, and nutritional imbal-
ance can contribute to problem wounds (Table 33-3).
Deficient intrinsic components often occur in combi-
nation in patients with problem wounds.
VASCULAR INSUFFICIENCY
Diseases associated with intrinsic causes of decreased
or abnormal circulation can be divided into arterial,
venous, and lymphatic insufficiency.
901
902 • GENERAL PRINCIPLES

TABLE 33-1 • ETIOLOGY OF SPECIFIC PROBLEM WOUNDS

Location Intrinsic Mechanical Extrinsic

Head and neck

Exposed skull S P
Osteoradionecrosis of the mandible P s
Orocutaneous fistula S P
Chest
Sternal wound P S
Bronchopleural fistula s P
Chest wall defect s P
Abdominal wall
Traumatic loss s P
Fistula s p
Exposed and infected mesh s p
Bone
Osteomyelitis p S
Nonunion s P
Exposed orthopedic hardware s p
Lower extremity
Exposed knee prosthesis s p
Venous ulcer p S
Achilles tendon rupture s p
Breast
Exposed breast implant s p
Perineum
Perineal trauma s p
Extirpative wound s p
Exposed vascular graft s p
Back
Exposed spinal hardware s p
Skin and muscle
Necrotizing soft tissue infection p s
Burn, frostbite, electrical s P
Envenomation s p
Extravasation s p
Pressure sore s p

P, primary; S, secondary.

Arterial Insufficiency are trauma, macrovascular disease (atherosclerotic

Adequate tissue oxygenation plays a critical role in
wound healing. In wound healing studies, it has been
shown by transcutaneous Po 2 (TcP02) monitoring that
suboptimal oxygen levels can prevent wounds from
healing appropriately.1 In 1982, White et al2 showed
that TcP0 2 values of more than 50 mm Hg predicted
success for various levels of amputations and for wound
healing without the need for additional reconstruc-
tive procedures; values of 40 mm Hg or less were
associated with continued wound problems and
complications after amputation. Proliferation of fibro-
blasts and deposition of collagen are directly propor-
tional to wound oxygen tension.3,4 Correction of
wound ischemia with supplemental oxygen leads to
an increased rate of collagen deposition, epithelial-
ization, and better healing of split-thickness skin grafts
(Fig. 33-1).5 Wound ischemia can arise from a variety
of causes. The common causes of vascular insufficiency
disease), microvascular disease (radiation exposure),
medication or illicit drug use, and vasospastic
disorders.
Hypovolemic shock after major trauma results in
poor peripheral tissue perfusion and oxygenation as
compensation to preserve blood flow to central organs
diminishes perfusion to the skin through peripheral
constriction. Decreased peripheral oxygenation occurs
in the early stages after trauma and returns late. It has
been shown that the parameters by which resuscita-
tion is measured (i.e., blood pressure, urine output,
and base deficit) are not reliable measures of periph-
eral perfusion.6 Thus, trauma patients who have been
"classically" resuscitated may in fact continue to have
compromised peripheral oxygen delivery portending
problem wounds. Human studies of trauma and
wound healing are limited, although Diegelmann et
al7 showed that patients with severe traumatic injuries
had deficient collagen production measured by

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image...

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 903

TABLE 33-2 • ETIOLOGY OF SPECIFIC PROBLEM WOUNDS

Intrinsic Mechanical Extrinsic

c
o
8
1 3 3,
1 -a

Caustic and Chem

Substance Exposur
1
1 >——
11 3
1
c
1 3 1
3
IS
o
*•*
1 o
••*
s
3 § b

111
c
I
§
i ! 11 o
••-4
3 6?
3
CO

Head and neck Exposed skull S s s p s

Osteoradionecrosis of the P s S s
mandible
- Orocutaneous fistula s s s s p
Chest Sternal wound s p s S s
Bronchopleural fistula s s p S s
Chest wall defect s P s s
Abdominal wall Traumatic loss s s s S S p
Fistula s s s p S s
Exposed and infected mesh s s P s s
Bone Osteomyelitis s p s s
Nonunion s s s P
Exposed orthopedic hardware s P s s
Lower extremity Exposed knee prosthesis s s P s
Venous ulcer P s s s
Achilles tendon rupture s p
Breast Exposed breast prosthesis s s P s
Perineum Perineal trauma s p
Extirpative wound s S s s P s
Exposed vascular graft s s P s
Back Exposed spinal hardware s s P s s
Skin and muscle Necrotizing soft tissue S P s s
infection
Burn, frostbite, electrical s s s p
Envenomation s P
Extravasation s P
Pressure sore s s s p s

P, primary; S, secondary.

hydroxy proline accumulation, which was only 40%
of normal at 14 days after injury. In addition to trauma
patients, it has been shown that intravascular volume
is often inadequate in patients undergoing elective pro-
cedures. 8 Arkilic et al9 have shown that supplemental
perioperative fluid administration significantly
increases tissue perfusion and tissue oxygen partial
pressures. Therefore, adequate perioperative fluid
administration may improve the ability of a wound
to heal.
Macrovascular disease leads to decreased blood flow
and delivery of oxygen. The most common macro-
vascular disease is atherosclerosis. Risk factors for
development of atherosclerosis include diabetes, age,
menopause, smoking, hypertension, obesity, and
sedentary lifestyle.10 The atherosclerotic plaque is a con-
sequence of focal accumulation of leukocytes and
smooth muscle cells within the intima of the arterial
wall. Plaques enlarge by an expansion of these cells,
accumulation of extracellular matrix, and deposition
of lipid.11 As these plaques grow, the artery wall
attempts to remodel such that the luminal size is
maintained. 12 When plaque formation overcomes this
remodeling process, blood flow is compromised and
ischemia ensues. This global ischemia leads to end-
organ ischemia, infarction, and tissue death. Wounds
associated with arterial insufficiency exhibit granula-
tion tissue, epithelialization, and decreases in strength.
When a wound is surgically manipulated with debride-
ment or attempted reconstruction, the metabolic

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904 I • GENERAL PRINCIPLES

7 i
3 concentration
"D
6 -

o 5 -i
-J
s E
<5 4 -
a.
1 o
tq 3 -
to
O
O 2 -

31 -

Po2 mm Hg Days after inoculation

B
FIGURE 3 3 - 1 . A, Relationship of leukocyte killing of Staphylococcus aureus and oxygen tension. B, Effect of increas-
ing oxygen concentration on bacterial clearance from wounds. (From Knighton DR, Halliday B, Hunt TK: Oxygen as an
antibiotic. The effect of inspired oxygen on infection. Arch Surg 1984; 119:199.)

requirements increase. The diminished blood flow is Martorell ischemic leg ulcers are a specific condi-
unable to meet this increased metabolic demand, tion associated with hypertension. This condition,
leading to an intrinsic cause of a problem wound. Arte- characterized in 1945 by Martorell,14 is described by
rial ulcers most commonly occur in male patients with pain disproportionate to the size of the ulcer and its
atherosclerosis, usually in association with cardiovas- specific location on the anterolateral leg above the
cular disease, diabetes, hypertension, or smoking (Fig. ankle; it is associated with a female predominance, long
33-2). Patients typically have symptoms of claudica- periods of standing, and poorly controlled hyperten-
tion and rest pain. The leg pain improves when the sion. It is suggested that the ischemic necrosis is a result
leg is dependent and is exacerbated when the leg is of hypertensive arteriolar disease. Duncan and Faris15
elevated. The base of the arterial ulcer generally does showed that patients with hypertensive ulcers have a
not bleed and has a punched-out appearance. Ulcers higher peripheral vascular resistance and concluded
associated with an ankle/brachial index of less than that this higher resistance may interfere with the com-
0.45 (normal range, 0.90 to 1.30) generally do not heal pensatory vasodilatation that normally occurs distal
without revascularization.13 to an arterial stenosis. In these patients, this exacer-
bates already poor tissue perfusion and subsequently
leads to ulcer formation.15,16
TABLE 3 3 - 3 • INTRINSIC CAUSES OF Radiation exposure is thought to have its greatest
PROBLEM WOUNDS effect on the microcirculation and dividing cells. The
damage from radiation is dose dependent and cumu-
Vascular insufficiency lative over time. In general, the more frequently cells
Trauma divide, the greater their sensitivity to radiation injury.
Macrovascular disease Wound healing cells most affected include endothe-
Microvascular disease lial cells, fibroblasts, and keratinocytes. Acute radia-
Medication or illicit drug use tion injury is manifested by vascular stasis and
Vasospastic disorders subsequent occlusion of the microcirculation in addi-
Cellular impairment
Macrophage tion to a decrease in the tensile strength and total
Neutrophil collagen deposition of the wound/ 7 On histologic
Platelet examination, subendothelial proliferation and medial
Keratinocyte wall thickening are seen in the blood vessel. Irradi-
Fibroblasts ated tissue characteristically has some degree of resid-
Endothelial cells
ual endothelial cell injury and progressive endarteritis,
Infection
Malignant disease which results in atrophy, fibrosis, and poor tissue
Nutritional imbalance repair. It has been shown experimentally that the ability
Amino acids of fibroblasts to proliferate is irreversibly injured by
Vitamins radiation.18 In addition, endothelial cell dysfunction
Minerals results in a lack of new blood vessel formation. The

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image...

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 905

FIGURE 3 3 - 2 . A and B, Avascular necrosis of lateral foot seen in ambulatory patient (intrinsic
factor: arterial insufficiency). See Figure 33-59. (From Mathes SJ, Nahai F: Reconstructive Surgery:
Principles, Anatomy, and Technique. New York, Churchill Livingstone, 1997.)

skin effects of chronic irradiation are due to the irre-
versible changes within the cell nuclei and subsequent
cytoplasmic dysfunction.19,20
Certain medications and drugs cause vascular
insufficiency by changes in the microcirculation.
Tobacco use causes cutaneous vasoconstriction as
shown by skin temperature measurements, plethys-
mography, and direct evaluation of the capillary bed.
Nicotine is the principal vasoactive component in
cigarettes, inducing endothelial wall injury, slowing
capillary blood flow, and causing the release of cate-
cholamines. 21 Nicotine also stimulates thromboxane
A2, a potent vasoconstrictor, and causes release of
carbon monoxide, which decreases the oxygen-
carrying capacity of the blood. 22 Platelet adhesiveness
increases with nicotine exposure, thereby raising the
risk of microvascular occlusion and tissue ischemia.
Many studies have shown an increased risk for com-
plications in surgical patients who smoke. For instance,
when effects of smoking on complications were eval-
uated in patients undergoing free TRAM flap breast
reconstruction, it was found that smokers had two
times the incidence of mastectomy flap necrosis than
nonsmokers did. Donor site complications were more
common in smokers (25.6% versus 10%), including
abdominal flap necrosis and hernia. 23 As in breast
surgery, smokers have a higher incidence of unsatis-
factory healing after aesthetic procedures, including
rhytidectomy and abdominoplasty. 24,25 Interestingly,
it appears that a history of smoking does not alter the
outcome of a microsurgical anastomosis, but it is
thought to alter the microcirculation of the flap as
well as the interface between the flap and the under-
lying tissues, which can ultimately compromise the
flap.26
Vasoconstriction can also occur from vasospastic
disorders such as Raynaud disease, which causes
episodic vasospasm resulting in occlusion of small
arteries and arterioles of the distal extremities in
response to cold exposure or emotional stimuli. 27 This
ischemia is manifested clinically by the sequential devel-
opment of peripheral blanching, cyanosis, and rubor
(Fig. 33-3). This condition can lead to skin necrosis
from arterial insufficiency, which is most commonly
seen as painful digital ulceration. These ulcerations
are usually associated with palmar and digital artery
obstruction with vasospasm. Raynaud patients are also
at an increased risk for wound problems after elective
surgery. Surgical procedures may trigger a vasospas-
tic episode, predisposing the patient to tissue ischemia
and tissue loss. For instance, clinical studies have
demonstrated flap necrosis after rhytidectomy and

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image...

906 I • GENERAL PRINCIPLES

tissue loss after elective hand surgery in patients with

FIGURE 3 3 - 3 . AandB, End-stage critical ischemia with
dry gangrene in two patients with Raynaud syndrome sec-
ondary to scleroderma (intrinsic factors: arterial insuffi-
ciency and impaired cellularfunction). (From Flavahan NA,
Flavahan S, Mitra S, Chotani MA: The vasculopathy of
Raynaud's phenomenon and scleroderma. Rheum Dis Clin
North Am 2003;29:275.)
documented vasospastic disorders.28
Venous Insufficiency
The estimated incidence of venous ulcers in patients
older than 45 years is 3.5 per 1000 per year.29,30 Thus,
venous ulcers affect up to 2.5 million people per
year in the United States.31 The risk factors for devel-
opment of venous ulceration include advanced age,
history of deep venous thrombosis, history of severe
lower extremity trauma, male sex, and obesity.32,33
Vascular incompetence, either in the superficial or in
the deep venous system, can cause venous insufficiency,
although it is disease of the deep venous system that
is the major cause of morbidity and mortality
in these patients.16 Venous reflux (through incompe-
tent perforating veins in the deep system), venous
obstruction, and calf muscle pump dysfunction
contribute to venous hypertension and the resultant
signs and symptoms of chronic venous insufficiency
(Fig. 33-4). A common complication of chronic

Normal Venous insufficiency

Superficial Deep Superficial Deep
vein vein vein vein

FIGURE 3 3 - 4 . Pathophysiology: venous insuffi-

ciency. A Muscle pump forces venous flow into
competent deep system with intact valves. B,
Muscle pump forces venous flow into superficial
system, resulting in venous hypertension in incom-
B petent dilated superficial venous system.

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image...

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 907

venous insufficiency is skin ulceration (Fig. 33-5).

These wounds develop secondary to pericapillary
fibrosis, tissue ischemia, and liberation of superoxide
radicals.34 In addition, increased pressure in the venous
system increases transendothelial and interendothe-
lial capillary leakage, resulting in tissue edema. This
edema may contribute to tissue hypoxia by increas-
ing the distance oxygen must diffuse from the nour-
ishing capillaries to reach cells.35 Skin breakdown is
usually associated with trauma or infection. The most
common location for these ulcers is over the medial
malleoli. These wounds are chronic and nonhealing,
and they often develop into problem wounds.

Lymphatic Insufficiency
The lymph system is a one-way drainage route
designed to rid the tissues of excess protein-rich inter-
stitial fluid. The normal lymph flow is 2 to 4 L/day.36
Lymph flow is influenced by the protein concentra- B
tion in plasma and interstitial fluid, local arterial and
venous pressure relationships, and capillary pore size
and integrity. Lymphatic disorders are characterized
by lymphedema (Fig. 33-6). Lymphedema occurs
when there is an imbalance between the production
of interstitial fluid and transport through the lym-
phatic system. Transport through the lymphatic system
can be disrupted secondary to congenital or acquired
disorders. Acquired disorders causing lymphatic
obstruction can occur from infection or from surgi-
cal dissection. The most prevalent worldwide cause
of lymphedema is filariasis, which affects 129 million
people. 37 Lymphatic filariasis results from infection
with the mosquito-borne filarial nematodes Brugia
malayi and Wuchereria bancrofti?* The complex life
cycle includes an infective larval stage carried by the
mosquito and an adult worm stage that can be found
in either the lymph nodes or lymphatics of the host
(Fig. 33-7). The offspring of the adults, the micro-
filariae, circulate in the blood. These microfilariae
can then be ingested by a biting mosquito, reinitiat-
ing the life cycle. Approximately 10% of patients
with filariasis enter the end stage of the disease, known
as elephantiasis. The obstruction of the lymphatic
system leads to massive swelling and skin ulceration. 39
These problem wounds are indistinguishable
from those ulcers that result from other causes of
lymphedema.
FIGURE 3 3 - 5 . Venous ulceration (intrinsic factor: vas-
The most common cause of lymphedema in the cular insufficiency). A Chronic venous ulceration secondary
to lower extremity venous insufficiency. B, Resection
United States is postsurgical.'10 The reported incidence requires excision of all abnormal fibrotic skin with preser-
of lymphedema after axillary node dissection is as high vation of underlying muscle and periosteum. C, Postop-
as %Wo.A* This risk increases with the addition of post- erative view at 6 months demonstrates stable wound
operative radiation therapy to the area of dissection. coverage at site of venous ulcerations with split-thickness
skin grafts. (From Mathes SJ, Nahai F: Clinical Applica-
The risk of lower extremity lymphedema after groin tions for Muscle and Musculocutaneous Flaps. St. Louis,
dissection for melanoma has been reported to be as CVMosby, 1982.)
high as 65%. 42 ' 43
Wounds that develop in extremities with chronic
lymph stasis often become problem wounds because

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Dr.Mustafa D.
908 I • GENERAL PRINCIPLES
FIGURE 3 3 - 6 . Primary lymphedema. A, Right leg demonstrates chronic lymphedema (lymphedema
praecox). B, Lateral view.
of the collection of interstitial fluid in the tissues.
Lymph stasis impairs local immune surveillance by
disrupting migration of immunocompetent cells and
stimulates disordered angiogenesis by promoting
development of a collateral lymphatic and vascular
network. This immunologically vulnerable area is also
predisposed to malignant transformation.44 Therefore,
a biopsy must be performed of any problem wound
existing within chronic lymphedematous tissue to rule
out carcinoma.
IMPAIRED CELLULAR FUNCTION
An impaired cellular response to injury represents an
intrinsic cause of a problem wound. Wound repair is
a complex process that requires several key cell types
working in concert. The cellular components include
macrophages, neutrophils, platelets, keratinocytes,
fibroblasts, and endothelial cells. The failure of func-
tion of any of these cells can result in wound healing
deficiencies.
Tissue macrophages are a primary component of
the inflammatory phase of wound repair because of
their capacity to produce inflammatory cytokines and
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Dr.Mustafa D.
a battery of growth factors. The macrophage also has
a role in stimulating fibroblast ingrowth and neovas-
cularization.45,46 In addition, the macrophage is one
cell among many responsible for phagocytosis. Phago-
cytosis is a process whereby foreign debris and necrotic
cells are cleared from the wound bed (Fig. 33-8).
Deficiencies of phagocytosis contribute to infection
and wound healing problems. Studies have shown that
wound healing can proceed normally in the absence
of both neutrophils and lymphocytes, but macrophages
must be present to trigger normal fibroblast produc-
tion and subsequent invasion into the wound. 47
Neutrophils function as immune cells that also
engulf foreign material and digest it with hydrolytic
enzymes and oxygen free radicals.48 Neutrophils
produce proinflammatory cytokines that serve to acti-
vate local fibroblasts and keratinocytes. Neutrophils
are the most numerous of the cellular elements in the
wound for the first 48 hours after wounding. Inter-
estingly, early studies have shown that the presence of
leukopenia at the time of wounding and during the
subsequent inflammatory phase has no effect on
wound debridement, fibroblast proliferation, or con-
nective tissue formation.47,49
image...

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 909

FICURE 3 3 - 7 . Lymphedema secondary to fiiariasis, a disorder caused by infection with larvae trans-
mitted to humans by mosquitoes. 4 and fi, Fiiariasis is a disease group affecting humans and animals
that is caused by nematode parasites of the order Filarioidea (most commonly termed filariae). Filarial
parasites are classified according to the habitat of the adult worms in the vertebral host. The cutaneous
group includes Loo loo. Onchocerca volvulus, and Monsonella streptocerca. The lymphatic group includes
Wucnereria bancrofti, Brugio malayi, and Brugia timori. The body cavity group includes Monsonella
perstans and Monsonella ozzardi. C, Stage III lymphedema secondary to fiiariasis: lympnostatic
elephantiasis.

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910 I • GENERAL PRINCIPLES

Bacterium

Pha

FIGURE 3 3 - 8 . Phagocytosis and destruction of engulfed bacteria consist of the following:

delivery of phagocytic cells to the site of infection; phagocytic adherence; ingestion; phagolyso-
some formation; intracellular killing; and intracellular digestion. Phagocytosis results from a
bacterium's initiation of engulfment by the process of endocytosis. The bacterium is ingested
in a membranous endosome called the phagosome. Digestive granules (lysosomes) merge with
the phagosome, release their contents, and form a structure called the phagolysosome. The
killing and digestion of the bacterial cell take place in the phagolysosome.

Platelets are responsible for the production of
growth factors during the first 48 hours of wound
repair. The factors released from platelets include
platelet-derived growth factor (PDGF), transforming
growth factor-)} (TGF-pl), fibroblast growth factor
(FGF), epidermal growth factor (EGF), and platelet-
derived angiogenesis factor. Thus, platelet dysfunction
precludes early activation of the wound repair process.50
Keratinocytes at the basal layer of a wound are the
principal source of the regenerating epithelium. In
response to injury, these cells undergo a sequence of
changes: detachment, migration, proliferation, dif-
ferentiation, and stratification. Impairment of any of
these steps inhibits the smooth and rapid completion
of epithelial surfacing, leaving the wound open and
susceptible to the environment. 51 The fibroblast is
present in virtually all tissues and is the most impor-
tant mesenchymal cell involved in wound healing. Its
roles are numerous and include regulation of tissue
repair and fibrosis, hematopoiesis, bone metabolism,
inflammation, and immune response.52*54 Fibroblasts
are solely responsible for the intracellular produc-
tion of procollagen, which eventually is cleaved to
collagen in the extracellular matrix. Disorders of
fibroblast function result in poor healing or excessive
scarring within wounds. Radiation has been shown
to directly affect fibroblast function; it causes intranu-
clear and cytoplasmic damage, limiting the prolifer-
ative potential of the fibroblasts. 55
Endothelial cells synthesize PDGF, FGF, and insulin-
like growth factor (IGF). These ceils are the corner-
stone of vascular wall remodeling. 56 On stimulation,
they proliferate and form new vascular sprouts, which
coalesce to form new vascular channels, bringing
oxygen into the wound bed. Disruption of this process
limits the ability of wounds to heal appropriately.
Therapies such as radiation therapy and chemother-
apy have detrimental effects on the cellular compo-
nents of wound healing. Radiation has been found to
have both acute and delayed effects on the ability of a
wound to heal (Fig. 33-9). The direct effects of radia-
tion are a function of the cumulative dose, and the
severity of the effects is directly related to the absorbed
dose.57 Tissue injury results from either direct damage
to the cellular DNA or indirect damage to the cellular
DNA from the formation of free radicals. Fibroblasts
are irreversibly altered by radiation therapy as meas-
ured by diminished collagen production. Collagen

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Dr.Mustafa D.
image...
33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE
FIGURE 3 3 - 9 . Osteoradionecrosis of the anterior
thorax (intrinsic factors: vascular insufficiency and infec-
tion). The patient underwent left radical mastectomy
and chest wall irradiation- See Figure 33-62. (From
Mathes SJ: Chest wall reconstruction. Clin Plast Surg
1995:22:187.)
production becomes deficient, and the cellular response
to wounding becomes inadequate to maintain normal
wound healing parameters. 57 Keratinocytes and
endothelial cells are also damaged, which is evidenced
clinically by a thin epidermis as well as by a lack of vas-
cularity of the irradiated wound bed. It has been shown
experimentally that the effect of radiation on neutrophil
function is that of diminished phagocytosis and super-
oxide production, which may account for the suscep-
tibility to infection and poor healing of irradiated
tissues.58
Chemotherapeutic agents exert their antineoplas-
tic effects by interfering with deoxyribonucleic acid
replication, ribonucleic acid production, protein syn-
thesis, or cell division.59 These combined effects neg-
atively influence wound healing by inhibit ing fibroblast
function or by decreasing collagen formation directly.
This directly decreases the strength of wounds and con-
tributes to their breakdown. It has been shown that
the most detrimental effects are observed when the
agents are given in the 2 weeks preceding surgery or
within 1 week after wounding. 60,6 '
INFECTION
Wound infection generally occurs when the bacterial
count in the wound exceeds 105 bacteria per gram of
tissue. This correlation of a critical number of bacte-
ria was initially based on a study of quantitative burn
wound biopsies that predicted skin graft failure.62
Whether the infection remains localized to the wound,
spreads to adjacent tissues, or becomes systemic
depends on the interaction of the invading microbes
and the host defenses. Bacteria may gain entrance into
skin and soft tissue directly, through dry or macer-
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Dr.Mustafa D.
911
ated skin, to initiate a problem wound, or they may
convert an existing simple wound into a problem
wound. Infection impairs the ability of the wound to
heal by several mechanisms. All phases of the wound
healing cascade are affected by infection.63 Infection
decreases tissue Po 2 and prolongs the inflammatory
phase. Significant infection (>10 5 bacteria) impairs
leukocyte chemotaxis and migration, phagocytosis, and
intracellular killing. Bacterial colonization impairs
angiogenesis and epithelialization.64 Last, microbial-
derived collagenase breaks down the collagen in the
wound, resulting in decreased wound strength and
contraction. 65 Factors to consider in managing an
infected wound are the source of the bacteria, rate of
microbial proliferation, pathogenicity (endotoxin
and exotoxin production), and bacterial resistance
(Table 33-4).
In addition to local wound infections, systemic sepsis
has detrimental effects on wound healing. Carrel,66 in
1924, first observed that the healing of war wounds
was delayed when the patient developed infection else-
where. Subsequently, it has been accepted that sepsis
is detrimental to generalized wound healing.67 The
cause of this phenomenon is not fully understood,
although it is thought that sepsis alters both the
inflammatory and the proliferative processes at remote
sites of injury.68
Necrotizing Soft Tissue Infections
Infections of the soft tissues occur commonly and
account for numerous hospital visits each year. Most
of these infections respond to oral antibiotic therapy
or a short course of intravenous antibiotics. However,
some infections overwhelm the skin and soft tissue,
leading to systemic sepsis, and do not respond to antibi-
otic therapy. These wounds progress rapidly with severe
soft tissue necrosis, which leads to the development
of a problem wound. In 1884, Fournier 69 described a
specific necrotizing infection involving the perineum
(Fournier gangrene). Fournier gangrene is now defined
as an abrupt, rapidly progressive, gangrenous infec-
tion of the external genitalia, perineum, or abdomi-
nal wall. In 1924, Meleney70 described a lethal and
rapidly progressing soft tissue infection, termed
Meleney gangrene, due to a microaerophilic strepto-
coccus. He also coined the term synergistic gangrene,
which is characterized by a symbiosis of anaerobic
streptococci and staphylococci (Fig. 33-10). 7I The
eponyms given to these necrotizing soft tissue infec-
tions through the years, although of historical impor-
tance, describe the same problem. Currently, there is
no accepted classification system for necrotizing soft
tissue infections. A necrotizing soft tissue infection is
often described on the basis of the tissue plane affected
and extent of invasion, the anatomic site, and the
causative pathogens. Deep soft tissue infections are
classified as either necrotizing fasciitis or necrotizing
912 • CENERAL PRINCIPLES
TABLE 33-4 • ANTIMICROBIAL AGENTS OF CHOICE
Organism
Gram-Positive Cocci
Staphylococcus aureus
Non-penicillinase-
producing
Penicillinase-producing
Beta streptococci (groups
Ar B, C, and G)
Alpha streptococci
(viridans
streptococci)
Streptococcus bovis
Enterococci
Endocarditis or other
serious infection
Uncomplicated urinary
tract infection
Streptococcus pneumoniae
Gram-Negative Cocci
Neisseria meningitidis
Neisseria gonorrhoeae
Non-p-lactamase-
producing
p-lactamase-producing
Gram-Negative Bacilli
Acinetobacterspp.
[Mima, Herellea)
Brucella spp.
Campylobacter jejuni
Enterobacter spp.
Escherichia coli
Uncomplicated urinary
tract infection
Systemic infection
Francisella tularensis
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Dr.Mustafa D.
Antimicrobial of Choice
Penicillin
A penicillinase-resistant
penicillin5
Penicillin (some add
gentamicin for serious
group B streptococcal
infections)
Penicillin
Penicillin
Penicillin (or ampicillin) +
gentamicin or streptomycin
Ampicillin or amoxicillin
Penicillin
Penicillin
Penicillin
Ceftriaxone, cefixime,
cefpodoxime
Imipenem or meropenem
Doxycycline (± gentamicin
or streptomycin)
Erythromycin
Imipenem or meropenem
Trimethoprim-
sulfamethoxazole or
amoxicillin-clavulanate
Third-generation
cephalosporin,"
cefoperazone, cefepime
Streptomycin or gentamicin
Alternative Agents
A cephalosporin,* vancomycin, imipenem,
erythromycin, neomacrolides,* fluoroquinolone*
A cephalosporin,* vancomycin, clindamycin, imipenem,
erythromycin, neomacrolides,' fluoroquinolone'
A cephalosporin," erythromycin, vancomycin
A cephalosporin,* vancomycin, erythromycin,
neomacrolides1
A cephalosporin,* vancomycin, erythromycin,
neomacrolides1
Vancomycin + gentamicin or streptomycin
Nitrofurantoin, fosfomycin, fluoroquinolone'
A cephalosporin,* levofloxacin, sparfloxacin,
grepafloxacin, trovafloxacin, erythromycin,
neomacrolides/ chloramphenicol, vancomycin,
cefotaxime or ceftriaxone (penicillin-resistant strains)
Ceftriaxone, cefotaxime, chloramphenicol, cefuroxime,
a sulfonamide (some strains)
Spectinomycin, ampicillin, amoxicillin, cefoxitin,
ceftriaxone, cefuroxime, cefotaxime, trimethoprim-
sulfamethoxazole, cefpodoxime, cefixime,
fluoroquinolone'
Cefoxitin, cefuroxime, amoxicillin-clavulanate,
spectinomycin, cefotaxime, trimethoprim-
sulfamethoxazole, fluoroquinolone'
Ampicillin-sulbactam, fluoroquinolone,' amikacin,
trimethoprim-sulfamethoxazole, ceftazidime
Doxycycline + rifampin, trimethoprim-
sulfamethoxazole + gentamicin, fluoroquinolone' +
rifampin
Fluoroquinolone,* doxycycline, clindamycin, gentamicin,
azithromycin, clarithromycin
Cefepime, fluoroquinolone,* ticarillin-clavulanic acid,
piperacillin-tazobactam, gentamicin, tobramycin,
piperacillin-aztreonam, amikacin, third-generation
cephalosporin," cefoperazone
Fluoroquinolone,' a cephalosporin,* a tetracycline,
ampicillin, amoxicillin
A cephalosporin,* ticarcillin, mezlocillin, piperacillin,
gentamicin, tobramycin, kanamycin, amikacin,
fluoroquinolone,' imipenem, aztreonam, ampicillin,
amoxicillin, ampicillin-sulbactam, ticarcillin-
clavulanate, piperacillin-tazobactam
Doxycycline, chloramphenicol, ciprofloxacin, rifampin
TtJWR^aacrKf image...

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 913

TABLE 3 3 - 4 • ANTIMICROBIAL AGENTS OF CHOICE—cont'd

Organism Antimicrobial of Choice Alternative Agents

Haemophilus influenzae
Meningitis Third-generation Ampiciilin (if p-lactamase negative), chloramphenicol,
cephalosporin" trimethoprim-sulfamethoxazole, fluoroquinolone*
Other infections Ampiciilin or amoxicillin,1 Trimethoprim-sulfamethoxazole, cefuroxime, cefaclor,
amoxicillin-clavulanate cefprozil, cefpodoxime, cefixime, cefamandole,
or ampicillin-sulbactam sulfisoxazole, fluoroquinolone*
Klebsiella pneumoniae A cephalosporin* (for serious Imipenem, meropenem, fluoroquinolone,* aztreonam,
infections, third-generation trimethoprim-sulfamethoxazole, cefuroxime,
cephalosporin") cefamandole, amikacin, gentamicin, tobramycin,
chloramphenicol, tetracycline
Legionella spp. Erythromycin ± rifampin or Azithromycin, clarithromycin, trimethoprim-
fluoroquinolone* sulfamethoxazole, doxycycline
Proteus mirabilis Ampiciilin Trimethoprim-sulfamethoxazole, gentamicin or
tobramycin, a cephalosporin,* imipenem,
meropenem, aztreonam, ticarcillin, mezlocillin,
piperacillin
Other Proteus spp. Third-generation Ampicillin-sulbactam, ticarcillin-clavulanate,
{P. rettgeri, cephalosporin," cefepime, piperacillin-tazobactam, ticarcillin, mezlocillin,
M. morganii, or fluoroquinolone* piperacillin, gentamicin, tobramycin, amikacin,
P. vulgaris) imipenem, meropenem, aztreonam, trimethoprim-
sulfamethoxazole
Providencia spp. Third-gene ration Gentamicin, tobramycin, netilmicin, ticarcillin,
cephalosporin," cefepime, mezlocillin, piperacillin, ampicillin-sulbactam,
or amikacin ticarcillin-clavulanate, piperacillin-tazobactam,
imipenem, meropenem, aztreonam, trimethoprim-
sulfamethoxazole, fluoroquinolone*
Pseudomonas aeruginosa Tobramycin orgentamicin Fluoroquinolone,* amikacin, imipenem, meropenem,
plus ticarcillin, azlocillin, aztreonam, ceftazidime, cefepime
mezlocillin, or piperacillin
Salmonella spp. Fluoroquinolone,' ceftriaxone Chloramphenicol, ampiciilin or amoxicillin,
trimethoprim-sulfamethoxazole**
Serratia marcescens Third-generation Ampicillin-sulbactam, ticarcillin-clavulanate,
cephalosporin," imipenem, piperacillin-tazobactam, ticarcillin, mezlocillin,
meropenem, or piperacillin, imipenem, meropenem, aztreonam,
fluoroquinolone' amikacin, gentamicin, tobramycin
Shigella spp. A fluoroquinolone* Trimethoprim-sulfamethoxazole, ampiciilin, nalidixic
acid
Yersinia pestis Streptomycin or gentamicin Doxycycline, chloramphenicol, fluoroquinolone'

Anaerobes

Anaerobic streptococci Penicillin Clindamycin, erythromycin, chloramphenicol, a

cephalosporin,* tetracycline, vancomycin
Bacteroides spp.
Oropharyngeal strains Penicillin Clindamycin, tetracycline, chloramphenicol,
metronidazole, cefoxitin, cefmetazole, cefotetan
Gastrointestinal strains Metronidazole Clindamycin, chloramphenicol, cefoxitin, cefotetan,
cefmetazole, ticarcillin, piperacillin, mezlocillin,
imipenem, meropenem, ticarcillin-clavulanate,
ampicillin-sulbactam, piperacillin-tazobactam
Clostridium spp. Penicillin Doxycycline, erythromycin, chloramphenicol,
clindamycin, imipenem, meropenem

"The term cephalosporin refers to the first-generation cephalosporins cephalothin, cefazolin, cephapirin, cephradine, cephalexin, cefaclor, and cefadroxil.
"The term neomacrolides refers to azithromycin, clarithromycin, and dirithromycin.
'Ciprofloxacin, ofloxacin, levofloxacin, sparfloxacin, grcpafloxacin, or trovafloxacin (or, for urinary tract infections, norfloxacin, lomefloxacin, or enoxacin).
*Methicillin, nafcillin, oxacillin, or dicloxacillin.
The term third-generation cephalosporin refers to ceftriaxone, cefotaxime, ceftizoxime, and ceftazidime.
'For strains that do not produce p-lactamasc.
"*Not approved for this indication by the U.S. Food and Drug Administration.
From Mandell GL, Bennett JE, Dolin R: Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases, 5th ed. Philadelphia, Churchill Liv-
ingstone, 2000:225.

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image.-
914 I • GENERAL PRINCIPLES
FIGURE 3 3 - 1 0 . Necrotizing soft tissue infection—syn-
ergistic gangrene (intrinsic factor: infection; extrinsic
factor: pressure). Synergistic gangrene of posterior thigh
extends into peritoneum from infected ischial pressure
sore in a paraplegic patient. See Figure 33-84. (From
Mathes SJ, Nahai F: Clinical Applications for Muscle and
Musculocutaneous Flaps. St. Louis, CV Mosby, 1982.)
myositis. Necrotizing fasciitis represents a rapid, exten-
sive infection of the fascia deep to the adipose tissue.
Wilson72 found fascial necrosis to be the most con-
sistent manifestation of necrotizing infections. Necro-
tizing myositis primarily involves the muscles and
spreads to the adjacent soft tissues. The organism most
commonly involved is Clostridium perfringensP These
infections are rarely due to gram-negative organisms
such as Pseudomonas aeruginosa or Vibrio vulnificus.
Infections that arise from clostridial species tend to
be more aggressive. Clostridia are obligate anaerobic,
spore-forming bacilli. These organisms are generally
found in soil, sewage, marine sediments, the gas-
trointestinal tract, and decaying animal and plant prod-
ucts.74 C. perfringens is responsible for the majority of
trauma-related infections; Clostridium septicum is
associated with spontaneous myonecrosis (gas gan-
grene). The hallmark of this infection is pain out of
proportion to the appearance of the wound. This pain
is due to the progression of the muscle destruction.
When it is suspected, either by laboratory culture or
in the operating room, aggressive debridement is of
primary importance. In advanced situations, the
muscle may appear black and necrotic. Clostridial
infections of the extremity often require urgent ampu-
tation to save the patient's life.
In necrotizing infections, polymicrobial infection
tends to be a more common finding than infection
with a single organism. There is a subset of intravenous
drug abusers who are at high risk for development of
necrotizing infections.75,76 These infections vary in
anatomic location, level of tissue involvement, pre-
disposing conditions, and offending organisms. Necro-
tizing soft tissue infections are fatal if they are not
recognized and treated early. Even with rapid diag-
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Dr.Mustafa D.
nosis and aggressive treatment, the mortality rate can
reach 75%. 77 Rapid diagnosis implies that the clini-
cian can recognize this deadly disease. Clinical signs
to suggest a necrotizing soft tissue infection include
hemodynamic instability, crepitation, skin necrosis,
bullae, and soft tissue gas on radiographic examina-
tion. 78 Other factors include a white blood cell count
greater than 15.4 x 109 L and serum sodium concen-
tration less than 135 mmol/L. 79 Treatment with
minimal debridement, incision and drainage plus
antibiotics, or antibiotics alone is associated with a
mortality rate of 80% to 100%. Elliot et al80 showed
that the risk factors for death include age of the patient,
female gender, extent of infection, delay in first
debridement, elevated serum creatinine level, elevated
blood lactate level, and degree of organ dysfunction
at time of admission. The risk factors for development
of necrotizing soft tissue infection include diabetes
mellitus, malnutrition, obesity, chronic alcoholism,
peripheral vascular disease, chronic lymphocytic
leukemia, steroid use, renal failure, cirrhosis, intra-
venous drug abuse, and autoimmune deficiency
syndrome.
Osteomyelitis
Osteomyelitis or chronic bone infection is character-
ized by a progressive inflammatory destruction and
new apposition of bone. 81 Osteomyelitis may result
either from hematogenous spread of a microorgan-
ism or by direct introduction from contiguous septic
foci.82 The Waldvogel classification system divides
osteomyelitis into categories of hematogenous, con-
tiguous, and chronic. 8 ' The more recently introduced
Cierny-Mader staging system is based on the status of
the disease process, including both the anatomic area
of bone affected and the physiologic status of the host.83
Injury is the most common cause of osteomyelitis, and
it is usually associated with an open fracture or occurs
after corrective orthopedic surgery.84 Trauma, ischemia,
and foreign bodies increase the susceptibility of bone
to microbial invasion by exposing sites to which bac-
teria can bind. 85 Patzakis et al86 found that open tibia
fractures have a 24% chance of infection without
antibiotic therapy, compared with a 4.5% infection
rate when they are treated with antibiotics.
Macrophages attempt to contain the infection and in
the process secrete enzymes that ultimately lyse the
surrounding bone. Infection spreads into the vascu-
lar channels, raising the intraosseous pressure and
impairing blood flow.84 As the infection becomes
chronic, ischemic necrosis of the bone results in sep-
aration of large devascularized fragments called seques-
tra. A wound with underlying osteomyelitis will
continue to be a problem wound until the infected
bone is debrided and the infection is treated with a
course of intravenous antibiotics. The identification
of the causative microorganisms is essential for
 33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE
FIGURE 33-1 1. Osteomyelitis of the skull (intrinsic
factors: vascular anomaly and infection). The patient has
previously undergone therapy for intracranial vascular
anomaly. See Figure 33-65.
diagnosis and treatment. A surgical sample or a needle
biopsy specimen of the infected tissue is required
because swabs from ulcers or fistulas are often mis-
leading.87 The bacteriology of these wounds shows that
Staphylococcus aureus accounts for more than 50% of
the isolates in osteomyelitis secondary to penetrating
injuries or surgical procedures.88 However, these infec-
tions are often polymicrobial and are likely to include
gram-negative and anaerobic bacteria (Fig. 33-11).
Although rare, squamous cell carcinoma is a well-
documented complication of chronic osteomyelitis.
In those patients with long-standing osteomyelitis, a
biopsy is warranted.89,90
The diagnosis of osteomyelitis is made largely from
the patient's history and physical examination findings.
Patients often have local symptoms such as pain and
erythema associated with a chronic open wound. If
there is suspicion of osteomyelitis, appropriate studies
should be obtained. Bone biopsy remains the "gold
standard" for diagnosis of osteomyelitis. This sample
should be sent for both microbiologic and histopatho-
logic evaluation. Blood tests often reveal leukocytosis
and elevations in the erythrocyte sedimentation rate
and C-reactive protein. Extremity osteomyelitis is often
evaluated with plain film radiography or bone scintig-
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Dr.Mustafa D.
915
raphy (technetium Tc 99m methylene diphosphonate).
Magnetic resonance imaging is helpful if the diagno-
sis remains unclear. The sensitivity and specificity of
magnetic resonance imaging are equivalent to or
greater than those of a bone scan. Other diagnostic
tests include ultrasonography and computed tomo-
graphic scanning. Ultrasonography can detect fluid
collections and surface abnormalities of the bone.
Computed tomographic scanning can reveal areas of
osteolysis in cortical bone, small foci of gas, and foreign
bodies.
Sternal Wound Infections
Complications after median sternotomy, such as insta-
bility, nonunion, and incision-related infection, occur
roughly 2% to 5% of the time.91 Infection with sternal
wound dehiscence has been associated with 50% mor-
tality in early series,92 but it more recently has been
shown to be 20% (Fig. 33-12).93 The increased use of
the internal thoracic arteries for myocardial revascu-
larization results in potential ischemia of the sternum
and further increases the risk of complications.94 Other
factors placing these patients at risk include diabetes,
immunosuppression, increased body mass index, and
previous chest wall irradiation.95 Median sternotomy
wound breakdown after cardiac surgery is a devastat-
ing complication leading to prolonged hospitalization,
increased hospital costs, and high associated morbid-
ity and mortality. Life-threatening complications of
sternal wound infections include mediastinitis, sepsis,
and infectious seeding of prosthetic heart valves and
FIGURE 3 3 - 1 2 . Sternal wound (intrinsic factors:
impaired cellular function and infection; extrinsic factor:
surgery). Diabetic patient with an anterior mediastinal
infection after a coronary artery bypass graft (left inter-
nal mammary artery). See Figure 33-67. (From Mathes
SJ, Eshima I: The principles of muscle and musculocuta-
neous flaps. In McCarthy JG, ed: Plastic Surgery. Philadel-
phia, WB Saunders, 1990:379.)
916 I • GENERAL PRINCIPLES
TABLE 3 3 - 5 • STERNAL WOUND INFECTION
CLASSIFICATION
Type Depth Description
la Superficial Skin and subcutaneous tissue
dehiscence
lb Superficial Exposure of sutured deep fascia
2a Deep Exposed bone, stable wired
sternotomy
2b Deep Exposed bone, unstable wired
sternotomy
3a Deep Exposed necrotic or fractured
bone, unstable, exposed heart
3b Deep Type 2 or 3 with septicemia
From Jones G, Jurkiewicz MJ, Bostwick J, et ah Management of ihe infected
median sternotomy wound with muscle flaps. Ann Surg 1997;225:766.
grafts.96*98 A classification of sternal wounds has been
proposed on the basis of their depth and exposure of
underlying soft tissues or organs (Table 33-5)."
MALIGNANT DISEASE
Malignant disease can affect wound healing, both
locally and systemically. Locally, a problem wound may
harbor an occult malignant neoplasm, causing wound
healing abnormalities; advanced cancers distant to a
wound may alter healing. Alternatively, long-standing
wounds may transform into a malignant neoplasm.
Malignant disease should always be considered
when a problem wound is treated. If any suspicion
exists, it is the obligation of the surgeon to rule out
cancer with a biopsy of the wound (Fig. 33-13). Indi-
cations for biopsy of a problem wound to rule out
cancer include history of a local or remote malignant
neoplasm, gross appearance of the wound, and length
of time the wound has been present. The most
common recurrent cancers are basal cell and squa-
mous cell carcinomas, although malignant melanoma
must also be considered. In-transit metastasis and satel-
lite lesions are manifestations of locoregional cuta-
neous recurrence and are characteristic of malignant
melanoma. 100 Patients with melanomas on the lower
extremity (>30%) seem more likely to develop in-
transit metastasis, whereas more than 30% of patients
with melanoma on the trunk and upper extremities
developed direct distant metastasis.101,102 The time
course for occurrence of satellite and in-transit metas-
tasis ranges from 16 to 19 months after diagnosis of
the primary tumor. 102 Advanced cancers distant to a
wound have also been associated with problem
wounds, possibly because of altered inflammatory cell
function by the advanced tumor burden. 103 In addi-
tion, patients with advanced cancer demonstrate
severe weight loss and malnutrition, which further con-
tributes to problem wounds.
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Dr.Mustafa D.
Long-standing chronic wounds may also induce
malignant change. An example of this occurrence is
termed a Marjolin ulcer. A Marjolin ulcer is a rare neo-
plasm that was originally described in the unstable scar
of a full-thickness burn, although it is now synony-
mous with malignant transformation of chronic ulcers
and sinus tracks as well as burn scars (Fig. 33-14). Most
of these ulcers are squamous cell carcinomas, although
basal cell carcinoma and melanoma are rarely seen.104,105
The latent period for malignant transformation ranges
from 1 to 75 years. Carcinoma arising from a chronic
wound is generally more aggressive than traditional
skin cancers are, and the rate of regional metastasis is
higher.' 06 Biopsy should be performed for chronic
wounds of more than 10 years* duration as well as
for those with exuberant granulation or bleeding. In
patients with osteomyelitis, 1 % will develop squamous
cell carcinoma within the sinus tracks of the wound. 107
Squamous cell carcinoma can also develop in acne
conglobata, dissecting perifolliculitis of the scalp,
hidradenitis suppurativa, and pilonidal sinus tracks.107
Leukemia represents a group of disorders charac-
terized by a large percentage of abnormal white blood
cells in the marrow and other organs. The leukemias
are classified as acute or chronic and are charac-
terized as myeloproliferative or lymphoproliferative,
depending on the predominant cell type. Cutaneous
involvement is common in certain types of acute
leukemias and may be a reflection of a capacity of these
tumors for tissue infiltration.108 The cutaneous man-
ifestation of leukemia is termed leukemia cutis. These
lesions often precede other clinical manifestations of
leukemia. In general, leukemia cutis shows a diffuse
infiltration of leukemic cells in the dermis and sub-
cutaneous tissue, often infiltrating between collagen
bundles. Extensive involvement and disruption of
FIGURE 33-1 3. A squamous cell carcinoma in a chron-
ically recurring ulcer of the lateral malleolus of more than
20 years' duration (intrinsic factor; malignant disease).
(From Casson PR, Robins P: Malignant tumors of the skin.
In McCarthy JG, ed: Plastic Surgery. Philadelphia, WB
Saunders, 1990:3614.)
image...

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 917

-— SSnBHBBnBS^HBBOi

-"ISP-

B
FIGURE 3 3 - 1 4 . Epidermoid carcinoma (Marjolin ulcer) developing in a 23-year-old burn scar (intrinsic factor:
malignant disease). A, Gross appearance. B, Microscopic appearance demonstrates piling up of excess epithelial
cells rather than an edge of progressively diminishing thickness. (From Peacock EE, Cohen IK: Wound healing. In
McCarthy JC, ed: Plastic Surgery. Philadelphia, WB Saunders, 1990:161.)

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Dr.Mustafa D.
918 I • GENERAL PRINCIPLES
FIGURE 3 3 - 1 5 . Osteoradionecrosis of the mandible
(intrinsic factor: vascular insufficiency). An orocutaneous
fistula developed at the site of radiation therapy for primary
treatment of carcinoma of floor of mouth. See Figure 33-
60. (From Mathes SJ, Nahai F: Reconstructive Surgery:
Principles, Anatomy, and Technique. New York, Churchill
Livingstone, 1997.)
blood vessels and skin adnexa are characteristic
findings. Cutaneous manifestations range from non-
specific rashes to necrotic ulceration.109 The ulcerat-
ing wounds do not respond to therapy because the
underlying leukemia is unrecognized. Aractingi et al110
found that the appearance of skin lesions on patients
heralded or was concomitant with acute transforma-
tion of their myelodysplastic syndrome.
Radiation therapy remains a common modality
of treatment of many malignant neoplasms. Conse-
quences of radiation therapy leading to problem
wound development include damage to the local soft
tissue and bone. This predisposes the patient to the
development of chronic, open wounds of the scalp,
osteoradionecrosis of the mandible, and orocutaneous
fistula (Fig. 33-15).
NUTRITIONAL DISORDERS
Nutritional disorders represent an intrinsic cause of
problem wounds. Wound healing is an anabolic event
that requires appropriate calorie intake.''' Severely mal-
nourished and catabolic patients have deficient wound
repair. Although this is clinically evident, objective data
are lacking."2 It has been shown experimentally that
chronic protein depletion impairs wound healing.113
It has also been shown in protein-depleted rats that
wound dehiscence is increased, which is reversible with
protein repletion immediately after wounding.114
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Powanda115 has shown that protein levels below 2 g/dL
in humans are associated with a prolonged inflamma-
tory phase and impaired fibroplasia. Surveys of patients
with pressure sores have shown a correlation between
low serum albumin and pressure sores.116,117
Patients with deficiencies of vitamins C, A, B6, Blt
and B2 or zinc have been shown to have wound healing
problems. Vitamin C or ascorbic acid deficiency
results in scurvy and has profound effects on wound
healing. Vitamin C is an essential cofactor for the
hydroxylation of proline and lysine residues necessary
for collagen synthesis.118 Vitamin C deficiency also
results in immature fibroblasts (lack of maturation),
failure of formation of mature extracellular materi-
als, marked production of alkaline phosphatase, and
formation of defective capillaries in the immature gran-
ulation tissue, leading to local hemorrhage (Fig. 33-
16).I!9 Interestingly, a normal number of fibroblasts
are present in the wound, but they produce inadequate
amounts of collagen. Vitamin A, or retinoic acid, is
important in several areas of wound repair, including
fibroplasia, collagen synthesis and cross-linking, and
epithelialization.120 In animal models, vitamin A sup-
plementation has been shown to reverse the impaired
healing that occurs with chronic steroid treatment.121,122
An oral dose of 25,000 IU daily or topical application
of 200,000 IU ointment three times a day is recom-
mended in severely injured patients to maintain
normal levels of vitamin A.123 Vitamin B6 or pyridox-
ine deficiency impairs collagen cross-linking.124
Vitamin B, (thiamine) and vitamin B2 (riboflavin)
deficiencies cause syndromes associated with poor
wound repair. Vitamin B| has been implicated as a
component of the inflammatory response of wound
repair.125 Vitamin B2 deficiency has been shown exper-
imentally to decrease the tensile strength and total
FIGURE 3 3 - 1 6 . Vitamin C deficiency (intrinsic factor:
nutritional disorder). A 16-year-old boy with purpura and
scattered ecchymoses over the lower extremities has a
3.0-cm area of induration and tenderness over the right
calf. A magnetic resonance image of the right calf showed
hemorrhage within the muscle without muscle disease.
On examination, he had persistent severe gingivitis and
interdental gingival proliferation. (From Bingham AC.
Kimura Y, Imundo L A 16-year-old boy with purpura and
leg pain. J Pediatr 2003:142:560.)
image...
33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE
TABLE 33-6 • VITAMIN AND MINERAL
DEFICIENCIES THAT AFFECT
WOUND HEALING
Vitamin Role in Wound Healing
C Collagen synthesis
A Collagen synthesis and cross-linking
Epithelialization
B6 Collagen cross-linking
B, Inflammation
B2 Collagen maturation
Zinc Epithelialization
Copper Angiogenesis
From Goodson WH III, HuntTK: Wound healingand nutrition. In Kinney
JM, Jeejecbhoy KN, Hill GL, et al, eds: Nutrition and Metabolism in Patient
Care. Philadelphia, WB Saunders, 1988:635.
collagen content of incisional wounds. l26 Trace metal
deficiencies, such as of zinc and copper, have been
implicated in poor wound repair because trace metals
act as cofactors for important enzymatic reactions. 120
Zinc deficiency results in poor epithelialization and
is often found to be deficient in chronic, nonhealing
wounds. Experimentally, it has been shown that re-
epithelialization is enhanced with the topical appli-
cation of zinc.127 Clinically, it has been established that
zinc supplementation in patients with low plasma zinc
levels promotes wound healing. Copper-sensitive
pathways regulate key mediators of wound healing,
such as angiogenesis and extracellular matrix remod-
eling.128 The specific targets of copper remain unclear.
It has been shown experimentally that topically applied
copper accelerates dermal wound contraction and
closure. The same study showed that copper induces
expression of vascular endothelial growth factor in
primary keratinocytes (Table 3 3 - 6 ) . m
Mechanical (Structural) Factors
Mechanical factors may prevent angiogenesis, impair
oxygen delivery, and delay wound healing. When the
base of the wound is nonviable or nonexistent, wound
healing cannot occur. Mechanical reasons leading to
problem wounds include cavity wounds that have no
base to begin wound healing and wounds that have a
dead or inert surface as their base. Other mechanical
causes of problem wounds are exposure of biomate-
rials and fistulous tracks (Table 33-7).
CAVITY W O U N D S
Cavity wounds cannot heal secondary to a large space
with an inherent inability of the wound to contract.
Persistence of this open wound provides an entrance
point for infection, which can become life-threaten-
ing. Anatomic areas susceptible to the development of
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Dr.Mustafa D.
919
cavity wounds include the chest wall, abdominal wall,
and perineum. Each of these wound cavities contains
critical organs whose function can be impaired when
they are exposed (Figs. 33-17 and 33-18).
PROSTHESIS EXPOSURE
Exposure of biomaterials is a mechanical cause of
problem wounds and represents a challenge for the
reconstructive surgeon. Examples of exposed bioma-
terials include vascular prostheses, breast implants,
tissue expanders, penile prostheses, mesh (polypropy-
lene, Gore-Tex, Marlex), joint prostheses, and ortho-
pedic hardware (Figs. 33-19 to 33-21). When these
biomaterials are exposed, a failure of wound healing
results because of the inert surface and inability of the
prosthesis to provide a matrix on which wound
healing can occur. The causes of implant exposure
include hematoma, infection, inadequate or unstable
soft tissue coverage, and trauma. When these bioma-
terials become exposed, complex treatment is gener-
ally required because wound healing will not occur
without correction of the underlying problem (e.g.,
hematoma or infection). Exposure of certain bioma-
terials can be a potentially life- or limb-threatening
problem. Prostheses that may result in problem wounds
include vascular prostheses, hardware stabilizing the
vertebral column, bone plates, and joint prostheses.
Exposure may result from wound breakdown sec-
ondary to infection or from unstable tissue coverage
secondary to poor perfusion or irradiation.
The evaluation of the patient should include an
assessment of the local wound as well as systemic
factors. An exposed or infected prosthesis in an
otherwise healthy individual is an easier problem to
manage and carries a more favorable outcome than in
a diabetic, debilitated, or immunosuppressed patient.
TABLE 3 3 - 7 • MECHANICAL (STRUCTURAL)
CAUSES OF PROBLEM
WOUNDS
Cavity wounds
Chest wall
Abdominal wall
Pelvis-perineum
Biomaterial exposure
Breast implant
Vascular prosthesis
Tissue expander
Penile prosthesis
Mesh
Joint prosthesis
Fistula
Pulmonary
Gastrointestinal
Genitourinary
Central nervous system
920 • GENERAL PRINCIPLES

FIGURE 33-1 7. Perineal cavity wound (intrinsic factor: infection; extrin-

sic factor: surgery; mechanical factor: cavity wound). A, The patient under-
went colectomy for ulcerative colitis; nonhealing of proctectomy site. B, The
sonogram demonstrates that the chronic wound extends into the pelvis to
the peritoneal resection. See Figure 33-75. (From Anthony JP, Mathes SJ:
The recalcitrant perineal wound after rectal extirpation. Arch Surg
1990; 125:1371.) B

Local evaluation focuses on the tissues surrounding
the exposed prosthesis. Evaluation of the viability of
the surrounding tissues, blood supply, infection, and
type of implant is essential for development of a treat-
ment plan.
Exposure of a prosthesis requires immediate atten-
tion and management. If the prosthesis exposure is
acute without the development of infection, antibi-
otic therapy (based on implant exposure with con-
tamination) and wound closure will often allow
implant salvage. If the tissue surrounding the implant
is infected because of prolonged prosthesis exposure
or the underlying infection resulted in wound break-
down, the implant must be removed. For exposure of
a vascular prosthesis, debridement and coverage with
vascularized tissue may be effective. Once the vascu-
lar prosthesis is infected, its removal is generally
required. If the vascular prosthesis is essential for limb
perfusion, extra-anatomic bypass may be required at
the time of removal. In the long bones, plate expo-
sure may be treated locally without wound closure if
the plate is providing anatomic alignment and bone
stability at the fracture or osteotomy site. However, if
bone viability is in question or stability has not been
achieved, plate removal is recommended, Bone
debridement and wound closure with vascular tissue
are recommended. External fixation distant from
the complex wound site will provide stable fracture
immobilization.
The use of tissue expansion in plastic surgery is a
common practice. A complication of expander use is
tissue breakdown with subsequent exposure of the
expander. As with other biomaterial exposures, the
causes of exposure include infection, inadequate soft
tissue coverage leading to wound dehiscence, and
trauma. The lower extremity has the highest incidence
of tissue expander exposure secondary to the inelas-
ticity of the skin and soft tissues. A study of 103 skin
expansion procedures and 207 placed prostheses on
the lower extremity had almost a 20% complication
rate.130 Gibstein131 reported that the complication rate
of tissue expansion is higher in children aged 1 to 12
years than in infants and adolescents.
Tissue expansion of the breast has played an inte-
gral role in breast reconstruction after cancer resec-
tion. Postoperative exposure of the breast prosthesis
is a devastating complication. The most common
reasons for expander failure are infection, inadequate

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Dr.Mustafa D.
image...

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 92

. il
r

.
^ki!

k.*~
FIGURE 3 3 - 1 8 . Thoracic cavity wound (intrinsic factors:
vascular insufficiency and infection; mechanical factor:
cavity wound). Radionecrosis extends into axilla and chest
wall. The patient underwent axillary dissection and radi-
ation therapy for melanoma. See Figure 33-74.
FIGURE 3 3 - 1 9 . Exposed, infected vascular prosthesis
(intrinsic factor: infection; mechanical factor: prosthesis
exposure). The patient underwent aortofemoral vascular
bypass surgery, and groin wound dehiscence from infec-
skin envelope size causing tension at the suture line tion exposed the vascular prosthesis. See Figure 33-80.
and breakdown of the overlying skin due to surgical (From Logon SE, Mathes SJ: Use of rectus abdominis mus-
technique, or radiation therapy. The incidence of infec- culocutaneous flap to reconstruct the groin defect. Br J
tion after breast reconstruction with use of expanders PlastSurg 1984;37:351. Reprinted with permission from
The British Association of Plastic Surgery.)
and implants ranges from 1% to 24%. ,32 Interestingly,
the incidence of infection after breast augmentation
ranges from 1% to 2%.133,134 Patients treated with
radiation therapy have a 4.8 times greater chance for
infection than do those not treated with radiation. 132
Common organisms cultured from infected expanders
include Staphylococcus aureus and Staphylococcus
epidermidis.liAAi6
Implantation of a penile prosthesis is a common
treatment of erectile dysfunction. The most common
cause of implant extrusion is infection. The frequency
of infection has been reported to range from 1.7% to
8.3% in primary implantation and to be higher in reop-
eration for revision or reimplantation.137"139 Subcuta-
neous extrusion of a penile prosthesis is a serious
complication and represents a problem wound.
Without adequate treatment, infection can spread,
leading to corporeal fibrosis, shortening of the penis,
and loss of function, and ultimately may result in penec-
FIGURE 3 3 - 2 0 . Breast implant exposure (mechanical
•
tomy. The most common mode of management of an
infected penile prosthesis has been total removal, factor: prosthesis exposure). Close-up of right inferior
lateral breast demonstrates loss of skin and subcutaneous
although salvage techniques have been advocated.140,141 tissue with silicone implant exposure. See Figure 33-78.

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Dr.Mustafa D.
922 • GENERAL PRINCIPLES

A B
FIGURE 3 3 - 2 1 . A, Exposed knee prosthesis and infected joint space after resection of
sarcoma and immediate knee reconstruction (intrinsic factor: infection; mechanical factor:
exposed prosthesis). B, Arteriogram of same patient reveals patent medial sural artery to
medial gastrocnemius for flap design (arrows). If a prosthesis failure occurs, the donor site
should be located within the potential amputation site. See Figure 33-79. (From Mathes
SJ, Nahai F: Reconstructive Surgery: Principles, Anatomy, and Technique. New York, Churchill
Livingstone, 1997.)

If tissue necrosis is present, debridement and soft tissue culosis. Thoracic trauma may result in large chest wall
coverage are necessary. This coverage can be accom- defects and lead to an empyema cavity and fistula. Pul-
plished with local musculocutaneous flaps or scrotal monary tract fistulas can occur as complications in
flaps. association with long-term tracheostomy or as a result
of esophageal or lung parenchymal surgery. A tra-
FISTULAS cheocutaneous fistula adds a difficult aspect to the
patient's care and may exacerbate respiratory disease.
A fistula is an abnormal communication between A pharyngocutaneous fistula is not uncommon after
two organ systems or between any organ and the
outside of the body. Fistulas occur under several cir-
cumstances. The cause may be a foreign body, malig-
nant disease, trauma, infection, epithelium-lined TABLE 33-8 • FISTULAS ASSOCIATED WITH
track, or distal obstruction. Fistulas may arise from PROBLEM WOUNDS
the pulmonary tract, gastrointestinal tract, geni-
tourinary tract, or central nervous system. Wounds Organ System Etiology
associated with these fistulas predispose to problem
wounds (Table 33-8). Pulmonary fistula
Trachea Long-term tracheostomy
The causes of pulmonary fistulas include those sec- Pharynx Total laryngectomy
ondary to primary parenchymal disease (malignant Lung parenchyma Tumor
neoplasia or infection), trauma, and complications of Gastrointestinal fistula
operative procedures. When pulmonary parenchymal Esophagus Trauma, inflammation
Intestine Trauma, inflammation
diseases, including cancer and infection, involve the Trauma, inflammation
Pancreas
chest wall, cutaneous fistulas may occur. Bron- Genitourinary fistula Tumor, inflammation, trauma
chopleural fistula is a severe complication that can Central nervous system Trauma, tumor, infection
occur in patients with severe infections such as tuber-

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Dr.Mustafa D.
 irnage...
33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE
FIGURE 3 3 - 2 2 . Pharyngoesophageal fistula in a patient
presenting with radiation necrosis and failed deltopec-
toral flap (intrinsic factor: vascular insufficiency: mechan-
ical factor: fistula). See Figure 33-61. (From Mathes S:
The pectoralis major flap. In Stark RB, ed: Plastic Surgery
of the Head and Neck. New York, Churchill Livingstone.
1985:949.)
pharyngolaryngeal surgery, with an incidence world-
wide from 7.6% to 50%.142 Patients with head and neck
cancer often have numerous comorbidities including
malnutrition, diabetes, and history of irradiation. 143
Other factors contributing to the development of a
fistula include tumor stage, tumor location, age of the
patient, type of operation, previous tracheotomy, and
concurrent neck dissection. 144 The development of a
pharyngocutaneous fistula is the most common and
troublesome complication in the early postoperative
period after free jejunal transfer for total laryn-
gopharyngectomy (Fig. 33-22). 145
In general, management of pulmonary fistulas
involves correction of the underlying disorder when
appropriate. This is followed by obliteration of the
fistulous track. Primary closure is often not possible
because of tissue loss, radiation damage, or infection.
In these circumstances, local muscle flaps are used.
Local options include the pectoralis major and latis-
simus dorsi; regional tissue, such as the omentum or
rectus abdominis, can be used. In the case of infec-
tion, appropriate antibiotic coverage is indicated in
combination with debridement and interposition of
vascularized muscle. This often involves thoracoplasty
in which ribs are removed to collapse the lung and
provide an entrance for the muscle flap.
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923
Gastrointestinal fistulas can occur anywhere from
the mouth to anus, including the oral cavity, neck,
small bowel, large bowel, hepatobiliary tract, and pan-
creas, although fistulas most commonly originate from
the pancreas or intestine. Pancreatic and intestinal
fistulas result from trauma, neoplasia, inflammation,
and distal obstruction and occur as complications of
intra-abdominal operative procedures. The incidence
of pancreatic fistula after trauma is reported in the 1 it—
erature as 5% to 30%. 146 Pancreatic fistula secondary
to elective pancreatic surgery (i.e., Whipple procedure,
distal pancreatectomy) has an incidence of 10% to
16%.147'149 Intestinal fistulas may arise from the small
or large bowel. Concomitant enterocutaneous fistulas
present a challenge in anterior abdominal wall recon-
struction. The morbidity and mortality rates increase
significantly when the abdominal wound is associated
with an enterocutaneous fistula, especially in the
setting of sepsis and malnutrition. 15° Enterocutaneous
fistula in the patient with cancer represents a difficult
problem in that the circumstances are often com-
plicated by prior surgery, radiation therapy, and
chemotherapy. 151 These fistulas result in skin break-
down and nonhealing wounds from the exposure of
the skin to the pancreatic or intestinal secretions
(Fig. 33-23).
Genitourinary fistulas can involve the bladder,
ureter, urethra, penis, or vagina. Genitourinary tract
fistulas can occur after oncologic pelvic operations,
from inflammatory processes, and after genitourinary
trauma. Contributing factors often include malnutri-
tion, history of radiation therapy with unstable
surrounding skin, tumor recurrence, and excessive
postextirpative dead space. Crohn disease is the most
common inflammatory disorder that affects the gen-
itourinary system. Genitourinary complications occur
in 4% to 35% of patients with Crohn disease, and
fistulas are the most common complication. 152 Recto-
vaginal fistulas are socially distressing for patients and
FIGURE 3 3 - 2 3 . Abdominal wall defect with enterocu-
taneous fistula and infected Marlex mesh (intrinsic factor:
infection; extrinsic factors: trauma and surgery). See Figure
33-77.
924 I • GENERAL PRINCIPLES

pose a challenge to the reconstructive surgeon. The
most common causes of rectovaginal fistulas are ob-
stetric injury (childbirth) and inflammatory processes
(Crohn disease).153 Other causesof rectovaginal fistulas
to consider are malignant disease (primary or recur-
rent) and radiation therapy.15*1 Treatment of recto-
vaginal fistulas first involves management of the
underlying medical condition, if this is applicable, and
then surgical obliteration of the fistulous track.
Central nervous system fistulas are characterized
by cerebrospinal fluid (CSV) leaks, which can also occur
from the peripheral nervous system. Central nervous
system fistulas can be congenital or acquired. CSF
fistulas arise most commonly after head trauma but
may occur as a complication of intracranial proce-
dures or infection. Traumatic CSF fistulas complicate
2% of all head traumas and 12% to 30% of all basilar
skull fractures.155,156 These fistulas result in problem
wounds secondary to the persistent CSF drainage with
local skin breakdown. Devastating consequences of a
persistent CSF leak are brain herniation and second-
ary infeciion of the central nervous system. CSF leaks
are also a significant complication after spine surgery.
This can result from tumor resection, infection, or
complications related to exposed hardware. When a
CSF fistula occurs after spine surgery, the risk of menin-
gitis and consequent morbidity increases (Fig. 3 3 '
24). 15? Unlike fistulas in other areas of the body, those
associated with the central nervous system require
expedirious surgical management.
Extrinsic Factors
Extrinsic factors are unfavorable systemic or environ-
mental factors that affect wound healing and may result
in the development of a problem wound. Extrinsic
causes of problem wounds include trauma, pressure,
temperature, caustic agents, and toxins. These causes,

D F
FIGURE 3 3 - 2 4 . Posterior cervical neck wound with CSF fistula (intrinsic factors: vascular insufficiency and infec-
tion; mechanical factor: fistula). A. Defect is secondary to osteoradionecrosis of cervical vertebral column. Local random
flaps from left shoulder have failed to provide stable coverage. B, Resection of nonviable tissue includes arachnoid (a).
Note the underlying radiation necrosis of posterior commissure of cervical cord (b). C Fascia lata graft used to restore
arachnoid continuity; design of posterior trapezius musculocutaneous flap. 0, Posterior trapezius musculocutaneous
flap inset into posterior neck detect. Muscle provides coverage of the fascia lata graft. The donor defect is skin grafted.
E, Postoperative posterior view at 3 years demonstrates stable coverage for osteoradionecrosis of cervical vertebral
column. F, Lateral view demonstrates flap inset. Preservation of anterior fibers of trapezius muscle provides function
and avoids shoulder droop. (From Mathes SJ, Nahai F: Clinical Applications for Muscle and Musculocutaneous Flaps.
St. Louis, CV Mosby, 1982.)

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33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE
TABLE 33-9 • EXTRINSIC CAUSES OF
PROBLEM WOUNDS
Trauma
pressuce
Tempe»3ture
Hyperthermia (burn)
Hvpothermia (frostbite)
Caustic and chemical substance exposure
Extravasation injury
Bnvenomation
Surgery
although extrinsic to the patient, often result in a
cascade of events that ultimately lead to intrinsic
deficiencies such as diminished oxygen delivery
(Table 33-9).
TRAUMA
Traumatic injuries leading to the development of
problem wounds can be acute or chronic in nature.
These traumatic wounds may be life-threatening sec-
ondary to exposure of vital structures such as the brain
and spinal cord, heart, or major vessels, which need
to be addressed rapidly. In most instances, once the
trauma team has controlled urgent life-threatening
conditions, post-traumatic defects are then recon-
structed on a semielective basis. However, exposed
nerves, vessels (especially those involving vein or
prosthetic grafts), and orthopedic hardware warrant
immediate flap coverage.
Trauma can be subdivided into blunt or penetrat-
ing trauma. Blunt trauma can result in a large amount
of tissue destruction, the extent of which is not always
obvious. Compartment syndrome can result from
blunt trauma and is defined as an increased pressure
within a limited anatomic space that compromises
circulation and neurologic function.158 Compartment
syndrome can occur in the extremities or intra-
abdominally. Increased intracompartmental pressure
causes compressive closure of the thin-walled venules,
resulting in hypertension at the venous end of the cap-
illary beds. If it is not recognized early, this compro-
mise in circulation can produce tissue necrosis or organ
failure due to lack of oxygen delivery. In the extremi-
ties, the normal intramuscular pressure is 0 to
8 mm Hg. The diagnosis of compartment syndrome
is largely clinical. Pain and paresthesias first appear at
pressures between 20 and 30 mm Hg.159 The pain is
generally described as out of proportion to the appar-
ent injury and progresses during a short time. Other
symptoms include pallor, pulselessness, and paralysis
(late symptom). Measurement of intracompartmen-
tal pressures can be accomplished in a variety of ways.
In general, either a catheter or needle is introduced
into the compartment, and the pressure is transduced
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Dr.Mustafa D.
925
to a manometer. The Stryker Quick Pressure Monitor
instrument* has been designed to measure intra-
compartmental pressures. This device measures the
pressure necessary to inject a small quantity of fluid.
Another technique uses a wick catheter. The wick
catheter technique uses polyglycolic acid suture wicks
connected to a pressure transducer and allows con-
tinuous measurement of intracompartmental pres-
sure. ly9 The critical intracompartmental pressure at
which one performs a fasciotomy is generally greater
than 30 mm Hg. Compartment pressures of 30 mm
Hg or greater for a period of 6 to 8 hours can cause
irreversible damage. 160 Once the compartment is
released, a large wound with exposed vital structures
or organ systems exists. The problem wound that
results from release of the compartment syndrome
relates to vascular insufficiency caused by intracom-
partmental pressures. This can be compared with the
problem wound formed by extrinsic pressure that
results in a pressure sore. The net result in both
instances is lack of capillary perfusion and poor
wound healing capacity.
Severe blunt abdominal trauma may lead to abdom-
inal compartment syndrome. This syndrome is the
result of massive bowel edema, third spacing of fluid,
intraperitoneal hemorrhage, or retroperitoneal
hematoma. 158 Measurement of intra-abdominal pres-
sures is warranted in patients who clinically have a
tense abdomen in combination with unexplained high
peak inspiratory pressures or oliguria in the face
of massive fluid resuscitation. Intra-abdominal pres-
sures of 25 mm Hg or more have been associated with
significant decreases in abdominal wall and intra-
abdominal organ perfusion.161 Measurement of intra-
abdominal pressure is accomplished by a variety of
means. Bedside measurement of intra-abdominal
pressure can be made by transducing pressure from
indwelling femoral venous, rectal, gastric, or urinary
catheters.162 Of these methods for indirect measure-
ment of intra-abdominal pressure, measurement of
urinary bladder pressures is the most commonly used
and is considered the gold standard because it is easy
to perform and minimally invasive.163 The treatment
of abdominal compartment syndrome is prompt
opening of the abdominal wound including the under-
lying fascia. The abdomen is subsequently left open
until the edema subsides. Frequently, a problem
wound develops as a consequence of the open
abdomen and loss of the abdominal domain. In addi-
tion, abdominal wound ischemia and underlying
organ system dysfunction may be present. There are
also circumstances in which abdominal compartment
syndrome can present postoperatively. It has been sug-
gested by Losken et al164 that a correlation exists
f
Strykcr Surgical, Kalamazoo, Michigan.
image...

926 I • GENERAL PRINCIPLES

between elevated intra-abdominal pressure and com-

plications after donor site closure in TRAM flap breast
reconstruction. The authors concluded that intra-
abdominal pressure greater than 20 mm Hg transiently
increases postoperative oliguria and tachypnea and
therefore predicts the increased likelihood of donor
site complications. These findings suggest that the ele-
vated intra-abdominal pressure adversely affects the
vascular perfusion of the abdominal wall. Abou-
Sayed and Mathes165 note that other factors must be
considered for donor site complications, including
the body mass index of the patient as well as other
comorbid factors.
Penetrating trauma results in the destruction of soft
tissues with a variable amount of underlying tendon,
nerve, bone, or vascular disruption (Figs. 33-25 and
33-26). Vascular disruption is the primary factor for
problem wound development. Devitalized soft tissue
is subsequently at risk for secondary infection. Major
vascular injuries, such as popliteal artery trauma, can
lead to problem wounds of the lower extremity or to
loss of the limb related to acute vascular insufficiency.
Although the entrance wound may be negligible, it
is critical to rapidly assess the underlying tissue
damage to prevent further tissue loss. Gunshot injuries
represent a specific type of penetrating injury. Depend-
ing on the caliber of the weapon and velocity of the
bullet, wounds from guns may range from minimal FIGURE 3 3 - 2 6 . Crush-avulsion injury to right pelvis and
soft tissue loss with underlying tissue destruction to lower extremity (extrinsic factor: trauma). The patient was
complete destruction of soft tissues in addition to crushed between train cars with resultant extensive soft
tissue and skeletal injuries. See Figure 33-89.

underlying muscle, bone, tendon, nerve, and blood

FIGURE 3 3 - 2 5 . Abdominal wall trauma (extrinsic
factor: trauma). Anterior view of shotgun wound with trau-
matic loss of abdominal wall and visceral injury and expo-
sure. See Figure 33-86. (From Steinwald PM, Mathes SJ:
Management of the complex abdominal wall wound. Adv
Surg 2001;35:77.)
vessels. These wounds present a challenge, not only
because of the tissue destruction but also as a result
of the penetration of functional structures, such as
the oral cavity. Unlike with penetrating trauma, avul-
sion injuries result in a large, readily definable defect,
although the viability of the avulsed tissue is some-
times questionable.
Other acute traumatic wounds occur from human
and animal bites, which may predispose the patient
to a problem wound. Human bite wounds often occur
as a fight wound in which the closed fist strikes a
person's mouth, causing a puncture wound of the
extensor tendon and its sheath. These injuries are not
always apparent at the time of examination but must
be sought if there is suspicion. Wounds are often treated
as "minor," given their small size, but poorly managed
human bites result in significant morbidity from infec-
tion.166 The resultant inoculation of the tendon sheath
causes tenosynovitis; when overlooked, this can result
in loss of function or even loss of the affected finger.
Bacteria isolated from human bite wounds are numer-
ous (Table 33-10). Commonly isolated aerobic
organisms include both alpha- and beta-hemolytic

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image...
TABLE 3 3 - 1 0 • BACTERIA ISOLATED FROM HUMAN BITE WOUNDS
Aerobes and Facultative
Achietobucter sp.
Branhamella catarrhalis
Corynebactehum sp.
Eikenella corrodens
Enterobacter cloacae
Enterobacter sp.
Escherichia coli
Haemophilus spp. (3)
Klebsiella pneumoniae
Micrococcus sp.
Moraxella sp.
Neisseria sp.
Nocardia sp.
Proteus mirabilis
Pseudomonas aeruginosa
Serratia marcescens
Staphylococcus aureus
Staphylococcus epidermidis
Staphylococcus saprophyticus
Streptococcus
alpha-hemolytic
beta-hemolytic
gamma-hemolytic
From Smith PF, Meadowcroft AM, iMay DB: Treating mammalian bite wounds. I Clin Pharm Ther 2000;25:85.
streptococci, S. aureus, S. epidermidis, Corynebacterium
species, and Eikenella corrodens.167 Commonly isolated
anaerobic organisms include Peptostreptococcusspecies,
Bacteroides (fragilis and nonfragilis species), Fusobac-
terium, Veillonella, Prevotella, Porphyromonas, and
Clostridium. Treatment involves early recognition fol-
lowed by incision and drainage of the affected digit
in addition to systemic culture-specific antibiotics.
A proven choice for oral or intravenous antibiotic
therapy remains the combination of a P-lactam anti-
biotic with a p-lactamase inhibitor.168 Other areas
susceptible to a problem wound formation are those
that have poor vascularity, such as the ear cartilage.
Common animal bites that occur annually are dog
and cat bites. Dog bites have the potential to cause
significant wounds secondary to the crushing-type
injury they cause. An adult dog can exert 200 psi of
pressure; some larger dogs are able to exert 450 psi.167
Thus, these wounds may present as problem wounds
given the size and associated bone, tendon, muscle,
nerve, or vascular injury. The cat's bite, although less
powerful than a dog's, can be equally dangerous
because cats have pointed teeth that allow inoculation
of deep tissues. The severity of the bite wound depends
partly on the area of the body affected. The risk of
infection is greater in those areas with a poor blood
supply. Common bacteria involved in dog bites include
Staphylococcus, Streptococcus, Eikenella, Pasteureiia,
Proteus, and Klebsiella (Table 33-11).' 69 Common
bacteria involved in cat bites include Pasteureiia,
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33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 927
Anaerobes Rare Pathogens
Acidaminococcus sp. Actinomyces sp.
Actinomyces sp. Clostridium tetani
Arachnia propionica Hepatitis B and C
Bacteroides sp. Herpes simplex virus
Clostridium sp. Mycobacterium tuberculosis
Eubacterium sp. Treponema pallidum
Fusobacterium sp.
Peptostreptococcus sp.
Prevotella sp.
Propionibacterium acnes
Veillonella sp.
Actinomyces, Propionibacterium, Bacteroides, Fusobac-
terium, and Clostridium (Table 33-12).169 The man-
agement of dog bites involves stabilization of the
patient and evaluation of the wound. A history of prior
rabies and tetanus vaccination should be sought
immediately. After the patient has received adequate
anesthesia, the wound is copiously irrigated and non-
viable tissue excised. Reconstruction of the defect is
generally done at a secondary procedure when appro-
priate antibiotic therapy has been instituted.
In treating patients with animal bites, it is impor-
tant to consider animal rabies. Rabies is an acute viral
infection of the central nervous system transmitted
in the saliva of biting animals. Wild animals are the
most common vectors in North America. Malaise,
anorexia, and nausea are early prodromal signs. There
is often a tingling and severe pruritus at the site of the
bite. After 2 to 10 days, frank neurologic signs appear.
Rabies is classically manifested by periods of hyper-
excitability and autonomic dysfunction (hyper-
salivation, piloerection, cardiac arrhythmias, and
priapism). 170 About 20% of patients may present with
flaccid paralysis.171 Treatment is supportive, and death
almost invariably occurs within 2 weeks after the onset
of symptoms. Only a handful of reports of human
survival have been documented. However, postexpo-
sure prophylaxis with rabies immune globulin and
active immunization with antirabies vaccine elicit high
titers of neutralizing antibodies in almost all recipi-
ents. Therefore, early recognition and treatment are
928 I • GENERAL PRINCIPLES

TABLE 33-11 • BACTERIA ISOLATED FROM DOG BITE WOUNDS

Aerobes and Facultative Anaerobes Rare Pathogens

Aeromonos hydrophila Actinomyces sp. Blastomyces dermatitidis

Acinetobacter sp. Bacteroides sp. Weeksella zoohelicum
Actinobacillus sp. Eubacterium sp. (formerly CDC group ll-j)
Bacillus sp. Fusobacterium sp.
Brucella canis Leptotrichia buccalis
Capnocytophaga canimorsus Peptococcus sp.
(formerly CDC group DF-2) Peptostreptococcus sp
CDC alpha-numeric groups Porphyromonas
EF-4, llr, M-5 Prevotella sp.
Chromobacterium sp. Propionibacterium sp.
Corynebacterium sp. Veilloneila sp.
Eikenella corrodens
Enterobacter cloacae
Enterococcus sp.
Escherichia coli
Haemophilus aphrophiius
Klebsiella sp.
Micrococcus sp.
Moraxella sp.
Neisseria sp.
Pasteurella multocida
Pasteurella "gas"
Proteus mirabilis
Pseudomonas sp.
Staphylococcus aureus
Staphylococcus epidermidis
Staphylococcus sp.
Streptococcus
alpha-hemolytic
beta-hemolytic
gamma-hemolytic

From Smith PF, Meadowcrofl AM, May DB: Treating mammalian bite wounds. J Clin Pharm Ther 2O0O;25:85.

the keys to management- In addition to vaccination, SURGERY

the wound must be thoroughly cleaned with soap and
water for 5 minutes or 1 in 20 dilution of chlorhexi-
dine or quaternary ammonium compound, after
which a disinfectant should be applied. Povidone-
iodine, aqueous iodine, or 40% to 70% alcohol may
be used.
Tissue injury may occur from elective surgical inter-
ventions. Postsurgical wounds may become problem
wounds by a disruption or an injury to the local or
regional blood supply. Along with proper atraumatic
tissue handling and selective blood vessel cauteriza-

TABLE 33-1 2 • BACTERIA ISOLATED FROM CAT BITE WOUNDS

Aerobic a n d Facultative Anaerobic Rare Pathogens

Acinetobacter sp. Bacteroides sp. Afipia felis

Capnocytophaga canimorsus Fusobacterium nucleatum Blastomyces
(formerly CDC group DF-2) Porphyromonas Francisella tularensis
Corynebacterium sp. Prevotella Plague
Enterobacter cloacae Propionibacterium sp. Rabies
Neisseria sp,
Pasteurella multocida Sporothrix sp.
Staphylococcus aureus
Staphylococcus epidermidis
Streptococcus sp.

From Smith PF, Meadowcroft AM, May DB: Treating mammalian bite wounds. J Clin Pharm Ther 2000;25:85.

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33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 929

tion, skin approximation must not be placed under
excessive tension to avoid skin and soft tissue necro-
sis. Skin necrosis from vascular disruption or exces-
sive tension at closure may lead to poor wound
healing and eventually a problem wound. Although
excessive tension is considered detrimental to wound
healing, early studies have shown that carefully applied
tension improves wound strength.172,173 This tension,
though, may be counterproductive if the suture is
pulled too tight. Suture tension that raises the inter-
stitial pressure in the center of the incision above cap-
illary pressure (approximately 30 to 40 mm Hg) has
been shown to cause necrosis in laboratory animals.174
Sanders175 showed that midline incisions closed with
wide bites, tied loosely, such that the wound margins
were brought together without excessive tension, had
25% more strength than incisions closed with narrow
bites tied as tightly as possible. When surgical wounds
break down or are unable to be closed primarily, the
resulting open wound has the potential to convert to
a problem wound. The most common intrinsic cause
of this is infection. Those wounds overlying a cavity
(mechanical) may expose underlying vital structures,
leading to organ system dysfunction. It has been shown
that acute fascial dehiscence is associated with mor-
talities as high as 50%. 176
When a surgical procedure involves elevation of skin
and subcutaneous tissue with disruption of deep fascial
and muscle vascular connections, the survival of the
subcutaneous tissue and skin depends on the blood
supply in the dermal-subdermal plexus. Cutaneous flap
survival is limited by the disruption of this plexus.
Dependable flap survival depends on the ratio of length
to width of the flap. This ratio varies from 5:1 in the
face to 1:1 in the lower extremity. When dissection in
this subcutaneous plane is combined with closure
under tension, tissue necrosis frequently occurs and
may result in problem wound development, particu-
larly if infection ensues.
Despite advances in antibiotics, antisepsis, anes-
thesia, and postoperative care and improved suture
materials, the incidence of serious abdominal wound
disruption remains largely unchanged. 177 A case-
control study by Riou et al178 showed that age older
than 65 years, wound infection, pulmonary disease,
hemodynamic instability, ostomy within the incision,
hypoproteinemia, sepsis, obesity, uremia, hyperali-
mentation, malignant disease, ascites, steroid use, and
hypertension were associated with abdominal wound
disruption. Patients with more than three risk factors
were at a significantly increased risk of wound failure;
those with five risk factors had an incidence of 30%,
and those with eight or more of these conditions
had a 100% wound disruption rate. The incidence
of abdominal wound complications is also greatly
dependent on the classification of the wound at the
time of surgery (Table 33-13).
PRESSURE
Excessive or prolonged tissue pressure represents an
extrinsic cause of a problem wound. Pressure necro-
sis is a function of the amount of pressure on the tissue
and duration of the pressure. It is estimated that 1.3
to 3 million adults have a pressure ulcer, with an esti-
mated cost of $500 to $40,000 to heal each ulcer.179,180
Incidence rates vary between clinical settings, with rates
of 0.4% to 38.0% in hospitals, 2.2% to 23.9% in
long-term care facilities, and up to 17% in home care
settings.181 Normal arteriole, capillary, and venule
pressures are 32, 20, and 12 mm Hg, respectively.182
The microcirculation is compromised when the tissue
pressure exceeds capillary perfusion pressure, approx-
imately 25 to 30 mm Hg. Muscle damage can occur
after 1 hour with pressures of 60 mm Hg.183 Pressure
generated under the ischial tuberosities while a person
is seated can reach 300 mm Hg, and sacral pressure
can range from 100 to 150 mm Hg while a person lies
on a standard hospital mattress.182,184,185 The ischial
region is the most frequent site of pressure ulceration
(Fig. 33-27). The scalp, sacrum, trochanter, and cal-
caneus can also be involved.
Pressure sores are characterized by deep tissue
necrosis and a loss of volume disproportionately
greater than the overlying skin defect.186 In addition
to the skin and soft tissue damage that occurs, the

TABLE 33-1 3 • ABDOMINAL WOUND CLASSIFICATION

Class Category Definition Infection Rate

l Clean Nontraumatic; no entry into oropharyngeal cavity or lumen of <5%

the respiratory, alimentary, or genitourinary tract
ll Clean-contaminated Entry into oropharyngeal cavity or respiratory, alimentary, or <2%-l 0%
genitourinary tract without significant spillage
Hi Contaminated Open, fresh, and traumatic wounds; major break in sterile <\ 5%-20%
technique
IV Dirty Traumatic wounds more than 4 hours old; perforated viscera; >30%
wounds with foreign bodies or devitalized tissue

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930 . I • GENERAL PRINCIPLES

recurrence is secondary to the inability to restore sen-

sation to the pressure sore area. Patients who suffer
pressure ulcerations secondary to a temporary disability
tend to recover when the disability resolves.

TEMPERATURE
Exposure to temperature extremes represents an
extrinsic cause of problem wounds. Temperatures
above 40°C can cause burn wounds with varying
degrees of tissue injury, depending on the tempera-
ture and length of exposure. Three zones of burn injury
have been described.190 The area closest to the heat
source receives the greatest damage and is termed the
zone of coagulation. This area consists of coagulated,
necrotic cells. Extending concentrically out from the
central zone of coagulation is the zone of stasis, which
FIGURE 3 3 - 2 7 . Right ischial pressure sore (intrinsic has marginal perfusion and questionable viability but
factor: infection; extrinsic factor: pressure). See Figure the ability to survive. The zone of hyperemia lies in
33-81. (From Mathes SJ, Nahai F: Clinical Applications the periphery and is the closest to normal tissue. This
for Muscle and Musculocutaneous Flaps. St. Louis, CV
Mosby, 1982.)
area has sustained the least injury and is characterized
by vasodilatation and increased blood flow in response
to the injury (Fig. 33-28). Factors determining whether
underlying bone is also frequently involved. Multiple the burn wound will become a problem wound include
risk factors are involved in the pathogenesis of pres- the involved structures, the presence of infection, the
sure ulcer formation. Intrinsic factors include age of
the patient, presence of chronic diseases (diabetes mel-
litus, peripheral vascular disease), immobility, mal-
nutrition, and sensory impairment. Extrinsic factors
include the external pressure, friction, shearing forces,
moisture, and infection. Pressure sores are graded I
to IV. Grade I represents a discoloration of intact skin,
including nonblanching erythema. Grade II represents
partial-thickness skin loss or damage involving epi-
dermis or dermis. Grade III represents full-thickness
skin loss involving damage or necrosis of subcutaneous
tissues; grade III does not extend through the under-
lying fascia or underlying structures. Grade IV repre-
sents full-thickness skin loss with extensive destruction
and tissue necrosis extending to the underlying bone,
tendon, or joint capsule. Although relatively superficial
lesions (grade I and grade II) heal in response to local
wound care, grade III and grade IV lesions are sus-
ceptible to the development of complications. Com-
plications of these high-grade pressure ulcers include
local infection, osteomyelitis, and bacteremia. Bac-
teremia associated with pressure ulcers is associated
with greater than 50% mortality.187,188
The clinical course of pressure sores in patients with
a temporary disability differs from that in patients with
a permanent loss of sensation (denervation). Dener-
vated skin is less susceptible to local temperature
changes and more likely than normal skin to ulcerate
because of high rates of collagenase activity. Paralyzed
patients tend to develop ulcers over anesthetic areas
larger (five times larger) than those in debilitated
patients with an intact nervous system.189 In patients
FIGURE 3 3 - 2 8 . Flame burn to anterior chest (extrin-
with a permanent loss of sensation, the frequency of sic factor: temperature).

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image...

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 931

skin and soft tissue cause local and systemic effects

that may result in a problem wound. In addition, med-
ications commonly given to patients may have unde-
sirable effects either directly on wound healing or
systemically, indirectly affecting the healing process.

Envenomotion
Caustic substances may be delivered by insect or reptile
bites, which result in problem wounds from toxin expo-
sure. The venomous exposure can act on the tissues
locally or as a neurotoxin. The most common insect
bite associated with severe tissue necrosis is that of
Loxosceles reclusa or the brown recluse spider (Fig. 33-
32). The toxins from the brown recluse spider cause
painful, necrotic, and slow-healing wounds (Fig. 33-
33). The mechanism for this skin necrosis is not entirely
understood but is thought to be dependent on the
victims neutrophil function. The Loxosceles venom acts
as an endothelial cell agonist, stimulating an inflamma-
tory response, which eventually leads to dysregulated
neutrophil function.194 Latrodectus or the black widow
spider can produce severe skin lesions that may neces-
sitate wound debridement and surgical coverage (Fig.
33-34). The local envenornation begins with pain and
pruritus that progresses to vesiculation with violaceous
necrosis, surrounding erythema, and ulcer formation.
The venom from the black widow spider is called a-
latrotoxin and is a potent neurotoxin. This neurotoxin
binds to presynaptic nerve terminals and stimulates

FIGURE 3 3 - 2 9 . Burn eschar, posterior trunk (extrin-

sic factor: temperature). Full-thickness flame burn involves
left posterior trunk.

surface area and location of the burn (i.e., joint involve-

ment), and the medical status of the patient (comor-
bidities) (Fig. 33-29). In addition, the late consequences
of burn wounds, such as hypertrophic scarring and
contractures, may contribute to problem wound
development (Fig. 33-30).
Prolonged hypothermia (central or core tempera-
ture of 35°C or lower) causes frostbite injuries to
exposed skin. It has been shown experimentally that
the tensile strength of a wound decreases by 20% in a
cold (I2°C) wound environment. 191 Mild hypother-
mia triples the risk of infection by reducing tissue
oxygenation.1 Severe hypothermia primarily affects
the vasculature as the blood vessels become severely
injured by a combination of direct cellular injury and
microvascular thrombosis, leading to progressive
dermal ischemia (Fig. 33-31).192-'93

CAUSTIC AND CHEMICAL

SUBSTANCE EXPOSURE FIGURE 3 3 - 3 0 . Electrical burn, scalp (extrinsic factor:
temperature). High-voltage electrical injury involves pos-
Exposure to caustic substances occurs from enveno- terior scalp and upper extremities. The exposed skull is
mation or extravasation injuries. These injuries to the treated with topical silver sulfadiazine. See Figure 33-85.

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 I • GENERAL PRINCIPLES
FIGURE 3 3 - 3 1 . Upper and lower extremity frostbite
(extrinsic factor: temperature}. A and B, Large bullae on
hands and feet of man with moderate hypothermia and
deep frostbite. (From Biem J, Koehncke N, Classen D,
Dosman J: Out of the cold: management of hypothermia
and frostbite. CMAJ 2003:168:305.)
a massive neurotransmitter release.' Clinically, a
lesion develops at the site of the bite with significant
pain. In addition to these local findings, patients also
have abdominal pain and lower extremity pain and
weakness within minutes to hours of envenomation
secondary to the systemic neurotransmitter release.
Venomous snakebites are an uncommon occurrence
in the United States. There are approximately 8000 ven-
omous snakebites reported each year.196 The venom
from a snakebite contains many toxic proteins and
enzymes that have potentially harmful consequences
(Fig. 33-35). The components of the toxins are
many and include procoagulants, anticoagulants,
hyaluronidases, RNases, DNases, postsynaptic toxins,
and presynaptic toxins.197 The majority of poisonous
snake envenomations occur from the bite of a pit viper
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(Fig. 33-36). This family of snakes includes rattle-
snakes, copperheads, and cottonmouths. Pit vipers are
identified by a heat-sensing pit anteroinferior to the
e>e, elliptical pupils, triangular head, and undivided
subcaudal scales. The other major groups of snakes
causing bites are the cobras and ^>ea .snakes. Their effects
may be neurotoxic, myotoxic or nephrotoxic. Rattle-
snake venom is significantly move potent than copper-
head or coitonmouth venom.
Rattlesnake venom is composed of several diges-
tive enzymes and spreading factors, which are respon-
sible for both local tissue necrosis and systemic, effects.
These wounds are often associated with local edema
and erythema. Rapidly progressive swelling is usually
associated with more severe envenomation. If intra-
muscular envenomation has occurred, local or diffuse
myotoxicity may result in compartment syndrome or
rhabdomyolysis. Wounds that progress to problem
wounds are those that are secondarily infected or large
envenomations with subsequent tissue necrosis. These
are especially problematic when they involve the distal
extremities, such as the hand or foot. These areas may
become significantly edematous, further retarding
wound healing and thus leading to problem wound
development. Copperhead and cottonmouth enven-
omation may cause effects similar to rattlesnake
envenomation, but it is usually less severe. Other
animals that produce toxins are scorpions, lizards, and
marine animals.
Extravasation
Intravenous fluid extravasation is defined as leakage
of injectable fluids out of the vein into the interstitial
space. Extravasation may be the result of a displaced
or malpositioned intravenous line or occur from
increased vascular permeability. Varying degrees of
injury may occur to the surrounding tissue, depend-
ing on the solution being injected. The substances that
most commonly extravasate are cationic solutions (e.g.,
potassium ion, calcium ion, and bicarbonate), osmot-
ically active chemicals (e.g., total parenteral nutrition,
hypertonic dextrose), antibiotics, and cytotoxic drugs.
Patients undergoing chemotherapy have a 4.7% risk
for development of extravasation.198 In children, the
incidence increases to 11% to 58%.'" The dorsum of
the hand is the most common site of extravasation in
the adult, which may result in a wound with exposed
extensor tendons (Fig. 33-37). Other common sites
are the antecubital fossa in an adult and the dorsum
of the foot and the scalp in neonates. The intravenous
fluids that most commonly extravasate to cause
necrosis in the infant are high-concentration dextrose
solutions, calcium, bicarbonate, and parenteral nutri-
tion. Newborn babies are at risk because of the
fragility and small caliber of their veins, their inabil-
ity to localize pain, and the system of delivery, which
pumps the intravenous fluid under pressure.200 After
image...

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 933

1 inch 1 cm

Black widow Brown recluse

A B

FIGURE 3 3 - 3 2 . Venomous spiders of North America (extrinsic factor: caustic and chemical sub-
stance exposure). A and C, Black widow spider (Latrodectus hesperus). B and D, Brown recluse
spider (Loxosceles rectusa). (C and D from Auerbach P: Wilderness Medicine. Philadelphia, Mosby,
2001.)

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934 I • GENERAL PRINCIPLES

FIGURE 3 3 - 3 3 . Brown recluse spider bite (extrinsic

factor: caustic and chemical substance exposure). A, Brown
recluse spider bite after 6 hours with central vesicle hem-
orrhage and gravitational spread of venom. B, Brown
recluse spider bite after 24 hours with central ischemia
and rapidly advancing cellulitis. (From Auerbach P:
Wilderness Medicine. Philadelphia, Mosby, 2001.)

FIGURE 3 3 - 3 5 . Rattlesnake bite (extrinsic factor:

FIGURE 3 3 - 3 4 . Black widow spider bites (extrinsic
factor: caustic and chemical substance exposure). Wheals
on skin surface from black widow spider bites are desig-
nated by arrows. (From Saucier JR: Arachnid envenoma-
tion. Emerg Med Clin North Am 2004;22:405.)
caustic and chemical substance exposure). A, Envenom-
ation in index and long finger proximal phalanges after
rattlesnake bite. Note the upper extremity edema 1 hour
after bite. B, Immediate compartment release for intrin-
sic dorsal and volar regions. The edema resolved in 48
hours after envenomation. C, Several days after rattlesnake
envenomation and intrinsic release of impending com-
partment syndrome. Full range of motion is noted in the
involved digits.

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image...

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 935

SPSS*"* * --^i •

#1* d i ftusra!

G
FIGURE 3 3 - 3 6 . Venomous snakes (extrinsic factor: caustic and chemical substance exposure). A Pit viper. B, Eastern
diamondback rattlesnake (Crotaius adamanteus). C, Western diamondback rattlesnake (Crotaius atrox). D, Mojave rat-
tlesnake (Crotolus scutulatus). E, Timber rattlesnake (Crotolus horridus). F, Prairie rattlesnake (Crotaius viridis viridis).
G, Southern Pacific rattlesnake (Crotaius viridis helleri). H, Tropical rattlesnake (Crotaius durissus durissus). I, King cobra
(Ophiophagus hannah). (Courtesy of Michael Cardwell/Extreme Wildlife Photography. From Auerbach P: Wilderness
Medicine. Philadelphia, Mosby, 2001.)

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936 1 • GENERAL PRINCIPLES
FIGURE 3 3 - 3 7 . Chemotherapeutic agent extravasation
at intravenous site (extrinsic factor caustic and chemical
substance exposure). The patient has an extensive wound
at the site of delivery of 5-fIuorouracil foi treatment of
lung cancer. See Figure 33-93.
extravasation, tissue necrosis progresses from chem-
ical toxicity, osmotic toxicity, or the effects of pres-
sure in a closed space. In most instances, the tissue
necrosis is underestimated.
The drug that most often causes an extravasation
wound in adults is doxorubicin (Adriamycin), a com-
monly prescribed chemotherapeutic agent. Doxoru-
bicin is directly cytotoxic. This cytotoxicity is amplified
by the release of doxorubicin-E>NA complexes from
dead cells, which causes further death. Cellular death
prevents the release of cytokines and growth factors,
which results in the failure of activation of the cells
important in wound healing.201,20'1 After extravasation,
edema, erythema, and induration are usually present
with variable amounts of tissue necrosis, the extent of
which may not be readily apparent on the surface. Along
with the soft tissue defect, the limb may have altered
function if there is injury to underlying nerves,
muscles, tendons, and blood vessels. When the extrava-
sation is in proximity to a major artery in the forearm
or leg, that extremity is at great risk for amputation
because of arterial thrombosis.
Medications
Certain medications that are commonly prescribed can
cause problem wounds. Medications can have a direct
effect (toxic) on surrounding tissues, causing tissue
necrosis, or may affect cells important to the wound
healing cascade, altering normal wound healing. Med-
ications that can cause tissue necrosis include warfarin
(Coumadin) and heparin. Common medications that
alter wound healing include steroids and chemother-
apeutic agents.
Warfarin has the potential to induce skin necrosis.
Warfarin-induced skin necrosis occurs in 0.01% to
0.1% of patients undergoing warfarin therapy.203,204 The
pathogenesis of this phenomenon is unknown, but
two theories exist. One theory is that warfarin has a
direct toxic effect at the dermovascular loop between
the precapillary arterioles and capillaries.201' The cap-
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Dr.Mustafa D.
illaries dilate and rupture, and the venules subsequently
thrombose, causing occlusion of the dermal and sub-
cutaneous venules that results in skin necrosis. The
other hypothesis is that warfarin causes an imbalance
between procoagulant and anticoagulant pathways.
Low levels of protein C or S, either functional or inher-
ited, are associated with the manifestation of symp-
toms in many patients. Proteins C and S are innate
anticoagulants within the body that balance the coag-
ulation cascade. Similar to the coagulation factors, they
are also vitamin K dependent; however, the half-life
of proteins C and S is shorter than that of the proco-
agulants. Warfarin affects proteins C and S before the
coagulation factors, thus leaving them unopposed,
causing a temporary state of hypercoagulability. This
phenomenon is generally seen in obese, middle-aged
women who are taking warfarin for treatment of deep
venoLis thrombosis or a pulmonary embolus. The areas
of skin necrosis tend to occur on the breasts, buttocks,
and thighs. The condition tends to develop rapidly
into full-thickness necrosis, which may lead to a
problem wound and significant disfigurement.
Another similar medication known to cause
problem wounds is heparin. Skin necrosis can occur
either at the site of injection or as a manifestation of
the heparin -induced thrombocytopenia syndrome. 206
Heparin-induced thrombocytopenia is an immune-
mediated complication associated with the use of
unfractionated heparin. The antibody-antigen
complex is composed of heparin and platelet factor
4. This complex activates not only platelets but also
the clotting system, leading to thrombin generation,
which results in a tendency toward both arterial and
venous thrombosis. Heparin-induced skin necrosis is
also caused by an immune complex mechanism and
is recognized to be strongly associated with heparin-
dependent platelet-activating antibodies, which may
occur with or without the development of thrombo-
cytopenia.207 These lesions generally present in areas
of subcutaneous heparin injection, although they may
occur distally.208 The time at onset is generally 2 to 5
days after heparin administration begins.209 The devel-
opment of heparin-induced skin necrosis should
result in immediate cessation of heparin therapy.
Although many drugs prescribed to patients have
the potential to delay wound healing, none has been
studied as extensively as steroids and chemotherapeutic
agents. Steroids have profound effects on wound
healing and may cause dehiscence of surgical incisions,
increased risk of wound infection, and delayed healing
of open wounds. Steroids produce these effects by
interfering with inflammation, fibroblast function,
collagen synthesis and degradation, deposition of
connective tissue ground substances, angiogenesis,
wound contraction, and re-epithelialization.210 Other
than avoidance of steroids, which may not be possi-
ble, depending on the disease state, vitamin A is effec-
image...
33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE
tive at overcoming the delayed wound healing seen
with steroids. Vitamin A has been shown to restore
the inflammatory response, to increase collagen syn-
thesis, and to promote epithelialization.21' The mech-
anism of action is poorly understood. The dose of
vitamin A that is generally given is 25,000 IU per day
orally or 200,000 IU ointment every 8 hours topically.
Chemotherapeutic agents have detrimental effects
on wound healing through the inhibition of dividing
cells. Along with the tumor cells, chemotherapeutic
agents affect the division of endothelial cells, fibro-
blasts, and keratinocytes of the wound. Normal wound
healing processes depend on the function of these cells
and their ability to liberate growth factors and to stim-
ulate angiogenesis. If the tumor treatment includes
chemotherapeutic agents, it is best to postpone their
use until 5 to 7 days postoperatively to prevent impair-
ment of the initial wound healing cascade.
DISEASE STATES ASSOCIATED
WITH PROBLEM WOUNDS
The second aspect of problem wound management is
assessment of the underlying disease state that may
contribute to delays in wound healing or potentiate
formation of a problem wound.
Connective Tissue Diseases
Connective tissue diseases are a spectrum of disorders
that can predispose to problem wounds. These disor-
ders are characterized by circulating antibodies or
immune cells that are targeted toward self antigens.
They are frequently associated with skin ulcers that
are commonly found on the lower extremity and lack
normal wound healing capacity. Common connective
tissue disorders associated with cutaneous wounds
include systemic lupus erythematosus, scleroderma,
and rheumatoid arthritis. Less common connective
tissue disorders include dermatomyositis, systemic
sclerosis, Sjogren syndrome, and Behcet disease.
SYSTEMIC LUPUS ERYTHEMATOSUS
Systemic lupus erythematosus is an autoimmune dis-
order of unknown cause. This disease occurs prima-
rily in women of childbearing age. Every organ system
can be affected. In one study, skin lesions developed
in 100% of patients observed for 5 years.212 The inci-
dence of leg ulceration has been reported to be
between 2% and 8%.213,214 The cause of ulceration is
thought to be multifactorial. Those causes thought to
be involved in the pathophysiologic process of problem
wounds include vasculitis, thrombosis, Raynaud
phenomenon, anticardiolipin antibodies, and venous
insufficiency. These ulcers typically appear over the
malleolar area and pretibial surface.213 Healing is
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937
further complicated by the fact that these patients are
likely to be taking systemic corticosteroids or other
immunosuppressive agents that suppress wound
healing.
SCLERODERMA
Scleroderma refers to several disorders characterized
by skin thickening due to excessive deposition of col-
lagen and proteoglycans in the involved tissues.215 As
with the other connective tissue diseases, the under-
lying cause is unknown. One study reported that more
than 35% of patients with scleroderma develop skin
ulcers.216 Scleroderma can be divided into two cate-
gories, systemic and localized. Systemic scleroderma
can be manifested as either limited or diffuse disease.
Limited scleroderma is typically preceded by Raynaud
phenomenon (see Fig. 33-3); it involves cutaneous scle-
rosis distal to the elbows, with gastrointestinal, pul-
monary, renal, and cardiac fibrosis. Diffuse systemic
scleroderma is characterized by simultaneous Raynaud
phenomenon and skin involvement proximal to the
elbow, with gastrointestinal, pulmonary, renal, and
cardiac fibrosis. Localized scleroderma is a cutaneous
limited fibrosis that manifests as plaque morphea,
generalized morphea, linear scleroderma, and deep
morphea. These ulcers tend to occur over bone promi-
nences (elbows, lower legs, malleoli, and calcaneus),
the dorsum of the proximal interphalangeal and
metacarpophalangeal joints, and the dorsal aspect of
the distal toes as well as the tips of the fingers.2,v'7
The cause of ulceration appears to be multifactorial.
Digit tip ulcers are most commonly caused by
ischemia; ulcers over the proximal interphalangeal and
metacarpophalangeal joints and elbows are probably
caused by contractures, tautness of the skin, thinning
of the skin, and vulnerability to trauma. Large, deep,
painful, punched-out lower leg and malleolar ulcers
are reported to be secondary to vasculitis.211*'219
RHEUMATOID ARTHRITIS
Rheumatoid arthritis is characterized by chronic
inflammatory synovitis that results in cartilage
destruction, bone erosions, and joint deformities. The
cutaneous manifestations of rheumatoid arthritis
include skin changes typical of vasculitis and leg ulcer-
ation in 8% to 9% of patients.220,221 The cause of the
ulceration is multifactorial and includes vasculitis, skin
atrophy, trauma, peripheral neuropathy, and venous
insufficiency. Methotrexate, a medication typically
given to treat rheumatoid arthritis, has also been
reported to cause skin ulcers.215 The ulcers associated
with rheumatoid arthritis typically appear over the
malleolar area and pretibial surfaces. The most
common problem wounds associated with rheuma-
toid arthritis are ulcerative lesions of the digits, which
may progress to gangrene. The cause of these problem
938 I • CENERAL PRINCIPLES
wounds appears to involve inadequate blood flow
as a result of intimal proliferation and vascular
occlusion.
Collagen Disorders
Disordered collagen production and deposition result
in abnormal wound healing. Hypertrophic scars are
raised scars that do not extend beyond the original
wound boundary (Fig. 33-38). These scars generally
form secondary to excessive tensile forces across the
wound; they are most common in wounds that cross
flexion surfaces and wounds of the extremities, breasts,
sternum, and neck. This fibroproliferative disorder is
characterized by up-regulation of collagen synthesis,
deposition, and accumulation. Scar hypertrophy is
more likely to occur in wounds that heal by second-
ary intention, particularly wounds that take more than
3 weeks to re-epithelialize.222 Hypertrophic scar
formation secondary to deep dermal burns often
develops into a problem wound.
In contrast to hypertrophic scars, keloids are a fibro-
proliferative disorder in which the scar extends beyond
the original wound edges (Fig. 33-39). Similar to hyper-
trophic scars, keloids occur on areas of the body that
FIGURE 3 3 - 3 8 . Hypertrophic scar (extrinsic factor:
caustic and chemical substance exposure). Burn scar con-
tracture and hypertrophy of neck and face.
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TABLE 3 3 - 1 4 • VASCULITIS CLASSIFICATION
Small- Vessel Vasculitis
Necrotizing vasculitis
Henoch-Schonlein purpura
Essential mixed cryoglobulinemia
Waldenstrom hypergammaglobulinemia purpura
Associated with collagen vascular disease
Urticarial vasculitis
Erythema elevatum diutinum
Rheumatoid nodules
Reactive leprosy
Septic vasculitis
Large-Vessel Vasculitis
Polyarteritis nodosa
Benign cutaneous form
Systemic form
Granulomatous vasculitis
Wegener granulomatosis
Allergic granulomatosis
Lymphomatoid granulomatosis
Giant cell arteritis
Temporal arteritis
Takayasu disease
Associated with collagen vascular disease
Nodular vasculitis
are subject to increased tension. Wounds on the ante-
rior chest, shoulders, flexor surfaces of the extremi-
ties, and anterior neck and wounds that cross skin
tension lines are most susceptible. Problem wounds
develop in these areas of increased skin tension when
areas of unstable skin develop from epidermal break-
down and subsequent abnormal wound healing. In
addition, hair follicles remaining in the keloid may be
subject to recurrent infections and may complicate
the healing process.
Vasculitis
Vasculitis is a general term that refers to segmental,
angiocentric inflammation and damage to the blood
vessel walls.223 The skin is often the first organ to
manifest signs of vasculitis with involvement of the
small to medium-sized vessels that supply nutrients.
Vasculitis can be idiopathic or associated with a drug,
infection, or underlying systemic disease.224 The
classification of vasculitis is generally based on the size
of the vessels involved, the histopathologic and clin-
ical findings, and the mechanisms or inciting agents
underlying the disease process (Table 33-14).225 The
cutaneous manifestations of vasculitis may range
from purpura to necrosis. Necrosis occurs in relation
to the intensity of the inflammatory reaction within
image...

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 939

FIGURE 3 3 - 3 9 . Prolific scar formation beyond site of original minor injury characteristic of keloid scar (intrin-
sic factor: fibroproliferative disorder). A, Keloid scar: posterior view, right shoulder. B, Keloid scar: lateral view,
right shoulder. C, Keloid: anterior chest. D, Keloid: posterior trunk.

the vessels. This inflammation then produces vascu-
lar compromise by interrupting the normal blood
flow.225 Given the pathophysiologic mechanism of vas-
culitis disorders, all subtypes have the potential for
necrosis and skin ulceration. Two types of vasculitides
that are likely to develop problem wounds are hyper-
sensitivity vasculitis (leukocytoclastic vasculitis) and
polyarteritis nodosa. The hypersensitivity vasculitides
involve small vessels and include the following clini-
cal syndromes: vasculitis associated with infection,
chemical or drug exposure, and connective tissue
disease; serum sickness; Henoch-Schonlein purpura;
erythema elevatum diutinum; and mixed essential
cryoglobulinemia with vasculitis. The clinical mani-
festations of these vasculitides are variable. These
lesions are generally round and regular in appearance.
Nodules with ulceration may persist for months.
The polyarteritis nodosa group of vasculitides
involves medium-sized muscular arteries. The exact
cause of this disorder is unknown, but it is thought
in part to be due to circulating immune complexes.226
Approximately 20% to 40% of patients with poly-
arteritis nodosa have skin involvement.227 A variant of
polyarteritis nodosa, periarteritis nodosa, is limited
to the skin. The lesions associated with polyarteritis
nodosa are 5- to 10-mm painful subcutaneous nodules
that occur along the course of blood vessels of the lower
extremities.

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940 I • GENERAL PRINCIPLES

Pyoderma Gangrenosum
Pyoderma gangrenosum is a relatively uncommon
destructive cutaneous lesion first described in 1930 by
Brunsting el ai.''° Pyoderma gangrenosum is most often
a cutaneous manifestation of ulcerative colitis or Crohn
disease, although it may be associated with rheuma-
tologic diseases, hematologic diseases, or malignant
diseases. Jt has been reported thai in 17% to 74%
of patients, pyoderma gangrenosum is associated
with an underlying disease. 20 The lesion begins as an
erythematous plaque that rapidly becomes a tender
necrotizing ulcer. The characteristic pyoderma gan-
grenosum ulcer has a purplish blue, undermined,
rolled border. The base typically has a cribriform or
honeycomb-like appearance. This ulcer is commonly
misdiagnosed, as there are no specific tests or pathog-
nomonic features of this disease. When it is identified,
treatment should be focused on the underlying con-
dition; surgical debridement will only result in a larger,
problem wound if the underlying disease state is not
adequately treated. Only after control of the underly-
ing disease (e.g., colectomy for ulcerative colitis) are
wound debridement and closure feasible. These
wounds tend to be small, although there have been
reports of lesions involving 15% and 25% of total body
surface area.230,231 These wounds may also be second-
FIGURE 3 3 - 4 0 . Pyoderma gangrenosum (intrinsic
arily infected,most commonly with Staphylococcusand factors: impaired cellular function and infection). The
Streptococcus. Thus, treatment should consist of both classic presentation of rapidly progressive, painful, sup-
local and systemic therapies. Local therapy consists of purative cutaneous ulcers with edematous, boggy, blue,
saline or benzoyl peroxide to gently d^bride the ulcer undermined, and necrotic borders. (From Habif TP: Clin-
ical Dermatology. A Color Guide to Diagnosis and Therapy,
and to decrease the bacterial colonization. Extensive 4th ed. Philadelphia, Mosby, 2004.)
or advanced lesions are generally treated with systemic
steroids or immunosuppression. After the underlying
disease state is controlled and the wound managed result. Fasciocutaneous and musculocutaneous flaps
locally, reconstruction can be accomplished (Fig. 33-40). have been described to cover the excisional defect.236*238
The musculocutaneous flap has been reported to be a
valid option for managing infected lesions because of
the abundant blood supply.239,240 Some investigators
Hidradenitis Suppurativa advocate the use of negative-pressure dressings in the
Hidradenitis suppurativa is a recurrent inflammatory treatment of hidradenitis suppurativa to secure skin
disease of the apocrine glands.232 It initially develops grafts firmly to the wound bed after radical excision,
from follicular occlusion with subsequent abscess, although the utility of this remains to be seen.241
inflammation, fistulous sinus tracks, and scarring.233,234
The sites most commonly affected are the intertrigi-
nal regions such as the axilla, groin, and genitoanal Immune Deficiency
region, although it can also affect the breasts, hips, and Immune deficiency can result from infectious
thighs (Fig. 33-41).235 Women are affected three times processes, such as human immunodeficiency virus
as often as men are. Given the potential size and area (HIV) infection, which causes AIDS, or be secondary
of involvement, these wounds may present as a problem to immunosuppressive medications as seen in trans-
wound. plant recipients. Frequently, people with HIV infec-
Initial treatment involves local wound care and tion develop chronic wounds, which become problem
antibiotic therapy. This may be followed by excision wounds in the setting of their intrinsic wound healing
of the area of high-density apocrine glands with deficiencies. These wounds may develop on their own
minimal undermining and direct closure at the site of or as a result of a surgical procedure. The risk of sur-
the hidradenitis wound. At the site of inadequate resec- gical wound complications increases with progression
tion of an area of infected glands, or if there is a recur- of the disease. Many studies have shown a greater inci-
rence, radical resection yields the best long-term dence of poor wound healing after laparotomy, anorec-

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image...

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 941

FIGURE 3 3 - 4 1 . Hidradenitis suppurativa (intrinsic factor:

infection; mechanical factor: cavity wound). A The axilla, with
high density of apocrine glands, is a common site of hidradeni-
tis. B, Hidradenitis involving groin; follicular excision predis-
poses to infection in glands.

tal surgery, and orthopedic surgery.242"244 The cause of

delayed wound healing is thought to be a low CD4*
T-cell count, presence of an opportunistic infection,
low serum albumin, and poor nutrition.245 In com-
paring biomechanical parameters in wounds of 11
patients with HIV infection to those of 11 control age-
matched wounds, Davis and Wastell242 showed that
the wounds of the patients with HIV infection had a
lower resilience, toughness, and maximum extension
compared with the control group by use of a ten-
siometer to determine how the wounds responded to
load and deformation. Resilience is the property of
the tissue that endures loads without inducing a tension
exceeding the elastic limit. Toughness is the property
of tissue enabling it to endure loads. The maximum
extension is the displacement of the tissue at the point
of wound rupture. The overall weakness of wounds
in the patient with HIV infection may be due to an
impairment of the underlying healing process that
results in poor collagen deposition and cross-linking •TO
(Fig. 33-42).
Immunosuppressive medications are a mainstay FIGURE 3 3 - 4 2 . Erosive herpes simplex secondary to
HIV infection (intrinsic factor: impaired cellular function)
of treatment in transplant recipients. Common med- (From Habif TP: Clinical Dermatology: A Color Cuide to
ications that affect wound healing include steroids, Diagnosis and Therapy, 4th ed. Philadelphia, Mosby,
azathioprine, cyclophosphamide, and antithymo- 2004.)
cyte globulin. Steroids inhibit wound healing by

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942 I • GENERAL PRINCIPLES
anti-inflammatory and immunosuppressive effects.
The anti-inflammatory effects of steroids occur
through inhibition of arachidonic acid metabolism and
by impairment of macrophage and neutrophil func-
tion. Steroids have also been shown to inhibit pro-
duction of procollagen by fibroblasts, delaying wound
contraction.2*6'247 Azathioprine, cyclophosphamide,
and antithymocyte globulin affect wound healing by
decreasing the number of inflammatory cells through
suppression of the bone marrow.
Neurologic Disorders
Neurologic disorders such as spinal cord injury,
peripheral nerve injury, and cerebral vascular accidents
predispose rhese patients to problem wounds. Patients
suffering a severe cerebral vascular accident or spinal
cord injury are initially bedridden because of the acute
neurologic insult. Over time, owing to loss of normal
neurologic function, particularly loss of sensation in
the area of bone protuberances of the pelvis and lower
extremities, these cutaneous areas are subject to pro-
longed periods of pressure with resultant skin and soft
tissue necrosis. Other factors that contribute to devel-
opment of these wounds are poor nutritional status,
immobility, depressed respiratory status, and incon-
tinence.2'18 The incidence of pressure sores in the spinal
cord-injured patient is 5% to 8% yearly; as many as
80% of spinal cord-injured patients have a history of
one or more pressure sores.249,250 Pressure sores are the
leading source of infection in this group of patients.
The neurologic insult and subsequent treatment and
recovery often take precedence while the development
of pressure ulcers goes unrecognized or they are inad-
equately treated. It is well known that pressure sores
pose a serious threat to spinal cord-injured patients,
especially in the immediate postinjury phase.251'253 The
outcome of patients with neurologic recovery is favor-
able because these patients have relief of the pressure
on the affected area, whereas those patients with irre-
versible injury continue to have pressure points and
are at risk for skin breakdown. Whether they are treated
with surgery or by conservative, nonsurgical measures,
pressure sores recur in 5% to 9 1 % of spinal cord-
injured patients (Fig. 33-43).254
Metabolic Diseases
Certain metabolic diseases predispose to problem
wounds. The most common metabolic diseases asso-
ciated with problem wounds are diabetes, obesity,
and gout.
DIABETES MELLITUS
The pathophysiologic process of diabetes mellitus and
poor wound healing is incompletely understood. Poor
wound healing in diabetics appears to be multifacto-
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FIGURE 3 3 - 4 3 . Sacral pressure sore (intrinsic factor:
infection; extrinsic factor: pressure). Quadriplegic patient
with sacral pressure sore. See Figure 33-82.
rial, associated with growth factor deficiencies,
impaired cellular function, microvascular disease,
and dysregulated glucose control. Diabetic microan-
giopathy is characterized by abnormal growth and
impaired regeneration of the microvasculature; it is
attributed to a number of aberrantly expressed growth
factors, possibly acting in combination to impair
wound healing. 255 Recent evidence suggests that
patients with diabetes mellitus have abnormal ker-
atinocyte growth factor and platelet-derived growth
factor (PDGF) function in their wounds.256-257 PDGF,
a powerful mitogen for many cell types, is believed to
play a major role in wound healing when it is released
from platelets at the site of injury. In diabetic patients,
it has been hypothesized that platelets release PDGF
prematurely, thereby impairing the ability of platelets
to initiate healing. Impaired cellular function is also
a component of defective diabetic wound healing. Th is
includes defective phagocytosis and migration of
inflammatory cells during hyperglycemia.258 Inability
of cells to use glucose disrupts normal aerobic metab-
olism, causing the fibroblasts and leukocytes of the
wound to become dysfunctional. These patients also
suffer from microvascular disease, resulting in periph-
eral ischemia and decreased subcutaneous oxygen
tension, leading to impaired wound repair. It has been
shown experimentally that correction of hyperglycemia
correlates with improved wound repair.25
The pathophysiologic mechanism of problem
wounds in patients with insulin-dependent diabetes
mellitus differs from that in patients with adult-onset
or non-insulin-dependent diabetes mellitus. Insulin-
dependent diabetes mellitus represents 20% of all dia-
betes mellitus; non-insulin-dependent diabetes
represents 80%. The pathophysiologic mechanism of
problem wounds in patients with insulin-dependent
diabetes (pancreatic beta cell dysfunction leading to
absolute insulin deficiency) relates primarily to
microvascular disease. The early changes in microvas-
cular function are present in young patients, long before
image...
33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE
the initial clinical presentation.260 The incidence of
wound complications in patients with adult-onset dia-
betes (insulin resistance) reflects not onlv inherent
vascular disease but also factors such as age, obesity,
and malnutrition. Most patients with non-insulin-
dependent diabetes are obese and inactive, and they
have higher incidences of atherosclerotic disease.201
The common clinical triad seen in these wounds is
neuropathy, ischemia, and infection. Neuropathic
ulcers are a serious complication of diabetes.362 At least
15% of people with diabetes will eventually develop a
lower extremity ulcer (Fig. 33-44).263 Distal poly-
neuropathy, encompassing motor, sensory, and auto-
nomic involvement, is one of the most important
factors in the development of diabetic foot ulcers.264
Boulton265 has classified diabetic foot ulcers according
to severity.
OBESITY
It is estimated that one third of the adult population
in the United States is overweight. Overweight is
w. i
FIGURE 3 3 - 4 4 . Diabetic foot ulcers (intrinsic factor:
impaired cellular function; extrinsic factor: pressure).
Ulcers on plantar surface of foot extend into metatarsal
phalangeal joints on first and fourth toes. See Figure
33-68.
Bin kilometrelik bir yolculuk ilk adimla baslar.
Dr.Mustafa D.
943
defined as a body mass index (weight [kg]/height (m2])
of 25 to 30 kg/m2. Obesity is defined as a body mass
index greater than 30 kg/nrV06 Obesity predisposes
patients to the development of problem wounds. The
cause of this deficient wound repair seems to be dis-
tinct from that in diabetic patients in that wound
healing is independent of blood glucose levels.267 Poor
wound perfusion and necrotic adipose tissue con-
tribute to poor wound repair. As the adipose layer thick-
ens, the blood flow to the skin becomes more tenuous
and less reliable. For example, Chang et al268 have shown
that obese and overweight patients undergoing breast
reconstruction with free TRAM flaps have significantly
higher total flap loss, flap hematoma, flap seroma, mas-
tectomy skin flap necrosis, donor site infection, donor
site seroma, and hernia compared with normal-weight
patients.
GOUT
Gout is caused by an inflammatory response to the
formation of monosodium urate crystals in joints,
which develop secondary to hyperuricemia. Hyper-
uricemia is due to the increased production or
insufficient elimination of uric acid by the body or the
increased intake of foods that are high in purines (such
as meats, seafood, dried peas, and beans).269 Exami-
nation of the synovial fluid under compensated, polar-
ized light microscopy is how one makes the diagnosis
of gout. Pathognomonic features are needle-like intra-
cellular and extracellular monosodium urate crystals,
which are engulfed by neutrophils.270 Medical man-
agement is the mainstay of treatment for an acute gouty
attack. The cutaneous manifestations of gout are tophi,
which are painful masses that represent precipitations
of urate crystals.271 Problem wounds develop when
these tophi produce destructive lesions, eroding into
cartilage, tendon, and bone, causing significant defor-
mity. The acute gouty attack must be managed med-
ically before reconstruction of the cutaneous lesion.
Organ System Failure
The failure of organ systems predisposes to problem
wound development. The organ systems to consider
are the cardiovascular, pulmonary, renal, and hepatic
systems. Cardiovascular insufficiency results in low
cardiac output, congestive heart failure, and periph-
eral edema. Patients with cardiovascular insufficiency
develop problem wounds from the intrinsic problem
of poor tissue perfusion. Problem wounds develop
as a result of pulmonary insufficiency because of
decreased oxygen delivery to the soft tissues. Renal
insufficiency causes uremia and results in impaired
host defenses and deficient wound healing. These
patients have an increased risk for problem wounds
because of intrinsic abnormalities. End-stage renal
l'eWttf'fcdtJW image...
944 I • GENERAL PRINCIPLES
disease is associated with a nutritional imbalance and
an increased risk for infection. It has been shown that
patients undergoing hemodialysis have less collagen
deposited in subcutaneous test wounds,272 and they
are known to experience greater wound morbidity.'75
Low subcutaneous oxygen tension is thought to be
responsible for wound healing problems in these
patients. Subcutaneous tissue oxygen tension was
studied in patients undergoing hemodialysis, and it
was found that the oxygen tension decreased from 52
mm Hg to 28 mm Hg. Hepatic insufficiency results
in intrinsic and extrinsic wound complications, poor
nutrition, and increased susceptibility to infection.275
Factitial Wounds
Factitial wounds may present as problem wounds as
the normal course of wound repair is intentionally
disrupted by the patient who gains gratification from
playing the sick role. When done for secondary gain,
it is referred to as malingering. Munchausen syndrome
is an example of a factitial disorder.276 Patients with
this syndrome typically travel from hospital to hos-
pital, feigning acute illness, and are willing to undergo
invasive diagnostic and therapeutic procedures.
Wounds that do not respond to standard treatment
and do not appear to have intrinsic, mechanical, or
extrinsic factors to explain their persistence as a
problem wound may represent factitial wounds. Cuta-
neous manifestations of Munchausen syndrome are
described under three subtypes: dermatitis artifact, der-
matologic pathomimicry, and neurotic excoriations.277
These wounds tend to have characteristic angular
borders and are found on areas of the body that are
easily accessible to the patient. Culture specimens from
these wounds commonly grow abnormal bacteria not
usually found at that site, such as coliform bacteria,
which originate from feces rubbed intentionally into
the wound to delay or to halt the normal wound healing
process. Factitial disorders are serious psychiatric ill-
nesses and as such should be treated appropriately.
The treatment consists of psychotherapy and behav-
ior modification, although relapse is common.
Acne Keloidalis Nuchae
Acne keloidalis nuchae is a chronic, scarring folliculitis
that affects mostly black patients.278,279 The most
common areas affected are the posterior aspect of the
neck and the occipital region of the scalp.280 The cause
of acne keloidalis nuchae is unknown. Some investi-
gators have proposed that irritation and subsequent
inflammation result from the recurving of hairs into
the skin.281 Others have suggested that shaving the neck
and constant rubbing of the neck and posterior region
of the scalp by collars may also exacerbate acne
keloidalis nuchae (Fig. 33-45).282,283The clinical course
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Dr.Mustafa D.
FIGURE 3 3 - 4 5 . Acne keloidalis (intrinsic factor:
impaired cellular function; extrinsic factor: pressure).
Chronic scarring folliculitis of posterior neck and occipi-
tal region of scalp. {From Habif TP: Clinical Dermatology:
A Color Guide to Diagnosis and Therapy, 4th ed. Philadel-
phia, Mosby, 2004.)
is progressive and leads to hypertrophic scarring,
chronic abscesses, draining sinuses, and hair loss.278
These late lesions are refractory to treatment and lead
to problem wounds. Surgical excision is the mainstay
of treatment for extensive lesions. Excision must
extend to the base of the hair follicles. Closure options
include primary closure, split-thickness skin grafting,
tissue expansion with local flap transposition, and
closure by secondary intention.280,284
Congenital Abnormalities
A congenital anomaly may be a problem wound at
presentation or become a problem wound over time.
These congenital abnormalities include aplasia cutis
congenita, branchial cleft cysts and sinuses, spina bifida,
cutaneous vascular anomalies, omphalocele, and
gastroschisis.
APLASIA CUTIS CONGENITA
Aplasia cutis congenita is a rare condition charac-
terized by the congenital absence of the epidermis,
dermis, and, in some patients, subcutaneous tissues.285
In approximately 20% of patients, underlying bone is
also absent. The incidence of this condition is 3 in
10,000 births. Although the scalp is the most common
location, the lesion may involve any body surface. The
management of this problem wound is difficult because
it is life-threatening given the high rate of complica-
tions. Death occurs in 20% of patients secondary to
hemorrhage or thrombosis of the superior sagittal
sinus, meningitis, and sepsis.286,287 Given this, conser-
vative management is risky. Definitive early wound
coverage is essential. The goal of management is to
provide stable soft tissue coverage of the defect to
prevent infection.
image...
33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE
BRANCHIAL CLEFT CYSTS AND
SINUS TRACKS
Branchial cleft cysts and sinus (racks are a result of
aberrant embryonic development. This congenital
anomaly must be included in the differential diagno-
sis of any child presenting with a neck lesion. Lesions
of the second branchial pouch commonly present as
a neck lump or discharging sinus that may develop a
secondary infection.288 Surgical excision is the treat-
ment of choice for branchial anomalies.
SPINA BIFIDA
Spina bifida, a congenital deformity occurs in the
lower back, and certain variants of this disorder may
present as a problem wound. Spina bifida denotes
incomplete fusion of the vertebrae dorsally. The
overall incidence of spina bifida is 1 in 800 live births.
Meningomyelocele is the most common variant. It has
a neural element consisting of spinal nerve, cauda
equina, or spinal cord, within a meninges-lined cystic
structure. The overlying skin is often tenuous and sus-
ceptible to breakdown, which exposes the underlying
structures. When the overlying skin breaks down,
emergent coverage is needed to prevent contamina-
tion of the nervous system. The plastic surgeon should
work closely with the neurosurgeon to develop a treat-
ment plan. Care must be taken to safeguard all neural
elements before closing or imbricating the meninges.289
Multiple techniques for closure have been described.
Small defects can generally be closed with local trans-
position or interposition flaps. Large defects (>5 cm
in diameter) are more difficult to manage, and simple
closure techniques, such as skin advancement flaps,
often break down.291 For these defects, latissimus
dorsi musculocutaneous flaps, paralumbar fasciocu-
taneous flaps, and gluteus maximus musculocuta-
neous flaps have been advocated.291"2 The ultimate
closure is tension free and durable and provides ade-
quate soft tissue coverage over the dural repair. These
patients must be closely monitored for tethered cord
syndrome because it can result in irreversible neuro-
logic deficits.
VASCULAR ANOMALIES
Vascular anomalies known to cause problem wounds
include hemangiomas, lymphatic malformations, and
arteriovenous malformations.
Hemangiomas represent the most common benign
tumor of infancy, with ulceration being the most fre-
quent complication.294 Ulceration carries the additional
risk of infection, hemorrhage, and scarring.
Lymphatic malformations are rare benign con-
genital tumors of the lymphatic system. These mal-
formations are composed of endothelium-lined
lymphatic cysts that vary in size from a few millime-
ters to more than several centimeters in diameter.295
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Dr.Mustafa D.
945
Lymphatic malformations occur most frequently in
the head and neck region.296
Arteriovenous malformations represent a difficult
reconstructive challenge. Vascular malformations
enlarge at an unpredictable rate and predispose the
patient to life-threatening hemorrhage, l-esions of the
head and neck are grossly visible and have the poten-
tial for significant disfigurement. Surgical excision, of
an arteriovenous malformation is difficult owing
to an increased risk of pressure hemorrhage, which
requires multiple teams for management. Given the
local invasive nature of an arteriovenous malforma-
tion and its ability to destroy and ulcerate bone, resec-
tion may result in a large defect (Fig. 33-46).
Pyogenic Granuloma
Pyogenic granuloma is an acquired vascular lesion that
closely resembles hemangiomas both clinically and on
microscopic examination.297 The natural history is one
of superficial ulceration and repeated episodes of
bleeding, giving it the name "band-aid disease."298
OMPHALOCELE
Omphalocele is a defect of the central abdominal wall
covered only by amniotic and peritoneal membranes
through which visceral organs herniate. Despite
advances in prenatal diagnosis and neonatal intensive
care, mortality in most series ranges between 13% and
40%.299300 Small to medium defects can be closed by
primary fascial and skin closure. Large abdominal wall
defects (>4 cm in diameter) with visceral herniation
represent problem wounds. Inability to reduce herni-
ation is secondary to a small abdominal cavity (Fig.
33-47). Early primary fascial closLire under tension
results in complications secondary to high intra-
abdominal pressure. Options for closure include local
transpositional skin flap coverage followed by delayed
secondary hernia repair, placement of a Silastic
chimney (silo) with staged reconstruction, and topical
therapy with epithelialization followed by secondary
ventral hernia repair. Fascial closure is difficult in
defects larger than 6 cm. In this situation, a Teflon or
silicone mesh may be sutured to the margins of the
fascial defect, effectively increasing the abdominal
domain. This reduces postoperative respiratory prob-
lems and allows subsequent growth and enlargement
of the abdominal wall.301 The mesh can then be
removed at the time of definitive reconstruction. Dunn
and Fonkalsrud302 reported excellent long-term func-
tional results with staged repair and silo reduction for
large omphalocele defects.
CASTROSCHISIS
Gastroschisis is a defect of the anterior abdominal wall
just lateral to the umbilicus. There is no peritoneal sac
as there is with omphalocele, so evisceration of bowel
image..

946 I • GENERAL PRINCIPLES

FIGURE33-46. Arteriovenous
malformation (intrinsic factor:
impaired cellular function). The
malformation involves the left
midface and temporal scalp.>4 and
C, Location of arteriovenous mal-
formation. Surgical attempts to
ligate vascular connections were
unsuccessful. B, Cerebral angiog-
raphy is used to visualize the direct
connection between the arterial
and venous systems that supplies
the low-resistance shunt for arte-
rial blood and exposes the venous
system to abnormally high pres-
sures, resulting in a system of
enlarged feeding vessels, the
tangled nidus of the arteriovenous
malformation itself, and enlarged
draining venous structures. This
patient's arteriovenous malfor-
mation was resected under car-
diopulmonary bypass with deep
hypothermic circulatory arrest.
The facial nerve was preserved.
D, Design of left vertical trapez-
ius musculocutaneous flap with
vascular pedicle outside the zone
of embolization treatment on the
descending branch of the trans-
verse cervical artery. E, Post-
operative lateral view at 1 year
demonstrates no evidence of
arteriovenous malformation re-
currence./; Anterior view demon-
strates preserved facial nerve
function.

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Dr.Mustafa D.
image...

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 947

FIGURE 3 3 - 4 7 . Omphalocele (intrinsic

factor: congenital abdominal wall defect). A and
B, A 3-hour-old infant with a 16-cm omphalo-
cele whose sac is thin and translucent. C, The
fascial defect measured 5 cm. The abdomen
was explored, and the cutaneous layer of the
abdominal wall was undermined extensively. The
large and small intestines were decompressed
to facilitate replacement. D, A postoperative
photograph at 3 weeks. Eand F, Follow-up pho-
tographs at 3V2 years. (From Shaw WW, Aston
SJ, Zide BM: Reconstruction of the trunk. In
McCarthy JC, ed: Plastic Surgery. Philadelphia.
WB Saunders, 1990:3675.)

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Dr.Mustafa D.
948 I • GENERAL PRINCIPLES

FIGURE 3 3 - 4 8 . Castroschisis (intrinsic factor: congenital abdominal wall defect). A, A 4-hour-old infant with a
4-cm gastroschisis defect. The stomach and almost all of the intestinal tract protruded through the defect with
the umbilical cord at its left edge. The intestines were shortened, malrotated, dilated, edematous, and purple.
B, The abdominal cavity was too small to accommodate the gastrointestinal tract. A polyester mesh sack (Mersi-
lene) lined with silicone rubber (Silastic) sheeting was sutured to the freshened edges of the defect. C, Beginning
on the second postoperative day, a suture was tied approximately 1 cm proximal to the suture at the apex of the
sack. This was continued every other day until the sack height was obliterated. Side-to-side plication sutures pro-
gressively narrowed the horizontal dimension of the defect. D, At 2 weeks of age, the abdominal defect was closed
in layers, and a gastrostomy tube was placed. (From Shaw WW, Aston SJ, Zide BM: Reconstruction of the trunk.
In McCarthy JG, ed: Plastic Surgery. Philadelphia, WB Saunders, 1990:3675.)

occurs through the defect during intrauterine life (Fig.
33-48). The bowel is edematous and matted, and it
has a fibrin coating due to amniotic peritonitis. Unlike
with omphalocele, urgent repair is necessary. Primary
closure of the abdominal defect is usually possible
except when there is significant bowel and mesentery
edema or the abdominal cavity is too small for the
viscera to be reduced. In these patients, prosthetic patch
repair and staged silo repair may be necessary.
MANAGEMENT OF THE PROBLEM
WOUND
Clinical Assessment
Clinical assessment of the problem wound includes
the following: wound etiology (intrinsic, mechanical,
extrinsic, or combination); associated disease states;
location, size, and depth of the wound; exposure of
vital structures; wound duration (acute versus
chronic); and underlying soft tissue and organ system
stability (stable versus unstable) (Fig. 33-49). With
information based on this clinical wound assessment,
it is possible to plan a management algorithm. Treat-
ment options include correction of the underlying
disease state, if possible, while a therapy is chosen that
may bridge the gap until definitive treatment can be
achieved. Management options may be local or sys-
temic. Local management includes dressings, topical
antibiotics, debridement (mechanical or enzymatic),
hyperbaric oxygen treatment, vacuum-assisted closure
device treatment, and soft tissue coverage. Systemic
management includes antibiotics, medications to
correct underlying disease processes (insulin, calcium
channel or P blockers, diuretics), nutritional supple-
mentation (total parenteral nutrition or enteral tube

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image...
33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE
Unstable wound
Wound problem
]
Organ system problem
Debridement Correct cardiovascular/pulmonary/
Wound care gastrointestinal problem (CHF,
Antibiotics revascularization, oxygen delivery)
T
Stable wound
i
Treatment
1
I
Surgical closure Conservative:
wound contraction
FIGURE 3 3 - 4 9 . Algorithm: converting an unstable
wound to a stable wound.
feedings), and treatment of organ system failure
(revascularization of an ischemic extremity or
hemodialysis for the patient in renal failure).
Timing
Timing is critical in management of a problem wound.
A decision has to be made about whether immediate
correction is needed, as is true for limb- or life-threat-
ening wounds, or elective treatment is possible. Elec-
tive treatment provides time for local wound therapy
and for further diagnostic studies to determine the
extent of the wound and the underlying organ system
involvement. An acute wound is defined as a wound
that is less than 8 hours old; a chronic wound is more
than 8 hours old.
The next determinations include wound stability
(stable or unstable), extent of the wound, and organ
system involvement. Wound stability can be deter-
mined by defining the limits of the wound and the
status of the underlying organ systems. An acute stable
woundis one that is not immediately limb or life threat-
ening. These wounds are either traumatic or opera-
tive resection defects and can be closed if there are no
intrinsic or mechanical factors precluding closure.
Traumatic acute stable wounds, if appropriately
managed, do not progress, and the underlying organ
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Dr.Mustafa D.
949
systems either are intact or are ready for definitive man-
agement at the time of wound closure. If intrinsic or
mechanical wound etiologic factors exist, these must
be corrected before or at the same lime as definitive
wound management. An acute unstable wound is one
that is potentially limb or life threatening. Definitive
management of these wounds is often delayed. Delayed
closure is required because of progression in wound
size and depth due to intrinsic and extrinsic factors
(e.g., trauma, infection). The wound may be associ-
ated with organ system dysfunction, leading to hemo-
dynamic instability of the patient. Therefore, in the
acute unstable wound, initial treatment must address
correction of failing organ systems, repair of injured
structures, debridement of nonvital structures, control
of systemic and wound sepsis, and precise definition
of wound size and depth. During this process of initial
treatment, the acute unstable wound is converted to
a chronic stable wound that can then be safely closed.
If injured organ systems cannot undergo definitive
repair because of the patient's instability, persistent
hemorrhage, or indecision regarding completeness of
organ and soft tissue debridement requiring a second
look, definitive repair of the problem is ill-advised until
injured organs are fully repaired. An example of an
acute unstable wound with a mechanical deficiency is
a groin wound with an exposed, infected vascular pros-
thetic graft. Wound closure is not feasible until the
infected graft is resected with repair by an autogenous
graft or restoration of vascular continuity by an extra-
anatomic bypass graft. If the exposed graft is not yet
infected, this unstable, limb-threatening wound may
also be managed acutely with soft tissue debridement
and immediate coverage of the prosthesis with a local
transpositional muscle flap.
A chronic stable wound has been present for a
minimum of 8 hours and is not rapidly progressing
in size and depth. Single or multiple intrinsic, mechan-
ical, or extrinsic factors relate to the difficulty of wound
closure. Organ dysfunction may exist, but the patient
is stable with regard to vital organ system function.
Although the wound is probably infected, the patient
does not demonstrate systemic sepsis. A chronic stable
wound always has the potential to convert to a chronic
unstable wound if sepsis develops or the wound
extends into vital structures, resulting in life-threat-
ening hemorrhage or organ system dysfunction. The
initial goals in management are simultaneously to
correct factors related to the cause of the wound, to
remove nonviable tissue, and to control chronic
infection while preparing plans for definitive wound
closure. On occasion, a chronic problem wound will
close while initial treatment is in progress.
After the wound is converted to a chronic stable
wound, local wound care can be used to bridge the
gap until definitive closure can be achieved. During
this interval, management is directed to prevention
HsWftf'fcStfW image...
950 I • GENERAL PRINCIPLES
of the conversion of a stable wound to an unstable
wound and correction of underlying organ system dys-
function, if it is present. It is after the wound is stable
that one can plan operative closure or continue local
wound care if rhe wound is effectively closing by con-
traction. Although conservative treatment options can,
in certain instances, serve as the definitive treatment
of a problem wound, conservative treatment is gen-
erally used as a means to maintain wound stability
and to define the extent of the wound so that definitive
surgical closure is possible. Conservative treatment to
maintain wound stability may be local or systemic.
Local treatments include dressing changes, wound
debridement, topical antimicrobial agents, wound irri-
gation systems, vacuum-assisted closure devices, and
growth factor application. Systemic treatments include
hyperbaric oxygen treatment and systemic antibiotic
therapy. Other systemic therapy is directed at cor-
rection of specific underlying organ dysfunction.
These therapies are frequently required to assist the
conversion of the unstable wound to a stable wound.
The treatment of underlying organ dysfunction
generally requires consultation with specialists in
internal medicine or specific medical subspecialties.
Diagnostic and therapeutic recommendations are
beyond the scope of this textbook, but they may
include addition of inotropic drugs to improve cardiac
output, nutritional supplementation by hyperali-
mentation or enteral tube feeding, or addition of a
diuretic to improve congestive heart failure and to
decrease peripheral edema.
Nonoperative Management
TOPICAL ANTIMICROBIAL AGENTS
Since the introduction of topical antimicrobial agents,
the mortality associated with burn wounds has sub-
stantially decreased. Historically, the most commonly
used agents have been mafenide acetate, silver sulfa-
diazine, and aqueous silver nitrate. Mafenide acetate
(Sulfamylon) penetrates wound eschars effectively and
has potent antibacterial activity against most species
of gram-positive and gram-negative bacteria, includ-
ing P. aeruginosa?03,30* The disadvantages of mafenide
acetate include severe pain with application, hyper-
sensitivity reactions, and metabolic acidosis caused by
inhibition of carbonic anhydrase.303 Silver sulfadiazine
(Silvadene) is commonly used for partial-thickness,
mixed partial-thickness, and full-thickness burn
wounds. Silver sulfadiazine is effective in controlling
local burn wound infection when it is combined with
burn wound cleaning and serial debridement. The dis-
advantages of silver sulfadiazine are that it does not
penetrate eschars well and can cause an idiosyncratic
neutropenia. Aqueous silver nitrate (0.5%) has largely
fallen out of favor because of its inability to penetrate
wounds effectively, large dressing requirements, and
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discoloration of the wound bed and surrounding
tissue. In addition, it can cause hyponatremia sec-
ondary to transeschar loss of sodium.305
IRRIGATING SYSTEMS
Irrigating systems are often used in acute unstable
wounds with a large bacterial load, both preoperatively
and postoperatively.306 They provide a way to non-
surgically debride and clean the wound with either
saline or antibiotic irrigation. Irrigation to remove
debris and lessen bacterial contamination is an essen-
tial component of open fracture care.307 Intraopera-
tive^, irrigation is applied with high pressure (2 to 10
pounds per square inch); postoperatively, it is used to
gently clean chronic wounds to control the antimi-
crobial load. The volume of the irrigation fluid is an
important factor; increased volume improves the
wound cleaning and decreases the bacterial load. High-
pressure flow has also been shown to remove more
bacteria and debris, thus lowering the rate of wound
infection compared with low-pressure irrigation.308
Pulsatile lavage is often used for debridement of
necrotic tissue and has been shown experimentally
to remove bacteria more efficiently than continuous-
pressure flow (Fig. 33-50).306
VACUUM-ASSISTED CLOSURE
Vacuum-assisted closure (VAC) exposes the wound
to subatmospheric pressure, typically 125 mm Hg
below ambient pressure. This subatmospheric pres-
sure enhances wound contraction by mechanically
pulling the wound together. In addition, it removes
excess fluid from the wound periphery.309 This nega-
tive pressure environment decreases local interstitial
pressure, thus restoring blood flow to those vessels
compressed or collapsed by the chronic edema, and
enhances the formation of granulation tissue (Figs.
33-51 and 33-52).310
The wound VAC system includes the placement of
sterile cell foam into the wound cavity. Two types of
foam are available, black polyurethane foam and white
polyvinyl alcohol soft foam. The black foam has larger
pores and is more effective in stimulating granulation
tissue and wound contraction; the white soft foam has
smaller pores, recommended for those wounds in
which the additional growth of granulation tissue is
not warranted or for patients who are not able to tol-
erate the black foam because of pain. A fenestrated
evacuation tube exits the foam connected to an
adjustable vacuum source, which generates the sub-
atmospheric pressure. The vacuum source is com-
puterized and can be programmed to deliver the
appropriate amount of pressure dependent on the
specific characteristics of the wound. This pressure may
be delivered continuously or intermittently. The foam
dressing and underlying wound are sealed with an
adhesive thin film, converting the open wound to a
image...

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 95

FIGURE 3 3 - 5 0 . A, Pulsatile jet irrigators are com-

monly used for the debridement of bone and tissue.
Treatment is accomplished with a hand-held device that
delivers a pulsed fluid at a measurable pressure to an
open wound, providing irrigation and debridement. The
instrument provides a range of intensities from gentle
pulsed lavage to more powerful irrigation with con-
current suction. Suction provides negative pressure
(-100 mm Hg, continuous). Pressure ranges from
4 to 15 psi. The irrigant should be normal saline 0.9%
(£2000 mL), warmed. B, Clinical photograph of pulsatile
lavage of open foot wound.

FIGURE 3 3 - 5 1 . Vacuum-assisted
closure (VAC), equipment and setup.
A, Foam with internal catheterthat will
be connected to VAC device. B, Cavity
wound of plantar surface of foot. C.
Lateral view of the wound demon-
strates irregular surface. Necrotic
tissue has been debrided.
Continued

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image...

952 I • GENERAL PRINCIPLES

e#
fc\\ •<
,

V— - - — ^ . '
•' *

' • » * . * /•
wt : J*.? -"• """.'•^ z..:. >

= Sl:

FIGURE 3 3 - 5 1 1 cont'd. D, Foam material is cut to fit the defect. Dressing mate-
rial covers the sponge and adjacent cutaneous margin of the defect to provide a seal.
E, Vacuum is applied to indwelling catheter. Negative pressure removes wound
exudates, helping to decrease interstitial pressures, which allows needed nutrient
exchanges to occur. It also enhances contraction of the healing wound and enhances
capillary ingrowth at the foam-wound interface. F, VAC is maintained in place on a
24-hour basis. Foam and dressing are changed daily.

controlled closed wound. The dressing is usually
changed at 48- to 72-hour intervals.
The wound VAC system is effective in treating a
wide variety of acute and chronic wounds.311 VAC
is currently used for pressure sore management,
traumatic wounds, burns, securing of skin grafts to
difficult recipient beds, wound dehiscence, large open
wounds, enterocutaneous fistulas, and chronic ulcers.
It has also been shown to be useful in deep chronic
wounds such as sternal wounds and complex abdom-
inal wall wounds (Table 33-15).
On histologic evaluation, VAC wounds show
increased angiogenesis and healthy tissue growth
compared with the inflammation and fibrosis seen with
wet-to-moist dressings. In a study of 24 patients with
nonhealing wounds, the VAC system increased the vas-
cularity and rate of granulation tissue formation com-
pared with standard dressings.312 Other studies have
shown that VAC treatment decreases wound tissue
bacterial levels.313 This decreased bacterial wound
load along with increased local tissue circulation and
oxygenation works to improve wound healing and can
be useful as a means to bridge the gap between an
unstable and a stable wound.
HYPERBARIC OXYGEN
Hyperbaric oxygen was first recommended by Valen-
zuela in 1887 for treatment of bacterial infections.314
Normal transcutaneous tissue oxygen levels are 40 mm
Hg. Tissue levels below 30 mm Hg significantly impair
normal metabolic activity and wound healing. Hyper-
baric oxygen therapy involves inhalation of 100%
oxygen at a pressure of more than 1 atmosphere, usually
2 to 2.5 atmospheres. The length of therapy is vari-
able, but it is generally done at 90-minute intervals

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33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 953

C D
FIGURE 3 3 - 5 2 . A, Clinical photograph of foot wound before VAC therapy. B and C, VAC therapy in place to
be connected to VAC therapy equipment. D, Wound is shown after VAC therapy.

once or twice a day. This therapy results in tissue oxygen
levels that are 10 times the usual levels (Fig. 33-53).315
This effect of hyperbaric oxygenation generates a favor-
able gradient for oxygen diffusion from functioning
capillaries to ischemic tissue sites.316 The biochemical
effects of hyperbaric oxygen are multiple. The effects
include leukocyte activation and increased oxygen free
radical production, enhanced fibroblast cell division,
increased collagen deposition, and capillary angio-
genesis.317 The indications for hyperbaric oxygen use
include refractor/ leg ulcers, venous stasis ulcers, dia-
betic ulcers (,if adequate vascular inflow is present),
radiation-induced soft tissue wounds, necrotizing
infections, compromised skin grafts and flaps, and
decubitus ulcers.318'324 Hyperbaric oxygen may be
used for the management of chronic stable problem
wounds or for the acute unstable wound in an effort
to convert it to a stable wound. Stable wounds include
the majority of lower extremity wounds (venous
stasis ulcers, diabetic ulcers), radiation-damaged
tissues, and compromised skin grafts and flaps. Acute
unstable wounds include deep soft tissue infections,
intravenous fluid extravasation, and burn wounds.
Several studies have attempted to determine whether
hyperbaric oxygen is of added benefit in management
of soft tissue infections. Life-threatening infections
such as clostridial myonecrosis and Fournier gangrene
have been evaluated for the effectiveness of hyperbaric
oxygen as part of the treatment regimen.322,325 These
studies have shown that along with aggressive debride-
ment and antibiotics, hyperbaric oxygen significantly
reduced mortality and need for repeated debridement.

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954 i • GENERAL PRINCIPLES

TABLE 33-1 5 • INDICATIONS FOR AND CONTRAINDICATIONS TO USE OF VACUUM-ASSISTED

CLOSURE

Indications Contraindications

Ulcers Necrotic tissue with eschar

Venous Osteomyelitis
Arterial Malignant neoplasm in wound
Neuropathic Fistulas to organs or body cavities
Wounds
Dehisced wounds
Superficial soft tissue wounds
Traumatic wounds

Although evidence suggests a beneficial effect of
hyperbaric oxygen in these series and animal studies,
no controlled, randomized, prospective clinical trials
have been done to date.
Limitations of hyperbaric oxygen therapy include
patients who have a problem wound but normal
transcutaneous tissue oxygen levels (-40 mm Hg),for
pressure sores), the delivery of oxygen and associated
benefits may be limited in these circumstances. In these
patients, surgical intervention to bring more blood flow
to the area is warranted. An untoward effect of hyper-
baric oxygen use is barotrauma, which may result in
tympanic membrane rupture, pneumothorax, or air
embolism.

FIGURE 3 3 - 5 3 . A, Monoplace hyperbaric chamber. B, Multiplace hyperbaric chamber (inside). (From Zamboni WA,
Browder LK, Martinez J: Hyperbaric oxygen and wound healing. Clin Plast Surg 2003:30:67.)

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image.,.
33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE
rily used for chronic stable wounds, although they are
also used for acute stable and unstable wounds. The
types of problem wounds associated with infection
may involve skin and soft tissue, cartilage, or bone.
These infections may be contained in a body cavity,
such as the cranium, the thorax, the mediastinum, or
the pelvis. Specific microbial flora is associated with
each of these areas of problem wounds, and so the
choice of antibiotic therapy should cover the common
pathogens. Initially, broad-spectrum antibiotics are
chosen until results of wound culture are available to
guide therapy. Antibiotics are primarily used to halt
the spread of bacterial infection and are unlikely to
convert an infected wound into a sterile wound. If a
chronic stable wound converts to an infected unsta-
ble wound, antibiotics are often used to help control
infection and improve the stability of the wound.
Chronic wounds may have unexpected flora and tend
to be polymicrobial. When wound stability is achieved,
systemic antibiotics are usually discontinued and local
wound care becomes the mainstay of treatment (see
Table 33-4).
Prolonged use of systemic antibiotics predisposes
to antimicrobial resistance and superinfection. For
example, antibiotic use is associated with Clostridium
difficile colitis, a devastating and debilitating con-
dition caused by a spore-forming gram-positive
anaerobic bacillus. It is responsible for 15% to 20% of
antibiotic-associated diarrhea. More than 90% of C.
difficile infections occur after or during antibiotic treat-
ment. Antibiotics act by disrupting the normal colonic
flora, allowing C. difficile to proliferate.326 In patients
who develop symptoms, the spectrum of C. difficile
disease ranges from mild diarrhea to fulminant
pseudomembranous colitis.327 A stool specimen with
the presence of leukocytes and C. difficile toxins
confirms the diagnosis. The typical treatment of C.
difficile colitis involves discontinuation of the causative
antibiotic and institution of oral metronidazole or,
alternatively, intravenous vancomycin.
Problem wounds associated with infection of
underlying bone require different considerations in
regard to antibiotic therapy. These are generally
chronic wounds that develop as a result of an open
injury to bone and surrounding soft tissue. The most
common pathogens isolated from these wounds are
S. epidermidis, S. aureus, P. aeruginosa, Serratia
marcescens, and Escherichia coli. Antibiotic therapy
along with debridement is often required in these
wounds. Although prolonged antibiotic therapy (4 to
6 weeks) has been advocated for the treatment of
chronic osteomyelitis, aggressive debridement with
muscle flap coverage reduces antibiotic duration to
7 to 10 days.82'328'330
Antibiotic-impregnated beads may be used as a
spacer before bone grafting. These beads allow the local
release of antibiotics into the wound without nega-
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Dr.Mustafa D.
955
tive systemic effects. Antibiotic beads have been
recommended for use in chronic osteomyelitis and in
acute musculoskeletal infections.331 The antibiotic is
incorporated into a bone cement polymer that con-
sists of polymerized polymethyl methacrylate, molded
or rolled into 3- to 10-mm spheres, which can be used
singly or strung onto surgical suture wire (Fig. 33-
54).3 2'333 These beads are then placed in the wound
after bone debridement, filling bone defects in addi-
tion to delivering a high concentration of antibiotic.
Antibiotic beads provide a system of specific local deliv-
ery of the antibiotic, potentially avoiding systemic side
effects.334 These beads may be used as the primary treat-
ment of a bone or deep soft tissue infection or as a
bridge to definitive reconstruction.
Operative Management
DEBRIDEMENT
The operative management of problem wounds begins
with adequate wound debridement. Debridement
involves the removal of devitalized, infected, or necrotic
tissue or fibrin from a wound. This may be achieved
pharmacologically (enzymatically) or surgically, in one
stage or sequentially.
Pharmacologic wound debridement uses prote-
olytic enzymes that serve to degrade necrotic debris.
The benefits of enzymatic treatment include that it is
noninvasive, causes little or no pain, and can be used
on an outpatient basis. Initially, the use of enzymes
for nonoperative wound debridement was appealing,
but increased clinical use has shown limitations. Enzy-
matic debridement is often slow and associated with
copious amounts of exudate, providing a medium for
bacteria. The results of enzymatic debridement are
highly variable. Bleeding problems associated with
aggressive enzyme treatment have proved difficult to
control. Subsequent studies have shown that enzymatic
preparations for wound debridement are highly vari-
able, dependent on the enzyme and the patient, and
work only in moist environments.335
Operative wound debridement is required for
obvious necrotic, infected, or nonviable tissue, espe-
cially when the extent of the abnormal tissue cannot
be established. The size and depth of a wound should
also be a consideration in choosing a debridement
method. Large deep wounds are better treated in the
operating room. The amount of debridement required
is variable, depending on the stability of the patient
(acute wound) and the intrinsic, mechanical, or
extrinsic factors present. An acute wound in a patient
with normal blood flow and good medical and nutri-
tional status will heal with appropriate care. Often,
debridement of problem wounds results in the con-
version of a chronic wound to an acute wound that
will not heal in the face of underlying intrinsic,
KeWttf'aStfW image...

956 I • GENERAL PRINCIPLES

FIGURE 3 3 - 5 4 . Infected nonunited tibial fracture with insertion of antibiotic-impregnated

beads (intrinsic factor: infection; extrinsic factor: trauma}. A and B, Insertion of antibiotic-
impregnated beads and microvascular latissimus dorsi muscle transplantation for wound cover-
age. C, Radiograph after second operation shows beads in bone defect. (From Nahai F: Soft
tissue reconstruction of the lower leg. Perspect Plast Surg 1987; 1:1.)

mechanical, and extrinsic factors. Correction of the
underlying deficiencies in association with wound
debridement is paramount. Multiple operative wound
debridements maybe necessary to achieve wound sta-
bility. To help differentiate viable from nonviable tissue
at the time of debridement, intravenous fluorescein
can be used. After infusion, one can inspect the area
of the wound with Wood's lamp to determine tissue
viability (Fig. 33-55 and Table 33-16). Debridement
and immediate closure are selected for wounds without
intrinsic, mechanical, or extrinsic deficiency. These
wounds must first be debrided to healthy bleeding
tissue to ensure that all nonviable tissue has been
excised. Sequential debridement is important when
there is an inability to accurately predict the amount
of nonviable tissue and extent of debridement required
at the initial operation. Segmental debridement allows
one to define the exact margins of the wound, poten-
tially preserving borderline tissue surrounding the
wound as well as allowing culture specimens to be

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33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 957

FIGURE 3 3 - 5 5 . Fluorescein test. A, Lower extremity avulsion injury with viability of flap in
question. B, Fifteen minutes after intravenous administration of 2 g of fluorescein Wood's lamp
delivers ultraviolet light to surface of questionable circulation. Absence of yellow-green fluores-
cence indicates absence of circulation and provides guidelines for resection of nonviable portion
of tissue.

collected and processed before wound closure. In
this situation, sequential wound debridement and
wound observation are important. During the course
of serial debridements, full-thickness biopsy culture
specimens and quantifications of the wound may be
obtained to assess the status of bacterial invasion.336
In burn wounds, it was determined that the burn
wound biopsy is a reliable procedure for quantitating
organisms and that changes in sequential samples give
an indication of the dynamics of infection.337 Debride-
ment with definitive management in a one-step pro-
cedure, if possible, limits the patient to one anesthesia,
reduces desiccation of the wound, shortens hospital
stay, reduces cost, and is useful if vital structures are
involved within the wound.
In patients with a history of radiation therapy, deter-
mination of the amount of tissue to be d£brided is a
difficult problem. In debridement of irradiated bone,
it is often difficult to define an endpoint. The level of
bone excision is often arbitrarily limited to the imme-
diate zone of injury. With radiation wounds, debride-
ment is generally followed with immediate flap
coverage because the zone of necrosis will continue
to expand the debridement margin if coverage is not
provided.
Operative wound debridement must be systematic
and thorough. Preoperative radiographs should be
considered if bone involvement is suspected. Abscess
cavities, if present, should be drained adequately.
Subjective criteria to determine skin viability include

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958 I • GENERAL PRINCIPLES
TABLE 33-16 • DEBRIDEMENT INSTRUMENTS
Tongue Knife and
Type of Debridement Blade Pickup
Chronic flat wound (gray
granulation tissue)
Preoperative split-thickness skin
grafting X
Necrotic soft tissue
Full-thickness burn (eschar)
Edge of bone (spicules)
Infected bone cavity with chronic
granulation tissue (marrow
cavity)
Infected bone cartilage with
adjacent vital structures _
Bone prominence contaminated,
infected outer cortex
color, temperature, and presence of bleeding on
stab wound. Objective criteria are obtained by visual
inspection with fluorescein dye, dermofluorometry,
surface temperature readings, photoplethysmography,
ultrasound Doppler and laser Doppler flowmetry,
and transcutaneous Po 2 monitoring.338 Fluorescein has
proved to be a consistent and reliable method to deter-
mine skin viability.339 Problem wounds associated
with an ischemic wound bed should not be overly
debrided until vascular inflow is corrected. The
surgical instruments appropriate for wound debride-
ment depend on the type of soft tissue involved.
Common instruments include a knife, scissors,
curets, rongeurs, osteotomes, and tongue blades
(Fig. 33-56).
The viability of the tissues during debridement is
an important factor to assess. Nonviable skin appears
dusky without capillary refill and does not bleed with
excision. Subcutaneous fat should appear yellow and
globular. Necrotic fat is dull in appearance with a gray-
brown to black color. Fascia is shiny white and sur-
rounds skeletal muscle. If the fascia appears healthy,
it is important not to violate this tissue plane; pene-
tration of this provides an avenue for bacteria to invade
the muscle. Skeletal muscle is dull red, contractile, and
vascular. Lack of contraction on stimulation, lack of
bleeding, or a dark red color warrants debridement.
Bone is hard and white if it is healthy. Cortical bone
is covered with periosteum, which is richly vascular-
ized. Bone with periosteum will form granulation tissue
and accept skin grafts, whereas bone without perios-
teum will not promote healing. Bone erosion repre-
sents an entrance point for infection and requires
debridement and coverage. Tendons are poorly vas-
cularized and have the potential to become infected
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Instruments
Humbly Osteotome
Knife Rongeur Curet Kerrison and Mallet
X
X
X
easily. Healthy tendons appear shiny white and are
covered by paratenon. The paratenon carries blood
flow to the tendon and should not be disrupted if it
is present. Tendons exposed within the wound
paratenon become necrotic and frequently require
debridement.
Acute unstable wounds generally require debride-
ment at the initial presentation along with manage-
ment of organ system injuries. Conversion to a stable
acute wound through debridement and management
of organ injuries allows wound closure. Similarly,
unstable chronic wounds require both the control of
infection through culture-specific antibiotic therapy
and serial debridement. When infection is controlled
and stabilization of a chronic wound is achieved, wound
closure maybe accomplished. In chronic wounds with
inadequate local circulation, debridement should be
associated with definitive procedures to provide local
wound perfusion.
Wounds associated with vascular insufficiency
should be revascularized, debrided, and closed as indi-
cated. In wounds with circulatory impairment (e.g.,
radiation injury), debridement should be performed
with immediate coverage with well-vascularized flaps.
In all instances, debridement must include all nonvi-
able tissues exposed to bacterial contamination before
wound closure.
RECONSTRUCTIVE PLANNING
The reconstructive ladder is a useful way to system-
atically plan problem wound reconstruction. Wound
coverage and stability are the first priority, followed
by functional reconstruction of the defect. An example
of this principle is a burn wound, which first demands
 33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE

B
FIGURE 3 3 - 5 6 . Debridement instruments. A, A tongue blade is used to remove
chronic granulation tissue containing excess fibrous ingrowth and paucity of
capillary ingrowth (gray granulation tissue}. Scraping with the edge of a tongue
blade restores the base to a capillary bed suitable for application of skin grafts.
The tongue blade will not disturb the deeper viable tissue plane. B, The Humbly
knife is useful to harvest skin grafts. In the fully open position, it will remove a
thin layer of tissue at the wound site. This technique removes nonviable layers
of tissue until capillary bleeding is observed. Continued

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960 I • GENERAL PRINCIPLES

FIGURE 3 3 - 5 6 , cont'd. C, A knife and pickup are useful to remove irregular

areas of necrotic and nonviable tissue. D, A rongeur is useful for removal of sharp
bone edges and spicules of nonviable bone.

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33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 961

FIGURE 3 3 - 5 6 , cont'd. E, A Kerrison instrument is useful to remove

nonviable bone adjacent to vital structures (e.g., cranial bone adjacent to
dura). F, A Kerrison instrument isalso useful for resection of necrotic sternal
edges adjacent to great vessels and mediastinal contents.
Continued

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962 I • GENERAL PRINCIPLES

FIGURE 3 3 - 5 6 , cont'd. G, A curet is useful to remove soft nonviable bone involved with osteomyelitis of long bones
and debridement of bone cavities (e.g., pelvis). H, A mallet and osteotome are useful in removing infected bone promi-
nences (e.g., bone prominences associated with pressure sores).

coverage, followed by reconstruction when both the RECONSTRUCTIVE LADDER

wound and the patient are stable.
Reconstructive treatment options begin simply and
become more complex as needed for a given defect
(Fig. 33-57). The first and most straightforward Complex / / 11 Distant flap
method is direct primary closure of the wound after
debridement. If the defect cannot be closed primarily,
the next option is wound debridement followed by Local flap
placement of a split-thickness skin graft. This can be
done for wounds with a large surface area, such as
burn wounds. Skin grafts are generally the first choice
for management of problem wounds. Skin grafts Skin grafts
are technically easy and provide for quick closure
(although skin grafts usually result in a noticeable
contour defect). Debridement with local tissue
rearrangement is the next option, followed by distant Simple / / II Direct closure
transposition flaps and microvascular composite tissue
transplantation. The majority of problem wounds
require distant flap coverage. The value of vascular- FIGURE 3 3 - 5 7 . Reconstructive ladder. The concept of
ized muscle as coverage for problem wounds has been the reconstructive ladder was proposed to establish pri-
well defined. A muscle flap consists of a muscle orities for reconstructive technique selection based on
the complexity of the technique and the defect require-
detached from its normal origin or insertion and trans- ments for safe wound closure. The reconstructive ladder
posed with an intact blood supply to another loca- provides a systematic approach to wound closure empha-
tion. Musculocutaneous flaps are a composite of sizing selection of simple to complex techniques based
muscle and overlying skin. The blood supply to the on local wound requirements and complexity. (From
skin occurs through musculocutaneous perforators. Matties SJ, Nahai F: Reconstructive Surgery: Principles,
Anatomy, and Technique. New York, Churchill Livingstone,
These flaps are considered the gold standard because 1997.) "

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image...
33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE
they are bulky, able to fill large defects and obliterate
dead space, malleable, and well vascularized. Chang
and Mathes340 compared the bacterial resistance of two
flap models in canines. With cranial-based paired flaps
consisting of either a random-pattern flap or a rectus
abdominis musculocutaneous flap, it was shown that
musculocutaneous flaps are more resistant to bacte-
rial infection. Injections of 8 x 106 bacteria into the
dermis in the three distal zones of cutaneous territory
of these paired flaps produced significantly increased
areas of necrosis in the random-pattern flap in com-
parison to the musculocutaneous flap. Furthermore,
the musculocutaneous flap recovered rapidly from the
bacterial inoculation with complete healing, whereas
the random-pattern flap showed signs of necrosis.
Thus, the well-vascularized muscle flap not only pro-
vides stable coverage but also serves as a delivery system
for leukocytes, oxygen, and antibiotics. Microvascu-
lar composite tissue transplantation is the most
complex method whereby a problem wound can be
closed. This technique is used when there is a large
defect to be reconstructed and local or regional flap
sources are inadequate or unreliable.
Another treatment option to consider in treating
problem wounds is local tissue expansion, which is a
modification of the reconstructive ladder. Skin and
soft tissue adjacent to the defect are preferred for defect
closure because of the similarity in skin color, texture,
and contour. The size, location, or zone of injury may
preclude the use of adjacent tissue for expansion.
Therefore, tissue expansion is somewhat limited, given
that many problem wounds have adjacent unstable
skin and often a concurrent infection. In this cir-
cumstance, the introduction of a foreign material
would add an additional risk. Tissue expansion does,
however, have a role at a secondary procedure. For
example, a wound may be treated with a skin graft
initially to close the wound. The surrounding skin is
then expanded at a secondary procedure for durable
skin coverage, with correction of the resulting contour
deformity.
Whenever it is indicated, closure of a problem
wound must not only preserve form but also restore
function. With appropriate flap selection, no functional
impairment should occur. In many instances, func-
tion-preserving techniques are used. Microvascular
composite tissue transplantation allows the use of
distant flap tissue and is preferable in regard to both
donor and recipient site results (Fig. 33-58).
Management of Specific
Problem Wounds
Most problem wounds are multifactorial in origin,
although there may be a specific inciting factor.
Common problem wounds are reviewed on the basis
of etiology and management recommendations.
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963
Flaps
Microsurgery Tissue expansion
FIGURE 3 3 - 5 8 . Reconstructive triangle. The recon-
structive triangle is a new paradigm more appropriate
than the reconstructive ladder for the sophisticated recon-
structive options now available. The individual surgeon's
judgment, experience, and familiarity with the various
techniques and flaps ultimately influence the selection of
reconstructive techniques. The reconstructive triangle is
a systematic approach to care of the patient through key
phases of management: defect analysis, assessment of
surgical options, identification of surgical goals, execu-
tion of the operative procedure, and result analysis or
outcome evaluation. (From Mathes SJ, Nahai F: Recon-
structive Surgery: Principles, Anatomy, and Technique.
New York, Churchill Livingstone, 1997.)
INTRINSIC
Specific problem wounds related to intrinsic defi-
ciencies include those associated with vascular
insufficiency, infection, cellular impairment, nutrition,
and malignant disease. The recognition of these
deficiencies is important in the management of
problem wounds.
Vascular Insufficiency
ARTERIAL. Arterial insufficiency may be acute or
chronic. Both acute and chronic arterial insufficiency
can lead to problem wound development.
The possibility of vascular disruption must be con-
sidered early in the management of a patient with
extremity trauma. A missed diagnosis or delay in diag-
nosis may have disastrous consequences leading to loss
of the limb. The circulation must be re-established
immediately either primarily or with an interposition
graft. If a graft is required, an autologous vein graft is
preferred over a synthetic graft, given the potential for
contamination. It is then essential to provide well-vas-
cularized coverage for the graft and vascular suture
lines with a local transposition muscle flap. Acute vas-
cular disruption may also be due to thrombosis of a
large vessel, producing critical ischemia that must be
corrected emergently.
Chronic arterial insufficiency is a more common
cause of problem wounds. Ulcers secondary to
arterial occlusion require correction of extremity
vascular inflow before reconstruction. In choosing
reconstruction, the patient's prognosis and lifestyle
964 I • GENERAL PRINCIPLES
must be taken into account. After correction of arte-
rial inflow, debridement and skin graft may be sufficient
to reconstruct a lower extremity problem wound. Alter-
natively, a more complex muscle or musculocutaneous
flap reconstruction may be used for the larger defect
with exposed bone. When microvascular composite
tissue transplantation is necessary to provide stable soft
tissue coverage, it can be performed during the initial
revascularization or as a second-stage procedure
(Fig. 33-59).
VENOUS. Venous insufficiency may lead to the
development of a problem wound. Surgical manage-
ment of the venous ulcer is first directed at correction
of underlying venous insufficiency. Treatment may
involve vein stripping, perforator ligation, valve trans-
position and transplantation, and valvuloplasty to
improve venous abnormalities.16 The most important
element of treatment is elevation and compression
(35 mm Hg pressure at the distal calf) of the extrem-
ity to improve the venous return and to lessen venous
hypertension.34,34' Compression therapy reduces or
eliminates edema; daily dressing changes d£bride the
wound in preparation for definitive management. The
types of compression vary. The Unna boot provides
both compression and debridement and is composed
of zinc oxide-impregnated gauze wrapped circum-
ferentially around the leg. Further management of
venous stasis ulcers includes excision and coverage with
split-thickness skin graft, skin substitutes, local trans-
position flaps, and microvascular composite tissue
transplantation.342,343 Split-thickness skin grafts and
skin substitutes have also been successfully used in con-
junction with vacuum suction to enhance fluid removal
and to secure the graft on the extremity.344 Wounds
are considered problem wounds when standard treat-
ment fails. These wounds tend to be the larger venous
stasis ulcers (> 12 cm2) and those associated with infec-
tion.345 Venous ulcers commonly harbor bacteria.
Common organisms include S. aureus and strepto-
cocci, although P. aeruginosa can be isolated. In fact,
venous stasis ulcers superinfected with P aeruginosa
can further increase the size of the ulcer and impede
healing.346,347 Infection should be aggressively treated
because these patients are susceptible to systemic
sepsis.348 In addition, comorbidities such as diabetes
and lower extremity arterial insufficiency can further
exacerbate an already problematic wound. Com-
pression therapy should be applied with caution in
patients with arterial insufficiency because it may
worsen tissue ischemia. Thus, all patients should have
the ankle/brachial index measured before compres-
sion therapy is initiated. The ankle/brachial index
should be above O.8.349 In addition to treatment of
the local wound, systemic factors such as oxygen
delivery, nutrition, and infection must be taken into
consideration.
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Venous hypertension must be corrected for long-
term success in reconstruction of venous ulcers. Small
wounds may be treated with debridement, Unna
boots, and skin grafts. Most small venous ulcers heal
with leg elevation and bed rest but recur when the
patient returns to ambulatory status. A Linton350 pro-
cedure with subfascial ligation of perforating veins,
wide resection of scar and subcutaneous tissue, and
skin graft coverage of tibial periosteum and leg muscles
will provide longer lasting results.
New techniques concentrating on deep venous
system reconstruction (valve transplants, vein replace-
ments) may offer correction of the underlying patho-
physiologic process, although this field of clinical
research is evolving. Microvascular composite tissue
transplantation offers an excellent solution for wound
coverage. However, the venous system of the flap must
be anastomosed to an incompetent venous system,
which predisposes the flap and surrounding tissue to
future venous hypertension and development of recur-
rent ulcerations.342,343*351
The type of coverage depends on the size and com-
ponents of the wound. Skin grafting would be inap-
propriate for those wounds involving tendon, bone,
or joints. Management is further complicated by the
lack of local muscle flaps available in the lower
extremity. This has prompted some surgeons to use
microvascular composite tissue transplantation to
manage the recalcitrant venous ulcer.
LYMPHATIC. Wounds that develop in lymphede-
matous extremities represent problem wounds.
Management first begins with establishment of the
underlying cause of the lymphedema and correction,
if this is possible. Upper extremity lymphedema is
often associated with a history of radiation therapy.352
Most patients are treated conservatively with local
wound care, physical therapy, pneumatic pumps,
and compression therapy.40 Topical or systemic antibi-
otics may be indicated in the treatment of these
wounds if there is clinical evidence of infection.
Patients with severe lymphedema refractory to con-
servative treatment causing recurrent episodes of
lymphangitis, intractable pain, lymphangiosarcoma,
and worsening limb function in addition to a non-
healing wound may benefit from surgical treatment.
Microsurgical approaches to improve the lymphatic
outflow, termed lymphatic-venous-lymphaticoplasty,
have been advocated.353 Theoretically, if the lym-
phatic drainage can be corrected and stabilized,
wounds in lymphedematous extremities could heal.
Although lymphovenous anastomoses and lym-
phatic grafting may restore lymphatic transport,
results have been variable. These techniques are indi-
cated in the subset of patients who have proximal
obstruction with preserved or dilated lymphatics
distally.354
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33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 965

FIGURE 3 3 - 5 9 . Revascularization and staged muscle flap transplantation for avascular necro-
sis of lateral foot (intrinsic factors: vascular insufficiency and infection). A and B, Site of avascu-
lar necrosis in ambulatory patient 5 days after saphenous-dorsalis pedis bypass graft for leg
revascularization. C, Arteriogram demonstrates revascularized dorsalis pedis as suitable receptor
vessel for microvascular flap transplantation. D, Foot debridement completed.
Continued

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image...

966 I • GENERAL PRINCIPLES

G H
FIGURE 3 3 - 5 9 , c o n t ' d . £ Latissimus dorsi muscle flap prepared for transplantation. F, Flap inset into defect and
revascularized with end-to-side anastomoses to dorsalis pedis vessels. C and H, Views at 6 months demonstrate stable
wound coverage. The patient has maintained ambulatory status. See Figure 33-2. (From Mathes SJ, Nahai F: Recon-
structive Surgery: Principles, Anatomy, and Technique. New York, Churchill Livingstone, 1997.)

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image...
33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE
RADIATION INJURY. Wounds associated with pre-
vious irradiation are commonly seen in the head and
neck, chest, perineum, and extremities.
Head and Neck. Osteoradionecrosis of the
mandible represents a problem wound that is becom-
ing more common as postoperative doses of head and
neck radiation increase. Long-term radiation therapy
leads to hypovascularityof the mandible, which results
in necrosis. Management of osteoradionecrosis of the
mandible is difficult because a functional reconstruc-
tion of the oral cavity must be achieved. The initial
approach includes debridement and antibiotic treat-
ment. This treatment will be effective only if there is
minimal soft tissue and bone involvement. Hyperbaric
oxygen and ultrasound therapy have also been sug-
gested as adjuvant treatments. 355,356 When there is
significant soft tissue and bone necrosis, conservative
management is unsatisfactory. In this circumstance,
microvascular flap transplantation provides an
adequate blood supply for healing after complete resec-
tion of necrotic bone and surrounding radiation-
damaged tissues.357 Reconstruction of the mandible
and surrounding soft tissue can be accomplished with
several osteocutaneous flaps. These include the fibula
osteocutaneous flap, radial forearm osteocutaneous
flap, scapular osteocutaneous flap, and iliac crest
osteocutaneous flap (Fig. 33-60). Choice of flaps
depends on the amount of bone loss and soft tissue
defect. The fibula has proved effective for large defects,
allows flexible contouring, and has a reliable skin
paddle. 358 More extensive defects may require two free
microvascular tissue transfers.359
Orocutaneous or pharyngocutaneous fistula is
another complication that can arise after patients are
treated surgically followed by radiation therapy for head
and neck cancers. If a fistula develops, conservative
wound treatment and delayed feedings may be
sufficient to control it. However, surgical intervention
consisting of muscle flap coverage may be necessary
to seal an orocutaneous or pharyngocutaneous fistula
(Fig. 33-61). Proper treatment of a pharyngocutaneous
fistula and wound dehiscence is important to avoid
exposure of the carotid artery. Exposure of the carotid
artery should be treated expeditiously with muscle flap
coverage, by use of a regional flap or composite tissue
transplantation. 360
Chest Wall. Chest wall problem wounds often
occur in radiation-damaged skin. Radiation therapy
is commonly delivered in variable doses either pre-
operatively or postoperatively in the management of
malignant tumors. Management of these wounds
involves aggressive debridement of all involved tissues
and reconstruction with vascularized tissue. Hyper-
baric oxygen can serve as a useful adjunct.361 The depth
or extent of the defect will influence technique selec-
tion. All chest wall regions—with the exception of the
sternum—that have absent skin or soft tissue may have
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967
viable muscle at the wound base. Long-standing radi-
ation wounds may involve the underlying ribs or
sternum; resection is required if these structures are
devascularized. A full-thickness defect of the chest wall
will always require flap coverage. A muscle or mus-
culocutaneous flap for coverage of defects that include
four ribs up to 6 cm in length will generally provide
a stable chest wall without significant paradoxical
motion. An omental or fasciocutaneous flap requires
structural support at the site of rib resection. This
support is provided by either autogenous tissue or
a permanent synthetic prosthesis. Extensive full-
thickness chest wall defects frequently require a
combination of synthetic material and muscle or mus-
culocutaneous, omental, or fasciocutaneous flap. 362
Local muscle flaps include the pectoralis major,
latissimus dorsi, serratus anterior, external oblique,
and trapezius (Fig. 33-62). Regional flaps include the
rectus abdominis muscle or musculocutaneous flap
and pedicled omental flap. Large defects without avail-
able local tissue require microvascular composite
tissue transplantation. 363,364 The surgical resection is
often larger than the area of planned resection given
the potential radiation damage to the surrounding
tissues. Inadequate resection of radiation-damaged
skin contributes to postoperative wound breakdown
and should be avoided.
Perineum. Extirpative operations of the perineum
often include preoperative or postoperative radiation
therapy. Without vascularized tissue reconstruction,
these wounds often break down, becoming problem
wounds. 365 Morbidity associated with the nonhealing
perineal wound remains the most common compli-
cation after proctectomy.366,367 After proctectomy, the
pelvic cavity also represents a mechanical problem
because it is lacking soft tissue for closure by wound
contraction. Management of the irradiated perineal
wound involves aggressive debridement and recon-
struction with a muscle or musculocutaneous flap.
Ideally, these wounds are reconstructed at the time of
extirpative surgery, although perineal wounds are often
closed primarily after extirpative surgery and break
down postoperatively. A bulky muscle flap fills the
perineal dead space and provides vascularized tissue
necessary for healing. Common muscle and muscu-
locutaneous flaps used include the rectus abdominis
and gracilis (Fig. 33-63).36a'369 The omentum also
provides vascularized tissue; however, it is often not
available because of intra-abdominal procedures
(e.g., colectomy) associated with the pelvic-perineal
wound. 370
Extremities. Extremity irradiation results in com-
plications, including fracture, edema, pain, fibrosis,
neuropathy, arterial thrombosis, joint immobility,
soft tissue necrosis, and chronic infection, in 6%
to 10% of patients. 371 A wound developing in an
Text continued on p. 974
 I • GENERAL PRINCIPLES

FIGURE 3 3 - 6 0 . Osteoradionecrosis of the mandible (intrinsic factor: vascular insufficiency; mechan-

ical factor: fistula). A, An orocutaneous fistula developed at the site of radiation therapy for primary
treatment of carcinoma of floor of-mouth. B, After wound debridement, mandible was resected between
parasymphyseal area and right angle of mandible. C, Donor site for vascularized fibula and combined
peroneal fasciocutaneous flap on left leg. Note osteotomy and insertion of plate in fibula before flap
transplantation to mandibular defect. D, Vascularized fibula and skin island based on peroneal artery
and vein for microvascular transplantation to oral cavity.

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33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 969

FIGURE 3 3 - 6 0 , c o n t ' d . E to C, Postoperative views at 1 year show successful bone replacement

and adequate chin projection. Skin island transplanted with fibula provided stable wound coverage.
H, Leg donor site also demonstrates good coverage. The patient has maintained ambulatory status.
See Figure 33-15. (From MathesSJ, Nahai F: Reconstructive Surgery: Principles, Anatomy, and Tech-
nique. New York, Churchill Livingstone, 1997.)

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VtJWH^aeldW image...

970 I • GENERAL PRINCIPLES

LfrW

FIGURE 3 3 - 6 1 . See legend on opposite page.

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HScPttf^d tf«f image...

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 971

FIGURE 3 3 - 6 1 , cont'd. Pectoralis major musculocutaneous flap for reconstruction of a pharyngoesophageal

fistula in a patient presenting with radiation necrosis and failed deltopectoral flap (intrinsic factor: vascular insuf-
ficiency; mechanical factor: fistula). A, Preoperative view. The patient had recurrent squamous cell carcinoma of
the larynx after primary radiation therapy, which necessitated laryngectomy. Complications secondary to poor
wound healing resulted in right-sided carotid rupture and necrosis of the anterior cervical esophageal wall. B,
The deltopectoral flap failed to provide stable coverage, d, site of deltopectoral flap inset; e, anterior wall defect
of the pharynx-cervical esophagus extending to the site of the tracheostomy. C, Deltopectoral flap excised; pha-
ryngeal-cervical esophageal defect (e) debrided. The left pectoralis major musculocutaneous flap is elevated with
a distal vertical skin island, a, superior aspect of skin island; b, inferior aspect. D, After flap transposition to the
neck, the skin island is inset in the defect with the superior edge of the skin island sutured to the esophagus at
the level of the trachea; the inferior portion is placed into the superior aspect of the pharyngeal defect. E, Skin
island tailored to fit defect in interior cervical esophagus. E One month after reconstructive surgery, the patient
demonstrated normal pharyngeal-esophageal continuity. C, Close-up view demonstrates stable coverage pro-
vided by skin grafts on the exposed deep surface of the pectoralis major muscle. See Figure 33-22. H,
Radiograph of barium swallow demonstrates restoration of pharyngeal-esophageal continuity with intact ante-
rior wall at the site of the pharyngeal-esophageal reconstruction with the pectoralis major skin island. (From
Mathes S: The pectoralis major flap. In Stark RB, ed: Plastic Surgery of the Head and Neck. New York, Churchill
Livingstone, 1985:949.)

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972 I • GENERAL PRINCIPLES

FIGURE 3 3 - 6 2 . Osteoradionecrosis of the anterior thorax (intrinsic factors: vascular insuffi-

ciency and infection). A, The patient underwent left radical mastectomy and chest wall irradiation.
B, Design of inferior oblique skin island for latissimus dorsi musculocutaneous flap to reconstruct
superior posterior chest for sequelae of chronic radiation therapy.

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image...

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 973

FIGURE 3 3 - 6 2 , c o n t ' d . C, Elevation of flap with overlying skin island. Retractors located on superior lateral chest
skin allow exposure of proximal muscle for completion of flap elevation. D, Debridement of left anterior chest wound
and second through fourth ribs between sternum and anterior axillary line. The flap is ready for inset into the defect.
E, After resection of left lateral sternum, second through fourth costal cartilages, and anterior ribs, reconstruction
achieved stable wound coverage and chest wall stability. See Figure 33-9. (From Mathes SJ: Chest wall reconstruc-
tion. Clin Plast Surg 1995;22:187.)

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974 I • GENERAL PRINCIPLES

FIGURE 3 3 - 6 3 . Radiation necrosis of perineum and pelvic cavity (intrinsic factor: vascular insufficiency; mechani-
cal factor: cavity wound). A, Perineum and sacral cavity after radiation therapy and abdominal-perineal resection for
carcinoma of the rectum. The wound extends from the perineum into the pelvic cavity to the level of the peritoneal
reflection. B, Elevation of bilateral gracilis muscle and gluteal thigh fasciocutaneous flap for wound coverage, g, gra-
cilis muscle; f, fascial surface of gluteal thigh flap. C, After removal of epithelium from distal half of gluteal thigh flaps,
flaps are used to fill pelvic cavity and provide skin coverage. The arrows indicate the site of flap de-epithelialization.
f, skin surface of gluteal thigh flap. D, View at 1 year shows stable wound coverage. The flap donor site was closed
directly. (From Mathes SJ, Hurwitz DJ: Repair of chronic radiation wounds of the pelvis. World J Surg 1986; 10:269.)

extremity that has been irradiated represents a problem Infection

wound. Irradiation is commonly used after resection
of soft tissue sarcomas to decrease the local recur-
rence rate. The management is similar to that of other
radiation wounds in that treatment involves debride-
ment of all necrotic, nonviable tissue and recon-
struction with a muscle or musculocutaneous flap.
The extremities do not provide many options for
muscle transposition flaps; thus, microvascular
composite tissue transplantation must be performed
(Fig. 33-64).372
Specific problem wounds related to infection include
necrotizing soft tissue infection and wounds with
underlying osteomyelitis.
NECROTIZING SOFT TISSUE INFECTION. Manage-
ment of the patient with a necrotizing soft tissue infec-
tion begins with aggressive fluid resuscitation to offset
acute renal failure and shock. Fluid resuscitation is
performed in conjunction with intravenous admin-
istration of broad-spectrum antibiotics. The patient

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33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 975

FIGURE 3 3 - 6 4 . Osteoradionecrosis of anterior thigh with exposed femur (intrinsic factors:

vascular insufficiency and infection). A, Site of prior resection of sarcoma and radiation therapy.
B, Wound debridement completed. The patient presented with drill holes in anterior surface
of femur made in an unsuccessful attempt to provide granulation tissue wound healing. Bone
is preserved in an attempt to salvage a functional extremity. C, Latissimus dorsi muscle trans-
planted to defect and revascularized end-to-side to profunda femoris artery and vein. The
exposed muscle is covered with skin grafts. D, View at 1 month demonstrates stable cover-
age of proximal two thirds of thigh after loss of distal flap. Continued

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976 I • GENERAL PRINCIPLES

FIGURE 3 3 - 6 4 , cont'd. E, Elevation of medial gastrocnemius muscle for transposition to remaining distal thigh
defect. Note release of muscle origin and insertion to allow extended arc of rotation to distal third of anterior thigh.
F, Flap inset into defect and exposed muscle covered with skin grafts. C, View at 1 year demonstrates stable wound
coverage provided by combined latissimus dorsi and medial gastrocnemius muscle flaps. The patient has had no recur-
rence of infection. H, Note well-healed donor site. The patient has remained ambulatory. (From Mathes SJ, Nahai F:
Reconstructive Surgery: Principles, Anatomy, and Technique. New York, Churchill Livingstone, 1997.)

should be promptly brought to the operating room
for aggressive debridement. Debridement should be
continued until grossly viable or noninfected tissue is
encountered. Failure to adequately debride infected
tissue results in increased patient mortality. Significant
bleeding must be seen at the skin and subcutaneous
fat edges to ensure complete excision of grossly
infected tissue. A thorough wound exploration is of
paramount importance at the time of debridement.
Continued debridement is required if blunt finger
dissection easily separates subcutaneous fat from the
fascia. After appropriate debridement, the patient
should be monitored in the intensive care unit and
returned to the operating room daily for assessment
of the wound and additional debridement if it is
needed. Intraoperative tissue and fluid specimens must
be sent for Gram stain as well as aerobic and anaero-
bic cultures with sensitivities. When the culture results
are returned, antibiotic coverage is changed appro-
priately. Studies of the cultured bacteria isolated from

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33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE
patients with necrotizing soft tissue infections reveal
that group A streptococcus is the most common
causative organism. It has been shown that the
outcome of patients with necrotizing fasciitis is
markedly improved when the initial debridement is
radical.373 Debridement should be repeated daily until
the wound bed and surrounding soft tissues appear
viable with bleeding edges and the patient is clinically
improved. A necrotizing myositis involves muscle in
addition to the skin and fascia. In this circumstance,
the necrotic muscle must be debrided to healthy viable,
bleeding, and fasciculating muscle. After debridement,
the wound is packed open with saline-soaked gauze.
These aggressive debridements often result in large soft
tissue deformities, which are definitively managed
when the infection is completely resolved. These large
problem wounds often require complex reconstruc-
tions to restore form and function. Coverage includes
split-thickness skin grafts and transposition, free
muscle, musculocutaneous, and fasciocutaneous flaps.
In general, initial wound coverage is by skin grafts;
flaps are used when coverage of exposed bone, tendon,
nerve, and vascular structures is required.
In addition to debridement, hyperbaric oxygen
therapy has proven benefits in clostridial infections.374
There are no concrete data as of yet whether hyper-
baric oxygen is effective for nonclostridial infections.
OSTEOMYELITIS. Treatment with aggressive de-
bridement to viable, noninfected bone is paramount.
The endpoint of bone debridement is marked by the
appearance of bleeding cortical bone. If removal of the
complete circumference of bone is needed, external
fixation maintains bone stability until a secondary pro-
cedure can restore bone continuity. The failure of
osteomyelitis to uniformly respond to antibiotics or
antibiotics in combination with debridement led to a
search for a more effective method of treatment. In
1946, Stark recognized the effectiveness of the muscle
flap in the management of an infected wound involv-
ing bone. 375 Currently, the muscle flap is widely used
for reconstruction. The basis for the use of the muscle
flap has been studied experimentally. Compared with
random-pattern flaps, the musculocutaneous flap
demonstrates superior resistance to bacterial inocu-
lation on both its skin and underlying muscle sur-
faces.376 Further studies demonstrated the delivery of
oxygen and leukocytes in the distal musculocutaneous
flap in response to bacterial inoculation.377,378
Once adequate debridement is accomplished,
muscle flaps provide stable and well-vascularized
coverage. The timing and type of coverage depend on
the size of the bone and soft tissue defects. After com-
plete debridement of the zone of bone infection,
immediate soft tissue coverage with a local pedicled
muscle flap or distant microvascular composite tissue
transplantation is undertaken (Fig. 33-65). Debride-
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Dr.Mustafa D.
977
ment with immediate flap coverage and culture-
specific antibiotic coverage have successfully treated
chronic osteomyelitis. With chronic osteomyelitis, the
debridement generally does not disrupt bone conti-
nuity. With successful treatment of the osteomyelitis,
the patient has adequate bone to maintain ambula-
tory status. With infected nonunion, bone continu-
ity is not preserved with the required debridement
and flap coverage. After the chronic wound is healed,
a number of options are available to establish bone
union. Defects measuring less than 8 cm may be
treated with cancellous bone grafts or used for syn-
ostosis between the tibia and the fibula. With more
extensive debridement, either cancellous bone graft-
ing or microsurgical vascularized bone transfer is
undertaken. Defects measuring less than 8 to 10 cm
are suitable for cancellous graft beneath the established
flap coverage. Longer defects are better suited for
vascularized bone transfer. Bone transport (Ilizarov
technique) may also be applicable for these defects.
Chronic unstable wounds may be aggressively
debrided and converted to stable wounds. When
wound stability is achieved, another option is either
continued systemic antibiotic treatment or definitive
wound closure with a musculocutaneous flap. Systemic
antibiotics, although often used, act only as a bridge
until definitive resection of grossly infected bone can
be achieved.
Antibiotic beads may be used at the time of bone
debridement and flap coverage. Antibiotic-impreg-
nated beads represent another treatment modality that
can be used on a temporary basis. The beads main-
tain a space deep to the flap for eventual bone replace-
ment and, through the delivery of antibiotics, further
contribute to the sterilization of the local environment.
In those patients in whom bone replacement and soft
tissue coverage cannot be achieved in one stage, the
use of antibiotic beads as a temporary spacer has been
helpful. It facilitates secondary bone replacement, at
which time the flap is elevated, the beads are removed,
and the preserved space is replaced with vascularized
bone.
C O M M O N SITES OF INFECTION
Sternum. The most common location of wound
dehiscence is the median sternotomy incision, followed
by the thoracotomy incision (Figs. 33-66 and 33-67).
Wound infections after median sternotomy with sub-
sequent dehiscence of the sternum cause problem
wounds for which plastic surgeons are often consulted.
Patients with these wounds generally have numerous
comorbid conditions that delay wound healing. The
management involves early, aggressive treatment with
debridement, coverage, and closure over drains. Ade-
quate debridement of the mediastinum is critical to
the success of the reconstruction. An uncontrolled
infection of the sternum may involve vascular and
mage...

978 I • GENERAL PRINCIPLES

FIGURE 3 3 - 6 5 . Osteomyelitis of the skull (intrinsic factors: vascular anomaly and infection).
A, The patient has previously undergone therapy for intracranial vascular anomaly. A vertical
trapezius musculocutaneous flap is designed for debridement defect coverage. B, Left vertical
trapezius musculocutaneous flap ready for transposition into defect. Bone debridement at
site of occipital cranial osteomyelitis is completed. C, Postoperative view at 6 months after
inset of trapezius musculocutaneous flap. Stable coverage is provided by the flap with no evi-
dence of recurrent infection. D, Function-preserving technique. Superior intact fibers maintain
left shoulder function. The donor site is closed directly. See Figure 33-11.

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HeWttf'SdtfW image..

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 979

FIGURE 3 3 - 6 6 . Chronic osteomyelitis of sternum (intrinsic factor: infection; extrinsic factor: surgery). A The patient
has longer than a 10-year history of sternal osteomyelitis after mitral valve replacement. B, Radiography demonstrates
mitral valve prosthesis and no anterior mediastinal extension of infection. C, Sternal debridement completed. The
right pectoralis muscle is elevated as a musculocutaneous flap based on segmental internal mammary pedicles, and
the muscle is split into superior and inferior muscle flaps. D, Superior half of turnover pectoralis muscle flap provides
coverage of superior half of sternal debridement site; inferior half of muscle flap covers inferior half of sternal debride-
ment site. The inferior half of the pectoralis major segmental muscle flap reaches into the inferior mediastinal defect.
E, Postoperative view at 6 months demonstrates stable coverage with no incidence of recurrent infection. F and C,
Despite use of pectoralis major muscle as a flap, the patient retains full range of motion of right upper extremity.
H, Two-year follow-up demonstrates stable coverage with no evidence of recurrent sternal infection.

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TfcWttf'aelCiW image...

980 • GENERAL PRINCIPLES

/
B

£#s
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FIGURE 3 3 - 6 7 . Sternal wound dehiscence and anterior mediastinal infection (intrinsic factors: impaired cellular
function and infection; extrinsic factor: surgery). A, Diabetic patient with an anterior mediastinal infection after a
coronary artery bypass graft (left internal mammary artery). B, After complete debridement of the left sternum and
partial debridement of the right sternum, the right pectoralis major muscle was elevated on the segmental vascular
pedicles from the right internal mammary artery. The muscle was split at the fourth intercostal space into two flaps
(a and b). C, Flap a was placed into the superior anterior mediastinum. Flap b completed coverage of the inferior
mediastinal defect. D, Postoperative view at 6 months. See Figure 33-12. (From Mathes SJ, Eshima I: The principles
of muscle and musculocutaneous flaps. In McCarthy JG, ed: Plastic Surgery. Philadelphia, WB Saunders, 1990:379.)

cardiac suture lines as well as prosthetic valves and
grafts, which have the potential to rupture under these
conditions.
The extent of debridement should include all
necrotic skin and subcutaneous tissues. The sternum
is debrided entirely if healthy bleeding bone is not
encountered. The surrounding cartilage should be
assessed for viability and debrided as necessary. After
debridement, the wound is pulse irrigated with 3 to 5
liters of antibiotic saline. Any remaining necrotic tissue
will be a nidus for continued nonhealing.
The reconstructive options for sternal wound cov-
erage include local or regional flap transposition. The
most common muscles in proximity to the sternum
used for coverage include the pectoralis major and
rectus abdominis muscles. These muscles maybe trans-
posed on their vascular pedicles to provide coverage
to the sternal defect. The pectoralis muscle, based on
the thoracoacromial vascular pedicle, can be transposed
over the defect. Based on their secondary segmental
pedicles from the internal mammary artery, the
muscles can be turned over into the sternal defect to
provide wound coverage. The rectus abdominis muscle,
based on the superior epigastric vessels, is also used
for sternal coverage. Another option for sternal
coverage is the omentum. The omentum is a large,

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image...
33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE
versatile flap that has documented immunogenic
properties.379,380 Hultman et al38' have shown that the
omentum can be harvested safely and used effectively
to reconstruct a variety of thoracic wounds.
The growing field of pediatric cardiac surgery has
led to an increase in infants and children with medi-
astinal wounds. A sternal wound infection can be a
life-threatening complication. 382 The treatment of
these wounds is similar to that of wounds in adults
and includes sternal wound debridement and muscle
flap closure.383,38'1 Of note, the cartilage and minimally
ossified bone of infants can desiccate readily and may
be easily contaminated, dictating aggressive debride-
ment to promote reossification. In addition, given the
size and development of the infant's muscles, more
than one flap is generally needed for coverage.383 Bilat-
eral pectoralis muscle flaps have been used success-
fully in this population of patients, although some
surgeons think that the muscle provides insufficient
coverage to the inferior portion of the wound and
others suggest that it may impair normal chest growth
and breast development. 385
Posterior Trunk. Elective operative procedures of
the spine can result in problem wounds. These midline
wounds may threaten the bony spine, which can com-
promise neurologic function. Thus, prompt coverage
is indicated. The cause of these wounds is likely to be
secondary to infection or unstable soft tissue cover-
age. Postoperative infection can lead to muscle necro-
sis, deep dead space, and exposure of hardware, bone,
and dura. In addition to a soft tissue deformity, the
components of these wounds may include one or all
of the following: bone, bone grafts, spinal cord and
branches, and vertebral column hardware. The result
of these potential exposures can be disastrous, espe-
cially when the dura is exposed. Without debridement
and coverage, these wounds result in significant mor-
bidities, such as spinal instability, neurologic com-
promise, and dissemination of infection to the central
nervous system. The area of infection needs to be
adequately d£brided, including nonviable bone, and
covered with an appropriate muscle flap. The use of
local transpositional flaps has provided stable soft tissue
coverage in some patients.386,387 When local muscles
are not available, microvascular composite tissue
transplantation to the lower back has been described
to cover large lumbosacral defects.388,389
Cellular Impairment
DIABETES MELLITUS. Lower extremity ulcers are
commonly seen in the diabetic patient. Poorly fitting
shoes are the main cause of ulceration. Initial treat-
ment includes management to reduce the pressure on
the prominent areas of the foot. Infection in the patient
with a diabetic ulcer must be treated aggressively.
Culture-specific parenteral antibiotic therapy gener-
ally controls the infection. After control of the infec-
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981
tion, an ischemia work-up is needed to evaluate the
vasculature of the lower extremity to determine if revas-
cularization is required. If vascular inflow is adequate,
or vascular reconstruction is not feasible, local debride-
ment, skin grafts, or a local flap may be effective in
providing stable coverage. If revascularization is under-
taken, the diabetic ulcer is evaluated for healing and
the need for further reconstruction.
Initial debridement can be accomplished at the time
of revascularization and then managed with local
wound care. Small defects with a healthy granulation
base may be skin grafted. Large defects with exposed
bone require microvascular composite tissue trans-
plantation. Flap transplantation can be staged 10 to
14 days after revascularization or done at the same time
as revascularization with use of the bypass graft as the
inflow for the muscle flap. Muscle transplantation to
the lower extremity has been a successful means of limb
salvage.390 Reliable muscles transferred to the lower
extremity include the rectus abdominis, latissimus
dorsi, and gracilis muscle flaps (Fig. 33-68).391,392
Nutrition
Nutrition is rarely an isolated cause of a problem
wound. More commonly, it represents a component
of the cause of poor wound healing. All patients with
problem wounds should have a nutrition evaluation
and supplementation as needed. Correction may
require hyperalimentation, tube feedings, or work-up
for malabsorption.
Malignant Disease
Problem wounds are secondary to extirpation of
malignant neoplasms. Reconstruction of these defects
depends on the anatomic area, the extent of the tumor
involvement, and the amount of resection. Examples
of difficult anatomic areas to reconstruct include the
head and neck and extremities. The chest wall and
perineum are covered in other sections.
HEAD AND NECK. Tumor excision from the head
and neck includes primary and recurrent skin and
mucosal cancers as well as intracranial tumors involv-
ing bone. Head and neck wounds after tumor resec-
tion represent problem wounds because of the size of
the resected tumor and surrounding soft tissues, vital
structures involved by the tumor, or exposure to radi-
ation used to treat the primary tumor. Reconstruc-
tion must focus on both form and function. Anatomic
areas to reconstruct include the scalp, forehead, orbit,
midface, oral cavity, mandible, and cervical esopha-
gus. Defects may involve any combination, making
reconstruction difficult. Large defects of the scalp can
be reconstructed with latissimus dorsi or omental flaps
that provide stable coverage and establish adequate
contour. Orbit defects can be large and deforming.
Depending on the extent of the orbital defect, the rectus
982 • GENERAL PRINCIPLES

FIGURE 3 3 - 6 8 . Diabetic foot ulcers (intrinsic factor: impaired cellular function; extrinsic
factor: pressure). A, Ulcers on plantar surface of foot extend into metatarsal phalangeal joints
on first and fourth toes. B, Debridement of plantar surface of first metatarsal phalangeal joint,
design of V-Y advancement flap based on medial plantar artery and associated veins. C, Flap
inset. D, Postoperative plantar view at 1 year demonstrates stable coverage with no recur-
rence of infection. See Figure 33-44.

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image...
33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE
abdominis muscle with or without a cutaneous portion
provides stable coverage. Extirpative defects of the oral
cavity represent a challenge to the reconstructive
surgeon. In addition to provision of stable coverage
of the defect, oral cavity competence and function
should be the goal. The radial forearm flap has been
the workhorse of oral cavity reconstruction. The
radial forearm flap is thin and pliable and has a long
vascular pedicle. Composite defects including the
mandible are best managed with the fibular osteocu-
taneous flap.
EXTREMITIES. Extensive tumor resection in the
extremities may involve soft tissues, nerves, and bone.
If the extent of resection is underestimated preoper-
atively, the reconstructive surgeon is confronted with
a problem wound in the acute setting. Nerve grafts,
bone grafts, and vascular repairs may be required in
addition to soft tissue coverage. Local tissues are often
inadequate for coverage that necessitates microvascular
composite tissue transplantation. Extensive muscle
resection may lead to a functional deficit requiring
functional reconstruction. For example, tumor resec-
tion about the knee often compromises the extensor
apparatus of the knee. The gastrocnemius muscle flap
can be used to provide stable knee coverage as well as
a means of extensor tendon reconstruction.
Two common carcinomas involving the extremi-
ties are sarcoma and melanoma. Soft tissue sarcomas
account for approximately 1% of all adult malignant
neoplasms and 15% of pediatric malignant neo-
plasms.393 Historically, the surgical treatment of extrem-
ity sarcoma involved amputation of the affected
extremity. However, studies have shown that amputa-
tion does not improve survival over limb-sparing
procedures. Limb-sparing techniques have made
complex reconstructions necessary.394 Studies show
good to excellent late results in patients undergoing
reconstruction with both pedicled and free flaps
(Fig. 33-69). 39W96
Brachytherapy is a term applied to the use of encap-
sulated radionuclides embedded into soft tissue close
to a tumor bed. Postoperative brachytherapy is com-
monly employed after cancer ablation in the extrem-
ity. An important concern postoperatively is delayed
wound healing.397 Therefore, management of these
wounds should include well-vascularized soft tissue
coverage (musculocutaneous flap) of the defect and
brachytherapy catheters. It has been shown that imme-
diate microvascular free flap reconstruction of sarcoma
treated with resection and brachytherapy reduced the
incidence of wound breakdown in the postoperative
period. 398
Perfusion chemotherapy for melanoma has been
used in certain high-risk patients. This has been com-
bined with hyperthermic perfusion with variable
results. L-Phenylalanine mustard or melphalan is the
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Dr.Mustafa D.
983
most common drug for limb perfusion. In conjunc-
tion with local and regional excisional surgery, hyper-
thermic perfusion offers a better chance for cure in
patients with thick tumors. Although it is of benefit in
certain subsets of patients, delayed wound healing is
evident in 10% to 30% of patients.399,400
POSTERIOR TRUNK. Tumor resection involving any
location on the back may result in a large soft tissue
defect that may include bone. Common resections
include skin cancers, giant congenital melanocytic
nevus, and tumors originating from the spinal cord.
Complete resections result in large defects. Defects
involving only the skin and subcutaneous tissue
require split-thickness skin grafting, whereas those
defects involving bone require a larger musculocuta-
neous flap for coverage. Patients requiring postoper-
ative radiation therapy after tumor excision benefit
from stable musculocutaneous coverage rather than
split-thickness skin grafting.
In general, the muscle flaps available for recon-
struction of problem wounds of the back include
the trapezius, latissimus dorsi, paraspinous, gluteus
maximus, and omentum. Cervical defects may be
closed with the trapezius muscle or musculocutaneous
flap. Upper thoracic defects can be closed with either
the trapezius or latissimus dorsi muscle flap or a com-
bination of the two. Midthoracic defects can be closed
with the trapezius, latissimus dorsi, or reverse latis-
simus dorsi muscle flap. The reverse latissimus dorsi
flap is based on perforating branches from the ninth,
tenth, and eleventh posterior intercostal arteries enter-
ing the muscle about 4 to 5 cm from the midline and
approximately 5 cm caudal to their respective origins
at the intercostal vessels.401 In addition, the paraspinous
muscles maybe used for midline defects. Lumbosacral
defects can be reconstructed with the latissimus dorsi,
either as a musculocutaneous advancement flap or with
a thoracolumbar fasciocutaneous extension, or the
gluteus maximus musculocutaneous flap in combi-
nation with the latissimus dorsi muscle. Sacral defects
can be covered with either single or bilateral gluteus
maximus musculocutaneous flaps. In patients in
whom local tissues are not available or the defect
is too large for coverage by local or regional flaps,
microvascular composite tissue transplantation may
offer treatment of a problem wound.
MECHANICAL
Specific problem wounds secondary to a mechanical
cause include wounds associated with surgical extir-
pation of tumor, cavity wounds, wounds with fistulas,
and wounds associated with prostheses.
Cavity Wounds, Fistulas, and Herniation
ABDOMINAL WALL. Open abdominal surgery puts
the patient at risk for development of a problem wound
984 I • GENERAL PRINCIPLES

FIGURE 3 3 - 6 9 . Congenital lymphangioma with wound ulceration (intrinsic factors: impaired cellu-
lar function and vascular insufficiency). A, Preoperative view of young patient with congenital lym-
phangioma. B, Tumor resection with preservation of neurovascular structures. C, Defect coverage
with microvascular transplantation of latissimus dorsi muscle. D, Postoperative anterior view at 1 year
demonstrates that skin grafts on muscle transplantation provide stable coverage. E, Shoulder function
is preserved. F, Posterior view; muscle transplant provided complete upper arm coverage.

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 image...
33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE
of the abdomen. A problem wound may develop from
an intrinsic deficiency, such as poor nutrition or infec-
tion, or it may be the result of surgical extirpation of
a large tumor that invades the abdominal wall. Infected
abdominal wounds can generally be managed with
intravenous antibiotics or drainage of an abscess. On
occasion, the infection will spread rapidly with severe
soft tissue necrosis, as in necrotizing fasciitis. Necro-
tizing fasciitis of the abdominal wall is a serious problem
with a high patient mortality. Management involves
debridement of large amounts of the abdominal wall.
The resultant defects can be enormous, including skin,
subcutaneous tissue, muscle, and fascia.
The failure of surgical wound closure with result-
ant hernia formation is a common problem. Ventral
hernia after abdominal surgery occurs in 10% of
patients; recurrence of ventral hernia after repair is 50%
(Fig. 33-70).402'404 In the case-control studies reported
by Riou et al178 and Makela et al,405 compared with
control patients, there was a greater risk for dehiscence
in patients with three to five of the following factors:
age older than 65 years, wound infection, pulmonary
disease, hemodynamic instability, ostomy within the
incision, hypoproteinemia, sepsis, obesity, uremia,
hyperalimentation, malignant disease, ascites, steroid
use, and hypertension.
Extirpation of tumors from the abdominal wall or
of those extending into the abdominal wall from the
intra-abdominal contents represents a challenge to the
reconstructive surgeon. One must take into consider-
ation the defect size and the involved tissue compo-
nents, tumor pathology, and stability of the remaining
skin. If the tumor is recurrent, the surrounding skin
has probably been subjected to radiation therapy, which
may alter treatment options.
Management of the midline abdominal wall prob-
lem wound requires analysis with regard to both the
defect and the reconstructive options. Depending on
the defect, options for closure include split-thickness
skin grafting, tissue expansion, intraperitoneal mesh
placement, components separation, regional flaps, and
microvascular composite tissue transplantation.
Autogenous tissues available for abdominal wall
reconstruction include the latissimus dorsi, rectus
abdominis, external oblique, tensor fascia lata, and
rectus femoris. Lower abdominal wall defects can
be managed with unilateral or bilateral tensor fascia
lata flaps (Fig. 33-70). 40M07 The tensor fascia lata flap
can also be expanded to increase the size and arc of
rotation as well as to facilitate donor site closure
(Fig.33-71). 408
Large fascial defects of the abdominal wall with
stable skin and soft tissue coverage are managed with
mesh reconstruction. Both nonabsorbable poly-
propylene mesh (Marlex and Prolene) and polytet-
rafluoroethylene mesh (Gore-Tex) are advocated for
abdominal wall reconstruction. 408 Prolene is relatively
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Dr.Mustafa D.
985
inert, has adequate strength, and unlike Gore-Tex
allows tissue incorporation and ingrowth of granula-
tion tissue.409 The mesh can be secured to the fascial
defect in a variety of ways. The mesh can be applied
externally as an interposition fascial replacement,
placed as a patch to reinforce direct fascial closure, or
placed intraperitoneally (Fig. 33-72). When mesh is
placed intraperitoneally, the repair is buttressed during
the period of tissue incorporation. The intraperitoneal
mesh is anchored to innervated, well-vascularized mus-
culofascial layers with interrupted, nonabsorbable U
sutures, which are passed through normal fascial layers
and tied on the external surface of the fascia.
Components separation uses bilateral, inner-
vated, bipedicled rectus abdominis-transversus
abdominis-internal oblique flaps, which are trans-
posed medially to reconstruct the central abdominal
wall (Fig. 33-73).410 This technique obviates the need
for regional flaps or placement of a prosthetic mate-
rial. Although it is useful, the reherniation rate is
relatively high in several series since the original de-
scription of this technique. 411 Other options include
endoscopically assisted components separation, whereby
one could minimize operative disruption of the mus-
culocutaneous perforators to the abdominal wall by
releasing the external oblique muscle through endo-
scopically placed ports rather than by dissection through
the perforators to the skin from the midline wound.412
Microvascular composite tissue transplantation
maybe used for extensive abdominal defects if distant
flaps with adequate arcs of rotation are not available
for transposition. A suitable recipient vessel must be
located in proximity to the abdominal defect (usually
within the groin). The flap selected for transplanta-
tion should have large size and a long major vascular
pedicle. Two common flaps used are the tensor fascia
lata and the latissimus dorsi flaps.
CHEST WALL. Problem wounds of the chest that
result in cavity formation may occur from trauma or
tumor extirpation. Further complicating factors
include a history of radiation therapy and develop-
ment of a bronchopleural or tracheoesophageal fistula.
The development of bronchopleural and tracheo-
esophageal fistulas after intrathoracic surgical proce-
dures can lead to recalcitrant problem wounds with
perioperative mortality rates as high as 15%.413,414
Traumatic defects of the chest wall include crush,
avulsion, and blast injuries. Massive traumatic defects
may involve the chest wall, pleural and mediastinal cav-
ities, spine, and abdominal wall. All of these defects
individually or in combination may lead to the devel-
opment of a problem wound. Chest wall defects
influence pulmonary function. A flail chest results when
four or more ribs are removed, necessitating chest wall
stabilization.
Text continued on p. 990
986 I • GENERAL PRINCIPLES

FIGURE 3 3 - 7 0 . Abdominal defect with skin graft coverage (intrinsic factor: vascular insufficiency; extrin-
sic factor: trauma). A, Major visceral injuries after motor vehicle accident. Abdominal compartment
syndrome required release of abdominal closure and split-thickness skin graft. B, Lateral view of ventral
hernia with skin grafts on viscera. C, Postoperative view 1 year after peritoneal Prolene mesh recon-
struction of abdominal wall. D, Lateral view: abdominal fascia continuity restored with Prolene mesh.

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T?ek*>ttf'9elcWimage...

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 987

FIGURE 3 3 - 7 1 . Infected Mariex mesh with ventral hernia (intrinsic factor: infection; extrinsic factor: surgery).
A, The patient underwent a gynecologic procedure and developed respiratory complication and abdominal dehiscence.
Repair with Mariex mesh subsequently led to exposure and infection. B, Lateral view. C, Infected Mariex mesh and
associated abdominal wall resected. D, Tensor fascia lata flap is prepared for transposition for reconstruction of central
lower abdominal fascial defect. E, Tensor fascia lata flap based on lateral femoral circumflex artery and associated
veins is transposed through a tunnel over the inguinal region. Vascularized flap is sutured into normal muscle layers.
F, Postoperative anterior view 1 year after abdominal wall reconstruction demonstrates stable coverage and success-
ful repair of ventral hernia. C, Lateral view demonstrates stable superior abdominal advancement coverage over tensor
fascia lata flap inset.

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988 I • GENERAL PRINCIPLES

FIGURE 33-72. Traumatic loss of

right lower quadrant abdominal
fascia. Previous attempts to repair
the hernia defect failed (extrinsic
factor: trauma). A, Recurrent hernia
secondary to blunt trauma, anterior
view. 8, Preoperative lateral view.
C, Mesh restores fascial continuity
between paraspinous musculature
and intact left anterior abdominal
muscle layers. D, Postoperative
anterior view at 1 year demonstrates
stable coverage over mesh repair.
£, Lateral view demonstrates
restoration of abdominal wall con-
tinuity. (From Mathes SJ, Steinwald
PM, Foster RD, et al: Complex
abdominal wall reconstruction: a
comparison of flap and mesh
closure. Ann Surg 2000;232:586.)

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33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 989

FIGURE 3 3 - 7 3 . Anterior ventral hernia with unstable

fascial defect coverage (intrinsic factors: vascular insufficiency,
malignant disease, and infection; extrinsic factor: surgery).
A, Preoperative view of woman with chronic incisional hernia
complicated by radiation damage after resection of a gastric
sarcoma. B, Posterior dissection plane, designed to preserve
anterior skin perforators. Bilateral rectus abdominis-internal
oblique musculocutaneous flaps will advance to close the
fascial defect (lateral sheath dissection with components
separation). C and D, Postoperative views demonstrate
stable soft tissue coverage and closure of fascial defect. (From
Steinwald PM, Mathes SJ: Management of the complex
abdominal wall wound. Adv Surg 2001:35:77.) D

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990 I • GENERAL PRINCIPLES
Tumors of the thorax may be confined to the pleural
space or the chest wall or may involve the pleural space
and the chest wall. The surgical excision of chest wall
tumors can result in a problem wound because of the
size of the resected defect, the location of the defect,
or an intrinsic deficiency of the patient. The tumor
may originate in and involve the chest wall, sternum,
mediastinum, or lung parenchyma. The depth or extent
of the defect influences the reconstructive technique.
Absence of costal cartilages and ribs (more than four
ribs extending over a 6-cm distance) may result in chest
wall paradoxical motion and requires a reconstruc-
tion to restore chest wall stability. In addition to the
defect, the surrounding tissue may be tenuous if radi-
ation therapy has been used in the chest wall.
Regardless of the cause, chest wall reconstruction
must restore the integrity of the chest wall and oblit-
erate all residual cavities and potential spaces with vas-
cularized tissues. This requirement includes not only
soft tissue but bone structure as well. Stabilization of
the chest wall can be established by a variety of syn-
thetic materials including Marlex, Vicryl, Gore-Tex,
and Prolene mesh.415 Prosthetic material is needed
when the defect is 5 cm or larger. The prosthetic
material must be secured under tension to restore the
skeletal stability.
Numerous tissues are available for soft tissue recon-
struction. These tissues may be locally available or
transplanted microsurgically. The latissimus dorsi
muscle, based on the thoracodorsal pedicle, is used
for anterior chest wall coverage, but it will also reach
defects of the ipsilateral superior, lateral, and poste-
rior chest. The pectoralis major muscle, based on the
thoracoacromial artery, may be used as a transposi-
tion flap, based on the thoracodorsal artery and asso-
ciated veins, or a turnover flap, based on perforators
from the internal mammary artery and veins, to recon-
struct anterior midline defects. The serratus anterior
muscle, based on the branches of the thoracodorsal
vascular pedicle, is primarily used for intrathoracic
defects because of its size, location, and arc of rota-
tion. The trapezius muscle, based on the descending
branch of the transverse cervical pedicle, is used for
superior and posterior midline chest wall defects. The
thoracoepigastric flap is a local fasciocutaneous flap
useful in chest wall reconstruction. Historically, the
thoracoepigastric flap has been used to cover exten-
sive defects relating to the extirpation of recurrent
breast cancers and postirradiation ulcers.416 It is thought
to be a simple and reliable technique. 417 The omentum
is a reliable option for chest wall reconstruction and
is considered the back-up in most situations. The left
or right omentum, on its gastroepiploic artery and
vein, can reach the anterior chest wall, providing well-
vascularized tissue for reconstruction. The surface area
of the omentum allows coverage of large defects and
accepts skin grafts without problem (Fig. 33-74). Unlike
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muscle flaps, the omentum requires mesh support over
the thoracic or mediastinal cavities.
Intrathoracic flaps are often indicated in patients
who need closure of bronchopleural fistulas, esophageal
fistulas, tracheoesophageal fistulas, empyema, expo-
sure of the great vessels or prosthetic materials, and
persistent air leaks. Tissues commonly transferred
intrathoracically include the pectoralis major, serra-
tus anterior, latissimus dorsi, and omentum. These
tissues assist in sealing fistulas, bolster bronchial
stump closures, and cover vascular or visceral repairs.
In addition, muscle flaps assist in the clearance of infec-
tion from the pleural cavity or mediastinum. 418
PERINEUM. Problem wounds involving the per-
ineum can occur in association with large perineal
resections for cancer or inflammatory bowel disease,
with trauma, or as a complication of surgery. The areas
that may be affected include the penis and scrotum,
vagina, anus, and pelvis.
After large colorectal or gynecologic resections,
patients often have large perineal wounds that cannot
be closed primarily. Perineal wounds developing after
abdominoperineal resection result in chronic puru-
lent drainage and intermittent episodes of sepsis that
are unresponsive to medical and surgical management.
This problem is in large part due to preoperative and
postoperative radiation therapy. Other risk factors
identified for development of a recalcitrant perineal
wound include resection for recurrent carcinoma and
presence of inflammatory bowel disease.419 Recurrent
cancer, radiation therapy, and inflammatory bowel
disease lead to local fibrosis with diminished vascu-
larity and impaired wound healing. Historically,
treatment options for these wounds have included
debridement and curettage, excision and primary
closure, and serial debridement with skin grafting.420,421
These methods all require multiple procedures and a
prolonged treatment period and are often unsuccess-
ful, especially in the presence of an irradiated field.
Successful closure of these problem wounds requires
a well-vascularized muscle flap to fill in the dead space
and to bring oxygenated blood into the wound. Muscle
flaps provide safe, effective, single-stage closure (Fig.
33-75).328 The muscle flaps most commonly used to
fill perineal defects are the rectus abdominis, gracilis,
and gluteus muscles. The use of these muscles results
in little or no functional deficit. The choice of the flap
depends on the following: the muscle flaps available
for use, the size of the defect to be reconstructed, and
the amount of skin required for closure. Muscle flap
availability depends on the patient's position during
the operative procedure, the status of each muscle's
vascular pedicle, and the surgical approach to the
wound. For those patients at risk for wound break-
down postoperatively, careful consideration should be
given to immediate reconstruction with a muscle flap.
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33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 991

FIGURE 3 3 - 7 4 . Thoracic cavity wound (intrinsic factors: vascular insufficiency and infection; mechanical factor:
cavity wound). A, Radionecrosis extends into axilla and chest wall. The patient underwent axillary dissection and radi-
ation therapy for melanoma. B, Forequarter amputation of right upper extremity and resection of right lateral chest
at site of radiation necrosis. C and D, Omental flap based on right gastroepiploic artery and vein ready for transposi-
tion to chest wall defect. Prolene mesh is used to close the thoracic wall defect. Note arc of rotation of omentum to
right chest defect. E, Omental flap tunneled through diaphragm to reach chest wall defect and sutured over defect to
seal chest defect and to provide vascularized coverage. F, Postoperative anterior view at 6 weeks demonstrates stable
coverage of complex wound with mesh, omental flap, and split-thickness skin graft. C, Lateral view. See Figure 33-18.

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 I • GENERAL PRINCIPLES

FIGURE 3 3 - 7 5 . Perineal cavity wound (intrinsic factor: infection; extrinsic factor: surgery; mechanical
factor: cavity wound). A, The patient underwent colectomy for ulcerative colitis; nonhealing of proctec-
tomy site. B, Elevation of gracilis muscle based on medial femoral circumflex artery and associated veins.
The pelvic cavity is debrided by curets. C, With the right leg abducted, an adequate arc of rotation is
observed for the muscle to fill the pelvic defect. D, Muscle is sutured into pelvic cavity. Note drain place-
ment (for 5 days). Skin is closed directly over muscles. E, Posterior view at 1 year demonstrates stable
coverage with no recurrence of infection. The patient has resumed normal activities as a health club
manager. See Figure 33-17. (From Anthony JP, Mathes SJ: The recalcitrant perineal wound after rectal
extirpation. Arch Surg 1990; 125:1371.)

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33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 993

Patients with inflammatory bowel disease may
develop problem wounds after bowel resection. Many
of these patients have a long history of steroid use. In
these patients, active inflammatory bowel disease
should be controlled medically before surgical inter-
vention. These wounds may present with a small bowel-
perineal fistula.422 As with soft tissue reconstruction
for carcinoma, these wounds are best managed with
vascularized muscle to fill the dead space after resec-
tion in conjunction with small bowel resection at the
site of the fistula (Fig. 33-76).
GASTROINTESTINAL TRACT. The presence of an
enterocutaneous or pancreatic fistula in association
with an abdominal wound represents a problem
wound. Every attempt should be made to protect the
abdominal wall from the fistula drainage. The amount
of drainage can be controlled to a certain degree with
the use of proximal nasogastric suction and intra-
venous hyperalimentation for nutritional support.
A radiographic evaluation of the fistula is indicated
to determine whether the fistula is secondary to
bowel discontinuity, visceral obstruction, malignant
disease, foreign body, radiation injury, or inflam-
matory bowel disease. The cause of the fistula should
be corrected before reconstruction of the abdominal
wall wound to prevent recurrence (Fig. 33-77).
Management of these wounds includes bowel rest,
total parenteral nutrition, octreotide, and control of
sepsis. The surrounding skin must also be protected

FIGURE 3 3 - 7 6 . Chronic wound of the posterior perineum (intrinsic factor: malignant disease).
A, The patient presents with chronic posterior vaginal wound. She is seen after resection of
vaginal cancer. Findings on wound biopsy demonstrated recurrent cancer. B, Radical hys-
terectomy and vaginectomy performed. Note design of skin islands for bilateral gracilis and
musculocutaneous flaps. C, Appropriate location of skin island is confirmed by location of gra-
cilis tendon of insertion. With traction on the tendon, the proximal muscle belly position in the
center of the designed skin island is confirmed. D, Bilateral gracilis musculocutaneous flaps
elevated and ready for transposition to pelvic extirpative defect. E, Bilateral Maps placed through
tunnels into pelvic defect. Continued

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image..

994 l • GENERAL PRINCIPLES

* * * * * *

H
FIGURE 3 3 - 7 6 , cont'd. F, Skin islands sutured
together in two thirds of skin islands to form vaginal cavity.
The donor sites are closed directly. The proximal skin island
is sutured to the introitus region to complete flap defect
closure after the distal ends of the flaps are rotated into
the pelvic defect. C, Postoperative view at 6 months
demonstrates stable pelvic wound closure with bilateral
gracilis musculocutaneous flaps. H, With retraction of prox- FIGURE 3 3 - 7 7 . Abdominal wall defect with enterocu-
imal gracilis skin islands, the reconstructed vaginal cavity taneous fistula and infected Marlex mesh (intrinsic factor:
is visualized. infection; extrinsic factors: trauma and surgery). A, Defect
of the abdominal wall is shown preoperatively. B, Design
of contralateral rectus abdominis musculocutaneous flap
for planned closure of fistula, wound debridement, and
abdominal wall reconstruction with vascularized fascia
(anterior rectus sheath). C, Flap inset with direct donor
site closure. See Figure 33-23.

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33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 995

from the continuous drainage to prevent further
skin breakdown. The rectus abdominis muscle trans-
position flap has been described to close complex ente-
rocutaneous fistulas.150 Although it is of theoretical
value, this technique is based on only a few reports
with short-term follow-up. Perineal fistulas develop-
ing after gastrointestinal surgery, such as procto-
colectomy, can be managed with interposed muscle
flaps with excellent results. Common flaps used in these
situations include the rectus abdominis and gracilis
muscles.423
Prosthesis Exposure
BREAST. Breast reconstruction with implants is a
common procedure. Complications associated with
implant reconstruction include exposure of the
implant. As with other prosthetic exposures, this rep-
resents a problem wound (Fig. 33-78). This implant

FIGURE 3 3 - 7 8 . Breast implant exposure (mechanical factor: prosthesis exposure). A, Preoperative view of patient
after augmentation with steroid injection. B, Close-up of right inferior lateral breast demonstrates loss of skin and sub-
cutaneous tissue with silicone implant exposure. C, Preoperative lateral view. D, Design of latissimus dorsi musculo-
cutaneous flap. E, Postoperative anterior view 6 months after implant coverage with latissimus dorsi musculocutaneous
flap. F, Postoperative lateral view. Note that the skin island of the flap provides stable coverage at the site of implant
exposure. G, Posterior view of flap donor site scar on right posterior trunk. See Figure 33-20.

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996 I • GENERAL PRINCIPLES
exposure may be associated with frank infection,
although exposure alone indicates only a prosthetic
contamination. Implant exposure is due to either active
infection or inadequate soft tissue coverage. Exposure
is generally at the mastectomy site. Management of the
exposed implant depends on the cause of the expo-
sure. If the skin edges become necrotic with subsequent
wound breakdown, simple wound care is appropriate
if muscle lies between the implant and incision. If the
implant is exposed at the incision, with early detec-
tion, wound debridement, implant and pocket irriga-
tion, flap coverage, and culture-specific antibiotic
coverage, it may be possible to salvage the implant. If
implant exposure is delayed with established peripros-
thetic infection, treatment involves immediate removal
of the implant followed by culture-specific antibiotics.
Delayed reconstruction can then be achieved at a
minimum of 6 months.134,424
KNEE. Knee joint exposure represents a problem
wound. This exposure may be the result of trauma,
tumor extirpation, or surgical reconstruction of the
knee. Wound infection and exposure of the prosthe-
sis, bone, or tendons can result in the removal of the
prosthesis, arthrodesis, and potential loss of the
affected limb. It has been shown by several investiga-
tors that early and adequate soft tissue coverage may
salvage the prosthesis (Fig. 33-79).425'427
Management of exposed extremity hardware
depends on the viability of the underlying bone. If the
underlying bone is stable, the plate can be removed,
B
FIGURE 3 3 - 7 9 . Exposed knee prosthesis (intrinsic factor: infection; mechanical factor: exposed prosthesis). A, Knee
prosthesis and infected joint space after resection of sarcoma and immediate knee reconstruction. B, Arteriogram of
same patient reveals patent medial sural artery to medial gastrocnemius for flap design (arrows). C, Design of trans-
verse skin island at distal medial gastrocnemius muscle.
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sterilized, replaced, and covered. If the underlying bone
is of questionable viability or the surrounding tissues
are nonviable, the plate must be removed and an alter-
native method of bone stabilization, such as external
fixation, substituted.
When one is confronted with this problem, the
surrounding tissues should be thoroughly debrided;
the prosthesis is sterilized in situ and covered with
a muscle or musculocutaneous flap. In addition to flap
coverage, an adequate irrigation system should be
placed for postoperative care. If purulent drainage
from the bone is seen and there is a clear lack of solid
fixation indicating that the infection has invaded the
prosthesis stem, the prosthesis must be removed.
VASCULAR. Vascular prosthesis exposure is an
uncommon but a serious and potentially devastating
complication of reconstructive vascular surgery.
Exposed vascular prosthesis or vasculature represents
a problem wound requiring immediate attention. The
most common area affected is the groin, after exposure
and dissection of the femoral vessels for lower extrem-
ity bypass operations. The incidence has been reported
to be 1.6% to 6% of all vascular procedures requiring
a groin incision. Breakdown of these wounds is a serious
threat to the patient and can lead to loss of limb or life.
Limb loss and mortality rates for this complication range
from 25% to as high as 75%, depending on the loca-
tion of the graft and extent of the infection.428 Pros-
thesis exposure may be secondary to a technical error
at the time of groin closure or an infection. The
* *
image...

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 997

H
FIGURE 3 3 - 7 9 , cont'd. D, Position of skin island located on distal aspect of medial gastrocnemius muscle. E, Flap
passed through tunnel to anterior knee space. F, Flap inset directly over prosthesis. Antibiotic irrigation catheters are
placed in the joint spaces. C, Flap inset completed. The patient received a 6-week course of culture-specific antibiotic
t"homn\/ W D n c t / M - w s t ' a t U / a w i c m r al- fi m c o t - h c H o m r m c f - r a f - a c c t - s h l A u u / M i n r l rrwiaricia T h e nation*- hac maint-ainaH a m h n -

prosthetic graft is either woven or knitted with numer- 33-80).429 Exposure is considered a surgical emergency,
ous crevices and interstices that afford a safe harbor for and stable graft coverage must be achieved.
bacteria. Patients generally present with an abscess or The management of an infected prosthetic graft is
purulent drainage from the wound, an anastomotic generally graft resection and debridement of the sur-
hemorrhage, or an anastomotic false aneurysm (Fig. rounding necrotic tissue. Ideally, replacement of the

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998 I • GENERAL PRINCIPLES

FIGURE 3 3 - 8 0 . Exposed, infected vascular prosthesis (intrinsic factor: infection; mechanical

factor: prosthesis exposure). A, The patient underwent aortofemoral vascular bypass surgery,
and groin wound dehiscence from infection exposed the vascular prosthesis. B, Groin wound
debridement included resection of infected graft and extra-anatomic bypass. Left (contralateral)
rectus abdominis musculocutaneous flap is designed for right groin coverage. C, Flaps elevated
with preservation of vascular pedicle to muscle: deep inferior epigastric artery and associated
veins. D, Flap inset. The donor site is covered with a skin graft.

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image...
i
FIGURE 3 3 - 8 0 , cont'd. E, Postoperative view at 6
weeks demonstrates stable right groin coverage provided
by rectus abdominis musculocutaneous flap. See Figure
33-19. (From Logon SE.MathesSJ: Use of rectus abdom-
inis musculocutaneous flap to reconstruct the groin defect.
Br J Plast Surg 1984;37:351. Reprinted with permission
from The British Association of Plastic Surgery.)
graft with an autogenous graft is done on graft resec-
tion to maintain distal perfusion. If an autogenous
conduit is not available, cryopreserved allograft vein
can be used or an extra-anatomic bypass may be indi-
cated. The functional outcome depends in part on the
indication for the bypass (critical limb ischemia versus
claudication). In certain circumstances, leaving the graft
in situ is the only option.
The functional outcome of the extremities affected
by exposed prosthetic grafts in the groin has been greatly
improved with muscle flap coverage.430 Management
of these wounds with a well-vascularized regional
muscle flap provides stable coverage. Early management
of vascular graft infections with intravenous antibiotics,
aggressive debridement, and coverage with a muscle
TABLE 33-1 7 • FLAP SELECTION FOR PRESSURE SORE COVERAGE
Sacrum
1. V-Y gluteus maximus
2. V-Y gluteus maximus (contralateral)
3. Readvance bilateral V-Y gluteus
maximus
Other gluteal flap
Transverse back flap
Modified from Foster RD, Anthony JP, Mathes SJ, et al: Flap selection as a determinant of success in pressure sore coverage. Arch Surg 1997;132:868.
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33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 999
flap has proved effective.430,431 Muscle flaps improve
healing time and decrease the bacterial counts in the
wound. Commonly used muscle flaps that provide stable
groin coverage include the sartorius, rectus femoris,
and rectus abdominis muscles. Other muscles and flaps
described include the gracilis, vastus lateralis, and
anterolateral thigh flap as well as the omentum. Graham
et al432 achieved a 94% flap survival rate and a 71 % limb
salvage rate using sartorius muscle. Mixter et al433
achieved a 9 5 % success rate using rectus femoris.
SPINE. Midline wound dehiscence in the back
with exposure of spinal stabilization devices represents
a problem wound. In patients requiring spinal stabi-
lization after oncologic resection, the breakdown may
relate to preoperative or postoperative irradiation. The
hardware must often be kept in place to maintain spinal
fusion and stability. Patients are subject to spinal insta-
bility, incapacity to assume the erect position, and
potential neurologic compromise. 434,435 In addition,
wound breakdown may expose the dura, which rep-
resents a surgical emergency. The use of muscle and
musculocutaneous flaps provides excellent soft tissue
coverage, obliterates dead space, controls infection, and
may salvage spinal hardware. 436 Muscle and muscu-
locutaneous flap options include the gluteus maximus,
latissimus, paraspinous, and trapezius muscles.437'440
EXTRINSIC
Pressure Sores
Aggressive surgical debridement is of critical impor-
tance in the treatment of pressure sores. Debridement
of the ulcer, underlying bursa, and involved bone fol-
lowed by soft tissue coverage remains the standard
approach. These wounds are often inadequately
d^brided before reconstruction, which lends itself to
failure. All involved bone should be adequately
ddbrided and sent for microbiologic cultures intra-
operatively. The flap used for coverage should be as
large as possible, with placement of the suture line
away from the area of direct pressure, and the flap
design should not violate adjacent flap territories to
preserve all future options for coverage (Table 33-17).441
Ischium Trochanter
Inferior gluteus maximus island flap Tensor fascia lata ± V-Y
Inferior gluteal thigh flap Readvance tensor fascia lata
Readvance inferior gluteal thigh flap Vastus lateralis
V-Y hamstring Rectus femoris
Gracilis Inferior gluteal thigh flap
Tensor fascia lata (expanded or delayed) Rectus abdominis
Rectus abdominis
image...
1000 I • GENERAL PRINCIPLES
Unfortunately, despite advances in surgical treatment
of pressure sores, authors have reported recurrence
rates as high as 80%.442,443
The most common causes of reconstructive fail-
ures are surgical technique, inadequate immobilization,
and inattentive turning of the patient postoperatively.
Given this high recurrence rate, some authors advise
an algorithm for flap selection based on the area to be
covered. Foster et al444 have found that appropriate flap
selection and management significantly improve the
success rates for pressure sore coverage. A study of
ischial pressure sores revealed that the inferior gluteus
maximus island flap and the inferior gluteal thigh flap
had the highest success rates, whereas the V-Y ham-
string flap and the tensor fascia lata flap had the poorest
healing rates (Fig. 33-81). Sacral coverage was best
achieved with the gluteus maximus musculocutaneous
flap, by either transposition or V-Y technique, and the
gluteal island flap, which had success rates of 97% and
9 1 % , respectively (Fig. 33-82).445 Trochanteric cover-
age was best obtained by the tensor fascia lata flap with
a success rate of 93%. 444
Permanently disabled patients often continue to
have breakdown of the wound despite the best efforts
of debridement and flap reconstruction. Standard
reconstructive options may have been used, but addi-
tional skin, subcutaneous tissue, muscle, and bone may
require additional debridement, leaving the patient
with a significant defect. In these circumstances, cov-
erage may be provided with a pedicled omental flap
to the sacrum or by microvascular composite tissue
transplantation (Fig. 33-83).446On occasion,advanced
infection may require hemipelvectomy or lower
extremity amputation with fillet of thigh flap. Although
it is thought of as an indolent infection, necrotizing
skin infection is a rare complication of a chronic sacral
decubitus ulcer (Fig. 33-84).447 Prompt recognition and
treatment are required because mortality from these
infections is more than 50%.
Temperature
BURN W O U N D S . Burn wounds may present as
problem wounds, depending on the size and location
of the burn. Burn wounds may also present as problem
wounds after reconstruction with subsequent wound
breakdown from failed skin grafting. The burned
trauma patient represents a complex management
issue. Between 5% and 7% of all patients admitted to
burn centers suffer from nonthermal trauma in addi-
tion to their burn injuries.448,449 These problem wounds
may have combined burns with underlying bone
fractures and nerve, tendon, or vascular disruption.
Systemic factors, such as burn wound sepsis, may also
contribute to nonhealing of burn wounds. Burn
wound sepsis develops in the local wound and is
difficult to manage because of the presence of dead
and denatured burn eschar, moist environment, and
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dysfunction of the immune system. Local wound sepsis
then leads to a generalized sepsis, which endangers the
patient's life. This complication underscores the need
for aggressive and adequate debridement.450
Debridement of these wounds should include all
nonviable or infected tissue. Tangential excision is the
technique of burn wound debridement. By use of a
guarded skin knife or dermatome, successive thin layers
of burn tissue are removed until all nonviable tissue
is excised as indicated by capillary bleeding. This
debridement should not be more than 20% of total
body surface area and should be done every 48 to 72
hours as needed until all burned tissue is excised. It
has been shown that early wound excision, topical
antimicrobials, and improved wound dressings have
decreased the incidence of burn wound sepsis. The
areas of burn excision are covered with thin cutaneous
split-thickness skin grafts, homograft skin substitute,
or cultured epithelium, depending on total surface area
of the burn and available donor sites.
Early wound excision is associated with a reduced
mortality rate and blood loss as the original tissue is
removed before the characteristically vascular tissue
is formed. Patients with circumferential wounds of the
extremities or chest wall must be monitored closely
for evidence of vascular or ventilatory compromise.
The eschar that develops forms an inelastic barrier
under which edema collects to a point at which tissue
pressure exceeds venous pressure. This represents a
surgical emergency, and escharotomy must be per-
formed. The escharotomy must be extended from the
proximal to the distal margin of the burned area; it
should be carried across involved joints and down
through the eschar and the superficial fascia to a
depth sufficient to allow the cut edges of the eschar
to separate.
Coverage of burn wounds depends on the remain-
ing soft tissue structure underneath. Superficial wounds
can be covered with autologous skin graft if sufficient
donor sites are available. Other coverage options
include allografts (cadaveric skin) and cultured epithe-
lium. When the area of the burn wound is large or
adequate autograft is not available, allograft is used.
Allograft prevents wound desiccation; promotes mat-
uration of granulation tissue; limits bacterial prolif-
eration in the burn wound; prevents exudative protein
and red blood cell loss; decreases wound pain, thereby
facilitating movement of involved joints; diminishes
evaporative water loss from the burn surface; and serves
to protect tendons, vessels, and nerves. Cultured
epithelium (keratinocytes) has also been used for cov-
erage in extensive burn wounds.451,452 The usefulness
of this therapy has been limited because of the length
of time it takes to culture a clinically significant amount
(3 to 4 weeks), the low resistance to mechanical trauma,
and the late occurrence of wound contraction and scar
formation.453
image...

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 1001

FIGURE 3 3 - 8 1 . Right ischial pressure sore coverage by inferior half of gluteus maximus muscle (intrinsic
factor: infection; extrinsic factor: pressure). A, Paraplegic patient with chronic right ischial pressure sore.
B, Design of skin island over right inferior half of gluteus maximus muscle. C, Debridement of left ischial pres-
sure sore including partial ischiectomy. The flap is elevated with use of only the inferior half of the gluteus
muscle. The superior half of the muscle is preserved. Overlying skin territory is elevated to ischium. Distal half
of skin island is de-epithelialized. D, Postoperative view at 6 months demonstrates stable coverage of left ischial
pressure sore with inferior half of gluteus maximus musculocutaneous flap. See Figure 33-27. (From Mathes
SJ, Nahai F: Clinical Applications for Muscle and Musculocutaneous Flaps. St. Louis, CV Mosby, 1982.)

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 • GENERAL PRINCIPLES

FIGURE 3 3 - 8 2 . Sacral pressure sore coverage by superior half of gluteus maximus musculocuta-
neous flap (intrinsic factor: infection; extrinsic factor: pressure). A, Sacral pressure sore. B, Debride-
ment of sacral pressure sore including resection of exposed outer table of sacrum. C, Elevation of
superior half of gluteus maximus musculocutaneous flap with division of mid-muscle and release of supe-
rior half of muscle's insertion. D, Arc of rotation of flap to sacrum. E, Muscle inset directly into defect.
The donor site is closed directly with a small area of muscle flap skin grafted to avoid tension at the
donor site closure. F, Postoperative view at 6 months demonstrates stable coverage at sacral defect
reconstruction site. See Figure 33-43.

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 33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 1003

FIGURE 3 3 - 8 3 . Sacral pressure sore extending into thoracic and lumbar space (intrinsic
factor: infection; extrinsic factor: pressure). A, Paraplegic patient has multiple failures for pres-
sure sore management. Both legs are amputated with anterior thigh flap coverage of pelvis.
Recent hemorrhage and infection of sacral defect extend into the posterior thoracic regions.
B, Debridement of sacrum, paravertebral tissue, and twelfth rib posteriorly. C, The patient
turned to supine position to elevate omental flap based on left gastroepiploic artery and asso-
ciated veins. D, Left colon mobilized and omentum tunneled through paravertebral region medial
to ureter to reach posterior thoracic-sacral defect. E, Omental flap inset into defect. Skin grafts
are placed on exposed portions of omentum. F, Postoperative view at 6 months demonstrates
stable coverage of posterior sacral-thoracic pressure sore.

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1004 I • GENERAL PRINCIPLES

^^^^

•
•

ML
j^k -*•
^mr \-
1^^^ " MX s»
&w\
V

FIGURE 3 3 - 8 4 . Synergistic gangrene from infected ischial pressure sore (intrinsic factor: infection; extrin-
sic factor: pressure). A, Synergistic gangrene of posterior thigh extends into peritoneum from infected ischial
pressure sore in a paraplegic patient. B, Emergency wound debridement includes right lower extremity ampu-
tation with preservation of anterior thigh muscles and overlying skin. C, Management in this septic patient
included emergency colostomy and multiple wound debridements, including excision of entire ischium. Ante-
rior thigh flap is preserved. Arc of rotation of flap is demonstrated. D, Postoperative view at 6 months. Stable
wound coverage is provided by the anterior thigh flap. Note transverse back flap used for sacral pressure sore.
See Figure 33-10. (From Mathes SJ, Nahai F: Clinical Applications for Muscle and Musculocutaneous Flaps.
St. Louis, CV Mosby, 1982.)

Even with expeditious management of burn
wounds, breakdown of the covered wound still occurs.
These patients suffer from poor nutrition as well as
hypovolemia, which contributes to poor wound
healing. Thus, the management of burn patients
should focus on adequate nutrition and volume
hydration.
Scalp. Burn wounds of the skull require standard
burn wound care as well as special attention to the
depth of burn on the involved scalp. A high incidence
of acute morbidity is associated with burns involving
the skull. Hunt et al454 showed that systemic or local
septic complications developed in 50% of all patients
who required bone debridement. Early management
requires recognition, protection, and preservation of
involved skull.455 Groenevelt et al recommended pre-
liminary coverage with a glycerol-preserved allograft
wound dressing; this significantly improves the
development of granulation tissue, which then accepts
an autograft at a later stage. Severe burns with large
areas of exposed calvaria represent a difficult problem
(Fig. 33-85). In a series of 119 children with full-
thickness calvarial wounds, the optimal management
was shown to be staged debridement of the desiccated
outer bone table. The wounds then quickly granu-
lated and were autografted without problem. 456 Some
authors suggest that when it is feasible, early excision
followed by immediate flap coverage is the procedure
of choice. This avoids multiple operative procedures,
and the vascularized muscle coverage lessens the
susceptibility to infection. Ideal tissue to transplant
to the scalp includes the latissimus dorsi muscle and
the omentum. 164,457 When burned calvaria remains
intact, flap coverage may provide stable coverage
without the necessity of bone debridement. Treatment
of exposed skull with topical antibiotic therapy may

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image..

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE

A B

FIGURE 3 3 - 8 5 . Electrical burn, scalp (extrinsic factor: temperature). A High-voltage elec-

trical injury involves posterior scalp and upper extremities. The exposed skull is treated with
topical silver sulfadiazine. B, The patient has severe electrical injury with bilateral upper
extremity amputations. Function-preserving technique is used for the trapezius musculocu-
taneous flap. The skin island is on the right posterior thorax. C, Arc of rotation of vertical
trapezius musculocutaneous flap to posterior scalp. D, Superior third of fibers left intact to
preserve shoulder function. Continued

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1006 I • GENERAL PRINCIPLES
FIGURE 3 3 - 8 5 , cont'd. E, Postoperative view at 6
weeks demonstrates stable skull coverage. The donor site
is intact. See Figure 33-30.
avoid the necessity for skull debridement due to
osteomyelitis.
Trauma
ABDOMINAL WALL. Acute traumatic abdominal
wall defects require immediate attention. Depending
on the mechanism of injury, there may be other organ
system injuries. The acute abdominal problem wound
can be divided into two categories: those associated
with unstable abdominal contents and those associ-
ated with stable abdominal contents.458 In the patient
with unstable abdominal contents (acute unstable
wound), urgent surgical intervention is frequently
required for intra-abdominal injury or disease (e.g.,
a shotgun wound to the abdomen or repair of a rup-
tured abdominal aortic aneurysm). Until the under-
lying organ system derangements are corrected or
stabilized, the unstable wound is treated with either a
temporary absorbable mesh or gauze packing with
scultetus-type support of the abdominal contents. This
treatment continues until the abdominal wound and
underlying organs are converted from an unstable to
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a stable wound, after which definitive closure can occur.
In the patient with an acute abdominal wall disrup-
tion with stable intra-abdominal contents (acute
stable wound), a decision can be made either to correct
the defect in the acute setting or to proceed with local
wound management and treatment of concurrent
medical illness while reconstruction of the abdomi-
nal wall is planned (Fig. 33-86).
Abdominal compartment syndrome most com-
monly occurs after blunt trauma, but it may occur after
an abdominal operation.459 The consequences of
abdominal compartment syndrome are profound and
affect many vital body systems. Hemodynamic, respi-
ratory, and renal abnormalities are hallmarks of
abdominal compartment syndrome. In addition, the
overlying abdominal wall is at risk for breakdown sec-
ondary to decreased perfusion. Recognition and
prompt decompression are critical to avoid disastrous
consequences. Management consists of urgent decom-
pressive laparotomy. The abdomen can then be left open
or temporarily covered with mesh. Definitive recon-
struction is deferred until a more optimal time.460 A
method of abdominal wound management described
for the open abdomen in abdominal compartment syn-
drome461 involves temporary placement of a vacuum-
assisted wound closure dressing. Once the edema
resolves, the abdominal wall fascia can frequently be
closed primarily.
When planning reconstruction of traumatic
abdominal wall defects, one must take into account
the defect components. This is often difficult in the
acute setting. These components include skin, subcu-
taneous tissue, muscle, and fascia. Large open wounds
with fascial defects can be managed with split-thick-
ness skin grafts; closed fascial defects can be managed
with intraperitoneal mesh placement.462,463 In addition,
the separation of parts technique, whereby sliding
rectus abdominis musculofascial flaps are advanced to
provide abdominal wall closure, has proved useful.
Other reconstructive options include local transposi-
tional flaps and microvascular composite tissue trans-
plantation (see earlier abdominal wall section).
HEAD AND NECK. Management of traumatic
wounds to the head and neck depends on extent of
soft tissue injury, status of underlying bone, and
whether there is exposure of the central nervous system
or a CSF leak. The airway, breathing, and circulation
in addition to neurologic injuries and emergencies must
be dealt with first, followed by management of soft
tissue injuries. Problem wounds can be associated with
large soft tissue defects (scalp or face avulsion), soft
tissue injury with underlying bone loss or commin-
uted fractures, facial nerve injury, or infection.
After the patient is stabilized, a thorough head and
neck examination is performed, including a complete
cranial nerve evaluation with documentation of any
image...

33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 1007

FIGURE 3 3 - 8 6 . Abdominal wall trauma (extrinsic factor: trauma). A, Shotgun wound with traumatic loss of
abdominal wall and visceral injury and exposure. Anterior view of abdominal wall before emergency explo-
ration. B, Wide excision of devascularized full-thickness abdominal wall and repair of visceral injuries. C, Intraperi-
toneal placement of Prolene mesh to re-establish abdominal wall continuity. D, After presentation of granulation
tissue through interstices of the mesh, split-thickness skin grafts provided cutaneous coverage directly on mesh.
Later elective surgery included colostomy closure and local flaps over Prolene mesh. See Figure 33-25. (From
Steinwald PM, Mathes SJ: Management of the complex abdominal wall wound. Adv Surg 2001 ;35:77.)

deficits. Adequate debridement of the wound is essen-
tial. All necrotic tissue and bone must be excised before
closure or coverage. Exposed cranium does not require
immediate coverage and can be managed with local
wound care until coverage is achieved. When a problem
wound involves exposure of the skull, the treatment
is based on the presence or absence of the periosteum.
If the periosteum is intact, a skin graft may be
sufficient. If the periosteum is absent, a vascularized
regional or distant flap may be needed for closure.
Cranial bone reconstruction is generally delayed until
flap coverage is accomplished and the patient has
recovered from the traumatic event.
Massive penetrating trauma to the face, commonly
seen after close-range, high-velocity gunshot or
shotgun wounds, requires complex reconstructive
procedures (Fig. 33-87). Once the airway is established
and hemorrhage is controlled, the complexity of the
wound is assessed. These wounds involve not only the
skin and soft tissues of the face and the underlying
facial skeleton but also the lining and other compo-
nents of the oral cavity and nasal passages. These

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1008 I • GENERAL PRINCIPLES
FIGURE 3 3 - 8 7 . Gunshot wound to the face (extrinsic factor: trauma). A, Traumatic loss of partial lower and
middle third of face. B, Postoperative view after staged reconstruction.
wounds may also extend into the cranial vault, result-
ing in CSF leaks or brain herniation. Draining CSF
is dangerous because this is a portal for infection.
Wounds involving the sinuses, especially the frontal
sinus, need to be surgically obliterated to protect the
anterior cranial vault.
Reconstruction of these defects must be well
planned. Several components of the reconstruction
must be addressed: the lining and integrity of the
oronasal cavity and air passages must be restored; lost
bone and soft tissues must be replaced; and an attempt
must be made to restore the competence of the oral
sphincter and to re-establish facial animation. The
reconstructions are often planned as multistage pro-
cedures and frequently require more than one flap with
a combination of local flaps, microvascular tissue trans-
plantation, and tissue expansion.
EXTREMITIES. Extremity wounds often present as
problem wounds, on the upper and lower extremity,
and involve soft tissues and bone as well as vessels and
nerves. Traumatic injuries of the extremities may
involve all essential components. Skeletal stability and
restoration of circulation are of paramount impor-
tance. The timing of soft tissue coverage will vary
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according to local conditions. Immediate coverage of
vascular grafts, orthopedic hardware, and bone
denuded of periosteum is essential.
Open Fractures. It is often difficult in high-impact
blunt trauma to delineate the zone of injury and the
viability of surrounding tissues (Figs. 33-88 and 33-
89). The possibility of vascular disruption must be con-
sidered early in the management of a patient with severe
extremity trauma. A missed diagnosis or delay in diag-
nosis may have disastrous consequences leading to loss
of the limb. The circulation must be re-established
immediately, and if a graft is required, an autologous
vein graft is preferred over a synthetic graft. Most choose
to fill the bone gaps at a secondary procedure to ensure
that the soft tissue envelope will be adequate to
provide coverage to the bone repair. Bone gaps may
be repaired with cancellous bone grafts, Ilizarov bone
lengthening, or vascularized bone grafts.
Lower Extremity Bone Nonunion. Bone nonunion
may be a component of a problem wound. These
wounds often develop after a traumatic injury involv-
ing soft tissue as well as the underlying bone. In a trau-
matic wound, nonunion may be secondary to infection
or disruption of the blood supply to the bone. Bone
nonunion may also occur after benign or malignant
 33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE

FIGURE 3 3 - 8 8 . Shotgun wound to upper extremity with bone and vascular injuries
(extrinsic factor: trauma). A, Sequential wound debridement; exposed vein graft for arte-
rial reconstruction and exposed humeral fracture with intramedullary rod. B, Design of
transverse thoracic flap. C, Elevation of transverse thoracic flap based on musculocuta-
neous perforators from pectoralis major and rectus abdominis muscle. D, Flap is inset over
defect after wound debridement, and fracture stabilization with medullary rod is com-
pleted. E, Early postoperative result. F, Flap provides stable coverage over defect in upper
arm. (From Mathes SJP Nahai F: Clinical Applications for Muscle and Musculocutaneous
Flaps. St. Louis, CV Mosby, 1982.)

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image...

1010 I • GENERAL PRINCIPLES

FIGURE 3 3 - 8 9 . Crush-avulsion injury to right pelvis and lower extremity (extrinsic factor: trauma). A, The
patient was crushed between train cars with resultant extensive soft tissue and skeletal injuries. B, Postoper-
ative view at 1 year demonstrates fracture and soft tissue healing with skin graft coverage on preserved mus-
culatures. See Figure 33-26.

tumor resection with placement of allograft material.
This nonunion occurs at the allograft-host junction.
Nonunion of the allograft-host junction after massive
allograft transplantation for patients with malignant
bone tumors is not an uncommon complication. Many
of these patients have been treated with either
chemotherapy or radiation therapy, and it has been
shown that patients treated with adjuvant therapy have
a higher incidence of nonunion.464"466 In addition to
the nonunion, many patients have an unstable soft
tissue envelope. Patients with traumatic wounds of the
lower extremity resulting in an infected tibial nonunion
are at risk for amputation of the affected extremity
(Fig. 33-90).
The management of bone nonunion involves
debridement of the nonviable bone and restoration
of bone continuity. Lower extremity bone continuity
may be restored with the techniques of Ilizarov or
autogenous cancellous bone graft placement. Ring et
al467 showed that if a well-vascularized soft tissue enve-
lope is present, bone grafting procedures are safe and
efficacious. If the skin and soft tissue envelope is not
adequate, bone debridement and simultaneous
microvascular flap transposition may be necessary
in a subsequent procedure to establish bone union.
After wound closure is accomplished, the Ilizarov tech-
nique may be best suited for the treatment of very
proximal or distal metaphyseal nonunions and
nonunions associated with large leg length discrep-
ancies (Fig. 33-91).
Achilles Tendon Rupture. The Achilles tendon is
the strongest tendon in the body. Defects of the Achilles
tendon are most commonly due to trauma.468,469
Difficulty in reconstruction arises after attempted
primary repair with subsequent infection and loss of
significant tendon substance. Loss of this tendon results
in impaired plantar flexion of the foot. Given the history
of trauma in most patients, an overlying soft tissue

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33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 1011

FICURE 3 3 - 9 0 . Open infected distal tibial fracture requiring staged wound management, flap cov-
erage, and vascularized bone transplantation (intrinsic factor: infection; extrinsic factor: trauma). A and
B, Infected fracture of distal tibia and ankle of 6 weeks' duration with medial wound harboring dead
bone and tendon. C and D, Composite defect of 12 cm after initial debridement.
Continued

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1012 I • GENERAL PRINCIPLES

FIGURE 3 3 - 9 0 , c o n t ' d . E, Latissimus dorsi microvascular transplantation and end-to-side anastomoses to poste-
rior tibial vessels 7 days after initial debridement. F, Osseous defect maintained with antibiotic beads for 5 weeks
before vascularized bone graft from contralateral fibula is anastomosed end-to-side to anterior tibial vessels. Fibula
from ipsilateral leg is transferred 3 weeks later (fourth operation). C and H, Postoperative views at 8 weeks show bone
union and graft consolidation. The patient has had no recurrence of infection. (From Nahai F, Cierny G: Dialogues: lower
extremity reconstruction: part II. Perspect Plast Surg 1988;2:115.)

defect may also be present. Initial local wound man-
agement may allow conversion into a stable, chronic
wound. For partial dehiscence of the tendon, local
wound contraction may allow healing with intact
tendon function. An option for complete tendon
disruption, and failed repair with local or distant
transposition flap coverage with a tendon graft, is
microvascular composite tissue transplantation with
a tendon graft or muscle incorporated into the tendon
defect. Local flap options include the medial plantar
flap, peroneus brevis muscle, gastrocnemius fascial flap,
and flexor hallucis longus flap. Tendon may be replaced
with strips of the tensor fascia lata, palmaris longus
tendon, plantaris tendon, or extensor carpi radialis
tendon.468,469 Microvascular composite tissue trans-
plantation includes the radial forearm, lateral arm,
tensor fascia lata, and gracilis flaps (Fig. 33-92).
Caustic Substance Exposure
INTRAVENOUS EXTRAVASATION. Although extrava-
sation is usually recognized early and remains local-
ized, certain subsets of patients develop severe necrosis
and a problem wound. The result of extravasation is
often more serious than the original injury and is often
underestimated. Extravasation into a closed com-
partment may lead to a compartment syndrome of
the affected extremity, and the patient must be closely
monitored for this complication. In addition to skin

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33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 1013

t *
B

D E F
FIGURE 3 3 - 9 1 . Open infected distal tibial fracture requiring wound and bone debridement, immediate flap trans-
plantation, and application of llizarov appliance (intrinsic factor: infection; extrinsic factor: trauma). A, Fracture site 1
month after injury. B, Preoperative arteriogram demonstrates patent posterior tibial artery (pt) and occluded peroneal
(pa) and anterior tibial (at) arteries. C, Rectus abdominis muscle flap ready for transplantation for wound coverage.
D, Flap inset into bone defect and skin graft placed on exposed muscle surface. E and F, llizarov apparatus in place.
The arrows indicate the site of debridement and flap transplantation. Continued

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1014 I • GENERAL PRINCIPLES

FIGURE 3 3 - 9 1 , cont'd. 0, Radiograph of proximal tibia. Proximal osteotomy (os) allows progressive migration of
proximal tibia into 6-cm bone gap to achieve bone union and preserve tibial length. H, Radiograph demonstrates new
bone formation within periosteal sleeve in proximal tibia (arrows) and advancement of distal tibia across site of bone
gap. / and J, Postoperative views at 1 year demonstrate stable wound coverage. Ilizarov technique achieved bone
union. The patient is ambulatory and without evidence of infection. K, Radiograph demonstrates tibial union at frac-
ture site. (From Mathes SJ( Nahai F: Reconstructive Surgery: Principles, Anatomy, and Technique. New York, Churchill
Livingstone, 1997.)

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 33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE 1015

FIGURE 3 3 - 9 2 . Infected Achilles tendon (intrinsic factor: infection; extrin-

sic factors: trauma and surgery). A, Chronic wound infection at Achilles tendon
rupture site after two attempts at repair. B, The gracilis muscle for microvas-
cular transplantation to site of Achilles tendon debridement. C, Gracilis muscle
inset after revascularization. The distal muscle is sutured to the gastrocne-
mius stump, and the proximal muscle is sutured to the remaining Achilles
tendon at the calcaneal insertion. Microvascular repair is performed at distal
tibial artery and vein. D, Postoperative lateral view at 2 years demonstrates
stable coverage provided by muscle flap with skin graft coverage. E, Poste-
rior view. F, Postoperative view at 4 years. Plantar flexion is fully recovered.
G, Foot dorsiflexes freely; there is no contracture. (From Mathes S: Man-
agement of chronically infected lower extremity wound by free gracilis muscle
transfer. In Brent B, ed: The Artistry of Reconstructive Surgery. St. Louis, CV
Mosby, 1987:711-717.)

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1016 I • GENERAL PRINCIPLES

necrosis, the extravasated substance may also cause a
local tissue reaction with scarring around tendons,
nerves, blood vessels, and joints.470 The severity of the
injury varies between extravasated substances and is
more severe in patients with intrinsic wound healing
deficiencies.
Several local, systemic, surgical, and nonpharma-
cologic treatments have been proposed for extravasa-
tion.471 Given the variable amount of soft tissue
involvement, early conservative therapy is recom-
mended. Nonpharmacologic treatment includes
immediate discontinuation of the infusion once
extravasation is suspected and attempted aspiration
of the fluid back through the same needle. Some authors
advocate liposuction and saline flush-out of the
affected area. If this is done early, it has been found
that this technique results in healing without any soft
tissue loss in the majority of patients.470 Given the
significant amount of tissue destruction that may
develop, some advocate early surgical excision and irri-
gation to avoid continued tissue breakdown.472 The sub-
sequent wound that results from debridement may
include significant soft tissue loss in addition to a vari-
able amount of tendon, nerve, or joint destruction.
Treatment will be tailored for the specific defect and
may include skin grafting, local muscle or fasciocuta-
neous flaps, tendon transplantation, or microvascular
composite tissue transplantation. Treatment must
also restore function of the affected extremity when
possible (Fig. 33-93).
ENVENOMATION INJURY
Snakebites. Treatment involves identification of the
type of snake responsible and stabilization of the patient
with adequate hydration with 2 liters of an isotonic
solution (see Figs. 33-35 and 33-36). Antivenom is deliv-
ered in those patients who have been judged to have
a significant envenomation as based on a progressive
clinical deterioration and for children younger than
12 years.473 Moderate to severe envenomations cause
systemic effects including vomiting, shock, coagu-
lopathy, renal failure, and altered mental status.
Antivenom is given more often for rattlesnake enven-
omation than for copperhead or cottonmouth enven-
omation. The dose of antivenom given depends on the
clinical severity of the envenomation.

FIGURE 3 3 - 9 3 . Chemotherapeutic agent extravasation at intravenous site (extrinsic factor: caustic and chem-
ical substance exposure). A, The patient has an extensive wound at the site of delivery of 5-fluorouracil for
treatment of lung cancer. 8, Postoperative view 3 months after debridement and skin grafts demonstrates
stable coverage. C, Range of motion preserved—full flexion. D, Full extension. See Figure 33-37.

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33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE
Treatment options for snakebites include incision
and suction, loose tourniquet, antibiotics and tetanus
prophylaxis, and debridement. 474 Incision and suction
have proved beneficial only in the first 45 minutes of
the bite. The incision is carried through the skin only
at the site of the fang entrance, after which suction is
applied. If a delay in transport to the hospital occurs,
a tourniquet should be loosely applied. A proximal
tourniquet will reduce the venom dissemination from
the affected limb by 50%. Tourniquets applied too
tightly will exacerbate the tissue loss in the affected
extremity.474 Antibiotics and tetanus prophylaxis are
appropriate for all patients. Rattlesnake fangs have been
shown to harbor gram-negative organisms, and
clostridial infections have been reported.475,476 Local
debridement occurs after the patient is stable and is
warranted in those patients with tissue necrosis. Some
authors recommend aggressive early local excision,476,477
whereas others advocate a more conservative
approach. 473,478 The involved extremity must be
evaluated for possible compartment syndrome.
Fasciotomy should be done if indicated by elevated
compartment pressures or subjective complaints of
pain, paresthesias, or compromised blood flow.
Spider Bites. Envenomations from two common
North American spiders may lead to problem wound
development. These two species are Latrodectus, which
includes the black widow spider, and Loxosceles, which
includes the brown recluse spider (see Fig. 33-32).
The adult female black widow spider is approxi-
mately 2 cm in length and shiny black with a red-orange
hourglass spot on the ventral abdomen. The male is
smaller and incapable of envenomating humans. 479 The
web of the black widow spider is irregular and low-
lying; it is commonly seen in garages, barns, outhouses,
and foliage throughout the continental United States.
The toxin of this spider is a potent neurotoxin (a-
latrotoxin) that opens presynaptic cation channels
(including calcium channels), causing increased release
of multiple neurotransmitters, which results in excess
stimulation of motor end plates. The predominant clin-
ical effects are neurologic and autonomic as well as
dermal necrosis at the site of envenomation. Within
30 minutes, the patient begins to exhibit systemic
symptoms. Symptoms include muscle cramping that
begins locally around the bite and progresses to
include large muscle groups, such as the abdomen,
back, chest, and thighs. Abdominal rigidity may mimic
an acute abdomen. Local effects are initially limited
to a small circle of redness around the immediate bite
site associated with sharp pain. This area generally does
not progress to tissue necrosis. Treatment involves sta-
bilization of the patient including airway, breathing,
and circulation, as needed. If a black widow bite is
suspected, a 10-mL dose of a 10% solution of calcium
gluconate should be administered during 15 to 20
minutes. The calcium gluconate should control the
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017
pain as well as confirm the diagnosis of a black widow
bite. The neurologic manifestations are treated with
a muscle relaxant such as diazepam. A 2.5-mL vial of
antivenom should be given to those patients with
significant envenomation. This treatment should be
weighed against the possibility of allergy to the
antivenom.
The brown recluse spider varies in size and can be
2 to 3 cm in length; it has characteristic violin-shaped
markings on its back. This spider is naturally nonag-
gressive and lives in attics, woodpiles, and storage sheds
throughout the southern United States. The spider
causes a local skin and tissue injury with envenoma-
tion termed dermonecrotic arachnidism. Loxoscelism
is the term used to describe the systemic clinical syn-
drome caused by envenomation from the brown
recluse spider. The brown recluse spider venom is cyto-
toxic and hemolytic. It contains at least eight compo-
nents, including enzymes such as hyaluronidase,
deoxyribonuclease, ribonuclease, alkaline phosphatase,
and lipase. Sphingomyelinase D is thought to be the
protein component responsible for most of the tissue
destruction and hemolysis caused by the brown recluse
spider envenomation. Along with the local tissue
destruction and hemolysis, the envenomation may
cause a coagulopathy, renal failure, and death. The bite
of the brown recluse shows a characteristic pattern.
Edema around the ischemic bite site produces the
appearance of an erythematous halo around the
lesion. At 24 to 72 hours, a single clear or hemorrhagic
vesicle develops at the site, which later becomes a dark
eschar. This erythematous margin continues to enlarge
peripherally secondary to the spread of the venom into
the tissues, causing extensive tissue destruction and
occasionally loss of the affected limb. Necrosis is gen-
erally more significant in fatty areas such as the but-
tocks, thighs, and abdominal wall. Treatment of the
brown recluse spider bite depends on the severity of
injury. Initial therapy should include application of a
cold compress, which functions to lessen the activity
of the temperature-sensitive sphingomyelinase D.
Dapsone, a leukocyte inhibitor, has been shown to be
effective in the management of the brown recluse spider
bite. A prospective study has shown that pretreatment
with dapsone, an antileprosy drug, not only reduced
surgical complications but also improved the outcome
of patients bitten by the brown recluse spider.480 Sur-
gical excision is limited to the infected or grossly
necrotic tissues.
THE FUTURE OF PROBLEM
WOUND MANAGEMENT
Topical Growth Factors
Growth factors are polypeptides that initiate cell
growth and proliferation. They have the ability to stim-
1018 I • GENERAL PRINCIPLES
ulate mitosis of quiescent cells. Although present in
small quantities in the wound environment, they have
profound effects. There are only a few studies in which
topical application of growth factors has been shown
to influence wound healing. The growth factors
involved in wound healing include PDGF, TGF-p, EGF,
FGF, and IGF. Platelets play a key role in the wound
healing process in that they are the primary source of
PDGF, TGF, EGF, and IGF. PDGF attracts neutrophils,
macrophages, and fibroblasts to the wound and serves
as a powerful mitogen. Investigators have exogenously
applied various growth factors to nonhealing wounds,
both in animal models and in human trials. In animal
models, application of b-FGF, TGF-p, and PDGF
increases both the rate of deposition of extracellular
matrix and the deposition and maturation of colla-
gen. The application of these growth factors also
increases the number and rate of formation of new
blood vessels. In humans, recombinant human PDGF-
BB has been shown to improve the overall healing
in lower extremity diabetic neuropathic ulcers in a
double-blind, placebo-controlled, multicenter study.
Complete wound healing occurred in 48% of the
treated group compared with 25% of the control
group.481 Human studies have shown that the appli-
cation of either PDGF or b-FGF to chronic wounds
decreased wound size by 19.6% and 10%, respectively,
compared with gauze-treated control wounds. Other
growth factors that show promise include TGF-P and
members of the FGF family. In the diabetic wound
model, application of b-FGF and PDGF restores the
ability of the wounds to produce granulation tissue
and close. Although PDGF is the only growth factor
approved for use in patients, it is likely others will be
approved for use.
Studies have not shown a tremendous effect of
growth factors on wounds; however, it is likely that
combinations of growth factors rather than a single
growth factor may provide the best wound healing
because the wound environment contains myriad
growth factors. Growth factors may prove beneficial
to the treatment of certain problem wounds that are
deficient in these factors. Specifically, chronic wounds
in debilitated patients may respond to the application
of topical growth factors.
Skin Substitutes and Stem
Cell Therapy
Skin substitutes have made significant advances in
recent years and may prove useful in the management
of problem wounds. Autologous skin grafts are still a
preferred method to treat skin defects, but donor site
morbidity and limited availability of autologous skin
remain problems. Expansion of skin produces a
limited amount of useful tissue, given that the
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expanded skin is largely epidermis and has minimal
dermal components.13M82,483 Current research is
directed at different materials and cells that can be
used to replace both epidermis and dermis. Skin sub-
stitutes may be derived from the process of tissue engi-
neering or from the propagation of one's own cells in
tissue culture. The composition of these skin sub-
stitutes varies from pure keratinocytes to a bilayer
dermal substitute. The use of epidermal grafts and epi-
dermal cell (keratinocyte) suspensions was first tried
in the animal model in the early 1950s. Currently, the
expansion of epidermis by the growth and matura-
tion of keratinocytes in culture is performed.484,485 A
small skin biopsy specimen can produce enough
autologous epithelium to cover the entire body surface.
However, on the body, the cultured epidermis often
blisters and sloughs because of slow restoration of the
basement membrane.486 In addition, replacement of
epidermis without the underlying dermis leads to
severe wound contractures and hypertrophic scars.
Restoration of damaged dermis remains a critical
unsolved problem.
Several dermal replacements based on synthetic
materials or cadaveric sources are in clinical use.487 A
bovine collagen- and shark proteoglycan-based dermis
(Integra) has been used primarily in burn patients for
more than a decade. This prosthetic dermis, available
in ready-to-use form, can cover large surface areas.488
Vascularization of this dermis takes 2 to 3 weeks, and
final epidermal coverage of the wound requires a thin
skin graft. The final result is functionally and aes-
thetically acceptable, but in the setting of acute burn
coverage, the engraftment rate of the material and high
cost have been problems. Despite its limitations, it is
the first promising dermal replacement to be widely
used and has a proven record of safety and efficacy.489
Cadaveric dermis with all of the cellular elements
removed is not antigenic and is not rejected by the
recipient patient. This human dermal matrix is com-
mercially available (AlloDerm) and functions much
like Integra with similar limitations of engraftment
and high cost. Both forms of dermal replacements are
more frequently used in delayed reconstruction of burn
patients rather than in the acute setting.490,491 The third
type of skin replacement uses a dermal matrix mate-
rial combined with mesenchymal cells (fibroblasts)
from an allogenic source (TransCyte), typically dis-
carded neonatal foreskin specimens,492,493 These prod-
ucts have the advantage of a matrix containing cells
that secrete growth factors and cytokines to acceler-
ate wound healing but have the disadvantage that the
recipient patient ultimately rejects the cells. Whether
these products are actually skin replacements or bio-
logic dressing is an issue because biologic dressing
would have limited use in patients with a large amount
of missing skin tissue. Apligraf, or "living skin equiv-
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33 • PROBLEM WOUNDS AND PRINCIPLES OF CLOSURE
alent," is a bilaminar skin equivalent produced by
seeding fibroblasts in type I bovine collagen
matrix.494,495 Human keratinocytes are then cultured
onto this medium and allowed to cornify. The result
is a two-layer living tissue with dermis and epithelial
components.
Cultured epithelial grafts are best suited for denuded
wounds that do not require additional tissue beyond
the epidermis. This treatment has been shown to be
beneficial in patients with large burn areas, traumatic
avulsion injuries, venous leg ulcers, and diabetic foot
ulcers and in neonates with epidermolysis bullosa and
giant congenital nevus. Studies have shown that
patients with extensive burns treated acutely with skin
1019
Electrical Stimulation
Certain investigators have advocated the use of elec-
trical stimulation in chronic wound healing. The basis
for this treatment is that intact skin possesses endoge-
nous electrical properties, with the surface more neg-
ative than deeper tissues.503 When the integrity of the
skin is disrupted, a potential difference between intact
and injured skin occurs during healing. Tissues sur-
rounding wounds are positively charged and attract
negatively charged cells, such as cells important in
wound healing—neutrophils, macrophages, fibro-
blasts, and keratinocytes. This process is termed gal-
vanotaxis. There are also data to suggest that electrical
stimulation may play a role in wound healing thr