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Plastic Surgery

Made Easy
Plastic Surgery
Made Easy

Prema Dhanraj
BSc MBBS MS (Gen Surg) MCh (Plastic) PDFBR (USA)
Professor and Head
Department of Plastic and Reconstructive Surgery
Christian Medical College and Hospital
Vellore, Tamil Nadu

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Plastic Surgery Made Easy


© 2006, Prema Dhanraj
All rights reserved. No part of this publication and DVD ROM should be reproduced,
stored in a retrieval system, or transmitted in any form or by any means:
electronic, mechanical, photocopying, recording, or otherwise, without the prior
written permission of the editors and the publisher.
This book has been published in good faith that the material provided by author
is original. Every effort is made to ensure accuracy of material, but the
publisher, printer and author will not be held responsible for any inadvertent
error(s). In case of any dispute, all legal matters to be settled under Delhi
jurisdiction only.

First Edition: 2006


ISBN 81-8061-786-6
Typeset at JPBMP typesetting unit
Printed at Gopsons Papers Ltd, A-14, Sector 60, Noida 201 301, India
I lovingly dedicate this book in fond memory of
my Mother and Father, Rosey and Dhanraj, who
taught me the value of life and to face difficulties
with strength, courage and grace. “Mum, Dad you
were a source of great inspiration through all my
difficult moments, in every step encouraging and
guiding me. Although you are not here today I
know and feel your guiding spirits which are as
strong and vibrant as ever. I also know that you
will be proud of all my achievements”. I thank God
for all His blessings and my wonderful family.
Foreword

It is indeed a previlege and honour to be asked by


Dr. Prema Dhanraj, Professor and Head of the Depart-
ment of Plastic and Reconstructive Surgery, Christian
Medical College and Hospital, Vellore to write a Foreword
to this book which is a creative work of Dr. Prema. But
there is another point of importance in my writing this
introduction.
THIS IS AN UNIQUE EVENT, as I believe that this
is the first time a patient who was treated by me
for burns, ultimately became a specialist in the dis-
cipline of plastic surgery and burns management,
and has written a book on burns.
The interaction between Dr. Prema and me began
when she was about eight or nine years old. She was
admitted in my surgical unit, Christian Medical College
and Hospital, with severe burns trauma. Her reconstruction
was a challenge to me and to my colleagues in my unit.
But this was not the only procedure. Prema underwent
several other procedures of excision and grafting and she
was discharged after five months, with a reasonably
satisfactory result.
Every single procedure caused pain at the time of
removal of dressings, and as a young girl she would,
of course, cry and be angry with some of the junior
viii PLASTIC SURGERY MADE EASY

doctors, if they removed the dressings in a hurried or


rough manner. When she was discharged, she had hardly
hair on her head, and there were yet some more pro-
cedures necessary on her face, which were done much
later.
During her stay in hospital I was impressed very much
by Prema’s fortitude under very difficult circumstances,
and her courage to overcome her handicap of a scarred
face. When Prema left CMC Hospital, I made two
promises to her. First, I promised to donate a part of my
hair to replace her lost hair. Secondly, I told her to become
a doctor and a specialist in plastic surgery with a specific
interest in the management of burns.
Thereafter I lost track of Prema for over fifteen years.
One day, a young lady walked into my office (I was the
Director of Christian Medical College and Hospital, Vellore,
by then), and said “Sir, I am your former patient, Prema.
I have come to make you fulfill your promises”. She
seemed to be a dynamic young lady, with charm and
poise. Of course, I recognized her immediately as my
former patient of almost two decades.
Prema then went on to say “ I have qualified to become
a doctor in my local city. Now I want you to make me a
plastic surgeon, with a special interest in burns”.
I was delighted to see her after so many years. Of
course, I could not fulfill my first promise of donating my
hair—I was quite bald by then and was in need of a
FOREWORD ix

donation myself !! But the second part of the promise I


fulfilled. Very soon, she joined the Department of Surgery
in CMC Hospital, Vellore, as a Surgical postgraduate
trainee in General Surgery, and passed the Master of sur-
gery examination in her first attempt, such a qualification
being a pre-requisite for further training and a Master’s
qualification in plastic surgery.
At CMC Hospital, Ludhiana, Dr. Prema received
excellent training and she really blossomed. She was an
excellent student and trained extremely well in the
speciality. She had skilled hands, but more so she had a
compassionate mind.
I received nothing but words of appreciation and
admiration from Dr. Prema’s teachers and colleagues. But
more so, for her patience in the Burns unit. I visited the
Burns unit in that hospital more than once (one of the
best Burns unit in India) and noticed the ‘look of adoration’
in the eyes of young women in that unit being treated for
burns. I could almost read the thoughts of these young
women—if you, Dr. Prema, like us, who also suffered
from severe burns, particularly of the head and face, could
make a success of your life as a doctor, then we
have also hope for our future.
That is the most important contribution Dr. Prema has
made, and continues to make, to the victims of burns,
young or old, men or women—restoration of hope among
those who have lost all hope, and who only looked
x PLASTIC SURGERY MADE EASY

forward to a bleak future of rejection, loneliness, depres-


sion, unhappiness and even suicide. Dr. Prema gives
courage, hope and the prospect of bright future to all the
unfortunate victims of burns, that makes them put away
all pessimistic thoughts and by her example she
demonstrates that all is not lost in life and that there
is yet a future.
To give hope to those who have lost hope, to give
courage to those who live in fear of the future, to give
confidence to those who have lost this gift and a purpose
and meaning to life—this continues to be Dr. Prema’s
mission.
More than once I have asked my former patient,
Dr. Prema the following question:
“Prema when you were my patient many, many years
ago, did you think that our future (yours and mine) would
be as has happened”. And her emphatic answer was “No,
Sir, but God has been good to me and to you”. She is
right, absolutely right.
Dr. Prema is not only a national figure, but is known
widely internationally. She has spent a few years in the
United States of America, adding to her knowledge and
skills in Plastic and Reconstructive Surgery. And more
recently, she has had a very good contact with an academic
center in Norway, some specialist doctors in the city of
Bergen, and in Ethiopia. She has established a training
program for doctors in Ethiopia to train under her in plastic
FOREWORD xi

surgery, particularly in the management of burns, in her


department of Plastic and Reconstructive Surgery here in
Vellore, supported by resources from Norway. Now her
department is recognized by the Medical Council of India
and the University in this State for the training of
postgraduate students in her speciality, leading to an M.Ch,
qualification. Thus, her knowledge and skills in the area
of her discipline is being shared not only within India but
also abroad.
I have briefly reviewed her book on Plastic Surgery. It
is ‘very easy’ to read and understand not only by doctors,
medical students, nurses and nursing students but also by
those who are not medically qualified.
This is the reason why I am so delighted to write a
Foreword to Dr. Prema’s book on Plastic Surgery. I would
like to conclude that Dr. Prema, her life and her
achievements are an example of the creative work of God
in a human being, and one cannot but wonder and feel a
sense of awe at God’s mighty power and accomplishment
through Dr. Prema and be grateful.
What of Prema’s future? What lies ahead of her? Is
the writing and the publication of this book the highest
point of her illustrious career so far? Certainly not ! I cannot
see “beyond the horizon—Prema’s horizon”. But I believe
firmly that Prema will achieve much in her life, of her
service to others, the unfortunate others and will be a
beacon of hope to many. Her talents are not merely in
xii PLASTIC SURGERY MADE EASY

her eyes and fingers, but in her mind also. And so there is
yet an acme in Prema’s life, the Mount Everest, for her to
conquer and I hope I will have the previlege of knowing
her entire career and lifetime of devoted work, perhaps
even writing another “foreword” to her autobiography!!

LBM Joseph
Retired Director and Professor of Surgery
Christian Medical College and Hospital
Vellore, India
Preface

Plastic and Reconstructive Surgery had its beginning


before Christ when surgeons in India reconstructed the
nose by transferring a flap from the forehead.
Plastic Surgery is a specialized area, but because of the
breadth of the discipline this book may be read by
Medical, Paramedical and Nursing students, as well as
speciality residents.
Most Interns, Senior House Surgeons and Residents
are not exposed to this speciality. Hence, it is more than
likely that they do not know what is done under the name
of plastic surgery. Many of them are bewildered when
they enter this new territory. This book is written to dispel
their confusions and misconceptions.

Prema Dhanraj
Acknowledgements

I would like to thank the many people, friends and my


colleague Dr. Ashish Gupta who enabled me to complete
this task. I am particularly grateful to my residents Dr. GI
Nambi, Dr. S Kumaran, Dr. Jeeth Isaac Jacob and
Dr. Sunil Babu Gotru who spent several hours at a time
for several weeks in gathering data and in organizing the
photographs, reviewing and proofreading the text. They
all deserve special thanks for their support in completion
of this book.
I thank all my Medical, Paramedical and Nursing
students who questioned me and were fascinated by the
creativity and artistic approach of Plastic Surgery. Their
enthusiasm inspired me to write this book in a simple
manner.
I specially thank my former surgeon and friend
Dr. LBM Joseph, who has been a source of great inspiration
for many years.
I thank M/s Jaypee Brothers Medical Publishers (P)
Ltd. for their help in this publication.
Contents

1. What is Plastic Surgery ....................................... 1

2. Wound Healing .................................................. 25

3. Skin and Subcutaneous Tissue ........................... 33

4. Skin Grafts ........................................................ 97

5. Skin Flaps ........................................................ 113

6. Muscle Flaps ................................................... 143

7. Fasciocutaneous Flaps ..................................... 155

8. Microsurgery ................................................... 159

9. Head and Neck ................................................ 163

10. Breast and Chest Wall Deformities .................. 227

11. Upper Extremity .............................................. 233

12. Lower Extremity .............................................. 239

13. Thermal Injury ................................................. 259

14. Aesthetic Surgery ............................................ 363

Index ............................................................................ 373


Chapter 1

What is Plastic
Surgery
2 PLASTIC SURGERY MADE EASY
DEFINITION
The term Plastic Surgery was coined by Vongraffe in 1818. The
word Plastic is derived from the Greek word “Plastickos” which
means to create, to shape, and to mould (The opposite of plastic is
elastic). Plastic Surgery is a multifacetted speciality that combines
form, function, technique and principle where deformities and
defects of the skin and underlying structures are dealt with. It is also
known as a problem solving speciality, as every patient presents
with a challenging problem requiring a unique solution.

Reconstructive Surgery
It is an attempt to restore the individual to near normal.

Cosmetic Surgery
It is an attempt to surpass the normal.
Plastic surgeons have to treat patients in a wholistic manner to help
them overcome not just their medical problems but also emotional
problems to improve self-esteem. Hence, the surgeon should be
flexible, creative, innovative, artistic and realistic. Most specialities are
limited by the area of the body or by age. Plastic Surgery transcends
all these. Plastic surgeons are, therefore, Craniofacial, Maxillofacial,
Reconstructive, Microvascular, General plastic, Hand, Cosmetic,
Oculoplastic and Burn surgeons.There is no limit to the number of
problems solved by the Plastic surgeon, the only limitation being the
patient’s needs and the surgeon’s imagination.
Craniofacial surgery is a discipline where congenital
deformities like Crouzon’s syndrome (Figs 1.1 and 1.2), Apert’s
syndrome and syndromes presenting with abnormal shape of the
bones of skull and face are corrected by repositioning and reshaping
these bones without any visible incisions on the face (Figs 1.3
and 1.4).
Microvascular surgery is a technique where large tissue is
taken from one part of the body to another for reconstruction by
connecting the vessels.This technique makes it possible even to re-
implant amputated parts of the body. The tissue transfer can be
only soft tissue (Fig. 1.5) or a composite of soft tissue and bone
(Fig. 1.6).
WHAT IS PLASTIC SURGERY 3

FIGURE 1.1: Crouzon’s FIGURE 1.2: Crouzon’s


preoperative postoperative

FIGURE 1.3: Apert’s syndrome FIGURE 1.4: Apert’s postoperative


preoperative showing incisions

Maxillofacial surgery is a discipline where facial bony


deformities are corrected. These deformities can be congenital or
acquired (Figs 1.7 to 1.9). This type of bony surgery is also
performed for aesthetic appearance of the face, where the bones
are reshaped to achieve the desired effect.
Reconstructive surgery is a vast field where defects and
deformities due to various causes are treated.The different
procedures performed can be for congenital, traumatic, infective,
malignant (Figs 1.10 to 1.12), burns (Figs 1.13 and 1.14)
and aesthetic purposes.
Aesthetic or cosmetic surgery is a discipline where body
sculpturing, nose surgery, face lift, breast enlargement and various
other surgeries are performed to give a better appearance to improve
the patients body image and self-esteem (Figs 1.15 and 1.16).
4 PLASTIC SURGERY MADE EASY

FIGURE 1.5: Radial


forearm freeflap

FIGURE 1.6: Free osteo


cutaneous flap

FIGURE 1.7: Preoperative FIGURE 1.8: Intraoperative showing


maxillofacial injury displacement of maxilla
WHAT IS PLASTIC SURGERY 5

HISTORY
Plastic surgery originated in India in
600 BC. Sushrutha is called the
“Father of Ancient Plastic Surgery”.
In 600 BC Sushruta described
operations of the nose and the ear
lobes. In India it was a common
practice to amputate the nose as a
mark of punishment. These patients
were operated by a group of people
called the koomas or the pot makers.
Knowledge of this Indian rhinoplasty
FIGURE 1.9: Postoperative after reached the west much later in
reduction maxillary fracture 1794.

FIGURE 1.10: Neck tumor preop FIGURE 1.11: Post excision tumor

FIGURE 1.12: Postoperative skin FIGURE 1.13: Preop burn


graft contracture neck
6 PLASTIC SURGERY MADE EASY

FIGURE 1.14A: Postoperative FIGURE 1.14B: Lady with Indian


release with STSG rhinoplasty in Vellore Fort

In the 14th century Italy used similar techniques by using tissue


from the arm and named it as Tagliacozzi arm flap for the
reconstruction of the nose. In the 20th century Herold Gillies of
England described tubed pedicle flaps. “Sir Herold Gilles” an ENT
surgeon is called the “Father of Modern Plastic Surgery”.
The first surgeon to publish a book on Principles and Practice
of Plastic Surgery is John-Staige Davis in 1924.

FIGURE 1.15: Depressed nose FIGURE 1.16: Postoperative


augmentation rhinoplasty
WHAT IS PLASTIC SURGERY 7

PRINCIPLES OF PLASTIC SURGERY


• Interpret the deformity in terms of loss and displacement of
tissues and the resulting functional impairment. Assess tissue
loss and the type of tissue involved
• Recreate the defect
• Plan and reverse plan, have a back up plan and if possible back
up of a back up plan
• The tissue to be transplanted should resemble the original tissue
• Repair of defect should not produce another visible deformity
• Always choose the most simplest technique and then progress
to complex methods
• Reconstructive ladder - planning includes the most simplest to
the most complicated procedure.

INJURIES
Facial injuries tend to be more common because there is no
protective covering. A facial injured victim often sustains multiple
injuries to other organ systems. Thus, suturing of facial injuries is
not an emergency and should be managed as soon as the patient’s
general condition is stable. Suturing skin lacerations on the face
may be complex.
Soft tissue injury of the face includes skin, muscle, nerves, blood
vessels and salivary glands.

Unique Characteristics of Face


• No protective cover
• High incidence of injury
• Rich blood supply
• Good lymphatic drainage
• Venous drainage is excellent as it is above the level of the heart
• Primary healing of the wound is good
• Muscles are attached to the skin to give beautiful facial
expressions and it deserves special attention due to its unique
function and aesthetic significance.
8 PLASTIC SURGERY MADE EASY
Challenges of a Surgeon
• To restore the face to preinjury appearance (Figs 1.17 and
1.18)
• Restoration of function (Figs 1.19 and 1.20)
• To return the patient to an active and productive life with minimal
aesthetic and functional disability.

Cause of Injury
• Motor vehicle accidents (Figs 1.21 and 1.22)
• Home and industrial accidents
• Assaults (Figs 1.23 and 1.24)
• Animal bites.

Investigations
• Plain X-ray: Waters’ view (PA) in prone position
• Reverse Waters’ view: Mento occipital position (when patient
cannot be placed in prone position)
• Orthopantogram (OPG)
• CT scan—visualizes both the soft tissue and bone.

Life-Threatening Facial Emergencies


• Respiratory obstruction—broken tooth, dentures, foreign body
and blood clots
• Hemorrhage—control with local pressure, dressing, application
of a clamp, ligation or packing
• Aspiration—oral secretion, gastric contents and blood.

Classification
• Soft tissue injury
• Soft tissue injury associated with fracture of bone
• Facial fracture without soft tissue injury

TYPES OF SOFT TISSUE INJURY


• Abrasion (Fig. 1.25)
• Avulsion (Figs 1.26 to 1.28)
WHAT IS PLASTIC SURGERY 9

FIGURE 1.17: Road traffic FIGURE 1.18: Postoperative


accident following reconstruction

FIGURE 1.19: Adherent skin in FIGURE 1.20: Intraoral view


thyroid carcinoma

FIGURE 1.20A: Cheek vascular FIGURE 1.20B: Post excision


tumor
10 PLASTIC SURGERY MADE EASY

FIGURE 1.21: Avulsion scalp FIGURE 1.22: Postoperative


rotation flap

FIGURE 1.23: Preop assault face FIGURE 1.24: Postoperative


following suturing

• Burn wound (Fig. 1.29)


• Contusion
• Laceration (Fig. 1.30)
• Punctured wound (Figs 1.31 and 1.32)
• Gunshot wound (Figs 1.33 and 1.34)

MANAGEMENT OF INJURIES
• Airway to be secured
• Cervical injury to be checked
• Hemorrhage to be controlled
• Shock treated
• Associated injuries evaluated
• Facial injuries to be tackled in the end
WHAT IS PLASTIC SURGERY 11

FIGURE 1.25: Abrasion FIGURE 1.26: Preoperative


avulsion face

FIGURE 1.27: Postoperative FIGURE 1.28: Scalp avulsion


avulsion face

FIGURE 1.29: Burn wound FIGURE 1.30: Clean laceration of


wound
12 PLASTIC SURGERY MADE EASY

FIGURE 1.31: Bullgore injury FIGURE 1.32: Postoperative


suturing

FIGURE 1.33: Gunshot wound FIGURE 1.34: Gunshot wound


with shattered mandible

A word of caution—Rule out head injury and cervical spine injuries


before facial lacerations are sutured.

General Treatment
• Injection tetanus toxoid 0.5 ml IM
• Tetanus immunoglobulin 250 units
• Systemic antibiotics
• Analgesics
• Anti-inflammatory drugs

Local Treatment
• Local anesthetic agent used is Lidocaine, maximum dose
which can be used is 5 mg/kg body weight of plain lidocaine or
7 mg/kg with adrenaline
WHAT IS PLASTIC SURGERY 13

FIGURE 1.35: Mid face degloving FIGURE 1.36: Sutured wound

• Clean the surrounding area with antiseptic solution


• Irrigate the wound with copious saline using syringe/asepto
syringe
• Debridement of the wound or freshening of the edges
• Closure of the wound in layers
• Oppose skin edges with a dermal suture to reduce tension
• Sutures are placed 1-3 mm apart and 1-2 mm from the edge of
the wound
• Skin edges should be everted for better dermal opposition
• Avulsion injuries should be thoroughly cleaned and sutured
for good approximation (Figs 1.35 and 1.36).

SUTURE LINE CARE


• Sutured wound should be washed with soap and water daily
• Anti-microbial cream to be applied locally
• Sutures to be removed on 5th day
• Adhesive tapes or steri strips applied on the skin to give support
• Long-term care - Moisturizing cream or oil to be applied along
the line of sutured wound to avoid hypertrophy of scar
• If the patient has the tendency for scarring, precautions are
taken to give pressure garments, silicone gel sheet and
moisturizing creams.

Suture Materials
• Natural or synthetic
14 PLASTIC SURGERY MADE EASY
• Absorbable or non-absorbable
• Braided or monofilament

Natural Material
• Catgut—Submucosal layer of sheep intestine
• Tensile strength lost in 7-10 days
• Moderate tissue reaction
• Absorbed in 60 days

Synthetic Material
• Vicryl
• Braided, has tissue reaction
• Absorbed in 90 days
• Tensile strength is 75% at 2 weeks
• Monocryl—is a monofilament synthetic suture, less prone to
infection
• Polydioxanone (PDS): A synthetic monofilament, absorbs in 6
months

Absorbable
• Catgut
• Polydioxanone (PDS)
• Polyglycolic acid (Dexon)
• Polyglactin (Vicryl)

Non-absorbable
• Nylon-monofilament
• Silk-braided
• Prolene
• Steel

Other Closure Materials


• Skin staplers
• Steri strips
• Simple adhesive tapes
• Glue-like cyanoacrylates
WHAT IS PLASTIC SURGERY 15
Transplantation
It means removal of a colony of living cells from donor area to
recipient site
• Autograft—This is transplantation of tissue from one location to
another in the same individual
• Allograft (Homograft)—This is transplantation of tissue between
different individuals of the same species
• Xenograft (Heterograft)—This is transplantation of tissue
between individuals of different species
• Isograft (identical twins)—This is transplantation of tissue
between genetically identical individuals.

Replantation
Surgical procedure where by tissue is replaced into its original site.

Implantation
Insertion of a foreign body into the tissue.

Barter Principle
Robbing Peter to pay Paul (skin borrowed from one area to
another).

SUN BLOCKING AGENT (SUNSCREEN)


A sunscreen is a photo protective agent designed to reduce the
effects of UV radiation from the sun. It acts by absorption, reflection
or scattering of solar rays. Upon application, sunscreen acts as filters
and inhibits the penetration of UV rays to the cells of epidermis and
dermis and thereby reduce pigmentation changes. The other photo
protecting measures are clothing and sun avoidance. A commonly
used sunscreen is para-amino benzoic acid (PABA). The most
common measure of sunscreen effectiveness is sun protecting factor
(SPF) of 15 or greater (SPF of normal skin is 13.4). Sunscreen
should be applied 15-30 minutes before actual solar exposure and
applied repeatedly.
16 PLASTIC SURGERY MADE EASY
Direct effects of sunlight has both acute and chronic changes on
the skin:
• Acute changes are—sunburn and tanning
• Chronic changes are:
• Premature aging
• Premalignant skin lesion
• Malignant skin lesion.

DERMABRASION
Dermabrasion or surgical planing consists of removal of the
epidermis and superficial dermis retaining the skin appendages to
allow for spontaneous re-epithelialization with minimal scarring.
This is a useful technique for surface irregularities following acne
scars. The goal is to sand down the normal elevated areas so that
the pits look less deep. Here the superficial layers of the skin, down
to the interface between the papillary and reticular dermis are
removed with a rapidly rotating dermabrader. The dermal papillae
are noted as fine sites of bleeding. Postoperatively the dermabraded
areas are treated with ointments.
Indicated commonly in acne scarring, best suited for fair skinned
people. It acts by leveling the edges of crater and thus a good
blending with surrounding tissue.
Dermabrasion is also done for over grafting on burn wounds.
The advantage is that the graft laid on the dermabraded surface has
less chance of contraction. The most simplest technique is to use
sand paper also known as emery paper which is autoclaved, rolled
on a bottle and gently scrapped to remove the most superficial
burned skin (Figs 1.37 and 1.38). Emery paper is available in
cream and black color. The best type of emery paper to use is cream
color with coarse granules (Fig. 1.39).

Complications
Hyperpigmentation, scarring and infection.
WHAT IS PLASTIC SURGERY 17

FIGURE 1.37: Post burn FIGURE 1.38: Postoperative


hypopigmented patch dermabration and sheet graft

FIGURE 1.39: Emery paper for FIGURE 1.39A: Dermabrasion


use as dermabrader

TATTOOING
Definition
Tattoos are permanent colors introduced in the skin by multiple
small needles dipped in coloring matter.

Types of Tattoo
• Cosmetic
• Traumatic
• Iatrogenic (placed for radiation)
• Camouflage
• Decorative
18 PLASTIC SURGERY MADE EASY

FIGURE 1.40: Blast injury face FIGURE 1.41: Postoperative


with traumatic tattoo scrubbing and suturing

Traumatic Tattoo
Traumatic tattoo seen after road traffic accidents and blast injuries
should be treated as early as possible as the particles get embedded
in the dermis. Delay in removal will result in permanent scarring
(Figs 1.40 and 1.41).

Cosmetic Tattoo
Cosmetic tattoo is performed using the pigment iron oxide in glycerol
and alcohol base. The pigment penetrates to the level of the dermis,
maximum fading occurs within 6 weeks. This can be repeated after
few months. Most commonly used for coloring nipple area after
breast reconstruction (Figs 1.42 and 1.43). It is also used for
tattooing the lip, both for lip lining and for vermillion filling.

Decorative Tattoo
Decorative tottoo can be removed using Q-switched lasers. Various
colors can be removed by using different types of lasers (Fig. 1.44).
WHAT IS PLASTIC SURGERY 19

FIGURE 1.42: Loss of nipple FIGURE 1.43: Postop cosmetic


areola region tattoo to the nipple areola region

FIGURE 1.44: Decorative tattoo


after removal

Camouflage Tattoo
Camouflage tattoo are used to treat portwine stain, burn scars, and
hypopigmented patches on the body (Figs. 1.45 and 1.46).
Tattoo is very effective for pigments deposited in the superficial

FIGURE 1.45: Preoperative FIGURE 1.46: Postoperative


camouflage for hypopigmented tattooing for hypopigmented lip
patch lip
20 PLASTIC SURGERY MADE EASY
dermis. Those involving the epidermis cannot be masked by
tattooing for they have no healthy skin surface where pigments can
be deposited.
Basic pigments are inorganic—White pigment (titanium oxide)
Red pigment (ferric oxide)

TISSUE EXPANSION
Tissue expansion is a mechanical process that increases the surface
area of local tissue available for reconstructive procedures. In 1957,
Neuman described tissue expansion. Tissue expansion is an
effective reconstructive modality and is ideal for reconstruction of
scalp defects allowing development of hair bearing tissue to cover
areas of alopecia (Figs 1.47 to 1.49).

Macroscopic Response
Progressive inflation of an expander increases the overlying tissue.

Microscopic Response
• Epidermis thickens by cellular hyperplasia with narrowed
intracellular spaces

FIGURE 1.47: Postelectrical burn


scalp with alopecia
WHAT IS PLASTIC SURGERY 21

FIGURE 1.48: Tissue expanded FIGURE 1.49: Final result


flap

• Dermis and subcutaneous tissue becomes thinner


• Muscles are pressed and stretched eventually becoming thin
• Vascularity increases dramatically.

Advantages
• Tissues of similar color and texture to that of donor site
• Sensate skin can be got for reconstruction
• Donor site deformity is less.

Complication
• Hematoma
• Infection
• Implant extrusion
• Implant exposure
• Discomfort
• Pain
• Pressure effects.

TISSUE ENGINEERING

Definition
It is the application of principles and methods of engineering and
the life sciences towards the development of biological substitutes
to restore, maintain or improve tissue function. It provides living
22 PLASTIC SURGERY MADE EASY
substitutes for medical and biologic application. It is the develop-
ment and manipulation of artificial implant, laboratory grown tissue
and cells, to replace or support the function of defective or injured
parts of the body.
It is a new field that seeks to provide a different solution to tissue
loss or deficiency.
Skin is the first tissue engineered organ for clinical use.

LASER (LIGHT AMPLIFICATION BY STIMULATED


EMISSION OF RADIATION)
History
Einstein thought that light could be generated via stimulation of
energy.
Maiman discovered Ruby crystals, and in 1965 CO2 and Argon
laser were developed.

Action
Light in contact with a surface can be:
• Reflected
• Absorbed
• Transmitted
• Scattered
Laser affects tissue via absorption and it is the absorbed portion
of light that has clinical use. Depth of penetration depends on wave
length, color, consistency of tissue, duration of exposure and spot
size of beam (distance measured from peak to peak).
Shortest wavelength has more scattering and less penetration.

Clinical Application
1. Vascular anomalies—Flashlamp pumped pulsed dye targets
selective absorption by blood vessels. Transmission occurs
through epidermis and dermis. Red blood cells undergo rapid
lysis. Ideal for portwine stain in infants and children. Darker
lesions in older children contain more deoxyhemoglobin
resulting in less absorption and thus less effective.
WHAT IS PLASTIC SURGERY 23
2. Cutaneous pigment—can be epidermal and dermal pig-
mentation. The targeted chromophore is melanin.
Q-switched ruby laser—can treat both epidermal and dermal
lesions
Nd:YAG and pulsed dye are also used.
3. Tattoo—melanocytes are destroyed
Q-switched laser penetrates to the level of upper papillary dermis
and targets ink particles based on their color
Nd:YAG Laser either green or infrared (effective for tattoo at
different wavelength)
Ruby laser—blue black
Alexandrite— Green
4. Hair removal—Melanin is the main chromophore targeted in
laser hair removal. Hypopigmentation is a side effect. Ten percent
regrows months after treatment.
5. Skin resurfacing (CO2 laser)—The targeted chromophore
is water. The direct effect for skin resurfacing is tissue vapo-
rization. It is useful in photoaged skin resulting in improvement
of fine wrinkles with a lasting result. Here, it causes thermal
ablation of epidermis and superficial dermis.
Erbium laser—Known as lunch time peel. It reduces fine
superficial wrinkles and gives much better results.
6. Acne scarring—Erbium YAG is specific for collagen and scar.

Complications of Laser
• Erythema
• Thermal burns
• Scarring
• Hypopigmentation and hyperpigmentation
• Infection
• Hypersensitive reaction to ointments.
Chapter 2

Wound Healing
26 PLASTIC SURGERY MADE EASY

DEFINITION
Wound is defined as a breach in the continuity of skin or mucous
membrane with or without the involvement of the underlying soft
tissues.

TYPES OF WOUND
Based on Duration
• Acute wound (Fig. 2.1)
• Chronic wound (Fig. 2.2)
(wounds that do not heal in 3 months).
Acute wounds—Acute wounds are those which proceed through
an orderly and timely reparative process resulting in faster restoration
of structural and functional integrity.
Chronic wounds—Chronic wounds are those which fail to proceed
through an orderly and timely reparative process resulting in delayed
or failure of restoration of structural and functional integrity.

Based on Mechanism
• Abrasion
• Bruise
• Contusion
• Hematoma
• Laceration

FIGURE 2.1: Acute clean cut FIGURE 2.2: Chronic wound


wound
WOUND HEALING 27

FIGURE 2.3: Contaminated wound FIGURE 2.4: Dirty wound

• Avulsion and degloving


• Puncture wounds

Clinical Types
• Clean wounds
• Contaminated wounds (Fig. 2.3)
• Dirty wounds (Fig. 2.4).

HEALING
Healing is the final stage of the response of the tissue to injury.
Healing comprises of regeneration and repair.

Types of Healing
• Primary healing (skin edges directly opposed)
• Secondary healing (wound edges left to heal by a combination
of contraction and epithelialization)
• Tertiary healing (Initially left open then closed as a secondary
procedure).
Primary healing or healing by first intention is seen in wounds
that are clean, with clear cut edges and closely approximated.
Delayed primary healing is seen in wounds that are contaminated
or poorly delineated. Here the skin and subcutaneous tissues of the
wound are left open for 3 to 4 days for the local defenses to act and
then the edges are approximated.
28 PLASTIC SURGERY MADE EASY
Secondary healing or healing by second intention is seen in
wounds which have tissue loss. Here the wound closes by contraction
and epithelialization.
Healing of partial thickness wounds involve epidermis and
the superficial dermis. Healing in these wounds occurs by
epithelialization in which epithelial cells from the dermal
appendages, hair follicles and sebaceous glands replicate to cover
the exposed dermis.

Mechanism of Healing
Epithelialization—is a process by which the keratinocytes migrate
and divide to resurface partial thickness loss of skin or mucosa.
Contraction—is a process in which there is mechanical reduction
in the size of the wound brought about by the myofibroblasts.

Connective tissue matrix deposition—is a process in which


the fibroblasts are recruited to the site of injury and produce
new connective tissue matrix composed of type 1 and type III
collagen.

Phases of Healing
The entire wound healing process is a complex series of events that
begins at the moment of injury and can continue for months to
years. This overview will help in identifying the various stages of
wound healing.
1. Inflammatory phase (2-5 days)
a. Hemostasis
• Vasoconstriction
• Platelet aggregation
• Thromboplastin makes clot
b. Inflammation
• Vasodilation
• Phagocytosis
WOUND HEALING 29

2. Proliferative phase (2 days to 3 weeks)


a. Granulation
• Fibroblasts lay bed of collagen
• Fills defect and produces new capillaries
b. Contraction
• Wound edges pull together to reduce defect
c. Epithelialization
• Crosses moist surface
• Cells travel about 3 cm from point of origin in all
directions.

3. Remodeling phase (3 weeks to 2 years)


a. New collagen forms which increases tensile strength to
wounds
b. Scar tissue is only 80 percent as strong as original tissue.

Growth Factors involved in Wound Healing


• Platelet derived growth factor
• Epithelial growth factor
• Fibroblast growth factor
• Transforming growth factor—alpha
• Transforming growth factor—beta
• Interleukin - 1
• Tumor necrosis factor—alpha

COMPLICATION
• Contracture
• Hypertrophic scars and Keloids
• Pyogenic granuloma
• Infection
• Dehiscence
• Scars—weak and painful
• Pigmentary changes
• Malignant changes
30 PLASTIC SURGERY MADE EASY

FIGURE 2.5: Healthy granulation FIGURE 2.6: Ready to take graft


tissue

FIGURE 2.7: Unhealthy pale FIGURE 2.8: Pale granulation not


granulation tissue ready for grafting

FACTORS DELAYING WOUND HEALING


Local Factors
• Blood supply
• Denervation
• Hematoma
• Infection
• Foreign body
• Excess movements

General Factors
• Age
• Anemia
• Malignancy
• Vitamin A and C, Zinc
• Corticosteroids
WOUND HEALING 31

GRANULATION TISSUE

Favorable (Figs 2.5 and 2.6) Unfavorable (Figs 2.7 and 2.8)
Young granulation (48-72 hours) Old granulation (> 72 hours)
Firm Thick, Slimy, Soggy
Flat Heaped up above the surface
Rough Soft, Friable
Bright red Pale
Bleeds on touch Avascular
No discharge Gelatinous/edematous
No sign of infection Purulent discharge
(Copper sulphate acts by removing exuburent granulations and hypertonic
saline solution helps to suppress the exuburent granulations.)
Chapter 3

Skin and
Subcutaneous
Tissue
34 PLASTIC SURGERY MADE EASY
ANATOMY OF SKIN
Functions of Skin
1. Protects from environment
2. Protects against microbial invasion
3. Protects against UV light
4. Prevents fluid loss
5. Regulates body temperature
6. Sensation.

Structure of Skin
Skin consists of two layers, the epidermis and the dermis
(Fig. 3.1).
A. Epidermis is derived from ectoderm and has no blood vessels
and is dependent on the underlying dermis for nutrition. It is
composed of stratified squamous epithelium.

FIGURE 3.1: Anatomy of skin


SKIN AND SUBCUTANEOUS TISSUE 35
i. Epidermis is composed of 5 layers.
Stratum corneum—contains non-viable keratinized cells
Stratum lucidum—present in palm and soles
Stratum granulosum
Stratum spinosum—prickle cell layer
Stratum germinatum—basal layer
ii. Cellular composition of epidermis
Melanocytes—Neural crest origin (produce melanin)
Langerhans—Bone marrow origin (antigen presenting cells)
Merkel cells—Neural crest origin (perception of light touch)
Keratinocytes
iii. Epidermal appendages are—Sebaceous glands, sweat
glands, apocrine glands, mammary glands and hair follicle.
They are often found deep in the dermis.

Glands Other name Location Most conc Secretions


Sebaceous Halocrine Entire body Face and scalp Sebum
Sweat Eccrine Entire body Palm and sole Sweat
Mammary Apocrine Entirebody Axilla and genitalia
Hair follicle Entire body Scalp,axilla and pubic
B. Dermis is derived from mesoderm and contains collagen,
elastic fibers, blood vessels, sensory structures and fibroblasts.
Dermis is composed of two layers, the more superficial papillary
dermis and the deeper reticular dermis.

IMPORTANT ARTERIES OF THE HEAD AND NECK (FIG. 3.2)


External Carotid Artery (8 branches)
• Superior thyroid
• Ascending pharyngeal
• Lingual
• Facial
• Occipital
• Posterior auricular
• Superficial temporal
• Maxillary
36 PLASTIC SURGERY MADE EASY

FIGURE 3.2: Head and neck blood supply

IMPORTANT ARTERIES OF UPPER EXTREMITY (FIG.3.3)


Subclavian artery becomes axillary artery at the outer border of
1st rib.

Axillary Artery
• Superior thyroid
• Thoracoacromial
• Lateral thoracic
• Subscapular
• Posterior circumflex humeral
• Anterior circumflex humeral

IMPORTANT ARTERIES OF THE LOWER LIMB (FIG.3.4)


• Common iliac artery
• External iliac • Inferior epigastric
• Deep circumflex iliac
• Internal iliac (10 branches)
SKIN AND SUBCUTANEOUS TISSUE 37

FIGURE 3.3: Upper limb artery


38 PLASTIC SURGERY MADE EASY

FIGURE 3.4: Lower limb arteries


SKIN AND SUBCUTANEOUS TISSUE 39
• Femoral (6 branches)
• Superior epigastric
• Superficial circumflex iliac
• Superficial external pudendal
• Deep external pudendal
• Profunda femoris
• Descending genicular artery
• Popliteal (7 branches)
• Lateral and medial superior genicular artery
• Lateral and medial inferior genicular artery
• Middle genicular artery
• Anterior and posterior tibial artery
• Anterior tibial
• Posterior tibial
• Anterior medial malleolar
• Anterior lateral malleolar
• Posterior tibial
• Medial plantar
• Lateral plantar
• Dorsalis pedis (continuation of anterior tibial).

BLOOD SUPPLY OF THE SKIN


Knowledge of blood supply is important for designing skin flaps
and incisions. Cutaneous arteries arise directly from the segmental
arteries or indirectly from the branches of the segmental arteries
(Fig. 3.5).
Cutaneous blood supply can be direct cutaneous or indirect
cutaneous. The subdermal plexus of vessels are the main supply of
skin, from here the arteries pass through the reticular dermis to
communicate with dermal and subepidermal plexuses.
Deep vessels arise from the aorta and divide to supply head,
neck, trunk and limbs.
The interconnecting system is composed of fasciocutaneous
perforating vessels and musculocutaneous vessels.
Fasciocutaneous blood supply is from the fascial plexus.
Branches from this plexus reach the skin as direct or indirect
perforators.
40 PLASTIC SURGERY MADE EASY

FIGURE 3.5: Skin blood supply

Angiosomes
An angiosome is a composite block of tissue supplied by a named
artery. Knowledge of the anatomy of blood supply is fundamental
to the design of skin flaps (Fig. 3.6).

FIGURE 3.6: Angiosomes

PHYSICAL PROPERTIES OF SKIN


The physical properties of skin are:
1. Viscoelastic properties
2. Skin tension
SKIN AND SUBCUTANEOUS TISSUE 41
3. Skin extensibility
4. Directional variations

Viscoelastic Properties
The viscoelastic properties are a combination of viscous and
elasticity.
Viscous—The material yields continuously under load without
recovering after unloading.
Elastic—The material regains its shape and dimension after
deformation.
The viscoelastic properties of skin are creep and stress
relaxation, contributed by the collagen fiber network, the elastic
fiber network and the interstitial fluid.
Creep—Creep is defined as the tissue extension or deformity over
a given length of tissue at a constant load.
Stress relaxation—Is defined as the decrease in retractive
force exhibited by a material when it is held at a given stretch over
time.

Skin Tension
Tension is defined as the force directed to stretch a material. Tension
is naturally present in the skin as a result of elastin fiber network
and the effect of gravity. Tension is responsible for the skin creases
and it varies in different parts of the body. wounds sutured along
skin creases have less tension causing thin scar and those sutured
across skin crease have more tension causing hypertropic scar. Skin
tension is high in the young age and is replaced by laxity in the
elderly.

Effects of Increased Tension


• Blanching and necrosis
• Rupture of the dermis
• Permanent stretching of skin
42 PLASTIC SURGERY MADE EASY
Skin Extensibility
Skin extensibility is functionally more important because it allows
for every movement of the body. Skin extensibility is mainly due to
the elastin fiber network. Relaxed skin elongates with the tension.
Like skin tension, skin extensibility is more in the young and is
replaced by laxity in the elderly and allows for the closure of the
wounds without importing distant tissues.

Directional Variations
The directional variations in skin were described by KARL LANGER
based on his experiments on fresh cadavers. The direction of the
skin creases depends on tension and elasticity.
They are unique such that:
• In same person varies at different sites
• In same site varies in different individuals
• In same site varies in different directions and therefore influen-
cing the shape of the skin incisions. Skin incisions along the
Langer’s lines produces a thin and cosmetically aesthetic scar.

SCARS
Definition
It is a dense avascular fibrous tissue formed as an end result of
healing. Any wound that penetrates the dermis will cause some
degree of scarring.

Types of Scar
• Depressed scar
• Step off scar
• Bevelled scar
• Mismatched scar
• Stretched scar (Fig.3.7)
• Hypertrophic scar (Fig.3.8)
• Bridal scar/Trapdoor scar
• Fine scar
SKIN AND SUBCUTANEOUS TISSUE 43

FIGURE 3.7: Stretched scar FIGURE 3.8: Hypertrophic scar

FIGURE 3.9: Surgical scar FIGURE 3.10: Extensive Keloid


scarchest
• Mature scar
• Immature scar
• Surgical or linear scar (Fig.3.9)
• Spreading scar
• Keloid scar (Figs 3.10 and 3.11).
Bridal scar or trap door scar—A semi-circular laceration tends
to cause bulging of the scar enclosed in the semi-circle. As the scar
44 PLASTIC SURGERY MADE EASY

FIGURE 3.11: Sternal keloid

contracts the skin may bulge with pin cushion effect. Scar has
wrinkling and raises the level of the tissue within the semi-circle.
Bevelled scar—A scar which tends to heap up in a ridge.
Contractions causes bulging of the superficial thinner side of the
bevel.
Depressed scar—A scar that causes mobile skin to adhere to
immobile deep structures results in fixation and indendation of the
scar skin.
Step off scar—When wound edges have been opposed
inaccurately a step off scar results.
Mismatched scar—When a laceration is closed inadequately, a
jog in the margin will be evident.
Stretched marks—formed when the dermis is stretched to the
point of disruption of collagen fibers. But the dermis remains intact.
The dermis forms a scar that is visible through the translucent
epidermis. Treatment is by removing the scar.
Mature scar—is light in color and flat.
Immature scar—Red, itchy or painful and slightly elevated.
Surgical or linear scar—Red raised itchy confined to the original
incision.
SKIN AND SUBCUTANEOUS TISSUE 45
Fine scar—Flat scar lying within or parallel to a skin wrinkle.
There should be no contour irregularity, distortion of adjacent
anatomic or aesthetic unit or pigmentary changes. Scar should be
parallel to the relaxed skin tension lines.

A Fine Scar Depends On


• Type of skin and location on the body
• Tension of wound closure
• Direction of wound
• Co-morbid condition and nutritional status of the patient
• Technique used

Hallmark of Obtaining Best Scar


• Atraumatic technique
• Debridement
• Ample irrigation
• Tension-free closure
• Eversion of wound edges
• Placement of scar in the same direction as skin lines
Scar has three components—Line, contour and color. A good
scar is one which is no more than a fine line, in level and even with
the surrounding surface and having the same color as the
surrounding skin.
Factors included in scar assessment (Vancouver scale).
Pigmentation, vascularity, pliability and height.
Clinical assessment—Color, contour, texture and distortion.

Factors Affecting Scar Contracture


Intrinsic Factors
• Skin looses its elasticity with increasing age
• Vitamin C deficiency—(needed for collagen synthesis)
• Zinc—needed for epithelial and fibroblast proliferation
• Iron and copper—necessary for normal collagen metabolism
46 PLASTIC SURGERY MADE EASY
Extrinsic Factor
• Lines of tension in the skin (Dupuytren 1832)
• Normal tension lines of the skin (Langer 1861)
• Relaxed skin tension lines (Borges)
• Amount of scar tension lines
• Position of scar and shape of scar

Enemies of a Plastic Surgeon (Remember as PRST)


Pressure, Raw area, Straight line and Tension.

Friends of a Plastic Surgeon


Z plasty and W plasty (Fig.3.12).

Skin Lines
Langer lines, Relaxed skin lines, Wrinkle lines, Lines of facial
expression. All these lines are perpendicular to the long axis of the
underlined muscles. Scars are less if they follow skin lines. Skin is
elastic, extensible and resilient.
Contour lines—Natural lines seen at the junction of two body
plains. Example, Cheek with nose.
Dog ear—Dog ear is excess bunching of skin seen when one side
of ellipse is longer than the other side of the wound. It tends to
flatten with time (Fig.3.13).

FIGURE 3.12: Z plasty FIGURE 3.13: Dog ear following


transposition flap
SKIN AND SUBCUTANEOUS TISSUE 47
Treatment
Scar revision. Wait for at least 18 months for the scar to mature
before performing scar revision.

Nonsurgical Methods
a. Contractubex ointment massaging has been found to be very
effective for controlling the itching and pain
b. Compression using pressure garments
c. Topical silicone gel sheet
d. Steroid injections (triamcinolone)
e. Make up camouflage
Scar may be improved by these measures, if not surgical
intervention should be carried out.

HYPERTROPHIC SCAR AND KELOID


Introduction
The word Keloid was derived from the greek word “chele “ which
means crabs claw. It describes the appearance of lesion with claw
like extension and the manner in which they expand by lateral
growth like a crab moving sideways. keloid and hypertrophic scar
occurs as a result of excessive healing leading to abnormal growth
of fibrous tissue of the dermis following trauma.

Incidence
• Pigmented races
• Particularly women during the child bearing period
• Particular regions of the body including sternum, shoulder, back
and ear lobe (Figs 3.14 to 3.19)
• There is no definite factor responsible for the development of
scars, although tension and inflammation are thought to be the
contributing factors. Hypertrophic scar and keloid affect about
4-15% of the general population.

Pathogenesis
• It occurs due to accumulation of excessive extracellular matrix
• It presents as red raised scar
48 PLASTIC SURGERY MADE EASY

FIGURE 3.14: Keloid ear FIGURE 3.15: Postkeloid


excision and RT

FIGURE 3.16: Keloid of the FIGURE 3.17: Ear keloid


left ear

• The predominant cells present in hypertrophic scars and keloids


are fibroblasts and mast cells. Increased number of mast cells in
these lesions are responsible for itching due to release of
histamine
SKIN AND SUBCUTANEOUS TISSUE 49

FIGURE 3.18: Keloid both FIGURE 3.19: Hypertrophic scar


ears

Clinical Findings
• Elevation due to extracellular matrix
• Itching due to excessive histamine production by mast cells
• Redness due to increased vascularity
• Growth of keloid—proliferation of fibroblasts in the keloid
dermis propagates the fibrosis.
Clinical Differences
Hypertrophic scar Keloid
1. Increased inflammatory Growth factor plays a role
phase of healing
2. Lesions are raised initially Remain elevated
and flatten spontaneously
with time
3. Scars are red, itchy and Scars are red, itchy, painful
painful. But confined to and extends sideways
original scar into normal skin
50 PLASTIC SURGERY MADE EASY
4. Increased collagen Markedly increased
collagen and vascularity
5. Treatment is by silicone Steroid injections, surgical
sheeting, pressure and excision followed by
surgical excision radiotherapy
6. No recurrence Recurrence common

Factors Responsible for Scar Hypertrophy


• Prolonged inflammatory phase during healing
• Infection
• Tension
• Scars placed across the relaxed skin tension lines
• Children are more prone for scars due to tight skin
• Dark race people

Prevention of Hypertrophy
• Placing all scars in the relaxed skin tension line
• Avoid wound tension
• All wounds to be closed before 2 weeks
• Prophylactic pressure therapy
• Silicon gel sheet application

Management
Hypertrophic Scars
a. Pressure therapy—Start using either elastocrepe bandage or
pressure garments as early as possible. This has to be worn
continuously twenty four hours a day. Pressure can be relieved
for 10-15 minutes for cleaning the skin. Pressure garment has
to be worn for a period of 6 months to 1 year.
Advantages
• Reduces edema and collagen synthesis
• Accelerates scar maturation process and remodeling of
collagen fibers.
Disadvantages
• Compliance is poor
• Blisters can form under the pressure garment
• Older scars respond very little to the pressure therapy.
SKIN AND SUBCUTANEOUS TISSUE 51
b. Topical application—Of hydrocortisone results in a marked
reduction in acute inflammation. The mechanism of action is
that of anti-inflammatory effect, that is suppression of
angiogenesis and reduction of edema.
c. Intralesional injection—This results in flattening of the lesion
and decreases symptoms of the scar. Small lesions are treated
with injection triamcinolone, intralesionally given at monthly
intervals, the dose can be adjusted according to the size of the
lesion varying from 10 to 40 mg each time for about 4-6 months.
Complication is atrophy of skin and subcutaneous tissue,
local depigmentation, necrosis, ulceration and systemic
Cushing’s syndrome.
d. Surgery—Is indicated when hypertrophic scar is extensive and
interferes with normal function. It should be supplemented with
an injection of triamcinolone in the wound edges during
excision followed by pressure garment. Elastocrepe bandage
should be used continuously to prevent further recurrence.
e. Silicone gel sheet—Silicone should be applied for twenty-
four hours. It should be removed often washed and reapplied.
It is effective in older scars. Use of silicone gel as an adjunct has
helped in flattening the scar. The scar eventually becomes soft,
supple and pain free.
Disadvantage—Is that the patients get contact dermatitis,
pruritis, redness, rashes and maceration due to reduced water
vapor transmission.
Mode of action—may be due to local rise of temperature,
changes in the hydration of the scar and release of silicone into
the scar.
f. Contractubex ointment—It exerts antiproliferative, anti-
inflammatory softening and smoothing action on indurated,
hypertrophic and painful scars. The action is by the deep
penetration of the water soluble gel base into the scar making it
soft and moist thereby preventing itching.
It should be gently massaged into the skin several times a day
until all the gel has been absorbed.
52 PLASTIC SURGERY MADE EASY
Keloids
Keloids deserve special attention in addition to the other modes of
therapy. Small lesions respond to intralesional triamcinolone
injections given at monthly intervals. Large lesions need excision
and split thickness skin graft followed by low dose radiation therapy
given in the immediate postoperative period to prevent recurrence.
The immediate complication is disruption of wounds.

Method of Injecting Triamcinolone


1 ml of triamcinolone (40 mg) should be mixed with 1/2 ml of
xylocaine (local anesthetic has the ability to inhibit both collagen
synthesis and collagen secretion) drawn in a luer loc syringe or
conventional 2 ml syringe with a 20 gauge needle. Inject directly
into the keloid or hypertrophic mass.

Complications
1. Local depigmentation
2. Dermal and subcutaneous atrophy of normal surrounding tissue
3. Large doses of triamcinolone results in iatrogenic Cushing’s
syndrome.

SKIN INFECTIONS
NECROTIZING FASCIITIS
(Syn: Meleney’s Gangrene or Fournier’s Gangrene)
It is a destructive invasive infection of the skin, subcutaneous tissue
and deep fascia.
It is due to a synergistic combination of gram-positive and
negative organisms involving the genitalia, groin and lower back.
This is a severe infection that is life and limb threatening. The
most common organism is group A beta hemolytic streptococci .
The group that is at risk are people with diabetes, elderly and the
immunocompromised.
Clinically, patient presents with fever, subcutaneous induration
leading to necrotic patches of skin (Fig. 3.20).
SKIN AND SUBCUTANEOUS TISSUE 53

FIGURE 3.20: Necrotising


fascitis

Treatment is by
• Vigorous surgical excision and skin grafting
• Broad spectrum intravenous antibiotics
• Careful monitoring in the ICU set up.

HUMAN BITE
Most commonly seen in the ear, nose and lip in south India due to
fight between two people. The most common organism involved is
alpha hemolytic streptococci, Staphylococcus aureus and Eikenella
corrodens.
Treatment is by thorough washing of the area
Injection Tetanous toxoid 0.5 ml IM
Broad spectrum antibiotic
A good debridement of the wound
Primary suturing depending upon the defect, If the defect is large a
flap may be required (Figs 3.21 and 3.22)

FIGURE 3.21: Human bite FIGURE 3.22: Island flap for one
stage reconstruction
54 PLASTIC SURGERY MADE EASY

FIGURE 3.23: Dog bite preoperative FIGURE 3.24: Postoperative


reconstruction with Abbe flap

DOG BITE
Commonly seen in children . The organisms involved are pasteurella
multocida, anaerobes and Staph aureus.
Treatment—
Wound—Thorough cleaning, debridement and local injection of
rabies immunoglobulins. Primary suturing of the wound or flap
reconstruction (Figs 3.23 and 3.24).
Antirabires vaccine on day 0, 3, 7, 28 and 90, deep IM, IV antibiotics.

BENIGN SKIN LESIONS


ADNEXAL TUMORS
Hair follicle Trichofolliculoma
Eccrine Syringoma
(Sweat gland Cylindroma (turban tumor)
Apocrine Cystadenoma
Sebaceous Nevus sebaceous of jadassohn
Epithelial cysts Epidermoid cyst
Sebaceous cyst
Milia
Dermoid cyst
Generalized Neurofibromatosis
Xeroderma pigmentosa
SKIN AND SUBCUTANEOUS TISSUE 55
Miscellaneous Hydradinitis suppurativa
Calcinosis cutis

HAIR FOLLICLE LESIONS


PILOMATRIXOMA (CALCIFYING EPITHELIOMA OF MALHERBE)
Derived from hair follicle Located on lower dermis and
subcutaneous fat
Age of onset Early childhood
Clinical appearance Extremely firm, flesh colored nodule
(hard subcutaneous nodules)
Positive Tent Sign (Stretching of
overlying skin reveals multiple peaks)
Location Most commonly involves head and
neck and upper extremities
Treatment Simple excision

TRICHOFOLLICULOMA
It is characterized by fluctuant nodules with a central pore. The
swelling is filled with keratin debris.

TRICHILEMMAL CYST (PILAR CYST)


It usually occurs in adulthood in the
scalp they are fluctuant flesh colored
and well circumscribed nodules (Fig.
3.25).

SWEAT GLAND LESIONS


CYLINDROMA (TURBAN TUMOR)
It is diagnosed by pink color lesions
which occur on the scalp of an elderly
person. It may be large and multiple
lesions. It is also known as “Turban
tumor” (Figs 3.26 and 3.27). FIGURE 3.25: Hair follicle
tumor
56 PLASTIC SURGERY MADE EASY

FIGURE 3.26: Turban tumor lateral FIGURE 3.27: Turban tumor


postoperative

SEBACIOUS GLAND LESIONS


SEBACEOUS ADENOMA
Onset is usually middle aged. It appears like yellow nodules and
commonly located on the head. Treatment is by local excision
(Figs 3.28 and 3.29).

FIGURE 3.28: Sebaceous FIGURE 3.29: Postoperative


adenoma excision and Transportion flap
SKIN AND SUBCUTANEOUS TISSUE 57

FIGURE 3.30: Sebacious nevus of FIGURE 3.31: Sebaceous


Jadassohn nevus of Jadassohn

SEBACEOUS NEVUS OF JADASSOHN


It is a congenital harmartoma of sebaceous gland (Figs 3.30 and
3.31).
Development of Basal cell carcinoma is 20%. Histiologically
cells are placed more deeply in the dermis.
Appears as elevated block which is
• Irregular
• Less verrucoid and pigmented
• Large plaque
• Yellow in color
• Cobblestone
• Not associated with CNS
• 15% undergo malignant change.

CYSTS
DERMOID CYST
Age of onset Birth, early childhood
Clinical features Fluctuant, flesh colored, well circums-
cribed lesion without punctum, cavity
58 PLASTIC SURGERY MADE EASY

FIGURE 3.32: Dermoid cyst post FIGURE 3.33: Dermoid cyst


auricular region temporal region

filled with keratinous debris lined with


all types of epidermal skin appendages
usually in a vestigial form (Figs 3.32
and 3.33).
Location Supraorbital ridge, lateral brow or
nasal midline.
Treatment Simple excision.

SEBACEOUS CYST (WENS)


Age of onset Adulthood
Clinical Features Fluctuant, flesh colored, well circums-
cribed with punctum
Cyst cavity filled with malodorous
keratinous debris (Fig. 3.34).

FIGURE 3.34: Sebaceous cyst


SKIN AND SUBCUTANEOUS TISSUE 59
Location Scalp (Except on Palm + Sole)
Treatment Excision along with the sac .
If infection is present then incision and
drainage and antibiotics and once the
infection settles a total excision along
with the sac to be carried out.

DERMAL LESION
LIPOMA
• It is a slow growing tumor composed of fat cells
• It may be encapsulated or diffuse
• It occurs at any age
• Clinically it appears as a soft single nodule or multiple and
lobulated, pseudofluctuation present
• Characterized by slipping edge
• It is painless
• Commonly present on the trunk and extremities, but can occur
anywhere in the body where fat is present
• The different types of lipoma are subcutaneous,subfascial,
intermuscular subserous, submucous and intraglandular (Figs
3.35 to 3.38).
• Treatment is by excision.

FIGURE 3.35: Lipoma back single FIGURE 3.36: Multiloculated


lipoma back
60 PLASTIC SURGERY MADE EASY

FIGURE 3.37: Lipoma breast FIGURE 3.38: Lipoma breast


postoperative

NEURAL TISSUE LESIONS


NEUROFIBROMATOSIS
Definition
It is a hereditary autosomal dominant genetic disorder that produces
pigmented scars, tumors of skin, peripheral nerves, subcutaneous
tissues and bony deformity.

Incidence
1: 3000.

Classification
Richardi classified neurofibroma into 7 types:
1. Generalised—Von Recklinghausen disease (Fig.3.39) (1882)
2. Central—Acoustic neurofibromatosis
3. Mixed tumors—intracranial, spinal or perispinal
4. Diffuse with pigmentation (Figs 3.40 and 3.41)
5. Segmental
6. Only café au lait spots
7. Late onset

Lesions
Primary Café au lait spot
Neurofibromas
Optic gliomas
SKIN AND SUBCUTANEOUS TISSUE 61

FIGURE 3.39: Generalized


neurofibromatosis

FIGURE 3.40: Diffuse FIGURE 3.41: Diffuse with pigmentation


neurofibromatosis

Secondary Seizures
Learning disability
Scoliosis

Clinial Types
• Cutaneous neurofibromas
• Subcutaneous neurofibromas
• Plexiform neurofibromas occurs in connection with 5th nerve
(Figs 3.42 to 3.45).
62 PLASTIC SURGERY MADE EASY

FIGURE 3.44: Plexiform


neurofibromatosis

FIGURE 3.42: Neurofibromatosis

FIGURE 3.43: Plexiform FIGURE 3.45: Neurofibromatosis


neurofibromatosis scalp

• Elephantiasis neurofibroma (subcutaneous fat is replaced by


fibrous tissue which is thickened, edematous and often
gelatinous)
• Pachydermatocele neurofibroma (coils of soft tissue hang
around root of neck)
SKIN AND SUBCUTANEOUS TISSUE 63
Signs and Symptoms (Remember as 15 ‘S’)
1. Spots—café au lait
2. Six in number
3. Size—1.5 cm (at least one should measure 1.5 cm)
4. Sex equal
5. Subcutaneous nodules
6. Swellings multiple
7. Sheath of the nerve involved
8. Situated along the course of a peripheral nerve
9. Sagging of the swellings due to involvement of the nerves
10. Skeletal abnormalities like scoliosis
11. Seizures
12. Speech impairment
13. Sarcomatous change (10%)
14. Schwann cells seen under microscope
15. Schwannoma common in NF-2
16. Lisch nodules—noncancerous tumors on the iris
17. Freckling in the armpit or groin

Treatment
Remove the neurofibromas for cosmetic purposes. Most often only
partial excision is possible.

Complications
• Deformity of soft tissue
• Sarcomatous transformation
• Hypertrophy of bones
• Loss of neuromuscular function results in drooping
• Recurrence is common.

MISCELLANEOUS
HIDRADENITIS SUPPURATIVA
• It is chronic recurrent inflammatory disease of apocrine sweat
glands
• Occurs in the axilla, groin, perineum or breast
• Involves the subcutaneous tissue and fascia
• Onset is usually after puberty
64 PLASTIC SURGERY MADE EASY
• Clinically it appears as nodu-
les with purulent discharge,
extensive scarring and sinus
tract and very painful.

Treatment
• Repeated cleaning of the area
and dressing with topical
antibiotic
• Incision and drainage for
abscess formation
• Wide local excision down to
the fascia and skin grafting.

CALCINOSIS CUTIS
FIGURE 3.46: Calcinosis cutis
Calcinosis cutis is a term used to scrotum
describe a group of disorders in
which calcium deposits in the skin due to local or systemic factors.
It is common in blacks. It arises in the second half of life. Treatment
is by excision and primary closure (Fig. 3.46).

NEVUS
EPIDERMAL NEVUS—(LINEAR NEVUS)
It is a congenital malformation of the epidermis (Figs 3.47 to
3.49).
• Appears yellow, brown, flat
• Verrucous or scaly plaque
• Arranged in a linear fashion
• Hyperkeratosis and acanthosis
• Associated with—mental retardation seizure disorder.

CONGENITAL MELANOCYTIC NEVI (CMN)


Definition
Nevi is defined as cutaneous malformation in which all the
constituents of the integument may take part (Figs 3.50 to 3.57)
SKIN AND SUBCUTANEOUS TISSUE 65

FIGURE 3.47: Linear nevus back FIGURE 3.48: Linear nevus

FIGURE 3.49: Small FIGURE 3.50: Giant nevus back


pigmented nevus

FIGURE 3.51: Nevus FIGURE 3.52: Postoperative


nevus
66 PLASTIC SURGERY MADE EASY

FIGURE 3.53: Small hairy nevus FIGURE 3.54: Excision and graft

FIGURE 3.55: Small hairy nevus FIGURE 3.56: Large hairy


nevus

FIGURE 3.57: Postoperative


excision with flap
SKIN AND SUBCUTANEOUS TISSUE 67
Nevus can be divided into—
• Junctional
• Compound
• Intradermal
• Blue nevi
• Hairy nevi

Giant Congenital Pigmented Nevus


It is a nevus present at birth commonly seen in darkly pigmented
people. It is divided into—small, intermediate and large.
Large is known as giant nevus with a diameter of 20 cm or
greater in adulthood.
Color ranges from tan to dark brown, bluish or black. Hair
growth can be fine, dark or coarse. Giant CMN may be extremely
rugose and their surface may be studded with pigmented nodules.
Multiple smaller nevi may be present called satellite nevi.
Incidence of malignant transformation within CMN is 2-4%.
Giant CMN range from 5-20% and mostly develop before puberty.
Melanoma arising within large CMN may develop deep in the dermis
and subcutaneous tissue and thus evade detection until late in the
progression of the lesion. These lesions can also have 4% extra
cutaneous melanomas.
Neurocutaneous melanosis is an association of a large CMN
with multiple small CMN (satellite) involvement. There may be
hydrocephalous, seizure and partial paresis. Majority of these
children with large CMN manifest before two years of age. When
neurological symptoms are present, prognosis is grave.
• Present at birth
• Extensive— Bathing trunk nevus
Vest type
Stocking type
Glove type
• Lesion may be Flat, elevated or verrucoid
Hair may be fine or coarse
• Three unique features include association with
Neurofibromatosis
Leptomeningeal melanocytosis and seizure
Melanoma including CNS—10%
68 PLASTIC SURGERY MADE EASY
Actual incidence of malignant transformation is from 2-4%.
Approximately 60% of malignant transformation occur before
the age of 10 years
Histologically, the lesion often tends to invade into the
subcutaneous fat.
Mortality from melanoma arising from giant congenital nevus is
very high (10%).

Treatment Option
• Excision and closure
• Serial excision
• Tissue expansion
• Excision and grafting

VASCULAR ANOMALIES
Classification
• Descriptive classification—Strawberry, Portwine, Salmon patch
• Embryological classification—Capillary, Venous, Arterial,
Arteriovenous
• Biological classification (Histological)—Hemangioma,
Malformation
A. Descriptive types—Salmon patch, Portwine, Strawberry
Salmon patch
• Named after the belly of salmon fish which is pink in color
• Present at birth
• Disappears by first year
Portwine
• Named after the color of portuguese wine
• Present at birth (Figs 3.58 and 3.59)
• Changes very little through out life (Figs 3.60 and 3.61)
• Located on the face in areas supplied by 5th nerve
• No tendency for spontaneous regression, becomes darker
with verrucoid eruptions (Figs 3.62 to 3.65)
• Associated with ‘Sturge-Weber syndrome’ which is an
intracranial involvement of choroid and pia mater with
hemangioma
SKIN AND SUBCUTANEOUS TISSUE 69

FIGURE 3.58: Portwine stain lip

FIGURE 3.60: Diffuse swelling


of lower lip post excision

FIGURE 3.59: Portwine one half of FIGURE 3.61: Portwine with


face swelling

Strawberry
• Normal at birth
• Appears at 1-3 weeks and rapidly increases upto 3 months.
It grows along with the child upto 1 year (Figs 3.66 to
3.68)
• Disappears by 7-10 years due to spontaneous regression
(Figs 3.69 and 3.70) showing signs of involution. It is
important to note that one should not intervene till
70 PLASTIC SURGERY MADE EASY

FIGURE 3.62: Skin changes in FIGURE 3.63: Portwine skin


portwine—verrucoid eruptions changes

FIGURE 3.64: Skin changes FIGURE 3.65: Skin changes in


portwine lateral view portwine stain
SKIN AND SUBCUTANEOUS TISSUE 71

FIGURE 3.68: Strawberry


hemangioma

FIGURE 3.66: Strawberry type

FIGURE 3.67: Strawberry type FIGURE 3.69: Resolving


hemangioma right eye

spontaneous regression takes place, as surgical intervention


results in severe deformity (Figs 3.71 and 3.72)
• Associated with “Kasabach-Meritt syndrome” which is
hemangioma with thrombocytopenia
• High serum levels of “Estradiol” in patients less than 1 year
of age and hence response to corticosteroid treatment is
high in infants
72 PLASTIC SURGERY MADE EASY

FIGURE 3.70: Involuting hemangioma FIGURE 3.71: Involuting type

B. Embryological classification—capillary, venous, arterial


and arteriovenous
Venous type
• Present at birth
• Consists of multiple venous channels (Figs 3.73 to 3.79)
• No tendency to involute
• Deep blue diffuse swelling with gigantism
• Slow compression and slow filling
• Increases in size against gravity
• Phleboliths may be palpable
• Associated with “Maffuci “ and “Blue rubber bleb”
syndrome
Arteriovenous Malformation
• Pulsatile swelling (Fig 3.80)
• Warm
• Thrill, Bruit and Continuous machinery murmur
C. Biological classification (Histological) Hemangiomas
and Malformations
1. Hemangioma
• Hemangioma (Strawberry)
SKIN AND SUBCUTANEOUS TISSUE 73

FIGURE 3.72: Surgical FIGURE 3.73: Venous malformation


intervention with poor results cheek

FIGURE 3.74: Venous FIGURE 3.75: Venous malformation


malformation of left cheek of upper lip
74 PLASTIC SURGERY MADE EASY

FIGURE 3.76: Venous malformation FIGURE 3.77: Venous Vascular


of lower lip malformation tongue

FIGURE 3.78: Lymphatico-venous FIGURE 3.79: Venous


malformation malformations of the hand

• Most common abnormal growth of infancy. They occur


in 1-2% of newborns
• About 80% of hemangiomas are noted in the first month
of life 80%—single tumor and 20%—multiple
SKIN AND SUBCUTANEOUS TISSUE 75

FIGURE 3.80: Arteriovenous


malformation of the upper lip

• Majority (60%) of hemangiomas occur in the head and


neck
• Male: Female ratio of 1: 3-5
• Red patch or a whitened area on the skin known as a
“herald spot” (quiet phase)
• First 4-8 months—grows rapidly (proliferative phase).
establishes new blood channels around itself and
appears cherry red or “strawberry” like
• Between 6-12 months—reaches a plateau and begins
to resolve around 18-24 months (involuting phase)
• Disappear—50% by 5 years, 70% by 7 years.
Histopathology
• Characterized by hyper cellular and endothelial
multiplication (Plump, rapidly dividing endothelial cells)
• Gradually with time cells flatten and mature
• Mast cells appear with progressive deposition of fibrous
tissue.
Management
• Wait and watch
• Systemic steroids—prednisolone 2 mg/kg/day
• Intralesional corticosteroids—Triamcenalone
76 PLASTIC SURGERY MADE EASY
• Intralesional (STD)—Sodium tetradecyl sulfate 0.1ml
at one site and the distance between two sites should
be 1 cm. A total dose of 1 ml should be given at any one
time. It acts by both tissue irritation and thrombosis
resulting in inflammation, fibrosis and obliteration of
vascular channels.
• Recombinant Interferon Alfa-2a. Used when heman-
gioma is not responding to steroid. The dose is 2-3
million units/m2 injected subcutaneous daily for 6-12
months.
• Laser therapy—Flash lamp pulsed dye.
• Surgical excision (wait till regression is complete).
Complication
• Ulceration
• Destruction
• Distortion
• Diversion of blood flow
• Obstruction of vital structures
• Bleeding
• Kasabach-Merritt phenomenon
Kasabach-Merritt phenomenon
• It is a life threatening complication of hemangioma
• Present at birth
• Located at trunk, shoulder, thigh and retroperitonium
• Involved skin is red purple and shiny
• Thrombocytopenia is profound
• Prothrombin time is increased
• Activated partial thromboplastin time is increased
• Risk of hemorrage is high.
2. Vascular malformation (Portwine, venous, arterio-
venous)
• Normal endothelial cell turnover. Present at birth and
grows with the child
• Malformations are true structural aberrations in the
development of the blood vessels themselves
• Found in 1-4% of the population
• Many are obvious at birth
SKIN AND SUBCUTANEOUS TISSUE 77
• Some undetected at birth are not recognized until
adolescence or adulthood
• Male female ratio—equal
Vascular malformations are subdivided into
I. Slow Flow
a. Capillary
b. Venous
c. Lymphatic
d. Combination
2. Fast Flow
a. Arterial—Aneurism,
b. Arteriovenous—AVM , AVF
I. Slow Flow
a. Capillary Malformation (Port-wine stain)
• Macular, red vascular stain obvious at birth and persists for life
• Sturge-Weber syndrome—Facial capillary malformation, ipsi-
lateral pial and ocular vascular malformation
• Trigeminal nerve -V1 dermatome
• Seizures, developmental delay
• Glaucoma, retinal detachment
• Treatment—Flash lamp pulsed dye laser.
b. Venous Malformation
• Congenital structural anomalies of venous channels within the
skin and other organs
• Enlarges proportionately with the child and do not regress
• May change with blood pressure and hormonal modulation
• The most common location is the lower limbs
• Skeletal deformities may occur in 35%
• Compressible, slow filling, more obvious in dependant position
• Episodic thrombosis, phleboliths
Treatment—Sclerotherapy, surgical resection and compression
bandages.
2. Fast Flow
a. AV Malformation
Most fast-flow malformation in children are arteriovenous
malformations.
78 PLASTIC SURGERY MADE EASY
Clinically one can feel warmth, pulsations, thrill, bruit, and
continuous machinery murmur. Ischemic skin changes, ulceration,
pain and intermittent bleeding may occur.
Treatment—Embolization followed by surgical resection 24-72
hours later.

Syndromes involving Vascular Malformations


• Klippel-Trenaunay syndrome—(Vascular gigantism)
Muscle hypertrophy, thickening of the skin, subcutaneous tissues
and bone.
Most often, they affect a single lower extremity (Figs 3.81 to
3.83).
A persistent lateral vein extending from the lateral malleolus to
the gluteal region is common.
• Maffucci syndrome
Multiple enchondromas.
Symptoms occur by puberty, No sex predilection exists.
Twenty percent of patients develop chondrosarcomas
• Blue “rubber-bleb” nevus (Bean) syndrome
Venous malformations involving the skin and gastrointestinal
tract.
Lesions manifest at adolescence.

FIGURE 3.81: Klippel-Trenaunay FIGURE 3.82: Angiomatosis skin


syndrome involving upper extre- changes
mity
SKIN AND SUBCUTANEOUS TISSUE 79

FIGURE 3.83: Postoperative


excision and STSG

• Von Hippel-Lindau disease


Congenital disorder characterized by capillary hamartomas
involving multiple organs.The retina and optic nerve are
involved most commonly.
• Osler-Weber-Rendu disease
Multiple system hereditary telangiectasias.
Recurrent hemorrhage, GI mucosal bleeds.

Hemangioma vs Vascular Malformations


• Time of appearance
Hemangiomas usually appear after birth.
Vascular malformations usually are present at birth.
• Color
Hemangiomas change color from a bright scarlet to a deeper
hue during the first year of life.
vascular malformations have a consistent purplish or bluish
color or no color at all.
• Texture
Hemangiomas have a firm, consistency like dough vascular
malformations often contain fluid-filled areas and are more
compressible. Some vascular malformations visibly pulse with
the heart beat.
• Change over time
Hemangioma usually resolve by themselves
Vascular malformations remain throughout life unless they are
removed by surgery or laser treatment.
80 PLASTIC SURGERY MADE EASY
• Associated Deformities
Skeletal deformities are rare with hemangiomas, but are
common with vascular malformations, especially lymphatic
malformations.
Pyogenic Granuloma—Also known as “ Band aid disease” .
It is a capillary hemangioma that has an intrinsic inflammatory
cell infiltrate. It arises spontaneously and has a relationship to
trauma, cherry red in color, friable and bleeds on touch.
Treatment is by curettage or excision.

PREMALIGNANT LESIONS
• Actinic keratosis or solar keratosis
• Bowen’s disease involves skin and mucous membrane
• Erythroplacia of queyrat—referred as Bowen’s disease of
mucous membrane. Affects glans penis
• Leukoplakia (white patch)
• Xeroderma pigmentosa
• Keratoacanthoma
• Radiation dermatitis
• Chronic scar (Marjolins ulcer)

XERODERMA PIGMENTOSA
Introduction
This condition occurs due to a deficiency of the enzyme thiamine
dimerase. Thiamine absorbs UV light and forms dimers. These
dimers cannot be broken down due to the enzyme deficiency . The
resultant build up of thiamine dimers induces defects in the structure
of DNA.
• The condition was first described by Hebra and Kaposi in 1874
• Termed by Kaposi in 1882, hence also known as Kaposi’s
disease
• A systemic disease that occurs primarily as a skin condition
(Figs 3.84 to 3.86)
• Rare genetic disease
• Transmitted via an incomplete sex linked recessive gene
• Extreme sensitivity to sunlight
SKIN AND SUBCUTANEOUS TISSUE 81

FIGURE 3.84: Xeroderma pigmen- FIGURE 3.85: Xeroderma


tosa with multiple skin cancer pigmentosa

FIGURE 3.86: Xeroderma


pigmentosa with melanoma

• Progressive drying, thining of skin, keratosis and malignant


changes like basal cell carcinoma, squamous cell carcinoma
and melanoma are common. Death is due to metastatic disease
• Management—Protection from sunlight and early aggressive
treatment of skin tumors.

Characteristic Feature (Remember as 4—P)


• Photosensitivity
• Pigmentation of skin
82 PLASTIC SURGERY MADE EASY
• Premature aging
• Prone for malignancies of skin

Pathophysiology
• Deficiency of the enzyme endonuclease
• Inability to repair the damaged DNA
• The factors that exaggerate the effects of UV light includes drugs
such as chlorpromazine, nitrofurantoin, mitomycin, azithromycin
and carcinogens such as benzopyrones.

Incidence
• 1: 2,50,000
• Equal sex incidence
• All races equally affected
• Usually seen at 1 or 2 years of age.

Clinical Features
Described in three stages:
Stage 1 Seen after six months of age
Seen in sun exposed areas
Scaly, freckling areas of increased pigmentation
Stage 2 Poikiloderma stage
Pigmentation, atrophy, telangiectasia and mottling
Stage 3 Malignancies such as squamous cell carcinoma, basal
cell carcinoma and malignant melanoma.

Problems Associated
Ocular manifestations seen in 80% of the patients. Increased
pigmentation of eyelids and loss of eyelashes. CNS manifestations
seen in 20% of the patients.

Course of the Disease


• Fatal before twenty years of age
• Two-thirds die before ten years of age
• The causes include multiple metastases.
SKIN AND SUBCUTANEOUS TISSUE 83
Treatment
• Protection from sunlight—They are called as “children of the
moon” as they can go out without protective covering after
sunset
• Always use two layers of cloth and broad brimmed hat
• Sun protection cream with maximum. Sun protecting factor
• Sun glasses with side coverings
• Examination by the physician every three months for early
detection of malignancies
• Early and adequate excision of all tumors
• Methylcellulose eyedrops as artificial tears.

MARJOLIN’S ULCER
It is a squamous cell carcinoma arising from a long-standing ulcer
either venous or a burnscar. It grows slowly as the scar is relatively
avascular. It is painless as scar tissue contains no nerves. Secondary
deposits do not occur in the regional lymph nodes as lymphatic
vessels have been destroyed. If the ulcer invades normal tissue
surrounding the scar, lymph nodes are liable to be involved and
malignant change—squamous cell carcinoma can occur (Fig.
3.87).

FIGURE 3.87: Marjolin


ulcer

MALIGNANT TUMORS OF SKIN


BASAL CELL CARCINOMA
Introduction
Basal cell carcinoma arises from cells of the basal layer of the
epidermis. It usually affects patients between 40 to 80 years. It
84 PLASTIC SURGERY MADE EASY
grows slowly, becomes locally invasive and penetrates deeper tissue
hence metastasis is rare. A history of a spot that never heals is a
typical complaint.

Etiology
Etiology is by ultraviolet radiation. It is the most common skin tumor.
Associated with predisposing conditions
• Sun exposure
• Advancing age
• Fair complexion
• Nevus sebaceous
• Albinism
• Xeroderma pigmentosa
• Ultraviolet radiation
• Unstable burn scar.

Incidence
Incidence is high in Australia due to ultra violet radiation derived
from sunlight.

Clinical Features
• Elevated above skin level
• Pearly translucent edges
• Pigmented
• Common on face
Based on gross appearance, Basal cell carcinoma is classified
into 5 types.

Types
• Nodular ulcerative carcinoma (Most common, single, rodent
ulcer) (Figs 3.88 to 3.90)
• Superficial basal cell carcinoma (multiple)
• Sclerosing basal cell (recurs frequently) (Fig.3.91)
• Pigmented basal cell
• Basal cell nevus syndrome.
SKIN AND SUBCUTANEOUS TISSUE 85

FIGURE 3.88: Basal cell FIGURE 3.89: Basal cell caricnoma


carcinoma pre-auricular region

FIGURE 3.90: Basal cell carcinoma FIGURE 3.91: Field fire type of
basal cell carcinoma

Nodular Ulcerative Type


• Most common type
• Undergoes central ulceration, ulcer surrounded by a pearly
rolled edge
• Temporary healing followed by further ulceration with serous
discharge and bleeding
• Spot which never heals, keeps scabbing over and breaking
down
86 PLASTIC SURGERY MADE EASY
• Slow growing, gradually erodes deeper tissues producing severe
disfigurement
• Does not metastasize. Dissemination by lymphatics and blood
stream does not occur.

Treatment
Radiation therapy, Surgery, Cryotherapy, Excision and local flap.

SQUAMOUS CELL CARCINOMA (Epithelioma)


Definition
Tumor originates from stratum spinosum of the epidermis.
Squamous cell carcinoma is a malignant tumor that arises from
some premalignant conditions (Figs 3.92 to 3.97).

Premalignant Condition
• Actinic keratosis
• Bowen’s disease
• Leukoplakia
• Keratoacanthoma

FIGURE 3.92: Squamous cell FIGURE 3.93: Jaw tumor


carcinoma cheek
SKIN AND SUBCUTANEOUS TISSUE 87

FIGURE 3.94: Squamous cell FIGURE 3.95: Squamous cell


carcinoma neck carcinoma back

FIGURE 3.96: Squamous cell FIGURE 3.97: Squamous cell


carcinoma groin carcinoma nose

Risk Factors
• Tobacco
• Alcohol
• Poor dental hygiene
• Chronic irritation
• Betel nuts

Etiology
• Solar radiation
• Chemical exposure
• Chronic ulcer
• Viral infection
• Radiation
88 PLASTIC SURGERY MADE EASY
Clinical Features
• More malignant
• More rapidly growing and occurs in
Pre-existing skin lesions
Post irradiation
Long-standing venous ulcers
Prolonged irritation of skin
• Irregular in outline
• Edges raised and everted
• Base indurated and attached to deeper structures
• Blood stained discharge
• Lymph nodes involved.

Types
• Verrucous—slow growing
• Ulcerative—rapidly growing

Spread
• Regional
• Distant metastasis

Treatment
• Wide excision and reconstruction
• Radiotherapy
• Chemotherapy

MELANOMA
Definition
Melanoma is a malignant tumor of melanocyte. It is the most serious
and life-threatening form of skin cancer which spreads often to
internal organs. It often arises in a mole and is associated with
excessive sun exposure, and is characterized by changing colors,
size and borders.
SKIN AND SUBCUTANEOUS TISSUE 89
Incidence
There has been a remarkable rise in incidence particularly in
Australia where 40 new cases are seen per 1,00,000 per annum.

Etiology
• Skin–Fair skinned individual
• Sunlight–Heavy exposure to sunlight
• Sex–(high incidence during reproductive period) Hormonal
factors
• Genetic
• Familial 3-6%
• More than half of cutaneous melanoma arise de novo
• The remainder occurs in association with a pre-existing melano-
cytic nevus

Changing mole—Suggestive of Melanoma


• Asymmetry
• Border notching
• Color variegation with black, brown, red, or white hue
• Diameter greater than 6 mm
• Elevation

Clinical Features
• Bleeding
• Ulceration (Fig.3.98)
• Increase in growth
• Itching
• Irregular margins
• Increased pigmentation
• Satellite nodules
• Pigmented halo
FIGURE 3.98: Melanoma foot with
ulceration
Clinical Classification
Type 1: Lesion is flat usually but a few nodules or papules may be
present. The color consists of brown and black shades admixed
with whitish, reddish and bluish gray (Fig. 3.99).
90 PLASTIC SURGERY MADE EASY

FIGURE 3.99: Melanoma type 1 FIGURE 3.100: Melanoma


type 2

Type 2: Lesion is just raised with papules and nodules. The color
consists of brown black admixed with bluish red gray and pink
(Fig. 3.100).
Type 3: The lesion is always raised and may be dome-shaped and
polypoidal. Color is usually uniform bluish black (Fig. 3.101).

Clinical Staging
In terms of the degree of advancement of the disease at the time of
presentation, 3 clinical stages are recognized.
Stage 1: The melanoma is confined to the primary site. Primary
lesion with or without satellite nodules with in a radius of 5 cm of
the primary (Fig. 3.102).
Stage 2: Metastatic involvement of a regional lymph node single
group or intransit cutaneous metastasis (Fig. 3.103).
Stage 3: Involvement of two or more group of lymph-node dis-
seminated cutaneous disease or visceral involvement (Fig. 3.104).
SKIN AND SUBCUTANEOUS TISSUE 91

FIGURE 3.101: Melanoma FIGURE 3.102: Melanoma foot stage 1


type 3

FIGURE 3.103: Melanoma stage 2 FIGURE 3.104: Melanoma with


cutaneous disease

Other Prognostic Risk Factors


In addition to tumor thickness and level of invasion, prognosis is
adversly affected by the following:
• Site – (BANS)
Upper back
Posterior arm
Posterior neck
Posterior scalp
• Ulceration
• Node involvement.
92 PLASTIC SURGERY MADE EASY
Investigation
• Biopsy
• Chest X-ray
• Liver function
• CT scan of all organs.

Classification
Clinicopathological
• Acral lentiginous melanoma—Rarest
• Superficial spreading type—most common
• Lentigo maligna melanoma
• Mucosal melanoma
• Nodular melanoma—Aggressive.

Acral Lentiginous Melanoma


• Sites—palms, soles, or beneath the nail plate (subungual variant)
• Pigment spread to the proximal or lateral nailfolds (Hutchinson
sign, a hallmark for acral lentiginous melanoma).

Superficial Spreading
• Flat or slightly elevated brown lesion, with black, blue, pink, or
white discoloration
• Irregular asymmetric borders
• Most common type, about 65% arises from a pre-existing nevus.
Common in the 4th or 5th decade. Horizontal growth is slow. A
nodule indicates a vertical growth with poor prognosis.

Lentigo Maligna
• 4-15% of cutaneous melanoma
• Sites—head, neck, and arms (sun-damaged skin)
• characterized by development of dark brown to black macular
pigmentation or raised blue black nodules.

Mucosal Melanoma
• Forms 1% of all melanomas
SKIN AND SUBCUTANEOUS TISSUE 93
• Sites—alveoli, palate, supraglottic region, lower and upper labial
mucosa, buccal mucosa and tongue
• Much less malignant (Hutchinson’s melanotic freckle)

Nodular Melanoma
• Most commonly seen on the legs and trunk
• Dark brown to black papule or dome-shaped nodule, which-
may ulcerate and bleed with minor trauma
• Has no horizontal growth. It is less common but more malignant.
Ulceration with bleeding is common.

Histological (Microstaging of melanoma)


This was introduced by Breslow and forms a reliable indicator of
prognosis and affects the local management of the disease. The
thickness of the lesion is measured in millimeter. Breslow, related
prognosis to the maximum thickness of the lesion as measured by
an ocular micrometer.

Breslow’s Microstaging
Thickness of lesion Nodal involvement 5-year survival
<0.75 mm 0 100%
0.76-1.5 10% 80-90
1.6-3.0 20 60
>3.0 40 <50

Clark’s Histological Level of Microstaging


Level 1: The atypical melanocytes are confined to the epidermis
(melanoma in situ)
Level 2: Extended into the papillary dermis but have not reached
the reticular dermis (Fig. 3.105)
Level 3: Penetrated the interface between the papillary dermis and
the reticular dermis but not extended into the reticular dermis
Level 4: Extended into the reticular dermis (Fig. 3.106)
Level 5: Reached into the subcutaneous fat.
94 PLASTIC SURGERY MADE EASY

FIGURE 3.105: Melanoma Clark’s level 2

FIGURE 3.106: Melanoma Clark’s level 4

Treatment
• Biopsy
• Treatment of primary tumor
• Treatment of regional LN
• Systemic chemotherapy
• Cytotoxic therapy—DTIC/dimethyl triazeno imidazole
carboxamide
• Bleomycin
• Immunotherapy
• Hormonal treatment—Tamoxifen, stilbesterol
SKIN AND SUBCUTANEOUS TISSUE 95
Surgery of the Regional Lymph Node
Melanoma disseminated from the primary site to regional lymph
node and then to distant sites.

Surgery for Metastatic Disease


• Regional metastases (intransit metastases)—surgery and intra-
lesional immunotherapeutic approaches, adjuvant radiotherapy.
• Distant metastases—surgery.

Prognosis
• The best indicator of prognosis is Breslow ‘s vertical tumor
thickness, which is measured histologically
• Thin lesion <0.8 mm carry excellent prognosis. Melanoma
with a thickness of more than 5 mm and with LN carry a poor
prognosis.

Recurrence and Spread—Four Types


• Local recurrence
• Locoregional spread to LN is common. Intransit metastases,
subcutaneous nodules in lymphatic pathway between primary
and regional nodes
• Systemic metastases—widespread subcutaneous deposits
together with pulmonary metastases
• Visceral metastases.
Chapter 4

Skin Grafts
98 PLASTIC SURGERY MADE EASY

HISTORY
Skin grafts originated in India 3000 years ago. In the 19th century,
various attempts at using different types of skin grafts were reported.
Although skin graft began many centuries ago, the present
knowledge differs only in the technique and accessory procedures.
1570 Fioravanti reported the successful tissue autograft.
1804 Baronio published his success on free transplantation
of skin on sheep.
1817 Sir Astley Cooper grafted full thickness skin from an
amputated thumb onto the stump for coverage.
1821 Bunger reported free skin autografting using Indian
method in which a piece of skin taken from the buttock
was transplanted to the nasal stump.
1844 Joseph Pancoast grafted autogenous Full thickness
skin from the arms to the nose and the earlobe.
1863 Bert’s experimental work on animal grafts were
successful and opened the way for the pioneers who
contributed the free skin graft.
1869 Reverdin stimulated worldwide interest in skin grafting
with his report of successful pinch grafts.
1870 Lawson, LeFort and Wolfe all used full thickness
grafts for eyelid ectropion.
1872 Ollier demonstrated the importance of dermis in skin
grafting.
1872 Reverdin reported use of his own skin as homografts
with good results.
1873 Thiersch used thin split thickness grafts 0.005 to 0.01
inches in thickness.
1877 Reverdin discussed skin grafting from pig to human
beings.
1881 Girdner reported the first clinical use of allograft by
harvesting a suicide victims skin to use for closure of a
burn wound.
SKIN GRAFTS 99
1888 Hubscher termed the early nourishment of skin grafts
as plasmatic circulation.
1893 Krause popularized the use of full thickness grafts
and known as Wolfe-Krause grafts.
1910 John Staige Davis reported use of allografts and
xenografts.
1938 Bettman reported successful use of allograft in 2
children with more than 60% TBSA burn.
1940 Medawar pioneering work on the histo chemical
aspects of the epidermis.
1941 Brown and McDowell popularized thick split
thickness grafts for treatment of burns.
1944 Webster reported the successful take of the refrigerated
skin graft.
1950 Brown and Fryer used allograft as biological dressing.
1951 Storey and Leblond reported that epidermis
undergoes growth and replacement throughout life.
1953 Regnell reported primary contraction to be greater in
full thickness grafts and least in thin split thickness grafts.
1954 Webster described dermal overgrafting.
1957 Silvetti used bovine skin grafts as a temporary
biological dressing.
1960 Ponten reported sensory pattern of skin grafts to
become that of the recipient wound bed rather than
that of the original graft donor site.
1961 Mir Y Mir reported serial dermabrasion or chemical
peel to reduce graft hyperpigmentation.
1964 Tanner, Vandeput and Olley expanded skin grafts
using skin mesher to be expanded upto 12 times its
original size.
1965 Bromberg et al established the method of treating
burns with pigskin.
100 PLASTIC SURGERY MADE EASY
1966 Morris et al reported beneficial effects of allografts.
1975 Epithelial skin culture technology was published by
Rheinwald and Green.
1976 Rudolph reported that the dermal component of
grafted skin exerts the influence on wound contraction.
1976 Rudolph and Milson reported the use of trypsin to
separate the two layers of the skin.
1979 Cultured human keratinocytes were grown to form an
epithelial layer for grafting.

ANATOMY
Skin envelops the entire surface of the body. It is the largest organ in
the body and constitutes 16% of the total body weight. As a result,
its total destruction is incompatible with survival. Skin serves as a
protective layer and controls temperature regulation. Skin varies in
character with age and location on the body. The thickness of skin
is dependent on age, sex, site and race. Skin is thinner in infants
and women compared to men. Skin varies from 5 thousandths to
150 thousandths of an inch in thickness. Skin is thin in the first
decade and again in the 5th decade. In between skin thickens
progressively. Skin is thin in certain areas of the body and thick
particularly in the palm and soles. The skin also looses its elasticity
with time.
The skin has two layers and differ in character. The outer most
thinner layer is the epidermis and inner most thicker layer is the
dermis. The two layers are connected by means of protoplasmic
processes and elastic fibers.

Epidermis
• Is of ectodermal origin
• It is avascular and depends on dermis for its survival
• Epidermis is a stratified squamous epithelium
• It has five layers and consists of stratum germinatum adjacent to
dermis, stratum spinosum, stratum granulosum, stratum lucidum
and stratum corneum. The more superficial layer is stratum
SKIN GRAFTS 101
corneum which is the dead and desquamating layer. Epidermis
undergoes growth and replacement throughout life
• The keratinized layer of the epidermis protects the body from
the environment
• The epidermal layer has two types of cells, they are keratinocytes
and melanocytes and takes part in melanin synthesis to
determine the color of the skin.

Dermis
• Is of mesodermal origin
• It has extensive vascular supply
• The predominant components of dermis are collagen, elastic
fibers and ground substance
• It has two layers a superficial or papillary layer and a deep or
reticular layer
• The papillary layer is characterized by widely separated collagen
fibers whereas the deep reticular dermis has dense coarser
collagen fibers
• The epidermal appendages like hair follicles, sebaceous glands
and sweat glands invade the dermis
• Sebaceous glands provide sebum which lubricates hair and
skin
• Sweat glands are of two types, i.e. eccrine and apocrine and are
under nervous control. Eccrine glands respond to emotions
and are important for temperature regulation and is odourless
whereas apocrine gland secretes continuously and has odour.

FUNCTIONS OF SKIN
• Protection—Protects the body from heat and cold
• Thermoregulation—Prevents heat loss
• Immunological—Prevents entry of micro-organism
• Secretory
• Excretory
• Neurosensory—for pain, touch to hot and cold
• Metabolic—production of vitamin D
102 PLASTIC SURGERY MADE EASY
SKIN GRAFTS
Definition
Skin graft is a segment of skin separated from the donor site and
transplanted to the recipient site devoid of its blood supply.

Classification
Skin grafts are classified as:
Autograft—Is a piece of skin taken from one site of the body and
transplanted to another site in the same person.
Allograft (Homograft)
• Is a piece of skin taken from another individual of the same
species
• It is used in extensive burns where autograft donor sites are
scarce
• It prevents protein and water loss
• It also decreases bacterial count and pain
• It is used as a test of readiness of a wound to accept an autograft
• Used as a temporary biological dressing in patients too sick to
undergo definitive autografting. Allografts though temporary
they do get vascularized before the rejection reaction. Although
O’Donoghue noted the difference in the angiogenic properties
of fresh skin allografts, he also noted that inspite of this difference
allografts were capable of neovascularization before it got
rejected
• Although it is an important skin cover, unfortunately the risk of
HIV transmission through cadaver allografts may outweigh the
benefits.
Isograft—refers to genetically identical donor and recipient
individuals such as twins in humans.
Xenograft—Is a graft taken from another species. Used as a
temporary biological dressing in cases of autograft and allograft
shortage. The advantages are that it is relatively low cost readily
available and can be easily stored. The commonest temporary
biological dressing is the pig skin.
SKIN GRAFTS 103
Types
Skin graft consists of whole of epidermis and a portion of dermis.
Depending on the depth of dermal involvement, skin grafts can be
either split thickness or full thickness grafts.

Split Thickness Grafts (Fig. 4.1)


• Involve the whole of epidermis and a small part of dermis
• Depending on the depth of dermal involvement it can be further
divided into thin split thickness skin grafts or thick split thickness
skin grafts.
• A very thin split thickness skin graft composed of almost pure
epithelium has great clinical application particularly in burn
patient who have had cultured skin during the acute phase of
care. Reconstruction on such patients is a challenge
• The average thickness of the graft is between 5-12/1000 of an
inch. Use of Alloderm as a dermal component and a very thin
epidermal graft as a cover can be successfully used in burn
patients.
• Advantages of thin split thickness skin grafts are that it can be
used in less than ideal wound bed and requires less optimal
vascularity.
• Disadvantages—It contracts and the graft is unstable.

FIGURE 4.1: Layers of skin


104 PLASTIC SURGERY MADE EASY
Partial Thickness
• Skin grafts are very useful in reconstruction of various burn
deformities.
• It contains more dermis so contraction is less.
• The average split thickness skin graft used is between 0.012-
0.018 inch.
• Split thickness skin grafts have a large number of cut blood
vessels on the undersurface of the graft and therefore “take” is
excellent .
• The donor site for split thickness skin graft can be any where in
the body. Since it includes only a portion of the dermis, the
epidermal appendages which are present in the dermis re-
epithelialize and result in spontaneous healing of the donor
site. Moreover skin can be harvested from the same site many
times.
• Advantages are that it can be used in large wounds with
questionable circulation.The grafted skin always maintains the
epidermal characteristics of the donor area.
• Disadvantages are that it tends to contract and has
hyperpigmentation of the graft. Depending on the setting of the
dermatome, translucency of the graft and the bleeding pattern
of the donor site one can refer to skin grafts as being either thin,
medium and thick. A very thin graft is transparent and has fine
bleeding points at the donor site.

Full Thickness Skin Grafts (Fig. 4.2)


• Includes epidermis and full
thickness of dermis with
varying portions of sweat
glands, sebaceous glands,
and hair follicles
• Since it includes the entire
thickness of the skin, it
retains all the characters of
the skin
FIGURE 4.2: Full thickness graft
• It resists contraction
• The texture and pigment closely resembles the normal skin.
SKIN GRAFTS 105
• The disadvantages are that it requires excellent vascularity
and therefore less useful in contaminated wounds, chronic
wounds and poorly vascularized bed.

Composite Graft
• Includes the full thickness of the skin and a portion of the
underlying tissue such as subcutaneous tissue and cartilage
• Common example of such a graft is for reconstructing the nasal
ala, where a wedge of skin, cartilage and skin is taken from the
ear.
• The risk of non-vascularization of this type of graft limits its size
and use since its blood supply comes through its margins instead
of its base.
• The other examples are full thickness eyelid and nipple grafts
• The survival of composite grafts can be improved by cooling
the graft to 5-10 degree centigrade.
• The safe size of the graft can be from 1.5-3.0 square centimeter.

Tissue Cultured Cells


• This technique requires a full thickness skin biopsy consisting
of a few square centimeter.
• The epidermal cells are separated from the dermis by using
trypsin. After an in vitro culture period of 3-4 weeks. The
autologous keratinocytes expand to approximately one square
meter available for wound coverage.
• The short comings of cultured epidermal cells are:
• It requires 3-4 weeks for culturing
• Very fragile and must be handled with extreme care
• Low rate of graft take
• Requires prolonged immobilization in order to facilitate
graft take
• Can blister and slough leads to less than optimal long-term
results and is very expensive.

SELECTION
Selection of the site and type of graft is an important decision in skin
grafting. During the acute phase of care obviously the most important
106 PLASTIC SURGERY MADE EASY
decision is to save life and hence split thickness skin grafts is the
choice of treatment for wound coverage. However, during the
reconstructive phase of burn care decision of the skin grafts becomes
more important for cosmesis, color match and preventing further
contractures.
• Epidermal grafts—Clearly are important in patients who have
had extensive burn wound covered with cultured skin during
their acute phase of care. Reconstructive surgery on such patients
is a challenge considering that there is no normal skin cover. In
these patients burn scar contracture release and resurfacing the
defect is successfully accomplished by using alloderm as a
dermal component and a thin epidermal layer of skin which is
in fact the cultured keratinocytes.
• Partial thickness skin grafts—Split thickness skin graft is
the first choice of treatment in wounds with questionable
circulation or large size of the defect following release of burn
scar contractures, despite many disadvantages like contraction,
abnormal pigmentation and lack of growth in children. It can be
taken from any where in the body including the scalp and
extremities. When possible it should be taken from the hidden
areas like the buttocks to camouflage the scars. If split thickness
skin grafts are required for the face then it should be taken from
either the scalp or supraclavicular areas. A graft taken from the
buttock or lower extremity should not be used on the face as it
tends to give a yellowish color.
• Full thickness skin grafts—Most often used for the face and
neck where cosmesis plays an important role. The donor site
for the face is usually from the post auricular or supraclavicular
region. The donor site is usually closed primarily. Large
dimensions of FTSG measuring 30 x 20 cm from the abdomen
and thigh to resurface the defect following release of burn scar
contracture of the neck has given excellent results. The donor
site is resurfaced with split thickness skin grafts. The other useful
donor site includes skin from the medial thigh with dark
pigmentation particularly in reconstruction of the areola. The
other areas are the elbow and groin crease.
SKIN GRAFTS 107
HARVESTING
Free Hand
• Humby knife—Is a common free hand dermatome for
cutting grafts. The basic maneuver is a gradual back and
forth movement. A roller is attached to the knife and the
distance between the blade and the roller is calibrated to permit
varying thickness of graft. Large pieces of skin can be taken in
the best of hands, however, the edges of the graft are always
irregular.
• Goulian—Is a smaller knife and very useful for taking grafts in
the outpatients setting.
• Scalpel—Is very useful for harvesting a full thickness skin graft
which is defatted using tenotomy scissors.

Power Dermatome
• Padgett—is an electric driven dermatome. It is lighter and easier
to use. It has a rapidly vibrating movement. The width of the
graft depends on the width setting of the dermatome. The
thickness of the graft is adjusted by setting the knob to
appropriate thickness.
• Zimmer—is compressed air driven.The advantage over electric
dermatome is that it allows control of blade speed.
• Castroviejo-It is a small electric dermatome. Very useful for
harvesting mucous membrane grafts.

Hand Driven
Drum dermatomes—Reese dermatome is precise when
compared to other drum dermatomes. It comes with a set of shims
and difficult to change thickness in midstream. The movement is by
gradual rotation of the drum over rotating blade.
Padgett dermatome—Is less precise than the Reese type, but it is
lighter and easier to use and allows re-calibration of depth while
cutting.
108 PLASTIC SURGERY MADE EASY

FIGURE 4.3: Meshed graft FIGURE 4.4: Sheet graft

MESHING OF GRAFTS
Skin grafts are meshed for various reasons. For example, when the
skin is insufficient as in extensive burns where skin can be meshed
to expand 6-12 times its original size.
• It is also useful when a lot of drainage is expected or
• When a convoluted surface is grafted
• The various instruments used for meshing grafts
• Simple hand-mesh using scalpel blade
• Zimmer skin graft mesher—where a plastic sheet is required for
the graft to be advanced through the instrument (Fig. 4.3)
• Mesher which does not require a plastic sheet for feeding the
graft into the mesher called the Brennen
Sheet grafts are used where cosmesis is required (Fig. 4.4).

CLINICAL APPLICATION
Preparation of Wound
For a graft to take it must have a vascular bed and proper preparation
of the wound. If the wound is infected then either debriding the
wound or jet lavage helps to reduce the bacterial count. To create a
SKIN GRAFTS 109
vascular bed temporary allograft can also be used for few days
before applying the autograft. Graft will not take on bare bone,
cartilage, bare tendon and irradiated surfaces. However, sometimes
it is possible to cover a denuded tendon or nerve with a skin graft
based on the bridging phenomenon if the area to be covered is
1 cm or less .

Fixation of Graft
In order for the graft to survive, there should be a good contact
between the graft and the recipient bed. This is achieved by either
suturing the graft to the bed, stapled or taped. Further to ensure
perfect contact bolster tie over dressing or circumferential wraps are
used. To avoid movement splints are very important particularly for
the extremities.

Vascularization of the Graft


The three steps are plasmatic imbibition, inosculation and
neovascularization.
Plasmatic imbibition—Immediately after the skin graft comes
into contact with the recipient bed it begins to absorb a plasma-like
fluid by capillary action. At the same time a fibrin network is formed
between the graft and the recipient bed. The whole process lasts
approximately for 48 hours during which time the fibrin bonds
cause graft to adhere to the recipient bed. But Clemmesen, Converse,
and Peer believe that serum helps to keep the graft moist at this
stage.
Inosculation—Is mouth to mouth contact of the blood vessels
from the recipient bed to the graft. This development of anastomosis
allows the flow of blood into the vessels establishing circulation of
blood.
Neovascularization—Once the circulation is established new
blood vessels start forming between the graft and the recipient bed.
The survival of graft initially is by vascular connection followed later
by vascular ingrowth.
110 PLASTIC SURGERY MADE EASY
Graft failure—Grafts can fail if there is infection or inadequate
graft bed. More over if there is hematoma, seroma or pus discharge
separating the graft from the recipient bed, graft take can fail. Finally
if there is shearing movement preventing the steps of vascularization,
grafts can again fail. Technical errors by placing the graft upside
down also results in complete rejection of take.

CHARACTERISTICS OF GRAFTED SKIN


Contraction
Skin grafts undergo two types of contraction, i.e. primary and
secondary.

Primary Contraction
It is the immediate recoil of the harvested graft and depends on the
elastic fibers present in the graft. For example, when a split thickness
skin graft is taken it has few elastic fibers and hence the immediate
contraction is very little and not noticeable. This can be overcome
by stretching the graft as it is sutured into place. Where as full
thickness skin grafts which contains more elastic fibers due to its
thick dermal component has more severe primary contraction. Davis
and Kitlowski found that split thickness skin grafts had 9% primary
contraction and full thickness graft had 41% contraction.

Secondary Contraction
Depends on the recipient bed. The thinner the graft more the
contraction. Thicker grafts have less tendency for contraction. To
certain extent this can be prevented by using splints. It is also noted
that split thickness skin grafts have 41% secondary contraction
whereas full thickness skin grafts has a minimum of less than 9%
contraction. Various authors feel that at least 75% of the dermis
should be incorporated in a split thickness skin graft to maximally
inhibit wound contraction. Rudolph noted inhibition of
myofibroblasts in the wound bed on application of skin grafts when
compared to non-grafted sites. Regnell noted the contracting
tendency of full thickness free skin graft to be more due to elastic
recoil of the graft.
SKIN GRAFTS 111
Pigment Changes
Skin grafts have a major pigment mismatch problem. Split thickness
skin grafts tend to darken although various treatment options are
available to lessen the pigmentation by avoiding UV light exposure
for 6 months, using sun blocking agents with a protective factor of
15 or more. The other methods are either serial dermabrasions and
chemical peels. Yet pigmentation changes continue to persist. Full
thickness skin grafts maintain the best pigment match and are
preferred in areas of face.

Graft Reinnervation
Skin grafts slowly regain normal sensation. Nerves grow into skin
grafts from wound margins. Sensation usually return between
1-6 months duration. Ponton found that grafts assumed the pattern
of innervation similar to the recipient tissue, whereas Fitzgerald at al
noted pattern to be that of the donor.

DONOR SITE
Split thickness skin graft donor site heals spontaneously by
epithelialization from the epidermal elements which are present in
the dermis like the hair follicle, sweat glands and sebaceous glands
in a week’s time (Fig. 4.5). The various types of dressings used for
donor site are scarlet red xeroform gauze, vasaline gauze and

FIGURE 4.5: Donor site


112 PLASTIC SURGERY MADE EASY

ointment impregnated gauze with bulky gauze on top. This bulky


dressing should be removed the next day and the graft is allowed to
air dry. A gentle heat lamp application speeds epithelialization.
Opsite an artificial semipermeable membrane can be used when
donor site is small. This results in improved reduction of pain.

STORAGE
Skin has to be stored to overcome the destructive effects of hypoxic
metabolism. On short-term basis skin grafts can be stored using
saline moist gauze. When stored by this method it can be preserved
for about 21 days. Long term is by freezing the graft with glycerol.
Allograft storage—Various skin banks have been developed to store
cadaver skin using glycerol and liquid nitrogen.
Chapter 5

Skin Flaps
114 PLASTIC SURGERY MADE EASY
INTRODUCTION
Flaps are not very difficult to execute, but it requires an
understanding of the different technique for moving tissues such as
knowledge of geometry, anatomy and biomechanics of skin for its
survival. Skin flaps are required where wounds do not permit the
use of grafts, such as poor vascular bed, contour deformity, bare
bone cartilage and tendon. The advantages of a flap are that it gives
an excellent color match. It is soft and pliable. The disadvantage is
that they are bulky in appearance.

DEFINITION
A skin flap consists of skin and subcutaneous tissue that is moved
from one part of the body to another with its blood supply intact.
Skin flaps get its blood supply from the dermal and subdermal
plexus.

HISTORY
The term flap was derived from the Dutch word “Flappe” meaning
anything that is hung broad and loose fastened only by the side.
1000 BC Pot maker family of India performed Indian forehead
flap for nasal reconstruction.
25 BC Celsus Introduced advancement flaps.
1597 Tagliacozzi performed the arm flap for nasal
reconstruction.
1814 Carpue performed forehead flap for nose reconstruct-
ion in less than 40 minutes.
1829 Fricke described the basic type of transposition flap
1837 Horner introduced Z-plasty.
1862 Wood performed groin flap.
1889 Manchot defined cutaneous territories based on blood
supply.
1893 Spalteholz described fasciocutaneous blood supply
to skin.
SKIN FLAPS 115
1898 Monks performed single stage island pedicle flap.
1904 Berger was the first to describe a true Z-plasty.
1914 Morestin described multiple Z-plasty.
1918 Gillies described the tube pedicle flaps.
1918 Esser described V-Y advancement flap
1930 Limberg described the geometric principles involved
in Z-plasty.
1931 Staige Davis noted improvement in the quality of
scar tissue following Z-plasty release of scar tissue.
1937 Ombredanne described the technique of W-plasty
and later in 1959 by Borges.
1953 Zimany introduced bilobed flap.
1963 Goldwyn et al performed groin free flap in dog.
1964 Bakamjian described delto-pectoral flap.
1970 Milton denounced the length to width ratio limitation
in skin flaps.
1972 Mcgregor and Jackson devised the groin flap and
classified skin flaps as either random and axial pattern.
1973 Daniel and Williams investigated the random pattern
flap and showed that increasing the width of a flap did
not increase the surviving length. They also defined
blood supply of skin to arise from two types of arteries.
1981 Ponten described fasciocutaneous flap.
1983 Esser’s concept of arterial flap was reintroduced.
1987 Palmer and Taylor proposed the concept of angio-
somes.

INDICATION
• Recipient bed with poor vascular bed
• Reconstruction of full thickness defect
• Re-operation through the flap to repair underlying structures
116 PLASTIC SURGERY MADE EASY
Pre-Requisites
• Choose the flap from the most simplest to complex
• Make a pattern, reverse plan to properly execute the flap
• Have a back up plan and back up of a back up plan
• Avoid bleeding, pressure, tension and kinking
• Do not cause deformity of secondary structures.

CLASSIFICATION OF FLAPS
a. Depending on the type of tissue composition
Cutaneous
Fasciocutaneous
Musculocutaneous
Osteocutaneous
b. Depending on the type of blood supply
Random flap and Axial flap
c. Depending on the type of movement
Tumbling, Waltzing, Caterpillar.

BLOOD SUPPLY
Blood supply of the skin can arise from Direct cutaneous,
Fasciocutaneous and Musculocutaneous arteries. The skin receives
its blood supply from either the perforator musculocutaneous
arteries or perforator direct cutaneous arteries that supply the dermal
subdermal plexus of the skin . These two arteries arise from the
major vessels of the aorta namely the segmental arteries, anastomotic
arteries and the axial arteries.

Branches of Vascular Tree


• Direct muscular
• Musculocutaneous
• Septocutaneous
• Fasciocutaneous
• Direct cutaneous
SKIN FLAPS 117
TYPES OF FLAP
1. Local
A. Those that rotate about a pivot point:
• Rotation
• Transposition
• Interpolation flap
B. Those that move forwards:
• Advancement flap
2. Regional flaps
• Tissue expanded flaps
• Island flaps
• De-epithelialized flaps and
• Interpolation flaps
3. Distant
• Direct flaps
• Indirect flaps

Local Flaps
Local flaps are raised from an adjacent tissue in such a manner that
the donor and the recipient areas are in continuity.

Rotation Flaps
Rotation flaps is a semicircular flap of skin and subcutaneous tissue
that rotate about a pivot point . The steps to design this flap (Fig.
5.1).
• Triangulate the defect by making an isosceles triangle
• Make the short side the base of the triangle

FIGURE 5.1: Rotation flap


118 PLASTIC SURGERY MADE EASY

FIGURE 5.2: Rotation flap FIGURE 5.3: Rotation flap


preoperative postoperative

• The defect and the flap together should form a semicircle or the
circumference should be five to eight times the width of the
defect. The base of the flap will be towards the apex of the
triangle
• The tissue is undermined and rotated about a pivot point to
close the defect
• If the tension is great a back cut may be made away from the
base
• The donor site is most often closed primarily
• This type of flap can be used to close scalp, sacral and facial
defects (Figs. 5.2 and 5.3)

Transposition flaps
• Fricke in 1829 described this
flap
• Flap is usually a rectangle of skin
and subcutaneous tissue that is
rotated about a pivot point into
an immediately adjacent defect
(Fig. 5.4)
• The design of this flap requires
the defect to be triangulated
• The flap should extend beyond
the defect because the flap FIGURE 5.4: Transposition
becomes shorter as it rotates flap
SKIN FLAPS 119
• The distance from pivot point to the far end of the triangle
should be the distance from pivot point to the flap length. (AB
=AC)
• The maximal possible movement of this flap is 90 degree from
its original position
• Closure of the donor site is usually by skin graft, direct closure
or another flap transposition can be either simple or right angle
transposition (Figs 5.5 to 5.14)
The different types of transposition flaps are Bilobed flap,
Limberg flap and Z-plasty.

FIGURE 5.5: Transposition flap FIGURE 5.6: Transposition flap


preoperative postoperative

FIGURE 5.7: Large defect scalp FIGURE 5.8: Postoperative large


transposition flap
120 PLASTIC SURGERY MADE EASY

FIGURE 5.9: Simple right FIGURE 5.10: Right angled


angled transposition flap transposition flap

FIGURE 5.11: Instep flap FIGURE 5.12: Nasolabial flap


transposed to heel defect

FIGURE 5.13: Nasolabial flap in


place
SKIN FLAPS 121

FIGURE 5.14: Simple sliding transposition to cover bony defect

Bilobed flap: Esser in 1918


described bilobed flap of equal size
and Zimany in 1953 described flap
of different size (Figs 5.15 to
5.17).
• This flap is basically two
transposition flaps
• Width of flap one is slightly less
than the diameter of the defect FIGURE 5.15: Bilobed flap
and that of second flap is
correspondingly less than flap
one

FIGURE 5.16: Parotid tumor FIGURE 5.17: Reconstructed with


excision bilobed flap
122 PLASTIC SURGERY MADE EASY
• Flap one rotates into the defect and flap two rotates into the
donor site of flap one and the donor site of flap two is closed
primarily
• This flap is best suited to reconstruct small defects on the face
• The design of the flap is to make the defect circular
• Draw three times the diameter of the defect.
• From the center of this line now draw a perpendicular line
which should be bisected at 45 degree angle
• The flaps are now designed in such a manner that the lines
form the center of each flap
• Each flap has 45 degree angle
• The disadvantage of this flap is the complex scar due to the
design of the flap and the pin cushioning effect.
Limberg flap (Figs 5.18 to 5.21)
• Limberg in 1946 designed this flap
• It is a type of transposition flap to close rhomboid defects
• The lesion is excised as a rhomboid
• The rhomboid defect has angles of 60 and 120 degree
• The orientation is such that the 120 degree angle is planned
where excess of skin is present
• A line is drawn from the outer point of the 120 degree angle
• The length of all the sides of the flap should be equal

FIGURE 5.18: Limberg flap FIGURE 5.19: Limberg flap


SKIN FLAPS 123

FIGURE 5.20: Abdominal wall FIGURE 5.21: Limberg flap


defect

• The flap is undermined and transposed into the defect


• The elevation of the flap should be beyond the base of the flaps
to achieve adequate transposition
• The disadvantage is the multiplicity of scars which do not fall in
ideal lines.
Z-plasty (Figs. 5.22 and 5.23)
• Horner introduced this flap in 1837
• Berger described this flap in 1904

FIGURE 5.23: Z-plasty after


FIGURE 5.22: Z-plasty transposing two triangular flaps
124 PLASTIC SURGERY MADE EASY
• Morestin in 1914 described multiple z-plasty
• Limberg in 1929 gave the geometric principles of z-plasty
• The basic principle of the Z-plasty is to transfer a lateral skin
excess transversely to lengthen the areas along the line of the
wound or a tight scar. The angle of the Z-plasty opens up and
the amount of lengthening increases. By curving the Z flaps an
extra tissue in the flap base augments flap vascularity which is
important in scarred tissue.
• Advantages of Z-plasty are that it lengthens the linear scar
• It realigns the scar within the lines of minimal tension
• Disperses the scar in different direction
• It redistributes the tension of the scar
• The classical Z-plasty is two triangular flaps of skin and
subcutaneous tissue of equal size and length with a 60 degree
angle
• Depending on the angles which may vary between 30 and 90
degree flaps can be designed to suit the area of reconstruction
• Variations in Z-plasty is indicated particularly in burn tissue
which has scar on one side and the other side has normal skin
where half Z-plasty procedure is performed consisting of an
incision and the flap fitting into this incision. Incision is made at
right angles to the defect
• The other type is the S-plasty used for web space correction.
Four flap Z-plasty (Figs 5.24 to 5.27)
This flap consists of a 90 degree Z-plasty which is then divided into
45 degree flaps thus converting Z-plast into four flap plasty. This
flap is commonly used for correction of the first web space in the
hand.
Five flap plasty (Figs 5.28 to 5.31)
• Hirshowitz in 1977 described five flap Z-plasty
• Is commonly used for correcting the scar contractures of the
axilla
• This flap is double opposing Z-plasty and a mid line incision
breaking the two Z-plasty transversly
• The triangular flaps of two Z-plasties and Y-V advancement flap
constitute the five-flaps
SKIN FLAPS 125

FIGURE 5.24: Four flap plasty

FIGURE 5.25: Four flap plasty FIGURE 5.26: Four flap preoperative
after

FIGURE 5.27: Four flap release


of first web space
126 PLASTIC SURGERY MADE EASY

FIGURE 5.28: Five flap plasty

FIGURE 5.29: Five flap plasty after transposing the flaps

FIGURE 5.30: Design of five


flap on web contracture

FIGURE 5.31: Post-


operative five flap
plasty
SKIN FLAPS 127
• D lies at the midpoint of the line AB which runs along the ridge
of the web GA and HB complete the outline of the two
Z-plasties
• The angles A and B are about 60 degree
• The incision DF opens as a triangular defect into which CDE is
advanced. The length DF is adjusted for the best fit
• The angles ADF and BDF are slightly larger and need trimming
of excess skin to fit into the triangle.
Six flap Z-plasty is an additional 45 degree angle flap drawn on
to each end of the central limb of a four flap Z-plasty to gain more
length (Fig. 5.32).

FIGURE 5.32: Design of six flap plasty

Seven flap plasty (Figs 5.33 to 5.35)


• The technique was described by Karacaoglan and Uysal in
1994
• This flap is designed so that flaps a,b,c,d, lie below the line A-B
• Flaps e, f, g, lie above the line A-B
• All flap tips meet at the middle of line A-B marked as point C
• The angle is 45 degree for flaps a,b,c,d, and 60 degree for flaps
e,f,g
128 PLASTIC SURGERY MADE EASY

FIGURE 5.33: Seven flap design

FIGURE 5.34: Perineal contracture FIGURE 5.35: Release perineal


contracture with seven flap plasty

• The flaps e,a,g,d, are transposed and flaps b,c,f, are interdigitated
as V-M plasty
• This flap has minimal morbidity with maximal benefit.
W plasty
• Ombredanne in 1937 described W-plasty
• Borges in 1959 to introduce concept of producing zig-zag scar
in asimpler way than Z-plasty
• This is commonly used for scars on the face to change the
direction of a linear scar and to break up the scar into multiple
fine suture lines
• This is aesthetically acceptable than the Z-plasty on the face

Advancement Flap
• Celsus in 25 BC introduced this flap
• Although there are various types of flaps, all have the same type
of movement that is sliding tissues forward
SKIN FLAPS 129
• The flap moves forward into the defect without the lateral
movement. Examples of this type of movement are the elliptical
and the direct closure. The various types of advancement flaps
are simple advancement flaps, bipedicle flaps V-Y and Y-V.
Simple advancement flaps (Figs 5.36 and 5.37)
• Is a rectangular or square flap of skin and subcutaneous tissue
that is moved forward into the defect.
• The length of the flap is gained by taking out burrow’s triangle
from the lateral side of the base of the flap.
• This allows the easy movement of the flap forward to fit into the
defect without any dog ear deformity.

FIGURE 5.36: Melanoma forehead FIGURE 5.37: Postoperative simple


advancement flap

Bipedicle flaps—These flaps are very useful in the scalp and


lower extremity reconstruction. Although it requires grafting of the
donor site and extensive undermining, it plays a great role in
reconstructing scalp defects with superior results in a single stage. It
is used mainly for elliptical defects. The length of the flap is twice the
length of the defect and the width of the flap is half the length of the
defect (Fig. 5.38).
V-Y flaps—“V” shaped incision is made and advanced to the
defect and the posterior incision is closed as a “Y”. This is very
useful for structures such as columella, vermillion border notching
and glabella flap. Running V-Y plasty has gained importance in
correcting the linear burn scar contractures since it does not require
undermining and can be transposed comfortably. This technique is
also very useful in closure of round defects (Figs 5.39 to 5.41).
130 PLASTIC SURGERY MADE EASY

FIGURE 5.38: Bipedicle flap FIGURE 5.39: V-Y plasty

FIGURE 5.40: V-Y plasty for web FIGURE 5.41: Y-V plasty
contracture
SKIN FLAPS 131
Y-V flaps—Most commonly used
for small contractures of the web
spaces.

Regional Flap
If there is a bridge of tissue between
the two flaps then it is called as a
regional flap.
Interpolation flap
• A flap taken from a nearby area
and transposed either above or
below the intervening skin
(Fig.5.42)
• The pedicle of the flap may FIGURE 5.42: Delto-pectoral
contain either only the skin, as an interpolation flap
subcutaneous tissue or it may
contain only the artery which supplies the flap.
• This flap can be used as a single stage when it is called as island
flap or two stages when it is called as pedicle flaps.
Tissue expanded flaps
• Newman in 1957 used rubber balloon for ear reconstruction
• Radovan introduced the concept of tissue expansion in 1976
• Its use for the reconstruction of various problems have become
well known alternative to a reconstructive surgeon
• This technique allows the surgeon to generate skin from the
normal skin with good color match, texture and sensibility
• Tissue expanded skin offers an alternative to distant flaps with
good results (Figs 5.43 and 5.44).
Island flap
• Monks described this flap in 1898
• Pedicle consisting of only the subcutaneous component
• There are two types of island flap depending on the blood supply.
In one, base is subcutaneous tissue and the flap pedicle is short
and arc of rotation limited. In the second type there is definite
vascular pedicle, so pedicle is long and arc of rotation more
• Tunnel is made from the defect to the pedicle base
132 PLASTIC SURGERY MADE EASY

FIGURE 5.43: Tissue expanded FIGURE 5.44: Tissue expanded


flap flap for cheek defect

De-epithelialized flap (Figs 5.45 to 5.48)


• Simple, quick, and one stage procedure
• The blood supply is from intradermal anastomosis

FIGURE 5.45: Bony defect FIGURE 5.46: De-epithelialized l


flap raised

FIGURE 5.47: Turn over FIGURE 5.48: Graft over the


de-epithelialized flap de-epithelialized flap
SKIN FLAPS 133
• Flap raised with an adequate base to length ratio (base unit=x,
flap unit =3x)
• Example 2 cm diameter defect
4 cm diameter flap
1 cm area left intact as base of flap.
Adipofascial flap (Figs 5.49 to 5.51)
Closure of the soft tissue defect remains a difficult problem. Local
adipofascial turn over flaps covered with a skin graft can be
successfully used to reconstruct such defects. The design of the flap
is determined by the size and the location of the defect. A flap to
base ratio of 4:1 is a safe index for flap survival. Flap‘s base should
be 1.5-2 cm and the flap should be 3 cm for the flap to be safe and
reliable.

FIGURE 5.49: Ulcer over the tendo Achilles

FIGURE 5.50: Adipofascial flap elevated

FIGURE 5.51: Adipofascial turnover flap


134 PLASTIC SURGERY MADE EASY

FIGURE 5.52: Bare bone

FIGURE 5.53: Fascial flap elevated

FIGURE 5.54: Fascial flap turned over the defect

Fascial flap (Figs 5.52 to 5.54)


Fascial flaps can also be used to cover bony defects.
Adipose tissue (Figs 5.55 and 5.56)
Adipose tissue can be raised to cover the defect
SKIN FLAPS 135

FIGURE 5.55: Hell defect

FIGURE 5.56: Adipose tissue turn over

Distant Flaps
Flaps raised from a distant site rather than the immediate
surrounding is called as distant flap.
When local and regional flaps are unavailable then distant flaps
can be used as alternative method of reconstruction. The different
types of transfer of flap include, the pedicle flap which is transferred
directly and the tube flap which is transferred by indirect method
either by waltzing, tumbling, and caterpillar method. Depending
on the content of the pedicle it can be either skin and subcutaneous
tissue or arteriovenous pedicle.
Tubed pedicle flaps—These flaps are seldom used now, but they
form a very important alternative to a surgeon when all other options
136 PLASTIC SURGERY MADE EASY
fail. They are staged and are
transferred via carriers. The wrist
is the most common carrier. With
the advent of free flaps tubed
flaps have become of historic
interest only (Fig.5.57).
Pedicle flaps—These flaps are
still used mainly for the
reconstruction of the head, neck, FIGURE 5.57: Tube pedicle
and extremities. Examples of flap
this type of flap are the groin flap,
deltopectoral, forehead flap, parascapular flap and washio flap.
The common factor in all these flaps is that they are axial pattern
flaps and are raised with fascia to have a well vascularized flap.
These flap can also be raised as a local random pattern flap to
resurface burn defects without compromising on the flap vascularity
(Figs 5.58 to 5.63).

FIGURE 5.58: Cross-leg flap FIGURE 5.59: A groin flap for single
finger
SKIN FLAPS 137

FIGURE 5.60: Multiple finger bone FIGURE 5.61: Groin flap for
exposed multiple finger

FIGURE 5.62: Exposed tendon dorsum of hand

FIGURE 5.63: Groin flap


138 PLASTIC SURGERY MADE EASY

FLAP DELAY
When the flap has to be extended beyond the boundaries of its
blood supply then the flap is delayed to increase vascularity thereby
increasing the length and reliability of the flap. This is done by
incising the flap on two parallel sides and undermining. Such flaps
require more than a single stage to transfer which is usually after 2-
4 weeks. By delaying, the flap is conditioned to survive on less
blood flow. The advantages are that the number of vessels are
increased due to the dilatation of the choke vessels (Figs 5.64
and 5.65).

FIGURE 5.64: Delay flap

FIGURE 5.65: Delay cross-leg flap after division


SKIN FLAPS 139
Advantage of Delay Flap
• Is to enhance flap circulation and ensure flap survival
• Greater length will survive
• Condition the flap to survive in a state of hypoxia by retraining
of vessels
• Delay upto 10 days.

PREFABRICATED FLAPS
flaps that are formed at the donor site with mixed element and then
grafted to the recipient site as a single stage (Fig. 5.66).

FIGURE 5.66: Prefabricated flap

ADVANTAGES OF FLAPS
• Functionally skin flaps are better because it has a potential to
grow with the patient
• Re-contractures are not very common.
• Does not require splints or long-term physiotherapy
• Very useful in non-compliant burn patient.

CHARACTERISTICS OF SKIN FLAPS


• Maintains color and texture
• Flaps are bulky and need thinning of flaps
140 PLASTIC SURGERY MADE EASY
• Resembles the donor site for hair growth and sebaceous
secretion
• Flaps take a longer time than grafts to get sensation, which
resembles the pattern of recipient site
• Pain temperature and touch sensations are restored later
• Although it provides a good cover, it often leads to pressure
sores particularly on the plantar surface of the feet due to
anesthetic nature of the flap for a long period of time before it
regains sensation
• Flap grows along with the growth of the body.

COMPLICATIONS
The various factors which can lead to flap failure are:
• Poor planning of flap and design
• Undue tension on flap
• Hematoma
• Pressure
• Torsion and kinking of pedicle
• Poor selection of patient
• Diabetes and hypertension.

PREVENTION OF COMPLICATION
• Use the most simple option
• Optimize patients health condition
• Cessation of alcohol, tobacco and NSAIDs preoperatively
• Gentle handling of tissues
• Good hemostasis
• Avoid torsion of pedicle and tension on flap.

MEASURES TO IMPROVE CIRCULATION IN SKIN FLAP


• During surgery—Avoid hypotension
Apply nitroglycerine paste on the flap
Use warm mops
• Dermaid ointment applied on the flap (vasodilator)
Anti-inflammatory drugs
• Intra-arterial prostacycline
SKIN FLAPS 141
TESTS OF SKIN FLAP PERFUSION
• Color of the flap
• Capillary bleeding
• Warmth
• Stab wound incision
• Doppler flow as bed side test
• Laboratory test
• Intravenous fluorescein dye tests by injecting 20 ml of 5%
sodium fluorescein 20 minutes after flap has been raised.
Immediate yellow fluorescence of the patients epithelial surface
is seen with an ultraviolet light in a dark room.

CONCLUSION
• Plastic surgery is a constant battle between blood supply and
beauty
• With all the tools available a plastic surgeon can repair many
defects and give the patient a good functional and cosmetic
outcome
• These techniques include an increasing element of risk as we
move up the reconstructive ladder. It is wise to start at the bottom
and work your way up trying the simplest technique that will
work.
Chapter 6

Muscle Flaps
144 PLASTIC SURGERY MADE EASY
INTRODUCTION
Muscle flaps are available all over the body and due to its rich
blood supply and bulk it is a very useful flap. Muscle flap can be
based on either superior or inferior pedicle . It can be detached
from its origin or insertion. It can be raised as a muscle flap or as a
composite flap. The decision to use myocutaneous flap should be
based on accurate assessment of the defect.
Myocutaneous flap is a compound flap in which muscle, fascia,
subcutaneous fat and skin are combined as one unit of tissue.

INDICATIONS
• Provides bulk to a large raw area and fills the cavity of the
wound, thus reducing the dead space.
• It is also indicated in infected wounds.
• It not only provides cover but also restores form and
function, for example, pectoralis minor muscle in facial palsy.
• It can be used as only muscle flap or myocutaneous flap or
as osteomyocutaneous flap.
• It can be transferred as a motor or sensory flap.

ADVANTAGES OF MUSCLE FLAP


• Good vascularity
• Provides bulk
• Reliable
• Safe
• High degree of resistance to infection

DISADVANTAGE
Sacrifice of a functional muscle.

CLASSIFICATION
Mathes and Nahai—1981. (Fig. 6.1)
Type 1 One vascular pedicle (Gastrocnemius—Figs 6.2 to
6.5, Tensor fascia lata—Figs 6.6 and 6.7)
MUSCLE FLAPS 145

FIGURE 6.1: Muscle types

FIGURE 6.2: Defect lower leg

FIGURE 6.3: Gastrocnemius flap


transposed-type-1 muscle
146 PLASTIC SURGERY MADE EASY

FIGURE 6.4: Island gas- FIGURE 6.5: Gastrocnemius island


trocnemius flap-type 1 muscle flap follow-up

FIGURE 6.6: Tensor fascia lata FIGURE 6.7: Tensor fascia lata
flap-type 1 muscle flap for groin-type 1 muscle

Type 2 One dominant pedicle


and one or more minor
pedicle (flaps cannot
survive on minor pedicles
alone) example—Rectus
femoris, Soleus and
Gracilis (Fig.6.8).
Type 3 Two dominant pedicles - FIGURE 6.8: Gracilis flap
gluteus maximus, rectus Type 2 muscle
abdominis (Figs 6.9 to
6.13).
Type 4 Segmental pedicles (sartorius, tibialis anterior)
MUSCLE FLAPS 147

FIGURE 6.9: Sternal wound FIGURE 6.10: Sternal wound with


rectus abdominis flap elevated muscle flap in place

FIGURE 6.11: Postoperative sternal FIGURE 6.12: Bilateral TRAM


wound closure flap-Type 3 muscle
148 PLASTIC SURGERY MADE EASY

FIGURE 6.13: TRAM flap in FIGURE 6.14: Breast tumor


place

FIGURE 6.15: Chest defect FIGURE 6.16: LD myocutaneous


flap-type 5

Type 5 One dominant pedicle and several segmental smaller


pedicles (flaps can survive on these segmental pedicles
alone) example—Latissimus dorsi (Figs 6.14 to
6.27)
Pectoralis major (Figs 6.28 to 6.31)
TANSINI contributed Latissimus dorsi flap for breast
reconstruction in 1906.
MUSCLE FLAPS 149

FIGURE 6.17: LD flap with FIGURE 6.18: LD flap moving into


vascular pedicle the defect

FIGURE 6.19: Breast FIGURE 6.20: Post op breast


reconstruction with LD flap reconstruction

FIGURE 6.21: Primary closure of FIGURE 6.22: Defect elbow


the defect
150 PLASTIC SURGERY MADE EASY

FIGURE 6.23: Good FIGURE 6.24: LD muscle flap elevated


debridment of the bone

FIGURE 6.25: LD flap in place with skin FIGURE 6.26: Degloving


graft injury arm

Tensor Fascia Lata


Origin —
ASIS
Insertion —
Iliotibial tract
Type —
1
Pedicle —
Lateral circumflex artery
Application —
Abdominal wall, groin, perineum and trochan-
teric sores
Disadvantage — Lateral knee instability
MUSCLE FLAPS 151

FIGURE 6.27: LD flap FIGURE 6.28: Carcinoma cheek with defect


pedicled into the defect

FIGURE 6.29: Pectoralis major FIGURE 6.30: PM flap in place


myocutaneous flap design Type -5

FIGURE 6.31: Postoperative PM


flap in place
152 PLASTIC SURGERY MADE EASY
Gastocnemius
Origin — Femoral condyle
Insertion — Fuses with soleus to form Achilles T
Type — 1
Pedicle — Sural artery branch of popliteal
Application — Defects over the knee and proximal third of tibia

Gracilis
Origin — Pubic tubercle
Insertion — Medial aspect of proximal tibia
Type — 11
Pedicle — Medial circumflex branch of profunda femoris
Application — Perineum, vaginal, penile and ischial sores

Rectus abdominis
Origin — Lateral head from pubic creast
Medial head from symphysis pubis
Insertion — Costal cartilages of 5th,6th,7th ribs
Type — 111
Pedicle — Major pedicle is superior epigastric artery (conti-
nuation of internal mammary artery)
Minor pedicle is inferior epigastric artery(branch
of internal illac artery)
Application — Breast reconstruction

Pectoralis major
It is a broad, flat, fan shaped muscle lying superficially on the anterior
chest wall. This is a reliable and very useful flap for most of the head
and neck reconstruction.
Origin — It has 2 origins, clavicular and sternal
Insertion — The fibers converge into a flat tendon to be
inserted into the lateral lip of the bicipetal groove
of the humerus.
Type —V
Nerve supply — Medial and Lateral pectoral nerves
MUSCLE FLAPS 153

Blood supply — Thoracoacromial artery, segmental minor pedi-


cles and perforating branches of internal
mammary artery
Function — The muscle is an adductor and medial rotator of
the arm
Use — Can be used as a musle or a myocutaneous flap
and osteomyocutaneous flap.

Latissimus Dorsi Flap


It is a flat triangular muscle situated on the back. This is the most
common flap used for reconstruction of breast in a single stage.
Origin — It arises from the spine of the lower 6 thoacic
vertebrae, thoracolumbar fascia, spine of lumbar
and sacral vertebrae and the posterior crest of
the ilium
Insertion — Into the intertubercular groove of the humerous
Type —V
Nerve supply — Thoracodorsal nerve
Blood supply — Thoracodorsal artery, segmental minor pedicles,
perforating branches from intercostal and lumbar
arteries
Function — Adductor and medial rotator of the humerous
Use — It is a very useful flap. It can be used as a muscle
or a myocutaneous flap.
Chapter 7

Fasciocutaneous
Flaps
156 PLASTIC SURGERY MADE EASY
It consists of perforators which pass upto the surface along the
femoral septa between adjacent muscles and then fan out at the
level of the deep fascia to form a plexus from which branches are
given off to supply the overlying subcutaneous tissue and the dermis.

HISTORY OF FASCIOCUTANEOUS FLAP


Pioneered by Ponten—1981
Championed by Tolhurst—1983
Investigated by Cormack
Lamberty—1984

CLASSIFICATION OF FLAP (FIG. 7.1)


On the basis of vascular pattern FC flaps are of 4 types—A, B, C, D.

Type A
Multiple Fasciocutaneous vessels entering the flap at its base. For
example—Sural artery flaps.

FIGURE 7.1: Fasciocutaneous flap classification


FASCIOCUTANEOUS FLAPS 157
Type B
Based on a single fasciocutaneous perforator entering the base of
the flap. For example—scapular/parascapular and gastrocnemius.

Type C
Supplied by multiple small vessels running in the fascial septa
coming out of the main vessel between the muscle.
For example—radial forearm flap.

Type D
Osteomyocutaneous free flap in which the fascial septum containing
the FC perforators to the overlying skin is removed in continuity
with the adjacent muscle and bone.
For example—Fibular graft.

Advantages of Fasciocutaneous Flap


• Do not require a delay procedure
• Length to breadth ratio of 3:1 with safety
• Provides mobility and ease of positioning
• Elevation of flap easy
• High reliability.
Chapter 8

Microsurgery
160 PLASTIC SURGERY MADE EASY
HISTORY
1912—Carrel won the nobel prize for Microvascular anastomosis
1969—Mclean and Buncke transposed a free omentum to the scalp
1973—Daniel,Taylor and O”Brien and associates reported use of
free groin flap for the lower extremity independently.

INSTRUMENT
• Microscopes and Loupes can be used depending on the size of
the vessel to be anastomosed
• Jeweler’s forceps, microneedle holder, microscissors—both
straight and curved, Acland clamps and vessel dilators.

SUTURES
• 8/0, 9/0, 10/0 and 11/0 nylon.

SOLUTIONS
• Heparinized saline for irrigation of vessel ends
• 2% lidocaine to prevent vasospasm
• Papaverin to counter act vasospasm.

PER OPERATIVE MEASURES


• Gentle technique to be followed
• Absence of blood flow through the anastomosis should be
managed by applying 5% lidocaine over the anastomotic site
• Keep warm gauze over it for 10 minutes
• Hydrate the patient well
• Keep the patient warm
• Keep the blood pressure above 100 mm of Hg
• Check for twist, kinking and compression
• If still not satisfied it is better to redoanastomosis.

Preventive Measures
• Prevent vasospasm
• Anticoagulants
• 10% dextran 40 acts as a volume expander and decreases
the stickyness of platelets
MICROSURGERY 161
• Aspirin 75 mg daily to inhibit platelet aggregation
• Heparin reduces platelet adhesion
The commonest type of microvascular flap used are radial fore-
arm flap (Fig 8.1) Latissimus dorsi mypcutaneous flap (Fig.8.2)
fibular osteomyocutaneous flaps (Figs 8.3 to 8.5).

FIGURE 8.1: Free Radial forearm FIGURE 8.2: Free latissimus dorsi
fasciocutaneous flap myocutaneous flap

FIGURE 8.4: Fibular graft -


Free osteocutaneous flap

FIGURE 8.3: Marking for fibular graft FIGURE 8.5: Fibular


osteocutaneous flap
162 PLASTIC SURGERY MADE EASY
Postoperative Measures
Check for color, temperature, tissue turgor, capillary return, bleeding
on pin prick and Doppler recording.

CLINICAL ASSESSMENT
Healthy flap will look Pink
Warm
Pulses felt
Soft
Tissue turgor present
Signs of poor arterial flow Cool
Flap with poor tissue turgor
Flap placid
Signs of poor venous flow Tense
Warm and cool
Bluish color
Increased tissue turgor
No flow Ischemia, edema and thrombosis
Reversible damage at 4 hours
Irreversible damage at 6-12
hours.
Chapter 9

Head and Neck


164 PLASTIC SURGERY MADE EASY

CLEFT LIP
ETIOLOGY
• Hereditary
• Familial
• Environmental factors
• Teratogenic drugs
• Idiopathic

EMBRYOLOGY (FIG. 9.1)


Normal facial development is completed in the third week of fetal
life. Fetal development is divided into those that occur between 4th
to 8th week of gestation (primary palate) and those that occur
between 8th to 12th week of gestation (secondary palate).

FIGURE 9.1: Embryology of lip


HEAD AND NECK 165
Primary palate forms upper lip, columella, alveolus and hard
palate upto incisive foramen.
Secondary palate forms rest of hard and soft palate posterior to
Incisive foramen.
In the 5th week of embryo all the major primordia involved in
the formation of the face is present. An elevation called frontal
process overhangs the stomodeum. Surrounding this stomodeum
there are several elevations—laterally maxilla, inferiorly mandible
and superiorly frontal process. Lateral to frontal process, thickenings
called nasal placodes appear. On each side of this nasal placodes,
inverted U shaped elevations appear called medial and lateral nasal
process.
The medial nasal process has medial part and lateral part.
The two sides of the medial part of the nasomedial process fuse
together to form upper lip philtrum and columella only.
The lateral part of the medial nasal process fuse with the
maxillary process to form the rest of the upper lip. The site of this
fusion remains as the philtral ridge failure of fusion between the
lateral part of the medial nasal process and the maxillary process
results in cleft lip.

ANATOMY
Normal (Fig. 9.2)
Lip Consists of symmetrical cupids bow and philtral ridge,
white skin roll and vermillion
Nose Straight columella and septum, symmetrical alar arches
and equal alar base
Muscle Orbicularis oris arises at each angle of the mouth and
ends by decussating in the midline with fibers from
opposite side.

Abnormal (Fig. 9.3)


Lip Cleft of the lip at the philtral ridge
Nose Deviated towards normal side there is stretching and
flattening of alar cartilage
166 PLASTIC SURGERY MADE EASY

FIGURE 9.2: Lip anatomy FIGURE 9.3: Abnormal anatomy

Muscle Fibers of orbicularis oris proceed horizontally from the


corner of the mouth and get attached to the base of
columella and alar base region (This is responsible for
the wide clefts as muscles abnormally attached pulls
the alar base apart from both sides)
Maxilla Severe displacement of the non-cleft segment, resulting
in the disparity between the level of the maxillary arch.

CLASSIFICATION
a. Davis and Ritchie (1922)—according to the position of the
cleft in relation to the alveolar process.
Group I—Prealveolar
II—Postalveolar
III—Alveolar
b. Veau (1931)
• Cleft of soft palate only
• Cleft of hard and soft palate
• Complete cleft of one side (cleft of soft palate, hard palate
extending through alveolus to lateral incisor tooth)
• Complete bilateral clefts
c. Kernahan and Stark (1958) Based on embryology
• Primary palate—Structures in front of incisive foramen
(premaxilla, anterior septum and lip)
• Secondary palate—From incisive foramen to uvula (hard
and soft palate)
HEAD AND NECK 167
d. Kernahan striped—Y classification
e. Balakrishna’s classification
• Group—I Cleft of the lip alone (Figs 9.4 to 9.6)
• Group—IA Cleft of the lip and alveolus (Figs 9.7 and
9.8)
• Group—II Cleft of the palate alone (Fig. 9.9)
• Group—III Complete cleft of the lip and palate (Figs 9.10
to 9.12)
• Bilateral complete lip and palate (Figs 9.13 and 9.14)

FIGURE 9.4: Incomplete cleft FIGURE 9.5: One week postoperative


lip following rotation advancement repair

FIGURE 9.6: Six months FIGURE 9.7: Cleft lip and


postoperative of the same patient alveolus
168 PLASTIC SURGERY MADE EASY

FIGURE 9.8: Two months follow- FIGURE 9.9: Cleft palate


up of the same patient

FIGURE 9.10: Complete cleft lip and FIGURE 9.11: Same patient after
palate 4 years follow-up

FIGURE 9.12: Same patient FIGURE 9.13: Bilateral complete cleft


after 5 years follow-up lip and palate
HEAD AND NECK 169

FIGURE 9.14: Bilateral cleft lip repair

PATHOPHYSIOLOGY
• Lip
• Inability to have a tight seal
• Malocclusion, alveolar defect and teeth deformities
• Palate
• Inability to separate nasal from oral
• Feeding difficulty because child is unable to create a negative
pressure and therefore cannot suckle the breast
• Regurgitation of food through nose
• Middle ear disease due to eustachian tube dysfunction
• Pierre Robin syndrome—Cleft palate, Micrognathia, Glosso-
ptosis.

GENERAL GUIDE LINES IN CLEFT LIP AND


CLEFT PALATE MANAGEMENT
When parents bring their child with cleft lip and palate deformity
a. Reassure the parents
b. Explain functional problems
c. Advise on
i. Feeding
ii. Timing of surgery

Reassure the Parents


Counsel the parents and dispel the guilt feeling, for they are usually
170 PLASTIC SURGERY MADE EASY
overcome with fear, guilt and wonder what they have done to
deserve such misadventure.
• Assure the parents that a satisfactory repair can be performed.
• Explain the incidence of the second child having similar
problems.
• To delay the next pregnancy so that adequate care can be given
to the deformed child.
• To point out the various functions affected by this anomaly like
chewing, swallowing and speech and that each will be dealt at
a separate time.

Functional Problem
i. Isolated cleft lip seldom presents with feeding problems
ii. Cleft palate child has many handicaps.
• Unable to develop intraoral negative pressure and cannot
suckle in a normal fashion, further on swallowing child expels
feeds through the nose.
• Develops continuous sore throat due to failure to warm and
moisten the inspired air.
• Due to improper function of tensor veli palatini muscle child
develops serous otitis media and can have ear discharge
(ENT check up).
• Children can also suffer from mastoiditis.
• The cleft segment of jaw usually collapses producing
malocclusion.
• Speech is often delayed and unintelligible.

Advice on Feeding
• Babies with cleft lip and palate requires special attention to
nourish them adequately.
• The child has to be held at an angle of 45 degree from the
horizontal during feeding to minimize aspiration and regurgi-
tation.
• To overcome child’s inability to suck properly, “Paladai” feeds
will have to be given at frequent intervals. Advise the mothers
to extract milk using breast pump and feed the child with this
milk using either spoon or paladai. Strict instructions to mother
HEAD AND NECK 171
to avoid using bottles as it requires frequent boiling to keep it
clean. Children can develop severe diarrhea due to infection.
• Child swallows a lot of air and therefore must be burped more
frequently during and after feeds. Great care is taken to give
slow feeds as frequently as possible to avoid aspiration.

Timing of Surgery
A child who is thriving well, free of infection can undergo surgery if
Rule of Ten is followed.
RULE OF TENS—CLEFT LIP
10 pounds (5 kg)
10 gm of hemoglobin
10 weeks of age
10,000 total WBC count (means free of infection).
Surgical repair—one stage repair of cleft lip and anterior palate
using Millards Rotation Advancement technique.

Goals
• Approximation without loss of natural landmarks
• Symmetry on both sides
• Scar along the natural lines
• Symmetric alar base
• The final result should be symmetrical
• Functionally and aesthetically natural looking.

Postoperative Care
• Restraining splints for 3 weeks to prevent disruption of repair.
• Spoon feed or paladai feeds for I month.
• I st post operative day wound to be cleaned with saline plus
hydrogen peroxide to take away the blood clots very gently.
From the second day onwards gentle cleaning with saline, and
apply a thin film of neosporin ointment.
• Suture removal on 5th day.
• Steri strips on the wound to support.
172 PLASTIC SURGERY MADE EASY
Postoperative Complication
• Infection
• Dehiscence
• Spreading scar
• Hypertrophic scar
• Whistle deformity

SYNDROMES ASSOCIATED WITH CLEFT LIP


Van der Woulde’s syndrome—Cleft lip associated with lip pits.

CLEFT PALATE
ETIOLOGY
• Genetic
• Environment—alcohol, smoking and teratogens

EMBRYOLOGY
Palatal development occurs between 7th and 10th week of
intrauterine life.
The palatal shelves of the maxilla are initially oriented vertically,
as the head grows and the neck extends, the tongue falls back
allowing the palatal shelves to move upwards. If this does not
happen then the two palatal shelves fail to make contact with each
other in the midline and cleft palate occurs.

CLASSIFICATION
1. Complete cleft palate—hard and soft palate (Figs 9.15 and
9.16)
2. Incomplete cleft palate—only soft palate (Fig. 9.17)
3. Submucous cleft palate—Bifid uvula, hard palate notching,
midline white line due to abnormal muscle insertion (Fig. 9.18)
4. Bifid uvula
HEAD AND NECK 173

FIGURE 9.15: Complete cleft FIGURE 9.16: Postoperative Wardill


palate Kilner-Veau push back method

FIGURE 9.17: Incomplete cleft FIGURE 9.18: Submucous cleft


palate

MUSCLES OF PALATE
1. Levator veli palatini—(elevates the soft palate and closes
the opening between the nasopharynx and oropharynx)
It arises from the petrous part of the temporal bone and is
inserted in the mid third of the soft palate. It interlaces with the
muscles from the opposite side especially palatopharyngeus. It
elevates and shifts the soft palate backwards. It contributes to
the lateral movements mesially and this is the basis of the
rationale for pharyngeal flap reconstruction in cleft palate
patients.
2. Tensor veli palatini—It arises from the scaphoid fossa at the
base of the medial pterygoid plate, it hooks around the hamulus
and widens towards the palate. It is of little importance to speech
174 PLASTIC SURGERY MADE EASY
and is therefore frequently sacrificed when the hamulus is
fractured in order to produce longer backward reaching palatal
flaps. It helps in opening and closing the eustachian tube. It
equalizes the pressure between the middle ear and
nasopharynx. It also fails to lift the soft palate due to abnormal
attachment. In cleft palate this action is lost and children present
with ear discharge eventually leading to chronic otitis media.
3. Muscularis uvulae—They lift and bend uvula backwards and
shortens it.
4. Palatoglossus—It is a small muscle arising from the transverse
fibers within the tongue and ascends to the palate forming
the palatoglossal arch. This is of importance to speech. It
narrows the pharyngo oral isthmus. It lifts the tongue and propels
food.
5. Palatopharyngeus—It arises in the palatal aponeurosis and
enters the lateral walls of the pharynx. This muscle is divided
into 3 parts. The function of this muscle is to narrow the
pharyngonasal isthmus by bringing the palatopharyngeal muscle
together.

BLOOD SUPPLY
• Greater palatine vessels
• Lesser palatine vessels

TIMING OF CLEFT PALATE SURGERY


• 10 Kg
• 10 gm of hemoglobin
• 10 months of age
• 10,000 total count
Timing of surgery in a cleft palate child is an important factor
and the object should be to have the child start speaking with a
normal speech mechanism and hence surgery should be done
when the infant is 10 months to one year old.
The child should be referred to a plastic surgeon for continuity
of care.
HEAD AND NECK 175
PROBLEMS
Child with cleft palate is often associated with:
• Upper airway obstruction
• Feeding difficulties
• Ear infection
• Speech

SURGICAL GOALS
• Closure of cleft
• To produce optimal speech
• Avoid ear infection
• To minimize facial growth disturbances

TREATMENT
• Von Langenbeck operation
• Intravelar veloplasty
• Wardill Kilner-Veau push back method
• Double opposing Z plasty

POSTOPERATIVE CARE
Airway—nasopharyngeal tube should be inserted at least for 24
hours, to make sure that the child does not go into respiratory
obstruction. This is very important particularly for children who
have undergone palatopharyngoplasty.
Sedation should not be given, as child can get obstructed.
Respiratory rate should be monitored.
Nursed in a lateral position to avoid aspiration pneumonia.
Bleeding should be watched for immediate postoperative period.
If there is a lot of oozing then child should be taken back to theater
for cauterization. If bleeding occurs on the 5-7 postoperative day,
then it is due to secondary infection and the child should be started
with IV fluids, antibiotics and adrenaline pack to stop bleeding.
Nurse the child in a lateral position to avoid aspiration.
176 PLASTIC SURGERY MADE EASY
Oral fluids should be started after four hours of surgery. Only
liquid diet to be given for 10 days. Gradually start on soft solids and
solids after two weeks.
Restraining splints for 2 weeks.

POSTOPERATIVE COMPLICATION (FIGS 9.19 TO 9.21)


• Bleeding
• Respiratory obstruction
• Secondary bleeding between
5th and 7th day
• Infection
• Dehiscence (Fig. 9.19)
• Necrosis (Fig. 9.20)
• Fistula (Fig. 9.21)
• Unintelligible speech

FIGURE 9.19: Wound


dehiscence

FIGURE 9.20: Palatal necrosis FIGURE 9.21: Palatal fistula

Pierre Robin Sequence


• Micrognathia
• Cleft palate
• Glossoptosis
HEAD AND NECK 177

VELOPHARYNGEAL INCOMPETENCE
Velopharyngeal incompetence is characterized by hypernasal
resonance, nasal emission and compensatory changes such as glottal
stops. The amount of air which passes into the nose increases, thus
adding the resonance of the nasal passages and paranasal sinuses
in the production of sound with the resulting hypernasal quality.
This is the typical “NASALITY” of the cleft palate speech.
In the presence of inadequate VP closure, the brain responds
by adopting compensatory articulatory patterns, which unfortunately
are maladaptive and can render speech unintelligible. During
articulation, movement of the soft palate and the pharyngeal walls
controls air entry into the nasopharynx. VPI results from inability to
fully close the space between the soft palate and the anterior wall of
the pharynx.
While speech therapy may help to improve and correct VP
closure and articulation errors, significant VP dysfunction due to
both functional and anatomic limitations of palate function and
pharyngeal form may require surgical intervention.
The primary causes of VP incompetence related to cleft palate
are:
• Unrepaired cleft
• Failure to repair
• Short or immobile palate
• Immobile pharynx
• Velopharyngeal incompetence may occur in absence of overt
cleft including
• Submucous cleft palate
• Neuromuscular disorders
• Palatopharyngeal disproportion
• Effect of adenoids and tonsils

Investigation
VP closure is assessed by:
• Videofluoroscopy
• Nasoendoscopy
178 PLASTIC SURGERY MADE EASY
Treatment
• Superiorly based pharyngoplasty.

Complication of Pharyngoplasty
Respiratory obstruction, sleep apnea and snoring.

Summary
The main factors of misarticulation, hypernasality or hyponasality
and nasal escape predetermine the extent of unintelligible speech.
A combination of proper surgical technique and speech therapy
can restore the speech to a near normal level.

SPEECH IN CLEFT PALATE


The main objective of cleft palate surgery is:
To achieve normal speech.
Speech that is articulated well with normal resonance.
The sphincteric action is by the levator palate, palatopharyngeus
and superior constrictor. The added bulk of a functioning musculus
uvulae also plays a role in VP closure.
VP closure (soft palate to posterior pharyngeal wall) is needed
to build up intraoral pressure for all the English letters except the
Nasal consonants “m”, “n”, “ng”. These nasal consonants are
produced with the lips closed and the air stream directed through
the nose.
All other consonants are divided into 2 main groups:
i. Those produced by a small explosion called “PLOSIVES”
such as “b”, “p”, and“t”.
ii. Those produced by the sounds of friction called
“CONTINUANTS” such as “s”, “sh” and “z”.
The two groups are further subdivided depending on whether
or not the vocal cords are being used, that is “VOICED” and
“UNVOICED”.
The main difference between voiced, “v”, “z” and unvoiced
continuants “s”, “sh” is the use of the VOCAL CORDS.
Unvoiced continuants are called SIBILANTS.
Voiced continuants are called FRICATIVES.
HEAD AND NECK 179
Closure of the velopharyngeal sphincter blocks airflow into the
nose during production of specific phonemes. A competent sphincter
is essential for the production of non-nasal sounds. In addition to
the repair of the levator muscle other factors that contribute to speech
improvement include:
a. Age at time of repair
b. Type of cleft
c. Hearing loss
d. Intelligence of child
Grading of Speech
a. Normal
b. Nasal emission, no articulatory errors
c. Nasal emission plus articulatory errors
d. Unformed or unintelligible speech

RARE CRANIOFACIAL CLEFTS


Tessier—1976 introduced the cleft numbering system (Fig. 9.22).
Clefts are numbered from 0-14 and follow constant lines through
eyebrow, eyelid, maxilla, nose and the lip. Facial and cranial clefts
are connected and they tend to add up to 14 (Ex—Facial cleft 6 will
have a cranial cleft pattern of 8 to add upto 14).

FIGURE 9.22: Tessier’s chart


180 PLASTIC SURGERY MADE EASY

Facial cleft Cranial cleft


Extend downwards from orbit Extend upwards from orbit
Numbered 1-7 Numbered 8-14
Cleft 0 Median cleft of upper lip. Associated with hypertelorism
(Figs 9.23 and 9.24).
Cleft 1 Begins in cupids bow, passes through the dome of
nostril and continued as cranial cleft number 13.

FIGURE 9.23: Cleft 0 FIGURE 9.24: Cleft 0

Cleft 2 Associated with hypoplasia


of middle third of alar rim
Cleft 3 Common cleft. Nasolacri-
mal system is interrupted
(Figs 9.25 to 9.27).
Cleft 4 It passes lateral to cupids
bow, philtrum and nasal ala
onto the cheek. It terminates
medial to the nasolacrimal
punctum. Clefts can be
unilateral or bilateral (Figs
9.28 to 9.31).
Cleft 5 It is known as oblique facial
FIGURE 9.25: Cleft-3
cleft as it is situated more complete
HEAD AND NECK 181

FIGURE 9.26: Cleft-3 Postoperative FIGURE 9.27: Cleft-3 after 4


years postoperative

FIGURE 9.28: Unilateral cleft 4 FIGURE 9.29: Unilateral cleft 4


182 PLASTIC SURGERY MADE EASY

FIGURE 9.30: Bilateral cleft 4 FIGURE 9.31: Bilateral cleft-4


postoperative
lateral on the face. It is one of the rarest. It courses lateral
to the cheek. It may be associated with coloboma of the
lower eyelid (Fig. 9.32).
Cleft 6 This is also known as incomplete form of Treacher
Collins syndrome. It is a maxillozygomatic dysplasia with
coloboma of lower eyelid (Figs 9.33 and 9.34).
Cleft 7 Also known as hemifacial microsomia or oromandi-
buloauricular syndrome. A depression is seen exten-
ding from the angle of the mouth to the ear (Figs 9.35
to 9.37).
Cleft 8 Cleft in the lateral canthus of the eyelids with coloboma.
Cleft 9 From this cleft onwards the superior aspect of orbit is
involved.
Cleft 10 Coloboma in the middle third of the upper eyelid.
Cleft 11 Cleft in the middle third of the hairline. Associated with
orbital hypertelorism.
Cleft 12 Cleft traverses the eyebrow.
HEAD AND NECK 183

FIGURE 9.32: Unilateral facial FIGURE 9.33: Cleft 6,7,8, Lateral


cleft-5 view

FIGURE 9.34: Cleft 6,7,8 FIGURE 9.35: Cleft-7


184 PLASTIC SURGERY MADE EASY

FIGURE 9.36: Cleft-7 FIGURE 9.37: Cleft-7


Cleft 13 Cleft traverses at the medial end of the eyebrow (Fig.
9.38).
Cleft 14 Mid line frontonasal encephalocele and orbital hyper-
telorism (Figs 9.39, 39A and 9.40)

FIGURE 9.38: Cleft 13 FIGURE 9.39: Cleft 14


Bil.frotonasal encephalocele preoperative nasal encephalocele

FIGURE 9.39A: CleftT 14 postoperative FIGURE 9.40: Cleft 14


follow-up after 4 years
HEAD AND NECK 185
Hypertelorism means the great breadth between the eyes. The
entire orbit and globe are displaced laterally.
Telecanthus means lateral displacement of the medial canthi.
The medial orbital wall is displaced but the globe is in normal
position.

CRANIOFACIAL ANOMALIES
APERT’S SYNDROME (ACROCEPHALOSYNDACTYLY)
Definition
Autosomal dominant inheritant disorder, most cases are sporadic.

Incidence
1 in 1,60.000 live births. Apert’s is characterized by syndactyly of
hands (Figs 9.41 and 9.42).

FIGURE 9.41: Apert’s with FIGURE 9.42: Apert’s with syndactyly


syndactyly
186 PLASTIC SURGERY MADE EASY
Clinical Features
Skull Craniosynostosis
Brachycephaly
Turricephaly—With a flattened forehead (short anterior
posterior skull dimensions—wide transverse dimen-
sions, increased projection of superior skull—Tower
shaped skull)
Bulging anterior fontanellae
Face Hypoplastic
Antimongoloid slant of palpebral fissure
Exorbitism, hypertelorism, ptosis, divergent strabismus
and ocular paralysis
Psuedomandibular prognathism
Oral Submucous cleft hidden in high arched palate
Crowding of dental arch
Anterior open bite with cross bowing of upper lip
Hand Symmetric syndactyly of the hands and feet.
Mental function Some degree of mental retardation.

Radiologic Findings
Increased digital markings of inner table of the calvaria

Treatment
• Orbitofrontal advancement.
• Syndactyly release.

CROUZON’S SYNDROME
Definition
Autosomal dominant disorder. Absence of syndactyly refers to
Crouzon’s (Figs 9.43 to 9.48).

Incidence
1 in 15000 live births.
HEAD AND NECK 187

FIGURE 9.43: Crouzon’s FIGURE 9.44: Crouzon’s postoperative


preoperative

FIGURE 9.45: Immediate postoperative FIGURE 9.46: Third postop


orbitofrontal advancement day orbital advancement

FIGURE 9.47: Cruzon’s FIGURE 9.48: Cruzon’s 4 years


postoperative 2 years postoperative
188 PLASTIC SURGERY MADE EASY

Clinical Features
Triad of
i. Bicoronal craniosynostosis
ii. Mid facial hypoplasia
iii. Exophthalmos
Skull Calvarial deformity
— Scaphocephaly (boat shaped)
— Trigonocephaly (wedge shaped)
— Oxycephaly
Copper beaten appearance of inner table of skull
Face Exorbitism, hypertelorism, nystagmus and strabismus
Shallowing of the orbital floor
Arched nose (parrot beak)
Pseudoprognathism
Oral Peg-shaped teeth, macrodontia
Anterior open bite (premature occlusion of molar teeth)
Bilateral crossbite—class 3 malocclusion.
High arched palate
Hands Normal

Radiologic Findings
• Premature synostosis of coronal, sagittal and lambdoid sutures
• Increased digital markings on the inner table of calvarium

Signs and Symptoms


Headache, hydrocephalous, epilepsy, increased intracranial
pressure, mental deterioration, optic atrophy and mental retar-
dation.

Treatment
Surgical correction—orbitofrontal advancement.
HEAD AND NECK 189
HEMIFACIAL MICROSOMIA
(1st and 2nd brachial arch syndrome)

Definition
It is a congenital condition characterized by the underdevelopment
of one side of the face . It is also known as 1st and 2nd branchial
arch syndrome.

Etiology
• Hereditary, environmental and Thalidomide intake.
• Results from bleeding in the temporal area in the embryo.

Incidence
1: 5000 live births
Characterized by
a. Underdeveloped
• Auricle
• Absent external auditary canal
• Macrostomia
• Absent parotid gland
b. Underdeveloped muscles-Masticatory muscles
• Facial
• Soft palate
• Tongue
c. Underdeveloped bone—Zygoma
• Temporal
• Maxilla
• Mandible
The deformities are remembered as “OMANS”
(Orbit, Mandible, Ear, Nerve facial, Soft tissue)

Clinical Findings
• Components of the syndrome are low-set ears, short mandibular
ramus, micrognathia, chin deviation, occlusal cant, and anterior
open bite.
190 PLASTIC SURGERY MADE EASY
• If epibulbar dermoids and vertebral anomalies are present, it is
termed Goldenhar syndrome also known as oculo-auriculo-
vertebral syndrome. Major features are underdevelopment of
auricle, maxilla, and mandible.
• Facial nerve is most commonly affected
• Transverse facial clefts are seen and vary in severity
• Hypoplastic or missing kidney
• Cardiovascular defects and limb anomalies seen in 50%.

Treatment
Individualized to the patient.

HEMIFACIAL ATROPHY (ROMBERG’S DISEASE)


Definition
It is an acquired condition, also known as Romberg’s disease. It is
usually unilateral (Figs 9.49 to 9.52).

FIGURE 9.49: Romberg’s FIGURE 9.50: Romberg’s


postoperative

FIGURE 9.51: Romberg’s disease FIGURE 9.52: Romberg’s syndrome


HEAD AND NECK 191
Etiology
• Unknown
• Viral infection
• Abnormality in sympathetic nervous system.

Clinical Features
Characterized by gradual wasting of one side of the face and forehead
• Starts in the paramedian area of face
• Progressive atrophy of skin, subcutaneous fat, muscle, and bone
• Severity depends on the age of onset. The younger the age, the
severe the deformity
• Nerves are unaffected
• An association with sympathetic stimulation has been
postulated, but the cause remains unknown.

Treatment
Bone and soft tissue augmentation. The various options available
for augmentation are
• Fat and derma fat graft
• Temperoparietal fascial graft
• Free tissue transfer
• The defect should always be over corrected to allow for
subsequent flap atrophy.

TREACHER COLLINS SYNDROME


(MANDIBULOFACIAL DYSOSTOSIS)
Definition
It is an inherited disorder with an autosomal dominant inheritance.
It causes bilateral abnormalities in structures derived from the first
and second branchial arches.

Incidence
It is 1: 25000 live births. It has an equal male and female incidence.
(Fig. 9.53).
192 PLASTIC SURGERY MADE EASY

FIGURE 9.53: Treacher Collins syndrome

Genetics
Fifty percent have a positive family history. Gene transmitted
primarily by mother. High incidence of miscarriage in families.
Increased paternal age implicated as a factor. Gene mapped to
chromosome number 5.

History
Earliest report of the disorder was by Thompson in 1846. Collins in
1900 described colobomas with malar deficiency. Franceschetti and
Klein in 1949 described the deformities of this syndrome and he
coined the term mandibulofacial dysostosis.

Clinical Features
According to Tessier’s classification, complete form of the syndrome
shows the presence of clefts 6,7,8.
Cranium—Flat parieto-occipital bone

Mid face— Antimongoloid slant of the palpebral fissures


Preauricular hair displacement
Colobomas of the lower eyelid
Malar defects
HEAD AND NECK 193
Other features
Macrostomia
Malocclusion
High arched palate
Cleft palate
Atresia of the lacrimal puncta
Absence of meibomian glands
Hypertelorism
Preauricular sinus
External auditory canal defects
Mandible— Mandibular defects— Type II malocclusion
Open bite deformity
Micrognathia
Other features
• Fish-like facial expression
• Deafness
• Sleep apnea and sudden infant death syndrome are common.
Radiological features
• Deficient zygoma
• Hypoplastic mandible and maxilla
• Antigonal notch on the ramus
Problems
• Airway
• Swallowing and feeding
• Defects of hearing and vision
Treatment
• Multispeciality craniofacial team approach
• Reconstructive work must be tailored to each individual and
timed to take into account their normal facial growth and
psychological needs.
Duplication of nose (Fig. 9.54)

BINDER’S SYNDROME (FIG. 9.55)


Nasomaxillary dysostosis characterized by:
• Hypoplastic nose and maxilla
194 PLASTIC SURGERY MADE EASY

FIGURE 9.54: Duplication of FIGURE 9.55: Binder’s syndrome


nose

• Underdevelopment of anterior nasal spine


• Atrophy of the nasal mucosa
• Columella may be small
• Anterior crossbite with class III malocclusion

GOLDENHAR’S SYNDROME
• Hemifacial microsomia
• Epibulbar dermoids
• Sometimes facial nerve may be abnormal
• Vertebral abnormalities

FIBROUS DYSPLASIA (FIGS 9.56 AND 9.57)


• It is a developmental derangement of bone due to abnormal
proliferation of fibroblasts
• It can be caused by trauma or complex endocrine disturbances
• It is usually located in the cranio-orbital, maxillary and mandi-
bular region
HEAD AND NECK 195

FIGURE 9.56: Fibrous dysplasia FIGURE 9.57: Fibrous dysplasia

• It becomes quite after puberty


• More common in women
• Clinically a slow growing swelling firm to soft in consistency
• Treatment is by shaving the soft avascular bone.

CHERUBISM (FAMILIAL FIBROUS DYSPLASIA) (FIG. 9.58)


Definition
Multiple areas of fibrous dys-
plasia within the mandible and
maxilla.

Age of Onset
1st year of life.
Etiology
Autosomal dominant.

Clinical Features
Symptoms begin in early
childhood and progress to
adolescence.
Bilateral painless enlarge-
ment of mandible and maxilla,
dental disruption with alveolar
bone loss. FIGURE 9.58: Cherubism
196 PLASTIC SURGERY MADE EASY
Treatment
Excision and reconstruction.

Faciomaxillary Injuries
Proper evaluation of polytrauma patient should be confirmed before
any operative procedure is undertaken.
Treatment of faciomaxillary injuries are divided into three
stages;
A. Emergency
B. Early
C. Delayed

EMERGENCY TREATMENT
1. Respiratory obstruction
• Frequently occur with panfacial fractures
• Bilateral parasymphyseal fracture of mandible (due to loss
of anterior tongue support)
• Hemorrhage associated with massive soft tissue swelling
Indication for tracheostomy
• Head injury patients requiring IMF
• Panfacial fractures
• Massive soft tissue swelling of floor of mouth or neck
• Patient’s with chest injury requiring IMF
2. Aspiration
Patient’s likely to aspirate are those with multiple fractures of
mandible involving floor of mouth, fracture of maxilla and
patients with profuse epistaxis.
3. Hemorrhage
Profuse bleeding may occur with any facial fracture commu-
nicating with nasal cavity.
Massive nasopharyngeal hemorrhage may be secondary to
cranial base fracture with intracranial arterial or venous sinus injury.
Techniques used for the control of profuse bleeding:
• Anterior and posterior nasal packing
• External compressive dressing
HEAD AND NECK 197
• Reduction of facial fracture and IMF
• Unilateral or bilateral ligation of external carotid and
superficial temporal artery
4. Multiple system injuries
Multiple specialty teams should try to do definitive treatment of
as many injuries as possible during emergency procedures.
The advantage of delayed treatment of facial injuries have been
inappropriately emphasized. Better cosmetic and functional
results are achieved with early treatment.
A complete primary and secondary survey should be done and
include following:
• Airway, breathing, circulation
• Cervical spine injury—X-ray films must include C -1 and C-2
and C-6 and C-7
• Chest X ray
• Head injury—evaluate GCS, ask CT scan if indicated
• Abdominal injury—peritoneal lavage or abdominal scan
• Extremity and pelvic injury.

EARLY EVALUATION AND TREATMENT


Radiographic Examination
Plain X-rays
• Waters’ view
• Towne’s view
• Skull—AP and lateral
• Mandible—AP and lateral oblique
CT scan should be obtained in frontobasilar, orbital, nasoeth-
moid, midfacial and mandible condylar fractures.
Physical examination
Complete clinical examination is very important for proper diagnosis
and treatment.
Always think there is a fracture under any laceration or bruise.
Always examine face in an orderly manner progressing from
either superior to inferior or inferior to superior.
198 PLASTIC SURGERY MADE EASY

DELAYED TREATMENT OF FACIOMAXILLARY INJURIES


Delayed treatment consists of definitive fracture or wound mana-
gement not achieved during early management.

ORBITAL FRACTURES
The weakest wall of the orbit is the medial wall (lamina papyracea).
The next weakest is the floor medial to infraorbital nerve. The
mechanism usually involves hydraulic pressure and blow to orbital
rim with a buckling force delivered to the orbital floor.
Pure blow out fracture is—fracture of orbital floor without orbital
rim fracture.
Orbital fracture is associated with ocular injuries in 10 -25% of
orbital fractures, therefore, detail eye evaluation by ophthalmologist
is mandatory.

Diagnosis
• Periorbital and subconjunctival hemorrhage
• Anesthesia of infraorbital nerve
• Diplopia most often in upper outer gaze due to entrapment of
inferior rectus muscle
• Enophthalmos
• Dystopia
• Ipsilateral epistaxis

Radiographic Evaluation
• Water’s view
• CT scan—axial and coronal view

Indications for Surgery


• Enophthalmos
• Entrapment with positive force duction test
• Dystopia
• Orbital floor defect > 2 cm on CT scan
HEAD AND NECK 199

FIGURE 9.59: Split face FIGURE 9.60: Split face

Treatment
Exposure of orbital floor by using subcilliary, transconjunctival or
orbital rim incisions and release of entrapped incarcerated tissue
with replacement or reconstruction of orbital floor using bone graft,
cartilage or silastic sheet.

NASAL BONE FRACTURE (FIGS 9.59 AND 9.60)


Nasal bone fractures are divided into those that occur due to frontal
impact and those due to lateral impact resulting in deviated fractures.
Frontal impact Nasal injuries are further divided into 3 categories:
Plane 1—The end of nasal bone and septum are injured.
Plane 2—The injury is more extensive involving the proximal
portion of the nasal bone and frontal process of the maxilla at the
pyriform aperture.
Plane 3—Nasal fracture involving one or both frontal process of the
maxilla extending upto the frontal bone. This is in reality a
nasoethmoido-orbital fracture.
200 PLASTIC SURGERY MADE EASY
Treatment
Plane 1—Injuries can be treated by closed technique.
Plane 2—Injuries increase support with external padded splint,
nasal packing or immediate bone graft.
Plane 3—Injuries require open reduction.

ZYGOMATIC FRACTURES (FIG. 9.61)


The body of the zygoma has five
attachments to adjacent structures.
• Laterally to the arch of the
temporal bone
• Superiorly frontal bone
• Medially maxilla
• Inferiorly maxillary alveolus
• Anterolateral orbit (to the
greater wing of the sphenoid).

Diagnosis FIGURE 9.61: Fracture zygoma


• Black eye and subconjunc- subconjunctival hemorrhage
tival hemorrhage
• Depression of the lateral canthus
• Depression of the malar eminence
• Step deformity and tenderness at the orbital rim
• Unilateral epistaxis
• Trismus (impingement of the zygomatic arch on the coronoid)
• Intraoral hematoma in upper buccal sulcus, step or irregularity
of the anterior maxillary wall
• Entrapment symptoms of orbital floor fracture
• Loss of sensation along the distribution of the Infraorbital nerve
• Globe dystopia or enophthalmos.

Investigation
• Caldwell’s view (fronto zygomatic junction)
• Waters’ view (lateral wall of the maxillary antrum, inferior orbital
rim and orbital floor) displacement at the zygomatico-frontal
junction cannot be assessed in this view
HEAD AND NECK 201
• Submento-vertex view (posterior displacement of the body of
the zygoma)
• CT scan—Has replaced the usual facial series

Treatment
Closed reduction—Ideally closed reduction is indicated for
isolated zygomatic arch fractures by Gillies’ temporal approach. A
simple fracture can also be reduced by using a bone hook which is
inserted under the zygomatic arch and yank it upwards and out-
wards.
Open reduction
Indication for Surgery
• Entrapment
• Vertical dystopia
• Trismus
• Deformity
• Numbness with medially impacted zygoma
Frontozygomatic region is exposed by Dingman‘s incision.
Inferior orbital rim is exposed either by subciliary or trans-
conjunctival incision. Zygomaticomaxillary region is exposed by
upper buccal sulcus.

MAXILLARY FRACTURES (LEFORT)


Maxillary fractures are classified according to LeFort into:
LeFort I—Separating the maxillary alveolus from the upper midfacial
skeleton.
LeFort II—Separating a central pyramidal shaped nasomaxillary
segment from the zygomatic and orbital portions of the facial skeleton
(Fig. 9.62).
LeFort III—A transverse fracture separating the facial bones from
the cranial skeleton through the orbits (the upper portion of the
zygomatico-frontal junction, the orbital floors and nasoethmoid
areas). Also known as craniofacial dysjunction (Fig. 9.63).
202 PLASTIC SURGERY MADE EASY

FIGURE 9.62: Maxilla LeFort 2 FIGURE 9.63: Panfacial fracture

Diagnosis
• Mobility of the maxillary alveolus
• Signs of zygomatic, orbital, nasal or nasoethmoidal-orbital
fractures
• Malocclusion
• Elongated and depressed midface
• Facial and eyelid swelling
• CSF leak, pneumocephalous and orbital emphysema in LeFort
II and III fractures. About 10-15% of LeFort fractures are
accompanied by palato-alveolar fractures.

Radiographic Evaluation
• Waters’ view
• CT scan

Treatment
LeFort I Fracture
• Closed reduction, IMF and Adams suspension from zygomatic
arch.
• Open reduction and internal fixation using plate and screw or
intraosseous wire with or without IMF using elastics.
LeFort II Fracture
• Open reduction of orbital rim and closed reduction of lower
midface, IMF and suspension of maxilla by wire from a point
above the highest fracture point.
• Open reduction and internal fixation using plate and screws.
HEAD AND NECK 203
Lefort III Fracture
• Open reduction of orbital rim and closed reduction of lower
midface, IMF and suspension of maxilla by wire from a point
above the highest fracture point.
• Open reduction and internal fixation using plates and screws.

MANDIBULAR FRACTURES (FIGS 9.64 AND 9.65)


Mandibular fracture is one of the most common facial bone fracture.
Approximately 1/3 of fractures occur in the condylar and
subcondylar region. More than 1/2 of all mandibular fractures are
multiple.

FIGURE 9.64: Mandible FIGURE 9.65: Fracture mandible


fracture fixing with plate and screws
Classification
1. Depending on the direction of fracture and favorability for
treatment fractures are classified as:
• Horizontal
• Favorable fracture directed downward and forward
• Unfavorable fracture directed downward and posterior
• Vertical
• Favorable
• Unfavorable
204 PLASTIC SURGERY MADE EASY
2. Depending on the presence or absence of serviceable teeth in
segments of mandible fractures are classified as:
• Class I—Teeth on both fragments
• Class II—Teeth on one fragment
• Class III—Edentulous

Diagnosis
• Pain
• Swelling
• Malocclusion—commonly crossbite
• Numbness in mental nerve distribution
• Intraoral hematoma
• Step discrepancy of lower border of mandible or in dentition
• Bleeding from ear is seen in condylar fracture
• Trismus

Radiographic Evaluation
• Panorex view (OPG) if patient can sit up, it shows entire mandible
and lower maxilla in one film
• PA mandible—For fracture of symphysis, body, ramus and angle
• CT scan

Treatment
• IMF remains the standard treatment of mandible fracture using
arch bar ligated to teeth for 4 to 6 weeks.
• Treatment of class I fracture—Often managed by IMF. Some
fractures are best managed by open reduction and internal
fixation using plates and screws.
• Class II and class III fractures generally require open reduction.

PANFACIAL FRACTURE
Panfacial fractures consist of combination of fractures. It is diagnosed
and treated by integrating the above individual components.

Treatment Principles
• First stabilize both horizontal and vertical portion of mandible.
HEAD AND NECK 205
• Relate maxilla to the mandible through proper occlusion (IMF)
using splints if required.
• Reduce upper facial fractures individually, starting laterally
(frontozygomatic) and progressing medially.
• Unite upper to lower midface at the LeFort I level.

HEAD AND NECK RECONSTRUCTION


The ultimate goal of reconstruction is to produce primary healing of
the defect in the fastest possible time with a minimal fistula rate and
allow oral feeding as early as possible. To achieve this goal we need
an interdisciplinary collaboration between Head and Neck surgeons,
Dental surgeons and Plastic surgeons to plan an ideal flap
preoperatively which is functionally and socially acceptable to the
patient.
The defects following resection of the tumor can be reconstructed
by one of the following methods:
1. Direct suturing—very small lesion
2. Local flaps
3. Regional flaps—Forehead, Cervicopectoral (Figs 9.66 and
9.67), Deltopectoral, Sternomastoid and Platysma (Fig. 9.68)
4. Free flap—Radial forearm (Fig. 9.69), Latissimus dorsi

FIGURE 9.66: Preoperative FIGURE 9.67: Postoperative


cervicopectoral flap cervicopectoral flap
206 PLASTIC SURGERY MADE EASY

FIGURE 9.68: Platysma myocuta- FIGURE 9.69: Radial


neous flap for submucous fibrosis forearm flap

5. Bony reconstruction can be either


A. Implant material
Space maintaining device
a. K-wire (Figs 9.70 and 9.71)
b. Custom designed metallic prosthesis
c. Titanium plate
d. Titanium tray
B. Autogenous bone graft
Non-vascularized
a. Iliac bone graft
b. Rib graft
Vascularized
a. Pedicle—PM flap with 5th or 6th rib
b. Free Microvascular
i. Radial forearm with radius
ii. Iliac crest (Fig. 9.72)
iii. Free fibular graft
HEAD AND NECK 207

FIGURE 9.70: Mandible tumor FIGURE 9.71: K wire for space


maintenance

1. Direct—Suturing is possible
for small lesions
2. Local flaps
a. Tongue flaps have played
a great role in the repair
of oral defects and can be
based either anteriorly or
posteriorly.
b. Nasolabial flaps have
been ideal for defects of
floor of mouth. FIGURE 9.72: Free iliac flap
3. Regional flaps
a. Forehead can be used both for lining and cover based on
anterior branch of superficial temporal artery either in a
single stage or two stages.
b. Deltopectoral flap is mostly used for cover based on the
perforating branch of internal mammary artery.
c. Cervico pectoral flap is used for cover of lower cheek defects.
d. Platysma myocutaneous flap is used both for lining and
cover particularly oral and midline neck defects.
e. Pectoralis myocutaneous flap—The discovery of this flap
represents a significant advance in reconstructive technique
for head and neck malignancy and has given the
reconstructive surgeon greater versality in timing and
performance of radical surgery. This is based on acromio-
thoracic artery. The skin paddle may be twisted through
208 PLASTIC SURGERY MADE EASY
180 degree if external skin cover is required or simply flip
flapped over for intraoral cover.
4. Free flap—Microvascular tissue transfer has changed the
fundamental approach to reconstruction as it has made extensive
reconstruction possible in one stage.
a. Latissimus dorsi myocutaneous flap is an excellent source
of tissue for any patient who needs tissue replacement in
the head and neck following major ablative cancer surgery.
A great mass of tissue can be transferred in the flap enabling
large defects to be filled in the head and neck region.
b. The distant transfer of living bone and soft tissue by
microvascular technique offers a reliable one stage method
of composite tissue repair.

RECONSTRUCTIVE PRINCIPLES OF EYELID


Eyelid reconstruction requires a minimum of 3 elements
• Outer layer of skin
• Inner layer of mucosa
• A semi-rigid skeleton interposed between them.
Upper eyelid requires
Movable tissue as it must open, close and blink regularly to assist in
lubrication and should have a stable margin.

Basic Principles in Lid Reconstruction (Figs 9.73 and 9.74)


1. Use lower eyelid to reconstruct the upper eyelid and use cheek
tissue to reconstruct the lower lid.
2. ¼ th principle is used for reconstructing the lids, because of lax
tissue ¼ tissue can be excised and closed primarily.
3. A wedge of full thickness of lower lid is turned up as a flap on a
vascular hinge and fitted into the defect in the upper lid, two
weeks later the hinge is divided.
4. Defects upto 50% of lower lid can be closed by using lateral
canthotomy and cantholysis to release lateral aspect of the lid
and advancement of lateral cutaneous flap.
5. Defects upto 75% of lower lid can be treated by cheek
advancement flap.
HEAD AND NECK 209

FIGURE 9.73: Eyelid reconstruction FIGURE 9.74: Eyelid


reconstruction

6. Defect greater than 75% can be treated by Mustarde cheek


rotation flap for cover and chondro-mucosal graft for stability of
lower lid.

FACIAL PALSY (FIG. 9.75)


• Facial nerves supplies
muscles of facial expression.
• Patients with injuries at or
distal to stylomastoid fora-
men have facial paralysis.
Facial nerve branches
• Frontal
• Zygomatic
• Buccal
• Marginal mandibular
FIGURE 9.75: Bell’s palsy
• Cervical
210 PLASTIC SURGERY MADE EASY
Etiology
• Congenital (Mobius syndrome)
• Traumatic (at birth, childhood)
• Tumors (cranium, facial cana , parotid and tumors of face and
neck)
• Iatrogenic injuries to facial nerve during surgery
• Infective—Herpes virus (Bell’s palsy).

Treatment
Immediate repair using sural nerve as a graft.
Nonoperative
• Protect eye with lubricating eyedrops, wearing dark glasses and
taping the eyelids at night
• Botox into the normal side of the face improves facial symmetry.
Surgical
• Static
• Temporary tarsorrhaphy
• Slings using fascia lata
• Dynamic
• Reanimation using cross nerve transfer
• Muscle transfer using Masseter by dividing the muscle into
3 slips and inserted
• Above the lip
• Into the commissure
• Below the lip
• Free muscle transplantation using gracilis, serratus anterior
or Pectoralis minor
• Temporalis muscle inserted around the eye.

EAR DEFORMITIES
Embryology
Auricle develops as a series of six hillocks from the first and second
branchial arches. External and middle ear are derived from 1st
mandibular and 2nd hyoid branchial arches. Inner ear appears at
3 weeks and is derived from ectodermal origin. External ear begins
to form at the 4th week of gestation.
HEAD AND NECK 211
Anatomy
Auricle lies between horizontal lines at the upper line of the orbit
and the nasal spine.
Length is 6 cm in adults. It reaches 85% of adult size at 8-10
years of age.
Protrudes about 30 degree from skull.
Distance between upper part of helix and temporal skin is 2 cm.
• Muscles
• 6 intrinsic and 3 extrinsic
• Blood supply
• Superficial temporal artery
• Posterior auricular artery
• Occipital artery
• Nerve supply
• Great auricular nerve
• Lesser occipital nerve
• Auriculo-temporal nerve
• Arnolds nerve—branch of vagus
Hearing problem—Human ear has a receptive portion (inner
ear) and a conductive portion (external and middle ear). Inner ear
is rarely involved in microtia, the problem is conductive deafness
due to the blockage of malformed middle and external ear.

Etiology
• Incidence -1: 6000 births
• Common in males
• Factors -
• Hereditary
• Tissue ischemia resulting from an obliterated stapedial artery
• Drugs like thalidomide
• Infection like rubella

Classification
According to Roger
1. Microtia
2. Lop ear (folding of scapha and helix)
212 PLASTIC SURGERY MADE EASY
3. Cup ear or constricted ear
4. Prominent ear
According to Tanzer
1. Anotia
2. Microtia
3. Hypoplasia of middle 3rd of auricle
4. Hypoplasia of superior 3rd of auricle
5. Prominent ear
6. Constricted ear
7. Cryptotia
1. Microtia
Type 1—Auricular component present but they are all of
miniature size
Type 2—Auricular components partially remain
Type 3—Most auricular components lacking
Type 4—No auricular components
Associated abnormalities
• Asymmetry of face caused by underdevelopment of
ipsilateral temporal, maxillary and mandibular bones due
to underdeveloped 1st and 2nd branchial arches.
• Atresia of external auditary meatus and hearing defects.
Preoperative counseling
• Technical limitations should be discussed with parents
• Surgery is performed at the age of 7 (rib growth should
permit a good framework)
• Many stages are required to complete the ear reconstruction
• Will not resemble the normal ear
Stages of Reconstruction
• Cartilage framework
• Lobule transposition
• Post auricular release and grafting
• Tragus construction
Figures 9.76 to 9.80 showing one stage repair of Microtia—
Fabrication of the rib cartilage, raising the temperoparietal fascial
flap, cartilage insertion, wrapping the fascia over the bare cartilage
and final closure of the skin.
HEAD AND NECK 213

FIGURE 9.76: Microtia FIGURE 9.77: Template with


cartilage

FIGURE 9.78: Temperoparietal FIGURE 9.79: Fabricated cartilage


fascial flap in place
214 PLASTIC SURGERY MADE EASY

FIGURE 9.80: Final skin closure FIGURE 9.80A: A constricted ear


2. Constricted ear—The characteristic features are small height,
flat antihelix and overhanging helical rim (Fig. 9.80A).
3. Prominent ear or protruding ear—There is a lack of
antihelical fold and conchal hypertrophy. Treatment is by
Mustarde suture to reduce the conchal projection.
Ear forms an angle of about 30 degree with the temporal
surface of the head. If the angle is more obtuse than it is called
prominent ear.
4. Cryptotia ear—(pocket ear) The root of the helix invaginates
into the temporal skin. Helical rim not elevated. Absence of
superior auriculocephalic sulcus posteriorly.
5. Stahl’s ear—Characterized by third crus that traverses the
scaphoid fossa.

RECONSTRUCTIVE PRINCIPLES OF LIP


Anatomy
Muscles of the lip are orbicularis oris, superior and inferior labial.
Oral competence is controlled by orbicularis oris muscle. The fibers
take its origin from the angle of the mouth and decussate in the
midline and insert into the philtral ridge of the opposite side.
Blood supply is from superior and inferior labial branch of facial
artery.
Nerve supply is from buccal and marginal mandibular branch of
7th cranial nerve. Infraorbital and mental nerves.
Lymphatic drainage—submandibular and submental nodes.
HEAD AND NECK 215
Goals of Reconstruction
• To use sensate flaps
• To maintain sphincteric action
• Obtain good opposition of both lips
• Provide sufficient opening for food and dental cleaning
• Aesthetically acceptable

Principles of Reconstruction
Isolated defects of the upper or lower lip are not accompanied by
trismus, however, defects of the angle of the mouth are often
associated with trismus.
Reconstruction follows 1/3rd principle—1/3rd defect of either
upper or lower lip can be closed primarily. Defect more than 1/3rd
requires borrowing of tissue from local or distant site (Figs 9.81
and 9.82).

FIGURE 9.81: Squamous cell FIGURE 9.82: Fan flap


carcinoma angle of mouth
216 PLASTIC SURGERY MADE EASY
Goals of Upper Lip Reconstruction
• Correct alignment of the white line
• Muscle approximation
• To minimize distortion
• Defects more than 1/3 require lip switch flap, Abbe flap from
lower to upper.

Philtral Region
Philtral region is very unique as it contains the philtral ridge and
philtral dimple. The best option to reconstruct this area is Abbe flap,
FTSG or composite graft from the ear.

Reconstruction of Lower Lip


• Goal should be to maintain sphinteric action of the muscle to
avoid evertion and drooling
• It should provide sufficient opening for food and for dental
cleaing
• Aesthetically should be acceptable.

BENIGN JAW TUMORS


AMELOBLASTOMA (ADAMANTINOMA)
Definition
Ameloblastomas are epithelial tumours of odontogenic origin. It is
a common disorder of the jaw. It is benign and locally aggressive. It
has the ability to recur and even metastasize.

Incidence
Forms 11% of odontogenic tumors.

Embryology
Originates from dental laminar rests, enamel organ, basal cells of
oral mucosa or epithelial lining of dentigerous cyst. When squamous
metaplasia is extensive and keratinization occurs the tumor is called
acanthomatous ameloblastoma.
HEAD AND NECK 217
Age of Onset
20 to 50 years.

Clinical Features
• Mandible is involved four times greater than maxilla (Figs 9.83
to 9.86)
• In both jaws tumor occurs in posterior region (80%)
• Tumor size ranges from 1–16 cm in diameter
• Slow growing, painless swelling. Pain being the feature in 1/3rd
cases
• Can also involve maxillary antrum.

Types
• Type I—Conventional ameloblastoma
• Type II—Unicystic ameloblastoma (less than 30 years) develops
in epithelial wall of dentigerous cyst
• Type III—Peripheral or extraosseous ameloblastoma arise from
basal layer of surface epithelium overlying a tooth bearing
portion of jaw.

FIGURE 9.83: Jaw tumor FIGURE 9.84: Ameloblastoma


218 PLASTIC SURGERY MADE EASY

FIGURE 9.85: Jaw tumors FIGURE 9.86: Massive jaw tumor

Radiological Features
Radiolucent unilocular or expansile multilocular lesions may or
may not be associated with the tooth.

Treatment
• Enucleation and curettage
• Segmental or radical resection
• Partial hemimandibulectomy (tumor involving ramus, angle or
high recurrence rate)
• Reconstruction depends on the type of excision. It can be costal
cartilage graft or microvascular fibular flap.

MISCELLANEOUS
PTERYGIUM COLLI (FIGS 9.87 AND 9.88)
It is a congenital defect in which there are thick folds of skin and
subcutaneous tissue on the lateral aspect of the neck extending
from the mastoid region to the acromion. Neck appears short, thick
and broad. Treatment is by Z-plasty.
HEAD AND NECK 219

FIGURE 9.87: Pterygium colli FIGURE 9.88: Pterygium colli

FIGURE 9.89: Torticollis FIGURE 9.90: Torticollis

TORTICOLLIS (FIGS 9.89 AND 9.90)


In this condition the sternomastoid muscle, deep fascia and deep
muscles are involved. The shortening of sternomastoid muscle
causes the head and neck to be immobile, the head gets tilted
towards the affected side and the chin is turned towards the opposite
side.
The cause is supposed to be angiofibromatous over growth.

Types
Congenital torticollis
• Resolves spontaneously in 3-9 months
• Physiotherapy and massage
• Requires sternomastoid tenotomy
Secondary torticollis—Transient torticollis seen in lymphadenitis.
220 PLASTIC SURGERY MADE EASY
TEMPEROMANDIBULAR ANKYLOSIS
Introduction
Temperomandibular joint ankylosis is an extremely disabling
condition from the view point of function, hygiene and cosmetic
appearance. An opening of less than 5 mm interincisor distance is
considered as complete ankylosis.

Classification
Ankylosis can be classified as
• True or intra-articular ankylosis
• False or extra-articular ankylosis

Etiology
• Can be due to trauma or infection
• A blow to the chin area not only damages the condylar head
but also results in degeneration of articular surfaces eventually
leading to fibrosis and ankylosis.

Clinical Features (Figs 9.91 to 9.94)


• The earlier the ankylosis, the greater the degree of deformity of
the face and is due to damage to the growth center of condyle.
• Fullness on the affected side, flat on the normal side, chin
deviated to the affected side, micrognathia, malocclusion with
cross-bite.
• In unilateral ankylosis there is some movement but in bilateral
ankylosis there is no movement, either side to side or protrusive
nor retrusive.
• when children come to us early, the deformity is less, when
children come to us late deformity is prominent.
• Bilateral symmetrical deformity has severe retrognathia and
micrognathia with a bird profile.
• Regardless of the type, the constant finding is the destruction of
the meniscus, atrophy of condyle and fossa, narrowing of the
joint spaces and formation of the thick fibrous adhesions.
HEAD AND NECK 221

FIGURE 9.91: TM joint ankylosis FIGURE 9.92: TM joint release with


sternoclavicular joint transfer

FIGURE 9.93: Severe retrognathia FIGURE 9.94: Deviation of chin


towards affected side
222 PLASTIC SURGERY MADE EASY
Investigation
OPG and CT Scan.

Orthopantogram Reveals
• Lack of definable condyle and glenoid fossa
• Condylar thickening
• Acute antegonial notching
• Absence of coronoid notch
• Bony spur at the angle of the mandible on the affected side
• Hypertrophy of the coronoids with impingement of zygomatic
arch.

CT Scan
CT scan shows the joint space on the normal side and the extent of
bony fusion on the affected side (Fig. 9.95).

Aim of Treatment
Both from the functional and aesthetic point of view it is important
to achieve effective release of ankylosis with simultaneous
mandibular advancement, good jaw movement and satisfactory
mastigatory function (Figs 9.96 to 103).
Anesthesia is always challenging and is by a blind nasal
intubation.

FIGURE 9.95: CT TM joint FIGURE 9.96: Malocclusion with


showing the bony fusion cross-bite
HEAD AND NECK 223

FIGURE 9.97: Postorthognathic- FIGURE 9.98: Premodel


correction surgery

FIGURE 9.99: Postmodel surgery FIGURE 9.100: Premodel surgery

FIGURE 9.101: Postmodel surgery


224 PLASTIC SURGERY MADE EASY

FIGURE 9.102: Preorthognathic FIGURE 9.103: Postorthognathic


surgery surgery

Discussion
TM joint ankylosis is a condition prone for recurrence following
many of the conventional options available for its treatment. Even
when recurrence is prevented, the problem of facial asymmetry
frequently remains. This has resulted in a continuing search for
newer approaches to the problem.
The various options available for the treatment of TM joint
ankylosis are:
• Gap arthroplasty—Simplest method of treating TM joint
ankylosis. But its major drawback is the possibility of recurrence
in more than half the patients so treated.
• Interpositional arthroplasty—Though the problem of
recurrence is less with either alloplastic material or autogenous
tissue, the static mandibular deformities often persist.
• Costochondral graft—Restores the functional cranioman-
dibular continuity with significant improvement in facial
symmetry.
HEAD AND NECK 225
• Sternoclavicular joint—The logical end point is to
reconstitute an anatomically complete joint. Snyder in 1971
was the first to explore the possibility of replacing TM joint by
sternoclavicular joint. He emphasized the structural similarity
between the two joints and noted the advantages of transferring
the growth center of the clavicular head in a growing child.
Siemssen in 1982 proved the feasibility of transfer and
suggested that the technique was also effective in correcting the
static deformity of the mandible. Siemssen’s technique, which
is a combined preauricular and submandibular approach to
remove the ankylosed joint. A superficial parotidectomy and
resection of styloid process to enable the relatively bulky
sternoclavicular joint to be transferred to the region of glenoid
fossa pedicled on sternomastoid and sternothyroid muscles.
This, however, was a complex procedures requiring long
operating hours, which finally led us to modify the technique to
make it simpler and less time consuming.
The rationale of our approach was to just take a thin sliver
of sternal bone in order to have a complete joint, a fragment so
small that it can be expected to be vascularized by its soft tissue
connections. This led us to several modifications:
• First of all with a small sternal fragment, the transferred joint is
not bulky and can fit into the space vacated by the TM Joint
• No need for parotidectomy
• No excision of styloid process
• No need to include sternohyoid muscle as a source of blood
supply to the sternal fragment
• No need for division of the sternal head of the sternomastoid
(its preservation is significant cosmetically and functionally)
• No need for preauricular incision as the developmental defect
associated with the ankylosis leaves the vertical ramus so short
that this incision affords adequate access to the joint itself.

Operative Steps
It consists of two parts:
• The first part is the radical resection of all bony connections
between the mandible and the cranial base.
226 PLASTIC SURGERY MADE EASY
• The second part is the transfer of the sternoclavicular joint
pedicled on the clavicular head of the sternomastoid muscle to
the subglenoid region.

Intraoperative Complications
• Troublesome pterigoid venous plexus oozing
• Pneumothorax

Recommendation
• Liquid diet for 4 weeks
• Acrylic screw exercise after that to increase the range of motion
of the joint after 6 weeks
• Mouth opening of 3 cm reduces to 2.5 cm presumably due to
muscle spasm.

Results
• Good mouth opening and moderate correction of retrognathia
• Minimal lateral deviation of the jaw on opening the mouth
• Good neck contour
• No significant disability related to shoulder function.
Chapter 10

Breast and Chest


Wall Deformities
228 PLASTIC SURGERY MADE EASY
Congenital
• Pectus excavatum
• Poland’s syndrome
• Unilateral breast—aplasia

Iatrogenic
• Burns of the chest
• Irradiation

Hormonally Related Breast Deformity


• Aplasia
• Hypoplasia
• Overgrowth
• Virginal hypertrophy of breast
• Juvenile fibroadenoma
• Gynecomastia

POLAND’S SYNDROME (1841)


Characterized by unilateral chest wall and upper limb abnormalities.
It is thought to be caused by kinking of the subclavian artery at the
6th week of gestation (Fig.10.1).
• Absence of sternocostal portion of the pectoralis muscle causing
flattening of chest wall
• Absence of anterior axillary
fold
• Hypoplasia of breast
• Lack of axillary hair
• Hand anomalies
• Goals of treatment
• Recreate anterior axil-
lary fold
• Add bulk to anterior
chest wall
• Build up breast FIGURE 10.1: Poland’s syndrome
BREAST AND CHEST WALL DEFORMITIES 229

GYNECOMASTIA
Definition
It is excessive development of the male breast

Questions to Ask
Duration, pain, any medica-
tion, weight gain, liver disease
and hyperthyroidism.
E xamine
• Breast—palpate for hard
and soft mass, nipple
discharge (Figs 10.2 to
10.4)
FIGURE 10.2: Unilateral
• Testes—Testicular tumor
gynecomastia
(Ultrasound)
• Liver for hepatomegaly
• Thyroid for nodules
• Nutritional status.

Etiology
• Physiologic
• Pathologic
• Pharmacologic FIGURE 10.3: Unilateral
gynecomastia

Physiologic
• Neonatal
• Pubertal
• Senile
• Imbalance between estro-
gen and androgen

Pathologic
• Cirrhosis
FIGURE 10.4: Bilateral
• Malnutrition
gynecomastia
230 PLASTIC SURGERY MADE EASY
• Hypogonadism
• Thyroid disease
• Testicular tumors

Pharmacologic
Spironolactone, Marijuana, Cimetidine, Diazepam, Reserpine,
Estrogen, Theophylline and Digoxine (Remember these drugs as)
Some men can develop rather excessive thoracic diameters.

Medical Therapy
• Testosterone can be effective if gynecomastia is secondary to
testicular failure
• Tamoxifen reduces gynecomastia
• Danazole decreases gynecomastia and pain.
Surgical therapy—Excision when the breast tissue is hard (Figs
10.5 and 10.6). Liposuction can be performed when the breast
tissue is soft (Figs 10.7 and 10.8) or a combination of both can
be performed.

Incision
Semicircular along the areola if glandular tissue has to be excised.
If the breast tissue is soft, a small stab incision is made in the
inframammary line and using either a syringe or suction liposuction
the fat is sucked out.

FIGURE 10.5: Bilateral FIGURE 10.6: Postoperative


gynecomastia
BREAST AND CHEST WALL DEFORMITIES 231

FIGURE 10.7: Bilateral FIGURE 10.8: Postoperative


gynecomastia liposuction
Complication
Hematoma, seroma, nipple necrosis and infection.
Chapter 11

Upper Extremity
234 PLASTIC SURGERY MADE EASY
CONGENITAL DEFECTS
Embryology
Human limb develops during the 4th week of gestation in the form
of lateral swellings called limb buds. Focal necrosis is important in
abnormal development.The timing and extent of necrosis determines
the results. Early focal necrosis before 3rd and 4th week prior to
limb bud formation results in upper limb absence.

Incidence
Common, occurs one in 625 live births.

Etiology
• Genetic
• Environmental
• Hereditary
• Drugs

CLASSIFICATION
Defects
• Amelia—complete absence of whole upper extremity from
shoulder girdle
• Phocomelia—hand articulates with shoulder girdle directly
• Absence of pectoral muscle—Poland’s syndrome is characterized
by absent pectoralis major muscle, nipple displacement,
underdeveloped breast, shortness of limb or anomalies of hand
and fingers
• Radial claw hand, Ulnar claw hand
• Absence of hand, Absence of digits
• Absence of ulnar segment, Absence of radial segment
• Absence of central segment—cleft hand, lobster hand, claw
hand.

Deformities
• Arthrogryposis—flexion deformity
UPPER EXTREMITY 235
• Brachydactyly—digital shortening (late development of middle
phalanx)
• Camptodactyly—crooked finger (affects PIP JOINT)
• Clinodactyly—lateral deviation deformity
• Duplication
• Ectrodactyly—absence of parts of hand
• Macrodactyly—(gigantism)
• Polydactyly—(Supernumerary digits)
• Syndactyly—(fused fingers).

Embryological Classification
• Failure of formation
• Failure of differentiation
• Duplication
• Overgrowth
• Undergrowth
• Constriction ring syndrome
• Generalized skeletal abnormalities and syndrome.

Syndactyly (syn in Greek means—together)


Embryology—Interlay mesenchyme fails to undergo necrosis
leading to persistence of overlying ectoderm.
Etiology
• Strong familial tendency—20%
• Males are common
• Associated with other deformities
• 3rd web space affected commonly
Incidence—1: 2000 births
Classification
• Simple—Webbing is of only skin
• Complex—Soft tissue and bony connections present between
the digits (Fig. 11.1)
• Complicated—Presence of bony union, abnormal phalangeal
segments constrictions and nubbins (Figs 11.2 and 11.3)
236 PLASTIC SURGERY MADE EASY

FIGURE 11.1: Bilateral syndactyly FIGURE 11.1A: Postoperative


unilateral syndactyly release

FIGURE 11.2: Unilateral syndactyly FIGURE 11.3: Bilateral


syndactyly of all fingers

Surgery—Separate the fingers by zig zag incisions and reconstruct


the cleft by using flaps both from palmar and dorsal surface. The
rest of the raw surface is closed
with full thickness skin graft. The
web is reconstructed with a
proximal based dorsal flap.

Polydactyly
Influence of excessive apical
ectodermal ridge in the hand
plate area is associated with
development of polydactyly. It is
represented by a soft tissue FIGURE 11.4: Polydactyly
UPPER EXTREMITY 237
appendage attached to a pre- or postaxial border digit (Fig. 11.4).
Treatment is by excision of excess tissue.

Camptodactyly
Incidence is 1% . It is flexion deformity of the PIP joint in an antero-
posterior direction due to deficiency of soft tissue on volar surface.
It commonly affects the little finger. The most common cause is
abnormal lumbrical or flexor digitorum superficialis muscle insertion.
Treatment is by splinting.

Clinodactyly
Characterized by lateral deformity of the finger in radioulnar plane.
Incidence is 1%. Usually affects the little finger. It is caused by
triangular shaped delta phalanx. Treatment is by wedge osteotomy.

Constriction Ring Syndrome (Streeter dysplasia, Annular


band syndrome, Amniotic band syndrome)

Classification
• Simple groove in the skin
• Constriction rings with deformity of distal part
• Constriction ring with fusion of distal part
• Intrauterine amputations (Figs 11.5 and 11.6)

FIGURE 11.5: Constriction band FIGURE 11.6: Constriction band


both legs correction one half of leg
238 PLASTIC SURGERY MADE EASY
Clinical classification
• Shallow—Only slightly noticeable on the skin
• Deep—Involves only skin
• Deeper—Involves the subcutaneous tissue and muscles
• Deepest—Extends into the bone
Incidence—1:15000
Pathogenesis
• Intrinsic theory—The band represents macerated sheets of
epidermis (streeter)
• Extrinsic theory—Intrauterine disruption of amnion (Torpin)
• Intrauterine theory—Intrauterine trauma causes hemorrhage
which leads to digital fusion.
Surgery—Z-plasty is performed to release the tight band at the
depth of the groove. The atrophic tissue along the side walls should
also be excised for a good release.

Ectrodactyly
Absence of parts of hand. Characterized by distal absence or
deficiency of phalanx or carpus.

Arthrogryposis
The joint is curved. The joint mobility gets limited due to contractures.
Treatment is by splinting.
Chapter 12

Lower Extremity
240 PLASTIC SURGERY MADE EASY

CONGENITAL DEFORMITIES OF LOWER LIMB


Cleft foot or lobster foot or partial adactyly—One or more
toes and parts of their metatarsals are absent and often the tarsals
are abnormal. First and 5th toes are usually present (Fig. 12.1).
Two typical manifestations are the lobster claw variety and
monodactyly type. Deficiency of radial rays only 5th digit remains,
absence of central ray
The other common congenital deformities of the foot are
syndactyly (Figs 12.2 and 12.3), constricting ring syndrome (Figs
12.4 to 12.6) and macrodactyly.

MACRODACTYLY
Definition
It is a rare condition of congenital idiopathic gigantism of one or
more digits (Fig. 12.7).

FIGURE 12.1: Cleft foot FIGURE 12.2: Syndactyly

FIGURE 12.3: Syndactyly bilateral FIGURE 12.4: Consrtiction band


foot
LOWER EXTREMITY 241

FIGURE 12.5: Preoperative FIGURE 12.6: Z-plasty release


constricting band

The other conditions which


can cause enlargement of the
digits are:
1. Hemangioma
2. Lymphangioma
3. Neurofibroma

Clinical Findings
• Enlargement of toe FIGURE 12.7: Macrodactyly
• Soft tissue hypertrophy is
greater on the plantar surface
than dorsal surface. This results in dorsal curvature of the digits
• X-ray will show enlarged metatarsal and phalanges.

Types of Macrodactyly
Static type where the enlargement is present at birth and
subsequent growth is proportionate to that of the individual. This is
the most common type.
Progressive type—Growth rate of the enlarged part is faster than
that of the child. This type is rare.

Problems
• Obvious functional limitations
• Psychologic effect
• Surgery is repetitive
242 PLASTIC SURGERY MADE EASY
Goal
1. To provide painless functional feet
2. Cosmesis
3. Reduce length and circumferential bulk
4. To maintain sensation and circulation
5. To preserve as much motion as possible
6. Epiphyseal arrest to control longitudinal growth
7. Partial digital amputation.

Important Points to Note


1. Blood vessels are either normal or slightly enlarged, so the digit
as a whole is poorly vascularized
2. Healing potential is reduced
3. Incidence of wound breakdown and infection is high.

Complications
1. Skin and flap necrosis
2. Loss of sensation

ULCER
Definition
It is a discontinuity of an epithelial surface or break in the continuity
of the skin and mucous membrane. It may involve all or part of the
dermis.

Classification
A. Clinical
• Spreading
• Healing
• Callous
B. Pathological
• Specific
• Nonspecific
• Malignant
• Also classified as (remember as MINT)
LOWER EXTREMITY 243
a. Metabolic Gout
Diabetes (Fig 12.8)
b. Malignant Rodent
Epithelioma
Melanoma (Fig.12.9)
c. Infective—Nonspecific Staphylococcus
Streptococcus
—Specific Tuberculosis
Leprosy
Syphilis
Soft chancre
d. Nutritional Arterial sclerosis
Earicose ulcer (Fig. 12.10)
Lymphatic obstruction
e. Neurotrophic Diabetes
Tabes dorsalis
Peripheral neuritis
f. Traumatic Pressure of splint

FIGURE 12.8: Diabetic foot FIGURE 12.9: Melanoma

FIGURE 12.10: Venous ulcer


244 PLASTIC SURGERY MADE EASY
LYMPHEDEMA
Definition
Accumulation of protein rich interstitial fluid within the skin and
subcutaneous tissues that occurs as a result of lymphatic dysfunction.

Classification
• Primary (Congenital lymphatic dysfunction)
• Secondary (Acquired precipitating cause)
a. Primary lymphedema—Allen’s classification
At birth
• Congenital sporadic
• Congenital familial (Milroy’s disease). Lymphedema con-
genita (Figs 12.11 and 12.11A)
At puberty—Congenital familial (Meige’s disease). Lymph-
edema precox (Fig. 12.12)
At middle age—Lymphedema tarda.
b. Secondary lymphedema
• Direct infestation of lymph node with Wuchereria bancrofti
• Infection and inflammation
• Damage or removal of regional lymph node by surgery,
radiation or tumor invasion

FIGURE 12.11: Congenital FIGURE 12.11A: Congenital lymphedema


lymphedema
LOWER EXTREMITY 245

Etiology
a. Primary
• Absent or hypoplastic lymp-
hatic channels
• Congenital abnormalities
• Fibrosis of lymph nodes
• Hyperplastic
• Obstructed lymphatics
b. Secondary
• Acute infections
• Athletes foot
• Block dissections
• Chronic inflammatory state
• Deep venous thrombosis
• Elephantiasis nonfilarial
FIGURE 12.12: Lymphedema
(podoconiosis) precox
• Filariasis
• Malignancies
• Surgical and trauma
• Superficial thrombophlebitis
• Snake and insect bites

Pathophysiology
• Lymphedema is confined to the subcutaneous tissue
• Extravasation of protein rich fluid occurs when fluid formation
exceeds lymphatic transport capacity
• High protein edema causes shifts in Starling’s equilibrium,
resulting in accumulation of more fluid giving rise to chronic
inflammatory state and consequent fibrosis
Leakage of protein into the interstitium results in raised tissue
oncotic pressure, which causes increase in interstitial protein and
fluid, leading to tissue hypoxia cell death eventually to chronic
inflammatory response and fibrosis.

Developmental Abnormalities
• Lymphatic aplasia
• Cystic hygroma
246 PLASTIC SURGERY MADE EASY
• Lymphatic and nodal hypoplasia/hyperplasia
• Lymphangioma.

Clinical Features
• Begins distally and progresses proximally over months to years
• Initially soft and pits easily. It gradually becomes nonpitting as
fibrosis develops and the tissue becomes indurated (Excess
protein oozing results in bacterial infection, cellulitis, inflam-
mation, fibrosis and additional lymphatic dysfunction)
• Symptoms—fatigue, pressure of limb and pain.

Signs and Symptoms


• Fatigue
• Edematous extremities
• Pain
• Buffalo hump, Edema of dorsum of foot
• Squared toes
• Stemmer’s sign
• Skin changes
• Ulcerations, raised nodules

Grading of Lymphedema (Brunner’s clinical grading)


Grade I—pitting edema. Decreases with limb elevation.
Grade II—Nonpitting edema, fibrosis and induration. Does not
decrease completely with limb elevation (Figs 12.13 to 12.15).
Grade III— Edema with skin changes and lymphorrhea (Figs 12.16
to 12.19).

Complications
• Secondary skin changes—dermatitis, hyperkeratosis, warty
verrucosis, ulceration with lymphorrhea and fungal infection
(Fig.12.20)
• Inflammatory—Recurrent lymphangitis, cellulitis, fibrosis of the
subcutaneous tissue and functional impairment (Fig.12.21)
• Malignant—Lymphangiosarcoma
• Post mastectomy lymphedema (Fig.12. 22)
LOWER EXTREMITY 247

FIGURE 12.13: Grade I FIGURE 12.14: Grade FIGURE 12.15: GradeII


lymphedema II lymphedema post conservative treat-
ment

FIGURE 12.16: Grade III FIGURE 12.17: Grade-III


lymphedema with skin changes lymphedema with skin changes
248 PLASTIC SURGERY MADE EASY

FIGURE 12.18: Grade III FIGURE 12.19: Grade III with severe
lymphedema skin changes hypertrophy of all the toes

FIGURE 12.20: Lymphedema FIGURE 12.21: Grade III with cellulitis


Grade III with hyperkeratotic
skin changes
LOWER EXTREMITY 249

FIGURE 12.22: Post mastectomy FIGURE 12.23: Lymphedema-vulva


lymphedema with skin changes

FIGURE 12.24: Lymphedema vulva FIGURE 12.25: Postoperative


excision

The other common sites of lymphedema are the vulva (Figs


12.23 to 12. 26), penis (Fig.12. 27) and scrotum (Figs12.28
to 12. 33).

Investigation
• CBC/ESR/serum proteins/blood urea/creatinine/electrolytes/LFT
• Isotope lymphography
• Ultrasound/CT/MRI
• Lymphangiography (Gold standard)
• Clinical trials everyday—limb volume, skin softness and limb
girth.

Management
• The primary treatment for lymphedema is nonsurgical
250 PLASTIC SURGERY MADE EASY

FIGURE 12.26: Genital lymphedema FIGURE 12.27: Penile


lymphedema

FIGURE 12.28: Peno-scrotal FIGURE 12.29: Side view


lymphedema
LOWER EXTREMITY 251

FIGURE 12.30: Scrotal FIGURE 12.31: Postoperative


lymphedema excision

FIGURE 12.32: Lymphedema FIGURE 12.33: Postoperative following


scrotum excision

• The aim of medical and surgical therapy is to reduce the swelling


and to prevent complications
• No treatment option is completely and permanently curative.

Conservative Management
• Bed rest and elevation of the affected limb
• Custom-fitted elastic compressive garments (sleeves or stockings)
• Measurements of water volume displacement are more precise
• Meticulous foot care
• Serial photography
252 PLASTIC SURGERY MADE EASY
Medical Management
• Antihistamine/anti-inflammatory agents
• Prophylactic antibiotic to control streptococcal infection once a
month for life long (Injection penidure 12 lakhs IM after test
dose)
• Diethylcarbamazine.

Surgical
• Numerous surgical procedures of which none is completely
curative
• Surgery does not obviate continued medical therapy.

Physiological (Lymphatic bypass)


• Skin bridge, omental pedicle (Gille’s)
• Enteromesenteric bridge—best lymphatic bypass.
• Lymphovenous/lymphonodal shunts
• Microlymphatico-venous shunts

Reduction Operations
• Sistrunck’s operation (1918)
• Homans operation
• Thompson’s operation
• Charle’s operation (1912)
• Liposuction
• Genital lymphedema (exisional reduction surgery)
• Penis (simple excision with circumcision)
From a physiologic stand point, surgery must reduce the
lymphatic load or increase the lymphatic transport capacity.
A. Procedure reducing the load for lymphatic clearance
a. Reduction of skin and subcutaneous tissue with primary
closure (Sistrunk and Miller’s operation)
b. Excision with wound closure by local flaps (Homans)
c. Wound closure with STSG (Charle’s) (Figs 12.34 and
12.35)
d. Wound closure with FTSG (Gibson)
LOWER EXTREMITY 253

FIGURE 12.34: Charle’s operation FIGURE 12.35: Front view

B. Procedure to increase lymphatic transport capacity


a. Creation of new lymphatics—Reconstruction of new
lymph vessels with threads (Handley used silk threads)
with the idea that their capillary action would enable them
to replace the missing lymphatics and to transfer excess
fluid to regress with normal circulation.
b. Drainage operations
• Through strips of fascia (Chitale)
• Through omental transfer (Gold Smith)
• Through skin flaps (Thompson)
• Through enteromesenteric bridging (Kinmonth)
• Through peripheral—Lymphatico-venous anastomosis
• Lympho-nodo-venous (Olszewski)

Complications
• Recurrent lymphangitis
• Cellulitis and sepsis
• Lymphangiosarcoma (Stewart-Treves syndrome)
254 PLASTIC SURGERY MADE EASY
Postoperative Management
• Limb elevation
• Postoperative pressure garments (30—40 mm of Hg) is
essential for good compression.

Prevention and Control


• Avoidance of mosquito bites (insect repellent and mosquito
nets)
• DEC prophylaxis.

LYMPHANGIOMA CIRCUMSCRIPTA
It is characterized by the presence
of small intradermal vesicles over-
lying a deeper lymphatic malfor-
mation. Treatment is by complete
resection and primary closure if it
is small, or total excision and split
thickness skin graft (Fig. 12.36).

PRESSURE SORE (BEDSORE,


PRESSURE ULCER)
Definition
Ulceration or maceration of tissues
due to prolonged pressure.
FIGURE 12.36: Lymphedema
Circumscripta scrotum
Epidemiology
It usually occurs in patients who are hospitalized, old debilitated
and bed ridden.

Location
It is commonly seen on the sacrum, heel, ischium, and trochanter
(Figs12.37 to 12.43).
LOWER EXTREMITY 255

FIGURE 12.37: Sacral FIGURE 12.38: Sacral pressure sore


pressure sore

FIGURE 12.39: Trochantric FIGURE 12.40: Pressure sore


pressure sore

FIGURE 12.41: Trochantric


pressure sore
256 PLASTIC SURGERY MADE EASY

FIGURE 12.42: Trochanteric FIGURE 12.43: TFL flap


bedsore

Pathogenesis
It can be due to intrinsic and extrinsic factors,
• Pressure, friction, old age, and malnutrition.
• Sores obtained in the lying position. Pressure transmitted to the
tissue particularly on bony points exceeds the capillary pressure
(35 mm of Hg) results in ischemia. Continuous pressure of
more than 2 hours can result in pressure sores.

Classification
• Grade I—Erythema of skin
• Grade II—Skin ulceration with necrosis of subcutaneous tissue
• Grade III—Above plus muscle necrosis
• Grade IV—Above plus exposed bone and joint.

Treatment
• Prevention
• Keep skin clean and dry
• Frequent turning of the patient every two hours
LOWER EXTREMITY 257
Surgical management
• Adequate debridement of necrotic tissue involving the soft
tissue, bone and wound covered with flaps.
• The various flaps used to cover the pressure sores are local
flaps, muscle flaps and myocutaneous flaps.
Chapter 13

Thermal Injury
260 PLASTIC SURGERY MADE EASY
INTRODUCTION
In India, approximately 7 million people sustain burn injury every
year and about 2 million people succumb to burn injuries. Burns
are caused by dry heat, hot liquids, chemical and electrical. Severe
burn is one of the most traumatic injuries a person can suffer and
still survive.

DEFINITION
Burns means thermal injury. It results in coagulative alteration of
proteins due to wide range of temperatures, ranging from the
lowest—that is frostbite to the highest—that is electrical injury. Thus,
both extremes of heat and cold can cause burn injury.

FIRST AID
The object of first aid is to extinguish the flames and bring down the
temperature to normal as early as possible.The damage is directly
proportional to the temperature of the burning agent and to the
duration of contact. A person whose clothes are on fire should not
run as it fans the flames. The oxygen supply in the air aggrevates the
burning process.
Water is the best option to put off the fire—if water is not available
then falling down on the floor and rolling over a blanket may be
useful. If nothing is available then roll on the floor or anything that
is available to put off the fire.
The advantage of pouring water is to cool the burn surface and
to prevent further destruction of deeper tissues. It stabilizes skin
mast cells which decrease histamine release thereby decreases
edema of the wound. It also controls pain. Once the fire is put out,
remove the burnt clothes, cover the burn wound with a clean sheet
and transport the victim to the nearest hospital. If transportation is
delayed for more than 30 minutes then start sips of water into
which a pinch of salt has been added. If facilities are available then
start intravenous fluids using dextrose saline.
THERMAL INJURY 261
CAUSES OF BURNS
a. Thermal or flame burns occur due to dry heat. Seventy five
percent (75%) occurs at home and are preventable.The heat
causes coagulation of the protein in the tissue.
b. Scald burns are due to hot liquids, mostly in children while
pulling down or knocking hot liquids onto themselves or by
stumbling onto a burning agent.
c. Chemical burns are caused by strong acids and alkali. It causes
tissue damage by denaturation of the cell protein. Chemical
burns are unique because there is continuous tissue damage. It
usually occurs at home where the acid is stored for use of cleaning
toilets. Homicidal burns are very common in India due to local
hooligans who throw acid on young female’s face when they
reject advances. Immediate removal of clothes and continuous
irrigation for at least 30 minutes with water is the most effective
measure of first aid management.
d. Electrical burns can be flash, arc or contact. The flash may
ignite clothes and hence burns may be superficial. In contact
burns the person comes in contact with live wires. The current
enters the body through nerves and vessels and exits at another
site.

ASSESSMENT OF BURN INJURY


Estimating Burn Size
For children under 12 years of age, Lund and Browder’s formula
chart is used to estimate the total body surface area burn involved.
For adults, Wallace’s “Rule of Nines” is commonly used.
According to this head and neck constitute 9% of TBSA, each upper
extremity is 9%, each lower extremity is 18% and anterior and
posterior trunk are 18% each, and 1% for the genitalia (Fig.13.1).
For all age groups palmar surface of the patient’s hand represents
1% of TBSA burns.

Estimating Burn Depth


The depth of burn determines the type of healing, besides being a
prognostic factor. Burn wounds are classified according to Boyer
262 PLASTIC SURGERY MADE EASY

FIGURE 13.1: Rule of nine

(1814) into three degrees and according to Dupuytren into six


degrees.
First-degree burns is characterized by epidermal involvement,
erythema and edema, typical example is a sunburn or touch of a
hot iron. This type of burn heals spontaneously in 7 days
(Remember as 3 E).
Second-degree burns are divided into superficial and deep
depending upon the involvement of the dermal structures.
Second-degree superficial burns involve the whole of
epidermis and a small part of the dermis (papillary layer). Clinically
blisters, blebs, bullae and blanching on pressure are seen (Fig
13.2). The wound looks pink in color because the dermal plexus
is seen through the burned surface. It is also painful. The wound
heals spontaneously in 7-14 days by regeneration of epithelial
cells that is, hair follicles, sweat glands and sebaceous glands (Fig.
13.3). Wound healing can be hastened by using skin substitutes
(Fig.13.4).
Second-degree deep burns involve the whole of epidermis
and varying depths of dermis including the papillary and the reticular
layer. It has pink white dry appearance and less painful.
THERMAL INJURY 263

FIGURE 13.2: Second degree FIGURE 13.3: Healed second


superficial burn with blisters degree superficial burn

FIGURE 13.4: Amnion on arm and FIGURE 13.5: Second degree


chest for second degree burns deep burns

Epithelialization occurs more slowly due to few epithelial structures


present in the reticular dermis (Fig. 13.5). If infection sets in, this
type of burns gets easily converted to third-degree burns.
Third-degree burns involves the whole of epidermis, the whole
of dermis and different depths of subcutaneous tissue. It appears
white, brown or black. The surface is dry and leathery. Coagulated
veins are seen on the surface (Fig.13.6), pain is characteristically
264 PLASTIC SURGERY MADE EASY

absent. Collagen, a protein pre-


sent in the dermis turns white on
burning, charring of this collagen
results in black color. This type of
burns will not heal spontaneously
and treatment is by excision and
grafting (Figs13.7 and 13.8).
FIGURE 13.6: Third-degree burns
with coagulated veins
PATHOPHYSIOLOGY
Burn Shock
Burn shock is both hypovolemic
and cellular and is characterized
by specific hemodynamic chan-
ges including decreased cardiac
output, decreased plasma
volume, decreased urine output,
increased extracellular fluid, and
increased edema. The primary
goal is to restore and preserve
tissue perfusion in order to avoid
ischemia.

Changes at Vascular Level

FIGURE 13.7: Third-degree burns


Immediately following burns
with pale granulations there is an increase in the capillary
permeability and this is due to the
inflammatory mediators. They act
by altering the membrane inte-
grity in venules leading to leakage
of fluid and protein from micro-
vessels. When this fluid is lost into
the skin it appears as blisters if
skin is intact or as exudates if skin
is lost. When this fluid is lost in
FIGURE 13.8: Third-degree burns subcutaneous tissue it causes
after complete eschar removal edematous swelling. The early
THERMAL INJURY 265
phase of burn edema is due to histamine, bradykinins, vasoactive
amines, prostaglandins and leukotriens. The late phase of edema is
due to increased extracellular fluid (ECF). The end result of the
changes in the microvasculature is disruption of normal capillary
barrier separating intravascular and interstitial compartments. This
results in severe depletion of plasma volume with a marked increase
in the extracellular fluid clinically manifested as hypovolemia.

Changes at Cellular Level


There is a systemic decrease in cell transmembrane potential. This
is due to an increase in intracellular sodium concentration and a
cellular swelling. If resuscitation is inadequate cell membrane
potential decreases resulting in cellular death. So resuscitation is
very important not only to correct hypovolemia but also to prevent
cellular death. While extravasation of fluid from vascular to extra-
cellular space is occurring there is release of potassium (K+) from
cells which are destroyed by burns and a shift of sodium (Na+) into
the intracellular space.
There is an increase in membrane permeability resulting in the
intracellular solutes to leak out of the cell—this is called “Sick Cell
Syndrome”. A fall in the sodium content of the ECF is due to—
damaged collagen in the burned area absorbing Na+ selectively
and the membranes of the damaged cells allowing Na to leak into
the cell and K+ to diffuse out. In burn patients the cell membrane
may become abnormal allowing K to leak out and Na to enter. This
condition is called Sick Cell Syndrome, which occurs late in the
shock period and is characterized by restlessness, disorientation
and over breathing. A 24-hour urine specimen shows a reversal of
the sodium to potassium ratio (normal approximately 2:1).
Treatment is to correct hypoxia, correct deficit of red blood cell
by transfusion, administering insulin 150-200 units and 1-2 L of
5% glucose daily. This treatment seems to have a beneficial effect in
restoring the cell membrane to normal.

Changes at Tissue Level


Injury to the tissue results in release of metabolic acid substance
into the circulation.The severity of acidosis can be predicted as it is
266 PLASTIC SURGERY MADE EASY
related to the amount of tissue destruction. Decreased blood supply
results in reduced tissue perfusion leading to poor oxygen supply
and retention of carbon dioxide eventually leading to lactic acid
production.
If well resuscitated with fluids, the capillary permeability recovers
its tone, fluid is reabsorbed and diuresis occurs. On the other hand
if not resuscitated well, patient goes into shock leading to decreased
blood flow to various organs like kidney, heart, skin and intestine.
Decreased blood flow to skin can result in skin becoming pale.
The capillaries passively dilate and fill with blood which becomes
deoxygenated and gives blue color to the skin.
Decreased blood flow to intestine results in passive dilation.
Absorption stops leading to vomiting. Decreased microcirculation
results in erosion, ulceration and bleeding.
The fluid loss results in fall in plasma volume. The natural
defense reaction of the body is to counter act this fall of plasma
volume in 3 ways:
1. By drawing fluid from undamaged part of extracellular space
2. By general constriction of blood vessels in the splanchnic area
and skin
3. By ingestion and absorption of fluid from the gut in response to
feeling of thirst.

SYSTEMIC RESPONSE TO LOCAL INJURY


Cardiovascular Response
Immediately following burns there is an increase in capillary
permeability due to inflammatory mediators like histamine,
serotonin, bradykinin, leukotriens and thromboxane resulting in
decreased cardiac output and decreased blood flow to various
organs. The loss of fluid continues at a rapid rate for some hours
and then gradually decreases in a day or two. Capillaries recover
their tone and permeability resulting in reabsorption of the edema
fluid leading to diuresis. Following burns toxic substances are
elevated such as potassium and enzymes that are toxic to
myocardium. Myocardium undergoes functional decompensation
during the acute phase and continues during the stress period.
THERMAL INJURY 267
Renal
Urine output is reduced due to hypovolemia. Increased amounts of
myoglobin and hemoglobin and other toxic products cause
decreased output. Increased secretion of ADH and aldosterone
lead to increased reabsorption of water into renal tubules and sodium
conservation resulting in concentrated urine. Renal problems can
be of two types:
1. Oliguric renal failure
2. High output failure

Oliguric Renal Failure


• Hypovolemia following burn injury results in decreased renal
perfusion and finally decreased urine output
• As in any trauma, increased ADH and aldosterone lead to
increased reabsorption of water and conservation of sodium
resulting in concentrated urine
• Increased amount of myoglobin and hemoglobin and other
toxic products decreases urine output.
High Output Failure
• Usually seen in impending septicemia. This is probably due to
initial increase in cardiac output and vasodilatation of renal
vessels
• Renal failure either pre-existing or secondary to other
complications.

Respiratory System
• In hypovolemic shock phase, respiration becomes shallow and
rapid due to lactic acidosis.
• Hyperventilation may lead to respiratory alkalosis.
• Circumferential burns on the chest may lead to shallow breathing
resulting in hypoxia.
• Infection leads to ARDS but the more likely cause is due to
inflammatory mediators from the burn wound. This explains
early respiratory signs even before infection sets in.
• Transient pulmonary hypertension due to inflammatory
mediators occurs.
268 PLASTIC SURGERY MADE EASY
• The other type is the direct injury by inhalation and burning
which results in reduced oxygenation, edema, obstruction and
further hypoxia leading to release of mediators such as
thromboxane which causes muscle constriction in bronchioles
eventually leading to ventilation perfusion imbalance,
inadequate peripheral perfusion, lactic acidosis and cellular
damage.
• The normal response to burns is hyperventilation. This results
from increased oxygen needs, ventilation perfusion imbalance,
restrictive process which reduces lung volume and increased
pulmonary resistance.
• Burn lung syndrome is insidious in onset. Manifests within 2-5
days and the first symptom is increased respiratory rate, difficulty
in breathing, rales and ronchi.
Investigations—Chest X-ray appears clear at first and later hazy
due to interstitial edema. Patchy infiltrates may also be seen.
Blood gas—Shows reduced oxygen and normal CO2 (interstitial
fluid blocks alveolar oxygen absorption but the high diffusibility of
CO2 makes it possible to be blown off). Predisposing cause is
overhydration.
Treatment—Antibiotics, high oxygen, bronchodilators, ventilatory
support (using peep—maintains residual pulmonary capacity in
edematous lung) and diuretics.
With better understanding and management of sepsis,
importance is given to early recognition and immediate aggressive
therapy to reduce progression to full blown septicemia. Treatment
priority follows the VIP format that is (Ventilation Infusion and
Perfusion).
Ventilation—A rising respiratory rate is the first indication of sepsis.
An arterial blood gas done at this time indicates a low partial pressure
of oxygen (tachypnea and tachycardia are among the body’s first
compensatory responses to sepsis). Importance is given to
administering oxygen to keep the arterial partial pressure of oxygen
to about 80-100 mm Hg. Patients who do not respond to a simple
increase of fractional inspired oxygen concentration and continue
to have refractory hypoxemia can be treated with face mask
THERMAL INJURY 269
continuous positive airway pressure (CPAP) therapy, which increases
oxygen without endo-tracheal intubation.
Infusion—In septic shock the circulating volume decreases
significantly as fluid shifts into the interstitial space, hence infusion
of electrolyte solution along with colloids, amino acids and fatty
acids are given to prevent circulatory collapse.
Perfusion—Adequate oxygen and fluid replacement helps in
improving perfusion. In addition, vasodilating drugs like dopamine
in small doses of 5 microgram/kg/min helps to maintain renal
perfusion. Antibiotics are started based on bacteriological monitoring
of the burn wound. Local measures to control sepsis is by slough
excision and dressing twice a day. Adequate nutritional support
with nasogastric feeds and parenteral supplementation like amino
acids, lipids and hyperosmolar glucose are needed to prevent
malnutrition.

Hematologic Changes
Altered capillary permeability allows loss of protein and electrolyte
leading to hemoconcentration. Anemia seen after burn injury at the
end of first week is due to
• Red cell destruction as a result of injury
• Damaged red cell agglutination, and inactivation by sludging
phenomenon
• Accelerated rate of hemolysis from increased red cell fragility
• Reduces half-life of red blood cells
• Reduced nutrition leads to reduced hemopoietic production
• Thrombosis of blood in capillaries in the burned areas
• Loss through wound donor site
• Hemolysis associated with septicemia
• Wound debridement and daily dressing
Significant changes occur in the red cell and in the clotting
system following burn injury. Initially there are elevated levels of
hemoglobin because of massive plasma loss. There is also red cell
destruction due to direct heat. The life span of RBC is also shortened
due to circulating factors. All this leads to progressive anemia during
the end of first week.
270 PLASTIC SURGERY MADE EASY
Gastrointestinal System
Hypovolemia can result in splanchnic vasoconstriction leading to
paralytic ileus. Bowel movement returns to normal after
resuscitation. Impairment of normal gut mucosa barrier function
may occur allowing gut bacteria and toxins to translocate from the
lumen to the lymphatics and mesenteric lymph nodes finally gaining
access into blood producing sepsis. Initial response is severe
splanchic vasoconstriction causing ileus, dilatation and ulceration
as a result of mediator release. Hyperactive GI system leading to
diarrhea results from administering broad—spectrum antibiotic and
high protein calorie diet.

Musculoskeletal System
Cell membrane gets damaged by burns and myoglobin is released
from muscle cells. Muscle wasting and osteoporosis may occur due
to prolonged immobilization.

Immune System
Injury damages the skin barrier function. Suppression of both the
cellular and humoral immunity leads to immunosuppression in
burn victims.
1. Nonspecific—skin first line of defense
2. Specific host immunity divided into —
• T-cell mediated cellular response
• B-cell mediated humoral response
Normally skin provides the first barrier to bacterial invasion. Its
normal excretion of sebum further provides bactericidal properties.
Burning removes outer layer and the local inflammatory response
leads to increase in prostaglandins. All proteins are depleted in the
first week following burns.
Impaired cellular immunity is suggested by lymphocytopenia,
delayed rejection of allograft and delayed response to normal
hypersensitivity antigens.

Metabolic Nutritional Response


Various hypermetabolic responses like increased oxygen consump-
tion, increased energy expenditure, increased rate of lipolysis,
THERMAL INJURY 271
increased protein catabolism and increased nitrogen loss are
seen.
Hypermetabolism results in increased oxygen consumption,
protein catabolism, hyperglycemia, decreased glucagons to insulin
ratio and negative nitrogen balance. Water holding lipid in the skin
is destroyed, and four times normal amount of water is lost through
skin. Increased water loss results in cooling of body and shivering
leading to additional heat expenditure. Hence, use of air conditioning
burn units are to be avoided.
Counter regulating hormones like glucagon, cortisol and
catecholamines are elevated and play a major role in the catabolic
response to injury. These endocrine mediators working with
inflammatory mediators are responsible for the various metabolic
responses in burns.
Protein metabolism—Following burns the urinary nitrogen begins
to increase in levels of 2-3 times normal urinary excretion and the
patient remains in negative nitrogen balance which continues until
wounds are closed. Since the main source of this nitrogen appears
to be from skeletal muscle extreme degree of muscle wasting can be
seen if vigorous attempts to maintain adequate protein and nitrogen
are not accomplished. Low protein is also responsible for delayed
healing and poor graft take.
Protein loss can be from:
• Loss in initial burn wound
• Reduced protein intake
• Continued loss from burn area
• Increased excretion of urinary nitrogen
• Infection
Carbohydrate metabolism—Hyperglycemia and glucosuria may
occur as the balance of insulin and catecholamine antagonism is
disturbed. There also appears to be insulin inhibition and resistance.
Fat and vitamins—Increased oxidation of fat in response to trauma
is one factor for weight loss.
After burn injury patients enter into severe catabolic state charac-
terized by elevated metabolic rate, increased protein mobilization
and gluconeogenesis. These changes lead to significant increase in
272 PLASTIC SURGERY MADE EASY
energy and protein requirement. Weight loss during this phase is
virtually inevitable unless aggressive nutritional therapy is instituted
soon after the burn, so nutritional support is as important as any
other aspect of management of burned patients.

ACUTE MANAGEMENT OF BURNS


Patients who need admission to the burn unit are:
1. Those with extremes of age
2. Burns more than 15%
3. Burns involving face, palms, soles and genitalia
Burns more than 15% should be admitted
• Obtain pertinent history—Time of injury and cause of injury
• Start Intravenous line
• Calculate fluid needs and adjust infusion rate
• Insert urinary catheter and monitor hourly urine output of 0.5-
1 ml/hour
• Start nasogastric feeds
• Determine extent and depth of burns
• Intravenous analgesics
• Tetanus toxoid 0.5 ml IM
• Tetglobe 250 units IM
• Systemic antibiotics—Intravenous injection of 10 lacs crystalline
penicillin every four hours after a test dose
• Draw blood samples for basic investigations like PCV, BBVS,
Serum electrolytes like NA, K and HCO3, CREATININE, and
RBS
• Check the weight/approximate weight
• Calculate the percentage of burns by Wallace Rule of Nine.

ELECTRICAL BURNS
Electrical burns are complex injuries and may affect multiple organs.
Most tissue damage is caused by heat generated by current flow
leading to progressive loss of viable tissue due to delayed thrombosis
of microvasculature. Prevention and treatment are important.
THERMAL INJURY 273
CLASSIFICATION
• Low voltage <1000 volts causes local tissue necrosis
• High voltage >1000 voltage causes deep muscle injury and
fractures
• Ultra high voltage seen in lightening injury , blast injury resulting
in cardiac arrest.

TYPE OF INJURY
It damages tissues in three ways—Flash, Arc or Contact
Contact burns are the commonest type of injury. This is due to
contact with a high voltage system converting electrical energy into
heat resulting in tissue damage. The current enters, traverses the
body and exits at another site. The final damage depends on the
pathway of the current through the body (Figs13.9 to 13.11).

FIGURE 13.9: Contact burns with FIGURE 13.10: Contact burns with
charred skin necrosed bone

FIGURE 13.11: Exposed


bones
274 PLASTIC SURGERY MADE EASY
Flash burns—The flash sets the clothing on fire and are usually
superficial and heals spontaneously.
Arc burns give rise to localized deep burns due to intense heat at
the termination of current flow. The current exists and re-enters skin
over a fixed joint to find the shortest pathway commonly seen on
flexor surfaces of the body.

PATHOPHYSIOLOGY OF SYSTEMIC CHANGES


As current passes through the tissues, heat is generated because
tissue is not a perfect conductor and acts as a resistance. The vessels
and nerves are good conductors of current while dry skin and bone
are poor conductors. Immediately after electric shock patient may
go into cardiac arrest or develop arrhythmias. Due to vascular
endothelial damage there may be occlusion, thrombosis and
progressive ischemia of the muscles.

CLINICAL FEATURES
Depends on mode of injury and duration of contact. If patient has
been thrown away or has had a fall, internal injury and fracture
should be suspected and excluded.
A crush type of syndrome is seen in the presence of significant
amount of dead muscle, this poses a risk of renal failure with the
precipitation of muscle break down products like myoglobin and
hemoglobin. If myoglobinuria persists for more than 6 hours—it is
a sign of major muscle loss requiring amputation or debridement.

MANAGEMENT
Emergency first aid is to disconnect from electrical supply by
switching off the power as early as possible.
• Rescue—Caution must be exercised by the rescuer so that he
does not become a part of the electrical circuit in attempting to
free a person still in contact with the live wire
• Use dry wood and push the victim away from current source
(please note if while the power is on and attempt is made to
remove the person it can be dangerous to the rescuer as the
current can arc as he approaches the victim)
THERMAL INJURY 275
• Take the patient to hospital for further management
• Cardiac and respiratory status are assessed, ECG should be
taken to check arrhythmias.
• Resuscitation—Calculating IV fluid is difficult in electrical burns
but the aim should be to clear the pigments like myoglobin and
hemoglobin, some advocate 7 ml/kg/% of burns. It is important
to maintain adequate organ tissue perfusion. If adequate fluids
are not given the chances that the patient would go in for renal
failure is high. This is due to the pigments which are break
down products of dead muscle, leading to damage of the kidneys
• Some advocate soda bicarbonate infusion in doses of
12.5 gm as IV bolus followed by 12.5 gm per hour to maintain
urine in alkaline range to prevent pigment precipitation in renal
tubules
• Urine output should be clear and maintained at 70-100 ml/
hour
• Forced diuresis with mannitol can also be tried
• Tetanus toxoid is given prophylactically
• If vascular impairment is noticed due to compartment syndrome
fasciotomy should be done immediately
• Surgical intervention—Escharotomy and fasciotomy are
frequently required to decompress the tense compartment
(Fig.13.12) Initial debridement should be aggressive as non-
viable tissue left behind can result in infection. Early excision
and skin grafting should be done if tendons and bones are
exposed. Charred extremities should be amputated as early as
possible (Fig. 13.13).

FIGURE 13.12: Electrical injury FIGURE 13.13: Electrical burn


requiring fasciotomy of forearm with gangrene of finger
276 PLASTIC SURGERY MADE EASY
COMPLICATIONS
• CNS—loss of consciousness
• Cardiac—ventricular fibrillation and cardiac arrest
• Injury to spinal cord with deficits ranging from localized paresis,
paralysis to quadriplegia.

REHABILITATION
• The devastating nature of injury makes rehabilitation very
important (Figs13.14 and 13.15)
• Long-term sequelae includes muscle fibrosis and peripheral
neuropathy which needs a lot of physiotherapy

FIGURE 13.14: Bilateral amputation FIGURE 13.15: Bilateral below


knee amputation

CHEMICAL BURNS
A chemical burn is unique because of continuous tissue damaging
effect by the chemical till it is completely washed off or neutralized.
Chemical injury may be accidental or homicidal. The extent of
damage is directly proportional to its concentration, volume and
THERMAL INJURY 277

FIGURE 13.16: Phenol burns of face FIGURE 13.17: Acid burns

FIGURE 13.18: Acid burns FIGURE 13.19: Acid burns

the duration of contact. Chemical burns generally involve the face


and eyes. The color of the skin is dark brown and black. The eschar
appears dry, adherent and insensitive to touch.
Chemical injury usually involves people at home, industrial
workers and those that are involved in chemical warfare [Phenol
burns (Fig.13.16)]. The acid trickles down from the face, although
the extent of injury is small, the destruction and deformity are severe
(Figs. 13.17 to 13.19).
278 PLASTIC SURGERY MADE EASY
FIRST AID MANAGEMENT
• Immediately remove all clothes and start continuous copious
irrigation with water for at least 30 minutes
• Early excisional surgery is necessary as spontaneous eschar
separation is delayed due to late development of subeschar
infection.
• Eye burns should be irrigated with water for a prolonged period
of time and an ophthalmologist should be called in as early as
possible for expert opinion to prevent blindness.

FROST BITE
It usually involves hands, feet, nose and ears. It is common in
unconscious patients.

CLASSIFICATION
Depending on the tissue destruction, it is classified into four degrees
First degree—involves superficial skin with edema and hyperemia
Second degree—superficial skin injury with pain, paresthesia and
vesicle formation
Third degree—Necrosis of skin
Fourth degree—Necrosis extends to deeper tissue.

FREEZING
It can be either rapid—where it causes damage and death of the
cells due to intracellular injury and slow freezing which causes
extracellular damage leading to dehydration from osmotic fluid
shift out of cells.

THAWING
It causes capillary leak and occlusion which leads to edema formation
and ischemia.
THERMAL INJURY 279
TREATMENT
Rewarming, elevation of affected part and prevention of infection.

TOXIC EPIDERMAL NECROLYSIS (TEN)


It is usually a reaction to antigenic
material that causes a split in the
epidermis resulting in necrosis of
skin. It is often drug induced. It
can also be caused by staphy-
lococcal infection. It is to be
treated like burns (Fig.13.20).

STAPHYLOCOCCAL
SCALDED SKIN
SYNDROME (SSSS)
A reaction to staphylococcal toxin
causes separation of the granular
layer of epidermis. This results in
desquamation, separation and
loss of epidermis over a wide
area. Clinical presentation of FIGURE 13.20: Erythema
SSSS is similar to TEN. The gangrenosa
mucous membrane and conjunc-
tiva are spared in SSSS in contrast to TEN. Systemic antibiotic should
be started early.

FLUID RESUSCITATION
INTRODUCTION
Fluid management is critical to the survival of a burn victim. In
1940’s hypovolemic shock was the leading cause of death. Today
with current knowledge of massive fluid shift and vascular changes,
the mortality has decreased considerably. A number of methods of
fluid resuscitation have been advocated. We will review the various
methods and present the rationale of each.
280 PLASTIC SURGERY MADE EASY
HISTORY
Moyer and Baxter used only crystalloids for resuscitation. He noted
that burn shock recovery occurred in all, but the hemo concentration
remained unchanged and the hematocrit was unresponsive. This
was the first evidence to state that burn shock is not only due to
hypovolemia but also influenced by extracellular sodium depletion.
It was also noted that the edema fluid contains protein in the same
proportion as that found in blood, this became the basis for
resuscitation with colloid fluid to increase the plasma volume. From
this, two things become evident, one to give salt solution and the
other to give colloid to increase plasma volume.
Although so many types of fluids are advocated, one thing was
clear, that edema fluid is accentuated by the amount and type of
resuscitation fluid. There was a consensus with regard to the
guidelines and type of fluid used during the resuscitation process.
The consensus was to give least amount of fluid necessary to
maintain adequate organ perfusion. As far as the optimum type of
fluid is concerned, replacement of extracellular salt lost into the
burned tissue and into the cell is essential for successful resuscitation.
Colloids should be given at the end of second 24 hours to maintain
the plasma volume.
Before we go to the type of fluid it is important to know the
composition of body fluids and certain terminology to understand
the basis for using different types of fluids.
Osmotic Gradient—Two different concentration of fluid,
movement is always from hypotonic to hypertonic.
Osmosis—Imbibe or absorb—Passage of a solvent through a semi
permeable partition into a more concentrated solution.
Transmembrane potential—A region of high potential impending
the movement of particle.

COMPOSITION OF BODY FLUIDS


Water is the most abundant constituent of the body, and represents
60% of total body weight. Water is distributed in two major
compartments—the intracellular (IC) and extracellular compartment
THERMAL INJURY 281
(EC). Intracellular is 40% and extracellular is 20% out of which 5%
is intravascular and 15% is extravascular or interstitial. The major
ECF particles are Na, Cl and HCO3. Total body sodium (Na) content
is a reflection of ECF volume. (Na influences the distribution of
water in the body). The major ICF osmoles are potassium (K),
phosphate and phospholipids.
Na is largely restricted to the extracellular compartment. Likewise
K is predominantly limited to ICF and necessary for normal cell
function. K is necessary for muscle activity primarily cardiac muscle.
K leaves the cell due to trauma.

TYPES OF FLUID
1. Sodium chloride solution contains 150 mEq of chloride which
is considerably higher than the normal serum levels (normal
level 95-105 mEq/l) and tend to increase the acidosis that occurs
following burns.
A. An isotonic electrolyte solution given intravenously ;
a. To a normal individual is distributed throughout the
ECC. If its electrolyte content is similar to ECF, it merely
expands the volume of ECF without any change in its
composition and quickly gets excreted by kidneys.
b. In hypovolemia due to whole blood loss only one
quarter of an administered crystalloid solution will
remain in the circulation while three fourths will be
distributed to the extravascular interstitial space.
B. In contrast plasma administered to the hypovolemic subject
remains largely in the circulation. Attempts to fill plasma
volume by isotonic crystalloid will result in edema of
unburned tissue whereas administration of colloid will result
in minimal non-burn edema.
2. Ringer lactate is a balanced salt solution most widely used
by those who rely solely upon a crystalloid solution. Ringer
Lactate solution with a sodium of 130 mEq/l has the advantage
of using a salt solution, but the disadvantage was the severe
hypoproteinemia leading to more edema formation (only salt
solution cause hypoproteinemia). It should not be used for
children and patients with inadequate urine output due to its
282 PLASTIC SURGERY MADE EASY
high K content (Ringer Lactate has Na-131, K -5, calcium-2,
chloride 111 and HCO3 -29).
3. Hypertonic salt solutions contains 240-300 mEq/l of
sodium. Although the advantage is the use of smaller total fluid
requirement the disadvantage is that the urine output is much
higher. Considering that urine output is the best guide for fluid
resuscitation it becomes unreliable. Secondly the edema is
increased both in burned and non-burned tissue due to shift of
water from intracellular into extracellular compartment.
4. Dextrose 5% becomes solute-free as soon as the dextrose is
metabolized. Water will reduce the osmolality of the extracellular
fluid causing an osmotic gradient across cell membrane and
thus enters the cells to produce intracellular edema. Fluid therapy
based on a sodium-free solution will cause death by intracellular
over hydration commonly called water intoxication. The
disadvantage of electrolyte-free solution is that they dilute the
serum sodium and accentuate the electrolyte problems.
5. Colloid—The advantage of administering plasma is that the
plasma proteins are very important for maintaining the plasma
volume and also in preventing edema formation. Tendency for
smaller total fluid replacement with less possibility of overload.
Replacement of albumin can minimize marked hypo-
albuminemia. Administration of immunoglobulins present in
the plasma enhances host resistance to infection. The
disadvantage is that only colloid resuscitation would be
expensive. Risk of anaphylactic shock may be present.
6. Dextran is a colloid consisting of glucose molecules
polymerized to form high molecular weight polysaccharides.
The advantage is that only less fluid is required for resuscitation.
40% is excreted by kidney, the disadvantage is that it carries risk
of allergic reaction and can interfere with blood grouping.
It is clear that all solutions are effective in restoring tissue
perfusion. Initially salt containing solutions levels not exceeding
160 mEq/l should be administered. Colloids should be given
24 hrs post injury to increase plasma volume (plasma would leak
out before that due to increased capillary permeability). The volume
of resuscitation fluid infused should be adequate for tissue perfusion
and should maintain a urine output of 0.5-1 ml/kg/hour. It is
THERMAL INJURY 283
important to emphasize that all of the resuscitaton formulas are
only guidelines.
Resuscitation is completed when there is no further
accumulation of edema fluid, which generally occurs between 18-
30 hours post burn. Maintenance fluid with potassium supplements
should be given because of the loss of intracellular potassium during
burn shock period.
The requirements for fluid calculation are Weight of patient,
Percentage of burns and Time of burns.

VARIOUS FORMULAS
1. Evans (1952)
Day-1—1 ml of colloid and 1 ml/kg/% of electrolyte solution +
normal requirement
Day-2—0.5 ml of colloid and 0.5 ml/kg/% of electrolyte solution
+ normal requirement
2. Brooke (1953)
Day–1—0.5 ml colloid and 1.5 ml/kg/% of electrolyte solution
+normal requirement
Day-2—0.25 ml of colloid and 0.5 ml kg/% of electrolyte solution
+normal requirement
3. Modified Brooke (1970)
Day-1—colloid nil 2 ml of electrolyte solution + normal
requirement
Day 2—0.5 ml of colloid and 1 ml of electrolyte solution +
normal requirement
4. Parkland (1968)
Day 1—No colloid, 4 ml of electrolyte solution (No normal
requirement)
Day 2—700-2000 ml of colloid and no electrolyte solution
(No normal requirement).

FLUID CALCULATION
First 24-hour-Burn requirement = Wt ×% of burns × 2
Plus Normal requirement =2500 ml
(lungs-500, skin-500 ml,urine-1400 ml, feces-100 ml)-Insen-
sible loss
284 PLASTIC SURGERY MADE EASY
(Example 50 kg × 50% × 2 =5000 ml
normal =2500 ml
Total =7500 ml
Second 24-hour
Burn Requirement = wt x% of burns × 1 (Half given as colloid
and half as crystalloid)
Normal Requirement = 2500 ml
Third 24-hour
5% D/S 2000 ml plus -N/S 500 ml + Inj Kcl 3 gms
we calculate the fluid requirement according to modified
Brooke’s formula (weight × percentage of burns × 2) + Normal
requirement
If the percentage of burns is less than 50% then calculate the
fluid requirement accordingly. For example, if the patient is 50 kg
and has 40% burns then the fluid calculation for the first 24 hours
will be
50 × 40 × 2 (4000 ml) + 2500 ml of Normal Requirement.
So a total of 6500 ml will be given for the first 24 hours which starts
from the time of burns and not from the time the patient is seen in
the emergency room.
It is dangerous to expand the interstitial space by more than
50% of the original size, so 50% should be the limiting factor for
calculating the fluid requirement irrespective of size of burns. In
burns involving more than 50% body surface area the capillary
permeability is at its maximum thus affecting both treatment and
prognosis and hence calculation should be for 50% only even if the
burns is over 50%.
Once shock phase subsides, diuresis and mobilization of sodium
occurs and urinary output increases. The enormous amount of
urine output is due to expanded extracellular fluid, which is excreted
out once edema subsides.
Fluid calculation is only a basic guide line. The best guideline is
hourly urine output of 0.5-1 ml/kg body weight/hour. Catheterize
the patient and adjust the IV fluids according to urine output.
Edema per se is very important as it
• Decreases tissue oxygenation
THERMAL INJURY 285
• Decreases blood flow
• Increases tissue ischemia
• Increases risk of infection
• Increases cardiac work load leading to cardiac failure
• Increases work of breathing leading to pulmonary insufficiency
The goals of fluid resuscitation are to restore and maintain
adequate tissue perfusion and oxygenation, avoid organ ischemia
and to preserve heat injured but viable soft tissue.

TESTS TO REFLECT PERFUSION


A. Clinical signs of optimal resuscitation
Urine output of >50 ml/hr
Pulse rate of <120/min
A calm patient
B. Laboratory
1. Persistent metabolic acidosis indicates inadequate perfusion.
This should be an indicator to increase fluid administration.
2. Urine must be non-glycosuric (hyperglycemia is commonly
seen following burns which leads to glycosuria and osmotic
diuresis resulting in dehydration).
3. Serial hematocrit determination can also be adjuncts to
determine the adequacy of resuscitation. Initial hematocrit
is followed by a later decrease in hematocrit that mainly
reflects re-expansion of the intravascular compartment with
fluid resuscitation.
4. Urine sodium normally should be 50-125 mEq/l/day, less
than 20 mEq of sodium/l of urine signals a plasma deficit
and reflects a volume deficit.

COMPLICATIONS
• Non-correctable metabolic acidosis in cases of delayed
resuscitation
• Hypernatremia due to inadequate resuscitation
• Hyponatremia when silver nitrate is used as topical agent
• Hyperkalemia due to RBC destruction
• Hypokalemia due to increased urinary K losses
286 PLASTIC SURGERY MADE EASY
• Prolonged hypovolemia after a delayed resuscitation resulting
in renal failure (try fluid challenge, mannitol and lasix).

BURN WOUND
FUNCTION OF SKIN
Skin is the largest organ in the body and acts as our first line of
defense and protects us from the outside world.
• Prevents loss of body fluids, electrolytes and protein
• Controls body temperature, allows rapid cooling and
vasodilatation of dermal vessels
• Functions as excretory and sensory organs and interprets pain,
touch, hot and cold
• It protects from weather, harmful environment and radiation
• It prevents entry of microorganisms and protects against infection
• It helps in production of vitamin D.
• It can feel the social interpersonal reactions, sexual interaction
and attraction.
Burn wound differs from other wounds in the following ways:
• Area of wound is extensive
• Burn wound is opened for long periods of time and does not
offer protection from pathogenic bacteria, as a result it easily
gets colonized by pathogenic bacteria
• Large amounts of devitalized tissue
• Exudes large quantities of water, serum and blood
Human skin can tolerate temperatures upto 40 degree, above
this level tissue destruction is obvious. The depth of burns depends
on temperature of the burning agent and the duration of exposure.
Burn injury can be direct due to heat or due to progressive dermal
ischemia following thrombosis.

JACKSON’S ZONE OF INJURY (FIG. 13.21)


1. Zone of Hyperemia—This zone shows minimal injury and
recovers over a period of 7-10 days with prominent
vasodilatation with increased blood flow.
THERMAL INJURY 287
2. Zone of stasis—In this zone,
most cells are initially viable.
Circulation becomes progres-
sively impaired leading to cessa-
tion of blood flow. Cells are
compromised in the beginning
and can be reversed after resus-
citation. According to Zawacki,
deeper portion of zone of stasis
can be reversed if properly
resuscitated. Exposure to air and
dehydration of this layer follow-
ing tangential excision without
skin cover prevents any recovery FIGURE 13.21: Jackson’s
of this zone as it undergoes zones of injury
dessication and necrosis (That is why following tangential
excision the wounds have to be covered).
3. Zone of coagulation—In this zone, central area of burn
wound, which is closest to the heat source, is characterized by
coagulation of cells. There is no blood flow and cells become
non-viable.

IMMUNOLOGICAL ASPECT OF BURN INJURY


• The first insult is injury itself —The burn patient is immuno-
compromised since inflammatory mediators play a major role
in both the local and systemic responses following burn injury
• The second insult is infection—It produces greater quantities of
inflammatory mediators, which cause tissue injury
• The third insult could be endotoxin absorbed from the wound
and from the gut
• The parameters are:
Increased Leukocytes
Increased serum C-reactive protein
Increased catecholamines
Decreased total protein
Decreased albumin
Decreased IgA, IgM and IgG
Disseminated intravascular system (coagulation, fibrinolysis with
consumption)
288 PLASTIC SURGERY MADE EASY
BURN WOUND EDEMA
Immediately following burns there is massive edema in the burned
and nonburned tissue. This is due to the inflammatory mediators
leading to increased capillary permeability. It also causes increased
hydrostatic pressure within the microvessels as a result of chemical
mediators, causing proximal vasodilatation or distal vasoconstriction.

ROLE OF MEDIATORS
Locally there is an increase in microvascular fluid flux into the
interstitial space resulting in an increase in osmotic pressure. There
is generalized impairment of cell membrane function. The local
mediators produced by the burn wound include histamine released
by both direct injury and by stimulation of mast cells causing
vasodilatation and an increase in capillary permeability of both the
capillary and venules leading to edema of burned and unburned
tissue, Oxidants and arachidonic acid metabolites all interact to
alter the capillary integrity and cell membrane permeability.
Thromboxane in the burn wound increases platelet aggregation
and vasoconstriction leading to dermal ischemia.

BURN INFLAMMATION
Inflammation begins when cell membrane phospholipids are
destroyed or are altered by thermal insult. Phospholipids are
converted to arachidonic acid. Inflammatory cells like neutrophils
and macrophages arrive. Neutrophils release oxygen-free radicals,
which in turn inflict damage to the cell membrane and also stimulate
activity of phospholipase A which triggers the arachidonic acid and
thus furthers inflammation. Blood flow at this stage is maximal that
is 7-10 days (surgery avoided at this stage).

BURN ESCHAR
Eschar is a denatured protein of the dermis and is a good medium
for bacterial growth. When it gets infected, it attracts leukocytes to
the interface between eschar and viable underlying tissue. The lytic
enzymes of these leukocytes start digesting the deep portion of
THERMAL INJURY 289
eschar, separation from viable
tissue occurs by 7-10 days.
Protein loss occurs at a high rate
through the eschar which impairs
nitrogen balance and wound
healing. Although the tissue with-
in the eschar is dead, it contains
toxins, which may diffuse into the
circulation causing distant organ
dysfunction and other problems
(Fig.13.22).

BURN BLISTER
A blister is formed by leakage of
fluid from heat injured vessels
deep to the zone of coagulation.
The fluid enters and collects in FIGURE 13.22: Burn eschar
the area of dermo-epithelial
junction and lifts off the epidermis away from the underlying
structures. Many of the mediators are located in the blister fluid and
are harmful. Remove blister fluid and retain the skin. Blister fluid
has inflammatory mediators and has detrimental effects. When
fibrogen molecules pass through the vascular compartment, it results
in clotting of blister fluid. Sometimes red and white mottling occurs
due to diapedesis of red corpusles.

MANAGEMENT OF BURN WOUND


Burn wound is sterile to start with, later on it becomes a breeding
site for the organisms to grow. Bacteria multiply in the dead tissue
producing putrefaction and the characteristic foul smell. Bacteria
also invades the living cells. Toxins are absorbed into the body
causing septicemia. Systemic and local antibiotic may not reach the
burn wound, as it cannot penetrate the dead tissue, thus care of the
wound becomes very important. By removal of all non-viable tissue,
prevention of wound dehydration and accumulation of purulent
secretion along with maintenance of environment, an environment
290 PLASTIC SURGERY MADE EASY
conducive to wound healing is achieved. In addition good nutrition
supplementation should be provided for early wound healing.
Circumferential burns and the leathery eschar produce chest
constrictions and compartment syndromes in the extremities or
distal ischemia and necrosis. Immediate escharotomy/Fasciotomy
should be performed in the mid lateral lines of the affected
extremities.
The main aim of local treatment is to minimize toxemia and
promote wound healing. As the wound gets infected, they manifest
signs and symptoms of toxemia such as rapid pulse, respiration,
high temperature, oliguria etc. The toxins are released from two
sources
a. From the bacteria that grow on the burned area
b. From the products of tissue breakdown
Burn wounds are either closed spontaneously or closed
surgically in a timely fashion. Wounds, which do not heal by 3
weeks, should be grafted to avoid scarring, repeated breakdowns
and pigmentation.
The ultimate goal in the management of burn patient is to heal
the wounds at the earliest. In partial thickness burns healing occurs
spontaneously by epithelial regeneration from the remnants of hair
follicle, sweat glands and sebaceous glands, whereas full thickness
burns heals by wound contracture and epithelialization from the
margins, leading to deformities and scarring and hence grafting
becomes necessary to obviate this problem.
Burn wound is cleaned and topical antimicrobial agent like 1%
silver sulfadiazine cream is applied generously once daily. Topical
antimicrobial agent is changed in the second week of burns or
when burn wound infection is suspected. Early excision of dead
tissue reduces the chance of bacterial colonization.

Topical Agent Commonly Used is Silver Sulfadiazine


Advantages
• Bacteriostatic
• Easy to apply
• Low toxicity
• Less painful to apply
• Infiltrates eschar wall
THERMAL INJURY 291
Disadvantages
• Adverse effect on the donor site
• Black staining
• Causes transient leukopenia
• Causes dilution hyponatremia
• Delayed eschar separation
• Depresses renal function
• Expensive
• Epithelialization is retarded.

Treatment of Superficial Burns


• Treatment of blister is controversial—Deroofing the blister,
removing the fluid and retaining the skin is important as the
blister fluid contains inflammatory mediators such as
thromboxane, known to be detrimental to the microcirculation
in the zone of stasis
• Best to rupture the blister, remove the fluid and retain the skin
as a biological cover

FIGURE 13.23: Amnion for back FIGURE 13.24: Amnion for chest
292 PLASTIC SURGERY MADE EASY
• If blister is already debrided, wound should be cleaned and a
non-adherent dressing/biological or synthetic dressing applied
(Figs 13.23 and 13.24).
• Wound heals spontaneously in about 2-3 weeks
• Superficial burns is highly susceptible to sun burn for a period
of 1-2 years. Patient should be cautioned about pigmentary
changes and advised sun protection both physical and chemical.
Use of caps, sun protecting factor creams (SPF of >15% to
avoid sun exposure).
• Burned skin is dry after healing and itching can be very severe
problem and adequate moisturizing cream will alleviate this
problem.

Treatment of Full Thickness Burn


• Complete destruction of all
epidermis and dermis.
• Break down of hemoglobin
results in many colors on the
wound.
• Appearance of skin may be
waxy, dry, leathery, charred or
translucent.Visible thrombosed
veins are seen often.
• Prompt burn wound excision
and autograft is the best option
(Fig. 13.25). The posterior
trunk and buttock are frequent
sites of burn wound infection
and hence the priority to
debride these two areas first
and graft.
FIGURE 13.25: Tangential
• The graft is meshed and if excison and grafting
adequate autografts are not
available the homografts are applied over the autografts at a 90
degree in a sandwich pattern.
• Approximately 6 units of blood for back, 4 for each extremity
and 2 units for hand alone has to be kept ready.
THERMAL INJURY 293
• Hemostasis is maintained by preparing large quantities of 5cc
of 1:1000 adrenaline to a liter of normal saline. This solution is
warmed and applied topically to the wound
• Large amounts of adrenaline are absorbed by the patient but
the incidence of adverse effect is low (this may be due to large
endogenous catecholamine release in these patients).

Methods of Surgical Wound Closure


• Primary closure
• Amputation
• Tangential excision
• Dermatome excision
• Degloving
• Cold scalpel electrocautery
• Enzymatic wound debridement.

Type of Burn Wound Excision


1. Early excision of full thickness burn tissue results in better
functional and cosmetic effect .
2. Tangential excision and autografting with split thickness skin
graft. It is sequential layer by layer tissue excision until living
tissue with punctuate bleeding is reached (Figs 13.26 to
13.27). The raw area is covered with meshed autograft
immediately (Fig. 13.28). This was first performed by Dr Zora
Janzekovic (1975). It removes all devitalized tissue and

FIGURE 13.26: Tangential excision FIGURE 13.27: Tangential excision


294 PLASTIC SURGERY MADE EASY
preserves viable tissue and
body contours are better
preserved. The drawbacks
are that tangential excision
involves massive blood loss.
This can be greatly reduced
if excision is performed in
very early post burn.
Vasoactive metabolites like
thromboxane, which is a FIGURE 13.28: Meshed graft
potent vasoconstrictor, are
elevated on day 1-3. The rationale for early excision is because
prompt wound closure has been shown to improve survival,
reduce length of hospitalization, curbs expenditure with fewer
metabolic complications.
3. Fascial excision performed in very deep full thickness burns
results in severe contour deformities.

Different Dressing
• Amniotic membrane
• Biobrane
• Collagen sheet
• Cultured skin
• Homograft
• Heterograft—Pig skin
• Synthetic skin
These different dressings protect the wound, maintain microbial
control and hastens wound maturation.

WOUND SEPSIS
Change in the patients general condition may be obvious.

Signs and Symptoms


• Hypotension
• Tachypnea
• Increased fever
THERMAL INJURY 295
• Tachycardia
• Hypo/or hyperglycemia
• Ileus
• Altered mental state, hypoxia, hypothermia
• Decreased urine output
Wound may be soft with surrounding cellulitis. Purulent
discharge may be present and healthy granulation tissue may
deteriorate.
The initial bacterial danger is due to beta hemolytic streptococci.
The rich vascularity of the inflammatory phase, edema and
neutralization of the bacterial defense mechanism of sebum, all
renders the burn wound prone to streptococcal invasion.
Human skin contains many organisms with which the individual
coexists and an equilibrium is established. In burn patient this
equilibrium is disturbed and sepsis occurs.
Host has 3 defenses—Skin, leukocytes and immune system
both humoral and cellular.
Humoral immunity is suppressed in severe burns as circulating
immunoglobulins are decreased due to loss of protein. Cellular
immunity is also impaired due to derangement of the products of
lymphocyte due to high cortisol level.
The persistent temperature and leukocytosis due to
inflammation alone make the addition of an infection difficult to
diagnose. Intermittent spiking fever usually initiated by burn wound
manipulation are the result of released pyrogens. There is no
relationship between the degree of temperature spike and the
presence of wound infection.
MRSA is a common cause of infection in burn patients and is
spread by hands of staff members and airborne particles resulting
in significant implication for treatment, posing a challenging problem
for burn centers.
Colonization of MRSA in burn wound, noses and hands of staff
members, and inanimate objects in Burn Unit prediposes burn
patients to high risk of cross infection. MRSA is usually considered
only a local wound problem but can cause severe systemic infection
in the immunocompromised burn patients. It may cause a
dissolution of grafted skin or induce multiple ulcers on an unstable
scar.
296 PLASTIC SURGERY MADE EASY
Basic infection control procedures of handwashing, extensive
cleaning and barrier nursing are not always sufficient to control the
transmission of MRSA in burn units. A period of closure allowing
extensive cleaning and disinfective procedures has to be carried
out in addition.
For nasal carriers—2% Mupirocin is used intranasally 4 times
daily for 5 days.
Local wound—MRSA efficiently eradicated by daily dressing
with Betadine/Dakins/Zepheran/Lysol and spirit.
Systemic life-threatening infection can be treated with
Vancomycin or Teicoplanin.

Policy to Follow
• Immediate culture of burn wound for patients referred from
other hospitals.
• Isolation of patients, use of disposable material, regular hand-
washing with soap and water/betadine scrub followed by spirit
wash.
• Regular and thorough cleaning of burns rooms and furniture
with soap and water, 7% Lysol and Dakins solution.
A period of closure coupled with strict nursing barrier seems to
have contributed to decrease in MRSA infection. Additional measures
to combat MRSA is by early surgical intervention and nutritional
supplementation which influences the control of wound sepsis.

Local Signs of Burn Wound Infection (Figs 13.29 to 13.31)


1. Abscess formation
2. Black or brown local areas of discoloration
3. Conversion of second degree burns to full thickness burns with
deepening of the wound
4. Change of color—purple, black, brown and blue
5. Erythema gangrenosa/eschar softening
6. Enhanced sloughing/or early sloughing and rapid eschar
separation of burned tissue
7. Focal signs of sepsis/Foul smell/focal areas of discoloration
8. Green color of pseudomonas infection/granulation deteriorating
9. Hemorrhagic patches in the subcutaneous tissue.
THERMAL INJURY 297

FIGURE 13.30: Local signs of


sepsis with abscess formation

FIGURE 13.29: Local signs of FIGURE 13.31: Local signs of


sepsis sepsis with blackish discoloration

CONCLUSION
Although there are many different types of burn wound, the extent
of tissue destruction is always dependent on the temperature,
duration of contact and the thickness of the involved skin. Burns,
which are unlikely to heal in less than 3 weeks, should be treated
by early excision and grafting. Benefits of this approach are many
and patients get optimal functional and cosmetic results.
Emphasis is placed on postoperative wound care.
• Graft care with moisturizing cream
• Splints to prevent flexion contractures
• Pressure garments to prevent hypertrophic scars
• Regular exercise both by physiotherapist and occupational
therapist
• Psychological counseling
298 PLASTIC SURGERY MADE EASY

SKIN SUBSTITUTES
INTRODUCTION
Skin substitutes for temporary covering has become a more frequent
requirement. The increased number of burn patients who survive
the acute phase are on the rise leading to wide spread practice of
early escharectomy. The extensive burns leave behind so few
available donor sites that their wounds cannot be covered by
autografts, hence tissue engineered grafts have become more
important. Construction of new tissue was first coined in 1987 in
USA. Biological substitutes restore, maintain and improve tissue
function. Three components of tissue-engineered constructs are
vascularization, extracellular matrix and cells.

ADVANTAGES OF SKIN SUBSTITUTES


• Hastens wound maturation
• Maintains microbial control
• Normalization of blood proteins and hematocrit levels
• Protects the wound
• Reduction of water, protein and electrolyte losses
• Reduction of heat dispersion
• Reduces pain

PROPERTIES OF SKIN SUBSTITUTES


• Adherence
• Absence of antigenicity
• Absence of local and systemic toxicity
• Biodegradability
• Compatibility
• Elasticity to permit motion of underlying tissue
• Flexibility and pliability
• Impermeable to exogenous microorganism
• Rapid adherence to wound surface
• Resistance to shear stress
• Tensile strength to resist fragmentation
THERMAL INJURY 299
TYPES OF SKIN SUBSTITUTES
1. Biological
• Homograft
• Heterograft-Pigskin
• Amniotic membrane
2. Synthetic
• Duoderm
• Opsite
• Omiderm
3. Biosynthetic
• Biobrane
• Transcyte
• Integra
4. Collagen-based dermal analog
• De-epithelialized allograft
• Alloderm
5. Culture derived tissue
• Apligraf (bilayer human tissue)
• Allogenic keratinocytes
• Cultured autologous keratinocytes
• Cultured allografts
• Collagen—glycosaminoglycan matrix
• Epithelial seeded dermal analog
• Fibroblast seeded dermal analog
• Polyglycolic or acid mesh

BIOLOGICAL
a. Allograft (Homograft)
• Used as a temporary burn dressing for Full Thickness Burns
• Immediate coverage for superficial burns
• Used as a test to determine the likelihood of autograft take
• Available biologic material include allograft and xenograft.
Allograft is the gold standard for temporary skin. The
pathological immunosuppression present in the early stages
of a severe burn injury protects allografts from rejection
during this period.There is a major problem of availability.
300 PLASTIC SURGERY MADE EASY
Advantages of allografts are
• Reduction in water, electrolyte and protein loss
• Reduction in energy requirements secondary to the
attainment of a closed wound reduction in wound infection
rates
• Reduction in pain
Disadvantages: Need for refrigerated storage conditions and
a limited effective shelf-life of 7-10 days at 4 degree, the viability
and take decrease with time and the possibility of disease
transmission is high.
Frozen skin
Advantages
• Maintains viability
• Can adhere to the wounds, viable and able to take and
stimulate vascularization.
• Showed to be less antigenic than fresh skin and this
permitted a lasting take.
Disadvantages
• Requires the creation of an expensive and complex
organizational operative and legislative system. Fear of
transmission of AIDS.
b. Heterografts (xenografts)
Bovine and porcine skin harvested and stored are used
extensively in burns. Porcine skin resembles human skin and
hence it is the most commonly used heterograft.
Advantages
• Used as temporary burn dressing
• Also available as a biosynthetic dressing off the shelf as E-Z
DERM
• Has all the properties of skin and it encourages
re-epithelialization
Disadvantages
• A lab set up is required for processing
• Not so effective in reducing bacterial population
• Adherence to wound bed is less
• Inosculation does not take place
THERMAL INJURY 301
• It undergoes progressive necrosis
• Strict immobilization is necessary.
c. Amniotic membrane—(Davis 1910)
Amnion exerts an angiogenic effect, which increases capillary
density of the wound bed. It enhances epithelialization in partial
thickness burns and promotes epithelial ingrowths from wound
margins in full thickness burn wounds.
Advantages
• It is easy simple and inexpensive, prevents heat and fluid
loss
• Set up required is simple
• Easy to apply, readily available, provides pain relief
• Can be used for all superficial burns where it promotes
healing
• Adheres well and Peels off spontaneously
• Has an angiogenic effect and increases capillary density
• Long-term glycerol preserved amniotic membrane is
available.
Disadvantage—cross infection is common and dangerous.

SYNTHETIC SKIN SUBSTITUTES


Omiderm is a thin transparent polyurethane based membrane. It
sticks to the moist wound surface. Its transparency facilitates easy
observation of the burn wound.

BIOSYNTHETICS (RATIONAL FOR DEVELOPING)


• Given the limitations of available biologic bilayer skin, the
development of engineered skin substitutes become necessary
using synthetic component
• Incorporating biological active components such as collagen,
glycosaminoglycan, keratinocytes and fibroblasts
Current bilayer skin substitutes are usually composed of :
a. A synthetic component
b. A biologically active component
302 PLASTIC SURGERY MADE EASY
Synthetic component—Advances in the technology has led to the
development of epidermal analogs critical for the function of both
temporary and permanent skin substitutes. Available synthetic
materials for skin substitutes are Silicone polymer, Polyurethane
polyvinyl, and Nylon.
• Initially collagen-based products lacked an outer synthetic
protective layer and were prone to environmental insults.
• An advance was addition of glycosaminoglycan to provide more
porosity and a more durable structure.
• Further advance was the development of a bilaminar structure
with an outer synthetic layer acting as a barrier and controlling
water vapor while the inner layer acting as a dermal analog.
• With current concepts the types of skin substitutes are classified
into Temporary and Permanent. The structure of dermal collagen
analog has changed.
• In the temporary skin substitutes the demal analog is not
incorporated.
• In the permanent skin substitute the dermal analog is
incorporated to varying degrees to restore a dermis.

Temporary Skin Substitutes


Rely upon incorporation into the wound by coagulum and
ingrowths of granulation tissue for adhesions. They can only be
temporary substitution and must be replaced by patients skin either
by re-epithelialization or skin grafts.
Example—Biobrane, Transcyte

Advantages
• Markedly reduces pain
• Decreases heat and water loss
• Decreases wound inflammation
• Prevents surface drying
• Increases the rate of epithelialization
• Decreases surface infection

Disadvantages
• Does not control deep infection
THERMAL INJURY 303
• Can seal bacteria
• Biologicals can transmit infection
Apligraf—Bilayer human epidermis and dermal analog. Epidermal
analog consists of cornified epidermal layer of neonatal allogenic
keratinocytes. Dermal analog is collagen matrix seeded with neonatal
fibroblasts.
Biobrane—Bilaminate membrane. Outer epidermal analog is of a
thin silicone film with barrier functions comparable to skin. Inner
dermal analog composed of nylon mesh bonded to a thin layer of
silicone. The nylon mesh is coated with collagen in order to aid
adherence to wound bed and fibrovascular ingrowths.
Cultured allogenic keratinocytes—Pregrown allogenic
keratinocytes. No acute rejection reaction. Healing noted is due to
secretion of growth factor.
Derma graft—It is a cryopreserved living dermal structure
containing neonatal allogenic fibroblasts on a polymer scaffold
dexon or vicryl. The fibroblast becomes confluent with a polymer
mesh secreting growth factors and dermal matrix protein thus
creating a living dermal structure.
Transcyte—Bilayer skin substitute. Outer epidermal analog is a
thin non-porous silicone film with barrier function. Inner dermal
analog is collagen coated nylon mesh seeded with neonatal
fibroblast in order to improve its healing properties. Subsequent
cryopreservation destroys fibroblasts but preserves activity of
fibroblast-derived products.

CULTURE DERIVED TISSUE


(PERMANENT SKIN REPLACEMENT)
As opposed to the bilayer concept of the ideal temporary skin
substitute, permanent skin replacement is much more complex.
Permanent wound closure relies on a subsequent epidermal graft
to the integrated allodermis. This may be from an autologous skin
graft or skin substitutes. Bilayer structure with biologic dermal analog
and either synthetic or biologic epidermal analog. Permanent skin
304 PLASTIC SURGERY MADE EASY
is biologically accepted by the wound bed and become permanently
incorporated into the healing wound. Example—Integra, Apligraf,
composite cultured skin either.
• Epidermis only—cultured epithelial autograft
• Dermis only—alloderm—allograft dermis
• Epidermis and fibroblasts
Alloderm—It is processed human cadaver skin from which the
epidermis is removed and the cellular components of the dermis
has been extracted prior to cryopreserved in order to avoid a immune
response. It allows grafting with split skin graft as a one-stage
procedure.
Epicel—Sheets of keratinocytes can be grown in vitro and then
applied to wounds. Epidermal layer replacement only 2-3 weeks
period to produce desired amount. Graft take on excised wound is
28-50% and on incorporate allograft dermis is 45-75%.
Integra—It is a bilaminar structure consisting of a cross-linked
bovine collagen and glycosaminoglycan coated one side with a
silicone membrane that provides epidermal function. The pore size
at 70-200 micrometer allows migration of patients own endothelial
cells and fibroblasts. After neodermis formation, the epidermal
analog silicone is removed and replaced with thin epidermal
autografts or cultured epithelial cells.

CONCLUSION
1. The scientific and practical approaches to replace skin temporary
or permanent are advancing at rapid rate.
2. These advances are due to advances both in the field of
bioengineering as well as increasing interest in optimizing the
outcome of burn wound.
3. The arena of temporary skin substitute is more concrete, easier
to categorize and determine efficacy with a bilayer structure and
commercially available.
4. Permanent skin replacement on the other hand is much more
complex –use of either bilayer products or replacement of either
dermal or epidermal elements are not yet commercially
available.
THERMAL INJURY 305

SEPTIC SHOCK
INTRODUCTION
Large open burn wounds containing necrotic tissue makes it
susceptible to infection. The microorganisms multiply and colonize
wounds easily due to the immunocompromised state of the patient.
Infection and septicemia should be suspected when patient shows
signs of disorientation, hyperpyrexia, hypotension, hypoxia, and
tachypnea.
Shock is defined as an abnormal physiologic state in which the
flow of blood is insufficient to maintain adequate nutritive perfusion
at the capillary level.
Sepsis is defined as a spectrum of clinical conditions caused by the
response of the patient to infection. It includes the full range of
response from systemic inflammatory response to organ dysfunction
to multiple organ failure and ultimately death.
Septicemia is a state of microbial invasion causing signs of illness.
The predominant feature of septic shock is arterial vasodilatation.
An imbalance of homeostatic mechanism leads to DIC (Homeostasis
is the maintenance of stable internal environment or maintenance
of equilibrium). There is a deficiency in several clotting factors due
to consumption of these factors. Respiratory failure is the most
important cause of death in patients with shock. It is called shock
lung syndrome and is characterized by pulmonary edema,
hemorrhage, atelectasis and thrombi formation. Renal failure
eventually leads to oliguria.

CLINICAL MANIFESTATION
• Hyperventilation is the earliest sign.
• Disorientation, confusion, GI manifestation such as nausea,
vomiting and diarrhea.
Laboratory—Blood lactate levels—rise early because of increased
glycolysis with impaired clearance of the resulting lactate and
pyruvate by the liver and kidney.
306 PLASTIC SURGERY MADE EASY
Metabolic acidosis—As hypoperfusion develops tissue hypoxia
generates more lactic acid contributing to metabolic acidosis.
Increased blood glucose levels.

Adult Respiratory Distress Syndrome (ARDS)


A rising respiratory sign is the first to indicate that the patient is going
into ARDS. Lung injury is characterized by increased permeability
of the alveolar membrane, diffuse alveolar damage, pulmonary
edema, dyspnea, severe hypoxemia and pulmonary infiltrates.

Clinical Phases of ARDS


Phase-1 characterized by altered tissue perfusion (partial pressure
of oxygen and carbon dioxide are normal or slightly decreased
with scattered rales.
Phase-2 hypocapnea.
Phase-3 severe hypocapnea and hypoxemia.
Phase-4 severe hypoxemia, metabolic acidosis.

Treatment of ARDS
With better understanding and management of sepsis importance
is given to early recognition and immediate aggressive therapy to
reduce progression to full blown septicemia. Treatment priority
follows the VIP format that is ventilation, infusion and perfusion.
A rising respiratory is the first indication of sepsis. An arterial
blood gas study done at this stage indicates a low partial pressure of
oxygen (Tachypnea and tachycardia are among the body’s first
compensatory responses to sepsis).
Ventilation—considering that ventilation has the highest priority
importance is given to administering oxygen to keep the arterial
partial pressure at about 80-100 mm of Hg.
Infusion—in septic shock circulating volume can decrease
significantly as fluid shifts into the interstitial space and hence rapid
infusion of electrolyte solution, colloid, amino acids, fatty acids and
10% dextrose should be given to prevent circulatory collapse .
THERMAL INJURY 307
Perfusion—adequate oxygen and fluid replacement helps in
maintaining or improving perfusion. In addition vasodilating drugs
like dopamine are started in small doses to maintain renal perfusion.
Appropriate antibiotics are started based on bacteriological
monitoring of the burn wound.
Topical antibiotic is used generously twice a day for local wound
care.
In addition close monitoring of respiratory rate, pulse rate, blood
pressure and urine output is maintained.
Patient who do not respond to this simple increase of fractional
inspired oxygen concentration and continue to have refractory
hypoxemia are to be treated with continuous positive airway
pressure (CPAP), this mode of treatment obviates the need for
endotracheal intubation and the subsequent infection (Fig.13.32).

FIGURE 13.32: CPAP


308 PLASTIC SURGERY MADE EASY
CPAP—is an effective supportive therapy in hypoxic respiratory
failure. It increases oxygenation without intubation. Patient is able
to communicate.
A number of measures are necessary in the treatment of sepsis
in burn patients, such as correct local care, nutritional support ,
environmental control and surgical therapy. All are necessary for
effective treatment.

NUTRITION
INTRODUCTION
After burn injury, patients enter into a severe catabolic state
characterized by elevated metabolic rate, increased protein
mobilization and gluconeogenesis. In burn patients these catabolic
changes lead to significant increase in energy and protein
requirements. Weight loss during this phase is virtually inevitable
unless aggressive nutritional therapy is instituted soon after the
burn. Weight loss of more than 10 percent has been shown to
increase mortality and a weight loss of more than 30 percent is
associated with almost 100 percent mortality (Fig.13.33).

FIGURE 13.33: Severe loss of FIGURE 13.34: Enteral


weight supplementation
THERMAL INJURY 309
Therefore, nutritional support is as important as any other aspect of
burn management. Nutritional support can be achieved by either
entral or parenteral routes . Parenteral nutrition is usually avoided
because of its expense and the high rate of complications. Nutrition
supplementation via a continuous nasogastric tube helps prevent
severe weight loss (Fig. 13.34).

DISTURBANCES IN METABOLISM
Following burn injury there is disturbances of carbohydrate, protein
and fat metabolism.
Carbohydrate—Burn patients have elevated blood glucose levels,
this is due to increase glucose production from gluconeogenesis.
The ability of burn patient to handle glucose is limited to 5 mg/kg/
min. Elevated blood glucose levels is due to elevated serum glucagon
levels. Elevated release of amino acids from muscles are utilized for
new glucose formation and this is responsible for the decrease in
the levels of amino acids in burn patients.
Fat—Increased lipolysis results in increased levels of serum fatty acids.
Protein—Protein is also altered. There is an increase in the rate of
protein anabolism. Protein break down exceeds synthesis. There is
marked muscle wasting in burn patients. Protein breaks into amino
acids. The increased rate of hepatic gluconeogenesis utilizing amino
acids explains the fact that serum amino acids are decreased.

Metabolic Response following Burn Injury (Flow Chart 13.1)


In response to anxiety, pain and fear, the hypothalamo-pituitary
axis releases:
• Elevated cortisol levels
• Elevated glucagon levels
• Elevated catecholamine levels
• Decreased insulin levels
Elevated cortisol results in increased mobilization of amino acids
from the muscles, raises blood glucose levels and neutrophils, at
the same time it reduces lymphocyte levels. The function of cortisol
is to regulate carbohydrate metabolism.
310 PLASTIC SURGERY MADE EASY
Flow Chart 13.1
THERMAL INJURY 311
Elevated glucogon raises blood glucose, converts glycogen to
glucose and also results in gluconeogenesis.
Elevated catecholamines stimulate glycogenolysis and gluco-
neogenesis, at the same time suppress insulin release.
All these elevated hormones lead to
1. Hypermetabolic state characterized by
• Hyperpyrexia
• Tachycardia
• Tachypnea
• Weight loss
The hypermetbolic state demands production of energy
from any source. In the absence of adequate exogenous source
available endogenous source is utilized.
2. Hyperglycemia
3. Altered carbohydrate metabolism—Causes increased
glucose levels and increased gluconeogenesis. Excess glucose
is converted to fat and CO2 production, hence carbohydrate
intake is limited to 5 mg/kg/min.
4. Accelerated fat and protein breakdown—Carbohydrate
reserve is limited for continued energy demands. Fat reserves
are utilized, but the process requires presence of carbohydrate
which is obtained from the mechanism of muscle protein.
5. Negative nitrogen balance
6. Insulin resistance—And hence glucose is not utilized.
By administering Very Early
Nutritional Supplementation
(VENS) it controls gluconeoge-
nesis, increases glucose utilization
and minimizes protein loss. More
over it is safe, well tolerated, limits
weight loss and controls secretion
of catecholamines and glucagon
thus reducing hospital stay FIGURE 13.35: Weight gain with
(Fig.13.35). supplement nutrition

THE GOALS OF AGGRESSIVE NUTRITIONAL SUPPORT


• Promote early anabolism and wound healing
312 PLASTIC SURGERY MADE EASY
• Prevent weight loss
• Improve Immunity
With increased understanding that the clinical outcome and
prognosis are influenced by patient’s nutritional status, the
importance of early nutritional supplementation to prevent the severe
catabolic state is realized. Simple nutrients like buttermilk should
be administered on the first day and gradually increase the strength
of the diet. This will help to minimize osmotic diarrhea. To overcome
the problems of diarrhea associated with this high protein calorie
diet, enteral supplementation is given in the form of a drip over 24
hours through a small nasogastric tube. This high protein calorie
diet seems to offset the ravages of hypermetabolism.

NUTRITION REQUIREMENT
Nutrition requirement is calculated by
Curreri formula = (25 cal × weight in kg) + (40 cal x% of burns)
Normal nutrition is necessary to maintain intestinal structure and
function and help preserve the intestinal mucosal barrier and thereby
prevent the translocation of bacteria and endotoxin from the gut to
the systemic circulation.
• Vitamins and minerals are necessary for wound healing and
skin maturation
• Fat-soluble vitamins (A, D, E & K) are stored in fat deposits.
They can be depleted during the prolonged course of a major
burn injury
• Water soluble vitamins (B,C) are not stored and are rapidly
depleted, if not constantly replaced
• Vitamin C-1000 gm/day should be given for collagen synthesis
• Vitamin B is needed to metabolize carbohydrate, fat and protein
• Zinc is essential for DNA synthesis (20% zinc is in the skin).

ASSESSMENT OF NUTRITIONAL STATUS


• Weight regularly
• Total lymphocyte count
• Serum Transferrin level
THERMAL INJURY 313
Total Count and Differential Count
Total lymphocyte count—a count below 3000/cubic mm reflects an
immunodeficiency state. It is an indicator of visceral protein status:
Example— If lymphocyte count is 40
Total count =5000
40 × 5000
—————— = 2000/cubic mm
100

Serum Transferrin (Serum Transferrin is calculated from TIBC)


Normal serum transferring value—2.04-3.60
Normal TIBC—230-380 microgram%
Calculate transferrin—0.8 × TIBC-43
More sensitive indicator of protein status—A transferrin level less
than 2 gm/L is associated with an increase incidence of bacteremia
in burns.
Evidence of malnutrition is calculated by
Usual wt – Actual wt
———————————— × 100
Usual wt

Example if 60-50
———— × 100 =16%
60
(Weight loss more than 10% loss over any given time period
has been taken as evidence of malnutrition)

ROUTES OF NUTRITIONAL SUPPORT


• Oral
• Enteral
• Parenteral
Earlier, the well-known paralytic Ileus had deterred attempts at
early enteral feeding. As a result burn patients were 3-4 days with-
out any nutrition of any kind and even when they took food by
mouth, calorie intake was far below demand and by this time the
rate of catabolism had already taken its toll. It was then realized that
very early nutrition supplementation is necessary not only to prevent
314 PLASTIC SURGERY MADE EASY
the severe catabolic state but also influence the clinical outcome
and prognosis.
We now administer simple nutrients like butter milk for all burn
patients on the first day of burn through a small nasogastric tube
and gradually increase the strength to full strength by day three.
From the 4th day onwards nutrition is calculated according to Curreri
formula. Parenteral nutrition support like hyperosmolar glucose,
amino acids and lipids are given via peripheral line to supplement
enteral feeds particularly during sepsis.

CONCLUSION
• The high protein calorie diet given very early seems to off set
the ravages of hypermetabolism
• Graft take is good
• Infection is reduced
• Patient gains weight
• Rapid wound healing

RECONSTRUCTIVE PRINCIPLES IN
BURN CONTRACTURES
Reconstruction of a burn patient is a complex and a lengthy process
that usually starts at the time of initial injury and often lasts from
years to a lifetime. The useful techniques during the acute phase
which help to minimize late reconstructive problems include
• Start active and passive mobilization and ambulation as soon
as possible
• Elevate and splint all limbs and joints
• Use darts to prevent linear contracture across joints
• Place graft seams that follow skin lines
• Place grafts on joints transversely
• Use sheet grafts whenever possible
• Avoid widely expanded mesh grafts
• Excise and graft all wounds that do not heal in 3 weeks of injury
• Use cosmetic units when necessary
• Start rehabilitation and pressure therapy as soon as possible
THERMAL INJURY 315
Non-surgical approach to burn reconstruction includes
• Compression by elastic bandage, tubular bandage and custom
fitted garments
• Silicone gel
• Steroids
• Masks and splints
In spite of all this, contractures and scarring remain, leading to
conflict in the timing of surgical reconstruction. The psychology and
rehabilitation prefer early reconstruction, whereas the wound
biology favors late reconstruction. Even though it is more rewarding
to do reconstructive procedures on the mature scar, in the patient’s
best interest, it is best not to wait for scar maturation.
Surgical treatment can be classified into essential surgery and
desirable procedures.
• Essential surgery is perfor-
med to preserve important
functions Exposed cornea
requiring eyelid reconstruction
Release burn scar contracture of
the neck that preclude general
anesthesia (Fig.13.36).
Oral contracture that interfere
with anesthesia, hygiene and
FIGURE 13.36: Essential
eating surgery
• Desirable procedures include
the type of reconstruction a patient envisions. At this time
patient’s priorities are the most important. Example—nose, burn
alopecia and scar revisions. These are performed after scar
maturation has occurred.

Reconstructive Principles Area-wise


• Face—The graft seams are placed along skin lines, custom
made face masks are worn continuously to give pressure evenly.
The disadvantage is that it is cumbersome and needs to be
worn 24 hours a day. Hypopigmented patch on the forehead
dermabraded and grafted using sheet graft to get the desired
esthetic result (Figs.13.37 and 13.37A)
316 PLASTIC SURGERY MADE EASY

FIGURE 13.37: Hypopigmented FIGURE 13.37A: Dermabrasion and


patch forehead sheet graft

• Eyelid reconstruction—Can be Extrinsic or Intrinsic. A very


important consideration is to eliminate extrinsic causes of
ectropion before concentrating on the eyelids. It is possible for
contracture of the face and neck to transmit forces to the eyelid
causing secondary problems. Once extrinsic problems are
corrected, the residual ectropion should be corrected, one at a
time either upper or lower as over correction is important
(Figs13.38 and 13.39).
It is preferred to use full thickness skin grafts for lower eyelid
and thin split thickness skin graft for upper eyelid. It is important

FIGURE 13.38: Ectropion of eye- FIGURE 13.38A: Reconstruction


lids hypopigmented forehead
THERMAL INJURY 317

FIGURE 13.39: Loss of eyebrow FIGURE 13.40: Mismatched graft


for a burned face

to choose the type of skin to be grafted on a burned face,


preferably a skin from the burned area should be taken to
match the rest of the face. A normal skin on a burned face looks
unacceptable even from a distance (Fig.13.40).
• Ear reconstruction—Although scarred tissue complicates ear
reconstruction; there are several advantages of burn ear over a
congenital ear. The burn deformity of the ear has all of the
cartilage but folded by contraction. Simple release is sufficient
to give a natural appearance.
The total absence of the helical rim is reconstructed with rib
cartilage graft (Figs 13.41 to 13.44). The reconstructed ear
should be protected for at least 2 months. We have designed a
protective ear cup using tea strainer with velcro straps
(Fig.13.45).The advent of vascularized temporal fascial flap
has been a major boon for burn patients.

FIGURE 13.41: Loss of helical FIGURE 13.42: Rib graft


rim
318 PLASTIC SURGERY MADE EASY

FIGURE 13.43: Shaping the rib FIGURE 13.44: Reconstruction


graft of helical rim

FIGURE 13.45: Protecting device made FIGURE 13.46: Loss of ear


of tea strainer lobe

Earlobe is often adherent to adjacent neck skin. Simple division


and closure is all that is needed for correction (Figs 13.46
and 13.47).
• Nasal reconstruction: The greatest projection and central
point of the face is the nose and successful correction is crucial
to the patient’s self-image. Two common deformities of the nose
are:
THERMAL INJURY 319

FIGURE 13.47: Reconstruction of FIGURE 13.48: Typical burned


earlobe from scarred burned tissue nose ectropion

FIGURE 13.49: Release ectropion FIGURE 13.50: Postoperative


and insertion of tubes picture with graft in place

Nasal ectropion: corrected with turn down flaps and full


thickness skin grafts (Figs 13.48 to 13.53).
Nasal stenosis: The scar is removed and skin graft is sutured
around a splint and placed in position for 6 months. Suction
catheters have been found to be a very useful alternative for
splints (Figs 13.54 to 13.54B).
320 PLASTIC SURGERY MADE EASY

FIGURE 13.51: Nasal ectropion FIGURE 13.52: Nasal ectropion post-


operative with rubber tube in place

FIGURE 13.53: Postoperative FIGURE 13.54: Nostril stenosis


correction nasal ectropion

FIGURE 13.54A: Rubber tube as FIGURE 13.54B: Release


splint for 6 months stenosis and graft
THERMAL INJURY 321

FIGURE 13.55: Microstomia FIGURE 13.55A: Postoperative


microstomia correction

FIGURE 13.56: Upper lip FIGURE 13.56A: Post release and


ectropion graft

• Oral commissure—Lateral margin of oral commissure, which


is at the end of nasolabial fold, is determined. A triangular
section of scar tissue is removed and the vermilion flap is
transposed. Splints are crucial (Figs 13.55 and 13.55A)
• Upper lip—Upper lip nasal unit can be corrected by release of
contracture and resurface with split thickness skin grafting or
Full thickness graft (Figs 13.56, 13.56A, 13.57 and
13.57A)
• Lower lip—Ectropion is corrected by release of the lower lip.
Partial vermilionectomy and wedge excision of the excess
vermilion to maintain tension of muscle. The raw surface is
covered with FTSG (Figs 13.58, 13.58A, 13.59 and
13.59A)
322 PLASTIC SURGERY MADE EASY

FIGURE 13.57: Hypo-


pigmented upper lip nasal
unit

FIGURE 13.57A: Upper lip


grafted patch

FIGURE 13.58: Lower lip FIGURE 13.58A: Lower lip


ectropion release and full thickness graft

• Neck contracture—Despite its obvious limitation, skin grafts


are most commonly used in extensive neck contractures. A
nasogastric tube for feeding and immobilization by postoperative
splinting is very essential for a good take (Figs 13.60 to
13.63)
• Axilla—The scar band can be either anterior or posterior. It
can involve the dome of the axilla or adherent to the chest wall.
Release contracture and reconstruction with local flaps rather
THERMAL INJURY 323

FIGURE 13.59: Lower lip FIGURE 13.59A: Release


ectropion ectropion and graft

FIGURE 13.60: Neck contracture FIGURE 13.61: Post release neck


contracture with graft
324 PLASTIC SURGERY MADE EASY

FIGURE 13.62: Front view neck FIGURE 13.62A: Neck contracture


contracture with graft

FIGURE 13.63: Neck contracture FIGURE 13.63A: Release neck


contracture with STSG

than using skin grafts is the best option (Figs 13.64 to 13.69)
• Lower extremity—creates a unique problem splinting with
early skin grafting prevents most of these contractures. However,
if contraction does occur, it is released using vertical and
transverse incisions, k-wire fixation and resurfaced with STSG
(Figs 13.70 to 13.73). Chronic non-healing ulcers or
recalcitrant ulcers in burn patients have been found to be due
to the tight skin. Treatment is by incisional release above or
below the ulcer. This seems to hasten the ulcer healing due to
the laxity of the skin.
THERMAL INJURY 325

FIGURE 13.64: Axilla contracture FIGURE 13.65: Release axillary


contracture with local flaps

FIGURE 13.66: Posterior axillary FIGURE 13.67: Release


fold contracture contracture with flaps
326 PLASTIC SURGERY MADE EASY

FIGURE 13.68: Axillary FIGURE 13.69: Five flap Z-plasty


contracture release of axilla

FIGURE 13.70: Post burn scar FIGURE 13.71: Release


contracture foot contracture and graft
• Breast—The goal is esthetic recontouring of the breast.
Secondary procedures like nipple and areolar reconstruction is
done at the peripubertal age. Surgical release of the breast is
carried out by inverted T incision and resurfaced with Split
thickness skin graft (Figs 13.74 to 13.79). Silicone inserts
and sternal straps help to improve scarring and shape.
Nipple areala region is tattooed by pigments and reconstruction
of nipple is by skate flap and areola by Full thickness pigmented
skin graft from medial thigh (Figs 13.80 to 13.83).
THERMAL INJURY 327

FIGURE 13.72: Post burn foot FIGURE 13.73: Release with vertical
and transverse incisions

FIGURE 13.74: Chest burns FIGURE 13.75: With entrapped


breast

FIGURE 13.76: Development of breast FIGURE 13.77: Entrapped


after release burns chest breast
328 PLASTIC SURGERY MADE EASY

FIGURE 13.78: Inverted t shaped FIGURE 13.79: Development


release and graft of breast

FIGURE 13.80: Absent nipple FIGURE 13.81: Tattoo of nipple


areola region

FIGURE 13.82: Reconstruction FIGURE 13.83: Projection of nipple


of nipple areola after reconstruction
THERMAL INJURY 329

FIGURE 13.84: Perineal FIGURE 13.85: Release


contracture contracture with 5 flap plasty

• Perineal contractures—
Are very common and can
be corrected by local flaps
(Figs 13.84 to 13.86).

CONCLUSION
Burn reconstruction is a very
rewarding field. For most
FIGURE 13.86: Postoperative
problems there is either a simple five flap plasty
solution or a complex solution.
The surgical challenge of reconstruction after burn injury takes on
an importance almost unmatched in any other area of reconstruction.
As burn surgeons we can all help the burn survivors to face the
society with confidence.

POST BURN AXILLARY CONTRACTURES


INTRODUCTION
Shoulder has the greatest range of motion of any joint. Maintaining
that posses many problems for the burn team. Early splinting,
positioning and motion of the arm to prevent contractures are very
important.
Post burn axillary contractures should be corrected as soon as
the diagnosis is established in order to avoid deeper tissue
330 PLASTIC SURGERY MADE EASY
involvement. Several techniques have been defined to release the
post burn contracture of the axilla. Axillary region is important
because it has multi-directional activity. Scar contractures restrict
various movements. Patients have problems with daily activities.
Scar tissue usually extends to the chest, back and upper arm
compounding the restrictions.

CLASSIFICATION
Axillary contractures are classified into 3 groups depending on the
involvement of the axillary fold.
Group I—Involving only the anterior or posterior axillary fold (Figs
13.87 and 13.88).

FIGURE 13.87: Group 1 axilla FIGURE 13.88: Group 1 release


cotracture with 5 flap plasty

Group II—Involving both the anterior and posterior fold but sparing
the apex of the axilla.
Group III—Most severe deformity where the complete axilla is
involved and attached to the chest wall (Figs 13.89 and 13.90).

TREATMENT
• Simple local flaps
• Transposition flaps (Figs 13.91 and 13.92)
• Regional faciocutaneous flaps
• STSG
THERMAL INJURY 331

FIGURE 13.89: Group 3 axilla FIGURE 13.90: Group 3 axilla


contracture contracture

FIGURE 13.91: Axilla contracture FIGURE 13.92: Local transposition


flap

The only condition which requires grafting is, when there is


extensive raw area either on the chest or arm on release.
Considering that skin grafts for post burn contracture release of
the axilla has a high recurrent rate, flaps have been the best choice.
Generally normal skin is mandatory to raise flaps, we perform flaps
which are reliable, safe and simple even when skin is burnt. The
use of flaps have been an invaluable option in preventing
recontractures.
We know that reconstruction of scar contracture is a challenge
for plastic surgeons. We use subcutaneous pedicle flaps for correction
332 PLASTIC SURGERY MADE EASY
of scar contractures and early release to avoid deeper tissue
involvement. Including subcutaneous tissue as a pedicle in the flap
has increased the survival of flaps.
Scar bands of either anterior or posterior axillary fold are
corrected by utilizing unburnt skin to break up the scar band using
multiple Z-plasties. The major short coming of Z-plasty is that scarring
at the base will jeopardize the circulation and tip necrosis is often
found. This can be avoided by using deeper dissection
subcutaneous pedicle flaps. For severe contractures a regional flap
like latissimus dorsi flap should be considered.

ADVANTAGES
• Postoperative immobilization is shortened
• Postoperative physiotherapy is reduced
• Hospitalization time is shortened
• Repeated releases are much less

POST BURN RECONSTRUCTION


OF FEET
INTRODUCTION
The survival of patients with major thermal injuries has drastically
increased in recent years. As our ability to save patients lives
increases, the concept of total rehabilitation becomes of paramount
importance. Burns to the ankle and foot represent some of the most
challenging problems in acute wound care, subsequent
rehabilitation and reconstruction.
Currently, great emphasis is given to proper positioning and
splinting to maintain mobility during the acute and reconstructive
phases of care. The lower extremity is important for static support of
the trunk and ambulation. Burn scar contractures not only affect
gait, but in very severe cases, may even preclude standing. The
human gait pattern is classified as normal, minor gait abnormality
and major gait abnormality.
The standard for reconstruction for burn scar contractures of
the feet is restoring the anatomy to normal and then obtaining soft
THERMAL INJURY 333
tissue coverage. The timing of reconstruction has been questioned.
However, if the deformity is progressive or causing a significant
functional deficit, reconstruction is initiated early.

ANATOMY OF THE FOOT


Foot is that area extending from toes to the lateral and medial malleoli.
The various subunits are dorsal surface, plantar surface and the
ankle. The skin over the dorsum of the foot is thin and supple. The
skin over the sole of the foot is firmly fixed to the deeper structures.
The plantar fascia along with the tarsal bones is very important to
stabilize the arch of the foot. Destruction of this fascia will disrupt
the arch support.

CLASSIFICATION
Dorsal Burn Scar Contractures
Blood supply of the dorsum of the foot is mainly by the dorsalis
pedis artery.
Nerve supply is from the superficial peroneal nerve, which supplies
the dorsum of the foot, and the deep peroneal nerve, which supplies
the first web space. The sural nerve supplies the lateral aspect of the
foot.
Skin of the dorsum of the foot is thin and loosely connected to the
underlying fascia The tendons in this region are located superficially.
Burns of the dorsum of the foot can result in distortion of the skin.
Dorsal contractures of the foot result in shortening of the skin,
often with enough force to cause hyperextension of toes and
subluxation or dislocation of the metatarsophalangeal joint. The
metatarsal heads become prominent on the plantar surface. The
long flexors of the toes result in flexion at the interphalangeal joints.
The accompanying shortening in the transverse axis often results in
narrowing of the forefoot with overriding of the toes.
Inversion contracture of the foot results from the contracting
band that extends from the leg to the foot on the medial side pulling
the foot into inversion.
334 PLASTIC SURGERY MADE EASY
Eversion contractures of the foot occurs when the contracting
band from the leg to the foot is on the lateral side pulling the foot
into eversion leading to callous formation and painful gait. This
results in an “Acquired talus deformity” where the scar contractures
pull skin into dorsiflexion with eversion of the foot and shortening
of the calf muscles.
Webbing contractures of the dorsal skin can occur in burns of
the forefoot resulting in overriding and deviation of toes. This is
managed with release and skin grafting or Y-V advancement flaps,
Z-plasty or V-Y flaps. Skin grafts and local flaps have proved
satisfactory for reconstructing almost all burn scars of the foot.

Plantar Surface Burn Scar Contractures


Blood supply of the plantar surface is by both the medial and
lateral plantar arteries. The lateral plantar artery is larger than the
medial plantar artery. The plantar arch is formed by the deep plantar
branch of the dorsalis pedis artery and the distal plantar artery.
Nerve supply of the plantar surface is by the plantar nerves, which
consists of medial calcaneal, which supplies the heel area, medial
plantar and lateral plantar nerves.
Skin on the plantar surface is very thick and firmly held on to
the underlying fascia by the fibrous septa. The plantar fascia consists
of strong fibrous layers that are oriented in longitudinal, vertical
and transverse direction. It extends from the calcaneal region to
attach to the plantar aspect of the proximal phalanges. The weight
bearing plantar surface is a challenging area to achieve soft tissue
coverage. Preservation of its sensation is important for maintaining
a stable weight-bearing surface.
An important feature of the foot is its longitudinal and transverse
arches. Destruction of these arches occurs in severe burn scar
contractures leading to reduced width and length of the foot. The
plantar surface is important to stabilize the arch of the foot.
Destruction of the plantar fascia as a result of burn injury can result
in disruption of the arch support.
THERMAL INJURY 335
Joint Deformities
Equino varus deformities occur when scar tissue following burns
results in flexion contractures at the tibiotarsal joint with heel cord
shortening. Later, capsular contractures develop. Prolonged
abnormal load on the joints results in subluxations and dislocations.
The ankle is usually in equinus position, with inversion of hindfoot
and equinus varus of forefoot. This can be corrected by tenolysis of
Achillis tendon, tendon lengthening or tenotomy. The established
equinus deformity can be corrected by calcaneal traction. This
deformity can be prevented if ankles are positioned properly.

TREATMENT
Nonsurgical
When the contracture is minimal, either simple skin traction or
Steinmann pins have been used to correct the contractures, although
this form of treatment alone is not applicable to most of the
contractures seen in the burn patients.

Surgical
1. Split thickness skin grafts continue to be the primary
method of coverage in reconstruction of the dorsal foot burns
when the underlying tendons are not exposed. In conditions
where the tendons are exposed, if it is a small area, then
debridement is sufficient to allow for the development of
granulation tissue. Then the use of split thickness grafts will
allow closure. One must bear in mind the fact that skin grafts
will not take on bare bone, cartilage or tendon.
Dorsal burns can result in extensive tissue deficiency and
require release and skin grafting both in the longitudinal and
transverse plane. A transverse incision across the dorsum of the
foot is performed proximal to the fifth metatarsal joint. This
maneuver releases longitudinal arch. The transverse arch is
released by making parallel release to the plane of the metatarsals
usually in line with the web spaces. If syndactyly is present, then
the incisions are carried into the web spaces. K-wire fixations may
be necessary to assure correct positioning of the
336 PLASTIC SURGERY MADE EASY
metatarsophalangeal joints. Postoperatively, elevation and splints
are continued until graft take is insured. Ambulation is started
with non-weight bearing initially, and gradually progressed to
full weight bearing. Silicone conformers and pressure garments
are fitted and worn continuously until grafts mature.
Plantar contractures are rare. Split thickness grafts have proved
satisfactory even on the weight bearing portions of the foot.
2. Flaps
a. Reconstruction of the foot using local tissue is limited by the
available skin in burn injuries. However, local random
pattern flaps have been used for coverage of small defects.
Dorsal foot burns with exposed tendon and deeper structures
require vascularized coverage using free tissue transfer,
Fasciocutaneous flaps and muscle flaps.
b. When the injury prevents the use of local flaps, regional or
distant flaps can be used if there is unburned skin in the leg.
Random pattern flaps like de-epithelialized turn over flaps
provide single stage flap cover in burns with full thickness
defect.
c. Cross-leg flaps are rapidly fading from use. When burn
injury prevents the use of regional flaps, then cross-leg flaps
have been used. Although rarely used in modern era,
certainly they form an important armamentarium for the
reconstructive surgeons.
d. Free flaps, when all other options are not possible,
microsurgical flaps definitely have a place in the reconstruction
of the complex foot injuries. The flexibility of design, transfer
of composite tissues and the increased vascularity make it an
useful alternative for reconstructing a burn foot.
3. Amputations
Appropriate treatment of extensive foot defect is complex.
Despite careful treatment, some patients inevitably require
amputation. In determining the level of amputation, one must
consider the optimal site for prosthetic fitting. The primary goal
should be to salvage as much of the foot as possible to minimize
functional loss. If the injury is severe resulting in either gangrene
or life-threatening infection, then amputation may be the only
choice.
THERMAL INJURY 337
PHYSIOTHERAPY AND SPLINTING
In the management of foot burns, proper positioning is a critical
step in the prevention of joint deformities. The detrimental effects of
poor positioning and contracture can result in multiple deformities.
Following reconstruction with skin grafts, there is an urgent need
for immediate and aggressive physiotherapy programs. Ambulation
is resumed one-week postoperatively after application of Ace wraps
to prevent shearing injury to the graft. Following discharge from the
hospital, these patients are advised about graft care and regular use
of splints to prevent further contractures.

PITFALLS
Obviously, burns of the foot, increases morbidity. Prolonged weight
bearing with abnormal loading on the joints can result in
subluxation and joint dislocation. The pitfalls of surgical intervention
include graft loss, joint pain and incomplete correction of the initial
problem.
Recontractures are quite common, particularly in children. Since
skin grafts do not always accommodate growth of a child, re-
contractures develop. Pitfalls in postoperative splinting can lead to
pressure sores and joint stiffness.

NURSING ISSUES
Grafting of the lower limb requires special nursing care. It is
imperative to make sure that the limb is elevated postoperatively to
reduce edema and subsequent graft failure. Proper positioning of
the splint has to be checked to avoid pressure sores. Strict bedrest
has to be ensured to prevent graft loss. The dressing change and
the use of silicone conformer and splint have to be taught to the
patient and relatives prior to discharge.

REHABILITATION ISSUES
Physiotherapists and occupational therapists continue to work with
the range of motion and muscle tone by providing daily exercise. In
addition to the wound, the other factors which affect outcome is
338 PLASTIC SURGERY MADE EASY
patient compliance, with the physical therapy program. Current
means for the prevention of additional deformities are proper
positioning with splints, exercise to maintain range of joint motion,
and the use of compression garments.
Regular follow-up is required to adjust pressure garments and
splints during the postoperative period.

LONG TERM GOALS


Foot burns should be given a high priority, although it forms a small
component of the TBSA. Burns of the foot can result in disabling
sequelae such as recurrent breakdown of grafts, improper shoe fit,
gait disturbances, prolonged absence from work, and the
development of fixed deformity of the foot. Our goal is to make sure
that our reconstruction provides a sensate cover to enable the foot
to function normally.

CONCLUSION
The ankle and the foot are specialized structures for maintaining
stability. In order to have proper function, these structures must be
stable and capable of bearing weight.
Priority treatment of the foot allows earlier ambulation and
rehabilitation. However, functional impairment processes,
appropriate release of contractures both in the longitudinal and
transverse arches and resurfacing with grafts are appropriate. The
postoperative rehabilitation program is crucial for a successful
surgical outcome. Consequently, patient compliance is the key to
maximizing our outcomes and preventing delayed complications
such as recurrence.

REHABILITATION OF HAND BURNS


INTRODUCTION TO HAND BURNS
These are common injuries caused by contact with various types of
thermal, chemical and electrical injury. The fundamental problem
in all types of burns is loss of skin. The complication and deformity
that follow burns of the volar surface of the hand are different from
THERMAL INJURY 339
the dorsal surface. Because volar skin is thicker, and so conservative
approach will suffice and even if skin graft is required, the problems
are less. Whereas dorsal burns are important as the skin is thin and
re-contractures is common requiring multiple revisions.

FACTS
Goals of treatment are no longer mere survival, but a meaningful
and worthwhile life. Growth spurt warrants repeated surgery.
Importance is given to post surgical program. There are many hurdles
in rehabilitation like poor compliance, no regular follow-up, non-
availability of splints and garments, hot climate and financial
constraints. To overcome these hurdles immediate rehabilitative
intervention with proper positioning using splints, exercise to
maintain range of motion in joints, maintenance of muscle strength
and muscle tone, and early mobilization are required. Great
prognosis has been made between the understanding of burn
wound and its impact on the function of the hand.

PATHOLOGY OF HAND BURNS


Following burns, the increased capillary permeability results in
outpouring of protein rich fluid, which soaks collateral ligaments of
small joints, connective tissue around tendons and broad expansion
of extensor mechanism. Even at this stage motion can prevent fibrous
fixation, but if immobilization continues, new collagen forms along
fibrin template and previously gliding surfaces become incarcerated
in a non-yielding fibrous cicatrix. Finally the collagen synthesis and
remodeling causes stiff joints.
The collateral ligaments of the MCP joints (shortest in the
extended position) become infiltrated with unyielding collagen, so
that they appear fat and short and unable to lengthen sufficiently to
allow the articular surface of the proximal phalanx to radiate around
the MC head. Moreover flexor tendons encased in a fibrous sheath
may be robbed of independent action by formation of inter-
tendinous adhesions.
340 PLASTIC SURGERY MADE EASY
CONTRIBUTING FACTORS TO POST BURN DEFORMITY
• Edema
• Wound infection
• Poor positioning
• Prolonged immobilization
• Delayed skin cover

AIM OF TREATMENT
One must realize that burn rehabilitation is the most important
aspect of burn care. The therapist’s role in the burn unit starts on the
day of admission and continues throughout hospitalization and
maintained during the prolonged convalescence almost for a period
of upto 2 years:
• To reduce edema and maintain range of movement
• To prevent deformity from contractures by correct positioning
and use of splinting
• To minimize scarring by using pressure technique
• To improve muscle strength.

CLASSIFICATION OF HAND DEFORMITY


A. Soft tissue deformity
Volar contracture
Dorsal contracture
Web space contracture
Adduction contracture (1st web space)
Hypertrophic scars
Contracture band
B. Joint deformity
Metacarpophalangeal joints (clawhand)
Proximal interphalangeal joint (Boutonniere)
Distal interphalangeal joint (mallet)
C. Nail deformity
D. Amputation
E. Complex deformity
THERMAL INJURY 341

FIGURE 13.93: Flexion FIGURE 13.94: Contracture


contracture of hand release with graft from the sole

Soft Tissue Deformity


1. Palmar burns—Are uncommon and easy to correct. Post-
operative pressure garments, silicone elastomere moulds and
splints are required to increase pressure on the palm and prevent
recontractures.skin graft from the sole will be ideal with perfect
color match (Figs 13.93 and 13.94).
2. Dorsal burns—when burn scars exist only on the dorsum of
the wrist, hand and forearm an extension deformity to the wrist
results. Skin graft is the best option (Figs 13.95 to 13.103).
3. Web spaces—Web space contractures and post burn
syndactyly involve only skin and are corrected by some form of
local tissue rearrangement. It is also necessary to provide
additional contoured pressure either underneath the glove using
silicon elastomere or on top of pressure gloves using web spacer
(Figs 13.104 and 13.105)
342 PLASTIC SURGERY MADE EASY

FIGURE 13.95: Dorsal contracture FIGURE 13.96: Dorsal


contracture release

FIGURE 13.97: Dorsal contracture FIGURE 13.98: MP extension


release with graft and IP flexion contracture

FIGURE 13.99: Post MP and FIGURE 13.100: Hyperextension


IP correction contracture
THERMAL INJURY 343

FIGURE 13.101: Post- FIGURE 13.102: Wrist flexion contracture


hyperextension deformity
correction

FIGURE 13.103: Wrist flexion release FIGURE 13.104: First web


with graft space contracture

Grading
Based on the distance the scar band extends along the length of
involved fingers, web space contractures can be graded as:
Grade I—extends upto 1/4th of the distance from MP to the PIP
joint
Grade II—upto one ½
Grade III—upto ¾
Grade IV—greater than ¾
344 PLASTIC SURGERY MADE EASY

FIGURE 13.105: Four flap release of FIGURE 13.106: Contracture


first web space band

4. Adduction contracture of the thumb


Involves muscle fibrosis, typically this occurs in the adductor
muscles of the first web space. To obtain a useful release some
fascia and muscle tissue will have to be divided. This contracture
is often associated with hyperextension at the MCP joint.
Contracted fascia, fibrous muscles and a luxated carpometacarpal
joint cause more serious problems. Superficial fascia over the
first dorsal interosseous and the adductor pollicis muscle is
contracted. Treatment is excision of fascia to release adduction
contracture.
5. Hypertrophic scar—wounds that heal from deep dermal
elements on the dorsal surface of the hand tend to develop bad
hypertrophic scars, which may deteriorate as scarring worsens.
So it is better to try to achieve a healed wound as swiftly as
possible.
6. Contracture band—A scar band can occur at any place
depending on the location of the scar. (Fig. 13.106)
THERMAL INJURY 345

Joint Deformity
1. MCP—Metacarpophalan-
geal joint (Clawhand)
• This is a typical deformity
resulting from unoppo-
sed contracture from a
dorsal hand burn
• MP joint extend due to
shortening of the colla-
teral ligaments associated
with edema and scar
formation
• PIP joint flex due to
stronger flexor tendons
• Wrists assume a position
of flexion FIGURE 13.107
• Distal DIP joints assume a flexed position.
Clawhand is due to contracted collateral ligaments. Collateral
ligaments arise from a tubercle near the dorsal surface of the
head of the metacarpal and pass obliquely down to a similar
tubercle near the volar surface of the proximal phalanx. The
distance between origin and insertion is most short during MCP
joint extension and most long as the joint is flexed to allow the
proximal end of the phalanx to sweep around the long curved
articular surface of the metacarpal head.
2. PIP—Proximal Interphalangeal joint (Boutonniere defor-
mity)
A stiff deeply burned PIP joint is unsuitable for tendon or joint
reconstruction. There is disruption of the central extensor slip.
Reconstruction of the extensor mechanism is needed. This
deformity results from either a disruption of the central slip of
the extensor mechanism or attenuation of transverse fibers of
the dorsal hood over the IP joint allowing the lateral band to
slip below the axis of rotation of IP joint. When this happens the
main force of extension transmitted through the lateral bands is
pulling below the axis of rotation of the joint producing flexion
of the joint. Arthrodesis in about 60 degree of flexion is a reliable
functional option.
346 PLASTIC SURGERY MADE EASY
3. DIP—Distal interphalangeal joint (Mallet)
Complete division of the terminal tendon beyond the insertion
of the oblique retinacular ligaments results in a mallet finger.
The distal phalanx is flexed at the DIP joint and cannot be
extended actively even with active extension of the PIP Joint.

Nail Deformity
Dorsal digital burn contractures cause unsightly eponychial retraction
and proximal nail exposure. These areas are subject to break down
with minor trauma. Reconstruction is by releasing the skin proximally
and recreating the fold and placing either a graft or flap.

Amputation Deformity
Common in patients with extensive burns. The fingers and thumb
can be effectively lengthened by deepening the web spaces,
phanlangization or pollicization.

TREATMENT
1. Non-surgical
2. Surgical
Intensive rehabilitation programs are extremely important during
the acute and reconstructive period to prevent severe deformities.
Maintain position of function (wrist extension of 30 degrees, MCP
in 90 degrees, and PIP joint in extension, thumb abducted and
opposed) along with early range of motion is necessary for a
functioning hand.

Nonsurgical Approach to Burn Reconstruction


• Compression
Elastic bandages (ace wrap)
Tubular bandages (tubi grip)
Readymade garments (jobst)
• Silicone gel sheet
• Steroid injections
• Masks
• Splints
THERMAL INJURY 347
Surgical
In spite of all these, if contractures do occur, then surgical intervention
is the only other option.
a. MCP joint stiffness—Dynamic splinting—knuckle bender
Operation—capsulotomy and collateral ligament excision
b. Interphalangeal joint—If disorder is due to extensor or
intrinsic tendon mechanism, arthrodesis in good position is all
that can be offered.
c. Attenuation of the extensor mechanism—Elevation of
volar displaced lateral bands is performed when extension of
PIP joint is week which is due to disruption of central slip of
extensor mechanism.

SPLINTING AND PHYSIOTHERAPY FOR THE BURNED HAND


Heat therapy, active and passive motion, dynamic and static splinting,
and other forms of physiotherapy are helpful only when the hand
has been released.
Maintenance of function in a burned hand can be achieved by
a carefully planned and supervised program of physical therapy
that is initiated upon admission continued throughout hospitalization
and maintained during a prolonged convalescence. Burned hands
are less painful under water which has a calming effect on the
patient as well as a lubricating effect, hence hydrotherapy is important
for easy movements (Figs 13.108 and 13.109).

FIGURE 13.108: Acute burns– FIGURE 13.109: Acute burns–


hydrotherapy treatment hydrotherapy treatment
348 PLASTIC SURGERY MADE EASY

Surgery is only 50% of the course of treatment. Patients should


receive hand therapy twice a day. Splints applied according to
individual needs. Skin care program must be outlined that will
soften grafts and provide lubrication so that cracking and ulceration
does not occur. Splints should be worn at night to maintain the
gains achieved during the day.

PRESSURE THERAPY FOR SCAR MANAGEMENT


There are various ways to apply local pressure to burn scars, pressure
therapy helps to reduce edema, diminish discomfort and itchy
problems and helps in scar maturation.
Ace wrap, coban, tubigrip, interim garments, silicon inserts,
and silicon gel are examples.

SUMMARY
• Role of OT/PT is to use a variety of therapeutic intervention in
order to promote a return to maximum independent living
• Management of burned hand represents a fascinating concept
of wound healing
• Multiple techniques are available with superior results
• The challenges have peaked
• Results have steadily improved
• Choice of correct modality of treatment remains the greatest
challenge.

ROLE OF COSMETICS IN BURN PATIENTS


The survival rate following extensive burns have increased and the
reconstructive techniques have significantly altered the appearance
by using the various nonsurgical and surgical methods. However,
the surgical disadvantages are many and limit aesthetic
reconstruction.
Face is the most important form of nonverbal communication
and in facial burns it may alter this form of communication. Our
goal is to minimize the psychological impact of the burn injury,
promote social rehabilitation and minimize visible scars. Cosmetic
THERMAL INJURY 349
therapy should become an integral part of overall management to
aid in patient’s wellbeing.

Nonsurgical
• Pressure garments
• Splinting
• Silicone conformers
• Moisturizing lotion

Surgical
• Scar excision
• Skin grafts
• Local flaps
• Tissue expansion
• Free flaps

Surgical Disadvantage
• Limited by available local tissue
• Poor color match
• Indistinct planes
• Scarring
• Pigmentation differences

Goals
• Minimize the psychological impact of burn injury
• Promote social rehabilitation
• Minimize visible scars
Cosmetic therapy should become an integral part of overall
management to aid in patient’s wellbeing.

Cosmetic Camouflage
Application of make up conceals scars and pigmentation changes.
Has no gender or racial limitation. Hypopigmented scars are
camouflaged with concealing creams (Figs 13.110 to 13.113).
Hyperpigmented skin grafts can also be treated by using bleaching
creams (Fig.13.114).
350 PLASTIC SURGERY MADE EASY

FIGURE 13.110: Hypopigmented FIGURE 13.111: Cosmetic


patches camouflage

FIGURE 13.112: Hypopigmented FIGURE 13.113: Cosmetic


patch palmar surface camouflage

FIGURE 13.114: Hyperpigmented


skin
THERMAL INJURY 351
Characteristics of Ideal Cosmetic
• Natural looking, opaque
• Easy to apply, waterproof
• Long lasting, fragrance free
• Available for use by all skin types
• Hypoallergenic and non-carcinogenic

Medical Make-up Specialist


• Knowledge of color blending and proper application
• Communicate well with patients
• Determine cosmetic needs of a patient in a sensitive and
nurturing way.

Camouflage Technique
Subtle Concealment
• Application of cosmetics confined to the lesion
• Advantages—less time consuming
• Pitfalls—color blending should be perfect to match the
surrounding skin.

Full Concealment
• Application of cosmetics extending beyond the boundaries of
the lesion
• Advantages—uniform color
• Pitfalls—time consuming and can give an unnatural appearance

Color Blending
• Select cream to match skin color
• Complimentary color helps to mask a particular skin problem

Key to Successful Make-up


• Perfect color blending
• Limit the number of products applied
352 PLASTIC SURGERY MADE EASY
Types of Make-up
• Foundation
• Corrective cosmetics
• Setting powder
• Compact powder
• Regular cosmetics
A. Foundation: Pigmented products invented in 1936 in the form
of cake make-up
Advantages
• Available for use by all skin types
• Good coverage
• Velvety look
Disadvantages
• Time consuming
• Rubbed off easily
• Stains clothes
• Not waterproof
B. Corrective make-up: Available in the early 1980’s for medical
community. They have a high concentration of pigments.
Advantages
• Opaque
• Waterproof
• Applied only over the lesion
• Natural look
Disadvantages
• Rubs off easily
Setting powder: Translucent colorless powder necessary to
stabilize corrective cosmetics.
Advantages
• Prevents smearing and rubbing off
• Long lasting
• Rub resistant
• Colorless
Disadvantages
• Time consuming
THERMAL INJURY 353
Compact powder: Pigmented powders and has the ability to
allow facial products to remain in place.
Advantages
• Absorbs oil and perspiration
• Imparts a non-shiny natural finish
• Smooth appearance
Disadvantages
• Need to use throughout the day to freshen the make-up
C. Regular cosmetics
Advantages
• Blush adds vitality to cheeks
• Lipstick adds color to lips
• Eye make-up enhances orbital region
Disadvantages
• They can never conceal defects
Benefits
• Restores confidence and self-image
• Survivors reintegrated into society
• Reintegration into society is a testimony to the beneficial
effects of cosmetics on improving the psychological outlook
of patients.

CONCLUSION
• Cosmetics is a useful adjunct to surgical intervention
• Lessens the impact of visible scars and pigmentation differences
• Enhances self-image and confidence.

PSYCHOSOCIAL REHABILITATION OF BURN SURVIVORS


Many people get afflicted with burns either by accident or injury.
These survivors experience great physical and psychological trauma.
Scarred figures and faces speak volumes of pain, despair and
loneliness, but their tales of struggle, woes and cares often go un-
noticed.
354 PLASTIC SURGERY MADE EASY
Many burn survivors fear being scorned or rejected and
sometimes begin to hide themselves in a world of their own.
Integrating back into society is difficult, and for many being accepted
by their own family members is a struggle.
An individual who has a positive self-esteem and has received
positive feedback from others has the advantage of falling back
upon these past experiences in life to overcome the situation. At the
time of injury every burns victim needs support, encouragement
and guidance for accepting his or her disability.
The extent of physical, emotional and psychological trauma is
dependent upon a number of factors, these include the kind of
burns inflicted, visibility and the invisibility of the disfigurement, the
way the patient gets burnt (accidental, inflicted by self, caused by
others) and the age of the individual. It is necessary that the burn
survivors be supported in accepting their new body image.
Most important of all burn survivors must be assisted to discover,
recognize and affirm their strengths and focus upon them. One
method of help is to increase sense of self-worth is through the
organization of self-help groups. These are informal groups run by
members who share a common illness or handicap.
Self-help groups provide the patients the experience of knowing
that they are not alone in their struggle. This helps them ventilate their
feeling of fear, anger and loneliness in a non-threatening atmosphere
and helps provide them the opportunity to learn practical coping
skills from the positive role models (i.e. those who have survived
accepted and are coping effectively despite their disability illness).
Families and spouses of the burn survivors also need support
and guidance and they can also be included in the self-help groups.
In some cases it becomes necessary to provide them individual
counseling to enable them to get over their psychological trauma
and to regain their emotional strength to face life effectively.
It is necessary to approach the pain and suffering of burn
survivors with sensitivity and strength. A great deal of emotional
support must be provided to help them to alleviate their fears,
anxieties and doubts throughout the rehabilitation period.
Therefore, one of the primary humanitarian duty of every individual
is to help the burn survivors to have hope and faith in the future
and to make them realize the gracious gift of a second life.
THERMAL INJURY 355

PREVENTION AND FIRST AID


MANAGEMENT OF BURNS
INTRODUCTION
Burn injuries are universal and incidence is on the increase with the
complexities of modern living and industrialization, since most of
the burns occur either at home or at the place of work. It becomes
important to know about Burn Prevention and First Aid
Management.
Burns is caused by a variety of agents like flame, hot liquids,
chemical and electrical. The priority of treatment is to stop the burning
process by using tap water, which reduces the severity in all types of
burns except electrical.
1. What causes burns?
Burns can be caused by flame, acid, hot liquids and electricity.
2. What to do immediately following burns?
Priority is to stop the burning process by using tap water
3. Can water cause blisters?
No. Blisters indicates that burns are superficial and will heal
spontaneously.
4. What to apply on the burnt surface?
Apply ointments like Neosporin, Soframycin, Silver sulfa-
diazine. Do not apply gention violet, ink, ghee, calamine, lotion,
salt, toothpaste etc.
The most effective course of action with regard to burns is to
prevent it from happening.

DO’S
• Pour water to stop the burning process
• If no water, stop, drop and roll.

DONT ‘S
• Do not play with matches, kerosene, fire cracker and electricity
• Do not pour kerosene or petrol to revive fire
• Do not leave gas inlet open when not in use
356 PLASTIC SURGERY MADE EASY
• If gas leak is suspected in the kitchen do not strike a match or
put the electric switch on, or smoke. Open the windows and
tighten all gas valves. If it is still leaking call gas company
• Do not use loose pressure cooker rubber (casket)
• Do not carry hot water on a slippery floor
• Never leave a child unattended in the bathroom
• Do not keep open fire near the bed on a winter night
• When you go on long leave, disconnect the plug of radio,
television and other electrical appliances
• Do not allow children near hot silencer
• Do not keep the test tube close to your face in Chemistry lab.

AVOID
• Avoid cooking on floor level
• Avoid leaving unattended hot liquids
• Avoid children playing in the kitchen
• Avoid wearing loose garments in the kitchen
• Avoid storing cooking materials across the stove
• Avoid using sari to handle vessels
• Avoid bending over the flame to put out fire
• Avoid keeping stove/candle near gas cylinder
• Avoid carrying hot things while children are around
• Avoid keeping mosquito coil near the bed
• Avoid open plug point
• Avoid live wires
• Avoid open bathrooms if immersion rod is used to heat water.

SMOKING
• Do not smoke in bed
• Do not throw matches/cigarette butts carelessly
• Do not smoke near flammable liquid or gases.

FLAME BURNS
• Remove the victim from the site of fire
• Pour water to cool the burning process
THERMAL INJURY 357
• Do not allow them to run as this adds oxygen to fire and increases
the flame
• Flames are either put out by water or smothered by rolling on
the ground or wrapping in a blanket which is removed as soon
as the fire is put out because it tends to retain heat.

SCALD BURNS
Hot water, milk, tea, oil spilling accidentally are the common causes
of burns in Indian kitchen. Hot liquid burns are very common in
children and is due to knocking of hot liquid onto them or by
stumbling onto a burning agent.
How to avoid—Keep children away from the kitchen, avoid using
tablecloth.
Treatment—Soaked clothes should be immediately removed and
cold water poured over the injured areas, apply ointments like
Neosporin.

ACID BURNS
Acid burns occur in laboratories and at home. They cause full
thickness burns. Immediate first aid management is by removing
the clothes and washing the burned area with copious amount of
water. (At least 20-30 minutes of washing is necessary to dilute the
chemicals). Take the patient to the hospital immediately.

ELECTRICAL BURNS
The rescuer must be careful so that he does not become a part of the
electrical circuit in attempting to free a person still in contact with a
live wire.
Use dry wood and push the patient away from current source
Keep the electric wire away from the child as they may bite the
live wire.
Take the patient to a hospital.
358 PLASTIC SURGERY MADE EASY
BURNS DUE TO FIRE CRACKERS
Causes serious injury to the eyes, face and hand
Fire works during festivals should be performed in the presence
of adults
During blast injuries sand or gunpowder particles may get
impregnated into the skin, so thorough cleaning of the wound is
mandatory.

CAR FIRE
Engine burning? Turn off ignition
Do not pour water in an empty hot car radiator, wait to cool or
keep the face away from the radiator while pouring water.

GENERAL MEASURES
• Once the patient is burnt
• Put off the fire
• Remove clothes
• Wrap in dry cloth
• Take the patient to the hospital
(Please note speed is not necessary in burns)

PREVENTION
Burn Prevention is the best burn care, burn injuries are physically
and emotionally devastating and a financial nightmare for families
and hospitals, and since most of the burns can be prevented, it is
our responsibility to inform the community about Burn Prevention.
Burn Prevention though not easy, is being designed to increase
awareness of burn dangers and it is hoped that these efforts will
reduce the incidence and severity.
A burn injury can happen to any one, so the best thing is to
prevent the injury. Secondly it takes only a moment for a tragic
accident to occur, but the effect lasts a lifetime. So take care of yourself
and those you love by being burn aware.
THERMAL INJURY 359
BURN UNIT
The concept of specialized burn unit was started in the USA some
50 years ago, along with it the importance was also given to medical
technology provided by multispeciality and multidisciplinary teams.
Burn unit is a specialized area within the hospital with a
specialized nursing team dedicated to burn patient care. If possible
burn unit should be part of a teaching hospital with ICU facility. It
should be staffed by a team of professionals with expertise in the
care of burn patients and includes both acute care, reconstruction
and rehabilitation. A burn team should also provide educational
programs regarding burn care to all health care providers and involve
in research related to burn injury.
The cost of running a burn unit is enormous. The overall design
of burns unit will depend on the required size and available finance.
The principles of prevention of infection in the burn unit are
more important than airborne spread. Handwashing is, therefore,
more important than complex air conditioning. Well-ventilated single
bedded rooms with ICU standards, monitoring and life support
equipment and above all a wash basin adjacent to the bed to wash
hands before and after touching the patient.
A burn unit will be treating patients in various stages of recovery
and all will not require the same level of care. It is, therefore,
important to have separate 4 ICU beds for very sick patients requiring
high dependency care, about 6 beds in a separate area for superficial
burns requiring less care and about 10 general beds for burn
reconstruction.
A good burn unit should be designed to provide the following:

FIRST FLOOR
1. Reception room
2. Prayer room
3. Maintenance department
4. Electrical department
5. Psychology department
6. Rehabilitation unit
7. Medical records
360 PLASTIC SURGERY MADE EASY
8. Photography department
9. Toilet for visitors
10. Elevators

SECOND FLOOR
1. Acute care ward with 4 beds having wash basins in the
rooms.The attached bathrooms preferably should have a
door outside to take all dirty linen, dirty dressings, bedpan
and other unsterile itmes, to prevent them from entering the
clean burn rooms. TV for entertainment.
2. Receiving room with resuscitation arrangement
3. Dressing room for patients attached with bathrooms to give
bath to the patients, for easy removal of dressing and so on
4. Nurses station with central monitoring equipments
5. Full laboratory
6. Blood bank
7. Main operation theater with changing rooms, Scrub rooms,
Recovery room, Launge for doctors, nurses and technicians,
Rest rooms and Bathrooms with shower
8. Pharmacy
9. Respiratory department
10. Laundry
11. Rest room for Doctors, Nurses and Technicians
12. Waiting rooms for relatives
13. Store rooms to store linen, dressing materials, IV fluids and
drugs
14. Playroom for children

THIRD FOOR
1. Reconstructive unit
2. Outpatient clinic rooms for the reconstructive patients
3. Library
4. Conference room
5. Seminar room
6. Dietary
7. Offices
THERMAL INJURY 361

IN SUMMARY
• A burn unit should be part of a teaching hospital
• Rooms should be spacious with wash basins in each room
• Dressing and operating rooms for small procedures
• ICU facility in all the rooms
• A well ventilated room large enough to have a bed with fittings
for IV stand, bed side table, chair for the patient, dressing table
and enough space to have a emergency ventilator and other
accessories.
Chapter 14

Aesthetic Surgery
364 PLASTIC SURGERY MADE EASY
The word cosmetic was derived from the word “cosmos” that is a
well organized system of universe (Opposite of cosmos is chaos).
Cosmetic was used to describe the nature of substances which had
the power to beautify the person especially the complexion. The
concept of cosmetic surgery derives from the Greek word
“cosmatikos” meaning to arrange or to add beauty. It is a branch of
surgery which concerns itself with the improvement of appearance
by the alteration of features.
It is said that the human face is an index of the human personality.
The face emotionally and functionally has one of the most important
part to play in a man’s personal and social life. Cosmetic procedures
have a greater part to play in restoring the confidence and personality
of a patient. Cosmetic surgery should be skillfully and artistically
applied to selected patients.
Commonly performed aesthetic surgical procedures are:
• Rhinoplasty—Incision is made inside the nostril for reshaping
the cartilage and bone
• Breast—Augmentation to increase the size of the breast using
Implant
• Reduction mammoplasty—to reduce massive enlargment of
breast tissue
• Mastopexy—Reshaping and lifting ptotic breast (hanging breast)
• Abdominoplasty—Tightening abdominal wall
• Liposuction—to remove excess fat.

RHINOPLASTY

Anatomy—The nose consists of paired nasal bones, paired upper


lateral cartilages and paired alar cartilages. Septum consists of
quadrangular cartilage, perpendicular plate of ethmoid, vomer,
perpendicular plate of maxilla and palatine bone.
Incisions—Rim, transcartilaginous, transfixion and inter-cartilagi-
nous.
Grafts—Rib, Iliac bone or calvarial bone.
Rhinoplasty is performed for depressed nose (Figs 14.1 to
14.6) using rib graft and iliac bone graft.
AESTHETIC SURGERY 365

FIGURE 14.1: Depressed nose FIGURE 14.2: Augmentation


rhinoplasty with rib graft

FIGURE 14.3: Severe FIGURE 14.4: Augmentation


depressed nose rhinoplasty with Iliac bone graft
366 PLASTIC SURGERY MADE EASY

FIGURE 14.5: Mild depression FIGURE 14.6: Augmentation


of nose using rib graft

Septorhinoplasty is done for gross deviation of the nose (Figs


14.7 to 14.12).
Implant—Nasal implants are also used for augmentation.

BREAST
Anatomy—Breast extends from the 2nd to the 6th rib and from
sternal edge medially to midaxillary line laterally. Nipple is located
in the fourth intercostal space.
Blood supply is from internal mammary artery, lateral thoracic
artery and intercostal perforators. Nerve supply is from intercostal
nerves.
AESTHETIC SURGERY 367

FIGURE 14.7: Deviated nasal FIGURE 14.8: Postoperative


septum correction of DNS

FIGURE 14.9: Worm’s eye view FIGURE 14.10: Postoperative


showing DNS septorhinoplasty
368 PLASTIC SURGERY MADE EASY

FIGURE 14.11: DNS FIGURE 14.12: Postoperative


septorhinoplasty

Breast augmentation—preoperative assessment of the type and


size of implant should be made. Commonly used implant is textured
(as capsule contracture is less). It can be either saline filled or silicone
gel filled. It can be placed either submuscular or subglandular (Figs
14.13 and 14.14).

FIGURE 14.13: Underdeveloped FIGURE 14.14: Post augmentation


breasts with breast implant

Incisions used can be inframammary, axillary and peri-areolar


(Fig. 14.15).
Complications are hematoma, seroma, infection, asymmetry
and implant rupture.

Reduction Mammoplasty
• Large breasts are both an emotional and physical burden (Fig.
14.16)
AESTHETIC SURGERY 369

FIGURE 14.15: Side view showing FIGURE 14.16: Virginal


the projection hypertrophy of breast

• Patients are self-conscious because of looks and comments


• In an effort to minimize her breast appearance a women may
have poor posture and try to wear tight restrictive brassiers
• Commonly seen in pubertal period due to virginal hypertrophy
• It causes pain in the shoulder and back with numbness of fingers
• Irritation and maceration of inframammary region
• Severe psychological problems
Surgery is performed by using the inferiorly based technique.
Breast is reduced to acceptable size keeping in mind the breast
function, lactation and sensation (Figs 14.17 to 14.23).
Complications are
Loss of nipple sensitivity
Necrosis of skin and fat
Hematoma
Inability to breastfeed
Infection

FIGURE 14.17: Lipoma of breast FIGURE 14.18: Peroperative


370 PLASTIC SURGERY MADE EASY

FIGURE 14.19: Postoperative FIGURE 14.20: Markings for


reduction mammoplasty reduction mammoplasty

FIGURE 14.21: A post reduction FIGURE 14.22: Markings for


mammoplasty reduction mammoplasty

FIGURE 14.23: Postoperative


AESTHETIC SURGERY 371

FIGURE 14.24: Ptotic breast FIGURE 14.25: Postoperative


mastopexy front view

FIGURE 14.26: Preoperative FIGURE 14.27: Postoperative


lateral view lateral view showing projection

Mastopexy—Here the breast is ptotic as it hangs due to loss of


elasticity.
Surgical procedure is by repositioning the breast tissue, reduction
of skin and redraping the skin and positioning the nipple areola
complex at a higher level (Figs 14.24 to 14.27).

ABDOMINOPLASTY
Abdominoplasty is indicated when there is excess skin and fat
resulting in a flabby abdomen.
372 PLASTIC SURGERY MADE EASY

FIGURE 14.28: Flabby abdomen FIGURE 14.29: Postoperative


abdominoplasty preoperative abdominoplasty

Surgical procedures—If the skin is not lax liposuction would be


the ideal procedure. If skin is excess then abdominoplasty either
mini or full abdominoplasty is performed (Figs 14. 28 and 14.29).
Complications are seroma, flap necrosis, infection, hematoma
and scar formation.

LIPOSUCTION
It is a surgical procedure performed to improve the appearance of
the body by aspirating fat. Lipoplasty is excision of excess skin and
fat along with tightening of the fascia. Liposuction can be syringe
type, suction type or power driven.
The solution used as infiltration is known as Tumescent
infiltration which is made up of 2% lidocaine 25 ml, 1:1000
adrenaline 1ml and ringer lactate solution 1000 ml.
At least 20 minutes should be given for the infiltration to act
before the procedure.
Index

A Bilateral gynecomastia 229


Acute management of burns 272 Bilateral syndactyly 236
Adult respiratory distress syndrome Breast 366
anatomy 366
306
blood supply 366
clinical phases of ARDS 306
breast augmentation 368
phase 1 306 Breast and chest wall deformities
phase 2 306 227
phase 3 306 Burn blister 289
phase 4 306 Burn inflammation 288
treatment of ARDS 306 Burn shock 264
cellular 264
infusion 306
hypovolemic 264
perfusion 307 Burn unit 359
ventilation 306 Burn wound 286
Aesthetic surgery 363 Burn wound edema 288
Ameloblastoma (adamantinoma) Burneschar 288
216
age of onset 217 C
clinical features 217 Camptodactyly 237
embryology 216 Causes of burns 261
incidence 216 chemical burns 261
Anatomy of skin 34 electrical burns 261
Angiosomes 40 scald burns 261
Apert’s syndrome 185 thermal or flame burns 261
Assessment of burn injury 261 Characteristics of grafted skin 110
estimating burn depth 261 primary contraction 110
estimating burn size 261 secondary contraction 110
Chemical burns 276
Assessment of nutritional status 312
Cherubism 195
age of onset 195
B clinical features 195
Barter principle 15 etiology 195
Benign jaw tumors 216 Classification of melanoma 92
Benign skin lesions 54 clinicopathological 92
374 PLASTIC SURGERY MADE EASY
acral lentiginous melanoma fat 309
92 protein 309
lentigo maligna 92
mucosal melanoma 92 E
nodular melanoma 93 Ear deformities 210
superficial spreading 92 anatomy 211
Cleft lip 164 embryology 210
anatomy 165 etiology 211
classification 166 Effects of sunlight 16
Balakrishna’s classification acute changes 16
167 sunburn and tanning 16
Davis and Ritchie chronic changes 16
Kernahan and Stark 166 malignant skin lesion 16
Kernahan striped 167 premalignant skin lesion 16
Veau 166 premature aging 16
embryology 164 Electrical burns 272
etiology 164 classification 273
Cleft palate 172 type of injury 273
classification 172 arc burns 174
embryology 172 contact burns 273
etiology 172 flash burns 274
Clinodactyly 237 Epidermal nevus (linear nevus) 64
Congenital melanocytic nevi 64
Cosmetic surgery 2 F
Craniofacial anomalies 185 Facial palsy 209
Craniofacial surgery 2 Faciomaxillary injuries 196
Crouzon’s syndrome 186 treatment of faciomaxillary
Culture derived tissue 303 injuries 196
alloderm 304 delayed treatment 198
epicel 304 early evaluation and
integra 304 treatment 197
Cysts 57 emergency treatment 196
dermoid cyst 57 Factors affecting scar contracture 45
extrinsic factor 46
sebaceous cyst 58
intrinsic factors 45
Fasciocutanoeus flaps 155
D Flap delay 138
Dermabrasion 16 Fluid calculation 283
Dermal lesion 59 first 24-hour 283
Disturbances in metabolism 309 second 24-hour 284
carbohydrate 309 third 24-hour 284
INDEX 375
Fluid resuscitation 279 padgett 107
composition of body fluids 280 zimmer 107
types of fluid 281 Head and neck reconstruction 205
colloid 282 Healing 27
dextran 282
factors delaying wound healing
dextrose 282
30
hypertonic salt solutions
282 general factors 30
Ringer lactate 281 local factors 30
sodium chloride 281 mechanism of healing 28
Frost bite 278 connective tissue matrix
classification 278 deposition 28
first degree 278 contraction 28
fourth degree 278 epithelialization 28
second degree 278
phases of healing 28
third degree 278
freezing 278 inflammatory phase 28
thawing 278 proliferative phase 29
Functions of skin 34 remodeling phase 29
types of healing 27
G delayed primary 27
Genital lymphedema 250 healing of partial thickness
Goals of aggressive nutritional 28
support 311 primary healing 27
Gynecomastia 229 secondary healing 28
Hemangioma vs vascular
H malformations 79
Hair follicle lesions 55 associated deformities 80
Harvesting 107 change over time 79
free hand 107 color 79
goulian 107 texture 79
humby knife 107 time of appearance 79
scalpel 107 Hemifacial atrophy 190
hand driven 107 Hemifacial microsomia 189
drum dermatomes-Reese Hidradenitis suppurativa 63
dermatome 107 Hypertrophic scars 50
padgett dermatome 107 contractubex ointment 51
power dermatome 107 intralesional injection 51
castroviejo 107 pressure therapy 50
376 PLASTIC SURGERY MADE EASY
silicone gel sheet 51 primary lymphedema 244
surgery 51 secondary lymphedema
topical application 51 244
Lymphedema vulva 249
I
Immunological aspect of burn M
injury 287 Macrodactyly 240
Implantation 15 types of macrodactyly 241
progressive type 241
J static type 241
Jackson’s zone of injury 286 Malignant tumors of skin 83
zone of coagulation 287 Management of burn wound 289
zone of hyperemia 286 Maxillary fractures (LeFort) 201
zone of stasis 287 treatment 202
John-Staige Davis 6
LeFort I fracture 202
LeFort II fracture 202
K
LeFort III fracture 203
Kasabach-Merritt phenomenon 76 Maxillofacial surgery 3
Keloids 52
Melanoma 88
clinical classification 89
L
type 1 89
Laser 22
type 2 90
clinical application 22
acne scarring 23 type 3 90
cutaneous pigment 23 clinical features 89
hair removal 23 clinical staging 90
skin resurfacing 23 stage 1 90
tattoo 23 stage 2 90
vascular anomalies 22 stage 3 90
complications of laser 23
etiology 89
Latissimus dorsi flap 153
Limb buds 234 incidence 89
Lipoma breast 60 Methods of surgical wound closure
Lower extremity 239 293
Lower limb arteries 38 Microsurgery 159
Lymphangioma circumscripta 254 Microvascular surgery 2
Lymphatico-venous malformation Muscle flaps 144
74
Muscles of palate 173
Lymphedema 244
classification 244 levator veli palatini 173
INDEX 377
muscularis uvulae 174 Prefabricated flaps 139
palatoglossus 174 Pressure therapy for scar
palatopharyngeus 174 management 348
tensor veli palatini 173 Prevention and first aid manage-
ment of burns 355
N Principles of plastic surgery 7
Necrotizing fascims 52 Psychosocial rehabilitation of burn
Neural tissue lesions 60 surivors 353
Nevus 64 Pterygium colli 218
Nutrition 308
Nutrition requirement 312 R
Curreri formula 312
Rare craniofacial clefts 179
Reconstructive principles area-wise
O
315
Orbital fractures 198
axilla 322
breast 326
P ear reconstuction 317
Panfacial fracture 204 eyelid reconstruction 316
Pectoralis major 152
face 315
Penile lymphedema 250
Physical properties of skin 40 lower extremity 324
Plastic surgery 2 lower lip 321
Polydactyly 236 nasal ectropion 319
Post burn axillary contractures 329 nasal reconstruction 318
classification 330 nasal stenosis 319
group I 330 neck contracture 322
group II 330 oral commissure 321
group III 330
perineal contractures 329
treatment 330
upper lip 321
Post burn reconstruction of feet 332
anatomy of the foot 333 Reconstructive principles in burn
classification 333 cntractures 314
dorsal burn scar Reconstructive principles of lip 214
contractures 333 anatomy 214
plantar surface burn scar goals of reconstruction 215
contractures 334 principles of reconstruction 215
treatment 335 Reconstructive surgery 2
nonsurgical 335 Rehabilitation of hand burns 338
surgical 335
aim of treatment 340
378 PLASTIC SURGERY MADE EASY
classification of hand deformity Sebacious gland lesions 56
340 Septic shock 305
amputation deformity 346 Skin and subcutaneous tissue 33
joint deformity 345 Skin flap 114
nail deformity 346 Skin grafts 102
soft tissue deformity 341
classification 102
contributing factors to post
allograft 102
burn deformity 340
facts 339 autograft 102
pathology of hand burns 339 isograft 102
treatment 346 xenograft 102
nonsurgical 346 types 103
surgical 347 full thickness skin grafts 104
Replantation 15 partial thickness 104
Rhinoplasty 364 split thickness grafts 103
anatomy 364 Skin infections 52
grafts 364 Skin substitutes 298
implant 366 advantages of 298
incisions 364
biological 299
Role of cosmetics in burn patients
allograft 299
348
amniotic membrane 301
Rule of tens—cleft lip 171
Rutes of nutritional support 313 heterografts 300
properties of 298
S types of 299
Scar 42 biological 299
components 45 biosynthetic 299
color 45 collagen-based dermal
contour 45 analog 299
line 45 culture derived tissue 299
types of scar 42 synthetic 299
bevelled scar 44 Speech in cleft palate 178
bridal scar trap door scar 43 Splinting and physiotherapy for the
depressed scar 44
burned hand 347
fine scar 45
Squamous cell carcinoma 86
immature scar 44
Staphylococcal scalded skin
mature scar 44
mismatched scar 44 syndrome 279
step off scar 44 Structure of skin 34
stretched marks 44 dermis 35
surgical or linear scar 44 epidermis 34
INDEX 379

Sunscreen 15 Thermal injury 259


Surgery for metastatic disease 95 Tissue expansion 20
Surgery of the regional lymph node macroscopic response 20
95 microscopic response 20
Sushrutha 5 Toxic epidermal necrolysis 279
Sweat gland lesions 55 Transplantation 15
Syndromes involving vascular Treacher Collins syndrome 191
malformations 78 Treatment of full thickness burn 292
blue “rubber-bleb” neyus (bean) Trochantric pressure sore 255
syndrome 78 Type of burn wound excision 293
Klippel-Trenaunay syndrome 78 Types of flap 117
Maffucci syndrome 78 distant flaps 135
Osler-Weber-Rendu disease 79 pedicle flaps 136
Von Hippel-Lindau disease 79 tubed pedicle flaps 136
Systemic response to local injury 266
local flaps 117
cardiovascular response 266
advancement flap 128
gastrointestinal system 270
hematological changes 269 rotation flaps 117
immune system 270 transposition flaps 118
metabolic nutritional response regional flap 131
270 de-epithelialized flap 132
musculoskeletal system 270 interpolation flap 131
renal 267 island flap 131
high output failure 267 tissue expanded flaps 131
oliguric renal failure 267 Types of wound 26
respiratory system 267 acute wounds 26
chronic wounds 26
T
Tattoos 17 U
camouflage tattoo 19 Ulcer 242
cosmetic tattoo 18 classification 242
decorative tattoo 18
clinical 242
traumatic tattoo 18
pathological 242
Temperomandibular ankylosis 220
Unilateral syndactyly 236
classification 220
clinical features 220 Unique characteristics of face 7
etiology 220 Upper extremity 233
investigation 222 Upper limb artery 37
Tests to reflect perfusion 285
clinical signs 285 V
laboratory 285 Vascular anomalies 68
380 PLASTIC SURGERY MADE EASY
classification 68 Venous malformation of upper lip
biological 72 73
descriptive 68 Venous malformations of the hand
embryological 72 74
Vascular malformations 77
fast flow 77
W
AV malformation 77
slow flow 77 Wound healing 25
capillary malformation 77 Wound sepsis 294
venous malformation 77
Vascularization of the graft 109 X
inosculation 109
neovascularization 109 Xeroderma pigmentosa 80
plasmatic imbibition 109
Velopharyngeal incompetence 177 Z
Venous malformation cheek 73 Zygomatic fractures 200

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