TENDON SURGERY

OF THE HAND
Editor-in-Chief

Jin Bo Tang, MD
Professor of Surgery, Founding Chair, Department of Hand Surgery,
Affiliated Hospital of Nantong University; Founding Chair, The Hand
Surgery Research Center, Nantong University, Nantong, Jiangsu, China

Editors

Peter C. Amadio, MD
Lloyd A. and Barbara A. Amundson Professor of Orthopedics, Consultant,
Department of Orthopedic Surgery, Mayo Clinic, Rochester, Minnesota, USA

Jean Claude Guimberteau, MD

Scientific Director, Aquitany Hand Institute, Pessac, France

James Chang, MD
Chief, Division of Plastic & Reconstructive Surgery, Professor of Surgery
(Plastic Surgery) and Orthopedic Surgery, Robert A. Chase Hand Center,
Stanford University Medical Center, Palo Alto, California, USA

Contributing Editors

David Elliot, MA, FRCS, BM, BCh

Hand Surgery Department, St Andrew’s Centre for Plastic Surgery, Broomfield
Hospital, Chelmsford, Essex, United Kingdom
Judy C. Colditz, OT/L, CHT, FAOTA
HandLab, Raleigh, North Carolina, USA
1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899

TENDON SURGERY OF THE HAND ISBN: 978-1-4377-2230-7

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Library of Congress Cataloging-in-Publication Data

Tendon surgery of the hand / editor-in-chief, Jin Bo Tang ; editors, Peter C. Amadio, Jean Claude
Guimberteau, James Chang ; contributing editors, David Elliot, Judy Colditz. – 1st ed.
   p. ; cm.
  Includes bibliographical references and index.
  ISBN 978-1-4377-2230-7 (hardcover : alk. paper)
  I. Tang, Jin Bo, 1963-
  [DNLM:  1.  Hand–surgery.  2.  Tendons–surgery. WE 830]
  617.5’75059–dc23
2012002534

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 DEDICATION

I dedicate this book to my parents, Cheng Hua Tang and Xiou Feng
Zhao; my wife, Xiao Tian; and my daughter, Yu-Qing. Their support,
understanding, and sacrifice are the most fundamental to my past work
and completion of this book.
I also dedicate this book to my colleagues all past and present members of
the Research Center and the Department. In particular, it is dedicated to
an inspiring professor and tendon enthusiast: Seiichi Ishii, who mentored
me in my first work on tendons.
Jin Bo Tang, MD

This book is dedicated to my wife, Bari, for her continuous emotional

support and understanding; to my clinical colleagues at Mayo Clinic, for
their daily inspiration and for their generosity in accommodating the
many demands that the creation of this book has required; and to my
many mentors in tendon surgery over the years, especially James M.
Hunter, MD, whose high standards of tendon surgical skill and creativity
I can only hope to emulate.
Peter C. Amadio, MD

I would like to thank two illustrious colleagues, Harold Kleinert and

Claude Verdan, for influencing my way of thinking in tendon surgery
and for lighting the path for me to perform vascularized tendon grafts.
They never wavered in their support for my work, and they encouraged
me to continue investigations.
Jean Claude Guimberteau, MD

I wish to thank my family—James Sr., Lily, Anthony, Barbara, and

Cecilia Chang; Harriet Roeder; and Julia, Kathleen, and Cecilia Roeder
Chang—for their constant love and support. I also wish to honor all the
research fellows, residents, and hand fellows at Stanford who have worked
so tirelessly; and my surgical mentors, Vincent Hentz, Neil Jones, and Roy
Meals, who have taught me so much about the hand.
James Chang, MD
 PREFACE
This book, Tendon Surgery of the Hand, is intended to
address the lack of a comprehensive and up-to-date text-
book on the basic science and clinical practice of tendon
surgery in the hand.
Tendon surgery is one of the most important topics
in hand surgery; its importance to hand function and
its allure to hand surgeons are well-reflected in the vast
number of investigations and publications devoted to
this topic. Surprisingly, however, no comprehensive
book on tendon surgery of the hand (or of other parts
of the body) has been published in the last 25 years,
despite revolutionary changes in the treatment of tendon
injuries and disorders. The only landmark book on
tendons is Hunter’s Tendon Surgery in the Hand, from
1987. Therefore, we organized a group of international
experts in tendon surgery to produce a new volume. The
idea of compiling such a textbook was initiated during
a conference in Manchester, UK, in 2006 and was sub-
sequently reshaped, with updated media technology, by
Elsevier with publication of both print and online
versions.
Since the mid-1980s, the clinical practice of tendon
surgery has evolved considerably, and a great number of
innovative techniques have emerged. They include a
myriad of novel repair techniques, use of new suture
materials, novel tendon sheath and pulley treatments,
vascularized tendon grafts, and the development of
various postoperative rehabilitation methods. With
regard to the basic science, a wealth of new knowledge
has been accumulated. Our knowledge of tendon
biology and biomechanics has increased greatly, and a
number of new research fields—such as gene therapy,
tissue engineering, stem cell delivery, and gene silenc-
ing—have emerged. Advancements in updated clinical
techniques and cutting-edge technologies in the basic
science of tendon surgery are comprehensively summa-
rized in this book.
This book contains a total of 46 chapters (41 print
and online chapters and 5 web-only chapters), orga-
nized in five sections: basic science, primary flexor
tendon surgery, secondary flexor tendon surgery, exten-
sor tendon repair and reconstruction, rehabilitation
of tendon surgery, and the future of tendon surgery.
We have aimed to include a worldwide selection of
iv
investigators, surgeons, and therapists to author the text.
These chapters are contributed by respected surgeons/
investigators from renowned centers and innovative sur-
geons who offer unique and insightful techniques.
It is our essential goal to offer comprehensive cover-
age of international perspectives and techniques cur-
rently used in tendon surgery of the hand. In particular,
the section on primary flexor tendon repair and reha-
bilitation is a genuinely international collaboration,
highlighting methods and protocols of different units;
it is sure to provide readers with an abundance of infor-
mation, allowing them to judiciously plan their own
treatments based on the surgical and post-surgical care
principles described in the chapters. Extensor tendon
injuries are another topic with various treatment options.
Considering the variety of techniques and rehabilitation
protocols currently used, we have planned the related
surgical and rehabilitation chapters to reflect diverse
approaches to the injuries. Further, multiple therapy
protocols were contributed from the leading hand units
across the world; these protocols are published online
to provide the readers with rich and authoritative refer-
ences for deciding on treatment course for extensor
tendon injuries.
We are greatly indebted to the contributors from 15
countries spanning four continents; their high quality
contributions are the cornerstones of this book. Notably,
we should give our earnest gratitude to Dr. David Elliot
and Ms. Judy Colditz, our guest editors. Not only are
both eminent educators with vast experience on tendon
problems—as a surgeon and a therapist, respectively—
but they are also keen editors who have tirelessly devoted
their effort to this book. Dr. Elliot contributed his own
crystallized experience in seven chapters of this book
and also edited a portion of the primary and secondary
repair chapters. Ms. Colditz coordinated and helped edit
the chapters relating to rehabilitation. Furthermore, we
greatly appreciate the surgeons and therapists who con-
tributed therapy protocols in the online appendix and
video clips to enhance the contents of this book.
Finally, we feel obliged to express our appreciation to
the Elsevier staff and editors, especially Dan Pepper,
acquisition editor; Don Scholz, senior content strategist;
Mary Beth Murphy, developmental editor; Heather
 Preface v

Krehling, content development manager; and Brandilyn master key concepts and techniques of tendon surgery
Tidwell, project manager. Without their advice on of the hand and aids in treatment planning of the
content and careful copyediting, it would not have been often worrisome problems relating to the tendon of
possible to accomplish this project. We also give our the hand.
great appreciation to the Elsevier art team for providing
superb color illustrations for this book, helping us Jin Bo Tang, MD
present our readers with a complex surgical topic in an Peter C. Amadio, MD
easily readable way. Jean Claude Guimberteau, MD
We hope that this textbook helps practitioners, James Chang, MD
fellows, residents, and medical students understand or
 CONTRIBUTORS
Roberto Adani, MD
Chief, Department of Hand Surgery, Azienda Ospedaliera
Universitaria Integrata Verona, Verona, Italy
Peter C. Amadio, MD
Lloyd A. and Barbara A. Amundson Professor of
Orthopedics, Consultant, Department of Orthopedic
Surgery, Mayo Clinic, Rochester, Minnesota
Kai Nan An, PhD
Professor of Biomedical Engineering, Department of
Orthopedic Surgery, Mayo Clinic, Rochester, Minnesota
Rohit Arora, MD
Associate Professor of Trauma Surgery, Department of
Trauma Surgery and Sports Medicine, Medical University
Innsbruck, Innsbruck, Austria
Morad Askari, MD
Assistant Professor of Surgery, DeWitt Daughtry Family
Department of Surgery, University of Miami, Miami,
Florida
Joseph Bakhach, MD
Clinical Assistant Professor of Surgery, Plastic and
Reconstructive Surgery Department, Hand and
Microsurgery Department, American University of
Beirut Medical Center, Beirut, Lebanon
Pierre-Yves Barthel, MD
Department of Hand and Reconstructive Surgery,
Emile Galle Surgical Center, CHU Nancy, Nancy,
France
Alexandros E. Beris, MD
Professor in Orthopaedics, Department of Orthopaedic
Surgery, University of Ioannina School of Medicine,
Ioannina, Greece
Nada Berry, MD
Assistant Professor, Department of Plastic Surgery,
Southern Illinois University, Springfield, Illinois
vi
Philip E. Blazar, MD
Assistant Professor of Orthopaedic Surgery, Department
of Orthopaedic Surgery, Brigham and Women’s Hospital,
Harvard Medical School, Boston, Massachusetts
Lance M. Brunton, MD
Assistant Professor of Orthopaedic Surgery, Department
of Orthopaedic Surgery, University of Pittsburgh Medical
Center, Pittsburgh, Pennsylvania
Robert E. Bunata, MD
Assistant Professor, Department of Orthopaedic Surgery,
Bone and Joint Research Center, University of North Texas
Health Science Center, John Peter Smith Hospital, Fort
Worth, Texas
Yi Cao, MD
Fellow, The Hand Surgery Research Center, Nantong
University, Nantong, Jiangsu, China
Francesco Catalano, MD
Associate Professor, Hand Surgery Division, Department
of Orthopedics, Gemelli Hospital of Rome, Catholic
University, Rome, Italy
James Chang, MD
Chief, Division of Plastic & Reconstructive Surgery,
Professor of Surgery (Plastic Surgery) and Orthopedic
Surgery, Robert A. Chase Hand Center, Stanford
University Medical Center, Palo Alto, California
Chuan Hao Chen, PhD
Professor, Department of Anatomy, Bengbu Medical
College, Bengbu, Anhui, China
A. Bobby Chhabra, MD
Charles J. Frankel Professor and Vice Chair, Department
of Orthopaedic Surgery, University of Virginia Health
System, Charlottesville, Virginia

Alphonsus K.S. Chong, MBBS, MRCS(Ed),
MMed(Orth), FAMS
Consultant Hand Surgeon, Assistant Professor,
Department of Orthopaedic Surgery, Yong Loo Lin School
of Medicine, National University of Singapore, National
University Hospital, Singapore
Sean P. Clancy, OTR/L, CHT
Program Coordinator, Hand Therapy, University of
Chicago Medicine, Chicago, Illinois
Judy C. Colditz, OT/L, CHT, FAOTA
HandLab, Raleigh, North Carolina
Monina Copuaco, OTC, CHT
Hand Therapist, Robert A. Chase Hand Center, Stanford
University Medical Center, Palo Alto, California
Massimo Corain, MD
Department of Hand Surgery, Azienda Ospedaliera
Universitaria Integrata Verona, Verona, Italy
Brandon E. Earp, MD
Department of Orthopedic Surgery, Brigham and
Women’s Hospital, Boston, Massachusetts
David Elliot, MA, FRCS, BM, BCh
Hand Surgery Department, St Andrew’s Centre for Plastic
Surgery, Broomfield Hospital, Chelmsford, Essex, United
Kingdom
Andrew E. Farber, DO
South Island Orthopaedic Group, Cedarhurst, New York
Felicity G.L. Fishman, MD
Department of Orthopaedic Surgery, Duke University,
Durham, North Carolina
Kristen E. Fleager, MD
Department of Orthopaedic Surgery, Stanford University
Hospital and Clinics, Stanford, California
Markus Gabl, MD
Department of Trauma Surgery and Sports Medicine,
Medical University Innsbruck, Innsbruck, Austria
Leesa M. Galatz, MD
Associate Professor, Shoulder and Elbow Service,
Washington University Orthopedics, Barnes-Jewish
Hospital, St. Louis, Missouri
Emily Grauel, MS
Virginia Commonwealth University School of Medicine,
Richmond, Virginia
Contributors vii
Robert R.L. Gray, MD
Assistant Professor, Department of Orthopaedic Surgery,
Miller School of Medicine, University of Miami, Miami,
Florida
Heather Griffiths, mscot(regnb), CHT
Certified Hand Therapist, Horizon Health Network,
Moncton, New Brunswick, Canada
Jean Claude Guimberteau, MD
Plastic, Hand Surgeon, Aquitany Hand Institute, Pessac
France
Hiroyuki Kato, MD, PhD
Professor and Chairman, Department of Orthopaedic
Surgery, Shinshu University School of Medicine,
Matsumoto, Japan
Ioannis Kostas-Agnantis, MD
Department of Orthopaedic Surgery, University of
Ioannina School of Medicine, Ioannina, Greece
Armin Kraus, MD
Division of Plastic and Reconstructive Surgery, Stanford
University Medical Center, Palo Alto, California
Richard D. Lawson, MBBS, FRACS
Director of Hand Surgery Research, Department of Hand
Surgery and Peripheral Nerve Surgery, Royal North Shore
Hospital, University of Sydney, Sydney, Australia
Fraser J. Leversedge, MD
Assistant Professor, Co-Director, Duke Hand and Upper
Extremity Surgery Fellowship, Department of Orthopaedic
Surgery, Duke University, Durham, North Carolina
Beng-Hai Lim, MD
Center for Hand and Reconstructive Microsurgery
(CHARMS), Singapore
Paul Y. Liu, MD
Clinical Professor and Chair, Department of Plastic
Surgery, Brown University Alpert Medical School,
Providence, Rhode Island
Marios G. Lykissas, MD
Division of Orthopaedics, Cincinnati Children’s Hospital
Medical Center, Cincinnati, Ohio
Mollie O Manley, MD, MS
Department of Orthopedics, University of Pittsburgh
Medical Center, Pittsburgh, Pennsylvania
viii Contributors
Michel Mansat, MD
Professor of Orthopedics and Traumatology, Department
of Orthopaedics and Traumatology, Toulouse University
Hospital, Toulouse, France
Pierre Mansat, MD, PhD
Professor of Orthopedics and Traumatology, Department
of Orthopaedics and Traumatology, Toulouse University
Hospital, Toulouse, France
Renzo Mantero, MD
Professor, Former Chief of Hand Surgery (Retired),
Ospedale San Paolo, Savona, Italy
Daniel P. Mass, MD
Professor of Surgery, Department of Orthopaedic Surgery,
University of Chicago, Chicago, Illinois
Antonio Merolli, MD, FBSE
Assistant Professor, Department of Orthopedics,
Universita Cattolica del Sacro Cuore, Rome, Italy
Arash Momeni, MD
Division of Plastic and Reconstructive Surgery, Stanford
University Medical Center, Palo Alto, California
Steven L. Moran, MD
Professor and Chair of Plastic Surgery, Professor of
Orthopedics, Division of Hand Surgery, Mayo Clinic,
Rochester, Minnesota
Nash H. Naam, MD, FACS
Clinical Professor, Plastic and Reconstructive Surgery,
Southern Illinois University and Southern Illinois Hand
Center, Effingham, Illinois
Lori Niemerg, OTR/L, CHT
Certified Hand Therapist, Department of Working Hands,
Southern Illinois Hand Center, Effingham, Illinois
Fiona H. Peck, MCSP
Burns and Plastic Surgery Department, Wythenshawe
Hospital, Manchester, Great Britain
Yeong-Pin Peng, FRCS
Department of Hand and Reconstructive Microsurgery,
National University Hospital, Singapore
Karen M. Pettengill, MS, OTR/L, CHT
Clinical Coordinator, NovaCare Hand and Upper
Extremity Rehabilitation, Springfield, Massachusetts
Brian C. Pridgen, BS
Department of Plastic and Reconstructive Surgery,
Stanford University Medical Center, Palo Alto, California
Mark A. Rider, MBChB, FRCS, FRACS
Department of Hand Surgery, SW Sydney Regional Hand
Institute, Sydney, Australia
Lorenzo Rocchi, MD
Hand Surgery Division, Department of Orthopedics,
Gemelli Hospital of Rome, Catholic University, Rome, Italy
Mario Igor Rossello, MD
Professor, Chief of Hand Surgery, Ospedale San Paolo,
Savona, Italy
Serge Rouzaud
Physiotherapist, Institut Aquitain de la Main, Bordeaux,
France
Michel Saint-Cyr, MD, FRCS(C)
Associate Professor, Department of Plastic Surgery,
University of Texas Southwestern Medical Center at
Dallas, Dallas, Texas
Robert Savage, MB, FRCS, FRCS Ed Orth, MS
Trauma and Orthopaedic Department, Royal Gwent
Hospital, Newport, Gwent, Great Britain
Ton A. R. Schreuders, PT, PhD
Rehabilitation Medicine, Erasmus University Medical
Center, Rotterdam, the Netherlands
Ombretta Spingardi, MD
Hand Surgery Department, Ospendale San Paolo,
Savona, Italy
Yu-Long Sun, PhD
Assistant Professor of Biomedical Engineering,
Department of Orthopedic Surgery, Mayo Clinic,
Rochester, Minnesota
Jun Tan, MD
Associate Professor of Surgery, Department of Hand
Surgery, Affiliated Hospital of Nantong University,
Nantong, Jiangsu, China
Jin Bo Tang, MD
Professor of Surgery, Founding Chair, Department of
Hand Surgery, Affiliated Hospital of Nantong University;
Founding Chair, The Hand Surgery Research Center,
Nantong University, Nantong, Jiangsu, China
Luigi Tarallo, MD
Department of Orthopaedic Surgery, Azienda Ospedaliera
Universitaria Policlinico Modena, Modena, Italy

Shian Chao Tay, PhD
Associate Professor, Department of Orthopaedic Surgery,
Associate Professor, Department of Biomedical
Engineering, Washington University, St. Louis, Missouri
Stavros Thomopoulos, PhD
Associate Professor, Department of Orthopaedic Surgery,
Washington University, St. Louis, Missouri
Michael A. Tonkin, MD, FRCS Ed Orth, FRACS
Professor of Hand Surgery, Head of Department,
Department of Hand Surgery and Peripheral Nerve
Surgery, Royal North Shore Hospital, Sydney Medical
School, University of Sydney, Sydney, Australia
Ghislaine Traber-Hoffmann, MD
Department of Ophthalmology, University Hospital
Zurich, Zurich, Switzerland
Shigeharu Uchiyama, MD
Associate Professor, Department of Orthopaedic Surgery,
Shinshu University School of Medicine, Matsumoto, Japan
Véronique van der Zypen, BSC PT
Certified Hand Therapist, Department of Orthopaedic,
Plastic and Hand Surgery, Division of Hand and
Peripheral Nerve Surgery, Inselspital, University of Bern,
Bern, Switzerland
Robert J. van Kampen, MD
Department of Plastic, Reconstructive and Hand Surgery,
University Medical Centre, Utrecht, the Netherlands
Gwendolyn Van Strien, LPT, MSc
Director, Hand Rehabilitation Consultancy, Den Haag,
The Netherlands, Director, Hand Therapy Unit, Lange
Land Hospital, Zoetermeer, the Netherlands
Contributors ix
Esther Vögelin, MD, PhD
Chief and Codirector, Department of Orthopaedic, Plastic,
and Hand Surgery, Division of Hand and Peripheral
Nerve Surgery, Inselspital, University of Bern, Bern,
Switzerland
Xiao Tian Wang, MD
Assistant Professor, Department of Surgery, Brown
University Alpert Medical School, Providence, Rhode
Island
Ya Fang Wu, MD
Lecturer, The Hand Surgery Research Center, Nantong
University, Nantong, Jiangsu, China
Ren Guo Xie, MD
Associate Professor of Surgery, Vice Chair, Department of
Hand Surgery, Affiliated Hospital of Nantong University,
Nantong, Jiangsu, China
Hiroshi Yamazaki, MD, PhD
Chief, Department of Orthopaedic Surgery, Aizawa
Hospital, Matsumoto, Japan
Jeffrey Yao, MD
Assistant Professor, Department of Orthopaedic Surgery,
Stanford University Medical Center, Palo Alto, California
Chunfeng Zhao, MD
Associate Professor of Orthopedics and Biomedical
Engineering, Department of Orthopedic Surgery, Mayo
Clinic, Rochester, Minnesota
 CHAPTER
1  
ANATOMY OF THE TENDON
SYSTEMS IN THE HAND
Robert J. van Kampen, MD, and Peter C. Amadio, MD
OUTLINE
This chapter describes the anatomy of the flexor and
extensor apparatus in the hand and wrist, supple-
mented with relevant clinical and biomechanical
features. It emphasizes the key importance of the reti-
nacular structures of the wrist and fingers and reviews
both normal anatomy and common variations of the
flexor and extensor tendons in the hand. Special atten-
tion is given to the vincula tendinea and pulleys sup-
porting the flexor tendons in the digital flexor
sheaths—in particular, the structure and biomechanics
of the pulley system. The key role of the A2 and A4
pulleys is emphasized. Finally, a closer look is taken
at the tendons and bands contributing to the extensor
mechanism, and their action on the metacarpophalan-
geal and interphalangeal joints is discussed.
The hand, with the carpus, is the most complex collec-
tion of interconnected joints in the human body, and a
large assembly of tendons carries out its extensive range
of motion. Distinctive groups of muscles execute the
actions of these tendons on the hand. Together with
numerous aiding structures, the tendons form an inge-
nious biomechanical system that gave humans the
ability to perform complicated tasks and develop dex-
terous professions that require sophisticated hand and
finger movement, like hand surgery. Treatment of hand
disorders is similarly delicate and complex; therefore, a
thorough understanding is essential to provide adequate
treatment.
FLEXOR RETINACULUM
On the volar aspect of the wrist, the carpal bones form
a deep excavation over which the flexor retinaculum
arches, creating the carpal tunnel. The tendons of the
flexor digitorum superficialis (FDS) and profundus
(FDP) and the flexor pollicis longus (FPL) pass through
this tunnel together with the median nerve.
This retinaculum inserts on the ulnar side into the
pisiform bone and the hook of the hamate and is
reinforced by the pisiform-hamate ligament. On the
radial side, the retinaculum firmly inserts into the volar
ridge of the trapezium (trapezial tuberosity) and the
tubercle of the scaphoid. Occasionally an insertion into
the styloid process of the radius can be seen.1,2
Controversial terminology surrounds this strong,
fibrous band that crosses the volar side of the carpus.
According to the Terminologia Anatomica, the term flexor
retinaculum carpi should be used. However, in textbooks,
the terms flexor retinaculum, transverse carpal ligament and
anterior/volar annular ligament are used for the same
structure.3
In hand surgery, it is often preferred to distinguish
between the different parts of the flexor retinaculum.
Stecco et al3 investigated its histological and anatomical
features. Continuous with the antebrachial fascia, a
fibrous reinforcement was identified at the volar side of
the wrist. After removal of this layer, another fibrous
layer was found, with strong lamina and histological
similarities to those of a ligament. According to Stecco’s
group,3 “ligament derives from Latin ligare (to bind) and
means a sheet or band of tough fibrous tissue connecting
bones.” They stated that “the role of the pulley for the
tendons of the flexor muscles is assumed above all” for
this deeper layer covering the carpal tunnel, and there-
fore the term transverse carpal ligament was suggested to
be the most appropriate.
In addition to the thickened continuation of the
antebrachial fascia and the transverse carpal ligament,
Cobb et al4 described a third, more distal segment com-
posed of an aponeurosis between the thenar and hypo-
thenar muscles. Based on their anatomical findings,
they advocate a more extensive release when dividing
the carpal ligament.
Tanabe and Okutsu5 endoscopically released the
flexor retinaculum in management of carpal tunnel syn-
drome and found that the mean distance between the
ends of the retinaculum increased from 1.3 mm to 6.6
mm if the distal fibers were also divided. They therefore
concluded that sectioning of the distal fibers is essential
for endoscopic carpal tunnel release.
3
4 Section 1:  Basic Science
EXTENSOR RETINACULUM
On the dorsal side of the wrist, a thickened part of the
deep antebrachial fascia is found, holding the tendons
of the extensor muscles in place. It works in continuity
with the volar carpal ligament and for the previous
stated reasons the term dorsal carpal ligament or posterior
annular ligament could also be suggested. However, the
term extensor retinaculum is most commonly used.
As studied by Taleisnik et al,6 the deep antebrachial
fascia begins to thicken proximal to the radiocarpal
joint and becomes the dorsal annular ligament, a compo-
nent of the extensor retinaculum of the wrist. Distally,
this supratendinous layer is continuous with the pretendi-
nous fascia of the hand. On the ulnar side, it inserts in
three distinct places: proximal around the flexor carpi
ulnaris tendon, the middle part into the triquetrum and
pisiform bone, and distally onto the fascia of the abduc-
tor digiti quinti and base of the fifth metacarpal.
The retinaculum attaches to ridges on the radius,
forming septa that divide the space below the extensor
retinaculum in six compartments through which the
extensor tendons pass. The six compartments are further
described in the section about extensor tendons.
Within the supratendinous layer, at the floor of the
fourth and fifth compartment, lies the infratendinous
layer, from which circular fibers form a tube around the
tendons within the compartments. In the sixth compart-
ment, a duplication of the infratendinous layer forms a
tube around the extensor carpi ulnaris (ECU) tendon
from the ulnar styloid to the triquetrum. This subsheath
stabilizes the tendon along the groove in the distal ulna
and contributes to the stability of the distal radioulnar
joint. Proximally, longitudinal fibers form the linea
jugata that reinforces the tendon to prevent subluxation
during full supination. The ECU subsheath is frequently
injured, typically in young athletes who play racket or
stick sports, which can result in recurrent subluxation of
the ECU tendon.7
FLEXOR TENDONS IN THE HAND
The tendons in the wrist have a relatively constant
arrangement with the median nerve. This arrangement
varies mainly when muscle or tendon anomalies are
present. It is important to keep these variations in mind,
because it can be confusing even for the experienced
surgeon. Usually, the median nerve can be found directly
under the tendon of the palmaris longus. Sometimes,
the nerve lies more superficial, next to the palmaris
longus tendon. The median nerve is also frequently
observed to split in the forearm.8
The palmaris longus tendon lies completely enclosed
in the deep fascia of the forearm between the superficial
veins and cutaneous nerves. The presence of this tendon
is highly variable, as its absence has been reported from
0.6% to 63.9% (either bilateral or unilateral) among
different populations all over the world.9 In humans,
this tendon is seen as rudimentary, and for that reason,
and its easy accessibility, the palmaris longus is often
used as a tendon graft.
To the radial side of the median nerve, the FPL tendon
can be found; to the ulnar side, the superficial flexor
tendons. When coursing through the carpal tunnel the
superficial flexor tendons are arranged in pairs, the
tendons to the middle and ring finger form the superfi-
cial pair, and the little and index finger tendons form
the deep pair. Dorsal to the superficial tendons lie the
flexor profundus tendons.2,8
In the case that the palmaris longus tendon is absent,
the tendon of the flexor superficialis indicis can some-
times be found between the superficial flexor tendon to
the middle finger and the median nerve. In other varia-
tions, the palmaris longus tendon can separate into two
or three tendons, the muscle can be doubled, the muscle
can be reversed or inverted, and partial or complete
insertion in the antebrachial fascia can be seen. Addi-
tionally, insertion into the pisiform bone, scaphoid,
flexor carpi ulnaris tendon, and muscles of the thenar
has been observed.8
Accessory slips for the FDS and FDP are frequently
observed, especially to the index finger. Slips arise from
the ulnar tuberosity to the superficialis tendon of the
index and middle finger, and from the annular ligament
to the superficialis tendon of the little finger. The super-
ficialis tendon to the little and index finger can be absent
and the index finger’s deep flexor tendon can divide into
two tendons or have a shared origin with the FPL.8
The flexor carpi radialis (FCR) tendon courses through
its own synovial sheath that forms a narrow osteofi-
brous tunnel when passing the trapezium. The radial
side of the tunnel is formed by the body of the trape-
zium and the volar side by the trapezial tuberosity. On
the ulnar side, the tunnel is separated from the carpal
tunnel by a thick septum. Distally, the FPL tendon pivots
around this septum. At the floor of the tunnel, the
tendon sheath lies in contact with the volar capsule of
the scaphotrapeziotrapezoid (STT) joint. The narrow
tunnel induces a higher risk of primary stenosing teno-
synovitis; however, because of the close relationship
with surrounding structures, tenosynovitis can also
occur secondary to traumatic or degenerative changes.
Tenosynovitis of the FCR tendon is not an uncommon
finding in arthritis of the STT joint, which can cause
additional pain to the baseline osteoarthritic pain.10,11
The FCR tendon is also suggested to play a role in
stabilizing the scapholunate joint through its close rela-
tionship between the FCR tendon sheath and the liga-
ments attached to the tuberosity of the scaphoid. The
tendon was thought to use the distal pole of the scaph-
oid as a pulley to increase its mechanical advantage and
prevent the scaphoid from rotating into flexion. Unlike
in previous hypotheses, Salvà-Coll et al12 found that
 Chapter 1:  Anatomy of the Tendon Systems in the Hand
loading the FCR tendon rotated the scaphoid in flexion
and supination, while rotating the triquetrum in flexion
and pronation. These opposite rotations are attributed
to relax the dorsal scapholunate ligament.
The FCR tendon inserts into the base of the second
metacarpal and gives off a strong, tendinous slip to the
third metacarpal. Frequently a small slip to the trapezial
tuberosity can be seen. Other variations are insertions
in both the trapezium and scaphoid and in the base
of the second, third, and fourth metacarpals. The FCR
muscle can even be absent. Insertion in the transverse
carpal ligament can also be seen and may cause confu-
sion with the palmaris longus tendon.8
The flexor carpi ulnaris (FCU) encloses the pisiform
bone, which can be seen as a sesamoid bone for this
tendon. The FCU attaches to the base of the fifth meta-
carpal and hamate, via the pisohamate and pisometa-
carpal ligaments. The pisohamate ligament creates an
additional tunnel, Guyon’s canal, between the hook of
the hamate and pisiform bone through which the ulnar
artery and nerve pass. Occasionally, the FCU tendon
doubles before inserting in the pisiform bone. The FCU
can also merge with the flexor superficialis or profundus
tendon.8
The FPL tendon passes through its own osseo-
aponeurotic canal and inserts at the distal phalanx of
the thumb. Sometimes an additional tendon to the
index finger is found. The FPL tendon can be absent, in
combination with a significant smaller thumb. Another
variation is splitting of the tendon into two or three slips
that insert into the scaphoid or flexor retinaculum.8
FLEXOR TENDON SHEATHS
Structure of the Sheath at Wrist and Palm
In the wrist, synovial sheaths allow the flexor tendons
to glide through the carpal tunnel. The sheaths begin
approximately 2.5 cm proximal to the transverse carpal
ligament and extend distally to the neck of the metacar-
pals. In the fingers, the flexor tendons are also sur-
rounded by sheaths. A considerable level of variation in
communicating patterns between these sheaths and the
digital flexor sheaths is observed.13
As reported by Fussey et al,13 the most common
pattern shows one common flexor tendon sheath or ulnar
bursa surrounding the tendons of the FDS and FDP. A
second sheath, forming the radial bursa, envelopes the
FPL tendon.
In most cases the little finger flexor sheath works in
continuity with the tendons along the phalanges. Like-
wise, the FPL tendon sheath accompanies the tendon
along the thumb as far as its insertion.13
Occasionally communications between the common
flexor tendon sheath and the second, third, and fourth
digital tendon sheaths are observed in the palm. Fur-
thermore, the ulnar and radial bursa can be found to be
5
SM SF PT SM SF SSCT
Tendon
Intrasynovial Extrasynovial ?
Tendon Tendon
Zone 2 Zone 3 Zone 4
Figure 1-1  Nutritional microenvironment of the flexor
tendon. In zone 2 the tendons are intrasynovial within the
digital flexor sheath. Zone 3, in the palm of the hand, is
extrasynovial tendon. In the carpal tunnel, zone 4, the
tendon is surrounded by a hybrid of both intrasynovial and
extrasynovial tissue. SM, Synovial membrane; SF, synovial
fluid; PT, paratenon; SSCT, subsynovial connective tissue.
connected. In case of an infection within the sheath, the
communication between the ulnar and radial bursa can
result in the “horseshoe abscess.”
In the carpal tunnel, the subsynovial connective
tissue (SSCT) connects the flexor tendons with the syno-
vial membrane of the ulnar bursa. It consists of fibrous
bundles parallel to the tendons, which in turn are inter-
connected by smaller microfibrillar fibers. By acting as
a sliding unit, the SSCT reduces friction and maintains
the integrity of the vascularity around the tendons. Non-
inflammatory fibrosis of the SSCT is the most common
histological finding in carpal tunnel syndrome, which
suggests injury to the SSCT to be an important etiologic
factor14 (Figures 1-1 to 1-4).
Structure of the Digital Flexor Sheath
The tendons of the FDP and FDS lie deep in the palm
of the hand, beneath the superficial palmar arch and the
superficial branches of the median and ulnar nerve.
There, the tendons are surrounded by several layers of
loose connective tissue. Vessels emerging from the
palmar arches traverse through this tissue toward the
tendons, forming the paratenon.
In a histological study of the flexor tendon sheath by
Cohen and Kaplan,15 two vascular systems are observed
to become organized in the paratenon; one adjacent to
the tendons, the other more peripheral. The develop-
ment of a “synovial-lined cleft” between these systems
creates a separation into a visceral and a parietal
synovium.
The parietal layer lines the wall of the tunnel through
which the tendon glides. As the layer continues distally,
the layer was found to be uninterrupted and reinforced
externally by dense bands of collagen. By maintaining
the tendons close to the bone and joint surface, these
bands act as a system of pulleys, facilitating efficient
finger movement. Between these reinforcements, the
thickness of the parietal synovium is greatest and is
called the membranous part of the tendon sheath.
6 Section 1:  Basic Science
I
I Flexor
I retinaculum
I Visceral synovium
II
I
II
III
III
IV IV
V
Figure 1-2  Flexor tendon zones. The zones are numbered
from distal to proximal. Zone 1 contains a single tendon, the
flexor digitorum profundus tendon. Zone 2 is the critical area
of the digital flexor sheath. It contains both the profundus
and superficialis tendons, and the area where the profundus
tendon penetrates the superficialis at the chiasm of Camper.
In the extrasynovial zone 3 the lumbrical muscles arise. Zone
4, the carpal tunnel, contains mixed intra/extrasynovial
tissue. Zone 5 is also extrasynovial, without the lumbrical
muscles. In the thumb, although we have marked zones 1 to
5, one may consider that zones 2 and 3 do not exist,
because there is only a single tendon, and no lumbrical.
The visceral layer or epitenon adheres to the tendon,
creating a synovial space between the two layers. It was
found to be supported by a thin cover of laminated col-
lagen. All structures entering the tendons are surrounded
by epitenon. In the opposite direction along these struc-
tures, the visceral layer works in continuity with the
parietal layer. The synovial layers extend distally to the
insertion of the FDP tendon, where they become
confluent.
VINCULA TENDINEA
On the palmar osseous side of the tunnel, vessels pro-
trude through the synovial layers, forming mesenterial
folds or mesotenon. These vascular bands connect the
dorsal side of the flexor tendons with the palmar side
of the flexor sheath. In consideration of their tendinous
structure, these bands are named vincula tendinea (vin-
culum derives from Latin and means “bond or link”).
Parietal synovium
Subsynovial
connective tissue
Tendon
Figure 1-3  Sliding unit in the carpal tunnel region has
both structures (i.e., paratenon and synovial sliding
mechanism). All layers from the flexor retinaculum to the
tendon are shown. The tendons in the carpal canal have a
subsynovial connective tissue and a bursa, containing
synovial fluid between the parietal and visceral synovium
(hematoxylin-eosin; original magnification, ×400). (From
Ettema AM, Amadio PC, Zhao C, et al: Changes in the
functional structure of the tenosynovium in idiopathic carpal
tunnel syndrome: a scanning electron microscope study,
Plast Reconstr Surg 118:1413-1422, 2006.)
Several variations in the vincula tendinea have been
observed. Ochiai et al16 studied the distribution patterns
of the vincula in the fingers of 35 human hands. Their
study showed that four transverse communicating
branches arising from the digital arteries enter the flexor
tendon sheath through openings in the pulleys, travel-
ing toward the vincula. The sites of entry are at the base
of the proximal phalanx, the neck of the proximal
phalanx, the base of the middle phalanx, and the neck
of the middle phalanx (Figure 1-5).
Two kinds of vincula were found within each digital
flexor tendon sheath: vessels arising from the transverse
communicating arteries protrude through the meso-
tenon forming short, triangle-shaped folds (vincula
brevia) and long, slender vincula longa (Figure 1-6).
The vincula brevia were found consistently in all dis-
sected fingers. The vinculum brevis superficialis (VBS)
arises from the volar plate of the proximal interphalan-
geal (PIP) joint and attaches to the decussation of the
superficialis tendon. The thin, triangle-shaped meso-
tenon of the vinculum brevis profundus (VBP) arises at the
distal third of the middle phalanx and attaches near the
insertion of the profundus tendon.
In contrast, several variations in the long vincula can
be found. Ochiai et al16 found the vinculum longum
superficialis (VLS) to have a radial, ulnar, or two-sided
origin at the base of the proximal phalanx. Absence of
the VLS was also observed, mainly in the middle and
ring fingers. They also mentioned that the vascularity of
 Chapter 1:  Anatomy of the Tendon Systems in the Hand 7

the profundus tendon is less in adults than in fetuses.

These findings can be a possible explanation for the
higher incidence of triggering in the middle and ring
fingers and in older patients.
For the vinculum longum profundus (VLP), Ochiai
et al16 found five types, named distal, middle, mixed,

A5

Distal C3
transverse
digital artery A4
Intermediate
C2
transverse
digital artery A3

Proximal C1
transverse
digital artery

A2
Branch to
vincular longum
superficialis (VLS)

Figure 1-4  Top, Loose vertical fibers join adjacent layers

in the subsynovial connective tissue (scanning electron A1
microscopy; original magnification, ×1100). Bottom, The
loose vertical fibers between adjacent layers are stretched
during flexor tendon movements (scanning electron Common
microscopy; original magnification, ×1000). (From Ettema digital artery
AM, Amadio PC, Zhao C, et al: Changes in the functional
structure of the tenosynovium in idiopathic carpal tunnel
syndrome: a scanning electron microscope study, Plast Figure 1-5  The tendon sheath contains the annular
Reconstr Surg 118:1413-1422, 2006.) pulleys A1 to A5 and the cruciate pulleys C1 to C3.

Flexor digitorum Vinculum longum Vinculum brevis

profundus profundus (VLP) profundus (VBP)

Dorsal

Flexor digitorum Vinculum Vinculum

superficialis longum brevis
superficialis superficialis
(VLS) (VBS)
Figure 1-6  The blood vessels enter the flexor tendons through the vincular system.
8 Section 1:  Basic Science
proximal, and absent to refer to the site of insertion at
the profundus tendon.
The distal type was found to be very rare; the middle
type was most commonly found and travels through the
decussation. The proximal type arises between the two
slips of the superficialis tendon and passes through the
bifurcation. The mixed type is similar to the proximal,
but no VLS is found.
The index finger most often had a radial or two-sided
VLS, and the middle type of VLP. In the long finger, no
predominant type was found. Most long fingers had the
middle type of VLP combined with the radial type of
VLS or a middle and proximal type of VLP in combina-
tion with two-sided VLP.
In the ring finger, the VLS was most commonly
absent, often in combination with mixed type VLP or
both mixed and middle types. The predominant type
for the little finger is the middle type of VLP and a broad
ulnar-sided mesotenon forming the VLS.
The area in which the vincula can be found is often
referred to as “no-man’s land” as surgical treatment of
flexor injuries often have poor outcome (see Figure
1-2). One possible explanation for these poor results
could be the disruption of the vincula, and thus blood
supply to the tendons. Amadio et al17 investigated the
relationship of the vincular status on final total active
motion after primary tendon repair and early mobiliza-
tion. This study showed a statistically significant decrease
in total active motion when the vincular system was
injured. Disruption (or absence) of vincula could there-
fore be an important prognostic factor of the outcome
of flexor tendon repair.
In the thumb, the vinculum breve forms a continuous
band with the FPL tendon proximal to its insertion. After
complete laceration of the FPL tendon at the interpha-
langeal joint, the intact vinculum produces some flexion
of the joint by its connection with the volar plate.18
THE PULLEY SYSTEM
The strengthening elements of the digital flexor sheaths,
called pulley, are condensation of dense connective
tissue and segmentally distributed along the digital
sheath. They serve to restrain the tendons from bow-
stringing and to accommodate maximum mechanical
efficiency of tendon excursion.
Several descriptions of these pulleys have been
reported.19-21 The popularly used nomenclature is based
on Doyle’s classic anatomical work.20
Strauch and de Moura19 investigated the pulleys in 72
fingers and found that a “complex synovial lined tube”
surrounds the flexor tendons to the central three rays.
At either edge two main “cul-de-sacs” enclose the
tendons. Between the pulleys are smaller cul-de-sacs,
which tend to flatten in extension, allowing for adjust-
ment in length of the sheaths in finger motion. Strauch
and de Moura19 described two sets of three annular
pulleys (termed annular proximal and annular distal)
and two cruciate ligaments (cruciate proximal and
distal). The first annular proximal (AP1) pulley origi-
nates just proximal to the metacarpophalangeal (MCP)
joint and ends at the middle of the proximal phalanx.
There it is overlapped by the proximal cruciate ligament,
which extends over the distal third of the same phalanx.
The second annular proximal (AP2) pulley is positioned
at the PIP joint; the third annular distal (AD1) pulley is
over the proximal third of the middle phalanx, where it
was overlapped by the distal cruciate ligament. At the
distal interphalangeal (DIP) joint is the second annular
distal (AD2) pulley; the third annular distal (AD3)
pulley is at the base of the distal phalanx.
A more commonly accepted description was given by
Doyle.20 After dissecting 80 digits, Doyle concluded
there are five annular (termed A1 to A5, from proximal
to distal) and three cruciate (C1 to C3, from proximal
to distal) pulleys (see Figure 1-5). The A2 pulley is the
largest pulley in the fingers, approximately 1.5 to 1.7 cm
long, which are located in the proximal part of the
proximal phalanx. This pulley has a distinct semilunar
and thick leading edge and the annular fibers are over-
laid with circular fibers. The second largest annular
pulleys are A4 pulley at the middle of the middle
phalanx and A1 pulley (at the level of the MCP joint);
the A3 pulley (at the PIP joint level) is rather narrow,
about 3 mm in length. The A5 pulley at the DIP joint
level is very small and sometimes indistinguishable.
Strauch’s most distal annular structure (AD3), a
pulley distal to the DIP joint, is not described by other
investigators, including Doyle.20 The second and fourth
annular pulleys were found to be always present—A3
and A5, respectively—in 80% and 90% of the speci-
mens. The cruciate pulleys sometimes are single oblique
bands or Y-shaped.
Lin et al21 further differentiated between pulleys that
attach to the bony floor of the digital canal formed by
the phalanges and pulleys that insert into the volar
plates covering the joints. The two annular bony pulleys
over the shaft of the proximal (A2) and middle phalanx
(A4) are the longest and strongest. These pulleys remain
nearly constant to the joint axis and shorten the least in
finger flexion.
In contrast, the distance between the volar plate
pulleys (A1, A3, and A5) and the joint axis showed a
significant increase in flexion of the fingers. The volar
plate pulleys also tend to have a greater shortening com-
pared to the bony pulleys. The cruciate pulleys attach at
one end to bone and at the other end to the palmar
plate. They show the most anatomical variation and
shortening.
Due to the concave shape of the volar shaft of the
phalanges, absence of the bony pulleys leads to bow-
stringing of the flexor tendon over this curvature. A
second form of bowstringing occurs over the joint, when
 Chapter 1:  Anatomy of the Tendon Systems in the Hand
in flexion. The A2 and A4 are not at an equal distance
on both sides from the PIP joint; the reason for this may
be to optimally control a combination of both joint and
bony bowstringing.21
The volar plate pulleys only restrain bowstringing
over the joint, and the cruciate pulleys seem to mainly
modulate force transmission, by increasing the moment
arm in flexion beyond 45 degrees. Absence of the A2
and A4 pulleys has the greatest effect on joint motion,
even when only the bony type of bowstringing is per-
mitted, by preserving the other pulleys that keep the
tendons close to the joint axis. The absence of the A3
pulley alone has minimal effect on joint motion.21
By remaining in close contact with the tendons that
glide through them, the pulleys generate friction. Zhao
et al22 found that the A3 pulley contributes to reducing
the gliding resistance of the tendons against the A2 and
A4 pulleys. By keeping the tendons close to the PIP joint
axis, the A3 pulley reduces the angle between the edges
of the pulleys and the tendons, which reduces gliding
resistance. This occurs mainly in greater angles of PIP
flexion. The presence of this pulley may prevent a
tendon repair site from buckling under the A2 pulley.
Two other structures also contribute to the pulley
system of the flexor tendons: the transverse carpal liga-
ment and the palmar aponeurosis.
The transverse carpal ligament arches over the flexor
tendons as they traverse toward the palm of the hand
and performs a pulley function by keeping the flexor
tendons in proximity of the wrist. After transsection of
the transverse carpal ligament in fresh-frozen cadavers,
Kline and Moore23 demonstrated that flexor tendons
move an additional 5.5 mm forward from the joint axis,
when flexing the wrist. The motion of the wrist required
a 25% increase of excursion for the FDP tendons and a
20% increase for the FDS tendons. As Kline and Moore
stated, this increase in excursion could clinically result
in decreased grip strength by reducing the remaining
tendon excursion over the other joints. Consequently,
the total active finger motion could decrease if maximal
muscle contraction is reached.
At the level of the MCP joints, the fibers of the palmar
aponeurosis and intertendinous septa form an archway
over the flexor tendons. By anchoring in the deep trans-
verse carpal ligament, this archway keeps the tendons
near the axis of the MCP joint and can therefore be seen
as an additional pulley—palmar aponeurosis (PA)
pulley.24 Manske and Lesker25 sequentially cut the PA
and the first and second annular pulleys in various orders
and studied the influence on joint motion. Cutting only
one of these pulleys resulted in minimal loss of function.
Increased loss of flexion was observed when one of the
annular pulleys was cut in combination with the PA
pulley. The A2 pulley was found to be the most impor-
tant as a single pulley, followed closely by the A1 pulley.
Although the PA pulley was the least important as a
9
single pulley, loss of function increased significantly
when this pulley was the final pulley to be cut.
INTRINSIC MUSCLES: THE LUMBRICALS
AND INTEROSSEI
An unusual muscle originates in the palm of the hand.
Instead of attaching to bone, the lumbrical muscle arises
from a movable medium, namely the FDP tendon and
inserts distally, after crossing the MCP joint, into the
extensor expansion.26 Although their origin is at the
profundus tendon, the lumbrical muscle covers a great
part of the superficialis tendon. The first and the second
lumbrical muscles are unipennate muscles and arise
from the palmar surface and radial sides of the tendons
of the index and middle fingers, respectively. The third
and the fourth are bipennate muscles that originate at
the contiguous side of the profundus tendons of the
middle and ring fingers and the ring and little fingers,
respectively. All pass at the radial side of the finger in
which they insert at the dorsal side of the MCP joint.26
The lumbricales are found to vary in number between
two and five. The most frequent variation can be seen
in the third lumbrical, as two tendons originate and
insert in the middle and ring fingers. Another variation
shows only one tendon from the third lumbrical to the
ulnar side of the middle finger.26
The main action of the lumbrical muscles is to keep
the fingers stretched as the MCP joint flexes. They act as
a moderator band between flexor and extensor mecha-
nism in the finger. When the flexor tendon is pulled, the
origin of the lumbrical muscle moves proximally, this
way the muscle is stretched. With the MCP joint in
flexion the lumbrical muscle pulls the interphalangeal
joints into extension, by moving the extensor mecha-
nism proximally.27
The interosseous muscles are numbered from radial to
the ulnar side of the hand. According to their relative
position to the intermetacarpal spaces, three palmar
and four dorsal interossei arise between the metacarpal
shafts. The palmar interossei are unipennate muscles that
arise on the opposite side relative to the middle finger
metacarpal and insert on the same side into the proximal
phalanx; therefore, the palmar interossei produce adduc-
tion of the fingers relative to the third ray.26
The dorsal interossei are composed of two muscle
bellies arising from the adjacent metacarpals. The
tendons on the ulnar side of the axis of the third ray
insert on the ulnar side of the proximal phalanx; on the
radial side of the middle finger, the tendon inserts on
the radial side of the proximal phalanx. In this way, the
action of the dorsal interossei is abduction of the fingers
relative to the middle finger.26
Variations in the interossei are seen in the number of
muscle bellies and insertions of the tendons. The palmar
interossei can be bipennate with two tendons inserting
in each corresponding side. One or even all palmar
10 Section 1:  Basic Science
interossei can be absent. The dorsal interossei are some-
times found to originate more proximal at the base of
the metacarpals or even at the carpalia. The insertion of
the tendon of the second dorsal interossei can be on the
ulnar side of the second metacarpal so that the abduc-
tion of the fingers is relative to the axis of the second
ray, instead of the third.26
CHIASMA TENDINUM OF CAMPER
After leaving the carpal tunnel, the flexor digitorum
tendons diverge and spread out to the fingers. As in
logical accordance with their names, the superficialis
tendon lies on top of the profundus. However, after
the tendons pass distal to the MCP joint, the profundus
tendon starts to penetrate through the bifurcated super-
ficialis tendon. At the middle part of the proximal
phalanx, the superficialis tendon divides into two slips
that rotate laterally.27 The most dorsal fibers of the
rotated slips emerge to the other side and, after crossing
each other, they finally insert at the lateral volar crest of
the middle phalanx. The other fibers of the lateral slips
continue on the lateral side and insert on the lateral
crest on the volar surface of the middle phalanx, where
they unite with the crossed fibers. The superficialis
tendon has a long insertion from the base of the middle
phalanx toward the neck.27
The profundus tendon passes through the tunnel
formed by the superficialis tendon at the level of the
proximal phalanx. The tunnel is narrowed by the vincu-
lum breve superficialis. The FDP tendon passes the volar
capsule of the DIP joint, to which it is firmly connected.
More distally, the tendon spreads out to insert widely
into the volar base and fat pad of the distal phalanx.27
This intersection of fibers of the FDS tendon forms a
plate beneath the flexor profundus and is called the
chiasma tendinum of Camper, named after the Dutch phy-
sician Petrus Camper, who gave a detailed description
of this structure in his book on the anatomy of the arm
and hand. The chiasma tendinum is an essential biome-
chanical element of the gripping function of the hand.
When longitudinal tension is applied to the deep flexor
tendon, the volar surface of the superficial tendon is
pushed against the A2 pulley. As grip is sustained, the
profundus tendon is compressed by the two slips of the
superficialis tendon. These mechanisms provide stabili-
zation of the interphalangeal joint, which aids in obtain-
ing grip on an object.28
EXTENSOR TENDONS AT THE WRIST
A detailed description of the extensor tendons and its
variations can be found in the anatomical textbooks
of Standring2 and Kaplan1 and Hunter.26 By passing
the wrist joint, the extensor tendons assist in extending
the wrist and, depending on their position toward the
median axis, provide radial or ulnar deviation. From
radial to ulnar, the tendons pass through grooves on the
JT
EIP
ECRB
ECRL
EDC EDM
APL
EPL
EPB
III IV V VI
Lister’s I II
tubercle
Retinaculum
Figure 1-7  The extensor retinaculum and extensor
tendons. Extensor tendons gain entrance in the hand from
the forearm through a series of six canals. The extensor
tendons are covered with a synovial sheath. APL, Abductor
pollicis longus; EPB, extensor pollicis brevis; EPL, extensor
pollicis longus; ECRL and ECRB, extensor carpi radialis longus
and brevis, respectively; EIP, extensor indicis proprius; EDC,
extensor digitorum communis; EDM, extensor digiti minimi.
Note the junctura tendinea (JT) connecting to the extensor
tendon of the ring fingers.
dorsal side of the distal radius in six compartments
formed by the extensor retinaculum (Figure 1-7).
Most radial in position, the abductor pollicis longus
(APL) tendon passes through the first compartment,
together with the extensor pollicis brevis (EPB) tendon.
It inserts on the radial side of the first metacarpal and
thereby induces abduction of the first ray of the hand.
Usually the APL has multiple slips. Common insertions
of these slips are the trapezium and the origin of the
abductor pollicis brevis or opponens muscle. In 71% of
100 dissections, Brunelli and Brunelli29 found that one
or two extra tendons in the first compartment belong
to a musculotendinous unit. By inserting in the trape-
zium, the main function of this unit is abduction of
the carpus and it was therefore named the “abductor
carpi” muscle. Brunelli and Brunelli consider that the
absence of this muscle, which was seen as abnormal,
leads to a higher risk of instability and arthritis of the
trapeziometacarpal (TM) joint, because of the loss of a
 Chapter 1:  Anatomy of the Tendon Systems in the Hand
force to balance the other abducting forces that pull the
base of the first metacarpal and cause a shearing effect
on the TM joint.
Other studies did not show a significant relationship
between supernumerary tendon insertions and TM joint
arthritis. However, the presence of a septum within the
first extensor compartment does seem to play a role in
the pathogenesis of TM arthritis.30
The EPB inserts into the base of the proximal phalanx
of the thumb. The tendon can be fused with the extensor
pollicis longus (EPL) or absent. It often has its own
subsheath within the first compartment. This may be an
important factor in de Quervain disease. The tendons of
the extensor carpi radialis longus (ECRL) and brevis
(ECRB) pass under the muscle bellies of the abductor
pollicis longus (APL) and EPB before passing under-
neath the dorsal carpal ligament, in the second com-
partment. Repetitive resisted extension of the wrist can
cause inflammation of the tenosynovium at this inter-
section, which is therefore called “intersection syn-
drome.” It was thought to be caused by friction of the
muscle bellies at the intersection; however, Grundberg
and Reagan31 demonstrated this inflammation is based
on stenosing tenosynovitis of the sheath of the radial
wrist extensors within the second compartment. The
radial wrist extensor tendons attach at the dorsal radial
aspect of the base of the second and third metacarpal,
respectively. Variations exist in the number of tendons
arising from the muscle bellies and cross slips between
these tendons. Occasionally, an extensor carpi radialis
accessorius can be seen with insertion into the bones or
muscles in the thenar region.
In the third compartment, EPL obliquely crosses the
long and short extensor carpi radialis tendons and
inserts into the base of the distal phalanx of the thumb.
The tendons to the thumb form a triangular interval
(anatomical snuffbox), wherein the radial artery can be
found. The EPL tendon goes around Lister’s tubercle,
which is a frequent site of chronic tenosynovitis. This
could eventually lead to “drummer boy’s palsy,” when
the EPL tendon ruptures.
The extensor indicis proprius passes through the
fourth compartment together with the extensor digito-
rum communis (EDC) tendons and joins the common
extensor tendon to the index finger, on the ulnar side.
Occasionally an extensor digitorum brevis manus
(EDBM) muscle can be found in the fourth compart-
ment, which can be confused with a ganglion. The
EDBM has the same insertion as the extensor indicis
proprius and could therefore be seen as variant of that
muscle.32
Through the fifth compartment, distally to the distal
radioulnar joint, runs the tendon of the extensor digiti
quinti proprius or extensor digiti minimi. It merges at
the proximal phalanx with the little fingers extensor
expansion.
11
The sixth compartment contains the ECU tendon,
which runs through a groove between the head and
styloid process of the ulna; after “encapsulating” the
pisiform bone, it attaches to the base of the fifth meta-
carpal. Frequently, a slip extends from the insertion to
the capsule of the MCP joint or the proximal phalanx
of the fifth digit.
VARIATIONS IN EXTENSOR TENDONS
TO THE FINGERS
Numerous variations exist in the extensor tendons to
the fingers. Zilber and Oberlin33 studied the pattern of
extensor tendons of 50 hands to determine the statisti-
cal distribution, combined with the results of previous
studies. In the most frequently encountered pattern, the
EDC provided one tendon to the index and middle
finger, two to the ring finger, and none to the little finger.
In this pattern there is a single extensor indicis tendon
and a double extensor digiti minimi tendon. A septum
is seen between the extensor digiti minimi tendon and
the EDC after they have emerged from the extensor reti-
naculum. Always observed is the extensor indicis tendon
lacking a junctura tendinum.
After reviewing the literature on variations in the
fingers extensor tendons, Zilber and Oberlin33 stated
that the different descriptions have certain contraindica-
tions, especially regarding the ring finger. A large varia-
tion was seen in the number of EDC tendons, ranging
from 5 to 12 tendons. The absence of a tendon to the
index finger is exceptional. The EDC tendon to the little
finger is often replaced by a structure arising from the
ring finger that joins the tendon of the extensor digiti
minimi at the level of the MCP joint. Some authors
describe this structure as a tendon and others as a junc-
tura tendinum. This may lead to differences in results
reported with respect to the EDC tendons to the fourth
and fifth fingers.33
The absence of the extensor indicis tendon is a rare
finding. An extensor medii digiti or extensor medii pro-
prius has been reported as a tendon for the middle
finger arising from the extensor indicis. The extensor
digiti minimi tendon can be absent with or without
substitution of a tendon from the EDC or ECU to the
little finger. The EDM can also be formed by two distinct
muscles or by one muscle with up to three tendons. The
two-tendon pattern is seen as the normal pattern. The
EDM can be identified by two tendons running in
the same sheath on the ulnar aspect of the wrist in 60%
to 90% of cases. This is important to know because this
extra tendon is useful for tendon transfers.33
Asymmetry is often seen between the right and the left
hand. Especially with respect to the EDM, this shows one
tendon favoring one hand more than the other in 20%
of cases. It is necessary to have thorough understanding
of these arrangements of the multiple extensor tendons
when performing tendon surgery33 (see Figure 1-7).
12 Section 1:  Basic Science
On the dorsum of the hand, the extensor tendons are
interconnected by tendinous bands called junctura ten-
dinea. The presentation of the juncturae shows several
variations. Most often an oblique slip branches off the
tendon of the ring finger to insert distally in the tendon
of the little and middle fingers. A thin transverse band
can be found between the middle and index fingers.
There are three types of juncturae: a filamentous trans-
verse or oblique band, a much thicker and well-defined
junctura, and a “y”- or “r”-shaped tendon slip.34
With the fingers in flexion, the juncturae restrict the
neighboring fingers from extending independently. This
especially accounts for the ring finger as the juncturae
originate at the tendon of the ring finger and course
distally35 (see Figure 1-7).
EXTENSOR MECHANISM OF THE FINGERS
Kaplan and Hunter26 and Smith35 thoroughly describe
the extensor mechanism of the fingers. As the common
digital extensor tendons approach the distal end of the
metacarpals, they spread out to form an aponeurosis
over the MCP joint and proximal phalanx, the extensor
expansion or dorsal hood. The tendon is fixed at the
midline of the MCP joint by a band of sagittal fibers
that arises volarly at the deep transverse metacarpal liga-
ment and the volar plate of the MCP joint. These sagittal
bands aid in the extension of the proximal phalanx and
restrict the tendon from moving proximally.26
Between the sagittal bands and the MCP joints run
the tendons of the interosseus muscles that insert at the
lateral tubercles on the base of the proximal phalanx.
These tendons allow for lateral deviation of the fingers.
By its connection with the extensor expansion, the inter-
ossei can flex the MCP joint. Fibers between the lateral
ligaments and the extensor expansion prevent the inter-
osseus tendons from luxating dorsally in extension. The
radial side of the proximal phalanx, slightly distal to the
lateral tubercles, normally also receives the insertion of
the lumbrical tendon.26
Distally, lateral bands formed by a continuation of
the interossei and lumbricales course to the sides of
the PIP joint and the middle phalanx (Figure 1-8).
Oblique slips attach to the base of the middle phalanx
and merge with the central tendon. The remaining
portion of the lateral bands continues at the sides of
the middle phalanx and turns dorsally near its head.
There the bands unite and continue as a wide band over
the DIP joint that inserts at the base of the distal
phalanx.36
Between the lateral bands of the interossei, distal to
the sagittal bands, transverse fibers arch over the dorsal
side of the proximal phalanx. The fibers of this interten-
dinous lamina gradually change from horizontal to
oblique from distal to proximal. The lamina courses
from the extensor tendon to the volar plate of the MCP
joint and acts as a flexor of the proximal phalanx.35
Central slip
Sagittal band
Interosseus
TRL Lateral
ORL band Lumbrical
Figure 1-8  Extensor mechanism lateral view. ORL, Oblique
retinacular ligament; TRL, transverse retinacular ligament.
Sagittal band locates dorsal and lateral to the MCP joint of
the finger. The tendons of the interosseus and lumbrical
muscles insert in the proximal phalanx and form the lateral
bands, which is interconnected with the central slip by the
sagittal band at the MCP joint.
At the base of the proximal phalanx the extensor
tendon infiltrates the dorsal lamina; the tendon trifur-
cates and spreads out over the PIP joint. At the distal
end of the proximal phalanx, fibers from the lateral
bands join the middle band or central slip. After cross-
ing the PIP joint, the central slip is fused with the
capsule and inserts at the base of the middle phalanx26,36
(Figure 1-9).
The central slip particularly extends the middle
phalanx, unless the MCP joint is in hyperextension.
When the PIP joint is flexed, the central slip contributes
to the extension of the proximal phalanx by dorsal dis-
placement of the middle phalanx on the head of the
proximal phalanx.36
A narrow, tendinous band arises at the volar aspect
of the distal end of the proximal phalanx. This oblique
retinacular ligament (ORL) courses obliquely to the
dorsal side of the middle phalanx, where it joins the
lateral bands to the distal phalanx. It helps stabilizing
the lateral bands and is also attributed to extend the DIP
joint in harmony with the extension of the PIP joint;
however, biomechanical investigations have refuted
this. This “link” ligament passes volar to the PIP joint
axis only when the joint is flexed; the same applies, in
greater extend, to the DIP joint. The oblique retinacular
ligament was observed only to aid in extension when
the DIP joint was flexed more than 70 degrees.37,38
At the PIP joint a homologue to the sagittal bands
originates from the volar aspect of the PIP joint. The
transverse retinacular ligament maintains the extensor
mechanism in position and pulls the lateral bands
volarly, in flexion of the PIP joint.26
Distal to the insertion of the central slip the dorsal
hood continues toward the distal phalanx as a thin
membrane between the lateral bands. This area covering
 Chapter 1:  Anatomy of the Tendon Systems in the Hand
LB
Central
slip
Triangular
ligament
Figure 1-9  Extensor mechanism dorsal view. LB, Lateral
band. The connections between the central slip and lateral
band are illustrated. The triangular ligament connects the
lateral bands over the dorsum of the middle phalanx.
the middle phalanx is called the triangular ligament (or
triangular lamina). It retains the lateral bands close to
each other by bonding them over the dorsum of the
middle phalanx (see Figure 1-8).
TENDONS IN THE THUMB
The FPL tendon courses through a groove on the volar
side of the first metacarpal, in its own flexor sheath. In
the volar capsule of the MCP joint, two sesamoid bones
are embedded, which firmly wedge the FPL tendon.
Distally the tendon inserts widely in a deep excavation
in the volar surface of the distal phalanx. It flexes the
interphalangeal joint of the thumb, as well as the MCP
and carpometacarpal (CMC) joint.2,39
The abductor pollicis brevis is inserted by a thin, flat
tendon into the lateral aspect of the MCP joint capsule
and unites with the fibers of the flexor pollicis brevis
(FPB) to the radial sesamoid. It moves the thumb ante-
riorly (abduction) and also contributes to opposition
and extension of the thumb.2,39 The FPB forms a tendon
near the MCP joint, to which it adheres, and inserts into
the lateral sesamoid bone and the lateral tubercle of the
proximal phalanx. It flexes the thumb towards the palm
of the hand. Some anatomists describe the medial part
13
A2
Oblique pulley
A1
Adductor pollicis
Flexor pollicis brevis, deep head
Synovial sheath
Figure 1-10  The flexor pollicis longus (FPL) pulley system
differs from the finger pulley system in that there is a strong
fibrous oblique pulley between the A1 and A2 pulleys. There
are no cruciate pulleys in the thumb.
of the FPB as one of the palmar interossei.2,39 The oppo-
nens pollicis inserts along the entire length of the lateral
side of the metacarpal bone of the thumb. It flexes the
metacarpal at the CMC joint and therefore contributes
to opposition of the thumb; a combination of actions
that brings the tip of the thumb and the other fingers
together. The abductor pollicis brevis, FPB, and oppo-
nens pollicis form the thenar muscles.2,39
The adductor pollicis tendon inserts in the first
annular pulley and the ulnar sesamoid at the MCP joint.
The volar plate is firmly attached to the proximal
phalanx, what gives the adductor pollicis the ability to
directly act on the phalanx. The adductor pollicis also
has an extension to the ulnar lateral tubercle and the
dorsal aponeurosis of the thumb. Its actions are adduc-
tion of the thumb and flexion of the MCP joint2,39
(Figure 1-10).
Some controversy exists about the pulleys of the
thumb. An annular pulley arises from the volar plate of
the MCP and interphalangeal joint. At the level of the
shaft of the proximal phalanx an oblique pulley can be
found. The proximal part of the oblique pulley shows
variation and is suggested to be seen as a separate trans-
verse pulley. These pulleys arising from the proximal
phalanx are most important in preventing bowstringing
of the FPL tendon. However, the oblique part alone does
not prevent bowstringing.40
14 Section 1:  Basic Science
On the dorsal side of the thumb the EPL tendon
courses over the ulnar side of the MCP joint. From there
it broadens, crosses the interphalangeal joint and inserts
widely into the base of the distal phalanx. It extends the
distal phalanx of the thumb and contributes to abduc-
tion and extension of the wrist.2,39
The EPB tendon is concealed by the dorsal aponeu-
rosis as it crosses the MCP joint and inserts in the dorsal
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human flexor tendon sheath, J Hand Surg (Am) 12:25–29,
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16. Ochiai N, Matsui T, Miyaji N, et al: Vascular anatomy of flexor
tendons. I. Vincular system and blood supply of the profun-
dus tendon in the digital sheath, J Hand Surg (Am) 4:321–
330, 1979.
17. Amadio PC, Hunter JM, Jaeger SH, et al: The effect of vincular
injury on the results of flexor tendon surgery in zone 2,
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18. Armenta E, Fisher J: Anatomy of flexor pollicis longus vincu-
lum system, J Hand Surg (Am) 9:210–212, 1984.
19. Strauch B, de Moura W: Digital flexor tendon sheath: An
anatomic study, J Hand Surg (Am) 10:785–789, 1985.
base of the proximal phalanx. Frequently an insertion
in the distal phalanx is observed. By acting on the CMC
and MCP joints the extensor pollicis brevis extends and
abducts the thumb.2,39 The extensor mechanism of the
thumb shows similarities with the expansion over the
fingers MCP joints. It is formed by EPL and EPB, and
the extensions of the abductor brevis on the radial side
and adductor on the ulnar side.2,39
20. Doyle JR: Anatomy of the finger flexor tendon sheath and
pulley system, J Hand Surg (Am) 13:473–484, 1988.
21. Lin GT, Amadio PC, An KN, et al: Functional anatomy of the
human digital flexor pulley system, J Hand Surg (Am) 14:949–
956, 1989.
22. Zhao CF, Amadio PC, Berglund L, et al: The A3 pulley, J Hand
Surg (Am) 25:270–276, 2000.
23. Kline SC, Moore JR: The transverse carpal ligament. An
important component of the digital flexor pulley system,
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24. Doyle JR: Anatomy and function of the palmar aponeurosis
pulley, J Hand Surg (Am) 15:78–82, 1990.
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of the Hand, ed 3, Philadelphia, 1984, JB Lippincott,
pp 98–102.
27. Kaplan EB, Hunter JM: Functional anatomy of the flexor
tendon system: The muscles and tendon systems of the
fingers. In Hunter JM, Schneider LH, Mackin EJ, editors:
Tendon and Nerve Surgery in the Hand, A Third Decade, St.
Louis, 1997, Mosby, pp 240–252.
28. Ijpma FF, van de Graaf RC, van Gulik TM: Petrus Camper’s
work on the anatomy and pathology of the arm and hand in
the 18th century, J Hand Surg (Am) 35:1382–1387, 2010.
29. Brunelli GA, Brunelli GR: Anatomical study of distal insertion
of the abductor pollicis longus. Concept of a new musculo-
tendinous unit: the abductor carpi muscle. Ann Chir Main
Memb Super 10:569–576, 1991.
30. Opreanu RC, Wechter J, Tabbaa H, et al: Anatomic variations
of the first extensor compartment and abductor pollicis
longus tendon in trapeziometacarpal arthritis, Hand (NY)
5:184–189, 2010.
31. Grundberg AB, Reagan DS: Pathologic anatomy of the
forearm: intersection syndrome, J Hand Surg (Am) 10:299–
302, 1985.
32. Ogura T, Inoue H, Tanabe G: Anatomic and clinical studies
of the extensor digitorum brevis manus, J Hand Surg (Am)
12:100–107, 1987.
33. Zilber S, Oberlin C: Anatomical variations of the extensor
tendons to the fingers over the dorsum of the hand: A study
of 50 hands and a review of the literature, Plast Reconstr Surg
113:214–221, 2004.
34. Von Schroeder HP, Botte MJ, Gellman H: Anatomy of the
juncturae tendinum of the hand, J Hand Surg (Am) 15:595–
602, 1990.
35. Smith RJ: Balance and kinetics of the fingers under normal
and pathological conditions, Clin Orthop Relat Res 104:92–
111, 1974.
36. Ubiana R: Anatomy of the extensor tendon system of the
fingers. In Hunter JM, Schneider LH, Mackin EJ, editors:
Tendon and Nerve Surgery in the Hand: A Third Decade, St.
Louis, 1997, Mosby, pp 547–550.
 Chapter 1:  Anatomy of the Tendon Systems in the Hand 15

37. Harris C Jr, Rutledge GL Jr: The functional anatomy of the
extensor mechanism of the finger, J Bone Joint Surg (Am)
54:713–726, 1972.
38. el-Gammal TA, Steyers CM, Blair WF, et al: Anatomy of the
oblique retinacular Ligament of the index finger, J Hand Surg
(Am) 18:717–721, 1993.
39. Kaplan EB, Riordan DC: The thumb. In Spinner M, editor:
Kaplan’s Functional and Surgical Anatomy of the Hand, ed 3,
Philadelphia, 1984, JB Lippincott, pp 124–142.
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the thumb: Anatomic and biomechanical study, J Hand Surg
(Am) 27:628–635, 2002.
 CHAPTER
2  
TENDON NUTRITION
AND HEALING
Peter C. Amadio, MD
OUTLINE
This chapter will review current knowledge on tendon
nutrition and healing. Tendon obtains nutrition from
both vascular sources and synovial fluid. The extracel-
lular matrix is the principal component of tendon
tissue, and is responsible for its material properties.
The major constituents are type I collagen; proteogly-
cans, principally decorin, but also aggrecan in the
gliding regions; fibronectin; and elastin. This matrix is
synthesized by tendon cells, or tenocytes. After tendon
injury, the extracellular matrix undergoes significant
changes, due to synthesis of new elements by the teno-
cytes, such as type III collagen, degradation of existing
elements by various matrix metalloproteases, and
remodeling of the resulting combination, under the
influence of cytokines as well as mechanical forces.
Physical factors, such as motion, loading and friction
affect the results of tendon repair. The concept of “safe
zone” was proposed to define the range of external
loading which does not disrupt the tendon repair
when the tendon is loaded during motion. Pharmaco-
logical manipulation of tendon healing, such as use
of 5-fluorouracil, may reduce adhesion formation
during tendon healing, and supplying stem cells or
cytokines may augment intrinsic healing capacity of
the injured tendon. Critical points are as follows.
Regarding nutrition, both synovial and vascular routes
are important; vascular route is affected by age and
injury, and the synovial route is affected by mobiliza-
tion. In healing, motion aids healing and reduces
adhesions. There is little evidence that loading, in the
absence of motion, is helpful, or that, once the tendon
is moving, more loading helps healing. We do know
that loading may lead to failure of the repair. The “safe
zone” involves enough loading to initiate motion but
not enough to risk the repair.
Traditionally, tendons have been thought of as being
inert, hypovascular structures.1,2 However, subsequent
research has shown that tendons are active metaboli-
cally, that tenocytes can replicate and heal experimental
injuries, and that adhesions, while common, are not
necessary for healing.3-6 This chapter will review current
knowledge on tendon nutrition and healing.
16
TENDON NUTRITION
Vascular Sources
Tendons have two sources of vascular nutrition. Extra-
synovial tendons are supplied by circumferential vessels
in the paratenon, a multilayered system elegantly
described by Giumberteau7 and illustrated in Chapter
31. Intrasynovial tendons, such as those in zone 2 in
the hand, are supplied through the segmental vincular
system.8-10 This segmental system results in predictable
watershed zones within the flexor tendon (Figure 2-1),
with intercalated regions on the palmar aspect of the
tendon with little in the way of blood supply. The
number and location of these zones also varies by digit,
with the ring finger generally having the fewest vincula.10
Synovial Fluid
Intrasynovial tendons have a second source of nutrition,
of course—synovial fluid. This mechanism is especially
important in avascular and hypovascular regions of the
tendon3,11-14 and is dependent on the pumping effect of
digital motion. Tendons whose vincula are absent or
damaged and that do not move are therefore deprived
of nutrition, an important consideration for tendon
repair and rehabilitation.
TENDON HEALING
Biology of Tendon Healing
The extracellular matrix (ECM) is the principal compo-
nent of tendon tissue and is responsible for its material
properties.15-17 The major constituents of the ECM are
type I collagen; proteoglycans, principally decorin, but
also aggrecan in the gliding regions18-21; fibronectin; and
elastin. This matrix is synthesized by tendon cells, or
tenocytes. These cells are surrounded by the dense
matrix; thus, although they are metabolically active,
they do not participate much in the tendon healing
process. Instead, undifferentiated cells in the epitenon
do the heavy lifting for tendon healing, proliferating,
migrating into the gap between the tendon ends, and
finally uniting the cut tendon ends22,23 (Figure 2-2).
Unfortunately, this is a two-edged sword; if these same
cells migrate away from the tendon, toward the tendon
sheath, they form adhesions, which restrict tendon

Figure 2-1  Tendon blood supply.
Figure 2-2  Epitenon cells migrating into the repair site 3
weeks after injury in a canine model of tendon injury
(hematoxylin-eosin, magnification ×100).
motion. Often this is indeed the case, as the relatively
ischemic tendon is surrounded by better vascularized
tissue, which sends out vascular buds under the stimula-
tion of vascular endothelial growth factor (VEGF).24-27
After tendon injury, the extracellular matrix under-
goes significant changes, due to synthesis of new ele-
ments by the tenocytes, such as type III collagen,28-30
degradation of existing elements by various matrix
metalloproteases, and remodeling of the resulting com-
bination, under the influence of cytokines such as
Chapter 2:  Tendon Nutrition and Healing 17
transforming growth factor (TGF)β as well as mechani-
cal forces. Manipulation of these processes, to augment
their action between the tendon ends while reducing
them at the tendon’s gliding surface, is the goal of much
research, as described later.
Healing of flexor tendons in zone 2 depends on the
ability of the injured tendon to recruit fibroblasts and
other cellular components to the site of injury.31 Nor-
mally these are circulating or locally derived undifferen-
tiated (i.e., stem) cells that are recruited to the injury
site by the expression of cytokines in the wound.24,27,32-34
Cytokine stimulation is also important in converting
these undifferentiated cells into the tendon phenotype,
characterized by the expression of markers such as
tenomodulin and scleraxis.35,36 Bone marrow–derived
stem cells (BMSCs) can also enter and participate in soft
tissue healing.37-39
EFFECT OF PHYSICAL FACTORS
Motion
Lacerated tendons that are immobilized, unless
extremely well nourished, will heal with adhesions.40-42
While these adhesions can remodel, especially in an
extrasynovial environment, in the region of the tendon
sheath such adhesions are invariably associated with
loss of motion. Thus, motion of flexor tendon repairs
in critical. Duran and Houser43 suggested observing
the repair intraoperatively and maintaining passive
motion sufficient to cause 4 mm of tendon gliding, and
separation of the profundus and superficialis repairs, if
both tendons are injured. Evans has discussed similar
concepts of limited active motion of repaired tendons.44
Loading
Clearly, some load must be applied to a flexor tendon
if it is to move. The loads applied to a tendon by passive
motion of a digit tend to be small, and tendons may
buckle instead of glide, especially if the tendon repair
has a high friction.45 A modification of the usual syner-
gistic passive motion protocol in which the metacarpo-
phalangeal joints are maintained in extension in both
the flexion and extension phases of motion seems to
provide better pull, on the order of 100 g, in both the
flexion and extension directions, and may be useful in
some cases.46,47 The use of higher loads, with active
motion protocols, is somewhat controversial.48-50 My
philosophy has been to tailor the loading to the stage
of healing, as emphasized by Groth,51 as further
described later.
Effect of Friction on the Results
of Tendon Repair
Animal studies over the past decade have shown
convincingly that high friction repairs with knots and/
or many loops on the surface, such as the modified
18 Section 1:  Basic Science
A B
Figure 2-3  A, Abrasion of sheath 6 weeks after MGH repair in an in vivo canine model (scanning electron microscopy,
magnification, ×300). Compare with B, a similar image from a tendon repaired with a modified Kessler suture.
Becker/MGH or Tsuge repairs, result in abrasion of the
tendon sheath (Figure 2-3) and adhesion formation,
even when factors such as rehabilitation method are
optimized.52-54 Thus, the goal should be to use a high-
strength, low-friction repair construct, such as the modi-
fied Kessler, Tajima, or Pennington repairs, and a
low-friction suture material, of which there are many.
Most recently, I have been using 3-0 polyester suture and
a modified Pennington design.
Impact on Postoperative Management:
Concept of the “Safe Zone”
Until the mid 1960s, most flexor tendon repairs were
immobilized postoperatively for three weeks. This
policy was based on the research of Mason and Allen,55
who had shown that canine flexor tendon repairs
decreased in tensile strength for three weeks postopera-
tively. Subsequent clinical work by Verdan,56 Kleinert
et al,57 and Duran et al58 showed that human flexor
tendon repairs could be safely mobilized with a combi-
nation of active extension and passive flexion.
The use of early mobilization after tendon repair has
resulted in improved outcomes for flexor tendon inju-
ries.56,58-62 In animal models,45,53,63-67 earlier mobiliza-
tion results in better final tendon gliding and tensile
strength. More recently, the fine details of mobilization
have been studied, specifically the effect of timing68-70
and the effect of differential motion of the wrist and
finger joints on tendon loading and tendon gliding
during the healing period.49,53,71 Active motion protocols
have also been used, although, interestingly, the clinical
results are not reliably better than passive protocols.72-75
Moreover, the addition of loading to motion in animal
models has been shown to have little effect on the final
result in terms of strength and motion.49,67,76 Thus, the
available evidence suggests that motion, not load, is the
critical factor.
Of course, there must be some load on the tendon if
it is going to move; at the very least, the load must be
sufficient to overcome the forces of friction. It is for this
reason that low friction repairs are important—they
minimize the load needed to initiate movement. Fric-
tion, though, is not the only concern. The force needed
to overcome joint stiffness and to flex traumatized,
edematous tissues must also be considered, as well as
the weight of the distal digit itself; often these latter
forces will far outweigh the frictional ones in magni-
tude, especially in an injured digits. So the minimum
force needed to load the tendon will be a combination
of the frictional force and the force needed to move the
joints and soft tissues. The energy needed to flex the
digit is often called the “work of flexion”.69,77,78
One might imagine that the maximum load that
could be applied is the load that represents the breaking
strength of the tendon, but that would be incorrect: long
before the tendon breaks, it begins to gap, and gapping
also increases friction, setting up a vicious circle that can
lead to later rupture. So, really, the upper bound is not
breaking strength but the force needed to create a gap,
which is usually much less.50,62,79-87 The difference
between the two forces—the force to initiate unloaded
digital flexion and the gapping force—represents the
“safe zone” in which rehabilitation can occur88 (Figure
2-4). Early on, this safe zone will be bounded by strictly
mechanical parameters, related to the anatomy and bio-
mechanics of the repair. Over time, though, the effects
of tendon healing are added in; the general effect is
usually to gradually widen the safe zone, enabling the
rational use of a graded resistance program as outlined
by Groth.51 The details of such programs are reviewed
in Chapter 38.
Unfortunately, in some cases, early mobilization after
tendon repair is not possible by any method. Common
examples include situations with complex hand injury,
in which motion might jeopardize bone, skin, nerve
or vascular integrity; patients who are uncooperative
due to age or mental status; or situations where the
tendon repair is deemed to be too tenuous to tolerate

Max strength
In Vitro
40N Initial strength of the repair
Max strength
1 wk. In Vitro
30
2 mm gap Initial “safe zone”
20
Initial gap Effect
10 of time
Friction 5
of the In Vitro
repair 0.2 Repair
Figure 2-4  The “safe zone” concept.
mobilization. In such cases, adhesions have been, up to
now, inevitable. It is possible, though, that the applica-
tion of a tissue engineered, biocompatible adhesion
barrier that is porous to nutrients might allow an immo-
bilized tendon to heal without adhesions. We are cur-
rently pursuing research to address this issue, using
carbodiimide derivatized hyaluronic acid and lubricin,
linked to collagen, as the proposed barrier, and hope to
have an update in time for the next edition of this book.
PHARMACOLOGICAL MANIPULATION
OF TENDON HEALING
Various pharmacological agents have been used in the
past in an attempt to modify adhesion formation. Ste-
roids, antihistamines, and beta-aminoproprionitrile
have not been shown to clinically decrease scar forma-
tion.89,90 Ibuprofen and indomethacin have been found
to have a small beneficial effect.91
The ideal pharmacological agent should have no
systemic side effects, should be limited to a single
application, and should be directed at growth factor
expression and ECM production. 5-Fluorouracil (5-FU)
may be such a drug. 5-FU is an antimetabolite that
is used not only as a cancer chemotherapeutic agent
but also to prevent adhesions in glaucoma filtration
surgery. The exposure of a surgical field to 5-FU pro-
duces a focal inhibition of scarring. Blumenkranz
et al92,93 has found that 5-FU is able to inhibit the pro-
liferation of fibroblasts in cell cultures and reduce retinal
scarring. Single exposures to 5-FU, for as short duration
as 5 minutes, can have antiproliferative effects on fibro-
blasts for several days. The suppression of fibroblast
proliferation has been observed for up to 36 hours
without signs of cell death.94,95 This time frame may be
adequate to inhibit tendon adhesions prior to begin-
ning postoperative motion protocols. Reversible pro-
longed inhibition of fibroblast function is attributed to
the drug’s inhibition of DNA and mRNA synthesis
through thymidylate syntheses. More important, these
Chapter 2:  Tendon Nutrition and Healing 19
Lubricated surface
Patch containing cells,
growth factors and collagen
Figure 2-5  Conceptual model of stem cell patch to
augment tendon repair.
effects appear to be focal to the site of application and
titratable in terms of length of action.96-98 A 5-minute
exposure to 5-FU has been shown to significantly
decrease postoperative flexor tendon adhesions in
chicken and rabbit models.99,100 This beneficial effect is
thought to be due to the downregulation of TGFβ and
modulation of matrix metalloproteinase (MMP)-2 and
MMP-9 production.101,102 The effect on surface lubrica-
tion is unknown. No adverse effect was noted on tendon
healing in these studies. It is presumed therefore that
the topical 5-FU does not penetrate to affect the cells
below the tendon surface. Topical application of 5-FU
may well have a role in improving the outcomes in
selected cases of tenolysis.
AUGMENTATION OF INTRINSIC
TENDON HEALING
Stem Cells
BMSCs delivered on collagen sponges improve healing
in animal models of tendon repair,103,104 and stem cells
from other origins have been shown to be effective
in enhancing repair in several other tendon injury
models.105-108 Current research is focused on optimizing
the isolation and differentiation of stem cells into the
tendon phenotype. In the future, it is likely that cells
derived from the patient’s own bone marrow, fat, skin,
or muscle will be used as a “patch” to augment tendon
repair (Figure 2-5). My colleagues and I are pursuing
one such option in our laboratory now: a mixture of
collagen, growth factors, and stem cells from the patient’s
own tissues and lubricated with an engineered surface
containing hyaluronic acid and lubricin.109-112 Such a
graft could also be used to bridge flexor tendon defects,
and, finally, replace like with like.
Cytokines
Growth factors are the chemical signals that direct the
migration and proliferation of the tendon fibroblast
during the healing process. The role of growth factors
has been examined extensively in cutaneous wounds
and other soft tissue processes, yet we are only begin-
ning to known the specifics involved in flexor tendon
healing.17,113 The factors that appear to be involved
20 Section 1:  Basic Science
include TGFβ, platelet-derived growth factor (PDGF),
basic fibroblast growth factor (bFGF), insulin-like
growth factor (IGF), epidermal growth factor (EGF),
and VEGF.27,114,115 These same growth factors have also
been shown to optimize tissue-engineered constructs
used for tendon repair.27,104,114-117 Growth differentiation
factor-5 (GDF-5), a member of the TGFβ superfamily,
has also been shown to accelerate tendon healing in
multiple animal models.118-120
TGFβ stimulates the formation of the ECM. It signals
fibroblasts to produce collagen and fibronectin,
decreases protease production, and increases the forma-
tion of integrins, which promote cellular adhesions and
matrix assembly. In normal tissue, TGFβ becomes inac-
tivated once wound healing is complete; however, it
may remain active in tendon adhesion formation, con-
tinuing the cycle of matrix accumulation.121,122 Modula-
tion of TGFβ has been reported to reduce peritendinous
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103. Butler DL, Jucosa-Melvin N, Boivin GP, et al: Functional
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108. Zantop T, Gilbert T, Yoder MC, et al: Extracellular matrix
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109. Zhao C, Sun Y-L, Amadio PC, et al: Surface treatment of
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tion improves extrasynovial tendon gliding in a canine
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modifications of extrasynovial tendon to improve its gliding
ability in a canine model in vitro, J Orthop Res 24:1555–1561,
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112. Sun YL, Yang C, Amadio PC, et al: Reducing friction by
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113. Singer AJ, Clark RAF: Cutaneous wound healing, N Engl J
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2007.
 CHAPTER
3  
TENDON FRICTION,
LUBRICATION, AND
BIOMECHANICS OF MOTION
Chunfeng Zhao, MD, Peter C. Amadio, MD, and
Kai Nan An, PhD
OUTLINE
Both physiological and pathological conditions
regarding tendon friction, lubrication, and motion are
discussed in this chapter. Tendon friction and lubrica-
tion mechanism vary according to tendon type. Intra-
synovial tendon, regularly located in high abrasion
areas, has less frictional force and greater durability
than the extrasynovial tendon. The lubrication mecha-
nism of the intrasynovial tendon is similar to that of
the articular cartilage. Proteoglycan, hyaluronic acid,
and phospholipid are the major lubricating compo-
nents. Extrasynovial tendon relies on the paratenon
sequential gliding phenomenon to reduce the direct
abrasion of the tendon with surrounding tissues.
However, this gliding unit is fragile. A hybrid of intra-
synovial and extrasynovial tendon occurs in the carpal
tunnel. Adequate tendon excursion is essential to
maintain normal muscle and joint function. An
increased tendon moment arm (such as bowstringing)
will affect both strength and excursion of the tendon.
A healthy tendon is essential to maintain the normal
functional performance of muscles and joints. Since the
tendons transmit both force and displacement from
muscle, the tensile strength of the tendon must be
strong enough to bear the range of anticipated loading,
and the tendon displacement must be long enough to
achieve full joint motion. Lose of either property would
not only jeopardize the tendon functional performance
but also affect muscle and joint function. Therefore, an
understanding of tendon friction, lubrication, and bio-
mechanics, in both physiological and pathological con-
ditions, is essential for clinicians who diagnose and treat
tendon disorders.
TENDON FRICTION
Tendon Friction in Physiological Conditions
When tendons glide against surrounding tissue, espe-
cially when passing through a series of pulleys in the
24
fingers, frictional force must be encountered. An et al1
developed a tendon/pulley gliding model to measure
the frictional force and calculate the frictional coeffi-
cient (Figure 3-1). If the impending motion of the cable
is from F1 to F2, then F2 is greater than F1 due to the
friction f, and f = F2 − F1. F2 is also related to F1 as F2
= F1eµø, where µ is the frictional coefficient. If a loga-
rithm is taken, LnF2/F1 = µø. If the values of F2, F1, and
ø are known and natural logarithms of F2/F1 are plotted
against angles in radians, the frictional coefficient can
be calculated as the slope of a line designed according
to the least-squares method.2
The assessment of frictional force at the tendon–
pulley interface with this method is an ideal model.
However, tendon gliding is far more complicated. In
classical theory, for friction without a lubricant, three
laws have been postulated3: (1) The frictional force is
directly proportional to the applied load; (2) frictional
force is independent of the apparent area of contact; and
(3) the kinetic frictional force is independent of the
sliding speed. However, these rules must be modified in
tendon, for several reasons. First, the tendon is a visco-
elastic tissue. Its properties are affected by the velocity
of tendon motion, and its surface deforms in response
to contact pressure. In addition, tendon is lubricated, at
least normally.
Moriya et al4 investigated three parameters that may
relate to tendon friction: temperature (4°C, 23°C, and
36°C), gliding velocity (2, 4, 6, 8, or 12 mm/sec), and
load (250, 500, 750, 1000, 1250, and 1500 g) applied
to the tendon using a flexor digitorum profundus
tendon and A2 pulley model. They found that the
tendon friction was proportional to load, but not,
within the ranges studied, to gliding velocity (Figure
3-2A and B). The temperature also affected the tendon
friction; the friction at 4°C was significantly higher than
that at body temperature, 36°C. This information is
useful to guide the experiments that relate to tendon
frictional testing. Some studies have also demonstrated
that tendon frictional force is dependent on joint posi-
tion or the direction of motion. Zhao et al5 found that
 Chapter 3:  Tendon Friction, Lubrication, and Biomechanics of Motion
70
65
60
55
50
45
40
35
20
15
10
5
0
Mechanical
actuator
and linear
potentiometer
Figure 3-1  Illustration of the tendon–pulley frictional measurement system, consisting of a mechanical actuator with a
linear potentiometer, two tensile load-transducers connecting distal (F1) and proximal (F2) to the A2 pulley, a mechanical
pulley (right), a Dacron cord, and a weight. FDP, Flexor digitorum profundus.
the friction at the flexor tendon–transverse carpal liga-
ment interface was significantly higher in wrist flexion
compared to the neutral position. Heers et al6 studied
the frictional force of the long head of the biceps tendon
during shoulder motion and found that the frictional
force during abduction was significantly higher than
that of adduction.
Tendon Friction in Pathological Conditions
The normal tendon frictional force is small. The fric-
tional coefficient of flexor tendon in zone 2, where two
flexor tendons are enveloped by flexor sheath with syno-
vial fluid between, is comparable to that of cartilage.7-9
However, the frictional force after tendon injury and
repair dramatically increases, which impairs tendon
function. Sutures create roughness of the tendon surface
and increase friction. Sutures also increase the volume
of the tendon, and postinjury edema can increase fric-
tion as well. Afterward, the biological healing between
tendons and surrounding tissue forms adhesions, which
increase the frictional force and may in some cases
totally impede tendon gliding.
Strategies to reduce the fictional force after tendon
repair have been studied.7,10-12 Surface friction of a
repaired tendon can be reduced by burying knots
between tendon ends, or locating the knots away from
the anterior tendon surface, choosing low friction suture
materials, and using fewer suture loops and strands.13,14
Using a canine in vivo model, Zhao et al15 found that
25
80 85 90 85 80 7
75 5 70
65
60
55
50
45
40
35
30
25
F1
F2 A2
pulley
10
5
α β
0
FDP
tendon
Load
a lower friction repair technique, the modified Kessler
repair, had fewer adhesions after 6 weeks compared to
a higher friction technique, the modified Becker repair.
However, these positive adhesion outcomes were com-
bined with higher rates of gap formation and rupture.
To balance the tensile strength and friction, several
studies have studied suture techniques with higher
tensile strength and lower friction. Momose et al16 used
a looped suture with a modified Kessler suture tech-
nique to repair flexor tendons and achieved high tensile
strength with relative low friction. Later, Tanaka et al17
demonstrated that the modified Pennington technique
possesses low friction and high strength.
Some alternative surgical techniques have been devel-
oped to minimize bulk after tendon repair. Resection of
one slip of the flexor digitorum superficialis (FDS)
tendon decreased the repaired flexor digitorum profun-
dus (FDP) tendon gliding resistance.18 Pulley plasty also
reduces friction.19 Trimming the pulley edge on an
oblique, rather than perpendicular to the long axis of
the bone, may also help the repaired tendon pass
through with less risk of triggering.20
The frictional force of a repaired tendon with a gap
has also been studied. The friction of repaired tendons
without gap mainly comes from surface roughness.
However, with gap formation, plowing friction, related
to surface shape, becomes dominant, which dramati-
cally increases the resistance. If a repaired tendon has a
3-mm or larger gap, the plowing frictional force may
26 Section 1:  Basic Science

increase sharply due to the trapping of the repaired
tendon edge on the pulley, eventually leading to repair
failure if the applied load exceeds the repair strength.21
The tendon frictional force may also increase in cir-
cumstances not related to tendon injury or repair. Joint
deformities that cause the tendon pulley gliding angle
FRICTION VS LOAD
1
0.8
Frictional force (N)
to increase, as in rheumatoid arthritis, also increase fric-
tional force.22 Trigger finger is another example where
increased bulk and decreased lubrication hamper
tendon gliding through the pulley. The integrity of the
flexor pulley system is also important to maintain
normal frictional force during finger motion. Resection
of the A3 pulley increases the gliding resistance between
tendon and A2 pulley.23 Increased carpal tunnel pres-
sure also increases tendon frictional force.24
Tendon Friction in Different Tendon
Surroundings

Tendons can be classified as intrasynovial and extrasy-

0.6 novial tendons based on their surrounding environ-
ment.25 Intrasynovial tendons are defined as tendons, or
0.4 parts of tendons, enclosed within a synovial sheath.
These tendons are lubricated by synovial fluid, and the
0.2 tendon surface is covered by a thin visceral synovial
membrane, the epitenon (Figure 3-3). The epitenon
0 cells are similar to synovial cells and secrete lubricants.
A 250 500 750 1000 1250 1500 (g) This unique structure effectively decreases friction,
reduces abrasion, and eliminates wear. Flexor tendons
FRICTION VS VELOCITY
in zone 2 area are typical intrasynovial tendons. Exten-
0.5
sor tendons in the dorsal wrist area, the long head of
0.4
the biceps brachii tendon, and the posterior tibial
Frictional force (N)

tendon at the medial malleolus are other examples of

0.3 intrasynovial tendons. In contrast, the tendons located
within subcutaneous soft tissues are extrasynovial
0.2 tendons. These tendons are covered by loose connective
tissue, called paratenon (see Figure 3-3). In addition,
0.1 some tendons have a hybrid type. Ettema et al26 reported
that flexor tendons in zone 4 (within the carpal tunnel)
0 have a unique structure, in which the subsynovial con-
2 4 6 8 10 12 nective tissue (SSCT), a paratenon-like structure, covers
B Gliding velocity (mm/s)
each flexor tendon. The SSCT and tendon are in turn
Figure 3-2  The frictional force of tendon is proportional to encased in a synovialized bursa. Therefore, the flexor
load applied to the tendon (A) but independent of the tendons in this region include both intrasynovial and
gliding velocity (B). extrasynovial gliding mechanisms (see Figure 3-3).

Figure 3-3  Left, Intrasynovial tendon region, Surrounding

the tendon surface is covered by epitenon, tissues
which includes several layers of epitenon cells
seeding on the surface (top, hematoxylin-
eosin stain). Middle, Extrasynovial tendon that Tendon
is wrapped by loose connective tissue,
paratenon (top, hematoxylin-eosin stain). Synovial
Epitenon Paratenon SSCT Bursa
Right, Hybrid region of the tendon that sheath
wrapped by paratenon and synovial sheath
bursa (top, hematoxylin-eosin stain).

Intrasynovial Extrasynovial Hybrid

portion portion portion
 Chapter 3:  Tendon Friction, Lubrication, and Biomechanics of Motion
2.0
FDP
PL
Friction force (N)
1.0
0 0
0 4 8 12
Load (N)
Figure 3-4  The slope of friction versus load for the
extrasynovial tendon (palmaris longus [PL]) was higher than
that for the intrasynovial tendon (FDP). (Data from Uchiyama
S, Amadio PC, Coert JH, et al: Gliding resistance of
extrasynovial and intrasynovial tendons through the A2
pulley, J Bone Joint Surg Am 79:219–224, 1997.)
Although the gliding ability of the paratenon is not
as durable as the epitenon, it serves as a cushion and
sliding sleeve to protect the tendons from surrounding
tissues, such as muscle, bone, and neurovascular struc-
tures. It also serves as a network to protect the vessels
and nerves that provide the nutritional supply of
tendons.27
Due to the differences of anatomy and structure
between intrasynovial and extrasynovial tendons, the
frictional force of extrasynovial tendons is much higher
than that of intrasynovial tendons.28,29 Uchiyama et al
found that the frictional force of the palmaris longus
tendon increased with increasing loads. In contrast, the
frictional force of FDP tendon was nearly independent
of the load applied to the tendon (Figure 3-4). Several
studies have demonstrated that the frictional force of
extrasynovial tendons increases rapidly with cyclic
motion,29-31 while intrasynovial tendons maintain a
constant frictional force even after 1000 cycles of tendon
motion (Figure 3-5).
Tendon surface morphology has been studied with
the use of electron microscopy. These studies show that
the intrasynovial tendon surface has a smooth surface,
with no collagen fibrils exposed on the surface. After
cyclic motion, this smooth surface is maintained. In
contrast, the paratenon on the extrasynovial tendon
surface wears off with cyclic motion, exposing increas-
ing amounts of collagen fibrils with increasing number
of motion cycles (Figure 3-6). One could argue that
extrasynovial tendon rarely glides against a pulley, but
this is only true normally. When an extrasynovial tendon
is used as a graft to reconstruct an intrasynovial tendon,
which is a common clinical situation, then the tendon
does glide against a pulley. While there are many reasons
27
0.8
0.7 PL tendon
FDP tendon
0.6
Friction (N)
0.5
0.4
0.3
0.2
0.1
0
200 400 600 800 1000
16 Number of cycles
Figure 3-5  The friction of the extrasynovial tendons rises
up rapidly with cyclic motion. The intrasynovial tendon
remains at the same level of frictional force even after 1000
cycles of tendon motion.
why tendons may form adhesions, increased friction is
certainly one of the major factors to consider, which
can be ameliorated if an intrasynovial graft is available.
Unfortunately, there are few intrasynovial tendons that
can be sacrificed for the purpose of tendon grafting. The
development of a tissue-engineered intrasynovial graft
is one object of our research.
TENDON LUBRICATION
Lubrication has been the focus of intense study in
articular cartilage, since cartilage degeneration is associ-
ated with mechanical abrasion and wear.32-34 Although
tendon does not bear as much compressive loading as
cartilage, the number of motion cycles experienced by
tendons is comparable to that of joints and was esti-
mated at over 1 million cycles per year.35,36 Therefore,
tendon lubrication is very important, especially for the
intrasynovial tendons in the hand, which experience
the most cyclic motion. Since the gliding structure of
the intrasynovial and extrasynovial tendon structure is
different, the lubrication mechanism is also totally
different.
Intrasynovial Tendon Lubrication Mechanism
As the intrasynovial tendon glides within a synovial fluid
environment, its lubrication mechanism is similar to
the cartilage in the articular joint, which associates two
lubricating phenomena (i.e., boundary lubrication and
fluid-film lubrication). Boundary lubrication mainly
relies on the tendon surface structure. The intrasynovial
tendon surface is covered by a highly resistant, tenacious
epitenon layer acting as a living boundary support load
and avoiding collagen wear. These cells also secrete
lubricants into the synovial fluid. In addition, some of
the secreted lubricants are bound to the intercellular
matrix, and thus remain adherent to the epitendinous
28 Section 1:  Basic Science

FDP tendon Before testing After 1000-cycle After 1000-cycle

A B C
PL tendon

D E F
Figure 3-6  The morphological appearances under scanning electron microscopy (SEM) of the intrasynovial tendon
(A, normal tendon before testing; B, after 1000 cycle motion in low magnification; and C, after 1000 cycle motion in high
magnification) display a smooth surface compared to the extrasynovial tendon (D, normal tendon before testing; E, after
1000 cycle motion in low magnification; and F, after 1000 cycle motion in high magnification paratenon on the extrasynovial
tendon surface wears off with collagen exposed under tendon cyclic motion against pulley).

surface. The extracellular matrix of the epitenon layer Core protein

has similar components and structure as the superficial
zone of the cartilage, including collagen, hyaluronic
acid, proteoglycans, and phospholipids. The structural Chondroitin
collagen in tendon is type I collagen. Hyaluronic acid sulfate
(HA) is an important component on the tendon surface.
Keratan
Proteoglycans bind to HA in the presence of HA binding sulfate
protein (Figure 3-7),37,38 forming large highly negatively HA
harged aggregates. These aggregates imbibe water to HA–binding
form a highly viscous layer to decrease friction and wear domain
during tendon motion. The major lubricating proteogly-
can on the tendon surface is lubricin.39,40 Phospholipids,
existing on the cell surface and extracellular matrix, are
also important for lubrication.41,42 These three compo- Proteoglycan
nents (i.e., HA, lubricin, and phospholipid) are present Hyaluronic
in the synovial fluid as well. acid (HA)
The removal of any of these three lubricating sub-
stances results in increased friction.43 Conversely, exog- Epitenon cell
enously applied lubricants on the tendon surface
decrease the frictional force, especially in combination, Collagen
and when chemically bound to the tendon Phospholipids
surface.29-31,44 Figure 3-7  Intrasynovial tendon surface structure.
Extrasynovial Tendon Lubrication
In contrast to intrasynovial tendon, the extrasynovial moves, the paratenon layer closest to the tendon starts
tendon has no synovial fluid environment. The lubrica- to move. This stretches the collagen fibers crosslinking
tion mechanism relies on the paratenon sliding unit.27 between the paratenon layers, leading to the next layer’s
The paratenon gliding mechanism of extrasynovial subsequent motion. This sequential small motion
tendon has been well studied recently, using flexor among paratenon layers effectively reduces the total
tendon in zone 4 as a model.26,45,46 When the tendon tendon excursion related to the surrounding tissue
 Chapter 3:  Tendon Friction, Lubrication, and Biomechanics of Motion 29

Outer paratenon
displacement

A B

Tendon displacement

Paratenon

Tendon

Figure 3-8  Extrasynovial tendon gliding mechanism. When a tendon moves from A to B, the paratenon layer that closes to
the tendon moves first and then transmit to the next layer by the connecting collagen fibers shown by the scanning electron
microscopy (SEM) left (relaxed) and right (stretched). This sequential motion of the multi–paratenon-layer motion decreases
the relative motion between tendon and surrounding tissue.

and decreases abrasion during tendon motion (Figure

3-8).47 Any pathological changes of the paratenon, such Toe region Linear region Failure region
as fibrosis, could alter this sequential motion pattern,
which in turn may lead to clinical problems. Indeed, a
Sress (N/ma)

disruption of this mechanism has been suggested as a

cause of carpal tunnel syndrome.26
BIOMECHANICS OF TENDON MOTION
Flexor tendons cross over multiple joints, including the
wrist, metacarpophalangeal (MCP) joint, proximal
interphalangeal (PIP) joint, and distal interphalangeal
(DIP) joint. Therefore, a large excursion is needed to
achieve full joint motion. Flexor tendons also bear large
tensile loads during forceful hand motion and experi-
ence a huge number of repetitive motion cycles during
routine activities. It is essential therefore to understand
the mechanical properties and motion characteristics of
the flexor tendons.
Mechanical Properties of Tendon
Mechanical properties of tendon are determined by its
basic structure, molecular organization, cellular arrange-
ment, and extracellular crosslinking. The tendon con-
sists of 60% to 80% water in its wet weight. The major
extracellular matrix is type I collagen, which is estimated
to comprise about 80% of the tendon’s dry weight.
Proteoglycans and elastin make up 1% to 5% and 2%
of the dry weight, respectively.48 Collagen’s hierarchical
structure has been well described. The collagen mole-
cule itself is a triple helix of polypeptide chains linked
by covalent and hydrogen bonds. Five crosslinked
Strain
Figure 3-9  Tendon mechanical properties can be typically
presented by its stress-strain curve, which includes three
phases: a toe region, a linear region, and a failure region.
collagen molecules form a microfibril, and groups of
microfibrils assemble a subfibril, which then combine
to form larger fibrils. Fibrils are packed in parallel
bundles with proteoglycans and water to form the fas-
cicles. The numbers of fascicles, which are wrapped by
the endotenon, compose a tendon bundle.48,49 Some
tendons have only one tendon bundle; others have
several. For example, the canine flexor digitorum pro-
fundus tendon in zone 2 has two bundles.50
The tendon stress-strain curve includes three phases:
a toe region, a linear region, and a failure region (Figure
3-9). The toe region is the initial loading phase, in
which a small axial load can reach a large elongation.
30 Section 1:  Basic Science
Creep
Elongation
Load
Constant load
Elongation
Load
A Time (load control)
Constant elongation
Stress
Elongation
relaxation
Load
Elongation
Load
B Time (displacement control)
Figure 3-10  A, Creep is the time-dependent elongation of
the tendon under a constant load. B, Stress relaxation
presents the concomitant decrease in load as the tendon is
subjected to a constant elongation.
This behavior is attributed to the collagen at the molecu-
lar level unfolding from an initial relaxed state. The
linear region demonstrates the fundamental tendon
mechanical properties, in which the tendon elongation
is constant under a given load. The slope of the stress
to strain represents Young’s modulus of elasticity. In
the failure region the collagen crosslinks gradually
break until complete disruption occurs. Since the
tendon is a viscoelastic tissue, the mechanical behavior
of tendon can be also characterized by creep and stress
relaxation. Creep is a time-dependent elongation of the
tendon under a constant load (Figure 3-10A). Stress
relaxation represents the concomitant decrease in load
as the tendon is subjected to a constant elongation
(Figure 3-10B).
In the normal tendon, Young’s modulus ranges from
1200 to 1800 Mpa, the ultimate strength ranges from
50 to 150 MPa, and the ultimate strain to failure ranges
from 9% to 35%.48 However, the true strain is probably
less. The strains noted in publication are measured from
the places where the tendon is gripped. More detailed
studies of strain within the tendon suggest that there is
always some slippage at the grips, and the intratendi-
nous true strain to failure is less.
Tendons are rarely subjected to within 30% of the
tendon ultimate force and stress values, even for the
most vigorous activity.51,52 This high safety factor may
explain why tendon rupture is usually at the muscle–
tendon conjunction or tendon–bone insertion, rather
than within the tendon substance,53,54 unless the tendon
is damaged by disease or trauma.55-57
Biomechanics of Tendon Motion
The flexor tendon excursion depends on the range of
joint motion and applied tension.58-60 In the pathologi-
cal condition, there are other factors, such as tendon
adhesions, joint contracture, bone shortening, or pulley
resections, that also affect excursion.61-63 Wehbe et al58
measured tendon excursion radiographically in 36
hands in which the flexor tendons were tagged with
buried wire sutures. The flexor digitorum profundus
tendon excursion averaged 32 mm and the flexor digi-
torum superficialis tendon averaged 24 mm with the
wrist in the neutral position. With wrist range of motion
added, the amplitude of the profundus tendon excur-
sion increased to 50 mm and the superficialis tendon to
49 mm.58
The correlation between tendon excursion and joint
motion has been well studied.64,65 For single joint
motion, the ratio of the joint motion and tendon excur-
sion is determined by the joint moment arm. Since the
moment arm is different for different joints, the relation
of tendon excursion and joint motion is different at
different joints. The larger the moment arm, the greater
the tendon excursion must be to produce a given angle
of joint rotation. For example, at the DIP joint, every 10
degrees of motion requires 1.2 mm of FDP tendon
excursion, while at the MCP joint every 10 degrees of
motion requires 2.2 mm of FDP tendon excursion.59
The tendon excursion also can be mathematically
calculated based on the joint moment arm.61,64,65 The
moment arm is defined as the perpendicular distance
between the joint center rotation and the central longi-
tudinal axis of the tendon (Figure 3-11). To best under-
stand the relationship between tendon excursion, joint
angular motion, and moment arm, the geometric
concept of the radian has been introduced (Figure
3-12).64 The basic concept is that the joint is like a
wheel, and the tendon is like a rope going around the
outer edge of the wheel. As the rope is pulled, the wheel
turns. For one complete rotation of the wheel (360
degrees) the rope must move the full circumference of
the wheel, which is 2πr. The moment arm, or distance
from the center of rotation to the closest point on the
tendon, is also the radius of the circle, or r, which means
that when the joint moves roughly 57.29 degrees
(360/2π), the tendon will have moved a distance equal
to r. This angular rotation, 57.29 degrees, is called a
radian.
The moment arms of the hand joints have been
reported with 12.5 mm at the wrist, 10 mm at the MCP
joint, 7.5 mm at the PIP joint, and 5 mm at the DIP
joint.64,66 Based on the angular motion of the finger
joints (MCP, 85 degrees; PIP, 110 degrees; DIP, 65
degrees), the excursion was calculated as 14.8 mm in
the MCP joint, 14.4 mm in the PIP joint, and 5.7 mm
in the DIP joint (see Figure 3-12). These results indeed
were similar to excursion that was experimentally
 Chapter 3:  Tendon Friction, Lubrication, and Biomechanics of Motion
Moment
arm
110° ~ 14.4 mm
140° ~ 30 mm
Figure 3-12  The FDP tendon excursion can be calculated by the joint moment arm and its range of motion based on the
principle that the excursion is equal to moment arm when joints move 57.29 degrees (1 radian).
measured using human fingers.58,59 This mathematical
calculation model provides a useful tool for the valida-
tion of in vivo measurement of tendon excursion.67-69
Tendon excursion is also dependent on the force
applied to the tendon. The excursion with active motion
is longer than the excursion with passive motion due to
the difference of the force applied to the tendon.60,70,71
Although joint passive motion can induce a pushing
force from distally towards proximally which is able to
create tendon motion, this passive tendon excursion is
limited by tendon buckling, if the resistance to passive
motion exceeds the passive force applied to the
tendon.71,72 In contrast, active motion not only elimi-
nates this tendon buckling effect but also elongates the
tendon viscoelastically, to create more tendon excursion
even without joint motion. In addition, the active force
on the tendon boosts the bowstring effect, especially
when the joint is in flexion position (Figure 3-13). This
bowstring effect will increase the tendon–joint moment
31
Figure 3-11  The moment arm is the
perpendicular distance between the joint
center rotation and the central
longitudinal axis of the tendon.
85° ~ 14.8 mm
65° ~ 5.7 mm
1 Radian = 57.29°
5 mm 7.5 mm 10 mm 12.5 mm
DIP PIP MP Wrist
arm, leading to a need for more tendon excursion to
produce a given arc of motion.
The flexor tendon–pulley system elegantly balances
the force generation and tendon movement.66 Tendon
excursion has an upper limit, so moment arms need to
be small to affect the most motion. However, tendons
transmit force, so moment arms should be big to apply
more force. The volar plate–based annular pulleys, A1,
A3, and A5, provide this flexibility, because the moment
arms begin short with the finger extended and then
gradually increase as the finger flexes, and the volar plate
bows away from the joint center of rotation. Using this
concept, many postoperative rehabilitation protocols
have been developed.71,73-76
The tendon motion or excursion can also be affected
by the tendon friction within the flexor sheath. This
effect may not be obvious since the normal frictional
force is very small. We have already discussed some
pathological conditions that cause the friction to
32 Section 1:  Basic Science
Moment arm
Figure 3-13  Moment arm of the PIP joint increases with
the joint flexion due to bowstring effect when a tension (10
Newton) is applied to the FDP tendon.
increase, potentially hindering tendon motion, such as
trigger finger or tendon repair.7,17,74,77-80
Mechanical resistance to tendon gliding is composed
of external sources of resistance and internal sources of
resistance. The external sources of resistance consists of
joint stiffness, surrounding soft tissue resistance, mass
of the digit, and resistance of antagonist muscles. The
internal resistance includes surface friction between
tendon and sheath, the bulk friction due to the fit of
the tendon within the flexor sheath, and biological
adhesions. The energy expended by internal resistance
in only a small portion (10%) of total work of flexion.
However, the internal resistance after tendon repair
increases 274% for low-friction repair techniques and
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 CHAPTER
4  
BIOMECHANICS OF CORE AND
PERIPHERAL TENDON REPAIRS
Jin Bo Tang, MD, and Ren Guo Xie, MD
OUTLINE
Surgical sutures with core and epitendinous stitches
are the mainstay of tendon repair. Adequate mechani-
cal strength is essential for a repair to resist gapping
and failure. A repair using conventional two-strand
core sutures is weak; repairs using four- or six-strand
core sutures are stronger. To ensure surgical repair
strength, a sufficient number of strands (four or more)
passing through the repair site, an optimal core suture
purchase (0.7 to 1.2 cm), appropriate suture calibers
(4-0 or 3-0), and optimal size (2 mm) of locking or
grasping anchors are essential. Maintaining a certain
baseline tension on the core suture during surgery
greatly benefits gap resistance. It should be realized
that repair strength decreases considerably as the
finger flexes, and traumatized tendon ends tend to
soften during the first 2 weeks postsurgery, thus reduc-
ing the holding power of the suture. The innately weak
and slow biological healing creates a “no gain” lag
period in tendon strength during the first 3 to 4 weeks
after surgery. We should ensure that the strength of
surgical repairs is greater than the forces generated
during unresisted active finger flexion (1 to 35 N for
a normal adult) plus a certain safety margin.
The gap resistance, ultimate strength, and stiffness of
repaired tendons are the primary parameters that define
the mechanical properties of a surgical repair. To evalu-
ate a surgical repair, the tendon is usually tested under
a single cycle load-to-failure or under cyclic loading;
both generate load-displacement curves. The cycle
numbers at which gapping occurs and the repair com-
pletely fails indicate performance of the repair.
Surgical repairs of the tendon are divided into end-
to-end repairs (for acutely lacerated tendons), repairs of
tendon–bone junctions, and tendon repairs by other
methods (such as interweave repairs for tendon grafting
or transfer). This chapter will be devoted to end-to-end
repairs for primary tendon surgery. These repairs have
received the most attention, and their success is most
dependent on repair mechanics. Strong surgical repair
is the mechanical basis of early tendon mobilization
and a prerequisite for biological healing.
The end-to-end repair commonly consists of two
parts: (1) core sutures that provide essential strength and
(2) peripheral sutures (also called epitendinous sutures)
that serve to “tidy up” the tendon approximation.
Strength of the repairs relates to the tendons’ resistance
to gapping at the repair site and to complete failure
during tendon movement, which consequently relates
closely to adhesions and ruptures of the tendons. The
essential goal of a surgical repair is to provide the tendon
with strength sufficient to withstand early active tendon
motion postsurgery but offering minimal resistance to
tendon gliding. A surgical repair should also be simple
(or at least uncomplicated) for most surgeons to learn
and to practice. Therefore, understanding the biome-
chanics of tendon repairs is imperative not only to
design and planning of an optimal repair technique but
also to its appropriate application to clinical cases and
to guide postoperative rehabilitation. Surgeons or thera-
pists should also be aware of the mechanical properties
of surgical repairs when establishing postoperative
therapies.
ESSENTIAL MECHANICAL REQUIREMENTS
OF A SURGICAL REPAIR
Forces generated during normal hand action range from
1 to 35 N, except tip pinch, according to in vivo mea-
surements.1 Schuind et al1 measured tendon forces up
to 6 N during passive mobilization of the wrist, up to 9
N during passive mobilization of the fingers, and up to
35 N during active unrestricted finger motion. There-
fore, a surgically repaired tendon should be able to
withstand at least 40 N, with power sufficient to resist
gap formation. The repair should be able to withstand
cyclic loads under both linear and curvilinear load con-
ditions. In vitro laboratory tests have shown that a con-
ventional two-strand core repair plus running peripheral
sutures yields a maximal strength of 20 to 30 N2; this is
lower than forces generated during normal hand actions
and explains why some such repairs are disrupted during
postoperative motion exercise. Studies have shown that
forces necessary to cause failure of four-strand repairs
are around or beyond 40 N3-5; six-strand repairs fail with
loads over 50 to 60 N.6,7
35
36 Section 1:  Basic Science

Clinically, patients are encouraged to start moving
the tendons in the first few days after surgery. Edema of
traumatized tissues (tendons, subcutaneous tissue,
sheath, and pulleys), bulkiness of the tendons, and the
normal healing responses of tissues increase the resis-
tance of the tendons. In the first 1 to 2 weeks, the tendon
ends tend to soften, which decreases their power to hold
the sutures. Therefore, a certain safety margin should be
maintained by increasing the baseline surgical repair
strength. Taking these points into consideration, one
expects a baseline ultimate strength of 40 to 50 N and
the capacity to resist gapping of 20 to 30 N for a surgi-
cally repaired tendon.
HISTORICAL REVIEWS
The main body of information regarding the biome-
chanics of tendon repair was accrued over the past few
decades; the principal contributing research groups are
summarized in Box 4-1. The investigatory topics
included (1) development of new repair methods; (2)
comparisons of existing repairs; (3) factors affecting
strength; and (4) new means to test or to record the
mechanical properties of the repairs. Human and porcine
tendons are the most common materials used in in vitro
tests of repair strength,2-5 though tendons from sheep,
rabbits, monkeys, and cows are also reported.7,8 Canine,
rabbit, and chicken are used in in vivo investigations.9-12
CURRENT TENDON REPAIR TECHNIQUES
Techniques currently available are, first, repair with core
and peripheral sutures. Core suture repairs are further
divided according to the number of strands passing
through the repair site: two-strand (conventional) and
multistrand (including four-strand, six-strand, and
eight-strand) repairs.2-8,13,14 Alternatively, suture repairs
can be categorized by type of tendon–suture junctions:
grasping, locking, and mixed grasping-locking repairs.
A repair is often referred to using the type of tendon–
suture junctions and the number of strands (e.g., a
locking four-strand repair). Peripheral sutures include
interrupted, simple running, locking running, cross-
stitch (Silfverskiöld),15 locking cross-stitch (Dona),16
interlocking horizontal mattress (IHM),16 and horizon-
tal mattress (Halsted) sutures.17 Second, repair can be

Box 4-1  Groups Contributing to Major Information of Tendon Repair Biomechanics

(Listed in Alphabetic Order of the Leading Investigators)

Amadio-Mayo Group: In vitro model: human, canine tendons; in vitro model: canine tendons
Gliding friction of the tendon against sheath and pulley (Uchiyama et al), gapping and resistance of grasping and locking
repairs (Tanaka et al), partial tendon repairs (Zobitz et al), effects of different repairs, knot sizes and locations (Momose
et al), and relation of gap sizes and gliding resistance (Zhao et al).

Gelberman–St Louis Group: In vitro and in vivo models: canine tendons

Significance of gap formation on adhesion and repair failure (Gelberman et al), effects of forces of rehabilitation on the
healing strength (Boyer et al), zone 1 flexor tendon repair including tendon–bone junction (Silva, Dinopoulos, et al), and
development of eight-strand repair (Winster et al).

Manske–St Louis Group: In vitro model: human, canine tendons; in vivo model: canine, chicken tendons
Development of tendon splint repair (Aoki et al), knot locations (Pruitt et al), cyclic loading (Pruitt et al), differences between
grasping and locking loops (Hotokezaka and Manske), effects of area of locking loops, suture sizes, and development of
the modified Pennington locks (Hatanaka and Manske), and tendon strength during early mobilization (Kubuta, et al).

Mass-Chicago Group: In vitro model and in vivo models: human tendons

In situ tendon repair strength in curvilinear test model using cadaveric hands (Komanduri et al), comparison of repair
strength of different techniques (Angeles et al), repair strength during cyclic load (Choueka et al), and partial tendon
repairs (Manning et al)

Tang-Nantong Group: In vitro model: human, porcine tendons; in vivo model: chicken tendons
Development of four- and six-strand repairs (Wang et al), effects of sizes and configurations of locks (Xie et al), core suture
purchase (Cao et al) and oblique or partial tendon cuts (Tan et al), effects of tension direction and tendon curvature
(Tang et al), strength of the healing tendon (Wu et al), and effects of a major pulley on strength (Cao and Tang).

Trumble-Seattle Group: In vitro model: human tendons

In situ test of repair strength in cadaveric hands and cyclic loading (Thurman et al), zone 1 tendon repairs (McCallister
et al), and repair with Fiberwire (Miller et al and Hwang et al).

Wolfe–Yale–New York Group: In vitro model: human tendons

Development of the cruciate repair (McLarney et al), cyclic loading test of locked repairs and gap formation (Barrie et al),
effect of peripheral suture purchase (Merrell et al), and comparisons of four-strand repairs with Teno Fix (Wolfe et al)
 Chapter 4:  Biomechanics of Core and Peripheral Tendon Repairs 37

completed with devices. The use of devices is not

common; methods include tendon splints,18 barbed
repair devices,19,20 and the Teno Fix device.21,22
Surgical repairs using sutures are the mainstay of
current clinical practice. In experimental settings, repairs
with use of the above-mentioned devices have yielded
impressive strength. The Teno Fix system, a stainless
steel rod connecting stainless steel soft tissue anchors
with screw threads in each end, was tested in vitro and
shown to have strength similar to or greater than a four-
strand repair.21 Clinical use of Teno Fix to repair zone 2
flexor tendons has been reported with good outcomes.22
However, Teno Fix is likely to make the tendon bulky
and may even impinge upon the already narrow and
swollen pulleys, which is a concern. Implanting a stain-
less steel rod not only risks increasing the volume of the Locking loop Grasping loop
tendon but also may require another operation to
Figure 4-1  Locking and grasping tendon-suture junctions
remove. A barbed suture device was reported to produce
have different interactions between the suture and tendon
strength equal to a four-strand core suture.19,20 There are fibers. Locking repairs tighten around tendon fibers under
similar concerns regarding repair bulkiness. The idea of tension, but grasping repairs tend to pull through tendon
placing a splint inside the tendon to bridge the cut ends fibers under tension.
was tested experimentally by Aoki et al,18 but this
method has not yet been used clinically.
TYPES OF TENDON–SUTURE JUNCTIONS
AND THEIR STRENGTH
In a broader sense, all parts of any sutures embedded
within tendon stumps constitute tendon–suture junc- Circle-lock Loop-lock
tions. However, the tendon–suture junction usually
refers to the site where the suture forms a “locking” or
“grasping” configuration to encompass the tendon sub-
stance. These sites are anchor points of the surgical
suture—by either grasps or locks on the tendon—that
help secure the power of surgical repairs. Cross-lock (embedded) Pennington-lock
Locking is defined as the configuration that tightens
around a bundle of tendon fibers when tensile forces
are applied to the suture ends (Figure 4-1).23 In con-
trast, grasping refers to the configuration that holds the
tendon fiber bundles but does not tighten around their
entire circumference and tends to pull through the fiber
Cross-lock (exposed) Grasp (non-lock)
bundles when tensile forces are applied to the suture
ends (see Figure 4-1). Figure 4-2  Different tendon–suture junctions: different
locking junctions and a grasping junction.
Grasping junctions are either open circle or open
loop. Locking junctions include cross-locks (either
exposed or embedded), circle-locks (looped or double- above are not met. In clinical settings, we should ensure
circled), and Pennington locks (original or modified) that the calibers of the suture are equal to or greater than
(Figure 4-2). Mechanically, the effectiveness of grasps 4-0, the suture purchase no less than 7 to 10 mm, and
or locks of a core suture is greatest when (1) suture the size of the lock or grasp equal to or greater than
materials are sufficiently strong—allowing the sutures 2 mm. These requirements are critical to the repair
to grasp or lock the tendon substance tightly without strength and are more important than whether a locking
disruption of sutures; (2) the anchor point is sufficiently or a grasping junction is used or which lock is incorpo-
distant from the tendon laceration—so grasps or locks rated into the repair.
will not slip; and (3) grasp or lock sizes are sufficient— When all the above conditions are met, grasping and
so the suture anchors to ample tendon substance. locking junctions provide reliable anchors for the suture
In other words, one should not expect a locking or in the tendon, although a locking repair is generally
grasping junction to be secure if all three requirements somewhat stronger than a grasping repair. In practice,
38 Section 1:  Basic Science
when the primary requirements of the repairs are met,
the differences in the strength between locking and
grasping repairs are actually narrow or insignificant.
Depending on the locks or grasps used, the strength of
repairs changes (usually less than 10 N).23-29 The increase
in strength brought about by incorporation of locking
anchors is much smaller than increases in strength
through other means—such as increasing the strength
of suture materials or the number of suture strands
passing through the repair site.2-7 From this perspective,
surgeons should pay ample attention to factors that
exert the greatest influence on strengths and ensure that
these requirements are met primarily. It is not appropri-
ate to rely on incorporating locks, hoping that this
measure alone increases strength, while neglecting other
more influential factors.
Whether various locks have different mechanical
strengths is under question. We tested the strength of
the different locks and found they have essentially the
same holding power.27 A cross-lock and a circle-lock are
identical in holding power; an exposed cross-lock and
an embedded cross-lock are the same as well.27 However,
our in vitro tests showed that the Kessler-type repairs
with the original Pennington locks are weaker than
repairs with cross- or circle-locks.28
Pennington locks are frequently incorporated in
Kessler-type repairs. Most surgeons believe that Pen-
nington locks help secure the repair. However, this con-
sideration actually lacks sufficient experimental support.
According to the definitions of Pennington30 in 1979,
in the locking configuration of the Kessler repair, “the
transverse suture component passes superficial to the
longitudinal component so that the sutures lock a
bundle of tendon fibers when tensile forces are applied
to the suture.” Pennington did not present its strength
data when describing this repair.30 In a letter communi-
cation directed to Pennington,31 Silfverskiöld com-
mented regarding this locking repair: “As to Dr.
Pennington’s claim that the locking loop design is
crucial to the tensile strength of the suture, I agree that
in theory this should be true, but in actual practice this
may not be the case. … Another practical consideration
is that even if one attempts to place the transverse part
superficial to the longitudinal part, to create the locking
design, it is often difficult to be certain of success.”
Practically, we agree that it is difficult for surgeons to
ascertain the relation of transverse and longitudinal
sutures in the repaired digital tendon clinically.
Hatanaka and Manske9,24 modified the Pennington
locking repair by placing some of the longitudinal
strands over the dorsal tendon surface, making locked
tendon–suture junctions confirmatively. The modified
repair is stronger than the grasping Kessler repair when
the suture calibers are 2-0 and 3-0 but not 4-0.24 It is
noteworthy that in an in vivo setting,9 the strength
gained by this modified locking repair was noted only
at days 3 and 21, not at days 7 and 14, even with the
2-0 suture. In other words, modified Pennington locks
do not improve repair strength during the second week
(days 7 to 14), when the tendon stumps usually soften
and most ruptures occur. We should be cautious in
relying upon Pennington locks to increase strength.
Recently we examined the effectiveness of the origi-
nal Pennington lock in a four-strand repair; we detected
no differences in strength between repairs with the Pen-
nington locks and those with random assignment of
grasping and locking. When a two-strand Kessler repair
with original Pennington locks was compared with the
repair with grasping anchors using 4-0 suture, our tests
indicated a modest difference (12%) in gap resistance
but no difference in ultimate strength.29 When compar-
ing two grasping anchors (open circle and open loop),
we found no difference in their gap resistance and ulti-
mate strength. Taken together, the evidence above leads
us to believe that differences between the grasping and
the original Pennington’s locking tendon–suture junc-
tions may not be substantial in a clinical setting, and
incorporating Pennington locks in multistrand repairs
does not appear to affect strength.
STRENGTHS OF CORE SUTURES
Strengths of core sutures have been tested extensively
both in vitro and in vivo and in single cycle load-to-
failure test2-14,23-28,32-34 or cyclic test setup.35-37 Using a
4-0 nylon suture, a two-strand repair has a strength of
about 20 to 25 N, a four-strand repair has a strength
of about 35 to 45 N, and a six-strand repair has a
strength of about 50 to 70 N. Thus we see the strength
is roughly proportionate to the number of strands
(Table 4-1).2-8,13,14,32-35 Strength is greatly increased when
suture caliber increases36-38 or stronger suture material is
used (see Table 4-1).38,39
The common core sutures are as follows:
1. Kessler-type repair: The two-strand modified Kessler
repair has been the most common over the past
decades. Four-strand Kessler repairs were devel-
oped, either as a double Kessler or as one Kessler
repair made with a double-stranded suture
(Figure 4-3).
2. Cruciate repair: The original cruciate repair is a
four-strand grasping repair (see Figure 4-3).4 Locks
can be incorporated to make a locking repair.14,35
3. Strickland repair: This four-strand repair consists of
a Kessler-type repair (with reinforced double-circle
locking anchors at four corners) and a simple
double right-angle suture (Figure 4-4).41,42
4. Savage repair and modifications: Savage repair is a
six-strand locking repair.32 Its modifications
include a six-strand single-cross repair, with one
cross-lock as suture anchor (see Figure 4-4).43
 Chapter 4:  Biomechanics of Core and Peripheral Tendon Repairs 39

Table 4-1  Some Biomechanical Tests Showing Increases in the Strength With the Number of Strands and the
Strengths of Repair Devices
Suture Materials Ultimate Gap Force (N)
Investigators Tendons Methods Core/Epitendinous Strength (N) (Gap Sizes)
Savage,32 1985 Procine 6-strand (Savage) 4-0 Ethibond 60–70 44 (3-mm)
2-strand (Kessler) 4-0 Ethibond 23 10 (3-mm)
18
Aoki et al, 1994 Human Tendon splint Dacron 81–84 20–31 (initial)
2-strand Kessler 4-0 Ethibond/6-0 26 14 (initial)
Prolene
Greenwald et al,7 1995 Monkey 4-strand (MGH) 5-0 Nylon/6-0 Nylon 30
2-strand (Kessler) 5-0 Nylon/6-0 Nylon 16
Thurman et al,35 1998 Human* 6-strand (Savage) 4-0 Tricron/6-0 79 (0.3 mm)
Surgilene
4-strand 4-0 Tricron/6-0 43 (0.3 mm)
(Strickland) Surgilene
2-strand (Kessler) 4-0 Tricron/6-0 34 (2.7 mm)
Surgilene
McLarney et al,4 1999 Human 4-strand 4-0 Ethobond/6-0 56 44 (2-mm)
(cruciate) Polypropylene
Barrie, et al,14 2000 Human* 4-strand 4-0 Ethibond/6-0 70 49 (3-mm)
(cruciate, grasp) Nylon
4-strand 4-0 Ethibond/6-0 79 52 (3-mm)
(cruciate, lock) Nylon
Xie et al,6 2002 Human 6-strand (Tang) 4-0 Supramid/6-0 60 45 (2-mm)
Nylon
Wang et al,33 2003 Porcine 6-strand 4-0 Supramid/6-0 62 46 (2-mm)
(M-Tang) Nylon
Cao and Tang,34 2005 Porcine 4-strand 4-0 Supramid/6-0 43 37 (2-mm)
(U-shaped) Nylon
Lawrence and Davis,39 2005 Human 4-strand 4-0 Fiberwire/6-0 81 63 (initial)
(single-cross) Nylon
Su et al,21 2005 Human Teno Fix Teno Fix 55 47 (2-mm)
Teno Fix/5-0 67 55 (2-mm)
Polypropylene
Hirpara et al,20 2010 Porcine 2 barbed repair Nitinol 58 30 (3-mm)
devices
Wu et al,28 2011 Porcine 4-strand 4-0 Ethilon/6-0 40 32 (2-mm)
(cross-lock) Nylon
*In situ test of the repair strength and gapping of flexor tendons in cadaveric hands under cyclic tension.

5. Becker repair and Massachusetts General Hospital
(MGH) repair: Becker et al44 used a series of cross-
stitches to repair a beveled tendon. The MGH
repair is its modification that uses four-strand with
a series of cross-stitches (cross-locks).7
6. Multiple looped sutures and their modifications: These
repairs are accomplished using Tsuge’s looped
sutures. Two or three groups of looped sutures can
be used. We typically used three groups of looped
sutures in repairing tendons (see Figure 4-4),45
and fewer looped sutures in modifications of such
repairs (Figure 4-5).33,34,46
7. Repairs with double-stranded sutures: These repairs
simplify surgical maneuvers (Figure 4-6). A
40 Section 1:  Basic Science
I I
II II
A III B III
Figure 4-3  Methods of making a two-strand modified
Kessler repair (A), and a four-strand cruciate repair (B).
A
C
D
Figure 4-4  Four-strand Strickland repair (A), six-strand
original Savage repair (B), six-strand modified Savage
(Adelaide) repair (C), and six-strand Tang (or three Tsuge)
repair (D).
number of configurations can be created and have
similar strength, except that the four-strand Kessler
repair is a bit weaker.28
Core suture configurations, as detailed above, vary enor-
mously. Practically, with an identical number of suture
strands passing through the repair site, the strength of
these sutures varies within a small range. To maintain
ideal strength, two factors are crucial to all core sutures:
(1) adequate suture purchase: a 7- to 10-mm purchase is
necessary to ensure optimal performance of a core
suture, and (2) secure locks or grasps: the locks or grasps
should be of a diameter of 2 mm or more and of suf-
ficient depth. Superficial or small locks or grasps are
pulled out easily.
A
B
C
D
E
Figure 4-5  Methods of making a modified six-strand
Tang repair forming an M configuration (M-Tang repair).
A U-shaped four-strand repair is made with one looped
suture (A-C), and another looped suture is used to complete
the six-strand repair (D and E).
STRENGTH OF PERIPHERAL SUTURES
Interrupted, running, or locking running peripheral
sutures are common in the clinic. These peripheral
sutures are usually adequate to smooth the tendon and
to help resist gapping (Figure 4-7).
Others are more complex, which some surgeons have
advocated to increase strength, rather than simply to
approximate the tendon ends. The cross-stitch suture
designed by Silfverskiöld et al15 is among the most
famous. Silfverskiöld’s group15 had good clinical results
with this suture combined with a two-strand modified
Kessler core repair. The cross-stitch suture does provide
the tendon with great strength, but we have a concern
 Chapter 4:  Biomechanics of Core and Peripheral Tendon Repairs
A
B A running peripheral suture with 2-mm purchase
C increase. The dorsal aspect of the tendon is also harder
D when a strong multistrand repair is used, supplementa-
Figure 4-6  Methods of making a variety of four-strand
repair using one needle carrying two suture strands (looped
or separated). These repairs achieve greater strength
with simplified surgical maneuvers. A, Cross-lock repair;
B, U-shaped repair; C, Kessler-type repair; and D, cruciate
repair. In A, B, and D, one needle carrying two separate
strands are used.
A
B increases53,54; and (10), above all, the holding capacity
C
D related to gap formation has rarely been discussed:
Figure 4-7  Methods of making peripheral sutures:
A, simple running; B, running locking; C, Silfverskiöld
(cross-stitch); and D, locking cross-stitch.
41
about its massive exposure of sutures over the tendon,
which may increase gliding resistance and the likeli-
hood of adhesions. Similarly, locked cross-stitch16 and
Halsted17 sutures give the tendon great strength. Com-
plexity of surgical maneuvers and suture exposures are
their major drawbacks. Nevertheless, several complex
repair methods, such as cross-stitch and locking cross-
stitches, are ideal options for repairing the thin, flat
extensor tendons.
generates optimal strength according to Merrell et al.47
Cross-stitch repairs usually have a purchase of 5 mm or
more. The number of runs of peripheral suture influ-
ences strength. However, increasing the number of runs
is difficult clinically, because the small diameter of the
digital tendon does not easily accommodate this
to access.
We prefer to use multistrand core repairs to give the
tendon strength, supplemented with interrupted or
simple running peripheral stitches. We believe that
tion of a complex peripheral suture such as cross-stitch
or Halsted repair is unnecessary. Giesan et al48 reported
not using any peripheral sutures with a six-strand core
repair in repairing flexor pollicis longus tendons.
FACTORS AFFECTING THE STRENGTHS
OF TENDON REPAIRS—SUMMARY
Factors affecting the strength of a surgical repair are as
follows (Figure 4-8): (1) the number of suture strands
across the repair sites—strength is roughly proportional
to the number of core sutures2-8,13,14,32-35; (2) the tension
of repairs—most relevant to gap formation and stiffness
of repairs46; (3) the core suture purchase2,3,49-51; (4) the
types of tendon–suture junction—locking or grasp-
ing14,23-29; (5) the diameter of suture locks in the
tendons—a small diameter of locks diminishes anchor
power5; (6) the suture calibers (diameter)36-38; (7) the
material properties of sutures39,40; (8) the peripheral
sutures15-17,52; (9) the curvature of tendon gliding paths—
the repair strength decreases as tendon curvature
of the tendon, affected by degrees of trauma and post-
traumatic tissue softening, is vital to strength. Following
are five important factors affecting the strength of
tendon repair.
IMPORTANT FACTOR 1—TENSION OF SUTURE
REPAIR AFFECTS GAP FORMATION
Peripheral sutures prevent tendon gapping. However,
another factor of perhaps equal importance and closely
initial tension of the core suture. In repairing a tendon,
we suggest that surgeons maintain a certain tension
across the repair site, rather than leaving the repair
42 Section 1:  Basic Science
Core sutures Curvature of the tendon
• Suture strands:
4 or 6 strands suggested
TENDON REPAIR
• Suture purchase lengths:
0.7 to 1.0 cm purchase suggested
• Tension of the repairs:
Slight tension (10% shortening
of tendon segment) suggested
• Suture calibers: 3–0 or 4–0
• Locking/grasping: locking preferred
Holding capacity of the tendon
• Sizes of the locks or grasp: >2 mm (tendon trauma, softening, etc.)
Figure 4-8  Summary of factors determining the strength of surgically repaired tendons.
tension-free. We tested the gap formation forces of the
repair under varying tension, which resulted in 0%,
10%, or 20% shortening of the sutured tendon segment.
The tendon with tension causing 10% shortening
reduced the chance of repair gapping, with significantly
increased gap formation forces. Increasing the tension
to cause 20% tendon shortening did further increase
gap resistance forces, but by a much smaller amount. A
four-strand core repair tensioned to cause 10% tendon
shortening, regardless whether a simple peripheral
suture is added or not, had identical gap resistance.
The gap resistance of a repair closely relates to its
tension status. Adding a slight baseline tension to the
repair site when the proximal tendon is temporarily
fixed to ease the tension during surgery results in appro-
priate tension after surgery, because this counteracts the
tension of muscle pull during active motion.46 Multi-
strand repairs are placed in different areas in the tendon
cross-section, which may evenly distribute tension
throughout the tendon and may not require a periph-
eral suture. This concept of “core suture–only” multi-
strand repairs, if practiced under certain repair tension,
is proper.
IMPORTANT FACTOR 2—SUFFICIENT
SUTURE PURCHASE AND LOCK (GRASP)
SIZE ARE ESSENTIAL
Length of core suture purchase is defined as the exit/entry
distance of the core suture from the cut ends of the
tendon. We tested how the length of core suture pur-
chase affects the strength of the transversely or obliquely
cut tendon.2,3,49 We examined the strength of porcine
flexor tendons with two-strand modified Kessler core
repairs with purchase of 0.4, 0.7, 1.0, and 1.2 cm and
with four-strand circle-locking repairs with purchase of
0.4 and 1.0 cm.2 As the suture purchase increased from
0.4 to 0.7, 1.0, and 1.2 cm, the gap and ultimate strengths
increased significantly. The strengths remained constant
with the purchase from 0.7 to 1.2 cm. The four-strand
circle-locking repairs with a suture purchase of 1.0 cm
were significantly stronger than those with a suture pur-
chase of 0.4 cm. In another study,3 we found that three
Material properties of sutures
STRENGTH Peripheral sutures
• Number of runs:
6–8 runs suggested
• Suture purchase lengths:
1–2 mm suggested
• Tension: slight tension
• Suture calibers: 6–0 or 5–0
four-strand repairs (double-modified Kessler, locking
cruciate, and modified Savage) had gained significant
resistance to gapping and ultimate strength as the length
of core sutures increased from 0.4 to 1 cm. We deter-
mined that the optimal core suture purchase for a trans-
versely cut tendon is between 0.7 and 1 cm (Figure 4-9).
In obliquely cut tendons, increasing the purchase
length to 1.2 cm improved the strength of a two-strand
modified Kessler repair and a four-strand locking cruci-
ate repair.49
The importance of core suture purchase was verified
by other investigators. Kim et al50 reported progressive
increases in the strength of double Kessler repairs as
purchase lengthened from 0.3, to 0.7, to 1, and 1.3 cm
in porcine tendons; they recommend 1 cm as the
appropriate purchase length. Using cadaveric hands,
Lee et al51 studied locking cruciate repairs, randomly
assigned to placement of 0.3, 0.5, 0.7 or 1 cm from the
cut edge of the tendon, with interlocking horizontal
mattress sutures. The tendons repaired at 1 cm had the
lowest increase in work of flexion (5.2%), the highest
2-mm gap force (89.8 N) and ultimate load (111.5 N).
In contrast, the tendons repaired at 0.3 cm had the
highest increase in the work (22.1%), the lowest 2-mm
gap force (54.6 N) and ultimate load (84.6 N). In fact,
all studies suggest an optimal core suture purchase of
1.0 cm (range: 0.7 to 1.2 cm).
As stated in previous paragraphs, sizes of locks and
grasps are another important factor; they should be
equal to or greater than 2 mm to guarantee anchors of
the sutures to the tendons (see Figure 4-9).
IMPORTANT FACTOR 3—STRENGTH DOES NOT
INCREASE DURING EARLY TENDON HEALING
Only a few investigations have been conducted of surgi-
cal repair strength in vivo, using animal models.9-14 Data
on the strength of the healing tendons in human
patients are not available. Urbaniak et al55 found that
the strength of repaired canine flexor tendons decreased
at week 2 postsurgery. With simulated postsurgical
motion, Boyer et al10 found no decrease in the strength
of the canine flexor tendons. In a chicken model,
 Chapter 4:  Biomechanics of Core and Peripheral Tendon Repairs 43

Weak
Weak
Diameter of locks: 1 mm

4 mm 4 mm
Strong
-optimal

Diameter of locks: 2 mm Stronger

Strong 7 mm 7 mm

A Diameter of locks: 3 mm
Strongest
-optimal

Three 10 mm 10 mm
locks
produce
equal Strongest
a b c power
Exposed X Embedded X Circle
B C 12 mm 12 mm
Figure 4-9  A, Sizes of the locks affect the repair strength significantly. We determined that the diameters of locks of 2 or
3 mm generate strength greater than those of 1 mm and recommend an optimal locking size of about 2 mm. B, Our
biomechanical tests of the strength of three different types of locks indicate no significant difference in the repair strength
with the three types of locks. C, We tested the strength of two- or four-strand repairs with core suture purchase lengths
ranging from 4 to 12 mm and found that repairs with the purchase lengths between 7 to 12 mm generate strength greater
than those with the purchase of 4 mm. We recommend the optimal core suture purchase of 7 to 10 mm. The purchase
length of 10 mm is optimal.

Hatanaka et al9 found no changes in the strength of the
healing tendons in the first 3 weeks. Our study12 using
chickens showed no significant changes in the strength
of the healing flexor tendon during the initial 4 weeks.
The strength of the digital flexor tendons in animal
models does not typically increase during the first 3
or 4 weeks postsurgery; under certain circumstances,
the strength may actually decrease slightly. This “no-
gain” lag period in strength in the initial weeks after
surgery is characteristic, reflecting the slow healing
responses of the tendon. Unfortunately, the slow bio-
logical healing response invites invasion of tissues
outside the tendon and development of adhesions,
resulting in gapping or rupture of the repairs during
early tendon mobilization.
IMPORTANT FACTOR 4—STRENGTH
DECREASES WHEN THE FINGER FLEXES
Because finger flexion is the key action of postsurgical
tendon motion exercise, the capability of a repair to resist
gapping or failure during finger flexion is important. To
understand how flexion affects the strength of tendon
repairs, we created two models to test (1) how the direc-
tion of tension on the tendon affects strength53 and (2)
how tendon curvature affects strength (Figure 4-10).54
Strength of the repairs decreased as the angles of pulling
became greater, and when the radius of the curvature is
smaller. These findings imply that repair strength
decreases as the finger flexes further, because both the
angles of tension on the tendon increase and the radii
of the tendon gliding curves decrease progressively. The
dorsal part of the tendon is subjected to greater tension
and may gap more easily during finger flexion. Placement
of sutures dorsally may favor gap resistance.
The clinical implications of these biomechanical
observations are that strength decreases as the fingers
are flexed progressively, and that repairs are weakest
when the finger is in marked flexion. Therefore, the final
part of finger flexion is when repairs are more vulnera-
ble to disruption. Catching of the tendon repair site by
the sheath or pulley edges during finger flexion may
trigger repair rupture.
IMPORTANT FACTOR 5—SOFTENING OF
TRAUMATIZED TENDON PARTS DECREASES
HOLDING POWER
It should be emphasized that tissue softening is crucial
to repair strength. Because most biomechanical studies
were in vitro, the influence of this factor could not be
reflected in these studies. Tissue softening renders the
repair weaker with decreases in both gap resistance and
maximal strength. As the locking or grasping anchors
move farther from the trauma area, tissue softening
decreases. Suture purchase of the core repairs should be
44 Section 1:  Basic Science

Pulley
F F′
A
F
F′
A B
1
2 F
Our model F

-INSTRON 4411 F1
C D F2

B
a
b
F F
Pulley
1′ Tendon E F
2′
Repair site
c F
Clamp

C G H

Finger flexion Force analysis

Figure 4-10  Left, The changes in the tendon arcs during digital flexion. A, The digital flexor tendons follow an arc of
increasing curvature as the fingers flex progressively during digital flexion. B and C, The curvature of tendon arcs is greater in
the distal (site 1) than in the proximal (site 2). As the finger flexes, the tendon curvature increases at each site close to the
joints (for example, site 1). Middle, Our test setup of the flexor tendon undergoing load to failure testing over a curve. By
changing the diameter of the pulley, we re-created different tendon curvature during tendon loading. We recorded substantial
decreases in the repair strength when the tendon curvature becomes smaller. Right, Differential loading conditions on the
tendons according to tendon curvature. A, The tendon is subjected to a linear load when pulled straight. B, The tendon is
subjected to both a linear and a bending force when pulled to glide over a pulley. The tendon is subjected to an angular
tensile load and bending forces. The bending force on the repaired tendon segment is greater in C (of a greater curvature)
than that in D (of a smaller curvature). E–G, The gliding curvature becomes increasingly greater, with increasingly greater
bending force on the repaired tendon segment; the tendon is easier to rupture. G, When the tendon arc approximates the
length of the core suture, the bending force is loaded entirely to the suture. The repair especially is prone to failure.
H, When the tendon glides over a remnant pulley with adjacent pulleys and sheath defects, tendon curvature is especially
small, and the repair is easy to disrupt.

sufficient to minimize the negative impact of tissue soft-
ening. Clinical evidence indicates that rupture of the
repair is most likely in the second week after surgery,56
thought to be related to softening of traumatized tissues.
TWO WAYS TO INCREASE STRENGTH—
MORE SUTURE STRANDS AND LARGER
SUTURE CALIBERS
Increasing the number of suture strands across the repair
sites is a popular means to increase strength. Repair with
four or six strands are most often used to provide proper
strength for early active tendon motion. Use of double-
or triple-stranded repair simplifies surgery.26,33,34 Increas-
ing suture caliber is another easy way to augment
strength. Clinically, repairs with 4-0 sutures are common.
Increasing the caliber from 4-0 to 3-0 adds 10-15 N to
the ultimate strength of two- or four-strand repairs (see
Table 4-1; Figure 4-11).36-39 Increasing the suture strands
from two to four is more efficient than increasing the
caliber from 4-0 to 3-0. We suggest either a 3-0 or a 4-0
suture for a four-strand repair, and a 4-0 suture for a
six-strand repair. However, rigidity of sutures increases
along with caliber. Sutures of 2-0 become more rigid;
sutures of this or greater caliber are rarely necessary.
Lawrence and Davis39 evaluated the mechanical prop-
erties of five nonabsorbable 4-0 sutures and a four-
strand locking repair with these sutures (Table 4-2). All
repairs failed by suture rupture at the locking loop.
Fiberwire and stainless-steel sutures and repairs were
stronger and stiffer than the other sutures. The results
 Chapter 4:  Biomechanics of Core and Peripheral Tendon Repairs 45

60
achieved by Prolene and Ethibond were similar with
Ultimate strength respect to gap and ultimate forces. The merits of Fiber-
4-0 suture
50 3-0 suture
wire have been reported by others40; knot security and
suture rigidity remain concerns. We expect to see the
40 development of strong yet flexible materials in the
Strength (N)

future.
30
2 mm gap forces TEST SETUP AND MEASUREMENTS OF
20
TENDON REPAIR BIOMECHANICS
The centerpiece of the test setup is a material testing
10 machine. Most data on tendon repair biomechanics
were generated using this machine, under either single-
0
cycle load-to-failure or cyclic loading conditions. Typi-
2-strand 4-strand 2-strand 4-strand
cally, a load-to-failure curve is generated (Figure 4-12),
Number of repair strands
which allows analysis of the failure load (called ultimate
Figure 4-11  Our test results of two-strand modified strength or maximal strength of the repair) and stiffness
Kessler repair and four-strand cross-lock repairs (using of the tendons. Stiffness is obtained by measuring the
double-stranded sutures) using 4-0 and 3-0 suture slope of the middle linear portion of the load-
(Ethilon). Increasing the suture caliber from 4-0 to 3-0 adds displacement curve. By calculation of the area under-
about 10 N to the maximal strength. Increasing the suture neath the curve, energy to failure of the repair can be
strands from two to four adds about 15 to 20 N to the obtained. The forces at which the gaps start to appear
maximal strength. The gap resistance of the repairs is or reach 2 or 3 mm are recorded as gap forces. Analyses
increased by increasing the caliber and the number of the of the curves generated when the tendon undergoes
repair strands.
cyclical loads help determine which repair tends to fail
in earlier cycles. Gap sizes can be monitored and
recorded continuously over loading cycles with a video

Table 4-2  Biomechanical Tests of Different Materials and Repairs With Varying Suture Calibers
Investigators Methods/Materials Ultimate Strength (N) Initial Gap Force (N) Stiffness (N/mm)
39
Lawrence and Davis Test of material properties of
sutures
4-0, Nylon 22 2.5
4-0, Prolene 25 5.0
4-0, Ethibond 25 8.2
4-0, Stainless steel 36 14.8
4-0, Fiberwire 37 11.0
39
Lawrence and Davis 4-strand (single-cross repair)
4-0, Nylon 46 36 6.0
4-0, Prolene 63 52 8.0
4-0, Ethibond 66 52 10.2
4-0, Stainless steel 87 66 11.9
4-0, Fiberwire 81 63 12.8
38
Taras et al 2-strand (Kessler repair)
5-0, Ethibond 16
4-0, Ethibond 22
3-0, Ethibond 31
2-0, Ethibond 41
46 Section 1:  Basic Science

Cyclic loading has been used rather extensively to

50 test the strength of repairs. Because this type of test
Ultimate imitates conditions of repetitive tendon loading in
40 strength
patients, it has yielded valuable information regarding

ion )
gap resistance and fatigue. One concern in interpreting

eg m
r r /m
Load (N)

30 the findings after cycling the tendon over hundreds and

ea (N
Lin ness
thousands of times continuously is that the test does
20 not simulate situations seen clinically in healing tendons
iff
St
Area = Energy
during the early period. Clinically, the tendon usually
10 moves only 20 or 30 times in each session of exercise;
to failure (J)
even ordinary daily life does not involve moving the
0 tendon over hundreds of cycles continuously. Testing the
0 10 20 30 repair strength or the gapping after more than 20 to 30
A Displacement (mm) cycles of tension appears to make more sense. We believe
that a single cycle of motion test provides the most
30 useful basic information; a test of the load-to-failure
Ultimate strength
strength after cyclic loading of a limited number (e.g.,
10 to 30) of cycles may generate information relevant to
20 Force of complete disruption
Load (N)

or peripheral sutures postsurgical exercise.

10
Tendon distraction during
peripheral suture disruption
0
0 5 10 15
B Displacement (mm)
Figure 4-12  A, A typical load-displacement graph
generated during a single cycle load-to-failure test. From the
graph, we can obtain ultimate strength, the energy to failure
(calculated from the area under the load-displacement
curve), and stiffness of the repairs (the slope of the linear
middle part of the load-displacement curve). B, Form this
graph, we can also determine the force at which peripheral
repairs fail completely and the tendon distraction during
peripheral or core suture failure. The initial, 1-, 2-, or 3-mm
gap formation forces are usually recorded to determine gap
resistance of the repair. These forces are measured during
tendon loading with the assistance of a video camera.
camera, allowing identification of repairs vulnerable to
gapping.
In situ testing of repaired tendons using cadaveric
hands, developed by Mass et al,57 Trumble et al,35 and
Wolfe et al,14 represents another means to measure the
mechanical properties of repairs. This test simulates a
curvilinear loading condition of the tendon within the
digits. Gap formation, gap forces, ultimate strength, and
work of flexion can be measured,14,35,57 and cyclic loading
on the tendon can be simulated as well.14,35 Measuring
the resistance to tendon movement over a pulley or a
segment of the sheath using a custom-designed device
is another innovative test setup developed by the Amadio
group.58 This test generates sensitive data on the differ-
ences among different repair methods, particularly with
respect to surface friction of the repair.
Gap resistance is an important measure, because a
repair with remarkable gaps is bound to fail, and
gapping impairs the healing process. Assessment of gap
forces (at the gap sizes of initial appearance, 2 mm, or
20 3 mm) or gap sizes under a certain load is necessary.
Nevertheless, the examiners should be aware that gap
formation forces are easily affected by the number of
runs of the peripheral sutures and tension status of the
surgical repair, two factors that should be standardized
to facilitate comparison of the gap resistance of various
repairs. The ultimate strength of a given repair, on the
other hand, is rather consistent in different studies. We
consider both parameters—gap force and ultimate
strength—essential measures of the mechanical perfor-
mance of a repair.
In our mechanical study settings, we load a 5-cm
segment of tendon in a material testing machine and
measure 2-mm gap formation force and ultimate
strength. Sometimes we also measure the initial gap
force and tendon stiffness; occasionally we include
energy to failure as well. The distraction of the tendon
during failure of the peripheral or core sutures is instruc-
tive as well. We believe that findings regarding tendon
stiffness are inconclusive. An increase in stiffness indi-
cates greater capacity to resist tendon deformation;
however, tendons normally have some elasticity.
Whether greater stiffness necessarily benefits a repaired
tendon is actually questionable.
CONSIDERATIONS IN THE DESIGN AND USE
OF REPAIR METHODS
Most surgeons use strong core sutures with simple epi-
tendinous sutures clinically; some others favor strength-
ening peripheral sutures. Rarely, surgeons try to adopt
both complex core and peripheral sutures, because the
tendon is hard to accommodate. Strength increases with
the complexity of peripheral or core sutures, but at the
 Chapter 4:  Biomechanics of Core and Peripheral Tendon Repairs
cost of more difficult surgical maneuvers, tendon bulki-
ness, and exposure of sutures or knots over the tendon.
With these considerations in mind, one should be careful
in designing and advocating complex suture techniques,
because they would not be widely accepted clinically and
the strength sometimes exceeds what is actually needed.
Assembling elements from existing methods to form a
complex (and “novel”) repair is not difficult. Such
methods may not have great practical value.
A novel and clinically acceptable repair should be
either (1) stronger than existing repairs (with an identi-
cal degree of complexity) or (2) simpler in surgical
maneuvers (without decreasing the strength). We favor
use of double-stranded sutures—either a loop at the end
or two separate strands, carried by a single needle, to
increase repair strength, with fewer needle-suture pas-
sages through the tendon and the same surgical
maneuvers.
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 CHAPTER
5  
BIOLOGY AND BIOMECHANICS
OF THE TENDON–BONE
INSERTION
Stavros Thomopoulos, PhD, and Leesa M. Galatz, MD
OUTLINE
The repair of tendon to bone presents a major chal-
lenge due to the disparity in the mechanical properties
of the two tissues. The uninjured insertion overcomes
this mechanical mismatch by attaching the two tissues
across a functionally graded insertion. This unique
transition develops between tendon and bone postna-
tally and is driven by both biological and mechanical
factors. Muscle loading, for example, is necessary for
the development of a well-organized, mineralized
insertion. Tendon–bone healing does not recapitulate
development. Healing is characterized by bone loss
and the formation of a fibrovascular scar, leading to a
repaired attachment that is prone to rupture. Current
treatment approaches for enhancing tendon–bone
healing focus on rehabilitation. Studies in animal
models, however, have demonstrated that a fine
balance must be reached between too much load
(which can lead to microdamage) and too little
load (which can lead to a catabolic environment) to
maximize tendon–bone healing. Future treatment
approaches may include delivery of growth factors
and/or mesenchymal stem cells to stimulate regenera-
tion of a functionally graded insertion. Ultimately, a
tissue engineered scaffold with a gradation in proper-
ties and seeded with the appropriate cells and biofac-
tors may provide a solution to the clinical problem of
tendon–bone healing.
The attachment of a compliant material like tendon to
a relatively stiff material like bone is a fundamental
engineering challenge.1 As is evident from the study of
attachment of engineering materials,2 potentially dam-
aging stress concentrations can be expected to arise at
the insertion if the tissue is not tuned to this stiffness
mismatch both at the macroscopic level (i.e., the
outward splay of the tendon) and the microscopic level
(i.e., the gradual stiffening of collagen molecules by
mineral crystals).
STRUCTURE AND FUNCTION OF THE
TENDON–BONE INSERTION
The gradual tailoring, or “functional grading,” of mate-
rial systems has been described in the engineering mate-
rials community as a way to minimize these stress
concentrations.3 A central concept to the formation of
a robust attachment between tendon and bone is that
smooth, monotonic transitions in mechanical proper-
ties are necessary for minimizing stresses. The tendon–
bone insertion site is a natural functionally graded
structure. Notably, this gradation is not maintained at
healing insertions, and the surgically repaired tissue is
prone to rerupture.4-6 Surgical technique and treatment
approaches should therefore seek to minimize stress
concentrations and thereby protect the repair site from
rupture.
MORPHOLOGY OF THE TENDON ENTHESIS
(TENDON–BONE INSERTION SITE)
Tendons insert into bone across broad fibrous transi-
tions or across short fibrocartilaginous transitions.7
Fibrous transitions are characterized by insertion sites
with large footprints (effectively distributing the forces
over large areas and reducing stresses) and by perforat-
ing mineral fibers (“Sharpey’s fibers”). Examples of
these attachments include the tibial insertion of the
medial collateral ligament and the deltoid tendon inser-
tion into the humeral head. Examples of the more
common fibrocartilaginous insertions include the
rotator cuff tendon insertions and the Achilles tendon
insertion. The structure, function, development, and
healing of fibrocartilaginous tendon–bone insertions
will be the focus of this chapter. These insertions are
characteristically short and occur across distinct fibro-
cartilage regions classically categorized into four zones
(Figure 5-1).7 The first zone consists of tendon; this
region is populated by fibroblasts and has properties
similar to those found at the tendon mid-substance. It
is composed primarily of well aligned type I collagen
49
50 Section 1:  Basic Science
Tendon
Insertion
site
Bone
Figure 5-1  The supraspinatus tendon–bone insertion in the rat (toluidine blue stain). Tendon attaches to bone across a
graded fibrocartilaginous transition.
fibers.8 The second zone consists of fibrocartilage; this
region is populated by fibrochondrocytes and is com-
posed of types I, II, and III collagen and the proteogly-
can aggrecan.8-11 The third zone is also populated by
fibrochondrocytes and is composed of mineralized
fibrocartilage. Here, the predominant collagen is type II,
and there are significant amounts of type X collagen as
well as aggrecan.8-11 The fourth zone consists of bone
proper; this region is populated by osteoblasts and
osteoclasts and is composed predominantly of mineral-
ized type I collagen. While the insertion site is typically
categorized into these four zones, changes in the tissue
are gradual and continuous, minimizing stress concen-
trations between the tendon and the bone. The com-
plexity of the tendon–bone insertion, however, results
in a difficult challenge for effective healing.
Gradations in Biomechanical, Compositional,
and Structural Properties Along the Tendon–
Bone Insertion Site
The tendon–bone insertion contains gradients in bio-
mechanical, compositional, and structural properties.
Between the unmineralized and mineralized fibrocar­
tilage of the enthesis is a narrow zone that darkens
markedly during tissue staining. This “line” was tradi-
tionally thought to represent a mineralization front, or,
mechanically, a boundary between soft and hard tissue.
Studies examining the supraspinatus tendon–bone
insertions of rats, however, have demonstrated grada-
tions in properties along the enthesis rather than an
abrupt change from mineralized to unmineralized
tissue. There was a variation in gene expression along
the length of the insertion; tendon-specific genes were
localized to the tendon proper, bone-specific genes were
localized to the bone proper and the mineralized por-
tions of the insertion, and cartilage specific genes were
localized to the insertion.12 Collagen fibers were less
oriented at the insertion compared to the tendon.12
Mineral content increased linearly from tendon to
bone.13 Biomechanically, both the elastic and viscous
behaviors of the tissue varied from tendon to bone.12
The tensile properties of the tendon, for example, were
stiffer than those of the insertion. Structure-function
relationships were also examined at the anterior cruciate
ligament–bone insertion.14 Microcompression was per-
formed to determine the compressive properties and
energy dispersive x-ray analysis was performed to deter-
mine mineral content along the ligament enthesis. The
calcified regions of the insertion exhibited significantly
greater compressive moduli than the noncalcified
regions. Based on these results, it is apparent that there
is a gradation along the tendon–bone insertion site with
regard to collagen structure, extracellular matrix compo-
sition, mineral content, and biomechanical properties.
Composition and Microstructure of the
Insertion Site Is Optimized to Minimize
Stress Concentrations
Mechanical models of the insertion demonstrate that
the orientation of the collagen fibers and their level of
mineralization are optimized to minimize stress and
strain concentrations. In one study, a finite element
 Chapter 5:  Biology and Biomechanics of the Tendon–Bone Insertion
model of the insertion was used to determine the role
of collagen orientation on stress and strain distribu-
tions.15 The idealized model showed that the micro-
structure serves to reduce stress concentrations and
material mass and to shield the insertion’s outward
splay from the highest stresses. Similarly, a model of the
medial collateral ligament femoral insertion demon-
strated that the direction of the principal tensile stresses
coincides with the direction of the collagen fibers.16 A
correlation was found between cell shape and mechani-
cal stresses, suggesting a direct relationship between
the stress field and cell activity. The effect of mineral
content on load transfer was modeled at the insertion
in a separate study.17 It was demonstrated that mineral
content and collagen fiber orientation combine to
give the tendon–bone transition a unique grading in
mechanical properties, supporting the idea for a func-
tionally graded, continuous tissue transition from
tendon to bone. An increase in mineral on collagen
fibers provided significant stiffening of the fibers. The
orientation of collagen fibers was the second major
determinant of tissue stiffness. The combination of
these two factors resulted in a variation of stiffness over
the length of the tendon–bone insertion similar to what
has been described from experimental testing.12,18 These
biomechanical models describe how tendon–bone
attachment is achieved in nature through a functionally
graded material composition.
DEVELOPMENT OF THE TENDON–BONE
INSERTION SITE
Studying the development of the tendon enthesis may
provide insights into the biological processes necessary
to form this complex anatomical site. These insights are
critical for the success of biological treatments or tissue
engineering solutions for tendon–bone repair. Animal
models indicate that the enthesis develops into a func-
tionally graded tissue postnatally,19-22 allowing a unique
opportunity to study and perturb its formation.
Role of Biological Factors
Several factors are important to the development of the
tendon–bone insertion site. Scleraxis is a transcription
factor expressed both in tenocyte progenitors and in
mature tendon cells and has been associated with
tendon and insertion site formation.23 SRY (sex deter-
mining region Y)-box 9 (SOX-9) is associated with chon-
drogenesis and has been localized in proliferating
chondrocytes.24 Parathyroid hormone–related protein
(PTHrP) and Indian hedgehog (IHH) drive chondrocyte
proliferation, but also form a negative feedback loop,
maintaining a population of proliferative cells at the
growth plate, available for further growth and differen-
tiation.25 These factors are seen in the growth plate of
developing bones and likely play a similar role at the
formation of the tendon enthesis, as many of the same
51
cell types and maturation processes are seen at both
anatomical locations.26
The developing growth plate contains cells that are
divided into distinct zones based on morphology and
mineral content.27 The zones are the reserve zone, the
proliferative zone, and the hypertrophic zone. The small
cells in the reserve zone proliferate and organize into
columns in the proliferative zone, and finally become
hypertrophic chondrocytes. It is at the leading edge of
the hypertrophic zone that calcium is deposited in the
zone of provisional calcification leading to mature
bone. Similar chondrocytes are seen at the developing
insertion site; these cells eventually mineralize to form
a tendon enthesis with a gradation in mineral.
The tendon–bone insertion site develops in the early
postnatal period.19-22 Mouse studies have elucidated the
time course of development of the tendon enthesis
using in situ hybridization.20,21 Collagens were localized
along the developing insertion. Collagen I was exam-
ined due to its prevalence in both tendon and bone.
Collagen II was examined due to its association with
chondrocytes, and hence the fibrocartilage region of the
insertion. Last, collagen X was examined due to its
reported expression by hypertrophic chondrocytes of
the growth plate. Rotator cuff tendon precursors were
juxtaposed to the humeral head at 15.5 days postcon-
ception. A transition zone between the developing
tendon and bone was not apparent until 7 days after
birth. Prior to 14 days postnatally, collagen I was con-
sistently expressed on the tendon side of the insertion
while collagen II was consistently expressed on the
humeral side, mirroring each other during these early
time periods. Collagen X was expressed at 14 days in
association with hypertrophic chondrocytes. As the
humeral head matured and mineralized, it began to
express collagen I, the main collagen type in mature
bone. A mature fibrocartilaginous insertion site was
formed by 21 days postnatally. This corresponded to the
completion of mineralization of the cartilaginous
humeral head. Similar results were seen at the develop-
ing Achilles tendon insertion of the rat21 and human.28
PTHrP has been localized to the insertion sites of
both tendons and ligaments.26 In the growth plate, it
is seen in proliferating chondrocytes, and is known to
be part of a negative feedback loop, preventing their
maturation into hypertrophic chondrocytes, which
then mineralize to form bone. Therefore, it plays an
important role not only in maintaining a population
of cells available for growth but also for preventing
inappropriate mineralization. It likely plays an analo-
gous role in maintaining a barrier between mineralized
and unmineralized tissues at the tendon to bone inser-
tion site. PTHrP works in concert with other factors.
IHH is secreted by proliferative chondrocytes before
they become hypertrophic chondrocytes. It binds to
the cell membrane receptor Patched 1 leading to the
52 Section 1:  Basic Science

accumulation of a transmembrane protein smoothened, used as controls. Many effects were observed due to
which leads to the production of PTHrP. These factors paralysis in bony development, soft tissue contracture,
are all localized to the developing tendon insertion muscle mass, and muscle force generation. Dramatic
site at 14 to 21 days, correlating to the onset of miner- changes were seen at the developing tendon–bone
alization of the humeral head. These factors are also insertion site due to unloading.
highly mechanosensitive.29 Specifically, their expression The sensitivity of bone to its mechanical environ-
is decreased when load is removed. ment was highlighted in this series of experiments.
SOX-9 and scleraxis are important factors in chon- Removal of load significantly decreases amounts of
drogenesis and tenogenesis, respectively.30 SOX-9 is bone mineral in the humeral heads of the paralyzed
localized to proliferating chondrocytes, but not in mice (Figure 5-2). These differences were not seen,
hypertrophic chondrocytes, and may play some role in however, until after the 14-day time point; large differ-
insertion site development. Serving as a marker for ences were seen comparing saline to botulinum toxin
many connective tissues, including ligaments, tendons, injected shoulders at 21, 28, and 56 days. In addition,
and joint capsules, scleraxis has been localized at the the botulinum toxin injected sides had larger numbers
developing insertion site and is required for teno­genesis. of osteoclasts lining the bone compared to the controls.
Scleraxis likewise has been shown to be highly sensitive Therefore, the decreased mineral content resulted not
to the mechanical environment, specifically, upregu- only from decreased mineral deposition, but also due
lated in stem cells exposed to tensile forces.31 to increased bone resorption.
Removal of load also impaired the formation of a
Role of Mechanical Factors graded fibrocartilaginous insertion site. At 14 days, both
A series of experiments using mice were performed to saline and botulinum toxin injected shoulders demon-
elucidate the effects of the mechanical environment on strated evidence of hypertrophic chondrocytes at the
the formation of the tendon–bone insertion site.19 Botu- insertion. However, by 21 days, the botulinum toxin
linum toxin A was injected to the shoulders of mice injected specimens showed a lack of fibrocartilage for-
within 24 hours of birth, simulating a neonatal brachial mation, disorganized collagen fibers, and persistence of
plexus injury and removing muscle load from the hypertrophic chondrocytes. The saline side, on the other
humeral head. Saline injections in the contralateral hand, had a well-developed transition zone with no
shoulders and a separate group of healthy mice were evidence of hypertrophic chondrocytes. The transition

Saline Botox

BONE VOLUME TRABECULAR THICKNESS TRABECULAR SPACING

6 0.30 0.8
Trabecular thickness (mm)

Trabecular spacing (mm)

Normal # Normal
0.25
Bone volume (mm3)

5 #
Botox Botox
Saline 0.6
4 # 0.20 # # Saline
*
3 # 0.15 0.4 #
* * #
* #
2 0.10 *
#* # Normal
*
# * # Botox 0.2
1 0.05
* Saline
# #
0 0 0
0 10 20 30 40 50 60 0 10 20 30 40 50 60 0 10 20 30 40 50 60
Time (days) Time (days) Time (days)

Figure 5-2  Bone volume and trabecular architecture were significantly altered in the Botox group compared to the Saline
and Normal groups at most timepoints during postnatal enthesis development (*significant difference Saline vs. Botox;
#significant difference Saline or Botox vs. Normal). (Adapted from Thomopoulos S, Kim HM, Rothermich SY, et al: Decreased
loading delays maturation of the tendon enthesis during postnatal development, J Orthop Res 25:1154–1463, 2007.)
 Chapter 5:  Biology and Biomechanics of the Tendon–Bone Insertion
zone remained disorganized and immature at 56 days
in the paralyzed specimens, whereas the saline group
had a mature, fibrocartilaginous, tendon enthesis. The
changes in fibrocartilage formation and bone formation
support the conclusion the mechanical environment
plays an important role in enthesis development.
TENDON–BONE REPAIR
Basic Science of Tendon–Bone Healing
Tendon–bone healing occurs through the generation of
a fibrovascular scar rather than regeneration of a graded
fibrocartilaginous transition (Figure 5-3).5,32-34 These
studies have focused on morphological and composi-
tional evaluations of the healing tissue. In an Achilles
tendon–bone healing study, surgical repair was impor-
tant to allow cells to reorganize the insertion site.33 At
8 weeks, the tendon was attempting to recreate the
insertion site. Low levels of type X collagen were found
in the fibrocartilage adjacent to bone, and this protein
was important in maintaining the interface between
calcified and noncalcified fibrocartilage. Similar histo-
logical findings were reported in a canine model of
tendon detachment.34 However, both models showed
that the structure and the composition of the healing
insertion did not approach normal by the longest time
points studied.
Investigators have also examined the mechanical
properties of the healing insertion site. One group
NORMAL
Tendon
Bone
Interface
Figure 5-3  A graded fibrocartilaginous transition is not regenerated at the healing supraspinatus tendon–bone insertion in
rats (toluidine blue stain). Rather, the interface is filled with fibrovascular scar tissue, forming an abrupt transition between
tendon and bone (orange lines indicate the borders of the fibrocartilaginous transition on the left and the abrupt interface
between scar tissue and bone on the right).
53
examined the strength of the rabbit patellar tendon–
tibia insertion site after the creation of a partial defect.35
Failure strength increased and approached normal over
a span of 12 weeks. However, the healing tissue in a
partial defect may have been stress shielded by the adja-
cent uninjured tissue. Another group found that the
strength of healing infraspinatus insertion site in goats
was only one third of the strength of the normal infra-
spinatus insertion at 12 weeks.36 This finding demon-
strates that although the histological appearance may
suggest the recreation of an insertion site, the strength
of the site may not be restored to normal. Another study
examined tendon healing in a bone tunnel.32 Strength
increased significantly between 2 and 12 weeks. After
this point, failure occurred somewhere other than the
insertion site. In a rat rotator cuff model, while the
structural properties reached two thirds of normal after
8 weeks of healing, the material properties remained an
order of magnitude weaker than control.5 The healing
tissue had a higher cross sectional area compared to
uninjured control, but was made up of poorly organized
type III collagen without a recreation of a fibrocartilagi-
nous transitional zone. Studies on canine flexor tendon
to distal phalanx repair indicated that insertion-site
healing demonstrates little improvement in repair-site
failure force from the time of suture through 42 days
following repair.37 A significant decrease was seen in
insertion site ultimate strength at 10 and 21 days
compared to time zero, indicating that a softening
HEALING
Bone
Interface
Tendon
54 Section 1:  Basic Science
phenomenon occurred in the early stages after repair.37
In all animal models, rather than regeneration of a func-
tionally graded transition between tendon and bone,
the interface was filled with fibrous scar tissue. These
findings demonstrate the considerable need for improve-
ment in the treatment of tendon–bone insertion site
injuries.
Bone Loss Following Tendon or
Ligament Injury
Bone loss following tendon or ligament injury has been
noted in a number of clinical studies and animal models.
In the rotator cuff, reduced bone mineral density was
seen in the humerus of patients 9 years after cuff rupture
and repair.38 These changes, however, were seen only in
patients who did not have full return of function, sug-
gesting that the bone loss was due in part to reduced
joint loading. In another clinical study of the Achilles
tendon, calcaneal bone loss was seen 4 to 12 months
after surgical repair.39 In a canine model of anterior
cruciate ligament transsection, a significant reduction in
bone mineral density was seen as early as 4 weeks
postinjury.40 Bone loss progressed through 10 weeks,
and then reached a plateau. Finally, a clinical study of
anterior cruciate ligament injury showed a 20% reduc-
tion in bone mineral density at 1-year follow-up for
patients who had surgical repair.41 Patients with less
severe injuries who were treated conservatively (i.e., no
surgery) showed only a 2% to 3% reduction in bone
mineral density. Significant bone loss was also demon-
strated in the canine flexor tendon model.42 Decreased
bone mineral density was seen at the distal phalanx
at 10, 21, and 42 days following injury and repair,
indicate that bone resorption may be a factor that con-
tributes to the low values of repair-site failure force
(Figure 5-4).42 Similar results were reported in the rat
rotator cuff model.43,44 Bone mineral density was signifi-
cantly decreased following tendon injury and repair.
A delay between injury and repair resulted in inferior
tendon–bone healing, in part due to decreased bone
quality.
Rehabilitation Based Treatments
As described earlier, tendon–bone healing is character-
ized by the formation of connective tissue with vastly
inferior biomechanical properties compared to normal,
uninjured tendon. A graded fibrocartilaginous transi-
tion between tendon and bone is not recreated. It is well
established that musculoskeletal tissues, including
tendon, bone, and cartilage, respond to their mechani-
cal environment. Similarly, as described earlier, the
development of a functional enthesis requires mechani-
cal loading. Therefore, significant efforts have been
made to enhance tendon–bone healing via rehabilita-
tion protocols (i.e., via control of the mechanical loads
across the healing insertion).
700
600
–21%
–40% –41%
500 *
BMD (mg/cm3)
400 * *
300
200
Control
100 Injury and repair
0
0 10 20 30 40
Time (days)
Figure 5-4  Dramatic bone loss was observed in the canine
distal phalanx after flexor tendon to bone repair. Decreases
in bone mineral density (BMD) were observed as early as 10
days after injury and repair. (Adapted from Silva MJ, Boyer
MI, Ditsios K, et al: The insertion site of the canine flexor
digitorum profundus tendon heals slowly following injury
and suture repair, J Orthop Res 20:447–453, 2002.)
Increased force is beneficial to healing in a variety of
clinical settings. Early mobilization improves healing
and function after anterior cruciate ligament reconstruc-
tion in the knee.45 Early passive range of motion
decreases adhesions and improves strength after flexor
tendon repair.46 Controlled static stress is beneficial to
medial collateral ligament healing in the knee.47 On the
other hand, excessive force and motion can be cause
microdamage and/or gapping and thus be detrimental
to healing.5 Optimizing the mechanical environment in
the postoperative setting is therefore critical for improv-
ing outcomes.
In order to determine the effects of a variety of activ-
ity levels on tendon–bone healing, rotator cuff repairs
were performed in rats.5 Rat shoulders were then immo-
bilized, allowed cage activity, or exercised. Shoulders
that were immobilized demonstrated superior collagen
orientation and biomechanical properties compared to
those that were exercised. The exercised rats had a greater
quantity of tissue, but the tissue was lower in quality.
The composition of extracellular matrix generated at the
immobilized insertion better resembled a normal, unin-
jured insertion. The immobilized group was superior to
the cage activity group, and the cage activity group was
superior to the exercised group. A second study using
this animal model investigated the effect of short and
long durations of these activity levels on the healing
insertion site.48 The activity level had no effect on the
biomechanical properties of the insertion site at the
early (4 week) time point. However, decreased activity
(i.e., cast immobilization) had a positive effect on
 Chapter 5:  Biology and Biomechanics of the Tendon–Bone Insertion
biomechanical properties at the late (16 week) time
point. In these studies, decreasing the activity level by
immobilizing the shoulder improved tendon–bone
healing, as measured by collagen organization and bio-
mechanical properties. These results demonstrate that
increased activity can be detrimental to healing.
However, it was not determined whether this was a
result of a positive effect due to low levels of loading in
the immobilized group or a negative effect due to high
levels of motion in the exercised group.
The notion of negative effects due to motion at the
healing rotator cuff insertion site were substantiated in
a subsequent study that examined tendon biomechan-
ics and joint range of motion in rat shoulders after
rotator cuff repair.49 Continuous immobilization was
compared to two different passive range-of-motion pro-
tocols for 2 weeks followed by a 4-week remobilization
period. Both passive range-of-motion groups had less
joint range of motion compared to the continuous
immobilization group. All joints were stiffer compared
to preinjury levels. No differences were found in tendon
collagen organization or mechanical properties in the
three groups.
As both high levels of load and high levels of motion
were found to be detrimental to tendon–bone healing,
the effect of decreasing load below that seen in immo-
bilized repairs was examined in a recent study.50 After
surgical injury and repair, rat shoulders in two groups
were immobilized. One experimental group had botu-
linum toxin A injected into the supraspinatus muscle to
completely remove load from the healing insertion site.
A second group was immobilized and had saline injec-
tions into the muscle. A third group had botulinum
toxin A injections and rats were allowed cage activity
after repair. The saline/casted group had greater scar
volume and cross-sectional area of the repair tissue at
the insertion site and improved structural properties
compared to the botulinum toxin–paralyzed groups,
demonstrating that complete removal of load from the
healing insertion site was detrimental to healing.
Although reduced loading (e.g., through cast immobili-
zation) can be beneficial to healing (presumably by
eliminating excessive motion at the repair site), some
load applied to the site via normal muscle contraction
is necessary for effective healing.
The beneficial role of cast immobilization coupled
with physiological muscle loading was corroborated by
a study using a canine model of flexor tendon repair.51
This study measured biomechanical properties, bone
density (of the distal phalanx), and gap formation after
a flexor tendon–bone repair. In the experimental group,
the proximal tendon was transected to remove all load
from the repair site. All repairs were immobilized post-
operatively and subjected to a standard flexor tendon
passive range-of-motion protocol. Muscle loading across
the repair-site resulted in improved biomechanical
55
properties and greater range of motion. There was no
difference in bone density between loaded and unloaded
specimens. As in the rat model, cast immobilization
resulted in a better outcome than complete removal of
load. When considering these studies together, it is clear
that a balance between too much and too little load is
important to maximize tendon–bone healing. Closer
investigation suggests that high levels of motion are
detrimental but physiological muscle loading is benefi-
cial. The role of loading is consistent with the premise
that musculoskeletal tissues not only respond to, but are
dependent on, some load for development, healing,
and homeostasis.
Biologically Based Treatments
Biologically based approaches for enhancing tendon–
bone healing have focused on one or more aspects of
the tissue engineering paradigm—the use of signaling
biofactors (e.g., growth factors), responding cells (e.g.,
mesenchymal stem cells), and scaffold microenviron-
ments (e.g., collagen matrices).52 Numerous studies
have attempted to enhance tendon–bone healing by
delivering growth factors to the repair site. As significant
bone loss has been demonstrated after tendon–bone
injury and repair, one approach has been to target the
bony side of the insertion for treatment. Bone morpho-
genetic protein 2 (BMP-2) is well established as a potent
stimulator of bone formation. One experiment demon-
strated that the healing of tendon in a bone tunnel
occurred through bone ingrowth into tendon.53 The
authors demonstrated an improvement in structural
properties of the tendon healing in a bone tunnel after
application of exogenous BMP-2. Preventing bone
resorption at the healing insertion using bisphospho-
nate treatment has also been effective in improving
healing.54 Promotion of fibrocartilage at the healing
insertion has also been attempted, but with limited
success. One study demonstrated that transforming
growth factor beta is critical for tendon–bone healing,
but its modulation was ineffective in improving
healing.55 A separate study showed that application of
articular cartilage to the healing insertion increases
fibrocartilage regeneration.56 However, the partial regen-
eration of a fibrocartilaginous transition did not lead to
improvements in the biomechanical properties of the
repair.
Cell based therapies also hold great potential for
enhancing tendon–bone healing. Adult mesenchymal
stem cells (MSCs) show excellent regenerative capacity,
including the ability to proliferate rapidly in culture and
the capacity to differentiate into a wide range of cell
types. Prior reports support the use of stem cells to
enhance healing in multiple tissues. Recent work showed
that MSCs transfected with a tenogenic factor were effec-
tive in improving rotator cuff tendon–bone repair in a
rodent animal model.57 The addition of naïve MSCs to
56 Section 1:  Basic Science

the healing rotator cuff insertion site did not improve σ = 0.29MPa σ = 1.60MPa σ = 2.41MPa
healing at the tendon attachment site. However, when High mineral
the MSCs were modified to overexpress the insertion-
site specific developmental gene membrane type 1
metalloprotease prior to delivery, rotator cuff healing
was significantly enhanced. Similar repair enhance-
ments were seen with the delivery of MSCs to a patellar
tendon defect and Achilles tendon models.58,59
A review of scaffolds currently used clinically for
rotator cuff tendon–bone repair revealed that further
work is necessary to optimize scaffold properties.60 Par-
ticularly lacking in the currently available scaffolds is an
appropriate recreation of the native tissue’s gradation in
properties. To address this lack of complexity, tissue
engineering work has focused on stratified and continu-
ously graded designs. In recent work, biphasic61 and
triphasic scaffolds62 were generated and seeded with Low mineral
multiple cell types. These studies demonstrated the
importance of signaling between the various insertion- ε=
site cell types for generation of a functional insertion.
0 0.02 0.04
Recent approaches have also attempted to create con-
tinuous gradients in properties to recreate the functional Figure 5-5  Strain maps of a nanofiber scaffold with a
gradation in mineral content under uniaxial tension.
grading that is seen at the natural tendon–bone inser-
Increasing strain is seen with increasing stress, with
tion. To this end, electrospun polymer nanofiber scaf-
localization at the compliant low mineral end.
folds were synthesized with gradations in mineral,
mimicking the mineral gradation seen at the native
insertion.63 The gradation in mineral content resulted in
a spatial variation in the stiffness of the scaffold (Figure
5-5). Similar results were reported using a cell-seeded provide a solution to the clinical problem of tendon–
collagen scaffold with a gradient in retrovirus encoding bone healing. A functionally graded material implanted
an osteogenic transcription factor.64 A tissue engineered at the time of surgical repair may provide mechanical
scaffold with a gradation in properties and seeded with stability and guide the repair process, leading to a suc-
the appropriate cells and biofactors may ultimately cessful attachment of tendon to bone.

References
1. Jones RM: Mechanics of Composite Materials, ed 2, Philadel-
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 CHAPTER
6  
GENE THERAPY FOR TENDON
HEALING
Jin Bo Tang, MD, Ya Fang Wu, MD, Yi Cao, MD,
Chuan Hao Chen, PhD, Xiao Tian Wang, MD, and
Paul Y. Liu, MD
OUTLINE
Weak intrinsic healing potential is the central issue
underlying difficulties of tendon healing and major
clinical problems associated with tendon surgery. Bio-
logical augmentation of the healing process has long
been sought. In the past decade, growth factor gene
therapy emerged as an attractive treatment modality.
Our work over the past decade has not only identified
appropriate genes as the therapeutic target and vectors
as gene-carrying vehicles but also assessed the effi-
ciency of transgene expression and sustained supply
of the growth factors in the healing tendon. In testing
the efficacy of growth factor gene therapy in vivo, we
found that injection of adeno-associated viral vectors
harboring basic fibroblast factor or vascular endothe-
lium growth factor cDNAs to the tendon during
surgery substantially increases tendon healing strength
in a chicken tendon cut and repair model. Transgenes
were expressed from postsurgical weeks 2 to 6, cover-
ing the critical healing period. In the healing tendons,
gene therapies increased the levels of growth factors,
promoted synthesis of extracellular matrix compo-
nents, decreased tenocyte apoptosis, and enhanced
cellular proliferation. These evidences show the
promise of gene therapies in the arena of tendon
repair. Our studies also indicate the possibility of
delivery of synthetic micro-RNA in limiting adhesions.
These findings may lay the groundwork for establish-
ment of methods to correct the insufficiency in intrin-
sic healing capacity of the tendon.
Improvement in tendon healing through biological
approaches, molecular manipulations in particular,1-8 is
a relatively new area of investigation related to flexor
tendon surgery. These biological manipulations are
intended to overcome a major obstacle to success in
tendon repair—low intrinsic healing potential. The
development of molecular treatment of tendon healing
has benefited from advances in biotechnology and
a recent exponential expansion in available genetic
information. We have noted that biological investiga-
tions are catching up with mechanical studies, making
an increasingly greater contribution to the efforts to
improve tendon repairs.9-29 From these biological inves-
tigations, we are rapidly accruing information regarding
the molecular mechanisms and efficacy of manipula-
tions of tendon healing, which may bear fruit in the
future.
Weak healing potential is a common problem in
tissues without a rich blood supply. At present, there is
a lack of effective treatment to ensure a prompt and
strong healing of these tissues. Finding treatments to
accelerate healing such tissues is of paramount signifi-
cance in regenerative medicine, sports medicine, reha-
bilitation, and in surgery. The treatments not only
benefit tendon repair in the hand but also benefit repair
and regeneration of tendons, ligaments, and tendon–
bone junctions throughout the body. Efforts to acceler-
ate healing of those tissues are expected to bring about
significant impacts in a number of medical specialties.
Laceration of digital flexor tendon is representative of a
wide spectrum of injuries that fail to heal reliably and
is an ideal setting for testing novel molecular therapies.
Work in this area holds promise for advancing the treat-
ment of tissue injuries due to trauma or sports or in
association with degeneration.
Of gene therapy applications in tissue healing, the
unique advantage is that this strategy necessitates
production of the encoded factors for a fairly short
period.30-32 Gene therapies traditionally aimed at curing
tumors or congenital diseases, in contrast, necessitate
long-term transgene expression, usually over the entire
lifetime. Such prolonged transgene expression is still a
difficult goal to reach reliably for chronic conditions,
which constitutes an obstacle to ultimate clinical success
in curing these diseases. However, for tissue repair, gene
therapy can establish a local, endogenous synthesis of
the authentically processed materials critical to the
healing. Long-term gene expression is neither necessary
59
60 Section 1:  Basic Science
nor desired.30 The required period of transgene expres-
sion for tissue healing exactly fits current possibilities
offered by gene therapy.
INNATE WEAKNESS IN INTRINSIC
TENDON HEALING AND “NO-GAIN”
PERIOD IN STRENGTH
Tissues nourished with rich blood supplies usually
acquire mechanical strength rapidly in the first and
second postsurgical weeks. However, the tendon healing
process is characterized by a “no-gain” period in strength
over the first 3 to 4 weeks (Figure 6-1)5,33-35 due to the
weak healing capacity, yielding slow healing responses
after injury. The innate weakness in tendon healing
relates to the following structural facts: (1) they lack
sufficient blood supply, (2) have sparse cellularity, and
(3) are mainly composed of tightly packed collagen
bundles. The characteristic no-gain period in strength is
the central issue underlying the difficulties and clinical
problems associated with tendon repairs. The goal of
present efforts through biological manipulations is to
elicit an earlier increase in strength, helping the tendon
“leap over” this lag period. Theoretically, this goal is
achievable through targeting major causes of weak
tendon healing, either by supplementation of cells
involved in healing or by increasing the activity levels
of growth factors. Because healing strength is structur-
ally based on collagen connections across the tendon
repair site, we expect that addition of specific cells or
growth factors will ensure speedy deposition and matu-
ration of collagens at the healing site, resulting in an
earlier gain in mechanical strength.
50
45
Further
steady gain in
40 the strength
Tendon strength (N)
35
Swift gain in
30 the strength
3 methods (e.g., liposomal, electroporation, sonopora-
25
20
15 No gain period
10 in the strength
2 Gene therapy is commonly considered a possible
5 treatment modality for patients with congenital defects
1
0 of key metabolic functions or patients with malignan-
0 1 2 3 4 5 6 7
Weeks
Figure 6-1  The tendon healing process is characterized by
a “no-gain” period in strength over the first 3 to 4 weeks.
The graph shows our data for the tendon strength obtained
from the complete cut and repair model of the FDP tendon
in chicken long toes. The tendon was repaired with a
modified Kessler method using 5-0 nylon suture. The
strength of the healing tendon can be divided into three
parts: no gain, swift gain, and further steady gain periods.
OVERALL CONCEPTS AND METHODS
OF GENE THERAPY
The central idea of gene therapy is the incorporation of
genes of interest into recipient cells to modify levels of
expression of the gene, for the purpose of treating
disease. The disorders requiring gene therapy are usually
refractory to conventional therapeutic approaches.
Although the clinical utility of these technologies
remains in its infancy, gene therapy has been used with
preliminary clinical success in some diseases. More trials
are currently under way and may generate evidence for
the utility of such techniques over a broader range of
medical problems. Gene therapy holds great promise
for incorporation into mainstream medicine.
The ideas behind gene therapy date back to the early
1970s. In 1972, Friedmann and Roblin advocated intro-
ducing exogenous genes to cure human diseases in an
article entitled, “Gene Therapy for Human Genetic
Disease?”36 Major advances were made in the technical
aspects of gene therapy in the 1990s. Over the past two
decades, investigators have taken logical steps of using
gene therapy to pursue curing diseases caused by single-
gene defects (e.g., cystic fibrosis, hemophilia, muscular
dystrophy, and sickle cell anemia) or in the treatment
of certain cancers. More recently, clinical work has
included a trial for treating Leber congenital amauro-
sis,37 a disease caused by mutations in the RPE65 gene.
The investigators proved the safety of subretinal delivery
of recombinant adeno-associated virus (AAV) carrying
the RPE65 gene and found a modest improvement in
vision of the patients.37 In another study, investigators
restored trichromatic vision to squirrel monkeys using
gene therapy to cure red-green color blindness.38 Other
investigators succeeded in treating adrenoleukodystro-
phy (ADL), a fetal brain disease, by delivering the gene
for the missing enzyme to patients via a lentiviral vector.39
Various techniques have been developed to achieve
successful gene transfer,32 including both nonviral
tion, shots from a “gene gun,” etc.) and viral vectors
(e.g., adenoviruses, AAVs, herpes simplex viruses, retro-
viruses, lentiviruses, etc.).
8 cies. Clinical success of gene therapy for congenital
diseases and cancers is hindered by problems such as
the short-lived function of the transgenes, immune
responses, side effects with vectors, the inability to treat
multigene disorders, and the risk of insertional muta-
genesis. However, these problems rarely constitute a
barrier to the use of gene therapy strategies for tissue
healing if gene delivery methods are appropriate. The
use of gene therapy in tissue repair or regeneration may
become “dark horses” in the field of gene therapy.
 Chapter 6:  Gene Therapy for Tendon Healing 61

Controlled-release drug delivery systems is another

BIOLOGICAL METHODS TO ENHANCE
TENDON HEALING
Theoretically, tendon healing may be enhanced through
biological means other than gene therapy. Nevertheless,
none of those methods can be claimed to be of practical
value until fully tested. The initial step in the test process
involves in vitro studies. The next step is in vivo experi-
mentation, which will generate preclinical data to
support the clinical trials, the last step in the test process.
One possible way to augment tendon healing is to
provide the tendons with exogenous cells, to ameliorate
sparse cellularity. A few such attempts have been made.
Direct delivery of bone marrow stem cells to healing
rabbit Achilles tendons produced some evidence of
increases in tendon strength.40 Investigators coated sur-
gical sutures with bone marrow stem cells and delivered
those cells to the tendon in vitro,6 but the in vivo effi-
cacy of this method has not been reported.
Growth factors, such as insulin-like growth factor-1
(IGF-1),9,10 platelet-derived growth factor-B (PDGF-B),20
and basic fibroblast factor (bFGF),20,23,25 have been
reported to promote tenocyte proliferation or collagen
synthesis. Direct supplementation of growth factors to
the healing tendons has failed to reliably improve
healing strength. Chan and colleagues41 injected bFGF
to rat cut patellar tendon and detected no effects on
ultimate strength of the tendon 7 and 14 days after
surgery despite increases in cell proliferation and type
III collagen production. Surgical sutures can be coated
with growth factors such as bFGF or growth differentia-
tion factor-5 (GDF-5).4,42 Surgical repairs using such
coated sutures improved the strength of the rabbit flexor
tendon only at a single time point (postoperative week
3) but failed to improve strength at other time points.4,42
way to provide the tendon with a prolonged supply of
growth factors.7,21 Growth factors can be incorporated
into polymers in vitro, and the impregnated polymers
are then implanted into the tissues, which may deliver
the growth factors continuously for a prolonged period
in a controlled fashion. This system holds promise for
use in tendon repairs, but research in this area is just
beginning. Growth factors (bFGF and PDGF-BB) have
been incorporated into fibrin matrices and the release
kinetics has been tested over a 10-day-period in vitro21;
bFGF and PDGF-BB were found to release gradually
from the fibrin matrices and to modulate cell prolifera-
tion and extracellular matrix synthesis in vitro. However,
this system loaded with PDGF-BB was not found to
improve the strength of the healing canine flexor
tendons at days 7, 14, and 42 after surgery.7 In a canine
model, bFGF delivered through fibrin heparin–based
controlled-release system stimulated cellular prolifera-
tion, promoted neovascularization and inflammation of
the flexor digitorum profundus (FDP) tendon in the
earliest stages after surgical repair, but it failed to improve
mechanical strength of the repair.43 This system remains
to be fully tested with respect to its effectiveness to
increase tendon strength in vivo.
GENE THERAPY APPROACHES—THE
FIRST STEP: CHOOSING GENES AND
DELIVERY METHODS
Over the past 10 years, we have directed our efforts toward
improving tendon healing through augmentation of
growth factor activity (Figure 6-2). To test the efficacy
of this approach, we faced two initial questions: (1)
what genes should be delivered, and (2) which are safe
and efficient gene-carrying vehicles for our purposes?

FLOW CHART OF OUR INVESTIGATIONS OF TENDON GENE THERAPY

Tissue reactions In vivo study Expression of

caused by different of efficacy of molecules
Characterization Tests of effects of vectors in tendons Construction of AAV2-bFGF involved in the
of effects of plasmid vectors AAV2-bFGF, gene therapy healing tendon
growth factors on harboring growth Efficiency of gene AAV2-VEGF, and apoptosis
tenocytes in vitro factors in vitro delivery by different and In vivo study
vectors in tendons DS-AAV2-VEGF of efficacy of Test of in vitro
vectors AAV2-VEGF engineered
Efficiency of gene
gene therapy miRNA gene
delivery by different
serotypes of AAVs therapy in vitro
and in vivo

(2002–2003) (2003–2004) (2004–2006, 2008) (2005–2010) (2007–2011)

Tang, Xu Tang, Wang Zhu, Cao, Chen, Tang Xin, Wang Cao, Wu, Tang Chen, Wu, Tang

Understand molecular biology of tendon healing Increase the healing strength Limit adhesions

Figure 6-2  Flow chart of our investigations of growth factor gene therapy to enhance tendon healing and micro-RNA gene
therapy to inhibit tendon adhesions over the past 10 years.
62 Section 1:  Basic Science
To answer the first question, we examined levels of
growth factors in the healing digital flexor tendons.
Growth factor genes with low levels of expression in the
healing process are considered targets of gene therapy.
In a chicken tendon laceration model, we examined the
levels of growth factors from day 3 to week 12 after
surgery. bFGF and PDGF-BB were found to have the
lowest expression in the early period28; VEGF and IGF-1
were expressed in modest amounts.28 Consequently, we
decided to target the bFGF gene initially, and the VEGF
gene secondarily.
Our answer to the second question—how best to
deliver the genes—was based on an essential consider-
ation: the intended therapy is aimed at the healing of
normal tissues, requiring only short transgene expres-
sion, rather than treating cancers or curing inherited
diseases. In this regard, safety issues of the vectors
should be the primary concern. With these consider-
ations in mind, we first eliminated retroviral vectors.
Lentiviral vectors and herpes simplex viral vectors were
next excluded, because of concerns of biosafety of len-
tiviral vectors (e.g., potentials of generation of
replication-competent lentivirus and oncogenesis) and
the narrow applications of herpes simplex viral vectors
(i.e., in the nervous system).44 Adenoviral, AAVs, and
liposome-mediated gene transfer thus became viable
candidates.
To move our decision process along, we implemented
three sets of studies to examine (1) tissue reactions in
tendons caused by the candidate gene transfer methods;
(2) efficiency of gene delivery to tenocytes using these
methods; and (3) duration and course of transgene
expression in healing tendons by these methods.
We used both rabbits and chickens to examine reac-
tions in the tendons elicited by three candidate methods.
Histologically, we observed dramatic tissue reactions in
both epitenon and endotenon areas after liposome-
mediated gene transfer. The reactions elicited by adeno-
viral vectors were also pronounced but less severe.
Tendons treated by AAV serotype 2 (AAV2) vectors dis-
played obvious cellular proliferation and thickening of
epitenon, but the reactions were almost completely con-
fined to the epitenon (Figure 6-3). We noted striking
similarity between cellular proliferation in the healing
process of tendons and that caused by the AAV2 vectors
(see Figure 6-3).26
Efficacy of liposome-mediated transfection and trans-
duction of adenoviral and AAV2 vectors was next tested.27
We found that tenocytes are not highly permissive in
cell culture settings; all these vectors were associated
with low efficiency of gene transfer in tenocytes, even
when test at high titers of vectors. From the later in vivo
studies, we understand that transduction rates of AAV
vectors in the cells of tissues are much higher than in
cell culture conditions. AAV2 and adenoviral vectors
have similar transduction efficiency, both more efficient
than liposome-mediated gene transfer. Because more
than 10 serotypes of AAV are currently available, all with
different cellular or tissue tropism, we compared trans-
duction efficiency of AAV1, AAV2, AAV3, AAV4, AAV5,
AAV7, and AAV8 vectors containing the lacZ gene. We
found that AAV2, the best characterized and most
popular AAV vector, has the highest efficacy of gene
transfer in tenocytes.27
We then examined the duration of expression of
transgene introduced by AAV2 vectors to the healing
flexor tendon. Using an in vivo chicken model, we
injected the vectors at two sites in each stump of cut
FDP tendon through lacerated tendon surfaces. We
found that expression of transgenes lasts beyond 4
weeks and peaks during the second week. Through the
presence of enhanced green fluorescent protein (EGFP)-
positive cells, we confirmed that injected vectors were
distributed to all layers of the tendon (see Figure 6-3).
Our above examinations, coupled with desirable fea-
tures of AAV vectors (nonpathogenicity, low immunity
in human beings, etc.),44-46 and evidence of their utility
and safety from reported Phase I clinical trials37,47-49 con-
vinced us that the AAV2 vector is a proper gene transfer
vector. Although AAV vectors, which have small packag-
ing capacity, accommodate up to 4 to 5 kb of DNA
insert,46 they are sufficient to package therapeutic cDNAs
encoding growth factors (usually less than 1 kb each)
to meet our needs.
To explore how to deliver vectors into the lacerated
tendon, we decided to directly inject the vector to
tendons and tried injections at either one or two sites
on the tendon stump. We found that injection at two
sites ensures better vector distribution and greater vector
delivery. The volume of the injections without spillage
of fluid out of the tendon was also tested. Injection of
5 µl liquid to each site on the stump was found appro-
priate in rabbit or chicken digital flexor tendons. In
addition, we decided to inject the tendon through the
lacerated tendon surface, avoiding injuries to the tendon
gliding surface.
Information gathered in the above trials established
our method of vector delivery to tendons (Figure 6-4).
Typically, we inject a total of 20 µl of vectors to four sites
(5 µl/site) into two stumps. The needle is inserted from
the cut surface of the tendon at the depth of about
5 mm.
THE SECOND STEP: TESTING THE EFFECTS OF
GROWTH FACTOR GENE THERAPY IN VITRO
We constructed AAV2 vectors harboring the bFGF or
VEGF cDNAs, by inserting the therapeutic construct
between the 5′ and 3′ inverted terminal repeat (ITR)
sequences under the cytomegalovirus (CMV) immediate-
early promoter (Figure 6-5), and examined the in vitro
efficacy of therapies using these vectors. We treated
the tenocytes with AAV2-bFGF or sham AAV2 vector
 Chapter 6:  Gene Therapy for Tendon Healing 63

Day 7

Cut and repaired tendons AAV2 treated

A B C

Day 14

Cut and repaired tendons AAV2 treated

D E F

Day 7 Day 14

G AAV2 treated H AAV2 treated

Figure 6-3  Tissue reactions and transduction efficiency of the AAV2 vectors. The tissue reactions during the tendon healing
(A, B, D, E) and those caused by AAV2 (C, F) are strikingly similar. The tendons treated with AAV2 vectors exhibit obvious
cellular proliferation and thickening of epitenon, but there are almost no tissue reactions in the endotenon area. Enhanced
green fluorescent protein (EGFP) expression was obvious in endotenon and epitenon areas at days 7 and 14 (G, H) after
injection of AAV2-EGFP into the tendon. *Epitenon area. (A and D, magnification ×100; B and E, ×200; all others, ×400).

(harboring the lacZ gene), with nontreated tenocytes as
the control.50 We assessed transgene expression, expres-
sion levels of the bFGF gene, and type I and III collagen
genes. Expression of the bFGF gene increased signifi-
cantly after AAV2-bFGF treatment. Expression of type I
and III collagen genes increased significantly after trans-
fer of the exogenous bFGF gene compared with that in
cells treated with sham vectors or in nontreated con-
trols. We concluded that delivery of exogenous bFGF
gene to tenocytes significantly increases the levels of
expression of bFGF and type I and III collagen genes.
Similarly, we tested the effectiveness of AAV2-VEGF and
found enhancement of collagen I production and pro-
liferation of tenocytes in vitro.
64 Section 1:  Basic Science

Lacerated tendons

FDS

cm FDP
5
0.

Pulley
Micro-injection
A syringe

C
Figure 6-4  Method of delivery of AAV2-bFGF to the tendon. A, How vectors were injected AAV2 to both stumps of the
tendon cut ends at the depth of 0.5 cm. The vectors were injected to two sites in each stump, at the center of the left and
right tendon bundle of the FDP tendon. B, Structures of flexor tendons and the major pulley in the area between the proximal
and distal interphalangeal joints in chicken toes, which are similar to those of the human tendons around the A2 pulley.  
C shows an example of injection of vectors through the lacerated tendon cross-sectional surface into the tendon. D shows
a microinjection needle used for vector injection.

AAV GENOMES AND VECTOR CONSTRUCTION

In the first set of experiments, a total of 104 toes from
52 chickens underwent surgery and were randomized
P5 p19 p40
into three groups, with 38 toes in each of two groups
and 28 toes in one group.5 The FDP tendon was tran-
5′ Rep Cap 3′ sected completely with a sharp surgical blade and was
ITR ITR subjected to one of three treatments: (1) AAV2-bFGF
injection (38 toes) in which a total of 2 × l09 particles
Promoter
of AAV2 containing the bFGF cDNA were injected into
Therapeutic construct
both stumps of the cut tendon ends; (2) AAV2-luciferase
injection (28 toes) in which AAV2-luciferase in the same
number of viral particles was injected into the tendon
Growth factor cDNA stumps; and (3) noninjection (38 toes) in which the
tendons did not receive injection. Immediately after the
Figure 6-5  AAV genomes and vector construction. A above treatments, the tendon was repaired surgically
therapeutic construct was inserted into downstream of a with a modified Kessler method using 4-0 suture. Post-
promoter, which replaces the Rep and Cap components of surgery, the toes were immobilized in semiflexion posi-
the wild-type AAV. tion by adhesive tapes for the first 3 weeks and were
released to allow free motion thereafter.
The FDP tendons from 20 toes of 10 chickens were
THE THIRD STEP: ASSESSMENT OF EFFECTS OF
cut and repair, for test of strength of repaired tendon
GROWTH FACTOR GENE THERAPY IN VIVO
immediately after surgery, and the 10 toes from 5
Over the past 5 years, we conducted four sets of in vivo chickens were not injured and were tested for work of
experiments to evaluate the effectiveness of growth toe flexion, to obtain time-zero strength and work of
factor gene therapy using chickens as a model. flexion data.
 Chapter 6:  Gene Therapy for Tendon Healing 65

We evaluated the outcomes at four time points from 14 120

2 to 12 weeks, with emphasis on variables reflecting p <0.001 p <0.001 p <0.05
12 100

Ultimate strength (N)

healing status and adhesions differently at early and late NS
10 NS NS
healing stages. Postoperative 2 and 4 weeks correspond 80
to the early healing period, and 8 and 12 weeks corre- 8
60
spond to the late healing period. At 2 weeks, tendons 6
were tested for strength and evaluated for healing status 40
4
and adhesions. At 4 weeks, the tendons were harvested 2 20
for strength tests and to score the severity of adhesions.
0 0
At 8 and 12 weeks, when the adhesions and healing had A 2 weeks 4 weeks 8 weeks
matured, we measured the tendon strength, work of toe
flexion, and scored adhesions. AAV2-bFGF treated
We found that the ultimate strength of repaired AAV2-lucifereas
No injection
tendons treated with AAV2-bFGF was significantly
greater than that of tendons treated with the sham-
vector or noninjection at 2, 4, and 8 weeks (Figure 6-6). 5 NS

Scores of adhesions (points)

The AAV2-bFGF treatment at 4 weeks increased the
strength to about 140% that of tendons treated with
sham-vector or noninjection. Statistically, the grading of
adhesions was the same among all three groups at 8
weeks and the treated tendons had less severe adhesions
at 12 weeks (see Figure 6-6). Work of toe flexion after
AAV2-bFGF treatment was not increased compared with
that of noninjection controls at 8 and 12 weeks.
In the second set of experiments, we examined the effects
of delivery of different amounts of AAV2-bFGF on
tendon healing. We examined the strength 4 weeks after
injection of 2 × l07, 1 × l08, 2 × l08, 4 × l08, 1 × l09, and
2 × l09 viral particles to each tendon and obtained a
range of vector amount (1 × l09 to 2 × l09 of viral
particles/tendon) that gives the best outcomes in terms
of healing strength.
In the third set of experiments, we expanded AAV2-
bFGF gene therapy experiments to include comprehen-
sive biomechanical evaluation of the healing strength
and molecular biological examinations at 10 postsurgi-
cal time points (day 0, weeks 1, 2, 3, 4, 5, 6, 8, 12, and
16). The purpose of this set of experiments was to obtain
a broader picture of the efficacy and mechanism of
AAV2-bFGF treatment. Three groups (AAV2-bFGF treat-
ment, sham vector control, and noninjection control)
were included, with a total of 134 chickens (268 toes)
used. The sample size ranged from 6 to 14 tendons at
each time point for each group. The results of this set
of studies are detailed in Figure 6-7. This set of experi-
ments offers further sound evidences of the effectiveness
of AAV2-bFGF: the tendons treated with AAV2-bFGF
showed an early increase in strength from postsurgical
week 1 through week 4, with percent strength gain of
40% to 70% over the non-injection controls (see Figure
6-7). The no-gain period in healing strength was effec-
tively corrected by AAV2-bFGF gene therapy. Transgene
expression was detectable from week 2 to 6, but the
expression ceased at weeks 8 or 12. The amount of bFGF
in the treated tendon returned to levels similar to those
in the noninjection control at 8 weeks. With AAV2-bFGF
p <0.05
4 p <0.05 p <0.05
3
2
B 2 weeks 4 weeks 8 weeks 12 weeks
AAV2-bFGF treated
AAV2-lucifereas
No injection
Figure 6-6  A, Ultimate strength of the repaired FDP
tendon at 2, 4, and 8 weeks postsurgery. The sample  
sizes were 10 to 12 tendons at each time point for each
treatment. At all the three time points, the strength of the
tendon treated with AAV2-bFGF was significantly greater
than that of the no-injection controls. B, Adhesion scores at
four time points. Sample sizes were 10 tendons at each time
point for each treatment. Adhesions were similar between
the treated tendons and no-injection controls at week 8.  
The treated tendons had less severe adhesions than the
no-injection controls at week 12. Adhesions were scored  
by criteria in Tang JB, Ishii S, Usui M, et al: Dorsal and
circumferential sheath reconstructions for flexor sheath
defect with concomitant bony injury, J Hand Surg (Am)
19:61–69, 1994.
gene therapy, tenocyte proliferation is increased, teno-
cyte apoptosis decreased, production of extracellular
matrix components accelerated, and the rate of degrada-
tion of extracellular matrix in the tendon decreased.
These molecular changes offer a mechanistic explana-
tion for the observed effects of AAV2-bFGF gene therapy.
In the fourth set of experiments, we tested the effective-
ness of AAV2 vector harboring VEGF cDNA on improve-
ments in healing strength. Thirty-six chickens (72 toes)
were used; transversely cut FDP tendons were injected
66 Section 1:  Basic Science

16
VEGF gene therapy is effective in correcting the insuffi-
AAV2-bFGF gene therapy ciency of intrinsic healing capacity and offers a thera-
14 peutic possibility for enhancing tendon healing.
12 GENE THERAPY ASSOCIATED
Ultimate strength (N)

WITH MICRO-RNA REGULATION

10
IN TENDON HEALING
8 Gain in the strength by
AAV2-bFGF gene therapy Adhesion formation is another major problem in
6 tendon healing. With the AAV2-bFGF or AAV2-VEGF
therapies described above, no increase in tendon adhe-
4
sions was recorded compared with sham vector-treated
AAV2-bFGF treated
2 Non-injection
or noninjection controls. However, morphologically
most treated and healed tendons still showed the forma-
0 tion of adhesions; the work of digital flexion did not
0 1 2 3 4 5 return to normal at postoperative 8 or 12 weeks. As an
A (Day) Weeks integral part of investigatory efforts, over the past 3
years, we explored the possibility of RNA interference
16 (RNAi) in reducing adhesion formations of tendon.8
AAV2-VEGF gene therapy Synthetic RNAi is an emerging and rapidly developing
14
field. Gene therapy incorporating siRNA or micro-RNA
12 (miRNA) is a new dimension to the field of gene therapy.
Ultimate strength (N)

Delivery of siRNA or miRNA to the healing tissues pres-

10
8 Gain in the strength by
AAV2-VEGF gene therapy
6
4 and scar formation, we aimed at silencing the TGF-β1
AAV2-VEGF treated
2 Non-injection
0 sequences of the chicken TGF-β1 gene and constructed
0 1 2 3 4 5
B (Day) Weeks
Figure 6-7  Effects of AAV2-bFGF and AAV2-VEGF gene
therapy on the tendon healing strength in a chicken tendon
cut and repair model. AAV2-bFGF and AAV2-VEGF gene
therapy substantially augmented tendon healing, helping the
tendon “leap over” the lag period in the early stage of the
tendon healing.
with AAV2-VEGF (2 × l09 viral particles to each tendon).
The results were evaluated at postsurgical day 0, and in
weeks 1, 2, 3, 4, 5, 6, and 8. We found that the AAV2-
VEGF treatment is basically as effective as AAV2-VEGF
treatment (see Figure 6-7).
To sum up our in vivo experiments, we found that
supplementing lacerated tendons with the bFGF or
VEGF cDNAs to produce supernormal amounts of bFGF
or VEGF (1) substantially increased growth factor activ-
ity within healing tendons, (2) promoted proliferation
(but inhibited apoptosis) of the tenocytes and produc-
tion of extracellular matrix critical to gain in strength,
and (3) significantly enhanced the strength of the healed
tendon. Moreover, production of supernormal amounts
of growth factors had ceased after healing was achieved.
Taken together, our evidence indicates that bFGF or
ents as an efficient tool to downregulate expression of
genes critical to tissue repair.
Because transforming growth factor (TGF)-β1 is a
master mediator and a major player in tissue fibrosis
gene and mitigating the effects of TGF-β1 during tendon
healing. We synthesized four pre-miRNAs according to
four plasmids containing these pre-miRNA sequences
and one control containing mock miRNA sequences
(Figure 6-8). Using cultured tenocytes of chicken digital
flexor tendons, we then screened the sequences that
effectively downregulate expression of the TGF-β1 gene.
We transfected cultured tenocytes with these plasmid
vectors and quantified expression of TGF-β1, type I and
III collagen, and connective tissue growth factor (CTGF)
genes using real-time polymerase chain reactions
(Figure 6-9). Subsequently, the plasmid miRNA that
most effectively silenced the TGF-β1 gene in vitro was
used to test its effectiveness on reducing adhesions in
vivo. The plasmid miRNA and the control were injected
into the injured tendons of 25 chickens. We found that
in both in vitro and in vivo settings, delivery of engi-
neered miRNA to the tendon downregulated expression
of the TGF-β1 gene but did not affect expression of the
collagen I gene.
In the healing tendon of chickens, we found that
TGF-β1 gene expression was downregulated 50% to
60% at weeks 1 and 6. At 6 weeks, collagen III gene
expression was reduced by 55%, and the CTGF gene was
downregulated by 25%. A smoother gliding surface of
the tendon with fewer adhesions was detected 6 weeks
after plasmid miRNA treatment compared with plasmid
mock miRNA treatment.
 Chapter 6:  Gene Therapy for Tendon Healing 67

Transcript degradation

Cytoplasm
Target
transcript or
Translational
repression
Exportin 5 (requires only partial
Pasha
complementarity)
Drosha Pre-miRNA
Pri-
miRNA RISC Argonaute
Dicer
Nucleus
A Mature miRNA

Insertion of pre-miRNA

BamH I
ds oligo

Xho I
Bgl II
Dra I

Dra I
Sal I

5′ miR flanking CAGG 3′ miR flanking

attB1 EmGFP region region
attB2
ACGA

TK pA
MV f1
PC or
i

SV
40
Spe

ori
pCDNA 6.2-GW/
ctinomycin

EmGFP-miR
EM7

(5699 bp)
Bla
sti
c
pU

C
id
in
or
i
B SV40 pA

5′ miRNA flanking region 3′ miRNA flanking region

AGGC T T GC T G A AGGC T G T A T GC T G pre-miRNA C AGGA C A C A AGGCC T G T T A C T AGC A C T

T CCGA A CGA C T T CCGA C A T A CG A C ds oligo G T CC T G T GT T CCGGA C A A T GA T CG T GA

Structures of engineered pre-miRNA oligo

5′G + antisense Sense ∆2 nt

TGCT Loop sequences CAGG
C target sequences target sequences

Figure 6-8  A, Biogenesis and biological effects of miRNAs. (Adapted from Mack GS: MicroRNA gets down to business,
Nat Biotechnol 25:631–638, 2007). B and C, Construction of a plasmid harboring in vitro engineered pre-miRNA to silence
expression of TGF-β1 gene of chickens in the tenocytes or in the healing tendon.

We also found downregulation of the type III
collagen and CTGF genes after plasmid miRNA treat-
ment, but type I collagen gene expression was not
affected in cultured tenocytes and in the healing
tendons. This treatment meets an essential requirement:
type I collagen, an essential contributor to tendon
strength, was not affected, while expression of the
TGF-β1 gene was inhibited. These findings warrant
further exploration of RNAi gene therapy in preventing
adhesions.
68 Section 1:  Basic Science

140
biomechanically in vivo, though they were successful in
increasing the cellular activities or promoting healing
120 potential in vitro.
We believe that in vivo findings from a series of our
Gene expression (%)

100
experiments provide support for future clinical trials,
80 laying a scientific ground for this treatment. Future
efforts will eventually determine the efficacy of these
60
p <0.001 p <0.001 p <0.001 gene therapy strategies in patients.
40 To expand the future scope of gene therapy for tendon
healing, the following needs to be considered: (1) We
20
tested only AAV2-bFGF and AAV2-VEGF treatments for
0 their ability to improve the healing strength. It is pos-
A TGF-beta Collagen I Collagen III CTGF sible that therapies involving other growth factors, such
as PDGF-BB or IGF-1, could be equally effective. For
140 tissues that generally lack growth factors, sustained sup-
plementation of any (rather than “specific”) growth
120
factors (by gene therapy or other delivery methods such
Gene expression (%)

100 p <0.01 as controlled release) would have a positive impact on

80
p <0.001
60 p <0.001
40
20
0 tion. Though we have considered the possibility of “dual
B TGF-beta Collagen I Collagen III
Figure 6-9  A, Silencing effects of the miRNA on the
TGF-β1 gene expression and downregulation of the collagen
III and CTGF genes in vitro; and B, 6 weeks after delivery of
the miRNA to injured digital flexor tendons.
FUTURE PERSPECTIVES
It is hard to speculate when gene therapy for tendon
healing will become a commonly available clinical
reality. Nevertheless, past investigations appear to have
identified a feasible path to overcome the slow biologi-
cal healing responses of the tendons reflected by the
“no-gain” period in strength. This is an important step
in biological augmentation of tendon healing. Previ-
ously, investigators have failed to augment tendon
healing reliably by other methods, and the effectiveness
was either small or could not be reproduced at other
time points. Most past efforts failed at increasing strength
healing strength. Nevertheless, exogenous factors such
as TGF-β or CTGF should not be supplied, because they
are likely to exacerbate adhesions. (2) The goal of
tendon repair is to restore normal function of the
tendon, but its resolution is often hampered by two
factors: weak healing strength and adhesion formation,
which may require simultaneous biological manipula-
CTGF regulation” by increasing the factors favoring strength
gain, while inhibiting factors responsible for adhesions,
this idea of dual regulation remains untested. We specu-
late that such manipulation of tendon healing may be
desirable in some clinical situations such as with exten-
sive trauma. However, biological prevention of adhe-
sions may not be necessary for clean-cut tendon injuries,
because strong surgical repairs, augmented by growth
factor gene therapy, if necessary, allow rigorous active
tendon motion, which may effectively limit adhesions.
Gene therapy to inhibit adhesions may become reserved
exclusively for cases of extensive tendon or peritendi-
nous damage in which adhesions are pronounced and
unavoidable, or hand trauma precludes early tendon
movement. (3) Regarding gene therapy using miRNAs
or siRNA, our efforts have offered only preliminary evi-
dences. Comprehensive in vivo experiments examining
effectiveness are necessary. The significance of these
treatments will become clear only when further investi-
gations have generated more information.

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in a rabbit model, J Hand Surg (Am) 35: 1825–1832, 2010.
43. Thomopoulos S, Kim HM, Das R, et al: The effects of exo­
genous basic fibroblast growth factor on intrasynovial flexor
70 Section 1:  Basic Science
tendon healing in a canine model, J Bone Joint Surg (Am)
92:2285–2293, 2010.
44. Monahan PE, Samulski RJ: AAV vectors: is clinical success on
the horizon? Gene Ther 7:24–30, 2000.
45. Erles K, Sebökovà P, Schlehofer JR: Update on the prevalence
of serum antibodies (IgG and IgM) to adeno-associated virus
(AAV), J Med Virol 59:406–411, 1999.
46. Daly TM: Overview of adeno-associated viral vectors, Methods
Mol Biol 246:157–165, 2004.
47. Mueller C, Flotte TR: Clinical gene therapy using recombi-
nant adeno-associated virus vectors, Gene Ther 15:858–863,
2008.
48. Aitken ML, Moss RB, Waltz DA, et al: A phase I study of
aerosolized administration of tgAAVCF to cystic fibrosis sub-
jects with mild lung disease, Hum Gene Ther 12:1907–1916,
2001.
49. Kaplitt MG, Feigin A, Tang C, et al: Safety and tolerability of
gene therapy with an adeno-associated virus (AAV) borne
GAD gene for Parkinson’s disease: an open label, phase I trial,
Lancet 369(9579):2097–2105, 2007.
50. Wang XT, Liu PY, Xin KQ, et al: Tendon healing in vitro: bFGF
gene transfer to tenocytes by adeno-associated viral vectors
promotes expression of collagen genes, J Hand Surg (Am)
30:1255–1261, 2005.
 CHAPTER
7  
TENDON TISSUE ENGINEERING
AND BIOACTIVE SUTURE
REPAIR
Brian C. Pridgen, BS, Jeffrey Yao, MD, and
James Chang, MD
OUTLINE
Tissue engineering is a field that aims to apply our
expanding basic knowledge of tissue biology to the
design of engineered tissue substitutes. Despite
advances in tendon repair, many patients still experi-
ence poor outcomes that can lead to lifelong disability.
Tendon tissue engineering and bioactive sutures are
well suited to address this clinical need. In injuries to
the hand that require interposition tendon grafts, the
need for autograft material may outstrip the supply in
a given patient, or the available autograft material may
lead to suboptimal outcomes for the patient. A tissue-
engineered tendon would be readily available as an
off-the-shelf product designed to optimize the healing
process and to recapitulate normal function. Design
of such a tendon requires a detailed understanding of
the tendon healing process as well as normal tendon
function and biology, including its structure and com-
position, cells and their role in tendon function, and
biomechanical properties of tendons. This under-
standing can then be applied to the four primary com-
ponents of a tissue-engineered tendon: cells, scaffolds,
growth factors, and mechanical manipulation. Injuries
requiring suture repair, whether or not an interposi-
tion graft is necessary, often have poor outcomes
despite advances in suture techniques and materials.
Current research into bioactive sutures loaded with
growth factors or cells offers a new strategy for strength-
ening and improving suture repairs of tendons.
Despite recent advances in flexor tendon repair surgery,
many patients still experience poor outcomes following
repair. This is often due to severe adhesion formation,
which may require tenolysis procedures to improve
motion. Additional causes of poor outcomes include
tendon rupture or failure at the repair site, due to either
suture pull-through, suture breakage, knot slippage, or
gapping at the repair site.
When graft material is required, repairs are currently
limited to autografts such as the palmaris longus,
plantaris, and toe extensor tendons. Limitations of
autograft harvesting include donor site morbidity and
additional anesthesia and operative time. In cases of
mutilating injuries to the hand (Figure 7-1), the demand
for graft material may outstrip the autograft supply in a
patient, leaving these patients without a good solution
for restoring hand function.
Although synthetic graft materials such as Dacron
grafts and Silastic rods have been used for tendon recon-
struction, outcomes are generally poor, and the life
span of these grafts tends to be short. Failure is typically
due to mechanical wear or rupture of the tendon–graft
interface. These synthetic materials are designed to
replace tendon tissue, rather than to regenerate it. Thus,
the resulting repair does not heal with tendon tissue
properly and does not support the ingrowth of cells
to promote biodegradation and remodeling of the
implant.
TISSUE ENGINEERING
One of the earliest articles broadly defining tissue engi-
neering was a 1993 Science article by Langer and Vacanti.1
In this article, they defined the nascent field of tissue
engineering as “an interdisciplinary field that applies
the principles of engineering and the life sciences toward
the development of biological substitutes that restore,
maintain, or improve tissue function.” They described
three general strategies of tissue engineering: (1) cells or
cell substitutes, (2) tissue-inducing substances such as
growth factors and delivery vehicles, and (3) cell-seeded
scaffolds. These principles have been applied to clinical
needs in hand surgery, resulting in commercially avail-
able products including engineered skin substitutes2
and allogeneic nerve grafts.3 However, a tissue-engineered
tendon is not yet available.
TENDON BIOLOGY
At their simplest, tendons can be thought of as thick
collagen ropes that transmit forces from muscles to act
across joints to move and stabilize them. Development
of a tissue-engineered tendon requires a much deeper
71
72 Section 1:  Basic Science
Figure 7-1  Mutilating injury to the forearm and hand with
significant soft tissue loss, including tendon damage. This
patient required extensive reconstruction and would have
benefited from a tissue-engineered tendon.
understanding. The mechanical properties of tendons
crucial to their proper functioning rely not only on
the structure and organization of its major collagen
constituents but also on the other extracellular matrix
components. At steady state, tendons are relatively
hypocellular and have low metabolic demands. During
times of injury and healing, cells and their nutritional
pathways play a critical role, and their activity is a major
determinant of tendon healing.
Structure and Anatomy
Collagen is the basic structural unit of tendons.4,5 It is
organized into a hierarchical structure of progressively
larger and more organized subunits to form the crimped
or sinusoidal pattern visible by light microscopy.
While collagen is the major constituent of tendons,
proteoglycans are critical to the biological and mechani-
cal functioning of tendons.6 Proteoglycans promote
hydration through hydrophilic subunits and mediate
interactions between structural units of the tendon,
which are important determinants of the viscoelastic
properties of tendons. Another important function of
proteoglycans is their role in promoting cell signaling
to mediate growth, proliferation, and migration.
Synovial sheaths around tendons are found in areas
subjected to mechanical stress in which efficient gliding
is mediated by synovial lubrication. Examples of tendons
of the hand with intrasynovial portions include the
flexor digitorum superficialis and flexor digitorum pro-
fundus tendons. These tendons have an intrasynovial
region in their more distal portions within the hand and
an extrasynovial region in their more proximal portions.
In addition to assisting with gliding in areas of high
mechanical stress, the synovial sheath also provides
nutrition by diffusion through synovial fluid. Extrasyno-
vial tendons are covered by the paratenon, a loose
connective tissue that carries the blood supply. This dis-
tinction is important because although overall outcomes
are generally unsatisfactory with injuries to intrasyno-
vial tendons and graft reconstruction, particularly in
zone 2, better outcomes are achieved when reconstruc-
tion is performed with intrasynovial autografts rather
than extrasynovial autografts.
Brockis and others made early observations about the
vascular supply to flexor tendons.7 They observed that
tendons receive their blood supply through the muscu-
lotendinous junction, the paratenon surrounding the
tendon in the extrasynovial region, the vincula within
the intrasynovial region, and the osteotendinous inser-
tion. In addition to vascular nutrition, the intrasynovial
portion of the tendon receives nutrition by diffusion
through the synovial fluid.8,9
Cells
Tenocytes, the primary cell type in tendons, are spindle-
shaped fibroblast-like cells oriented along the long axis
of tendons that are responsible for the production and
maintenance of the extracellular matrix of the tendon.
As they mature, their metabolic activity and energy
demand decrease. This enables tendons to carry loads
and maintain tension for long periods of time without
becoming ischemic and necrotic. However, during
injury and repair, this slow metabolic rate leads to pro-
longed healing.
Tendon Healing
Tendons heal slowly because of their hypocellularity,
hypovascularity, and low metabolic rates.10 This pro-
longed healing process requires immobilization to
reduce the risk of tendon rupture or gap formation. The
duration of this immobilization must be balanced
against the risk of adhesion formation. Modulating this
healing process to create a strong tendon repair with
minimal adhesion formation requires an understanding
of the three stages of tendon healing: inflammatory,
proliferative, and remodeling.4,10
The inflammatory stage occurs within the first 24
hours and is characterized by recruitment of inflamma-
tory cells. The proliferative stage begins as tenocytes are
recruited to the site of injury and begin to produce
extracellular matrix components, including collagen
type III. After several weeks, the remodeling stage begins.
The randomly organized extracellular matrix produced
during the proliferative stage is organized into parallel
fibrils, while the collagen type III production decreases
and collagen type I production increases. As healing is
completed, tenocyte number and metabolism then
begin to decrease.
Extrinsic Versus Intrinsic Healing
It was originally thought that tendons must heal by an
extrinsic process in which ingrowth of new cells occurred
through vascularized adhesions to surrounding tissue.11
It was later demonstrated that intrasynovial tendons
could heal by a process mediated by cells intrinsic to
the tendon.12,13 This suggested that adhesion formation
 Chapter 7:  Tendon Tissue Engineering and Bioactive Suture Repair
might not be necessary for tendon healing if cells within
the damaged tendon are available to mediate repair.
TENDON TISSUE ENGINEERING
Tissue engineering a tendon requires an understanding
of the basic science of tendon healing and tendon func-
tion. This knowledge can then be applied to designing
and choosing the components of a tissue-engineered
tendon, which can include cells, a scaffold, growth
factors, and mechanical manipulation (Figure 7-2),
some or all of which can be used to create the final
tissue-engineered product.
Cells
As the machinery responsible for tissue repair and main-
tenance, cells are a necessary component of a tissue-
engineered construct in order to achieve functional
restoration of the tendon. Despite this clear goal of a
tissue-engineered construct, the steps necessary to
achieve this goal remain uncertain. Questions research-
ers continue to face include determining the appropri-
ate cell type and cell source and determining the site of
cell seeding.
Cell Type and Cell Source
Selection of the cell type and cell source for seeding of
the tendon construct is an important decision that must
consider (1) the ease of harvest of the chosen cell type
without inflicting collateral morbidity at the donor site,
(2) the ability to culture and expand the cells in vitro,
and (3) whether the chosen cells will achieve functional
restoration of the tendon. Cell types that have been
considered include tenocytes, dermal fibroblasts, and
mesenchymal stem cells.
Tenocytes are the predominant cell type of native
tendon. Thus, they should be capable of restoring func-
tion of a tissue-engineered tendon construct. In a study
using unwoven polyglycolic acid scaffolds seeded with
hen tenocytes, Cao and colleagues demonstrated that
Cells Scaffold
Cell type Biologic scaffolds
Cell source Synthetic scaffolds
Site of cell seeding Acellularized scaffolds
Autogenous vs.
allogeneic cells
Growth factors Mechanical manipulation
IGF-I Continuous strain
TGF-β Cyclic strain
VEGF Intermittent strain
PDGF
bFGF
Figure 7-2  Components of a tissue-engineered tendon
and some of the considerations necessary for each of these
components. A final tissue-engineered tendon product may
contain some or all of these components.
73
tenocyte-seeded scaffolds resembled native tendons in
histologic structure, collagen arrangement, and breaking
strength.14 However, tenocytes may not be a practical
source of cells because autologous tendon harvest
required for their isolation results in donor site morbid-
ity. They also expand very slowly in culture, which may
make them further impractical due to a lengthy in vitro
expansion time following cell isolation and before
seeding of the tendon construct.
Human dermal fibroblasts are another terminally dif-
ferentiated cell type that closely resembles tenocytes and
have been widely considered as a candidate cell line for
tendon tissue engineering. Like tenocytes, dermal fibro-
blasts are derived from the mesoderm, have similar
morphology, and have similar extracellular matrix pro-
duction capacity. Harvest of autologous dermal fibro-
blasts through a simple skin biopsy would cause
minimal morbidity or expense, which is a notable
advantage over tenocytes, and they are easily and rapidly
expanded in culture. In a study comparing human teno-
cytes and human dermal fibroblasts, each cell type was
isolated and grown separately on a polyglycolic acid
scaffold.15 The authors found no difference in a number
of outcome measurements comparing tenocyte-seeded
and dermal fibroblast–seeded tendon constructs, includ-
ing gross structure, histology, collagen deposition, col-
lagen fibril diameter, and construct strength. These
results suggest that dermal fibroblasts may be a suitable
substitute for tenocytes, which will also avoid the prob-
lems with using autologous tenocytes.
Mesenchymal stem cells (MSCs) are a multipotent
cell line present in adult bone marrow and adipose
tissue that may be cultured as undifferentiated cells
or driven to differentiate into mesenchymal lineages
including tenocytes, osteoblasts, chondrocytes, and adi-
pocytes.16 Although harvest of MSCs from bone marrow
is invasive, provides low yields, and requires time con-
suming and expensive in vitro expansion in culture, it
does not carry the donor site morbidity of tenocyte
harvest. Several groups have demonstrated improved
tendon strength, remodeling, and tissue formation
when seeded with bone marrow–derived MSCs.17-19
Adipose-derived MSCs, on the other hand, are easily
obtainable in sufficient quantities with minimal mor-
bidity, and they have been shown to have a similar dif-
ferentiating potential to bone marrow–derived MSCs.20
One of the concerns with the use of MSCs is the risk for
undesirable differentiation down nontenogenic lines.
Several authors have noted ectopic bone formation with
MSCs used for tendon tissue engineering,18,21 although
another group modulated MSC differentiation by over-
expressing Smad8 to promote tenogenic differentia-
tion.22 Further research will be necessary to better
understand MSC differentiation and replication. This
may include identifying possible subpopulations of
MSCs with predispositions to differentiate down a
74 Section 1:  Basic Science
particular lineage and to better characterize tenocyte
markers to verify proper differentiation.
Site of Seeding (In Vivo versus In Vitro)
Much research has focused on seeding scaffolds with
cells in vitro prior to implantation. This offers a possible
advantage of providing a cell population intrinsic to the
tissue-engineered construct that may initiate the healing
process. This may mediate an intrinsically mediated
healing process that may result in fewer adhesions,
while promoting more rapid healing at the repair site,
remodeling, and engraftment. Many of the previously
mentioned studies have successfully demonstrated cell
attachment to the surface of tendon scaffolds. However,
there has been limited success with establishing cell
populations deep to the surface of tendon scaffolds.
Some groups have attributed this to the tight weave of
the scaffold matrix, which inhibits cells from migrating
deeper into the tendon.23 Another possible explanation
could be poor nutritional supply deeper into the tendon
in the absence of the native intratendinous vascular
supply or nutrition by diffusion of synovial fluid. This
may be of particular concern for newly seeded cells that
are metabolically more active than native tenocytes,
thus inhibiting them from migrating deeper from the
surface. Despite the difficulty with seeding deep to the
surface, it has been shown that host cells infiltrate and
replace seeded cell populations in a time-dependent
manner.24 Further work will be needed to understand
the importance of establishing cell populations deep to
the surface of the tendon and how to promote seeding
deeper into the core of the tendon.
Another option would be to implant an acellular
scaffold and to rely on the patient’s body to cellularize
the graft. To allow more rapid healing at the repair
site, remodeling, and engraftment, some groups have
attempted to accelerate this process of in vivo seeding
by using guided regeneration. This includes the use of
growth factors or using an acellularized tissue scaffold
that contains important biomolecules. Advantages to
this approach include avoiding in vitro cell expansion
and seeding, which would be expensive and time con-
suming, carry infectious risks to patients, and involve
regulatory hurdles. Challenges to this approach include
requirement of a detailed understanding of the biology
of tendon healing and the temporal distribution of key
growth factors. Additionally, as the seeding process
would be dependent on extrinsic cells, this may mediate
adhesion formation.
Autogenous versus Allogeneic Cell Seeding
Much of the research in tendon tissue engineering has
focused on using autogenous cells for seeding of the
scaffold. This approach avoids problems with immuno-
logic incompatibility and rejection of the grafted cells.
It also reduces concerns of infection transmission,
although in vitro manipulation carries some risk of
infectious contamination.
The greatest concern with the use of allogeneic cells
is the risk of immune rejection due to incompatibility
with the recipient. However, recent work has shown that
the use of allogeneic MSCs avoids an immune response
in recipients. Possible explanations for this include low
expression of MHC-II and disruption of leukocyte
function.25
The use of allogeneic cells presents a number of
advantages over autogeneic cells. First, an existing supply
of allogeneic cells would eliminate the need for a time-
intensive and costly harvest and in vitro expansion of
autogeneic cells. Having this existing supply would
allow clinicians to more rapidly seed a scaffold and to
provide definitive repair without a staged process of cell
harvest, in vitro cell expansion, and implantation.
Second, there may be some regulatory advantages to
using allogeneic cells. By having a large bank of cultured
cells, cell samples could be removed for safety testing
without significantly reducing the cell count and neces-
sitating further in vitro expansion, as would be neces-
sary for safety testing of autogeneic cells. Last, MSCs
have been shown to decrease in number, life span, and
proliferative capacity with increasing donor age.26 This
age-related decline of MSCs may make autogeneic MSCs
an impractical option for seeding of a scaffold in older
patients. An available source of allogeneic MSCs from
younger donors would avoid this problem.
Scaffolds
Cultured cells alone are incapable of replacing the func-
tion of a tendon. They require the three-dimensional
scaffolding of the extracellular matrix in tendons. In
addition to providing an attachment site for cells, the
tendon extracellular matrix provides the mechanical
properties to the tendon and has attached signaling
molecules important for cell growth, proliferation, and
migration. The role of a scaffold in tissue engineering is
to provide a three-dimensional biocompatible and bio-
degradable construct to support growth, proliferation,
and migration of cells and to allow remodeling by
cells without the production of toxic or inflammatory
degradation products. The scaffold should provide
mechanical strength sufficient to permit postoperative
mobilization therapy without rupture of the tendon
graft. Scaffolds have been produced from natural bio-
logic materials, synthetic materials, or acellularized
cadaver tissue.
Biologic Scaffolds
Because collagen is the primary component of tendons,
it has been widely investigated as a possible scaffold for
tendon tissue engineering. As the natural major con-
stituent of tendons, collagen is highly biocompatible
with safe degradation products, and it supports cell
 Chapter 7:  Tendon Tissue Engineering and Bioactive Suture Repair
attachment and proliferation better than synthetic
materials.27 Collagen scaffolds may be made either as a
gel or as a sponge. Collagen gels alone do not possess
inherent mechanical strength to act as a suitable scaf-
fold; they must be used with a supporting material, such
as suture.18 Collagen sponges possess superior mechani-
cal strength but have inferior cell attachment pro­
perties.28 Some groups have combined the superior
cell-seeding characteristics of collagen gels with the
superior mechanical characteristics of collagen sponges
in a joint gel–sponge construct.29 While these scaffolds
have the advantages of being easily manufacturable with
natural nonimmunogenic materials, they lack GAG sig-
naling molecules and do not have the mechanical
strength of native tendon.
Synthetic Scaffolds
The most commonly used biodegradable synthetic scaf-
folds for tendon tissue engineering are polyesters,
including polylactic acid (PLA), polyglycolic acid (PGA),
and their copolymer polylactic-co-glycolic acid (PLGA).
The ability to manufacture them synthetically permits
researchers to manipulate the material properties of
the scaffold to achieve the appropriate balance of
degradability and scaffold mechanical strength and to
create a surface environment that encourages cell attach-
ment, migration, and proliferation. A study by Lu and
coworkers compared the suitability of PLA, PGA, and
PLGA as a scaffold for ACL reconstruction.30 They found
that although PGA initially was the strongest of the
three materials, it rapidly degraded with in vitro cell
culture, which would put such a graft at risk of rupture
if used in vivo. When seeded with ACL fibroblasts, the
PLA scaffold supported the greatest number of cells
with normal morphology. In a different study by
Ouyang and colleagues, they observed that PLGA
scaffolds supported the greatest attachment and pro­
liferation of bone marrow–derived MSCs.31 Groups
continue to use a variety of scaffolds with no agreement
yet in the literature, which could attributable to a variety
of factors, including differing manufacturing specifica-
tions of the polymer scaffolds, cell types used, culture
conditions, or mechanical testing parameters. Other
observations that have been made using synthetic scaf-
folds include the use of a fibronectin coating to over-
come the surface hydrophobicity of the scaffolds to
promote cell attachment30; the use of knitted scaffolds,
rather than braided scaffolds, to promote improved cell
attachment and ingrowth19; and electrospinning of
nanofibers to promote cell attachment, proliferation,
and migration.32
Despite the advantages of having a manufacturable
and easily modified synthetic scaffold and the many
recent advances made in this field, there are a number
of disadvantages that remain. Although polyester scaf-
folds are degraded by hydrolysis into naturally occurring
75
metabolites, including glycolic acid and lactic acid,
these metabolites are acidic and may give rise to sys-
temic or local reactions.33 Such a reaction may promote
an inflammatory response that may delay healing by
killing cells, disrupting the newly forming neotendon,
and promoting adhesion formation. Another hurdle to
the implantation of synthetic scaffolds is their poor
mechanical strength. They are typically far weaker than
native tendon, and it takes several weeks of in vitro or
in vivo culture with cells before these constructs begin
to approach the strength of native tendon.14,19 If in vitro
maturation of the scaffold is performed, this will be
expensive, put the tissue-engineered construct at risk of
infection, and require the patient to wait for an extended
period of time for the repair if autogeneic cells are used.
If in vivo maturation of the scaffold is performed, this
will put the patient at risk for adhesion formation and
joint contracture with prolonged immobilization to
prevent rupture of the weak graft.
Acellularized Scaffolds
One of the disadvantages of biologic and synthetic scaf-
folds is that they are biologically inert; they lack the
signaling molecules necessary to promote cell migra-
tion, cell proliferation, and extracellular matrix produc-
tion. Although molecules may be incorporated into
these structures, tendon biology is not yet well under-
stood enough to entirely recapitulate the local
environment.
Native tendon, on the other hand, contains many of
these signaling molecules in the form of proteoglycans.
Native tendon also possesses the mechanical strength
necessary to withstand normal loading forces without
the need for lengthy in vitro or in vivo neotendon
formation, unlike many of the biological or synthetic
scaffolds. However, native tissue containing these bio-
logical and mechanical advantages cannot be grafted
from one individual to another because of the existing
immunogenic cellular material. Instead, the tissue must
be acellularized to remove the immunogenic compo-
nents without compromising the signaling molecules,
mechanical strength, and biocompatibility.
A number of groups have produced a scaffold from
fresh tendons treated with detergents to remove immu-
nogenic cellular material (Figure 7-3).34,35 They demon-
strated that these acellularized tendons retained the
biochemical signaling molecules and mechanical prop-
erties important for proper biological and mechanical
functioning of the tendon. They went on to show that
these scaffolds are capable of supporting the attachment
and growth of allogeneic cells, suggesting that these
acellularized tendon scaffolds may be suitable for clini-
cal use in tendon tissue engineering. Other tissue that
has been considered for producing an acellularized scaf-
fold for tendon tissue engineering include acellular
dermal matrix36 and human umbilical vein.37
76 Section 1:  Basic Science
B
Figure 7-3  Acellularization of a full-length human tendon.
A, Untreated control tendon showing nuclear staining with
a fluorescent nucleic acid stain. B, Acellularized tendon
showing removal of nuclear material.
Growth Factors
The temporal distribution of growth factors during the
healing process is still being investigated, but it is known
that they play an important role in mediating the tendon
repair process. Well-studied growth factors involved in
tendon healing include insulin-like growth factor-I
(IGF-I), transforming growth factor-β (TGF-β), vascular
endothelial growth factor (VEGF), platelet-derived
growth factor (PDGF), and basic fibroblast growth factor
(bFGF).4,38 These growth factors have roles in inflamma-
tion, cell migration and proliferation, collagen produc-
tion, angiogenesis, and remodeling of the tendon.
Methods of growth factor delivery include seeding of
genetically engineered cells, loading with vectors har-
boring the genes of interest, or direct delivery of growth
factors. Although much progress has been made, further
research will be required. A better understanding of
the temporal changes and role of growth factors in the
different stages of healing will be necessary. Further
research into delivery methods will also be necessary to
determine a method that is safe, efficacious, and cost
effective.
Mechanical Manipulation
Mechanical strain is known to be an important con-
tributor to tenocyte function, maintenance of a teno-
genic phenotype, and collagen production.39 One group
noted in a series of studies the role of mechanical
loading on PGA scaffolds seeded with human dermal
fibroblasts.15 They found that mechanical loading
promoted maturation of collagen fibers with parallel
Figure 7-4  A bioreactor designed to accommodate a
full-length human flexor tendon. The system can be
connected to a motor and programmable control system
that permits continuous, cyclic, and/or intermittent strain to
be applied.
alignment and that this collagen was composed pre-
dominantly of collagen type I typically found in tendon
rather than collagen type III typically found in skin,
suggesting a phenotype switch of the dermal fibroblasts
to a tenogenic cell type. They also noted the improved
strength of their tissue engineered constructs following
mechanical loading. A study by another group demon-
strated that intermittent cyclic strain, rather than con-
tinuous strain, promoted greater cell proliferation, type
I collagen production, and maintenance of tenocyte
morphology.40 They then went on to demonstrate that
acellular tendon scaffolds re-seeded with cells and then
subjected to intermittent cyclic strain are stronger than
re-seeded tendons that were not subjected to strain. An
example of a tendon bioreactor is shown in Figure 7-4.
BIOACTIVE SUTURE
Once a tissue-engineered tendon is developed, it must
be interposed into the defect and then sutured into
place. Following repair, patients should initiate early
postoperative mobilization therapy to reduce adhesion
formation. However, the benefits of early mobilization
must be weighed against the risk for gap formation,
which can lead to delayed healing and reduced tensile
strength at the repair site. Recent advances in suturing
 Chapter 7:  Tendon Tissue Engineering and Bioactive Suture Repair
A B
Figure 7-5  Seeding of mouse embryo pluripotential cells onto FiberWire suture. A, Control suture with no coating and few
adherent cells. B, Suture with poly(L-lysine) coating mediating cell adhesion. C, DAPI staining of cells adherent to the suture.
techniques and suture material have improved the
strength of tendon repairs, but the risk of gap formation
with early mobilization has not been eliminated. Addi-
tionally, the trauma from suture repair has been impli-
cated in creating acellular zones and inflammation that
delay tendon healing.41
Several groups have investigated the use of bioactive
suture to augment tendon repairs. The two primary
strategies under investigation are to modulate cells
present at the repair site through growth factors incor-
porated into the suture or to attach cells directly onto
the suture with the intention of seeding them to the
repair site.
Multiple groups have investigated the use of suture
as a drug delivery device. An in vitro study using epi­
dermal growth factor seeded onto Mersilene suture
demonstrated increased cell proliferation along the
coated suture.42In another study, bFGF was loaded onto
a nylon monofilament suture used to repair rabbit
tendon injury.43 The bioactive suture increased strength
of the repair and promoted cell proliferation at the
repair site. A third group used growth differentiation
factor-5 to coat sutures and achieved similar results to
the previous groups, demonstrating increased strength
of the tendon repair and enhanced cell proliferation.44
Another group has attempted to address directly the
problem of the acellular zones at the site of suture repair
by incorporating pluripotential cells into the suture.45
These pluripotential cells have been shown to be deliv-
ered to a tendon repair–reconstruction site (Figure 7-5)
as well as along the entire path of the suture. The cells
References
1. Langer R, Vacanti JP: Tissue engineering, Science 260:920–
926, 1993.
2. Lou RB, Hickerson WL: The use of skin substitutes in hand
burns, Hand Clin 25:497–509, 2009.
77
C
survive the trauma of passage through acellularized
tendons, proliferate, and remain metabolically active.
These cells repopulate the acellular zones shown to sur-
round suture material in repaired tendons, and may
thereby accelerate healing. Animal studies to evaluate
the use of bioactive sutures are currently ongoing.
These techniques will be beneficial both for direct
repair of tendon ends or for placement of a tissue-
engineered interposition graft. By promoting early
healing and cell proliferation at the repair site through
the use of bioactive sutures, early tensile strength may
be increased and overall healing time decreased. This
may permit earlier initiation of safe postoperative
mobilization with minimal risk of gapping or tendon
rupture.
CONCLUSION
Despite many of the recent advances in flexor tendon
repair, many patients still experience poor outcomes.
Adhesion formation leads to reduced mobility. Large
defects require autograft harvesting, which carries mor-
bidity and may be insufficient in extensive mutilating
injuries. Traditional suture repair requires delayed post-
operative mobilization due to the risk of gap formation.
Continuing research in tendon biology has increased
our understanding of tendon structure, function, and
healing. The application of this basic science research
through the use of tissue-engineering principles has led
to the development of many technologies that promise
to one day improve the repair and reconstruction of
flexor tendon injuries.
3. Whitlock EL, Tuffaha SH, Luciano JP, et al: Processed allografts
and type I collagen conduits for repair of peripheral nerve
gaps, Muscle Nerve 39:787–799, 2009.
78 Section 1:  Basic Science
4. James R, Kesturu G, Balian G, et al: Tendon: Biology, biome-
chanics, repair, growth factors, and evolving treatment
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injury and repair, J Biomech 37:865–877, 2004.
6. Doroski DM, Brink KS, Temenoff JS: Techniques for biologi-
cal characterization of tissue-engineered tendon and liga-
ment, Biomaterials 28:187–202, 2007.
7. Brockis JG: The blood supply of the flexor and extensor
tendons of the fingers in man, J Bone Joint Surg (Br) 35:131–
138, 1953.
8. Lundborg G, Holm S, Myrhage R: The role of the synovial
fluid and tendon sheath for flexor tendon nutrition. An exper-
imental tracer study on diffusional pathways in dogs, Scand
J Plast Reconstr Surg 14:99–107, 1980.
9. Abrahamsson SO, Lundborg G, Lohmander LS: Tendon
healing in vivo. An experimental model, Scand J Plast Reconstr
Surg Hand Surg 23:199–205, 1989.
10. Sharma P, Maffulli N: Biology of tendon injury: healing,
modeling and remodeling, J Musculoskelet Neuronal Interact
6:181–190, 2006.
11. Potenza AD: Critical evaluation of flexor-tendon healing and
adhesion formation within artificial digital sheaths, J Bone
Joint Surg (Am) 45:1217–1233, 1963.
12. Matthews P, Richards H: The repair potential of digital flexor
tendons. An experimental study, J Bone Joint Surg (Br)
56:618–625, 1974.
13. Lundborg G: Experimental flexor tendon healing without
adhesion formation: A new concept of tendon nutrition and
intrinsic healing mechanisms. A preliminary report, Hand
8:235–238, 1976.
14. Cao Y, Liu Y, Liu W, et al: Bridging tendon defects using
autologous tenocyte engineered tendon in a hen model, Plast
Reconstr Surg 110:1280–1289, 2002.
15. Deng D, Liu W, Xu F, et al: Engineering human neo-tendon
tissue in vitro with human dermal fibroblasts under static
mechanical strain, Biomaterials 30:6724–6730, 2009.
16. Pittenger MF, Mackay AM, Beck SC, et al: Multilineage poten-
tial of adult human mesenchymal stem cells, Science 284:143–
147, 1999.
17. Young RG, Butler DL, Weber W, et al: Use of mesenchymal
stem cells in a collagen matrix for Achilles tendon repair,
J Orthop Res 16:406–413, 1998.
18. Awad HA, Boivin GP, Dressler MR, et al: Repair of patellar
tendon injuries using a cell-collagen composite, J Orthop Res
21:420–431, 2003.
19. Ouyang HW, Goh JCH, Thambyah A, et al: Knitted poly-
lactide-co-glycolide scaffold loaded with bone marrow
stromal cells in repair and regeneration of rabbit Achilles
tendon, Tissue Eng 9:431–439, 2003.
20. Lee RH, Kim B, Choi I, et al: Characterization and expression
analysis of mesenchymal stem cells from human bone marrow
and adipose tissue, Cell Physiol Biochem 14:311–324, 2004.
21. Harris MT, Butler DL, Boivin GP, et al: Mesenchymal stem
cells used for rabbit tendon repair can form ectopic bone and
express alkaline phosphatase activity in constructs, J Orthop
Res 22:998–1003, 2004.
22. Hoffmann A, Pelled G, Turgeman G, et al: Neotendon forma-
tion induced by manipulation of the Smad8 signalling
pathway in mesenchymal stem cells, J Clin Invest 11:940–952,
2006.
23. Whitlock PW, Smith TL, Poehling GG, et al: A naturally
derived, cytocompatible, and architecturally optimized scaf-
fold for tendon and ligament regeneration, Biomaterials 28:
4321–4329, 2007.
24. Thorfinn J, Saber S, Angelidis IK, et al: Flexor tendon tissue
engineering: temporal distribution of donor tenocytes versus
recipient cells, Plast Reconstr Surg 124:2019–2026, 2009.
25. Ryan JM, Barry FP, Murphy JM, et al: Mesenchymal stem cells
avoid allogeneic rejection, J Inflamm (Lond) 2:8, 2005.
26. Stenderup K, Justesen J, Clausen C, et al: Aging is associated
with decreased maximal life span and accelerated senescence
of bone marrow stromal cells, Bone 33:919–926, 2003.
27. Qin T, Yang Z, Wu Z, et al: Adhesion strength of human
tenocytes to extracellular matrix component-modified
poly(dl-lactide-co-glycolide) substrates, Biomaterials 26:
6635–6642, 2005.
28. Butler DL, Juncosa-Melvin N, Boivin GP, et al: Functional
tissue engineering for tendon repair: A multidisciplinary
strategy using mesenchymal stem cells, bioscaffolds, and
mechanical stimulation, J Orthop Res 26:1–9, 2008.
29. Juncosa-Melvin N, Boivin GP, Gooch C, et al: The effect of
autologous mesenchymal stem cells on the biomechanics
and histology of gel-collagen sponge constructs used for
rabbit patellar tendon repair, Tissue Eng 12:369–379, 2006.
30. Lu HH, Cooper JA, Manuel S, et al: Anterior cruciate ligament
regeneration using braided biodegradable scaffolds: In vitro
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31. Ouyang HW, Goh JCH, Mo XM, et al: Characterization of
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C 20:63–69, 2002.
32. Sahoo S, Ouyang H, Goh JC, et al: Characterization of a novel
polymeric scaffold for potential application in tendon/
ligament tissue engineering, Tissue Eng 12:91–99, 2006.
33. Böstman OM, Pihlajamäki HK: Adverse tissue reactions to
bioabsorbable fixation devices, Clin Orthop Relat Res 371:216–
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34. Cartmell JS, Dunn MG: Effect of chemical treatments on
tendon cellularity and mechanical properties, J Biomed Mater
Res 49:134–140, 2000.
35. Tischer T, Vogt S, Aryee S, et al: Tissue engineering of the
anterior cruciate ligament: a new method using acellularized
tendon allografts and autologous fibroblasts, Arch Orthop
Trauma Surg 127:735–741, 2007.
36. Adams JE, Zobitz ME, Reach JS, et al: Rotator cuff repair using
an acellular dermal matrix graft: an in vivo study in a canine
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37. Abousleiman RI, Reyes Y, McFetridge P, et al: Tendon tissue
engineering using cell-seeded umbilical veins cultured in a
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tendon and ligament healing, Sports Med 33:381–394, 2003.
39. Yang G, Crawford RC, Wang JH: Proliferation and collagen
production of human patellar tendon fibroblasts in response
to cyclic uniaxial stretching in serum-free conditions,
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40. Riboh J, Chong AKS, Pham H, et al: Optimization of flexor
tendon tissue engineering with a cyclic strain bioreactor,
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41. Wong J, Alyouha S, Kadler K, et al: The cell biology of suturing
tendons, Matrix Biology 29:525–536, 2010.
42. Rohrich RJ, Trott SA, Love M, et al: Mersilene suture as a
vehicle for delivery of growth factors in tendon repair, Plast
Reconstr Surg 104:1713–1717, 1999.
43. Hamada Y, Katoh S, Hibino N, et al: Effects of monofilament
nylon coated with basic fibroblast growth factor on endoge-
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44. Dines JS, Weber L, Razzano P, et al: The effect of growth dif-
ferentiation factor-5-coated sutures on tendon repair in a rat
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2011.
 CHAPTER
8  
INDICATIONS FOR PRIMARY
FLEXOR TENDON REPAIR
Jin Bo Tang, MD
OUTLINE
Injuries to the flexor tendons occur in the digits, palm,
wrist, or distal and mid-forearm. Repairs of flexor
tendons in the digital sheath area are technically
demanding. When wound conditions are favorable,
primary tendon repair is preferable in terms of ease.
However, it is important that primary repairs be per-
formed by experienced surgeons. Alternatively, a well-
accepted strategy is to postpone the repair for a few
days, or even 1 to 2 weeks, to the delayed primary
stage, for an experienced surgeon to become available.
Repairs during either the primary or delayed primary
stage produce comparable clinical outcomes.
Primary and delayed primary flexor tendon repairs
are indicated in clean-cut tendon injuries with limited
damage to the peritendinous tissues or a wound that
can be converted to a clean-cut wound. Neurovascular
injury is not a contraindication to primary repairs.
Loss of soft tissue coverage over the tendon or the
presence of fractures is a borderline contraindication.
Local defects in skin and subcutaneous tissues can be
covered by flap transfer. A simple fracture limited to
the phalangeal or metacarpal shaft can be securely
fixed with screws or mini-plates and the tendons can
be repaired.
Serious crush injuries, severe wound contami­
nation, extensive loss of soft tissues, or extensive
destruction of pulleys and tendon structures are con-
traindications to primary tendon repairs.
Injuries in the flexor tendons can occur in the digits,
palm, wrist, or distal and mid-forearm. Tendon repairs
in the digital sheath area are most technically demand-
ing and controversial. The advent of primary flexor
tendon repairs within the synovial sheath region should
be credited to pioneers of nearly half a century ago,
including Verdan1 and Kleinert and colleagues.2,3 Prior
to that time, over most of the previous half century,
primary tendon repair was not advocated and surgeons
were accustomed to removing the tendons entirely and
grafting in new tendon.4,5 The reports of Verdan and of
Kleinert and his colleagues on primary flexor tendon
repairs followed by early mobilization established that
the lacerated digital flexor tendon can be treated by
direct end-to-end repairs when wound conditions are
favorable.1-3
ANATOMICAL DIVISIONS
By virtue of their anatomical features, the flexor tendons
in the hand and forearm are divided into five zones,
which delineates the fundamental nomenclature for
flexor tendon anatomy and surgical repairs.1,3,6 In the
1990s, the most complex areas—the flexor tendons
within the digital sheath—were subdivided by Moiemen
and Elliot7 and by Tang.8 The zoning is described in
Box 8-1, and its relation to the locations of pulleys is
shown in Figures 8-1 and 8-2.
ETIOLOGIES AND EVALUATION
OF TENDON INJURIES
Tendons can be injured through open wounds, caused
by sharp cuts or machine injuries, as closed ruptures
after fractures, through other bony problems, or even
spontaneously, without history of injury or clear etiol-
ogy. Severe forms of tendon injury can present as part
of compound injuries due to major trauma to the
extremities. Surgically repaired tendons may disrupt
during functional exercise.
Tendon injuries often present as open injuries and
are associated with a variety of open wounds. Open
trauma with deep, narrow traumatic laceration should
raise suspicion of concomitant tendon injuries. Such a
diagnosis can be missed if surgeons do not carefully
evaluate active motion of the potentially involved digits.
When a tendon is partially cut, the fingers may still func-
tion well in many cases, easily causing such cuts to be
neglected. Some larger partial cuts of the tendon may
be detected through triggering during finger flexion.
Large open traumas deep enough to reach the bony
structures are usually accompanied by tendon injuries,
which are not difficult to diagnose. Open trauma to the
palm or wrist areas is frequently accompanied by tendon
injuries. Trauma to the wrist area may injure only a part
81
82 Section 2:  Primary Flexor Tendon Surgery

Box 8-1  Nomenclature for Flexor Tendon

Anatomy in the Hand and Forearm
1
Zones of Finger Flexor Tendons (Verdan)
1 From the insertion of the FDS tendon the terminal
insertion of the FDP tendon
2 From the proximal reflection of the digital synovial
sheath to the FDS insertion 2
3 From the transverse carpal ligament to the digital
synovial sheath
4 Area covered by the transverse carpal ligament
5 Proximal to the transverse carpal liagment 1

Zones of Thumb FPL Tendon 2 3

1 Distal to the IP joint
2 From the IP joint to the A1 pulley 3
3 The area of the thenar eminence
4

Zone 1 in Fingers (Moiemen and Elliot)

1A The very distal FDP tendon (usually <1 cm)
1B From zone 1A to distal margin of the A4 pulley
1C The FDP tendon within the A4 pulley 5

Zone 2 in Fingers (Tang)

2A The area of the FDS tendon insertion
2B From the proximal margin of the FDS insertion to
Figure 8-1  Zoning of the digital flexor tendons.
the distal margin of the A2 pulley
2C The area covered by the A2 pulley
2D From the proximal margin of the A2 pulley to the
proximal reflection of digital sheath
Transverse metacarpal ligament

of the wrist flexors, without interfering in normal finger

Vertical septa

aponeurosis

and wrist flexion. However, injuries to the majority of

Palmar

the wrist flexors cause weakness of wrist flexion and/or A1 A2 C1 A3 C2 A4 C3 A5

render active finger flexion impossible.
The levels of division of the tendons often do not lie
immediately deep to the finger skin lacerations. The
location of the distal tendon ends depends on the posi-
tion of the fingers at the time of injury. If the finger
is lacerated in flexion, the distal end of the tendon is
2D 2C 2B 2A 1C 1B 1A
drawn distally as the finger is extended. If the finger is
lacerated in extension, the distal tendon end is usually Zone 2 Zone 1
found at the site of the laceration. The proximal tendon
Figure 8-2  Pulleys and subdivisions of the digital flexor
end often retracts to into the palm because of the pull
tendons (zones 1 and 2).
of the muscles. When the laceration is in the distal
half of the fingers, the vincula to the tendons may
prevent the proximal tendon from retracting. Therefore,
the proximal end of the lacerated flexor digitorum patients are asked to actively flex the fingers. Inability to
superficialis (FDS) or flexor digitorum profundus (FDP) actively flex the finger proximal interphalangeal (PIP)
tendons sometimes retracts over only a short distance or distal interphalangeal (DIP) joints using the specific
and is still found within the digital sheath. The proximal tests shown in Figures 8-4 and 8-5, when passive motion
end of the lacerated flexor pollicis longus (FPL) tendon is complete, indicates that the FDP or FDS tendon (or
usually retracts to the thenar area, or even more proxi- both) is completely severed.
mally, due to the vigorous pull of the muscle. In making decisions about treatment, surgeons
During examination, any changes in resting position should consider the condition of the hand thoroughly.
of the fingers should be closely observed (Figure 8-3). Tendon injuries often present as a part of compound
In assessment of function of the FDP and FDS tendons, injuries with open wounds. Nerve and vascular injuries
 Chapter 8:  Indications for Primary Flexor Tendon Repair
Figure 8-3  Change of the resting position of the digits
indicates complete laceration (or disruption) of the digital
flexor tendon. The picture showing a case of complete cut of
the FDP tendon 2 weeks after primary skin closure without
tendon repairs.
Figure 8-4  Active flexion of the DIP joint indicating
integrity of the FDP tendon. Loss of active flexion of the DIP
joint indicates FDP tendon injury.
Figure 8-5  Normal function of the FDS tendon in the
middle finger is shown. Loss of active flexion of the PIP joint
while the flexion of the other fingers is blocked indicates loss
of FDS function, hence complete severance of the tendon.
83
are the most commonly associated injuries and soft
tissue defects may also be present. Injury to a single
artery in the digit does not need repair, but it is essential
to repair the lacerated digital nerve even when the con-
tralateral one is intact.
Wound contamination can be a serious problem. All
wounds should be thoroughly washed and débrided. If
the wounds have clear signs of contamination, thor-
ough washing of the wounds, débridement, and intra-
venous infusion of antibiotics are necessary. The tendons
should be repaired during the delayed primary stage,
after inflammation has been controlled. For such
patients, intravenous administration of antibiotics is
indicated and status of tetanus immunization should
be evaluated. If tendon injuries are accompanied by a
fracture, these can be treated on the same day or sepa-
rately on different days. The fracture can be treated first
by internal fixation, and the tendons can be repaired
after 1 week, or even later.
Closed rupture of the tendons presents as the inabil-
ity to actively flex the digits without an open wound.
Forced extension during active flexion of the finger can
cause avulsion injury of the FDP tendon at its insertion
to the distal phalanx, which is called “Jersey” finger.
Tendon rupture from chronic attrition may occur in
rheumatoid diseases, Kienböck disease, scaphoid non-
union, hamate fracture, or distal radius fracture. Tendon
rupture may also occur spontaneously without clear eti-
ology. Closed rupture of the pulleys usually presents in
special populations engaged in forceful flexion of the
fingers, such as rock climbers. Clinically, patients can
actively flex the fingers but present signs of tendon bow-
stringing of the involved fingers.
Radiographic examination should be routine for
patients with large wounds and suspected of having
compound injuries. Ultrasound or computed tomogra-
phy should be used for patients suspected of having a
closed tendon injury or closed pulley disruption.
TIMING OF TENDON REPAIR
Primary tendon repair is end-to-end repair performed
immediately after wound cleaning and débridement,
usually within several to 24 hours after trauma. Delayed
primary repair is defined as end-to-end repair performed
days to weeks after tendon injuries (usually within 3, or
even 4, weeks after tendon lacerations), after immediate
closure of the wounds without tendon repairs. When-
ever possible, acutely lacerated flexor tendons in the
hand and forearm should be treated primarily or during
the delayed primary stage. The ideal situation is that a
patient with digital flexor tendon lacerations is brought
into the clinic soon after injury, an experienced surgeon
is readily available, and surgery begins within a few
hours (Figure 8-6). In particular, a tendon injured in
critical areas (such as zone 2) should not be repaired by
an inexperienced surgeon. In such cases, tendon repair
84 Section 2:  Primary Flexor Tendon Surgery

Primary repair Delayed primary repair Secondary repair

Do:
Within a few hours or one
day after injury
Experienced surgeons are
available
Do:
A few days or within 2 to 3
weeks after injury ideally
After edema subsided and
infection controlled
Do:
3 to 6 months later
Tendon grafting
Staged reconstruction
Pulley reconstruction

Not do: Not do: Not do:

Experienced surgeons are Over 4 weeks after injury Passive joint motion
not available generally not ample
Skin conditions
not good
• Primary and delayed repairs have comparable outcomes. Risk of infection exists
• Avoid primary repairs by inexperienced surgeons.
• Primary wound closure followed by tendon repair in later
days by experienced surgeons is a standard practice.

Lengthy loss of tendon substance, extensive pulley

Go
When: destruction, serious wound contamination, or
unstable fractures or joint destruction. to

Figure 8-6  Flow-chat of the decision-making process for primary or delayed primary tendon repairs in zone 2 flexor tendon
repair.

should be delayed until an experienced surgeon is avail-
able (see Figure 8-6). Inadvertent damage to the tendon
structures by inexperienced operators may introduce a
second “injury” to the tendon system, which may render
the tendons difficult to repair at subsequent operations,
even in the hands of an experienced surgeon. So far, no
clinical data have shown that delayed primary surgery
within a few days to 1, or 2, weeks after injury, per-
formed by an experienced surgeon, are inferior to
primary surgery in terms of outcomes. In deciding
between primary and delayed primary repairs, I advise
to always place the expertise of the operators before the
exact timing of the repairs.
No clinical investigations have actually validated the
best time for primary or delayed primary repair. My
preferred period of deliberate delay is 4 to 7 days, when
the risk of infection can be properly addressed and
edema has reduced substantially.9,10 Delay of the repair
beyond 3 to 4 weeks may cause myostatic shortening of
the muscle–tendon unit; for these late cases, lengthen-
ing the tendon within the muscles in the forearm can
ease the tension.11
Rupture of the repaired flexor tendons after surgery
can be re-repaired if the rupture occurs within a few
weeks up to a month after surgery; secondary tendon
grafts may be the only choice for ruptured cases in the
presence of obvious retraction of the tendon end(s),
extensive scarring when both tendons ruptures or exten-
sive scarring around the intact FDS tendon when the
FDP tendon alone ruptures.12, 13
INDICATIONS
Indications for primary or delayed primary end-to-end
tendon repairs are clean-cut tendon injuries or tendon
injuries in a wound that can be converted to a clean-cut
wound, with limited damage to peritendinous tissues.
Simultaneous injuries to the nerves and arteries are
common and are not a contraindication for primary
repairs.
“Clean-cut” wounds, the simplest clinical situation
associated with digital tendon lacerations, are a prime
indication for primary flexor tendon repair.6,10 A “clean-
cut” wound is one in which the structures are injured
through a clean and tidy cut, usually a single transverse
or oblique laceration in the digits, palm, or distal
forearm, often produced by a knife or a piece of glass.9
The cut should also be “clean” in terms of contamina-
tion and infection. Anatomically, the tendon(s) is “only”
severed, and without tissue defect. The cut tissues may
even align well (Figure 8-7). This is the best indication
for primary repair, with the greatest likelihood of rela-
tively uncomplicated repair, rehabilitation and satisfac-
tory outcome. Such wounds are often accompanied by
divisions of the digital neurovascular structures.
Crush injuries to a very limited segment of the fingers,
palm, or wrist produce untidy skin and subcutaneous
injuries and tendon wounds (Figures 8-8 and 8-9).
Such wounds are also good candidates for primary
repairs, because the soft tissue wounds and tendons can
be converted to those associated with a clean-cut wound
through débridement of nonviable tissues and direct
wound closure. However, these injuries have a greater
potential for contamination. Primary tendon surgery is
possible, although more difficult than with a truly clean-
cut wound. Phalangeal fractures are rarely associated
with a clean-cut flexor tendon laceration but can be part
of a crush injury. A simple and stable fracture in the
phalangeal shaft can be securely fixed internally, thus
presenting no contraindication to primary tendon
repair.
 Chapter 8:  Indications for Primary Flexor Tendon Repair
Figure 8-7  Clean-cut digital flexor tendon laceration and primary repair. The tendon was tidily severed without loss of
tendon substance. Primary tendon and nerve repairs are indicated. (Courtesy of Department of Hand Surgery, Nantong
University.)
Figure 8-8  Injuries in the distal palm area, resulting in
untidy wounds, lacerations of flexor tendons to multiple
fingers, and injuries to neurovascular bundles. Primary
tendon and nerve repairs are indicated.
Figure 8-9  Injuries to the distal forearm and wrist area,
producing lacerations of multiple wrist and digital flexor
tendons and the median nerve. Primary tendon and nerve
repairs are indicated.
85
Severity of tendon injuries ranges from isolated
partial to complete divisions of either the FDP or FDS
tendon, to complete severance of both tendons, to com-
plicated tendon injuries in multiple fingers involving
soft tissue or bone injuries. Although isolated partial
FDS tendon injuries usually do not need surgical repair,
complete FDP tendon laceration in the distal half of the
fingers do. A partial FDP tendon cut through over 80%
of its diameter is also an indication for surgical repair
and is treated similarly to a complete tendon cut.
Tendon lacerations through 50% to 80% of the tendon
diameter require surgical repair to lessen the chance of
tendon triggering during finger motion and to increase
strength. A partial cut of less than 50% of the tendon
diameter may not need surgical suture, or the cut sites
can simply be trimmed to smooth the tendon surface.
Complete lacerations of both flexor tendons in one, or
multiple, digits are typical indications for primary repair,
and tendon injuries accompanied by other tissue
damage constitute some of the borderline indications
discussed later.
BORDERLINE INDICATIONS
Borderline indications to primary or delayed primary
repairs have been less thoroughly addressed. Loss of soft
tissue coverage over the tendon or the presence of frac-
tures is a borderline indication. Five clinical situations
represent borderline indications to tendon repair.
1. Localized soft tissue injuries: crush, or compression,
injuries on the palmar aspect of the fingers some-
times lead to localized soft tissue defects. The
underlying flexor tendons may present with a
short traumatic defect, or such a defect may arise
after débridement of nonviable, ragged tendon
tissue. This situation includes no contraindica-
tions to primary repair if the soft tissue defect is
less than one-third the length of the fingers and
the tendon loss is less than 1.5 to 2 cm. In my
experience, the FDP tolerates shortening by up to
86 Section 2:  Primary Flexor Tendon Surgery
1.5 to 2 cm. The soft tissue can be repaired with
a local, or free, flap transfer and the tendon is
repaired by direct end-to-end suture. Flap transfer
provides fresh and vascularized tissue coverage,
roughly similar to the original subcutaneous
tissue. However, a tendon with a defect length
close to 2 cm is hard to draw together. Direct
end-to-end suture of the tendon should be accom-
panied by a procedure to reduce the tension on
the tendon when the surgeon is less experienced
with dealing with tendons with a defect. In such
cases, intramuscular tendon lengthening through
a forearm incision may release the tension.11
Lengthening of the tendons at the wrist level may
be also needed for this degree of tendon loss.
When the tendon is repaired directly, care should
be taken to prevent repair rupture when starting
early active tendon motion. Early active motion
and its progress to full active digital flexion should
be delayed.
2. Injuries including a simple and stable fracture: A
simple, stable fracture in the phalanx or metacar-
pal is not a contraindication to primary tendon
surgery. Fractures in the shafts of more than one
metacarpal bone may sometimes accompany a cut
digital flexor tendon. These injuries do not pre-
clude primary tendon surgery, providing the frac-
tures are simple, limited to the shaft and do not
involve the joints. Internal fixations in the palm
with mini-plates, screws, or K-wires usually ensure
a stable reduction, but early postoperative exercise
may have to be less aggressive. What are seen more
frequently, however, are tendon injuries associated
with fractures involving joints in more than one
phalanx, with crush, or abrasion, of the overlying
soft tissues. These skeletal injuries are contraindi-
cations to primary tendon repair, because fractures
involving joints tend to be unstable, the soft tissue
wounds are always contaminated and early post-
operative tendon mobilization is either difficult or
not feasible. However, some surgeons still perform
tendon repair and mobilize the hand after surgery
under these conditions.
3. Rupture of tendon repairs: Ruptures of primarily
repaired flexor tendons have been noted in
most case series incorporating early active finger
mobilization. I approach the ruptured tendon
repair as I would a primary tendon repair. At least
half of the segment, if not the entire segment,
encompassed by the original sutures should be
trimmed off, because the ends are softened and
ragged, which decreases the holding power of the
subsequent re-repair. The length of tendon seg-
ments that I trim off is about 0.8 to 1.0 cm (0.5 cm
or less on either end). This amount of shortening
is of no biomechanical consequence to the FDP
tendon, even if the tendon has already been
trimmed by a similar amount at the initial surgery.
In my experience, the FDP tolerates shortening by
up to 1.5 to 2 cm. The ruptured FDS tendon
should be removed. Re-repair of both tendons is
impractical, and shortening of the FDS, particu-
larly within zone 2, is mechanically disadvanta-
geous. The digital sheath system is usually less
elastic, narrow, and inclined to collapse after
primary repair rupture. Rupture of a repair within
one month after the initial repair is always worth
an attempt at re-repair. However, by one month
after primary repair, re-repair is rarely indicated, as
ruptured tendons are likely to be surrounded by
adhesions and their healing potential is limited,
particularly if repaired under increased tension.
4. Delayed repairs: All estimates of the “best timing”
for primary flexor tendon repair suggested so far
have been empirical. I do not have a rigid “best”
time frame in mind, as previous suggestions
regarding the timing of primary repair are not con-
sistent and may not be imperative. My clinical
impression is that treatment outcomes after delay
for such a short period are almost identical to
those associated with primary repair promptly
after the trauma. Upon re-opening of the wound,
the cut tendon ends still appear fresh and no col-
lapse or fibrosis of the sheath is seen. The tendons
can be treated as if they were freshly cut. However,
when the surgery is postponed further beyond that
period, the tendon ends may be rounded, with
varying degrees of adhesions present, and the elas-
ticity of the sheath is likely to be reduced, making
repair more difficult. Although a delay of more
than 1 month would rule out direct end-to-end
repair surgery, the report of McFarlane and col-
leagues showed that direct end-to-end repair after
a delay for 1 to several months can been possible
without undue tension.14 For these late cases, the
tendon may be lengthened within the muscles in
the forearm to ease the tension on the proximal
tendon end.11 Of note is one situation in which
repair delayed more than 1 month is still feasible
(i.e., a wound around the PIP joint level in which
the FDP tendon has been cut but the long vincula
connecting to the proximal cut tendon has not
been severed). In this instance, retraction of the
FDP tendon is limited. When the wound is opened,
the retracted proximal end is found locally within
the sheath and the tendon can be repaired with
relative ease.
5. Massive soft tissue damage: Generally, this is a con-
traindication to primary flexor tendon surgery,
and I discourage primary repairs under this
circumstance. However, such situations can be
broken down further into: (1) extensive soft tissue
 Chapter 8:  Indications for Primary Flexor Tendon Repair
damage without apparent loss of tendon sub-
stance and (2) soft tissue damage with loss of a
significant length of tendon. The former injury
may still leave room for primary tendon repair,
providing the surgeon is prepared to carry out sec-
ondary tenolysis later. This borderline indication
is controversial and has not been well defined.
Although the decision is difficult, we must balance
the merits of primary repair and early mobiliza-
tion, followed by tenolysis if necessary, against
those of secondary tendon grafting. It may be
acceptable, to repair these injured tendons primar-
ily and prepare the patient for the possibility of
tenolysis. Nevertheless, these cases should be
managed carefully in order to prevent wound
References
1. Verdan CE: Primary repair of flexor tendons, J Bone Joint Surg
(Am) 42:647–657, 1960.
2. Kleinert HE, Kutz JE, Ashbell TS, et al: Primary repair of lacer-
ated flexor tendons in “No Man’s Land”, [abstract] J Bone Joint
Surg (Am) 49:577, 1967.
3. Kleinert HE, Schepel S, Gill T: Flexor tendon injuries, Surg
Clin North Am 61:267–286, 1981.
4. Bunnell S: Repair of tendons in the fingers and description
of two new instruments, Surg Gynecol Obstet 26:103–110,
1918.
5. Bunnell S: Repair of tendons in the fingers, Surg Gynecol Obstet
35:88–97, 1922.
6. Kleinert HE, Verdan C: Report of the Committee on Tendon
Injuries (International Federation of Societies for Surgery
of the Hand), J Hand Surg (Am) (5 Pt 2):794–798,
1983.
7. Moiemen NS, Elliot D: Primary flexor tendon repair in zone
1, J Hand Surg (Br) 25:78–84, 2000.
87
infection, and should be handled by surgeons
with considerable experience in tendon repairs.
Such repairs should not become routine.
ABSOLUTE CONTRAINDICATIONS
Absolute contraindications to flexor tendon repair are
severe contamination, signs of infection, bony injuries
involving joint components and long defects of
the flexor tendons, including extensive destruction of
pulleys. Serious crush injuries, extensive loss of soft
tissues, or fractures involving multiple bones, particu-
larly at different levels or which cannot be stabilized
adequately by internal fixation, are also contraindicative
to primary tendon repairs.
8. Tang JB: Flexor tendon repair in zone 2C, J Hand Surg (Br)
19:72–75, 1994.
9. Tang JB: Clinical outcomes associated with flexor tendon
repair, Hand Clin 21:199–210, 2005.
10. Tang JB: Indications, methods, postoperative motion and
outcome evaluation of primary flexor tendon repairs in Zone
2, J Hand Surg (Eur) 32:118–129, 2007.
11. Le Viet D: Flexor tendon lengthening by tenotomy at the
musculotendinous junction, Ann Plast Surg 17:239–246,
1986.
12. Dowd MB, Figus A, Harris SB, et al: The results of immediate
re-repair of zone 1 and 2 primary flexor tendon repairs which
rupture, J Hand Surg (Br) 31:507–513, 2006.
13. McFarlane RM, Lamon R, Jarvis G: Flexor tendon injuries
within the finger. A study of the results of tendon suture and
tendon graft, J Trauma 8:987–1003, 1968.
14. Elliot D, Barbieri CH, Evans RB, et al: IFSSH Flexor Tendon
Committee Report 2007, J Hand Surg (Eur) 32:346–356, 2007.
 CHAPTER
9  
TREATMENT OF THE FLEXOR
TENDON SHEATH AND PULLEYS
Jin Bo Tang, MD
OUTLINE
The flexor sheath system consists of a continuous
synovial sheath and segmental pulleys. The pulleys are
arranged in either cruciform or annular patterns over-
lying the membranous synovial sheath. The synovial
sheath provides the tendons with a smooth gliding
bed and the pulleys strengthen the sheath and main-
tain the proper mechanics of tendon motion. The
digital sheath system is closed and compact, making
it structurally comparable to a compartment of the
extremities. The traumatized and edematous tendon
can be easily compressed by the tightly closed sheath,
resulting in poor tendon healing, adhesion formation,
and loss of integrity of the sheath.
The guiding principle in treating the sheath is not
to narrow the injured, or opened, sheath and not to
compress the repaired tendons. Closure of the injured,
or opened, synovial sheath is not necessary, unless
such openings are long. Venting of a part of the A2
pulley and the A4 pulley, under the condition of the
other annular pulleys and the remainder of the syno-
vial sheath being intact, improves outcomes and does
not produce a clinically significant functional distur-
bance. The length of such active release of the sheath–
pulley complex should not exceed 2 cm.
Pulley-release procedures should not be carried out
without thorough mastery of pulley anatomy and rec-
ognition of the borders of these pulleys during dissec-
tion. Releasing multiple pulleys (cruciate and annular)
or leaving a lengthy defect, or opening, in the synovial
sheath and pulley system is harmful and impairs
digital function. Losses of significant length of the
sheath or multiple pulleys should be reconstructed.
The synovial sheath and segmental pulleys are a
prominent feature of the flexor tendon system in the
hand. Because injury to the sheath occurs in all flexor
tendon lacerations in the digits and we cannot approach
the tendons without violating the sheath surgically, con-
siderable investigations have been devoted to this topic
over decades.1-33 The significance of proper treatment of
the sheath—the rigid and condensed annular pulleys in
88
particular—has received great attention in efforts to
optimize the outcomes of flexor tendon surgery.
ANATOMY
The digital flexor sheath is a closed synovial system
extending from the distal part of the digits to the meta-
carpophalangeal (MCP) joint levels of the digits. The
sheath consists of membranous portions of continuous
synovial sheath (called simply the “sheath”), and con-
densed retinacular components (the “pulleys”). A layer
of thin, smooth, and continuous membrane covers the
inner surface of the entire sheath and pulleys. Pulleys
are segmentally located and overlie the membranous
lining. The pulleys include annular pulleys (condensed,
rigid, and heavier annular bands), cruciate pulleys
(filmy cruciform bands), and the transverse palmar apo-
neurosis pulley (Figure 9-1).1
In each of the four fingers, there are five annular
pulleys (A1, A2, A3, A4, and A5), three cruciate pulleys
(C1, C2, and C3), and one palmar aponeurosis (PA)
pulley.1-3 The A1, A3, and A5 pulleys originate from the
palmar plates of the MCP and proximal and distal inter-
phalangeal (PIP and DIP) joints, respectively. The A2
and A4 pulleys originate from the middle portion of the
proximal and middle phalanges, respectively. The broad-
est is the A2 pulley, which covers the proximal two-
thirds of the proximal phalanx and encompasses the
bifurcation of the flexor digitorum superficialis (FDS)
tendon. The A4 pulley is located at the middle of the
middle phalanx. The A2 and A4 pulleys are structurally
the most critically located and, functionally, the most
important.
The length of the A2 pulley is about 1.5 to 1.7 cm
and the length of the A4 pulley is about 0.5 to 0.7 cm
in the middle finger of an average adult. The diameter
of the flexor sheath is at its narrowest at the level of the
A4 pulley and in the middle and distal parts of the A2
pulley. The A2 and A4 pulleys appear as white con-
densed bands; they are easily recognizable, because
both are remarkably denser and more rigid than their
adjacent flexor sheath. The A1 pulley, with a length of
about 1.0 cm, is located proximal to the A2 pulley; in
some instances, both A1 and A2 pulleys merge to form
 Chapter 9:  Treatment of the Flexor Tendon Sheath and Pulleys
PA A1 A2 C1 A3 C2 A4 pulleys
A tendon mechanics. Manske and Lesker2 investigated the
A4
A1 C2
A3
A2 C1
B is relatively unimportant. Doyle and Blythe3 found sig-
Digital pulley system
PA A1
A2
C1 A3 C2 A4 C3 A5
C Chapter 10. Here, Box 9-1 summarizes the work of other
Figure 9-1  The anatomy of the flexor pulleys and synovial
sheath of the fingers (A), with the finger flexed (B), and the
concertina effect on the sheath during finger flexion (C).
a compound pulley complex. The A3 pulley is located
palmar to the PIP joint, is short (0.3 cm) and difficult
to distinguish from the synovial sheath.
In the thumb, there are three pulleys (A1, oblique,
and A2) with no cruciate pulleys. The A1 pulley (0.7 to
0.9 cm in length) is located palmar to the MCP joint.
The oblique pulley (0.9 to 1.1 cm) spans the middle
and distal parts of the proximal phalanx. The A2 pulley
(0.8 to 1.0 cm) is close to the insertion of the flexor
pollicis longus (FPL) tendon.
FUNCTION
The synovial sheath offers a smooth gliding bed and
provides synovial nutrition to the tendons. Mechani-
cally, the pulleys serve to strengthen the sheath and hold
the flexor tendons close to phalanges and their joints.
The annular pulleys act as a fulcrum, optimizing the
mechanical efficiency of digital flexion. The more com-
pressible cruciate pulleys allow for digital flexion with
condensation of the fibro-osseous sheath at the inner
part of flexed fingers (called the “concertina effect”) (see
Figure 9-1). Both forms of pulley prevent anterior dis-
placement (i.e., bowstringing) of the tendon during
finger flexion.
89
In the finger, the A2 pulley is the strongest in respect
of preventing anterior displacement of the tendons and
is at the most critical location. The A2 and A4 pulleys
are most important in maintaining the biomechanics
of the tendon gliding, although the other sheath com-
ponents do contribute to the maintenance of tendon
mechanics. Absence of a series of pulleys will affect
roles of the A2, A1, and PA pulleys and found that
absence of any two, or all three, pulleys resulted in
tendon bowstringing. Tang and Xie20 investigated the
roles of the A3, C1, and C2 pulleys and found that these
pulleys help to restrain tendon bowstringing.
In the thumb, the proximally located A1 pulley and
the oblique pulley are the most important functionally.
The distally located A2 pulley of the thumb is thin and
nificant decrease in motion of the distal joint of the
thumb when both the A1 and the oblique pulleys were
removed, but loss of either alone did not noticeably
affect the motion of this joint.
HISTORICAL REVIEW
A review of the conceptual changes regarding roles and
treatments of the sheath, pulleys in particular, are pro-
vided by Elliot, together with his commentaries in the
groups that influenced our studies, the time sequence of
our investigations, and evolving philosophies, leading
to current treatment guidelines.4-29
INVESTIGATIONS
Over two decades, I have organized and conducted a
series of investigations to explore the basic science and
to develop clinical treatments relevant to the flexor
sheath and pulleys. My investigations proceeded after
starting with a study of the methods of sheath recon-
struction in 1988 under the instruction of an exemplary
hand surgeon, Professor Seichii Ishii.
My interest was developed in the studies of the
methods of sheath treatment and their effects on tendon
gliding, followed by an anatomical study of the flexor
pulleys. Over the past decade, I have been joined by a
group of capable colleagues in studying the effects of
pulleys and pulley incisions on tendon biomechanics
and tendon biology.
Investigation of Sheath Treatment—Excision,
Repair and Reconstruction
In the 1980s, there was an upsurge in awareness of the
importance of synovial nutrition of the tendon and in
attempts to restore the integrity of the injured synovial
sheath. My first study was on sheath excision, closure,
and enlargement plasty using a graft. However, the find-
ings did not support particular benefit from direct
closure of the opened sheath, but, instead, indicated
90 Section 2:  Primary Flexor Tendon Surgery

Box 9-1 Some Major Steps Toward Current Treatments of Sheath and Pulleys Over the Past 25 Years

1985:  Lister, in a review, advocated sheath closure and described the method to create sheath flaps to assess the tendon
and accommodate surgical repairs.4 This review had a great impact on later clinical practice of sheath closure.

1985:  Strauch and colleagues compared the results of sheath closure with vein grafts with sheath excision in chickens.
They found improved digital motion after restoration of sheath integrity.5

1986:  Peterson and Manske compared the mechanical and histologic outcomes of sheath repair and excision in a chicken
model. They concluded that closure of the flexor sheath does not improve tendon gliding.6,7

1987:  Saldana and colleagues compared surgical closure (42 fingers) and opening (48 fingers) of the sheath after tendon
repairs in zone 2 in a comparative perspective study. There was no statistical difference between the results of the patients
with the two treatments.8

1988:  Manske, in a review, stated, “It should be kept in mind that a water-tight closure of the tendon sheath may in fact
narrow the diameter of the fibro-osseous canal and reduce its volume.”9

1990:  Tang, Ishii, and Usui compared the mechanical and histological results of sheath repair, excision, and enlargement
sheath plasty by autogenous grafts using chickens. Tendon gliding was not improved after sheath closure, but was
improved after enlargement plasty. They considered that the fibro-osseous digital sheath is comparable to the fibro-
osseous muscle compartments in the extremities, and proposed a “digital sheath syndrome” to explain pathophysiology
in the tendon after tight sheath closure.10

1990:  Gelberman and colleagues compared sheath reconstruction and excision in canines treated by early motion reha-
bilitation, and substantiated that sheath repair—either by suture or graft—does not improve the biomechanical, biochemi-
cal or morphologic features of the tendons.11

1990:  Savage measured tendon excursion, profundus tendon flexion force, and tendon bowstringing using five cadaveric
hands after varying combined excisions of the annular pulleys. He stated, “In an otherwise intact digital fibrous flexor
sheath, A2 and A4 pulleys were no more important mechanically than the other pulleys.”12

1994:  Tang and colleagues reported that closure of the sheath did not improved tendon gliding in chickens at multiple
time-points of delayed primary repair.13

1995:  Tang studied the anatomy of the A2 pulley specifically, using cadaveric hands, by measuring the tendon excursion
after midline incisions through part of the A2 pulley, and the vertical and horizontal diameters of distal, middle, and proxi-
mal parts of this pulley. He proposed the partial release of the pulley and stated, “To improve tendon healing and gliding,
procedures for A2 pulley release, including incision of the critical portion to free tendon motion or enlargement of the A2
pulley, can be performed.”14

1996:  Tang, Shi, and Zhang examined the effects of sheath narrowing and enlargement on tendon excursions, healing,
and adhesions using chickens. They demonstrated that the diameter of the surgically repaired sheath exerts great influ-
ences on tendon function.15

1998:  Kwi, Ben, and Elliot reported the clinical results of zone 2 flexor tendon repairs in 185 fingers in 166 patients together
with lateral release of the A2 and A4 pulleys. They showed practicability of active partial release of these pulleys. They
stated, “It was necessary to vent the A4 pulley between 10 and 100% of its length in 71 (56%) of the fingers and to vent
the distal edge of the A2 pulley by 4 to 10 mm in 10 (8%) of the fingers.”16

1999:  Tang and colleagues reported 1-year follow-up of the finger motion after simple partial release through the one-half
to two-thirds portion along the midline of the A2 pulley or with enlargement pulley plasty in 16 fingers. No tendon bow-
stringing was noted. They advocated “partial release of the A2 pulley up to 1/2 or 2/3 lengths of the A2 pulley under the
condition that other pulleys are intact.”17

1998, 1999:  Tomaino, Mitsionis, and colleagues performed cadaveric studies to substantiate that partial release of the
A2 and complete release of the A4 pulley do not significantly alter tendon mechanics.18,19

2001:  Tang and Xie, in a cadaveric study, showed that loss of an A3 pulley does not affect tendon biomechanics, but cruci-
ate pulleys and synovial sheath restrain tendon bowstringing. They advise not creating lengthy sheath defects, given the
integrity of major annular pulleys.20
 Chapter 9:  Treatment of the Flexor Tendon Sheath and Pulleys 91

2002:  Elliot, in a review, highlighted the feasibility of pulley-venting. He stated: “In reality, … as the A2 pulley is of sufficient
length that one can excise any one-third of it to allow repair and free movement of the repair and still have a pulley which
is one or more centimetres in length, and thus, functional.” Regarding the sheath, he stated: “It is now our practice after
zone 2 repairs to simply lay the sheath back over the tendons without suturing, after adequate venting of the A2 and A4
pulleys to allow free running of the repairs.21

2002:  Amadio, Zhao, Paillard, and colleagues investigated gliding resistance of the FDP tendon after resection of one
slip of the FDS tendon and Kapandji pulley plasty, and found that both pulley plasty and resection of one slip of the FDS
reduce gliding resistance.22

2003, 2007: Tang, Xie, Xu, and colleagues investigated tendon repairs within and proximal to a major pulley using chick-
ens. Worse results of surgeries were noted in the pulley area.24 They compared the results of simple pulley incision, Kapandji
pulley plasty, and excision of one slip of the FDS and found no improvement of tendon gliding after Kapandji pulley plasty.25

2004:  Tanaka, Amadio, An, and colleagues investigated gliding resistance of the tendon and pulley strength after the A2
pulley was excised successively by 25%, 50%, and 75%. Their data support the clinical practice of partial pulley excision,
up to a limit of 50%.26

2007:  Tang, in a review, highlighted the critical roles of proper and sufficient release of critical annular pulleys in achieving
predicable functional recovery. He outlined precisely the lengths and areas to be release in different locations of injuries.
He considered that proper release of the pulley may be even more effective in reducing repair ruptures than use of a strong
repair.27

2009:  Cao and Tang compared the strength of the repaired tendon with the A2 pulley intact or vented at varying digital
flexion. They recorded that the strength decreased significantly when the pulley was intact.29 Rupture of the healing
tendons was significantly more frequent when the pulley was intact.28

that enlargement of the sheath accommodates tendon

gliding more effectively than direct closure of the sheath
after tendon repair.
In this study, we used 90 long toes of 45 white
Leghorn chickens to compare the effect of enlargement
sheath plasty—interposing a patch of grafted sheath
from the extensor retinaculum area into a longitudinal
opening of the sheath, without excising the digital
sheath—with two treatments: sheath excision or direct
sheath closure after longitudinal incision.10 Tendons in
zone 2 were completely cut and surgically repaired
either primarily or at the delayed primary stage (3 days
after tendon division).
We found that 6 weeks later, in toes with primary
repair, sheath enlargement produced greater tendon
excursion than sheath excision or closure, but no differ-
ence was found between the latter two treatments. In the
toes with delayed primary repair, the tendons with
sheath enlargement had the greatest gliding, and those
with the sheath closed directly had the worst gliding. The
sheath that had been closed during delayed primary
repair have dissolved among the extended adhesions.
Conclusions: We concluded that enlargement sheath
plasty by a graft improves tendon gliding. Direct closure
of the sheath does not improve tendon gliding, and may
in fact impair tendon gliding at the delayed primary
stage.10 We considered the digital sheath comparable
to the fibro-osseous compartments of the extremities
(Figure 9-2). A concept of “digital sheath syndrome” to
DIGITAL SHEATH: A MINIATURE COMPARTMENT
Tight closure of the sheath/pulleys
Compress the edematous tendons
Digital sheath syndrome
FDS • Poor tendon healing (ruptures)
FDP • Adhesion formations
Sheath narrowing • Destruction of closed synovial sheath
Avoid compression to repaired tendons!
Tendons are edematous after surgery.
Figure 9-2  Consequences after tight closure of the sheath
or pulleys.
explain the pathophysiological changes in the tendons
was proposed to describe the triad phenomena fre-
quently associated with tight closure of the sheath,
namely: (1) loss of integrity of the directly closed sheath;
(2) increased peritendinous adhesions; and (3) worsened
tendon healing. These considerations are further sup-
ported by a subsequent study to deliberately narrow the
sheath and compare this with direct closure of the
incised sheath, partially excised the sheath or sheath
enlargement by an interposition graft.15
92 Section 2:  Primary Flexor Tendon Surgery

Clinical application: Between 1989 and 1991, we
treated 21 fingers in 17 patients presenting with zone 2
tendon injuries and a graft was taken from the sheath
covering the extensors in the wrist or with a part of the
dorsal retinaculum to reconstruct and enlarge the trau-
matically defected sheath (Box 9-2).31 The size of the
graft was made greater than the size of the real defect.
Box 9-2  Some Major Clinical Reports of Case
Series of Sheath or Pulley Plasty Procedures
1993:  Tang, Ishii, and Zhang reported 21 fingers in 17
patients with enlargement sheath reconstruction using
autografts during delayed primary tendon repair in zone
2. No repair ruptures were noted in this case series.31
2005:  Bakhach and colleagues reported a new
procedure—flexor pulley Omega plasty, which consists
of releasing the lateral attachment of the pulley to
increase the internal volume (the flexor tendon gliding
space) in the A2 and A4 pulley localities. They consid-
ered that “this procedure respects the anato­mical con-
tinuity of the pulley and its mechanical properties.”31
2009, 2010:  Bunata and colleagues presented his
experimental data in cadavers32 and, subsequently, nine
fingers of primary pulley enlargement plasty using auto-
grafts.33 No repair ruptures were found.
Among 21 fingers with such grafts, 7 fingers were rated
excellent (33.3%), 11 good (52.4%), and 3 fair (14.3%).
No tendon rupture occurred.
Investigation of the Anatomy of the A2 Pulley
and Clinical Partial A2 Pulley Release
In 1993, I reviewed the results of flexor tendon repairs
in different subdivisions of the zone 2, and noted that
the worse outcomes were most frequently associated
with zone 2C (A2 pulley area) injuries. This finding
prompted me to specifically observe the A2 pulley
anatomy and the mechanics of FDS and FDP tendon
motion under the A2 pulley.
I dissected 40 fingers of 10 cadaveric hands. The
transverse and vertical diameters of the A2 pulley were
measured at its distal border, middle, and proximal
border.14 The excursions of the FDP tendons and
maximal finger flexion were measured after incision
through volar midline of the proximal half, and then,
the whole length of the A2 pulley.
Anatomically, the distal and middle parts of the A2
pulley are the narrowest. Movement of the FDP tendon
is restrained by both the A2 pulley and the FDS tendon
(Figures 9-3 and 9-4). Mechanically, given the integrity
of the other annular pulleys, incision of half of the A2
pulley resulted in only minimal (0.7%) loss of total
flexion of motion; complete division of the A2 pulley

A2

IID
IIB
IIC
A2

FDS bifurcation Double sheath for FDP

Figure 9-3  The anatomy of flexor tendon zone 2C, i.e., the A2 pulley area. The gliding of the FDP tendon is restricted by
both the rigid and narrow A2 pulley and the bifurcating FDS tendon which surrounds the anterior, lateral, and dorsal aspects
of the FDP tendon. The presence of such a “double sheath” restricting motion of the FDP tendon is a unique anatomical
feature in this locality, which contributes to difficulties of surgery and recovery of tendon function after surgical repair.

CHANGES IN SHEATH DIAMETER: A2 PULLEY

Distal A2 Middle A2 Proximal A2 Proximal to A2

S FDS FDS FDS

FDP FD
FDS S FDP
FD FDP FDP

Most narrow Most narrow Relatively large Relatively large

Very restrictive Very restrictive Less restrictive Less restrictive

Figure 9-4  The anatomy of the A2 pulley: changes of sheath diameter in the locality covered by and proximal to the A2 pulley.
 Chapter 9:  Treatment of the Flexor Tendon Sheath and Pulleys
resulted in a larger (2.3%) loss of flexion. Incision of part
of the A2 pulley did not lead to tendon bowstringing.14
Conclusions: The distal and middle parts of the A2
pulley are particularly restrictive to tendon gliding.
Partial A2 pulley release affects digital motion insignifi-
cantly and does not cause tendon bowstringing.14 Based
on the findings, I proposed procedures for partial release
of the A2 pulley to release compression of the repaired
tendon under the pulley.
Clinical application: From 1994, I started to partially
incise the A2 pulley along its volar midline when repair-
ing the tendons in this area; the length of the release
was either the distal or proximal half to two-thirds.
Before partial release of the A2 pulley, the other annular
pulleys were confirmed to be intact and uninjured. In
carrying out these A2 releases, a part of the A2 pulley
was always retained. In 1998, we examined the outcome
of 16 fingers with FDP tendon repairs and partial release
of the A2 pulley.15 No functionally disturbing tendon
bowstringing was noted after this procedure. Although,
from a rigorous viewpoint, the tendon would displace
after even minor releases of the pulley after incision
through its midline, such changes are insignificant clini-
cally and are well within the compensatory reserves of
the tendon system for normal function.
Investigations of the Effects of Integrity of
the A2 Pulley in Chicken Models and Partial
A2 and A4 Pulley Releases in Clinical Cases
Between 2000 and 2011, my colleagues and I studied (1)
different results of tendon repairs after tendon injuries
within, or proximal to, the A2 pulley; (2) the biome-
chanics and adhesions of tendons after repair of a single
slip of bifurcated FDS tendon, incision of the A2 pulley,
Kapandji pulley plasty, and direct pulley closure; (3)
tendon gliding and the work of digital flexion after
flexor tendon repair together with sheath enlargement
by a graft, sheath incision, or sheath closure with delib-
erate narrowing; (4) tendon gliding resistances in
tendon repairs with the pulley released and intact; (5)
tendon repair strengths with the pulley released and
intact; and (6) relative contribution of an intact A2
pulley and edematous subcutaneous tissue to resistance
to active tendon movement. All studies were carried out
in the chicken toe model and involved more than 260
chickens. The study methods were detailed in previous
reports.23-25,28,29
Conclusions: (1) tendon repairs located under the A2
pulley have significantly worse gliding excursion and
more adhesion formation than those proximal to the
pulley; (2) release of the A2 pulley or resection of one
slip of the FDS tendon produces greater tendon excur-
sions, smaller work of digital flexion and less adhesion
formation than closure of the pulley. Kapandji pulley
plasty does not improve tendon gliding more than a
simple pulley incision; (3) narrowing of the sheath
93
produces significantly worse tendon gliding and
increased work of digital flexion. Incision of the sheath
produces identical results, regardless of whether the
sheath is closed by a graft; (4) tendon gliding resistance
decreases substantially after release of the pulley in the
postoperative period; (5) tendon repair strength
increases significantly when the pulley is released com-
pared with the pulley intact; and (6) presence of an
intact A2 pulley contributes more substantially to
increase in the resistance to active tendon movement
than edematous subcutaneous tissue.
Clinical application: My colleagues and I have contin-
ued the practice of partial A2 pulley release thus far. I
further defined the length and location of the sheath
pulley which can be released without causing clinical
problems of tendon bowstringing.27 In this period, we
reviewed more than 40 cases of release of part of the A2
pulley or the A4 pulley. We did not detect tendon bow-
stringing sufficient to cause clinically perceivable func-
tional disturbances after partial and limited pulley
release procedures, given the integrity of the other
pulleys. Proper release of these pulleys, together with
strong surgical repairs, even without very strictly super-
vised postsurgical motion in our recent case series, led
to good or excellent recovery of finger flexion when the
tendon wounds were clean or could be converted to
clean wounds.
TREATMENT GUIDELINES
The guideline for treating the sheath is not to narrow the
sheath and not to compress the repaired tendons. Surgically,
priority should be given to avoiding narrowing of the
tendon gliding space, rather than complete restoration
of sheath integrity. Complete closure of the sheath is
insignificant to tendon function and, thus, is not a
necessity during primary tendon repair. During delayed
primary repair, sheath closure is usually not possible
due to sheath contracture. However, a lengthy defect in
the sheath would impair tendon mechanics and, thus,
should be avoided.
INDICATIONS AND OPERATIVE METHODS
Direct Closure
Direct closure of the sheath, usually performed with
interrupted 5-0 suture, may be indicated at primary
repair in a clean-cut wound without sheath defect. I
personally do not close the sheath if it appears likely
to be difficult, but do avoid leaving a lengthy sheath
opening or defect (greater than 2 cm). Possible benefits
of direct closure of the sheath may be avoiding catching
of the repaired tendons on the cut edges of the sheath
and avoiding invasion adhesions to the tendon repair
site. However, closure of the sheath is not necessary to
nutrition and healing of the tendon. Clinically, there is
no clear evidence of improvement of tendon gliding
94 Section 2:  Primary Flexor Tendon Surgery
after sheath closure. In delayed primary repair, sheath
contracture usually makes direct closure impossible.
Excision
Sheath excision has been a practice of hand surgeons for
decades and comes from the era when outside adhesions
were considered necessary to tendon healing. However,
it is equally appropriate, or even more appropriate, to
leave it unrepaired. I leave the sheath unrepaired in most
cases at primary repair but excise a part of an already
thickened, or contracted, sheath at delayed repair.
Sheath Reconstruction by Grafts
Sheath defects can be reconstructed by grafting a sheath
with extensor retinaculum.30,33 The graft, with the syno-
vial aspect facing the tendons, is sutured with 5-0 inter-
rupted sutures to the in situ sheath. In performing such
grafting, I emphasize that the graft size should be greater
than the size of the defect, to avoid potential compro-
mise to the repaired tendons. Sheath enlargement plasty
by a graft may decrease resistance to the tendon and act
as a barrier to adhesion invasion. If the laceration
extends over the entire length of the A2 pulley, such a
graft of extensor retinaculum may both improve gliding
and decrease tendon bowstringing.
In the early 1990s, I reconstructed digital sheath
defects by harvesting an autograft.30 During the last 10
years, I have not reconstructed sheath defects using graft
as I have changed to partially releasing the A2 pulley
together with part of the adjacent synovial sheath,
without recourse to grafts. Without this reconstructive
A5 C3 A4 C2 A3 C1 A2 A1
Tendon laceration
Tendon laceration
Tendon laceration
Tendon laceration
Figure 9-5  Proposed sites and lengths of sheath-pulley releases in primary or delayed primary flexor tendon repair in the
fingers, which allow access to the tendons and release constriction to tendon gliding, but do not produce loss of tendon
function due to tendon bowstringing.
procedure, the surgery is simpler, and outcomes are
similar, in my experience.
Venting of the Major Pulleys
(such as the A2 and A4)
Venting a part of the A2 pulley or the entire A4 pulley
has been advocated by a number of surgeons to improve
gliding of the repaired tendons.14,16,21,34-36 Those reports
have shown that such venting does not lead to tendon
bowstringing, given the integrity of other parts of the
sheath, including the other annular pulleys.14,16,21,27,34-36
Venting of the most constrictive part of the pulley
substantially decreases gliding resistance and avoids
catching of a bulky repair on the pulley edge. Of par­
ticular note, several recent reports showed no repair
rupture in the cases that underwent venting of the major
pulleys.27,34-36
In my experience, given the integrity of the other
annular pulleys, the A2 pulley can be vented through
two-thirds of its length, either distally or proximally.
The A4 pulley can be vented entirely (Figures 9-5
through 9-8). The degree of the venting should be such
as to ensure that the passive digital motion during
surgery allows the tendon repaire site to glide freely
distal to or under the vented pulley. Whether the vented
part of the pulley needs to be excised or trimmed is still
questionable. Because the A2 pulley is thick and rigid,
if the release by an incision is judged to be insufficient,
it may be appropriate to remove a part of the incised
portion of the pulley, or a part of the pulley is trimmed
to form an oblique or oval opening.
Sheath-pulley release
Sheath-pulley release
Sheath-pulley release
Sheath-pulley release
 Chapter 9:  Treatment of the Flexor Tendon Sheath and Pulleys 95

A B
Figure 9-6  A case of venting of the entire A4 pulley when tendon passage under this pulley is difficult (A and B).

Pulley

Pulley

B
Figure 9-7  A case of venting of the A2 pulley through the
midline. The distal 60% of the A2 pulley was vented.

The function and treatment of the condensed sheath Shortened

parts, i.e., the pulleys, are complex and may even be part of
confounding. Most information on this subject has been the pulley
derived from investigations over the past two decades.36,37
C
Here, I summarize the current understanding of the
function and treatment of pulleys (1) Most pulleys (includ- Figure 9-8  Three methods of releasing pulleys: A, midline
ing at least a part of the A2 pulley) should be preserved to incision; B, lateral incision; C, shortening (partial resection).
maintain normal digital function: most of the annular
pulleys, including at least part of the A2 pulley, should
be preserved during tendon repair. Individual minor
annular pulleys (A1, A3, PA, or A5) are not essential
96 Section 2:  Primary Flexor Tendon Surgery
functionally and, thus, may be incised to allow access to
the tendons. The A2 and A4 pulleys are the most impor-
tant functionally, but maintenance of the majority of the
other pulleys still is necessary for normal tendon func-
tion. (2) A part of the A2 pulley or the entire A4 pulley can
be incised without clinically significant loss of digital func-
tion: given that the other annular pulleys and adjacent
sheath are intact, the integrity of part of the A2 or the
entire A4 pulley is not as important as previously
believed;4 incision of part of the A2 or the entire A4
pulley does not result in remarkable functional distur-
bance. Therefore, part (but not all) of the A2 pulley or
part, or all, of the A4 pulley is expendable when the
other pulleys and most of the sheath are uninjured. (3)
Lengthy defects or incisions in the sheath should be avoided:
lengthy sheath defects lead to tendon bowstringing. The
allowable length of defects, or incisions, is less than
approximately 1.5 to 2 cm, depending on size of the
fingers. In exposing the lacerated tendon, we should
avoid incising a lengthy part of the sheath. Though not
commonly seen, the lengthy traumatic opening in the
sheath should be closed partially to reduce the length
of sheath opening, and the large defect should be recon-
structed. (4) Cruciate pulleys become important when
annular pulleys are lost: cruciate pulleys do not play a key
role in restraining tendon bowstringing in normal
fingers, but they do restrain the tendons when adjacent
annular pulleys are destroyed. If the annular pulleys are
intact, it is not necessary to repair the cruciate pulleys.
On the other hand, if the annular pulleys are not intact,
care should be taken to preserve the cruciate pulleys and
synovial sheath. (5) Two pulleys should be preserved in the
thumb: in the thumb, at least two pulleys should be pre-
served for better FPL function. Venting of either the A1
pulley or the oblique pulley in the presence of one of
the two pulleys and an intact A2 pulley is clinically
acceptable. (6) Two or three strong annular pulleys should
be preserved in secondary tendon surgery: during secondary
tendon grafting or tenolysis, at least two, or three, strong
annular pulleys at critical locations should be preserved
or reconstructed. Preservation of the A2 and A4 pulleys
is essential in secondary surgery.
My own practice has evolved. I no longer repair an
opening in the sheath except in some of very clean
wounds and at primary tendon repair. In delayed repair,
the sheath frequently has contracture, thickening, or is
embedded in immature adhesions. It was rarely possible
to close the sheath directly. In fact, I have not encoun-
tered a case in which the sheath could be approximated
easily without tension. I no longer continue my practice
of sheath plasty by interposing a graft and consider that
this procedure may not yield better results than the
much easier procedure of simple cutting, or venting, the
pulley. It is my current preference to simply incise a
part of the sheath-pulleys without performing any
reconstructive procedures, when the pulleys constitute
obstacles to repaired tendon passage or are judged to
restrict tendon gliding during surgery.
CONSIDERATIONS
In the late 1980s, at the start of investigations of the
sheath, I was initially puzzled by a variety of suggestions
of sheath treatment by different surgeons. Over the past
two decades, I came to believe that the sheath and
pulleys can be treated by a more simple and straightfor-
ward principle. Although valid and theoretically sup-
ported, complicated repairs, or reconstructions, of the
synovial sheath are not a necessary part of the surgery.
Over the years, my practice has evolved from reconstruc-
tion of the lost synovial sheath, to leaving the injured
sheath unrepaired, and to intentional venting of the
critical part of a pulley that is too narrow. After I reviewed
my cases of pulley release and pondered the importance
of venting a part of the pulley to lessen resistance to
tendon motion, and compared it to a strong surgical
repair, another part of my past work, I came to realize
and became gradually convinced that a properly per-
formed pulley release is important and may even be a
vital step in improving the function of the tendons. This
procedure will probably be proved to be a key to com-
plete avoidance of repair rupture, eventually becoming
a critical step in reaching the elusive goal of predictable
outcome of flexor tendon repair.
It is very likely that outcomes of some of past cases,
treated by experienced and inexperienced surgeons
alike, have been affected by the way in which the pulleys
were treated, yielding a general impression of “unpre-
dictability” of flexor tendon repairs. When patients were
treated by inadvertent venting of the pulleys or the par-
tially lacerated pulleys were left unrepaired (which was
not unusual in cases treated by inexperienced physi-
cians), they may have achieved good results inexplica-
bly. Conversely, when surgeons strictly followed the
instruction to maintain the entire A2 pulley, repairing
both FDS and FDP tendons specifically, the cases had
unpredictably poor outcomes, even when the surgeons
were experienced. This remains a bold interpretation in
respect of the “unpredictability” of the outcome of past
cases, but I believe this is, at least, partly true.
My final comment is that pulley-release surgery
should be attempted only with precise mastery of pulley
anatomy and recognition of the borders of these pulleys
during dissection. Releasing of multiple pulleys (cruci-
ate and annular) or leaving a lengthy defect or opening
in the synovial sheath and pulleys is harmful and
impairs digital function. Such losses of a significant
length of the synovial sheath with multiple pulleys
should be reconstructed. My observation of operations
in a number of units in different countries has made
me aware that a significant number of surgeons have
not precisely mastered the anatomy of these pulleys.
I strongly advise that surgeons working in this field
 Chapter 9:  Treatment of the Flexor Tendon Sheath and Pulleys
review relevant anatomical descriptions in textbooks
or journals to obtain a clear and detailed knowledge of
the pulleys before performing these releases. Without
good mastery of the anatomy and clear recognition of
the major pulleys during surgery, (1) pulleys could be
References
1. Doyle JR: Anatomy of the finger flexor tendon sheath and
pulley system, J Hand Surg (Am) 13:473–484, 1988.
2. Manske PR, Lesker PA: Palmar aponeurosis pulley, J Hand
Surg (Am) 8:259–263, 1983.
3. Doyle JR, Blythe WF: Anatomy of the flexor tendon sheath
and pulleys of the thumb, J Hand Surg (Am) 2:149–151,
1977.
4. Lister G: Indications and techniques for repair of the flexor
tendon sheath, Hand Clin 1:85–95, 1985.
5. Strauch B, de Moura W, Ferder M, et al: The fate of tendon
healing after restoration of the integrity of the tendon sheath
with autogenous vein grafts, J Hand Surg (Am) 10:790–795,
1985.
6. Peterson WW, Manske PR, Bollinger BA, et al: Effect of pulley
excision on flexor tendon biomechanics, J Orthop Res 4:96–
101, 1986.
7. Peterson WW, Manske PR, Kain CC, et al: Effect of flexor
sheath integrity on tendon gliding: A biomechanical and his-
tologic study, J Orthop Res 4:458–465, 1986.
8. Saldana MJ, Ho PK, Lichtman DM, et al: Flexor tendon repair
and rehabilitation in zone II open sheath technique versus
closed sheath technique, J Hand Surg (Am) 12:1110–1114,
1987.
9. Manske PR: Flexor tendon healing, J Hand Surg (Br) 13:237–
245, 1988.
10. Tang JB, Ishii S, Usui M: Surgical management of the tendon
sheath at different repair stages. Biomechanical and morpho-
logical evaluations of direct sheath closure, partial sheath
excision, and interposing sheath grafting, Chin Med J (Engl)
103:295–303, 1990.
11. Gelberman RH, Woo SL, Amiel D, et al: Influences of flexor
sheath continuity and early motion on tendon healing in
dogs, J Hand Surg (Am) 15:69–77, 1990.
12. Savage R: The mechanical effect of partial resection of the
digital fibrous flexor sheath, J Hand Surg (Br) 15:435–442,
1990.
13. Tang JB, Ishii S, Usui M, et al: Flexor sheath closure during
delayed primary tendon repair, J Hand Surg (Am) 19:636–
640, 1994.
14. Tang JB: The double sheath system and tendon gliding in
zone 2C, J Hand Surg (Br) 20:281–285, 1995.
15. Tang JB, Shi D, Zhang QG: Biomechanical and histologic
evaluation of tendon sheath management, J Hand Surg (Am)
21:900–908, 1996.
16. Kwai Ben I, Elliot D: “Venting” or partial lateral release of the
A2 and A4 pulleys after repair of zone 2 flexor tendon inju-
ries, J Hand Surg (Br) 23:649–654, 1998.
17. Tang JB, Shi D, Shen SQ, et al: An investigation of morphol-
ogy and function of flexor tendons in zone IIc in the hand
and treatment of flexor tendons, Chin J Surg (in Chinese)
37:639, 1999.
18. Mitsionis G, Bastidas JA, Grewal R, et al: Feasibility of partial
A2 and A4 pulley excision: Effect on finger flexor tendon
biomechanics, J Hand Surg (Am) 24:310–314, 1999.
19. Tomaino M, Mitsionis G, Basitidas J, et al: The effect of partial
excision of the A2 and A4 pulleys on the biomechanics of
finger flexion, J Hand Surg (Br) 23:50–52, 1998.
97
insufficiently released and the procedures made ineffec-
tive, (2) the entire A2 pulley could be released, cutting
a series of annular pulleys, or (3) a lengthy segment of
injured sheath is left unattended, resulting in significant
loss of finger function.
20. Tang JB, Xie RG: Effect of A3 pulley and adjacent sheath
integrity on tendon excursion and bowstringing, J Hand Surg
(Am) 26:855–861, 2001.
21. Elliot D: Primary flexor tendon repair: Operative repair,
pulley management and rehabilitation, J Hand Surg (Br)
27:507–513, 2002.
22. Paillard PJ, Amadio PC, Zhao C, et al: Pulley plasty versus
resection of one slip of the flexor digitorum superficialis after
repair of both flexor tendons in zone II: A biomechanical
study, J Bone Joint Surg (Am) 84:2039–2045, 2002.
23. Tang JB, Wang YH, Gu YT, et al: Effect of pulley integrity
on excursion and work of flexion in healing flexor tendons,
J Hand Surg (Am) 26:347–353, 2001.
24. Xu Y, Tang JB: Effects of superficialis tendon repairs on lacer-
ated profundus tendons within or proximal to the A2 pulley:
An in vivo study in chickens, J Hand Surg (Am) 28:994–1001,
2003.
25. Tang JB, Xie RG, Cao Y, et al: A2 pulley incision or one slip
of the superficialis improves flexor tendon repairs, Clin Orthop
Relat Res 456:121–127, 2007.
26. Tanaka T, Amadio PC, Zhao C, et al: The effect of partial A2
pulley excision on gliding resistance and pulley strength in
vitro, J Hand Surg (Am) 29:877–883, 2004.
27. Tang JB: Indications, methods, postoperative motion and
outcome evaluation of primary flexor tendon repairs in Zone
2, J Hand Surg (Eur) 32:118–129, 2007.
28. Tang JB, Cao Y, Wu YF, et al: Effect of A2 pulley release on
repaired tendon gliding resistance and rupture in a chicken
model, J Hand Surg (Am) 34:1080–1087, 2009.
29. Cao Y, Tang JB: Strength of tendon repair decreases in the
presence of an intact A2 pulley: Biomechanical study in a
chicken model, J Hand Surg (Am) 34:1763–1770, 2009.
30. Tang JB, Zhang QG, Ishii S: Autogenous free sheath grafts in
reconstruction of injured digital flexor tendon sheath at the
delayed primary stage, J Hand Surg (Br) 18:31–32, 1993.
31. Bakhach J, Sentucq-Rigal J, Mouton P, et al: The Omega
“Omega” pulley plasty. A new technique to increase the diam-
eter of the annular flexor digital pulleys, Ann Chir Plast Esthet
50:705–714, 2005.
32. Bunata RE, Kosmopoulos V, Simmons S, et al: Primary
Tendon sheath enlargement and reconstruction in zone 2: An
in vitro biomechanical study on tendon gliding resistance,
J Hand Surg (Am) 34:1436–1443, 2009.
33. Bunata RE: Primary pulley enlargement in zone 2 by incision
and repair with an extensor retinaculum graft, J Hand Surg
(Am) 35:785–790, 2010.
34. Al-Qattan MM, Al-Turaiki TM: Flexor tendon repair in zone
2 using a six-strand “figure of eight” suture, J Hand Surg (Eur)
34:322–328, 2009.
35. Giesen T, Sirotakova M, Copsey AJ, et al: Flexor pollicis
longus primary repair: Further experience with the Tang tech-
nique and controlled active mobilisation, J Hand Surg (Eur)
34:758–761, 2009.
36. Tang JB: Clinical outcomes associated with flexor tendon
repair, Hand Clin 21:199-210, 2005.
37. Amadio P, An KN, Ejeskar A, et al: IFSSH Flexor Tendon Com-
mittee report, J Hand Surg (Br) 30:100–116, 2005.
 CHAPTER
10  
VENTING OF THE MAJOR
PULLEYS
David Elliot, MA, FRCS, BM, BCh
OUTLINE
Review of the history of the management of the flexor
tendon sheath over the last half century is necessary
to understanding why venting the pulleys has met
with such resistance among hand surgeons. The
author’s clinical research illustrating why venting of
the A2 and A4 pulleys is necessary in clinical practice
is then described. This is followed by review of other
subsequent research supporting the practice of venting
these pulleys as a necessary surgical activity to ensure
safe rehabilitation of primary repairs of the digital
flexor tendons.
To repair flexor tendon injuries in zones 1 and 2, it is
inevitable that the tendon sheath be opened for access.
Over the past 40 years, treatment of the sheath on
completion of the tendon repair(s) appears to have
been determined partly on theoretical grounds and
partly by interpretation of the tendon healing research
at the time.
HISTORY
After primary repair, the subsequent discrepancy
between the external diameter of flexor tendons and the
internal diameter of the tendon sheath was first dis-
cussed by Mason in 1940.1 He pointed out the impor-
tance of excision of the sheath adjacent to the primary
repair and over a sufficient length to allow free gliding
of the repair. In 1958, Verdan2 again highlighted this
point, stating that “the sheath is excised over a distance
of about two to three centimeters, the amount of the
sheath to be resected was determined by estimating the
physiological gliding amplitude at this level.” Ketchum,3
in 1977, also mentioned the need to excise a portion of
the sheath. Although these authors were writing when
it was assumed that adhesion formation between the
tendons and the subcutaneous fat was necessary to
achieve repair of the sutured tendon, a secondary need
for adequate sheath excision to allow free movement of
the repair is clear.
98
Following identification of a synovial means of nutri-
tion and repair of injured flexor tendons, complete
repair of the flexor tendon sheath was advocated both
to reestablish the synovial environment of the tendon
and to diminish formation of adhesions, no longer
believed to be necessary for tendon healing and recog-
nized to be a hindrance to movement.1,4-8 The method-
ology of complete closure of the sheath following
primary tendon repair was elaborated by Lister.9 The
zeal to completely close the flexor sheath waned in the
1980s and 1990s from a lack of supportive evidence that
this is either necessary or beneficial.10-16
Various authors at this time pointed out again that
repaired, and thereby thickened, flexor tendons might
not move freely in the closed tendon sheath, because of
the increased diameter of the repaired tendon and/or
narrowing of the sheath by the process of closing it.1,16-22
The problems identified after complete closure of the
sheath were (1) complete immobility of the repair and
(2) (more likely) snagging of the repair on the edges of
adjacent pulleys during tendon movement. Such an
impediment to full mobility might be expected to cause
either a loss of range of motion of the digit or a rupture
of the repair during early postoperative mobilization,
depending on the vigor with which the hand was reha-
bilitated. It was suggested that it might be necessary to
partially release or “vent” the sheath laterally to achieve
a free-running repair.1,17,21 Strickland (1986) described
and illustrated the technique of lateral “venting” pulleys
but thought that this was only necessary when a particu-
lar bulky repair came to lie adjacent to a pulley, which
restricted its full excursion.21 In most instances, he con-
sidered that complete sheath closure without this
maneuver was possible. Schneider (1985) wrote that
“excising a portion of the sheath in badly damaged cases
may be required to allow free mobility of the tendon
juncture” and also admitted having been forced to
remove the A4 pulley on rare occasions with delayed
repairs.23 There has been no work done since Strickland
(1986) to identify any useful difference between split-
ting the pulleys laterally and in the midline.

Throughout all of these reports, there was a palpable
reluctance to condone such venting of pulleys as, in
practice, this would usually entail partial division of the
A2 or the A4 pulleys, the complete integrity of which
was believed to be of great importance in maintaining
the mechanical efficiency of the flexor system.13,24-27
Toward the end of this period, and coinciding with the
waning of the enthusiasm for complete closure of the
flexor sheath, Savage (1990) questioned the absolute
need to preserve the A2 and A4 pulleys completely.20
Tomaino and his colleagues subsequently lent support
to Savage’s work.28,29
AUTHOR’S CLINICAL RESEARCH
There was also a degree of imprecision in these reports
as to which pulleys should be vented and by how much
and how often such releases were necessary. With this
background, we designed a prospective study to examine
those zone 2 injuries in which this problem arises most
commonly, namely those occurring between the proxi-
mal end of zone 1 and the distal edge of the A2 pulley,
designated zones 2A and 2B by Tang (1994)30 in his
proposed subdivision of the original zone 2 described
by Verdan and Michon (1961)31 and modified to its
present form by Kleinert and Weiland (1979).32 Over a
period of 29 months, 126 consecutive fingers with zone
2A and 2B flexor tendon injuries were repaired as part
of the routine emergency workload of our unit by senior
trainee plastic and orthopedic surgeons, who had been
briefed to vent the A2 or A4 pulley as necessary to
achieve sound tendon repairs and to allow the repaired
tendons to move passively through their full excursion
before closing the finger.33 Whenever possible, tendon
repair was carried out through the wound of the tendon
sheath with only sufficient further opening of the sheath
as necessary to allow tendon suture. In zones 2A and
2B, this usually requires release of part of the A3 pulley,
either distal, proximal, or both distal and proximal to
the initial wound. As the A3 pulley and the adjacent C
pulleys were not then considered essential to the pres-
ervation of full flexor mechanical function, particular
efforts to preserve this part of the tendon sheath were
not made and its fate was not recorded. When tendons
were injured close to, or under the A4 pulley, extension
of the tendon sheath wound to allow placement of the
intratendinous core suture often required some degree
of venting of the A4 pulley. A tendon injury adjacent to
the distal edge of the A2 pulley does not usually require
venting of the distal A2 pulley for repair as the tendons
can be drawn out distal to the pulley to undertake the
repair(s). In those fingers that were cut in partial flexion,
the tendon injury was identified more distally when the
finger was in the extended position necessary for surgi-
cal repair and was reached either by extending the
primary opening or, more commonly, through a sepa-
rate window of the sheath more distally. Fingers injured
Chapter 10:  Venting of the Major Pulleys 99
in flexion in zones 2A and 2B are those in which the
repairs of the flexor digitorum profundus (FDP) tendon
are likely to impinge on the proximal edge of the A4
pulley on finger extension. In fingers injured in exten-
sion, the tendon injury lies immediately beneath the
laceration of the sheath. These repairs are liable to
impinge on the distal edge of the A2 pulley on flexion
of the finger. After completion of each repair, the finger
was moved passively through a full range of motion and
the repair observed for catching on the proximal edge
of the A4 or distal edge of the A2 pulley. When catching
occurred, the appropriate pulley was vented along one
edge for as much of its length as was necessary to allow
a full and unimpeded range of motion of the repair. The
degree to which the A4 pulley had been vented was
expressed as a percentage of the total length of the
pulley. Venting of the distal edge of the A2 pulley was
measured and expressed in millimeters as expressing
this as a percentage of the whole of the A2 pulley would
have involved unnecessary opening of the base of the
finger and palm of the hand to measure the full length
of the A2 pulley. After venting of the pulleys, and achiev-
ing free movement through the full range of motion of
the finger, the sheath was laid over the flexor tendons,
hemostasis was achieved, and the skin of the finger was
closed. The fingers were then mobilized using the variant
of the controlled (early) active motion regimen we rou-
tinely use and have described previously.34
Of the 126 consecutive zone 2A and 2B injuries with
at least one tendon completely divided, 85 (67%) were
cut in flexion and 40 (32%) were cut in extension. The
position of the injury was not specified clearly in one
finger (1%). In eight cases (6%), the record of the find-
ings at surgery was unclear. A variable degree of venting
of the pulleys was necessary. In general, the length of
the pulleys is proportional to the length of the digit.35
The average length of the A2 pulley is between 18 and
20 mm.26,36 In this study, the A2 pulley was vented dis-
tally for between 4 and 10 mm, which represents 20%
to 50% of its average length. The degree of venting of
the A4 pulley ranged from 10% to 100% of its length
with a mean of 52%. In 14 cases, the A4 pulley had to
be completely divided. In all of these cases, the site of
division of the FDP tendon was in zone 2A close to, or
under, the A4 pulley. In all 14 cases, the surgeon par-
tially vented the A4 pulley and the assistant flexed the
distal interphalangeal (DIP) joint while holding the
proximal interphalangeal (PIP) joint straight to deliver
the distal stump from under the remainder of the A4
pulley and allow insertion of the core suture. In some
cases, complete division of the pulley was necessary to
insert the core suture into the distal end of the tendon.
In some, it was only necessary to partially vent the
pulley for access but the repaired tendon then impinged
on the distal remnant of the pulley on full finger exten-
sion and it was necessary to complete the division of
100 Section 2:  Primary Flexor Tendon Surgery
A B
the pulley to allow full mobility. In many instances,
repair of the FDP tendon at this level can be achieved
while leaving a small distal part of the pulley, with the
repair then moving through a full range of motion
without impinging on this remnant. It is questionable
whether pulley remnants of less than 10% to 20% of the
original length will continue to function adequately as
a pulley and do not snap during early mobilization. In
one case in this study, and in one subsequent case, the
FDP division was beyond the A4 pulley when the finger
was fully extended (Figure 10-1), requiring pulley
venting from distal to proximal to allow full passive
mobilization of the repair.
It was noted during the study that the length of the
flexor digitorum superficialis (FDP) insertion was vari-
able and that the relationship of the insertion of the FDS
tendon and the A4 pulley was inconstant. In examina-
tion of the latter relationship, we found that the FDS
insertion lay immediately beneath the A4 pulley in 22
cases (73%), whereas the FDS insertion was entirely
proximal to the A4 pulley in eight fingers (27%). Given
that Tang’s zone 2A is defined as the insertion of the
Figure 10-1  A, Division of both flexor tendons in zone
2B of the left ring and little fingers. B, The sheath has
been penetrated at the A3 pulley level. C, The FDP tendon
has been divided distal to the A4 pulley when the finger is
extended.
FDS tendon to the middle phalanx, this helps explain
the need for different degrees of venting of this pulley
and how the FDP division could occasionally be distal
to the A4 pulley. Although the original definition of the
boundary between zone 1 and zone 2 was the distal
edge of the FDS insertion into the middle phalanx,31
there would be benefit in redefining it as the proximal
edge of the A4 pulley. This would both simplify discus-
sion of zone 1 and zone 2 injuries and bring this part
of the classification into line with the definitions of the
more proximal boundaries in the classification, which
are all defined in terms of the pulleys.
In summary, given the brief that two requisites—
good flexor repairs and a full range of motion passively
of all three finger joints after completion of the repairs—
were necessary, our senior fellows (all experienced in
this surgery and the surgeons most likely to carry out
this type of surgery in most specialist hand units) found
it necessary in clinical practice to vent the A2 or the A4
pulley in 81 fingers (64%), either to perform the flexor
tendon repair(s) or to allow the repairs to run freely
without snagging, or for both indications. This study of

A B
routine flexor tendon repairs in zone 2 would suggest
that both the frequency and the degree of venting of
the A2 and A4 pulleys necessary in clinical practice are
greater than the earlier literature would suggest. The
inviolability of the A2 pulley was further undermined
by laboratory studies in chickens by Tang and his col-
leagues, which provided evidence of improved gliding
excursions and reduced resistance to motion of repaired
tendons after partial incision of the A2 pulley.37 Venting
of the A4 pulley, particularly in its entirety, is, arguably,
the more important debate, as the A2 pulley is so long
that it is unlikely that removal of any one-third of it will
cause bowstringing. Whether one vents the A4 pulley as
much as needed to allow full and free passive move-
ment of the repair or leaves the distal part of the A4
pulley intact and accepts a loss of full extension of the
DIP joint is a moot point, and one’s practice in this
respect will depend on how much credence one gives to
the research showing no absolute need for the A2 and
the A4 pulleys to always be completely intact. In this
study, we had hoped to confirm whether the practice of
dividing the A4 pulley entirely is harmful to long-term
flexor tendon function. This was thwarted by 5 of the
14 patients with complete A4 venting choosing to ter-
minate their follow-up before meaningful measure-
ments could be taken.
This study is incomplete in that it did not examine
the function of the fingers after full recovery to deter-
mine whether this policy of pulley venting leads to any
loss of range or power of flexion. From other studies
carried out in our unit during the same period and with
the same policy of pulley venting occurring as the
routine of the unit, it is unlikely that range of motion
was significantly affected. However, alteration of the
mechanical relationship between the tendons and the
Chapter 10:  Venting of the Major Pulleys 101
Figure 10-2  A, Clinical picture of distal
bowstringing of the flexor tendons of the
finger following secondary flexor tendon
surgery in which the C1, A3, and C2 pulleys
were excised for access and the A4 pulley
A4
subsequently snapped during tenolysis of
the distal FDP tendon. B, Diagrammatic
A3 illustration of the removal of the C1, A3, C2,
and A4 pulleys.
A2
skeleton could have given rise to changes in power of
flexion, not measured in our other studies.
DISTAL BOWSTRINGING
Visible distal bowstringing, which is a rare problem,
only occurs when there is a complete absence of the
sheath beyond the A2 pulley (Figure 10-2). This is
mostly an iatrogenic problem resulting from secondary
flexor tendon surgery that should not occur in primary
flexor tendon surgery if we retain all, or most, of the
sheath. In secondary flexor surgery, our entry into the
tendon sheath to visualize the tendons is usually
between the distal edge of the A2 pulley and the proxi-
mal edge of the A4 pulley, and this often leads to exci-
sion of much, or all, of the A3 and the adjoining C
pulleys. Later in the dissection, we find the A4 is often
not only small and very flimsy, but also tightly bound
to the underlying profundus tendon. During the subse-
quent tenolysis, it is too easy to snap the A4, leaving no
pulley system beyond the distal edge of the A2 pulley.
Visible distal bowstringing then occurs. We now rou-
tinely start all secondary surgery by keeping some of the
scarred sheath around the PIP intact as an A3 pulley, in
case we snap the A4 pulley later in the dissection. While
this paragraph digresses into secondary flexor tendon
surgery, it makes the point that we should aim to pre-
serve as much as possible of the sheath between the A2
and A4 pulleys when exploring flexor tendon injuries
distal to the A2 pulley when the finger has been cut in
flexion, whether in a primary or secondary surgical
setting. These observations are supported by the results
from a human cadaveric study by Tang and Xie.38
Although this study found the actual A3 pulley itself to
be of little importance compared with the surrounding
sheath and C pulleys, it did suggest that the sheath
102 Section 2:  Primary Flexor Tendon Surgery
Figure 10-3  The right little finger after primary repair of
both flexor tendons in zone 2B by a middle-grade trainee
with a two-strand Kessler core suture and a Silfverskiöld
circumferential suture. Full DIP joint extension could only be
achieved by venting two-thirds of the A4 pulley.
adjacent to the A3 pulley plays an important role in
preventing tendon bowstringing at the PIP joint.
So, the question remains unanswered as to whether
the clinical practice of venting pulleys has any deleteri-
ous effect on long-term flexor function. Conversely, the
long-term effect of retaining the A4 pulley in its entirety
in respect of loss of DIP extension is unknown but, pos-
sibly, more immediately obvious. The larger core and
circumferential sutures we are now using would seem
likely to lead to greater need for venting pulleys, both for
access and then to allow the repairs to move, as the new
sutures create added bulk at the repair site (Figure 10-3).
Discussion of the acceptability of venting pulleys has
continued into this century. The argument for preser­
vation of all pulleys has been supported indirectly by
two reports following the philosophy of Messina and
Messina39 of accepting the change in diameter of the
repaired tendon as inevitable and attempting to enlarge
References
1. Mason ML: Primary and secondary tendon suture. A discus-
sion of significance in tendon surgery, Surg Gynecol Obstet
70:392–404, 1940.
2. Verdan CE: La reparation immediate des tendons fleuchis-
seurs dans le canal digital, Acta Orthop Belg 24 (suppl III):15–
23, 1958.
3. Ketchum LD: Primary tendon healing: A review, J Hand Surg
2:428–435, 1977.
4. Amadio PC, Hunter JM, Jaeger SH, et al: The effect of vincular
injury on the results of flexor tendon surgery in zone 2,
J Hand Surg (Am) 10:626–632, 1985.
5. Eiken O, Hagberg L, Lundborg G: Evolving biologic concepts
as applied to tendon surgery, Clin Plast Surg 8:1–12, 1981.
6. Lister GD, Kleinert HE, Kutz JE, et al: Primary flexor tendon
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7. Lister GD: Indications and techniques for repair of the flexor
tendon sheath, Hand Clin 1:85–95, 1985.
the relevant pulleys to accommodate the larger
tendon(s).40,41 Most clinicians who have tried to enlarge
pulleys at some period in their career are probably sus-
picious of the ability of the small sutures one has to use
in such repairs to withstand the forces involved in early
active motion, making it seem likely that it is the
remainder of the intact flexor sheath that is actually
functioning to restrain the tendon(s) against the skele-
ton of the finger. This being so, is the pulley reconstruc-
tion actually necessary?
THE SIGNIFICANCE OF PULLEY VENTING
Perhaps more realistic to clinical practice has been the
policy of Tang and his colleagues in China,42 which
takes the writings from this unit33,43 on this subject a
quantum step farther. This team not only describes
exactly what part of the tendon sheath should be, and
can be safely, vented for tendon repairs at different levels
of injury in the finger, including complete division of
the A4 pulley whenever necessary, but also raises the
need for such venting to that of a necessity if we are to
overcome the unpredictability of outcome of primary
flexor tendon repair in zones 1 and 2. In 2007, in a
review of primary flexor tendon surgery, Tang made the
statement, “It is, thus, obvious to me that even a multi-
strand tendon repair should be accompanied by proper
and sufficient release of the critical part or the entire
pulley in the vicinity of the repair, to eliminate the
danger of overloading the tendon as a result of tendon
gliding against the pulley rim or constriction by the nar-
rowest pulley parts.”42 In analyzing the critical points of
primary flexor tendon surgery, Tang considered appro-
priate release of the pulleys as probably most important,
followed by the use of strong repairs to increase the
margin of safety. He considered closure of the synovial
sheath of least importance and repair of the strong
annular pulleys over, or proximal to, edematous tendon
repairs to be positively harmful.
8. Matthews P, Richards H: Factors in the adherence of flexor
tendon after repair, J Bone Joint Surg (Br) 58:230–236, 1976.
9. Lister GD: Incision and closure of the flexor sheath during
primary tendon repair, Hand 15:123–135, 1983.
10. Chow JA, Thomes LJ, Dovelle S, et al: A combined regimen
of controlled motion following flexor tendon repair in “no
man’s land,” Plast Reconstr Surg 79:447–455, 1987.
11. Gelberman RH, Woo SLY, Amiel D, et al: Influences of flexor
sheath continuity and early motion on tendon healing in
dogs, J Hand Surg (Am) 15:69–77, 1990.
12. Lister GD, Tonkin M: The results of primary flexor tendon
repair, J Hand Surg (Am) 11:767, 1986.
13. Peterson WW, Manske PR, Kain CC, et al: Effect of flexor
tendon sheath integrity on tendon gliding: A biomechanical
and histological study, J Orthop Res 4:458–465, 1986.
14. Peterson WW, Manske PR, Lesker PA: The effect of flexor
sheath integrity on nutrient uptake by primate flexor tendons,
J Hand Surg (Am) 11:413–416, 1986.

15. Saldana MJ, Ho PK, Lichtman DM, et al: Flexor tendon repair
and rehabilitation in zone II: Open sheath technique versus
closed sheath technique, J Hand Surg (Am) 12:1110–1114,
1987.
16. Tang JB, Ishii S, Usui M, et al: Flexor sheath closure during
delayed primary tendon repair, J Hand Surg (Am) 19:636–
640, 1994.
17. Duran RJ, Houser RG: Controlled passive motion following
flexor tendon repair in zones 2 and 3. In AAOS Symposium
on Tendon Surgery in the Hand, St Louis, 1975, Mosby, pp
105–114.
18. Manske PR: Flexor tendon healing, J Hand Surg (Br) 13:237–
245, 1988.
19. Peterson WW, Manske PR, Dunlap J, et al: Effect of various
methods of restoring flexor sheath integrity on the formation
of adhesions after tendon injury, J Hand Surg (Am) 15:48–56,
1990.
20. Savage R: The mechanical effect of partial resection of the
digital fibrous flexor sheath, J Hand Surg (Br) 15:435–442,
1990.
21. Strickland JW: Flexor tendon injuries. Part 2: Flexor tendon
repair, Orthop Rev 15:701–721, 1986.
22. Tang JB, Shi D, Zhang QG: Biomechanical and histological
evaluation of tendon sheath management, J Hand Surg (Am)
21:900–908, 1996.
23. Schneider LH: Flexor Tendon Injuries, Boston, 1985, Little,
Brown, pp 47–75.
24. Barton NJ: Experimental study of optimal location of flexor
tendon pulleys, Plast Reconstr Surg 43:125–129, 1969.
25. Doyle JR: Palmar and digital flexor tendon pulleys, Clin
Orthop Relat Res 383:84–96, 2001.
26. Doyle JR , Blythe W: The finger flexor tendon sheath and
pulleys; anatomy and reconstruction. In AAOS Symposium on
Tendon Surgery in the Hand, St Louis, 1975, Mosby, pp 81–88.
27. Rispler D, Greenwald D, Shumway S, et al: Efficiency of the
flexor tendon pulley system in human cadaver hands, J Hand
Surg (Am) 21:444–450, 1996.
28. Mitsionis G, Fischer KJ, Bastidas JA, et al: Feasibility of partial
A2 and A4 pulley excision: Residual pulley strength, J Hand
Surg (Br) 25:90–94, 2000.
29. Tomaino M, Mitsionis G, Basitidas J, et al: The effect of partial
excision of the A2 and A4 pulleys on the biomechanics of
finger flexion, J Hand Surg (Br) 23:50–52, 1998.
Chapter 10:  Venting of the Major Pulleys 103
30. Tang JB: Flexor tendon repair in zone 2C, J Hand Surg (Br)
19:72–75, 1994.
31. Verdan CE, Michon J: Le traitement des plaies des tendons
flechisseurs des doigts, Rev Chir Orthop et Repar l’App Mot
47:290–296, 1961.
32. Kleinert HE, Weiland AJ: Primary repair of flexor tendon
lacerations in zone II. In Tendon Surgery of the Hand, Verdan
C, editor, Edinburgh/London/New York, 1979, Churchill
Livingstone, pp 71–75.
33. Kwai-Ben I, Elliot D: “Venting” or partial lateral release of the
A2 and A4 pulleys after repair of zone 2 flexor tendon inju-
ries, J Hand Surg (Br) 23:649- 654, 1998.
34. Elliot D, Moiemen NS, Flemming AF, et al: The rupture
rate of acute flexor tendon repairs mobilised by the con-
trolled active motion regimen, J Hand Surg (Br) 19:607–612,
1994.
35. Idler RS: Anatomy and biomechanics of the digital flexor
tendons, Hand Clin 1:3–11, 1985.
36. Zancolli EA, Cozzi EP: Atlas of Surgical Anatomy of the Hand,
New York, 1992, Churchill Livingstone, pp 327–345.
37. Tang JB, Wang YH, Gu YT, et al: Effect of pulley integrity on
excursions and work of flexion in healing flexor tendons,
J Hand Surg (Am) 26:347–353, 2001.
38. Tang JB, Xie RG: Effect of A3 pulley and adjacent sheath
integrity on tendon excursion and bowstringing, J Hand Surg
(Am) 26:855–861, 2001.
39. Messina A, Messina JC: The direct midlateral approach with
lateral enlargement of the pulley system for repair of flexor
tendons in fingers, J Hand Surg (Br) 21:463–468, 1996.
40. Bunata RE: Primary pulley enlargement in zone 2 by incision
and repair with an extensor retinaculum graft, J Hand Surg
(Am) 35:785–790, 2010.
41. Dona E, Walsh WR: Flexor tendon pulley V-Y plasty: An alter-
native to pulley venting or resection, J Hand Surg (Br) 31:133–
137, 2006.
42. Tang JB: Indications, methods, postoperative motion and
outcome evaluation of primary flexor tendon repairs in Zone
2, J Hand Surg (Eur) 32:118–129, 2007.
43. Elliot D: Primary flexor tendon repair: Operative repair,
pulley management and rehabilitation, J Hand Surg (Br)
27:507–513, 2002.
 CHAPTER
11  
THE OMEGA “Ω” FLEXOR
PULLEY PLASTY
Joseph Bakhach, MD
OUTLINE
In this chapter, we present our methods for the Omega
plasty used to treat A4 and A2 digital flexor pulleys in
primary or delayed primary tendon repair. This proce-
dure expands the inner diameter of the annular pulleys
of the flexor sheath, but anatomically it does not
disturb the integrity of the pulleys. During surgery one
lateral attachment of the annular pulley is entirely
released from the corresponding anterior phalangeal
bony surface. Our clinical series includes 34 Omega
pulley plasties performed in 34 fingers of 27 patients.
In 15 patients, 19 pulley plasties were performed with
primary repair of flexor tendon rupture, while in the
remaining 12 patients, 15 Omega pulley plasties were
done concomitantly with delayed primary tendon
repair. Among the 34 fingers, 7 fingers subsequently
needed tenolysis 3 months after initial surgery. After
7-month mean follow-up, excellent results were seen
in 29 fingers (85%), and good in 5 fingers (15%)
according to Strickland criteria. The advantage of this
subperiosteal surgical release is that it increases pulley
diameter and inner volume, which accommodates
better tendon gliding.
The surgical management of traumatic flexor tendon
injuries, especially in zone 2 (sometimes called “no
man’s land”), has always been a controversial subject.
These injuries in zone 2 are accompanied by injuries to
the digital fibrous sheath. The later the injury is attended
to, the more fibrosis and collapse of the digital sheath
are likely. The methods for repairing the functional
flexor unit (i.e., the finger flexor tendons and their fibro-
osseous sheath) are still evolving, testifying to the ana-
tomical as well as the functional complexity of this
structure.
The conservative camp proposed the concomitant
repair of the digital fibrous tube with the primary suture
of the flexor tendon injuries to restore the sheath integ-
rity and avoid the formation of adhesions.1,2 However,
the failure of the fibrous sheath to heal and, more dra-
matically, the risk of creating a constriction to tendon
104
gliding have led several surgeons to abandon this
approach.3-8
The repair of injured digital flexor tendons, either
primarily or secondarily, is accompanied by an increase
in the diameter of the tendon where sutures are placed,
increasing resistance to movement.9 To avoid this risk,
several authors10-12 prefer to deal with the fibrous sheath
structure and propose a partial or a complete resection
of the A2 or A4 annular pulleys.
Enlarging the digital fibrous sheath by “venting” the
pulley is attractive theoretically.12 However, even if it
does improve the local mechanical conditions around
the tendon repair site, incision into the pulley structures
may decrease digital flexion to a certain degree. Ana-
tomic work has showed that the most remarkable loss
of function is caused by resection of the annular pulleys
A2 and A4.13 We thus began to imagine technical inno-
vations that would resolve this conflict more specifically
without affecting the integrity of the annular pulleys.
The Omega (“Ω”) pulley plasty we describe consists
of releasing one lateral pulley attachment from its cor-
responding lateral phalangeal bony surface. The most
relevant fact is that this technique preserves the ana-
tomical integrity of the pulley and its continuity with
the periosteum and the floor of the digital fibrous
sheath. If one attachment is released, the annular pulley
moves palmarly and rotates transversally, enhancing
its internal space. This procedure may provide better
gliding conditions for repaired flexor tendons. We
named this technique for pulley plasty Omega, or “Ω,”
reflecting the anatomical shape of the annular pulleys
cross-sectionally.
METHODS AND OUTCOMES
Anatomy of the Fibrous Digital
Sheath Tunnel
Though the anatomy of the digital fibrous sheath is
familiar, we review some points that are important for
explaining the Omega (“Ω”) pulley plasty. The pulleys
segmentally distributed along the synovial sheath differ
by their sites of insertion and their plasticity.14 The

annular pulleys A1, A3, and A5 (also called articular
pulleys), are attached to the palmar joint plates of the
metacarpophalangeal (MP), the proximal interphalan-
geal (PIP), and the distal interphalangeal (DIP) joints,
respectively. The lengths of these pulleys change during
digital motion, with an approximate 50% retraction
after full digital flexion,13,15 whereas the A2 and A4
pulleys (bone pulleys) insert on the lateral phalangeal
crests in continuity with the lateral periosteum and with
the floor of the digital fibrous sheath tunnel. The A2
pulley is situated in the middle and proximal part of the
proximal phalanx, and the A4 pulley in the middle third
of the middle phalanx. The lengths of the A2 and A4
pulleys change somewhat (less than 25%) during digital
flexion.
All the relevant biomechanical studies to date agree,
giving functional priority in finger flexion to the A2 and
A4 pulleys.13,16 It is on these two pulleys that the pulley
plasty is performed during tendon repair in zone 2,17
more precisely in zones 2B and 2C.18
Operative Techniques
Pulley plasty during tendon surgery in zone 2 may be
necessary under two circumstances: (1) primary tendon
repair that generates an immediate impingement on or
impediment to the digital fibrous sheath tunnel and (2)
delayed management of injured tendons with a col-
lapsed and retracted digital fibrous sheath over the
injured area.
Omega Plasty of the A4 Pulley
For a description of the operative technique, we con-
sider a case of primary repair of an injured flexor digi-
torum profundus (FDP) tendon in zone 2B with the
finger in an intermediate flexed position. The wound is
cleaned. The digital fibrous sheath is exposed through
classic oblique incisions on both sides of the cutaneous
wound. The collateral neurovascular pedicles are dis-
sected and protected. The second cruciform (C2) pulley
is opened, and the stumps of the tendon are located.
If the finger is in an extended position, the distal
tendon stump is retracted and hidden completely under
the A4 pulley. It is necessary to flex the DIP joint to
expose the tendon and to place the two stumps in the
operative field (Figure 11-1).
The tendon suture is completed with the Kleinert
technique using Prolene 4-0 suture material with an
epitendinous continuous running suture using Prolene
6-0. The suture technique itself is not important, and
different methods can be used. After the reestablish-
ment of tendon continuity, finger extension brings the
sutured part of the tendon under the proximal edge of
the A4 pulley, where a conflict process obstructs the
tendon from sliding beneath the pulley. An A4 expan-
sion pulley plasty becomes necessary to free the tendon
motion.
Chapter 11:  The Omega “Ω” Flexor Pulley Plasty 105
Figure 11-1  A patient with FDP tendon injury in zone 2B
with the finger in an intermediate flexed position. The DIP
joint was passively flexed to bring the distal stump out of
the A4 pulley into the operative field.
The ulnar digital neurovascular bundle is retracted
and the entire ulnar phalangeal bone attachment of the
A4 pulley is exposed. The ulnar periosteum is sharply
incised along the body of the middle phalanx and freed
progressively from dorsal to palmar. The ulnar pulley
attachment is then reached and freed from the ulnar
phalangeal crest until it has been totally liberated
(Figure 11-2).
Despite the total release of the pulley insertion, the
integrity of the fibrous sheath is fully preserved, with
complete continuity between the pulley and the ante-
rior periosteum of the phalanx, which forms the floor
of the digital fibrous tunnel. This release produces a
lengthening of the pulley circumference and conse-
quently an enhancement of its internal diameter. This
induces the rotational movement of the tendon gliding
tunnel, which is the basic rationale of the Omega pulley
plasty.
Then we verify sliding of the tendon passively, par-
ticularly the suture area of the tendon through the proxi-
mal ring of the enlarged A4 pulley, by extending gently
the DIP joint (Figure 11-3). In case of any remaining
resistance, it is necessary to carry out a complementary
release of the periosteum flap until perfect concord
between the pulley volume and the tendon is achieved.
Finally, the expanded pulley is left free and no sutures
are placed to fix the pulleys to other structures. The
digital neurovascular bundle is placed back, and the C2
pulley is left to heal spontaneously.
In case of delayed primary management of an injured
tendon, the retracted and collapsed annular pulley is
expanded using the same plasty technique. Two tendi-
nous stumps are integrated within the expanded pulley.
106 Section 2:  Primary Flexor Tendon Surgery

B
A

D
C
Figure 11-2  A, B, The annular pulley is firmly fixed by two lateral attachments to the anterior crests of the phalanx.
C, D, Releasing one lateral attachment allows a rotational upward movement, increasing the internal diameter of the pulley.
B, D, Demonstrations in a cadaveric finger. Arrows indicate the side of release at the pulley attachment to the phalanx.

A B
Figure 11-3  After the Omega plasty, passive extension of the DIP joint brings the suture area into the proximal edge of the
expanded A4 pulley, confirming free gliding of the tendon. A, Finger semiflexed. B, Finger extended.

Omega Plasty of the A2 Pulley
The same operative technique is applied to the A2
pulley, with some adjustments due to the length of the
A2 pulley, which can be three to four times the length
of the A4 pulley. In our cases, when an A2 pulley plasty
was necessary, the conflict was located at the distal ring
of the A2 pulley. In all such cases, the Omega plasty
started on one side at the distal end of the pulley and
extended proximally. In our cases, the Omega plasties
in the A2 pulley were partial and never exceeded 50%
of the pulley length.
On each side of the expanded pulley, the synovial
sheaths injured during the initial trauma are opened
surgically to expose and repair the tendons, then left to
heal spontaneously. We prefer not to repair these syno-
vial flaps in order to avoid any constricting scar.
Postoperative Care
After surgery, we protected the pulley with an external
ring skin bandage on the middle phalanx for an A4
pulley, or on the proximal phalanx for an A2 pulley, and
adopted either the Kleinert or Duran protocol of post-
operative digital motion.
Outcomes
Between 2005 and 2007, we carried out 34 Omega
pulley plasties (34 fingers) in 27 patients; 20 men and
7 women, with an average age of 34 years.18 There were
11 index, 9 middle, 7 ring, and 7 little fingers. In 15
patients, 19 Omega pulley plasties were performed
immediately after injury together with primary flexor
tendon repairs. In the other 12 patients, 15 Omega
pulley plasties were carried out secondarily in the
delayed primary stage concomitantly with management
of the neglected injured flexor tendons. Among the total
34 plasties, 26 Omega pulley plasties involved the A4
pulleys and 8 involved the A2 pulleys. In 5 fingers, it
was necessary to make a proximal incision on the distal
palmar crease in order to find the retracted FDP tendon.
In 2 fingers the flexor digitorum superficialis (FDS)
tendon was also injured, and in one finger there was a
neck fracture of the proximal phalanx.
It was necessary to perform tenolysis in 4 cases (7
fingers) at the third month postoperatively because of
the persistence of a deficit in the active flexion of the
DIP joint despite the adapted physiotherapy.
The average period of follow-up was 7 months (range,
4 to 9 months) after tendon repairs and pulley plasty.
According to the Strickland classification, “excellent”
results of active motion were achieved in 29 fingers,
whereas the other 5 fingers achieved “good” results.19
DISCUSSION
The volume discrepancy between the repaired flexor
tendon in zone 2 and its digital fibrous sheath has long
been a concern among surgeons.20 This discrepancy,
Chapter 11:  The Omega “Ω” Flexor Pulley Plasty 107
which is obviously the origin of the resistance phenom-
enon during tendon sliding, has prompted a number of
authors to propose sheath excision in order to enlarge
the digital fibrous sheath.21,22 On one side, there is the
conservative stream, which preaches the sealing of the
digital fibrous sheath, opposed by those who advise its
resection. Between those two extreme attitudes, there is
a mixed position.23 It consists in freeing the pulleys as
necessary, thus making it possible to widen the digital
fibrous tube and to permit tendon sliding movement
without resecting the pulleys.
The work of Kwai Ben and Elliot12 is interesting. They
pointed out the frequent discrepancies between the
repaired flexor tendon volume and the diameter of its
digital fibrous tube. In a series of 126 fingers with
tendon injuries in zone 2A and 2B,12 71 fingers (56%)
required venting of the A4 pulley. In 10 fingers (8%) a
partial lateral section of the A2 pulley was performed,
extending 20% to 50% of its length.
This technique of venting the pulley, either partial or
total, practiced to permit the surgical tendon suture or
to facilitate normal sliding of the tendon, has been
accepted by the scientific community. Nevertheless, it
remains unsatisfactory from a biodynamic point of
view, because it eliminates a fundamental structure of
the tendon physiology.
There are numerous clinical situations in which a
conflict arises between the digital fibrous tunnel and its
contents. As far as the tendon rupture is concerned, the
position of the finger (extension or flexion) at the time
of the trauma should be determined. A rupture of the
FDP tendon in zone 2B or 2C with the finger extended
will generate a conflict between the tendon and the
distal ring of the A2 pulley. However, the rupture of the
FDP tendon in zone 2B with the finger in a flexed posi-
tion will bring the distal tendon stump under the A4
pulley and will make it difficult to reach for surgical
repair. The Omega plasty is done on the A4 pulley in
order to ensure the adaptation of the pulley volume to
that of the repaired tendon, avoiding any resistance and
offering normal tendon sliding (Figure 11-4).
In cases of neglected tendon injuries, the trauma to
the digital fibrous sheath and the retraction of the
tendon stump lead to fibrous sheath retraction and
pulley collapse along the gap between tendon ends
(Figure 11-5). This may require an Omega plasty of
the constricted pulley. It must be noted that about
half of our cases concern secondary repair of the rup-
tured tendon. This reveals, even today, ignorance of
tendon pathology on the part of non-specialized hand
surgeons.
After its release, the anatomical architecture of the
digital fibrous sheath (particularly the anatomy of the
A2 and A4 pulleys, with their bony attachments) allows
pulley enlargement and the creation of better condi-
tions for tendon sliding. The unilateral release of the
108 Section 2:  Primary Flexor Tendon Surgery
A B
pulley attachment does not impair its biomechanical
properties; we preserve the continuity of the pulley with
the phalangeal periosteum on one side and the second
pulley-to-bone attachment on the other. After surgery,
tissue healing will restore the continuity of the detached
pulley with the phalangeal crest. We have confirmed the
restoration of normal solidity of this new attachment in
the cases that required secondary tenolysis. Indeed, the
pulleys seemed to have regained their anatomical con-
tinuity and normal solidity, which was tested in the
presence of tendon motion during surgery of tenolysis.
Past investigations indicate that during digital flexion,
the pulleys are subject to stress from the flexor
tendons.13,24 Nevertheless, the threshold of tendon
rupture is far from being reached; that would require 7
times as much stress as occurs during digital grasp.25
Moreover, Mitsionis et al26 showed that the section of
half of the A2 or A4 pulley does not alter any bio­
mechanical properties, while Tang27 has recorded a
Figure 11-4  Rupture of the FDP tendon in zone 2B with
the left index finger in a flexed position. A, B, An Omega
plasty is performed on the total length of the medial A4
pulley attachment, allowing normal gliding of the repaired
tendon through the expanded pulley during surgery.  
C, Complete recovery to normal flexion of the index finger
after surgery.
decrease of 9% simulated active range of digital motion
after total section of the A2 pulley, and Savage28 assures
us that the A2 or A4 pulley can be removed, provided
the remaining digital fibrous sheath remains intact.
According to these previous reports, we believe the
Omega pulley plasty creates no risk of pulley rupture
and does not generate significant disturbance in tendon
biomechanics.
We maintain that preserving the anatomical integrity
of the pulley and one of its two attachments is sufficient
to maintain biomechanical properties. Intraoperative
observations of the expanded A2 and A4 pulleys show
that the newly healed bone insertion is sufficiently solid
to maintain the deep flexor tendon on its axis during
digital flexion.
The technique of pulley expansion that we describe
here completely preserves pulley integrity. It respects the
internal surface of the pulley and does not increase the
risk of tendon adhesions. After this procedure, it is not

* ample sliding of the tendon repair site inside the
A A4 pulley.
B release of the pulley from one side of its bony attach-
Figure 11-5  Delayed primary repair of a FDP tendon
injury in a left ring finger. A, Collapse of the A4 pulley
(indicated by an asterisk) over a tendon gap. The end of the
proximal tendon is indicated by an arrow. B, Recovery of
the finger motion after pulley plasty performed on its one
attachment to the phalanx to increase pulley volume and
tendon gliding.
References
1. Lister GD: Incision and closure of the flexor tendon sheath
during primary tendon repair, Hand 15:123–135, 1983.
2. Lister GD, Tonkin M: The results of primary flexor tendon
repair with closure of the tendon sheath, J Hand Surg (Am)
11:767, 1986.
3. Amadio P, Hunter JM, Jaeger SH, et al: The effect of vincular
injury on the results of flexor tendon surgery in zone 2,
J Hand Surg (Am) 10:626–632, 1985.
4. Lister GD: Indications and techniques for repair of the flexor
tendon sheath, Hand Clin 1:85–95, 1983.
5. Eiken O, Hagberg L, Lundborg G: Evolving biologic concepts
as applied to tendon surgery, Clin Plast Surg 8:1–12, 1981.
Chapter 11:  The Omega “Ω” Flexor Pulley Plasty 109
necessary to specifically modify protocols for postopera-
tive rehabilitation that we use.29,30 The only necessary
precaution is to protect the pulley plasty with an exter-
nal ring skin bandage.
Our experience indicates that the extent of pulley
release must be carefully considered. We accomplished
the release gradually with intraoperative assessment of
expanded pulley. In our series, all Omega plasties on the
A2 pulley required a partial release not exceeding 50%
of the pulley’s attachment length, while the Omega
plasties of the A4 pulley required a complete release in
60% of our cases. In the remaining 40%, the release did
not extend more than the two thirds the length of the
Approximately 20% of operated fingers required
tenolysis by postoperative month 3 because of a persis-
tent loss of active flexion of the DIP joint. Presumably,
the loss of DIP joint motion was associated with the use
of Kleinert protocols. Rehabilitation began the day after
tendon release, and recovery of complete digital flexion
was obtained, on average, by the third month after the
tenolysis. These tendon adhesions varied depending on
the extent of the initial finger trauma and were gener-
ated by the healing processes around the repaired
tendon. In no cases could these adhesions be correlated
to the Omega pulley plasty itself.
SUMMARY
The Omega plasty of the fibro-osseous annular pulleys
(A2 or A4) is a simple and reliable procedure. The
ment increases the spatial volume within the pulley and
accommodates greater motion of the repaired tendon.
This procedure may create favorable conditions for
recovery of tendon gliding and active digital flexion.
Tendon injuries are frequently accompanied by conflicts
and resistance to tendon gliding produced by the
annular pulleys. We are confident of the safety and
utility of this new technique, which may be considered
in primary, delayed, or secondary repairs of the flexor
tendons in zone 2.
6. Saldana MJ, Ho PK, Lichtman DM, et al: Flexor tendon repair
and rehabilitation in zone II: open sheath technique versus
closed sheath technique, J Hand Surg (Am) 12:1110–1114,
1987.
7. Tang JB, Ishii S, Usui M, et al: Flexor sheath closure during
delayed primary tendon repair, J Hand Surg (Am) 19:636–
640, 1994.
8. Tang JB, Shi D, Zhang QG: Biomechanical and histologic
evaluation of tendon sheath management, J Hand Surg (Am)
21:900–908, 1996.
9. Manske PR: Flexor tendon healing, J Hand Surg (Br) 13:237–
245, 1988.
110 Section 2:  Primary Flexor Tendon Surgery
10. Peterson WW, Manske PR, Dunlap J, et al: Effect of various
methods of restoring sheath integrity on the formation of
adhesions after tendon injury, J Hand Surg (Am) 15:48–56,
1990.
11. Tomaino M, Mitsionis G, Basitidas J, et al: The effect of partial
excision of the A2 and A4 pulleys on the biomechanics of
finger flexion, J Hand Surg (Br) 23:50–52, 1998.
12. Kwai BI, Elliot D: “Venting” or partial lateral release of the A2
and A4 pulleys after repair of zone 2 flexor tendon injuries,
J Hand Surg (Br) 23:649–654, 1998.
13. Lin GT, Amadio PC, An KN, et al: Functionnal anatomy of
the human digital flexor pulley system, J Hand Surg (Am)
14:949–956, 1989.
14. Moutet F: Les poulies de l’appareil fléchisseur: anatomie,
pathologies, traitement, Annales de Chir Main 22:1–12, 2003.
15. Lin GT, Cooney WP, Amadio PC: Mechanical properties of
human pulleys, J Hand Surg (Br) 15:429–434, 1990.
16. Cleveland M: Restoration of the digital portion of a flexor
tendon and sheath in the hand, J Bone Joint Surg 15:762–765,
1933.
17. Verdan CE, Michon J: Le traitement des plaies des tendons
fléchisseurs des doigts, Rev Chir Orthop et Répar 47:290–296,
1961.
18. Tang JB: Flexor tendon repair in zone 2C, J Hand Surg (Br)
19:72–75, 1994.
19. Bakhach J, Mouton P, Panconi B, et al: The Omega pulley
plasty. A new technique to increase the diameter of the
annular flexor digital pulleys, Ann Chir Plast 50:705–714,
2005.
20. Mason ML: Primary and secondary tendon suture. A discus-
sion of the significance of technique in tendon surgery, Surg
Gynecol Obstet 70:392–404, 1940.
21. Ketchum LD: Primary tendon healing: a review, J Hand Surg
2:428–435, 1977.
22. Verdan CE: La réparation immédiate des tendons fléchisseurs
dans le canal digital, Acta Orthop Belg Suppl III 15–23, 1958.
23. Strickland JW: Flexor tendon injuries. Part 2. Flexor tendon
repair, Orthop Rev 15:701–721, 1986.
24. Manske PR, Lesker PA: Strength of human pulley, Hand
9:147–152, 1977.
25. Schuind F, Garcia-Elias M, Cooney WP, et al: Flexor tendon
forces: in vivo measurements, J Hand Surg (Am) 17:291–298,
1992.
26. Mitsionis G, Fischer KJ, Bastidas JA, et al: Feasibility of partial
A2 and A4 pulley excision: residual pulley strength, J Hand
Surg (Br) 25:90–94, 2000.
27. Tang JB: The double sheath system and tendon gliding in
zone 2C, J Hand Surg (Br) 20:281–285, 1995.
28. Savage R: The mechanical effect of partial resection of the
digital fibreous flexor sheath, J Hand Surg (Br) 15:435–442,
1990.
29. Kleinert HE, Kutz JE, Cohen MJ: Primary repair of zone 2
flexor tendon lacerations. In AAOS Symposium on Tendons
Surgery in the Hand. St Louis, 1975, CV Mosby, p 91–104.
30. Duran RJ, Houser RG: Controlled passive motion following
flexor tendon repair in zones two and three. In AAOS Sympo-
sium on Tendons Surgery in the Hand. St Louis, 1975, CV
Mosby, p 105–114.
 CHAPTER
12  
TENDON SHEATH AND PULLEY
ENLARGEMENT
Robert E. Bunata, MD
OUTLINE
This chapter presents the results of clinical experience
and laboratory studies related to the idea of enlarging
and then repairing a major pulley and closing the
sheath at the time of primary flexor tendon repairs.
This procedure is intended to give room for the more
bulky tendon repairs to slide while providing an intact
sheath and pulley system that guides the repair and
prevents bowstringing. The clinical data on a series of
patients and a description of the surgical technique are
presented, and the laboratory studies provide biome-
chanical findings regarding tendon gliding, triggering,
and bowstringing after this procedure. This chapter
deals with an alternate solution to the problem of
getting a bulky flexor tendon repair to glide freely
without triggering while maintaining the adequate
sheath support that is required for efficient finger
flexion. This solution is at odds with the axiom of
keeping as much as possible of the major A2 and A4
pulleys intact, and instead cuts an obstructing pulley,
subsequently repairing it with a slight enlargement.
The history of dealing with this problem started with
the earliest attempts at primary flexor tendon repair and
continues to the present time. When Kleinert and col-
leagues published their successful primary tendon
repairs in zone 2 combined with early motion in 1973,
he initially resected a window of tendon sheath.1 Ten
years later, Lister and coworkers advocated closure of the
tendon sheath following a limited, pulley preserving
tendon exposure.2 In 1983, they advocated complete
closure of the sheath so that catching of the repair on
an edge of sheath would be avoided, and in 1985 Lister
described replacing a deficient sheath with a fascial graft
to accomplish closure.3,4 However, others realized that
tight sheath closure might restrict the free gliding of the
sutured tendons.5,6
This author first used the procedure of pulley enlarge-
ment in 1985 for a patient whose bulky tendon repair
would not glide into or through the A4 pulley. Contrary
to the dictum of A2 and A4 pulley preservation, the
entire A4 pulley was cut. Because of concern that bow-
stringing could result, the A4 pulley was repaired with
a slight enlargement using a fascial graft as Lister recom-
mended for a deficient sheath. This seemed to solve the
problem of providing a nonrestrictive gliding environ-
ment for the repair while adequately restoring impor-
tant sheath support. The result of that surgery was
surprisingly good. Since then this technique has been
applied to either the A2 or A4 pulleys in a total of 12
fingers in 9 patients, which represent the more difficult
patients treated over a 20-year period.7
Since those developments early in the history of
primary repairs of flexor tendons, attention and research
have made tendon repairs stronger to prevent rupture if
subjected to increased resistance. Stronger repairs are
often more bulky and can make gliding even more dif-
ficult and catching more likely. Even the strongest repair
might rupture if an exposed edge of pulley that com-
pletely blocks motion is encountered.8 Venting has
become an accepted method of sheath management,
being a way to preserve enough of the essential pulleys
while improving tendon gliding. Venting allows free
gliding to occur only within the vented area, and the
repair must often reenter a tight, restrictive sheath,
exposing the repair to catching on an edge of sheath or
to traversing an area of resisted gliding.
Other methods that have been suggested to solve the
same problem include removal of one slip of flexor
digitorum superficialis (FDS), pulley enlargement by
V-Y plasty, and pulley release from the underlying
phalanx.7,9-18 Tang and colleagues have shown complete
pulley incision with or without graft repair in chickens
reduces work of flexion even after the effects of time and
healing are included.12,19,20 Tang8,11 and Elliot10 have even
recommended completely cutting the A4 pulley as stan-
dard clinical practice despite the continuing belief that
at least some of the A2 and A4 pulleys are essential to
preventing bowstringing and preserving the efficiency of
finger flexion.
Because of the encouraging results in the clinical
patients, during the past 5 years laboratory investiga-
tions have been conducted to explore how this tech-
nique affects gliding within the enlarged sheath,
triggering, and bowstringing. These are summarized
below along with the surgical technique and the clinical
outcomes.
111
112 Section 2:  Primary Flexor Tendon Surgery
SURGICAL TECHNIQUE
Operative Techniques
The flexor tendon sheath is exposed and examined with
the finger in full extension. Tendon and sheath injuries
are evaluated and the anticipated excursion of the
repaired tendon is identified. If the flexor digitorum
profundus (FDP) lies within the A4 pulley or if both
tendons might have to pass under the A2 pulley, sheath
and pulley enlargement might be needed, and the
sheath, including any part of a pulley, is opened far
enough to provide adequate exposure for easy tendon
repair. The sheath injury is extended distally until, with
the help of distal interphalangeal joint flexion, a core
suture can be placed in the FDP stump. The sheath/
pulley incision is placed lateral to the volar midline,
leaving enough sheath tissue to secure a suture and
adjusting the incision to fit the conditions of the original
injury. The distal FDS is always longer than the FDP and
readily visible with this exposure. The proximal tendons
are retrieved. If needed, the proximal sheath/pulley is
incised far enough to allow room so that an easy tendon
repair can be performed. Both tendons are repaired.
In the series, all tendons or tendon slips were repaired
with a two-strand modified Kessler repair using 3-0
suture. The suture was performed starting in the distal
tendon segment with a 1-cm longitudinal insertion and
a locking loop followed by the transverse pass and a
grasping loop leading back to the tendon end. The iden-
tical pattern was used in the proximal tendon segment.
This allowed easy tensioning until the ends abutted
without bunching and there was no gapping when
placed under manual tension. The triple-throw sur-
geon’s knot was buried inside the repair. All repairs were
reinforced and smoothed with a circumferential
running, alternately locked, 6-0 nylon suture, making
10 to 12 passes around each tendon and 6 to 8 passes
around each tendon slip. The 6-0 suture was tied with
one triple-throw square knot on the external lateral
tendon surface. A stronger repair can be substituted if
preferred.
Once the tendons are sutured, the excursion of the
repairs is checked by passively extending the finger and
by pulling on the tendons through a palm incision to
flex the finger. If any intact sheath or pulley tissue
restricts the full excursion of the repair pulley, enlarge-
ment may be indicated and the sheath/pulley incisions
are extended even if this means completely incising an
entire major pulley. If an entire A2 or A4 pulley is cut,
the entire sheath is repaired and closed with an extensor
retinaculum graft in an attempt to reestablish the incised
major pulley in order to limit bowstringing and guide
the tendons into the sheath without snagging.
The graft is obtained through a transverse skin inci-
sion on the dorsum of the wrist extending from the
second to the sixth compartments of the distal extensor
retinaculum. A transverse ellipse of extensor retinacu-
lum 5 mm wide × 30 mm long is removed. Any septal
remnants are excised and any defects repaired to present
a smooth, synovial lined graft. The 5-mm gap in the
donor site retinaculum is closed side-to-side with
absorbable, interrupted sutures, and the wrist skin inci-
sion with subcuticular absorbable suture. The elliptical
graft is trimmed to fit to the retinacular sheath and
pulley defect of the finger and sutured in place, synovial
side toward the tendon repairs, with a running horizon-
tal mattress, alternately locked, 6-0 nylon suture under
enough tension to support but not restrict the gliding
of the tendons. This usually requires a 2 mm enlarge-
ment and the graft requires about 20 suture passes per
side for closure. Additional injuries or lacerations in the
tendon sheath are closed with everting, interrupted 6-0
sutures.
Clinical Outcomes
Seven of the nine patient were followed to an adequate
follow-up ranging from 3 months to 11 years.7 All seven
patients (nine digits) were treated as primary flexor
tendon repairs in zone 2 preferably with the surgery
delayed 2 or 3 days to be confident that the wound was
not contaminated. All were managed postoperatively
with Kleinert’s original rehabilitation protocol, which
was begun immediately following surgery in the recov-
ery room. The final total active interphalangeal joint
motion of the nine digits averaged 127.5° of a possible
maximum of 175° (Table 12-1). The final range of
motion ranged from 65° to 175°. The scores according
to the Strickland-Glogovac system were three excellent,
two good, two fair, and two poor.21 There were no
tendon ruptures despite the use of a two-strand core
repair. Two fingers in one patient required a tenolysis,
and one finger in another patient had a secondary skin
scar lengthening. These secondary operations improved
finger motion. Only three of the nine digits attained full
PIP joint extension, with the average lack of extension
(flexion contracture) for the nine fingers being 21°.
While the Kleinert rehabilitation protocol has been
associated with developing flexion contractures, they
may be the result of bowstringing if the grafts stretched
with time and/or use.7 One finger, the right ring finger
of patient 3, had visible and palpable bowstringing
when seen at follow-up post tenolysis. Another finger,
the right little finger of patient 4, had clinical evidence
of bowstringing at follow-up.
The two patients with bowstringing merit comment.
The sheath repair of right little finger of patient 4 may
have been too loose because even a limited enlargement
of the small fifth digit sheath can be disproportionately
large. The right ring finger of patient 3 had no evidence
of bowstringing at 6 months, immediately before a
tenolysis to improve flexion was performed. When seen
18 years later, this finger had midline skin callous
 Chapter 12:  Tendon Sheath and Pulley Enlargement 113

Table 12-1  Patient Information About Injuries, Operations, and Follow-Up

Age(y)/ Digit(s) Tendon(s) Pulleys PIP Joint DIP Joint
Patients Gender Injured Repaired Incised Follow-Up Motion Motion TAM Grade
1 54/M L middle FDP/FDS Mid-A2, A3, A4 11 yr 30/105 0/85 160 Excellent
2 18/M R little FDP/FDS Mid-A2, A3, A4 2 yr 45/90 0/90 135 Good
3 21/M R ring FDP A3, A4 6 mo 0/90 20/34 105 Fair*
R little FDP A3, A4 30/90 25/40 75 Poor
4 17/M R ring FDP/FDS Mid-A2, A3, A4 5.5 yr 15/100 15/50 120 Fair
R little FDP/FDS Mid-A2, A3, A4 50/90 20/45 65 Poor**
5 20/M R middle FDP/FDS A2, A3 3 mo 0/100 0/65 165 Excellent
6 45/F L ring FDP/FDS A2, A3 1.5 yr 20/95 0/70 145 Good
7 15/M R index FDP/FDS Mid-A1, A2, A3 3 yr 0/115 0/60 175 Excellent
M, Male; F, Female; R, Right; L, Left. Graded by Strickland-Glogovac method.21
*Finger without clinical observable tendon bowstringing 6 months after tendon repair before tenolysis, but had clinically observable
bowstringing when examined 18 years after tenolysis.
**Finger with clinically observable bowstringing after primary surgery.

formation directly over underlying flexor tendons which
were distinctly prominent during gripping. The PIP joint
had complete extension and 95° flexion; the DIP joint
motion was 30/65°. Possible explanations for this may
be: (1) there was bowstringing present at 6 months that
was not detected, (2) the sheath function was damaged
during the tenolysis, or (3) the graft stretched from
heavy use over the following 18 years.
BIOMECHANICAL STUDIES
Uchiyama and colleagues’ method of testing resistance
of an isolated segment of the tendon/tendon sheath
provides the opportunity of observing and testing the
effects of sheath enlargement and repair on gliding resis-
tance and triggering.22 Using a tensioning force (F1)
through a load cell attached to the distal FDP and an
activating force (F2) through a proximal load cell, force
recordings as seen in Figure 12-1A, are obtained. The
difference in force between the load cells is the gliding
resistance (the friction between the tendon and the
sheath).
Gliding resistance measurements in our laboratory
for the normal, uninjured A1 through A3 segment has
averaged about 0.4 N (see red line in Figure 12-1A).
After the FDP is cut and repaired with a two-strand 3-0
core suture and running, locked 6-0 epitenon suture,
gliding resistance increases to 1.25 to 1.5 N, or by 200%
to 250% (see blue line in Figure 12-1A). These values
are similar to what others have found for various tendon
suture techniques.18,23-28 Experiments done in our labo-
ratory revealed that either venting (50% or 66%) or a
2-mm sheath enlargement and repair reduces the resis-
tance to approximately 1.0 N, or by 22% to 31% from
the tendon repair resistance level (see green line in
Figure 12-1A).
Study of the effect of venting and pulley enlargement
on the incidence of triggering in the force recordings
(see Figure 12-1B) revealed that after the bulk of the
tendon was increased by tendon repair, triggering
occurred in some fingers. Venting alone had a variable
effect on the incidence of this triggering, but closing the
sheath with enlargement provided smoother gliding of
the repair and reduced the incidence of triggering.3,29,30
Regarding bowstringing, in a preliminary, unpub-
lished study of nine cadaver fingers, total range of
motion (TROM) in the uninjured state was compared
to the motion after cutting the A4 pulley plus additional
sheath for the distance equal to the FDP excursion, and
then to the motion after that sheath was repaired with
a 2-mm-wide fascial graft. Cutting the sheath reduced
the finger TROM to 93.8% of normal. Repairing the
sheath and pulleys enlarged by 2 mm brought the loss
of TROM to 99.3% of the uninjured state. This suggests
that a 2-mm enlargement may preserve acceptable finger
flexion efficiency. We have not tested how well the
pulley repair holds up under stress and with time. With
more tension on the tendons or with time, the pulley
repair may stretch. This technique of the pulley repair
requires further study to evaluate the need or benefit of
strengthening or reinforcement.
DISCUSSION
Considering the three goals of sheath and pulley man-
agement during primary zone 2 flexor tendon surgery
of providing a good gliding environment, avoiding trig-
gering, and minimizing bowstringing, this experience
with sheath enlargement and repair may offer insight
into future research and clinical practice, especially with
regards to the benefits of a closed sheath. The surgeon
has the option and obligation to reconsider decisions
114 Section 2:  Primary Flexor Tendon Surgery

8 8

F2 tendon repair

7 7

A B

6 F2 sheath 6
enlarged
F2

Uninjured
Force (N)

Force (N)
5 5

F1 F1
C

4 4

3 3

2 2
25 30 35 40 45 50 22 27 32 37
A Time(s) B Time(s)

Figure 12-1  Force recordings generated using Uchiyama et al testing technique. F1 is tensioning force; F2 is activating
force. A, Resistance recordings during tendon gliding in a simulated digital flexion cycle. Red, force recorded without tendon
injuries; blue, force tracing after the FDP tendon has been cut and repaired; green, force tracing after the sheath has been
enlarged. B, An example of the force recordings when triggering occurs. Orange, gliding resistance (F2). An increase (A) in
gliding resistance followed by a sudden drop (B), associated with a disturbance in F1 (purple, C), called an echo, indicate
triggering.

throughout an operation. During primary repair, pulley
and sheath enlargement may be a useful choice to
provide repaired tendon with adequate tendon gliding
amplitude.
Use of the technique of sheath enlargement should
be carefully considered. More basic and clinical investi-
gation is needed before it can be considered an
established procedure. The procedure carries the risks of
increasing the sheath injury, cutting a major pulley,
obtaining a distant graft, and inserting a graft of uncer-
tain strength to repair the cut pulley, but for those
patients in which a strong repair plus venting do not
permit adequate tendon excursion, complete pulley
enlargement may become an option.

References
1. Kleinert HE, Kutz JE, Atasoy E, et al: Primary repair
of flexor tendons, Orthop Clin North Am 4:865–876,
1973.
2. Lister GD, Kleinert HE, Kutz JE, et al: Primary flexor tendon
repair followed by immediate controlled mobilization,
J Hand Surg (Am) 2:441–451, 1977.
3. Lister GD: Incision and closure of the flexor sheath during
primary tendon repair, Hand 15:123–135, 1983.
4. Lister GD: Indications and techniques for repair of the flexor
tendon sheath, Hand Clin 1:85–95, 1985.
5. Manske PR: Flexor tendon healing, J Hand Surg (Br) 13:237–
245, 1988.

6. Strickland JW: Flexor tendon surgery. Part 1: Primary flexor
tendon repair, J Hand Surg (Br) 14:261–272, 1989.
7. Bunata RE: Primary pulley enlargement in zone 2 by incision
and repair with an extensor retinaculum graft, J Hand Surg
(Am) 35:785–790, 2010.
8. Tang JB: Indications, methods, postoperative motion and
outcome evaluation of primary flexor tendon repairs in Zone
2, J Hand Surg (Br) 32:118–129, 2007.
9. Elliot D, Moiemen NS, Flemming AF, et al: The rupture rate
of acute flexor tendon repairs mobilized by the controlled
active motion regimen, J Hand Surg (Br) 19:607–612, 1994.
10. Elliot D: Primary flexor tendon repair: operative repair, pulley
management and rehabilitation, J Hand Surg (Br) 27:507–
513, 2002.
11. Tang JB: Clinical outcomes associated with flexor tendon
repair, Hand Clin 21:199–210, 2005.
12. Tang JB, Xie RG, Cao Y, et al: A2 pulley incision or one slip
of the superficialis improves flexor tendon repairs, Clin Orthop
Relat Res 456:121–127, 2007.
13. Messina A, Messina JC: The direct midlateral approach with
lateral enlargement of the pulley system for repair of flexor
tendons in fingers, J Hand Surg (Br) 21:463–468, 1996.
14. Paillard PJ, Amadio PC, Zhao C, et al: Pulley plasty versus
resection of one slip of the flexor digitorum superficialis after
repair of both flexor tendons in zone II: A biomechanical
study, J Bone Joint Surg (Am) 84:2039–2045, 2002.
15. Zhao C, Amadio PC, Zobitz ME, et al: Resection of the flexor
digitorum superficialis reduces gliding resistance after zone II
flexor digitorum profundus repair in vitro, J Hand Surg (Am)
27:316–321, 2002.
16. Dona E, Walsh WR: Flexor tendon pulley V-Y plasty: An
alternative to pulley venting or resection, J Hand Surg (Br)
31:133–137, 2006.
17. Bunata RE, Kosmopoulos V, Simmons S, et al: Primary tendon
sheath enlargement and reconstruction in zone 2: An in vitro
biomechanical study on tendon gliding resistance, J Hand Surg
(Am) 34:1436–1443, 2009.
18. Tanaka T, Amadio PC, Zhao C, et al: The effect of partial A2
pulley excision on gliding resistance and pulley strength in
vitro, J Hand Surg (Am) 29:877–883, 2004.
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19. Tang JB, Wang YH, Gu YT, et al: Effect of pulley integrity on
excursions and work of flexion in healing flexor tendons,
J Hand Surg (Am) 26:347–353, 2001.
20. Tang JB, Cao Y, Wu YF, et al: Effect of A2 pulley release on
repaired tendon gliding resistance and rupture in a chicken
model, J Hand Surg (Am) 34:1080–1087, 2009.
21. Strickland JW Glogovac SV: Digital function following flexor
tendon repair in zone II: A comparison of immobilization
and controlled passive motion techniques, J Hand Surg (Am)
5:537–543, 1980.
22. Uchiyama S, Coert JH, Berglund L, et al: Method for the
measurement of friction between tendon and pulley, J Orthop
Res 13:83–89, 1995.
23. Tanaka T, Amadio PC, Zhao C, et al: Gliding resistance versus
work of flexion–two methods to assess flexor tendon repair,
J Orthop Res 21:813–818, 2003.
24. Tanaka T, Amadio PC, Zhao C, et al: Gliding characteristics
and gap formation for locking and grasping tendon repairs:
A biomechanical study in a human cadaver model, J Hand
Surg (Am) 29:6–14, 2004.
25. Zhao C, Amadio PC, Zobitz ME, et al: Gliding resistance after
repair of partially lacerated human flexor digitorum profun-
dus tendon in vitro, Clin Biomech 16:696–701, 2001.
26. Zhao C, Amadio PC, Tanaka T, et al: Effect of gap size on
gliding resistance after flexor tendon repair, J Bone Joint Surg
(Am) 86:2482–2488, 2004.
27. Paillard PJ, Amadio PC, Zhao C, et al: Gliding resistance after
FDP and FDS tendon repair in zone II: an in vitro study, Acta
OrthopScand 73:465–470, 2002.
28. Coert JH, Uchiyama S, Amadio PC, et al: Flexor tendon-
pulley interaction after tendon repair. A biomechanical study,
J Hand Surg (Br) 20:573–577, 1995.
29. Amadio P, An KN, Ejeskar A, et al: IFSSH Flexor Tendon Com-
mittee report, J Hand Surg (Br) 30:100–116, 2005.
30. Bunata RE, Simmons S, Roso M, et al: Gliding resistance and
triggering after venting or A2 pulley enlargement: A study
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J Hand Surg (Am) 36:1316–1322, 2011.
 CHAPTER
13  
CLINICAL PRIMARY FLEXOR
TENDON REPAIR AND
REHABILITATION
A The Bern Experience
Esther Vögelin, MD, PhD, Ghislaine
Traber-Hoffmann, MD, and
Véronique van der Zypen, BSC PT
OUTLINE
In this chapter we present our experience with treat-
ment of zone 2 flexor tendon repair using a six-strand
repair technique combined with postoperative place-
and-hold exercise. The six-strand Lim/Tsai repair
technique combined with place-and-hold exercises
demonstrated better digital function compared to a
two-strand repair without place-and-hold exercises.
Range of motion in the Lim/Tsai repair group appeared
to be increased without a higher rate of ruptures but
with a shorter rehabilitation period. The fact that the
two groups differed in both suture techniques and
rehabilitation programs made it impossible to know
whether the better results in the group of Lim/Tsai
were due to the six-strand repair or the place-and-hold
exercises or both. Despite the obvious benefit of early
active mobilization, an active motion protocol may
not always be possible to apply in a substantial number
of patients due to concomitant injuries, the quality of
the surgical repair or patient factors (swelling, pain,
limited compliance). Since August 2006 a staged reha-
bilitation program (“stop and go”) was introduced
within our unit using early active controlled flexion
(green), place-and-hold (yellow), or passive flexion
exercises (red) introduced by Kleinert-Duran. Our
experience using the six-strand suture repair technique
and “stop and go” is outlined.
Functional results after flexor tendon repair in zone 2
have markedly improved over the past three decades.1-4
However, a big dilemma of flexor tendon repair in zone
2 remains the challenge between scar formation and
116
risks of rupturing the repairs. Not only repair techniques
but also postoperative mobilization require a balance
between these two extremes.
The repair that Lim and Tsai advocated5,6 was found
to have the mechanical strength required for unrestricted
active finger flexion in vitro.5,7 We used the Lim/Tsai
repair with an early active tendon motion regimen and/
or place-and-hold exercise between 2003 and 2005. We
noted that despite the need to mobilize repaired flexor
tendons early, an active motion protocol may not be
possible to apply in a substantial number of patients
due to concomitant injuries, the quality of the surgical
repair, or patient factors such as swelling, pain, or lack
of compliance. We therefore started a staged rehabilita-
tion program using the “stop and go” principal in the
style of a traffic signal: early active controlled flexion
(green), place-and-hold (yellow), or passive flexion exer-
cises (red) depending on different factors of the patient
such as the severity of injury, the ease of repair or the
postoperative compliance.
Since August 2006, we have combined the six-strand
Lim/Tsai suture repair with “stop and go” method of
postsurgical rehabilitation in all flexor tendon repairs,
and these methods remain our current practice of treat-
ment of tendon injuries in zone 2.
METHODS AND OUTCOMES
Patients
We reviewed and compared results of three cohorts of
patients with flexor tendons repairs in zone 2 in the
Hand Surgery Department of the University Hospital
of Bern. From 2003 to 2007, a total of 76 patients
 Chapter 13A:  The Bern Experience 117

Table 13(A)-1  Patient Details

Groups Lim and Tsai Method Kessler Method
Core suture method Lim and Tsai (six-strand) Modified Kessler (two-strand)
Postoperative care Kleinert-Duran regimen with place-and-hold Kleinert-Duran regimen
exercises
Patients 46 (8 women, 38 men) 25 (8 women, 17 men)
Age (range) 32 years (13–74 years) 38 years (16–82 years)
Injured hand Dominant 22 10
Nondominant 24 11
Unknown — 4
Injured digits 51 (13, 9, 7, 22)* 26 (6, 7, 6, 7)*
Tendon injuries
  Isolated complete FDP 24 10
  Complete FDP and partial FDS 9 3
  Complete FDP and complete FDS 18 13
Neurovascular damage (digits) 3 13
Therapy delay (range) 0.5 day (0–2 days) 0.3 day (0–1 days)
*The numbers given in the parentheses are in the order of the index, middle, ring, and little fingers.

underwent a six-strand zone 2 flexor tendon repair and
early active motion (51 digits in 46 patients) and “stop
and go” rehabilitation protocols (35 digits in 30
patients).
The results were compared to the results of zone 2
flexor tendon repair with the two-strand modified Kessler
repair combined with a Kleinert-Duran regimen in 25
patients (30 digits) between 1998 and 2002.1 Both
groups included consecutive patients who sustained
sharp and complete flexor digitorum profundus (FDP)
tendon lacerations in zone 2, with or without concomi-
tant flexor digitorum superficialis (FDS) tendon lacera-
tions or neurovascular damage. Injured tendons in these
patients were repaired surgically within 2 days after
trauma and postoperative therapies of the patients were
continued for a minimum of 8 weeks (Table 13[A]-1).
During the follow-up, grip strength (kg) was mea-
sured using a hand-held Jamar Dynamometer (Preston,
Jackson, MI). Total active motion (TAM) of each oper-
ated finger without secondary surgery was recorded. The
flexion of each involved joint was measured first when
the patient attempted to make a complete fist; the exten-
sion deficits were measured afterward. The original
Strickland grading system was used to assess final TAM.8
The functional results were recorded at a mean of 12
weeks postoperatively in both groups (range: Lim/Tsai
repair group, 9 to 17 weeks; Kessler repair group, 8 to
16 weeks). The follow-up period was determined on the
basis of collected data of the Kessler repair group; the
retrospectively collected data of this group provided
exact TAM values up to 12 weeks. After 12 weeks, the
patient files often contained only qualitative statements
without mentioning the degrees of TAM or only giving
the remaining extension deficits.
In case of an extension lag resisting physical therapy,
treatment with an extension splint was started only 5
weeks after surgery. The need for secondary surgery,
occurrence of tendon rupture, dehiscence, contracture
of joints, and the use of extension splints were com-
pared in both groups. A tendon rupture was defined as
a complete gap separation without any detectable
tendon function clinically. When the tendon remained
in continuity due to scar formation and still showed an
impaired function, we defined it as a dehiscence. Their
diagnosis and difference could be confirmed during
secondary surgery.
From August 2006 to June 2007, we treated 30 con-
secutive patients with flexor tendon injury in zone 2
using the Lim/Tsai surgical repair and the postsurgical
“stop and go” motion protocol. Exclusion criteria into
this review were the same as given earlier1; 26 long
finger injuries (involving 25 FDP and 14 FDS tendons)
and 9 thumbs were included. The surgeon initially
decided on which rehabilitation protocol was used,
taking in account the severity of the injury and the
quality of the repair.
In this most recent cohort of patients, we imple-
mented a new motion protocol—“stop and go” pro­
tocol, as detailed in Figure 13(A)-1. At the end of the
therapy (postsurgical 3 months ± 1 week) the outcome
118 Section 2:  Primary Flexor Tendon Surgery

DECISION MAKING AND REHABILITATION

Day 0 Repair reliable and free of tension?

No Unclear Yes

RED: passive flexion, YELLOW: place and hold, GREEN: early active
active extension passive tenodesis flexion

Cobra splint (30° wrist flexion, MCP 0° extension), rubber band fixed to injured finger.
Day 0 to 1
Therapy starts for all: passive flexion, active extension

Patient compliant? Injury site free of additional tissue resistance?

No Yes

Control of exercises: passive Place and hold exercise,

Day 2 to 5 wrist tenodesis exercise under
flexion, active extension
surveillance of therapist

Patient compliant?

Day 6 to 24 No Yes

Tenodesis exercise with active

flexion. Active flexion in splint

3 to 5 weeks postoperatively: splint completely removed, rubber band fixed to wrist bandage

Week 3.5 Continue exercises according to red/yellow/green, wrist free active motion

5 weeks postoperatively: rubber band removed

Week 6 to 8 Continue exercises, full active flexion without resistance.

8 weeks postoperatively: start of exercises against resistance

Week 9 to 12 Increasing resistance step by step to regain force. If necessary passive full extension

12 weeks postoperatively: full resistance allowed

Figure 13(A)-1  Decision making and rehabilitation.


Figure 13(A)-2  Technique of the six-strand core and running suture tendon repairs.
was measured using the original Strickland classification
for the fingers and the Buck-Gramcko classification for
the thumbs.
OPERATIVE TECHNIQUES
After Bruner zigzag incisions, the core suture was
achieved with the six-strand Lim/Tsai5,6 double-loop
technique with polyamid (4-0 Supramid; S. Jackson,
Alexandria, VA) and an epitendinous running suture
with polypropylen (5-0 Prolene) (Figure 13[A]-2). The
two slips of the FDS tendon were repaired with the use
of simple core Kessler sutures with polyamid single
suture (4-0 Supramid). No repair of the tendon sheath
was performed.
POSTOPERATIVE CARE
Therapists decide after consulting the surgeon as to
which protocols to be used depending on postoperative
hand conditions (swelling, pain) and the compliance of
the patient. Therapists may change the protocols during
the process of rehabilitation (see Figure 13[A]-1).
The Staged Rehabilitation Group:
“Stop and Go”
Conditions for the “stop and go” program are that the
patient is older than 12 years and that the patient speaks
Chapter 13A:  The Bern Experience 119
and understands German, French, or English. “Stop and
go” is used for lesions in zones 1 to 4; the wrist teno-
desis exercises are not performed for zone 5. Immedi-
ately after surgery, all patients receive a dorsal “cobra”
splint in 30° to 40° wrist flexion, with metaphalangeal
(MP) and interphalangeal (IP) joints in 0° (Figure
13[A]-3A).
Red: Passive Flexion, Active Extension.
The patient is instructed to perform passive flexion
(three times a day) and active extension (hourly) of all
fingers. The extension of involved digits should reach
the dorsal splint (0° in all finger joints) (Figure 13[A]-
3B–E). The goal of passive flexion is to make the
involved digits reach the palm.
The exercises are monitored by hand therapists at
least once a week, and continue to postoperative 3.5
weeks. The splint is then removed to allow active mobi-
lization of the wrist. The rubber band is fixed to a wrist
bandage for another 1.5 weeks. After 5 weeks the patient
is instructed to actively flex and extend fingers. Exercises
against resistance or passive full extension are not yet
allowed. If a passive extension deficit is noted, a static
or dynamic extension splint is adapted. At 8 weeks,
exercises against slight resistance are started. Over the
next 4 weeks, the resistance is gradually increased. Full
120 Section 2:  Primary Flexor Tendon Surgery

A B C

D E F

G H I
Figure 13(A)-3  A, Cobra splint and rubber band. B–E, Passive flexion. F, Place and hold (yellow). G, H, Tenodesis exercise
(yellow and green). I, Active flexion (green).

resistance is allowed after 12 weeks. The passive flexion
and active extension (red) is a basic program. The yellow
and green programs described next are built up on it,
with addition of active motion components.
Yellow: Place and Hold
To the basic program (red), place-and-hold exercises are
added. The place-and-hold exercises are done after the
basic exercises to decrease tissue resistance. In doing
place-and-hold exercises, all fingers are passively flexed
and actively hold in the flexed position for one second
(Figure 13[A]-3F). During the therapy session, the
splint is removed to perform wrist tenodesis exercises to
initiate tendon gliding: active extension of the wrist
while the fingers stay relaxed (Figure 13[A]-3G–I). After
3.5 weeks, the splint is removed. The rubber band is
fixed to a wrist bandage and the exercises are continued
in the same way. After 5 weeks, the therapy is continued
in the way as described in the red protocol.
Green: Early Active
In addition to the basic exercises, the patient starts cau-
tiously with active flexion in the splint to reach a middle
position (every joint around 60° flexion).
If the patient is cooperative and able to follow the
directions given by the surgeon/therapist, he is instructed
to remove the splint and to perform the wrist tenodesis
exercise with active finger flexion: active wrist extension
with complete active finger flexion without resistance.
When the patient is not considered to be compliant, he
is “downgraded” to the yellow or even the red protocol
at any time in the course of therapy.
The control and progression of rehabilitation remain
the same as for red and yellow.
OUTCOMES
Our results of the two- and six-strand repair are sum-
marized in Table 13(A)-2. The assessment of range of
Table 13(A)-2  Results of Repairs of Completely Lacerated FDP Tendons Using Two Suture Methods
Evaluations
TAM PIP + DIP joints
MP + PIP + DIP joints
Extension deficit
PIP + DIP joints
Extension
Grip strength Injured hand
Uninjured hand
Difference (uninjured-injured)
Duration of therapy
*The numbers given in the parentheses are ranges. NS, not significant.
Chapter 13A:  The Bern Experience 121
motion, evaluated by the original Strickland classifica-
tion system, rendered 21 of 50 excellent and 18 of 50
good results in the group of Lim/Tsai repair compared
to 4 of 21 and 5 of 21 in the group of Kessler repair. The
TAM of the group of Lim/Tsai was 141.4°, which is
significantly better (p = 0.013) than the TAM of 123.3°
in the Kessler group. In the group of Lim/Tsai, 14 of 50
fingers (12 of 45 patients) (28%) necessitated an exten-
sion splint compared to 8 of 21 fingers (8 of 20 patients)
(38%) in the group of Kessler. On average, extension
splinting was applied around 8.5 weeks postoperatively.
The average extension lag was 20.7° in the group of
Lim/Tsai and 18.8° in the group of Kessler before splint-
ing. Twelve weeks postsurgery, the remaining extension
deficits of the interphalangeal joints were 12° and
16.4°, respectively, demonstrating no statistically sig-
nificant difference between the two groups. Using the
linear model, in the group of Lim/Tsai, the grip strength
was significantly better (p = 0.02), and the average time
of treatment for long fingers was significantly shorter
compared to the group of Kessler (p < 0.0001).
In the staged rehabilitation (“stop and go”) group,
48 flexor tendon repairs in 26 long fingers and 9 thumbs
were evaluated after 3 months; 14 fingers were treated
with the green, 9 fingers using the yellow and 3 using
the red protocol. Of 9 thumbs, 6 were rehabilitated with
the green, 1 with the yellow and 2 with the red protocol.
Nine (35%) flexor tendon repairs were rated excellent,
7 (27%) good, 6 (23%) fair, and 4 (15%) poor using
the original Strickland criteria. The mean active range
of motion at the end of therapy was 90° of flexion and
10° hyperextension for the MP joint, whereas it was
90° of flexion but an extension lag of 10° for the PIP
joint and 43° of flexion and full extension for the DIP
joint. Grip strength compared to the contralateral hand
was 72%.
The results of the FPL repair were good or excellent
in 90% (6 excellent, 2 good, 1 fair) of digits. The mean
Lim and Tsai Group Kessler Group p values
141° (90°–195°)* 123° (75°–190°) .013
232° (190°–290°) 213° (155°–290°) .013
23/50 digits 11/21 digits NS
12° (5°–30°) 16° (10°–25°) NS
14/50 digits 8/21 digits NS
34.6 kg (14–60 kg) 30.3 kg (14–60 kg) NS
45 kg (22–70 kg) 46.3 kg (22–66 kg) NS
10.4 kg (−40 to 40 kg) 16.1 kg (−6 to 34 kg) .02
112 days (62–230 days) 209 days (83–496 days) <.001
122 Section 2:  Primary Flexor Tendon Surgery

Table 13(A)-3  Results of Staged Rehabilitation After Flexor Tendon Repairs in 26 Fingers and 9 Thumbs
26 Fingers (Strickland Criteria) 9 Thumbs (Buck-Gramcko Criteria)
Functional Grades Results Protocol Functional Grades Results Protocol
Excellent 9 (35%*) 9 green Excellent 6 (66%) 6 green
Good 7 (27%) 4 green, 3 yellow Good 2 (18%) 1 yellow, 1 red
Fair 6 (23%) 6 yellow Fair 1 (9%) 1 red
Poor 4 (15%) 3 red, 1 green Poor 0 —
Grip Strength 72% compared to the opposite Pinch Strength 85% compared to the
site opposite site
*Percentage of the fingers rated in each grade is given in the parentheses.

Table 13(A)-4  Tendon Injury Sites and Complications Using Tang’s Division of Subzones
Numbers of Lacerations Within Time of Secondary Surgery (Months
Groups Complications Age Finger Tang’s Subzones After Last Surgery)
Lim/Tsai 2 (out of 51 fingers) 1 tenolysis — 1 rupture
30 Long 2B 9 months — —
26 Index 2B — — 2 months
Kessler 6 (out of 26 fingers) 1 tenolysis 2 dehiscence 3 ruptures
53 Index 2B 9 months — —
18 Long 2D — 7 months —
46 Ring 2B — 7 months —
30 Long 2D — — 2 months
59 Long 2B — — 4 months
82 Ring 2B — — 1 month

active range of motion of the thumb was 61° of flexion
and 5° hyperextension in the MP joint and 39° of
flexion in the IP joint but with a slight extension lag of
5° (Table 13[A]-3).
COMPLICATIONS
All eight patients requiring secondary surgery had com-
plete lacerations of both the FDP and the FDS tendons.
Table 13(A)-4 details the injured finger and the lacera-
tion site within zone 2 according to Tang’s subdivision
of zone 2.9
Lim/Tsai Group
One 30-year-old patient with impaired flexion and
extension of the middle finger required a tenolysis
with FDS resection 9 months after primary repair. One
patient sustained a rupture of the repaired index FDP
and was reconstructed with a palmaris longus tendon
graft 2 months after the primary repair. The rupture
rate in the group of Lim/Tsai was 1 of 51 fingers (2%)
and the complication rate including tenolysis was 2 of
51 (4%).
Kessler Group
The rupture rate in the group of Kessler was 3 of 26
fingers (11%). The complication rate was 6 of 26 fingers
(23%). The complication rate (including dehiscence and
tenolysis) was significantly lower (Lim/Tsai: 4%; Kessler:
23%) in the group of Lim/Tsai repair (p = 0.048).
In the staged rehabilitation group “stop and go” the
rupture rate was 2 of 48 (4%). One rupture occurred
while the patient was fighting with others during a
nightmare.
DISCUSSION
Gill and colleagues5 conducted a human cadaveric study
and showed the superiority of the Lim/Tsai four-strand
repair over two- or four-strand repair techniques with
regard to tensile strength. Xie and coworkers7 compared
different six-strand suture configurations and showed
that in vitro the modified Savage and the Tang suture
have greater tensile strength than the Lim/Tsai suture,
but they also concluded that the Lim/Tsai suture has the
mechanical strength for unrestricted active finger flexion.
The loop-suture technique simplifies flexor tendon

repair compared to the modified Savage repair and does
not use superficial knots like the Tang suture. Given the
tensile strength of the Lim/Tsai suture, our comparison
of the six-strand and two-strand repair techniques1 dem-
onstrated a better outcome without increasing the risk
of tendon ruptures using place-and-hold exercises post-
operatively in the Lim/Tsai suture group. This group
demonstrated a significantly better TAM. There was no
increased rate of ruptures, nor did it differ significantly
between the two groups. Even without a statistically rel-
evant difference, there may still be a clinical difference
given the drop of the rupture rate from 11% to 2%
between the Kessler and the Lim/Tsai groups. The
rupture rate in group of Lim/Tsai and in the group of
Kessler is in line with the published rupture rate of 4%
to 10% in zone 2 mentioned in the review of Tang.10
Furthermore, the overall complication rate (including
tenolysis and dehiscence) was significantly lower in the
group of Lim/Tsai.
Tang and colleagues11 performed a biomechanical
study showing that gliding curves of a small diameter
and gliding over the rim of a major pulley are associated
with an increased rupture risk. Dowd and coworkers14
stated that these characteristics were typically found in
zone 2B repairs and repairs of tendons in the little finger
(zone 2B defined by Tang9: subzone from the proximal
margin of the FDS insertion to the distal border of the
A2 pulley). In the clinical study by Dowd and col-
leagues,12 32 of 42 fingers requiring rerepair had injuries
in zone 2B and/or in the little finger. In our study, no
repair ruptured in the small finger. Four of six patients
with ruptures or dehiscences, had undergone repair in
zone 2B (see Table 13[A]-4), which seems to support
Dowd and colleagues’ conclusion of zone 2B as the repair
site at highest risk. The remaining two patients required
repairs in zone 2D (subzone from the proximal border
of the A2 pulley to the proximal margin of zone 2).
Using the original Strickland classification, the group
of Lim/Tsai demonstrated 39 of 50 (78%) good and
excellent results compared to 9 of 21 (43%) in the group
References
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tendon repair in zone II using a six-strand double-loop tech-
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2. Strickland JW: The scientific basis for advances in flexor
tendon surgery, J Hand Ther 18:94–110, 2005.
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Chapter 13A:  The Bern Experience 123
of Kessler. Compared to the 50% to 100% good and
excellent results of other studies,13-21 the outcome in
the group of Kessler repair seemed to be rather poor.
The results of the group of Lim/Tsai are in line with the
above mentioned reports of zone 2 tendon repairs, espe-
cially in view of the longer follow-up of at least at 6 to
12 months in these studies. The only report on Lim/Tsai
sutures with place-and-hold exercises in zone 2 is by
Lim and Tsai.6 They achieved 81% good/excellent results
after 7 months assessed by the revised Strickland criteria
compared to 100% of good/excellent results in the
group of Lim/Tsai and 91% in the group of Kessler after
3 months in our series when using the revised Strickland
criteria.
We evaluated a six-strand suture repair technique and
the benefit of place-and-hold exercises on digital func-
tion compared to a two-strand repair without place-
and-hold exercises. In an additional group of patients,
“stop and go” early active mobilization protocol pro-
duced better outcomes compared with the previous
patient groups with place-and-hold or passive flexion
and active extension protocols. In nearly 50% of the
patients, the surgeons and the therapists decided not to
use the early active (green) but rather the place-and-hold
(yellow) or Kleinert/Duran (red) rehabilitation program
despite the use of a strong six-strand repair. The actual
effects of wound conditions and swelling on the resis-
tance to tendon gliding can be difficult to estimate in
due course. In our experience, it is better to have a few
options for the rehabilitation protocols to select accord-
ing to patients’ wound conditions and degree of hand
swelling. Furthermore, we should consider the capabil-
ity of the patient to perform the exercises to reduce the
likelihood of repair ruptures.
Our experience with “stop and go” protocols indi-
cates that the protocols allow individual adjustments of
postoperative rehabilitation, thus optimizing outcomes
after flexor tendon repair. With these protocols, rehabili-
tation can be adapted to different patients’ conditions,
leading finally to good and excellent results.
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24:1315–1322, 1999.
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repair, Atlas Hand Clin 1:65–76, 1996.
7. Xie RG, Zhang S, Tang JB, et al: Biomechanical studies of 3
different six-strand flexor tendon repair techniques, J Hand
Surg (Am) 27:621–627, 2002.
8. Strickland JW, Glogovac SV: Digital function following flexor
tendon repair in Zone II: A comparison of immobilization
and controlled passive motion techniques, J Hand Surg (Am)
5:537–543, 1980.
9. Tang JB: Flexor tendon repair in zone 2C, J Hand Surg (Br)
19:72–75, 1994.
10. Tang JB: Clinical outcomes associated with flexor tendon
repair, Hand Clin 21:199–210, 2005.
124 Section 2:  Primary Flexor Tendon Surgery
11. Tang JB, Xu Y, Wang B: Repair of strength of tendons of
varying gliding curvature: A study in a curvilinear model,
J Hand Surg (Am) 28:243–249, 2003.
12. Dowd MB, Figus A, Harris SB, et al: The results of immediate
re-repair of zone 1 and 2 primary flexor tendon repairs which
rupture, J Hand Surg (Br) 31:507–513, 2006.
13. Bainbridge LC, Robertson C, Gillies D, et al: A comparison
of post-operative mobilization of flexor tendon repairs with
“passive flexion-active extension” and “controlled active
motion” techniques, J Hand Surg (Br) 19:517–521, 1994.
14. Baktir A, Turk CY, Kabak S, et al: Flexor tendon repair in zone
2 followed by early active mobilization, J Hand Surg (Br)
21:624–628, 1996.
15. Cullen KW, Tolhurst P, Lang D, et al: Flexor tendon repair in
zone 2 followed by controlled active mobilisation, J Hand
Surg (Br) 14:392–395, 1989.
16. Elliot D, Moiemen NS, Flemming AFS, et al: The rupture
rate of acute flexor tendon repairs mobilized by the con-
trolled active motion regimen, J Hand Surg (Br) 19:607–612,
1994.
17. Klein L: Early active motion flexor tendon protocol using one
splint, J Hand Ther 16:199–206, 2003.
18. Lee H: Double loop locking suture: a technique of tendon
repair for early active mobilization. Part II: Clinical experi-
ence, J Hand Surg (Am) 15:953–958, 1990.
19. May EJ, Silfverskiold KL, Sollerman CJ: Controlled mobiliza-
tion after flexor tendon repair in zone II: A prospective com-
parison of three methods, J Hand Surg (Am) 17:942–952,
1992.
20. Silfverskiold KL, May EJ: Flexor tendon repair in zone II with
a new suture technique and an early mobilization program
combining passive and active flexion, J Hand Surg (Am)
19:53–60, 1994.
21. Small JO, Brennen MD, Colville J: Early active mobilisation
following flexor tendon repair in zone 2, J Hand Surg (Am)
14:383–391, 1989.
 B The Chelmsford Experience
David Elliot, MA, FRCS, BM, BCh
OUTLINE
This chapter reviews the research into primary flexor
tendon surgery chronologically through from 1989 to
2010 in the Hand Surgery Unit of the St Andrew’s
Centre for Plastic Surgery, Chelmsford, UK, explaining
the changes made and the thinking behind them.
Movement should be instituted with care and judgment.
In the first week, it will prevent the incision from healing
and encourage infection. If begun late, adhesions will
already have immobilized the tendon. Rough, extreme and
continuous movements will cause fibrin and scar tissue to
form and bind the tendons, and also cause the sutures to
cut out. Rest favors a natural repair, with a minimum of
inflammatory reaction, but, also, allows adhesions to form
to all raw surfaces. Movement encourages the formation
of synovial membranes over the raw surfaces. It would
seem that a moderate amount of intermittent movement,
with as long an excursion as practical, interspersed by rest,
will yield the best results.
Sterling Bunnell MD, San Francisco, 1918
HISTORY
Although Bunnell (1918) wrote on primary repair and
early, albeit guarded and intermittent, active mobiliza-
tion, his subsequent experience in the 1920s presum-
ably led to the dictate that flexor tendons divided in the
tendon sheath of the fingers should not be repaired
primarily but treated by delayed tendon grafting. This
practice dominated the practice of flexor tendon surgery
for 40 years. The past 50 years is notable for the reversal
of this policy and recognition that results after primary
or delayed primary flexor tendon repair, that is within
a few days of tendon division, can be better than after
delayed tendon grafting, provided early surgery is com-
bined with early mobilization of the repaired tendons,
a change largely pioneered by Verdan,1 Young and
Harman,2 and Kleinert and colleagues.3 Although there
is ongoing debate about the details of technique, the
central tenet of modern flexor tendon surgery is to repair
and move the flexor tendons within a few days of injury.
While all flexor tendon surgery is complicated, it is
simplest in the newly injured and unscarred digit and
the results of correctly rehabilitated primary repairs are
likely to be the best attainable.
THE ST. ANDREW’S UNIT
As a basis for modern practice, this is only likely to
improve results if surgery is carried out by adequately
trained surgeons and followed by early mobilization by
skilled hand therapists, not general physiotherapists.
The Chelmsford unit has tried to progress along these
lines for the past 20 years in both respects. The growth
of specialist hand therapy during this period, both
within the unit and, more generally, throughout the
United Kingdom, has been an essential factor in this
change. The development of a dedicated all-day trauma
theater and increasing numbers of consultant hand sur-
geons and training surgeons at a senior (fellow) level
involved in this surgery have also been integral to main-
taining the quality of service with increasing numbers
of referrals. Emergency services locally are arranged to
relocate these injuries almost entirely to our unit from
the surrounding accident and emergency departments
of several large peripheral towns and the suburbs of East
London, which have a combined population of around
4 million people.
THE PROBLEMS OF PRIMARY FLEXOR
TENDON REPAIR
Repair of the divided flexor tendon to achieve normal,
or near normal, function is a problem that has not yet
been solved. Primary flexor tendon surgery remains
technically difficult, with each result still being uncer-
tain. There have been about 20 methods of assessing
flexor tendon results described in the hand literature
since 1950.4 This repeating need to reevaluate our
methods of assessment has come not from attempts to
keep up with improvement of the results over the years
but from a repeating need to quantify how much we
should reasonably downgrade our expectations to
accommodate for the imperfections of our treatment.
Over and above the actual technical difficulties of repair-
ing tendons, we face the complications of rupture and
adherence of repairs during healing and these two prob-
lems have dominated thought on this subject for a
century. “Spot-welding” by scar adhesions can occur
anywhere along the length of a flexor tendon, but it is
a particular problem in the fingers themselves, where
the flexors are confined within the tendon sheath in a
system as finely bored as the pistons in an engine. This
requires that the tendons be mobilized throughout the
125
126 Section 2:  Primary Flexor Tendon Surgery
period immediately after repair when tendon continuity
depends almost entirely on the strength of the sutures,
as healing of the flexor tendon takes about 3 months.
Unfortunately, this period is sometimes longer than that
for which the hand can be kept free of activities, or
accidents, liable to snap the repair. In this unit, our
main research interests have been to eliminate rupture
of the tendons while maintaining a policy of enthusias-
tic early active mobilization. The assumption support-
ing this philosophy is that the results will be better with
increasing early movement through the first 5 weeks,
albeit within the protective environment of a dorsal
splint, provided the sutures hold and rupture does not
occur. Our research over 20 years has aimed at liberating
rehabilitation from unnecessary constraints while, coin-
cidently, reducing the rupture rate after primary repair.
EARLY ACTIVE MOBILIZATION
The author’s interest in early active mobilization comes
from his training with McGrouther in Glasgow, then
with Brown and Black in Newcastle, prior to arrival in
the Chelmsford unit. The latter part of my training coin-
cided with the publishing of an article by the hand
surgeons in Belfast, not far away, in which they described
mobilization after routine zone 2 flexor tendon repairs
in a Kleinert traction splinting system but without the
elastic bands (i.e., actively moving the fingers when
flexing as well as when extending).5 This was not actually
new as many before had either never used rubber bands
or tried to get rid of them,6-25 although always stressing
the use of some variant of suture technique to make the
repair stronger, presuming this would be necessary to
withstand early active movement. What the Belfast sur-
geons identified was the fact that the sutures did not
need to be stronger to allow early active mobilization
in both directions. The desire to be free of the rubber
bands had been prevalent for years, largely because of
the problems arising from the flexed resting position of
the proximal interphalangeal joints in Kleinert traction
and, also, because of the difficulties in managing Klein-
ert traction. It was also realized that many patients never
actually used the rubber bands to passively flex but
simply flexed their fingers actively, even when the bands
were correctly tensioned, which was often only for 5
minutes after leaving the therapy department. This stim-
ulated me to repeat the Belfast experiment. This is
recorded in an article26 comparing patients mobilized in
a passive flexion-active extension, or “Kleinert” regimen,27
with patients mobilized in an active flexion-active exten-
sion, or “Belfast” regimen,5 after the same repair with a
two-strand modified Kessler core suture and a simple
running circumferential suture. This study, performed
between 1986 and late 1987 (although only published
much later), and the study from Sheffield, UK, reporting
the results of their repeat of the Belfast experiment28
convinced me that this was the way forward for
rehabilitation, in respect of simplifying rehabilitation to
a level commensurate with the availability of therapy in
our own unit and likely to be available worldwide. The
results of these, and subsequent reports throughout the
1990s, confirmed a rupture rate of around 5% when
using variants of the Belfast regimen,5,26-30 which was
similar to that reported at the time by units worldwide
using the Kleinert regimen.26,29,31-35
PASSIVE MOBILIZATION
The other alternative to the Kleinert technique of mobi-
lization, introduced in the United States by Duran and
Houser (1975) and supported by Strickland and Glogo-
vac (1980), in which the fingers were only mobilized
passively by a therapist, or the patient’s other hand,
was never popular in the United Kingdom as it was
very labor (therapy) intensive, with no seeming advan-
tages.36,37 A common debate at the time which, to my
knowledge, has never been settled, was whether the
tendons actually moved significantly with this regimen
or simply bunched up as the fingers were passively
flexed. Another factor that made it unattractive was the
fact that the first report included a 14% rupture rate,36
while the second had only 56% good and excellent
results,37 both of which are unacceptable compared with
published results at the time using the Kleinert regimen
and, subsequently, the Belfast regimen. The most
common use now of the Duran Houser idea is in helping
Kleinert and Belfast regimens push for better results at
the extremes of movement.
ST. ANDREW’S EARLY RESULTS—FINGERS
Our own early results using a two-strand Tajima modi-
fication of the Kirchmayer, or Kessler, core suture19,38 of
3-0 or 4-0 polypropylene (Prolene), in which the suture
is tied with a single intratendinous knot, a simple con-
tinuous running circumferential suture of 5-0 or 6-0
nylon (Ethilon), or polypropylene, and a modification
of the Belfast regimen (Figure 13[B]-1), were reported
in 1994.28 Over a period of 31 2 years, 233 patients were
treated for complete divisions of flexor tendons in zones
1 and 2 within 24 hours of admission following emer-
gency referral. The patients included 58 complete
tendon divisions in 58 fingers in 54 patients in zone 1
and 259 tendon divisions in 166 fingers in 149 fingers
in zone 2. A later study extended this survey to include
508 patients with 840 acute complete flexor tendon
divisions in 605 fingers treated in the same manner
between June 1989 and December 1996.29 These reports
were both focused on the problem of rupture. In the
first report, an overall rupture rate of 5.8% was achieved,
with a rupture rate for zone 2 injuries of 5.4% and for
zone 1 injuries of 6.8%, confirming our belief that the
regimen was safe for use as an alternative to Kleinert-
type regimens for mobilization of zone 1 and 2 finger
flexor tendon injuries. In the larger survey, after

A negligible differences in the number of patients with
B ing results in the early 1990s, although having little
Figure 13(B)-1  Original Billericay/Chelmsford variation of
the Belfast splint with (A) the fingers resting in extension,
and (B) the fingers actively flexing.
exclusion of 68 patients who did not complete the
8-week rehabilitation program, 440 patients with 728
complete tendon divisions in 526 fingers were assessed.
Twenty-three patients suffered rupture of 28 tendons in
23 fingers, an overall rupture rate of 4%. One hundred
and twenty-nine fingers with zone 1 injuries had a
rupture rate of 5% and 397 fingers with zone 2 injuries
had a rupture rate of 4%. The good and excellent results
in the final year of the first study, assessed using the first
Strickland method of assessment,37 of 62.5% for zone 1
injuries and 79.4% for zone 2 injuries confirmed that
these rates of rupture were not being achieved at the
expense of increased protection and poor mobility.
These studies confirmed that early active motion was as
safe as any current regimen, with results comparable to
those of previous studies in terms of both rupture and
mobility in a considerable number of fingers, most
other studies in the literature being much smaller in
size. At the time, we wrote that we believed the Belfast
type of rehabilitation was both simpler and less expen-
sive to maintain than the Kleinert type of rehabilitation
regimen. We were no longer concerned about the safety
of the Belfast regimen, something, which still persists
elsewhere, particularly in the United States. However, we
Chapter 13B:  The Chelmsford Experience 127
had also reached the conclusion that argument over
which was the best of the two active regimens was prob-
ably unproductive.
THE 5% RUPTURE RATE
Throughout this period, we were concerned by the
seemingly static state of acute flexor tendon repairs
being reported worldwide in those units publishing
results. With few exceptions, most studies discussing
acute flexor tendon repair and early mobilization
reported a rupture rate of between 3% and 6%. In
studies of less than 100 patients, these figures indicated
ruptured tendon repairs in different units in different
countries and continents, using a multitude of suture
techniques and variations of the basic regimens of early
postoperative mobilization. Even taking into account
the variations in methods of assessment used at the
time,4,39-41 the similarity of the results in different studies
showed that an adequately trained, but not necessarily
experienced, surgeon, using a routine repair of divided
flexor tendons, whether using the Kirchmayr/Kessler
core suture or following the technique described by
Tsuge,42,43 and with good therapists, would achieve 70%
to 80% excellent, or good, results and suffer a rupture
rate of about 5%. The only identifiable way of improv-
effect on rupture rate, seemed to be to increase post­
operative supervision, generally believed to be the
explanation of the excellent results achieved by Chow
and his colleagues, dealing with military personnel.32 It
was thought at the time that this was unattainable in
civilian practice, until the civilian surgeons and thera-
pists in Göteborg, in Sweden, showed that—with a
stronger technique of circumferential suturing and a
more rigorous therapy regimen, incorporating features
of the Kleinert, the Duran-Houser, and the Belfast
regimens—this was not true.44 However, this study still
included two ruptures in 55 repairs: stronger sutures
and more complex rehabilitation still had not solved
the problem of rupture of primary repairs.
ETIOLOGY OF RUPTURES
Our second article was intended to look further at this
seemingly unconquerable rupture rate by examining the
third factor in the problem of rupture: the patient. We
analyzed the 23 patients whose primary repairs rup-
tured between 1989 and 1996: two tendons ruptured
during sleep, four patients had an accident that was not
their fault, and five patients claimed they were exercising
as instructed at the time of rupture. There were reasons
to doubt the truth of this information in three cases.
However, we gleaned definite information that 11
patients’ repairs ruptured while using the hand for a
variety of tasks, ranging from lightweight activities such
as lifting a newspaper to unreasonable activities such as
128 Section 2:  Primary Flexor Tendon Surgery

moving a wardrobe. In other words, just under 50% of

the ruptures had occurred as a result of patient noncom-
pliance. This injury mainly occurs at an age and in a
social group for which improving compliance is likely
to be difficult. Nevertheless, all patients have subse-
quently been told the causes and incidence of failure
before 2 months, with need for further surgery, by the
author on the morning after surgery as a routine. In this
era, it would seem reasonable that the patient should
have the likely consequence of noncompliance spelled
out clearly before rehabilitation begins!
The group labeled “uncooperative patients” includes A
adults and children who do not cooperate and small
children who cannot. As adults constitute by far the
greater proportion of patients who sustain flexor tendon
injuries, they are the major concern. In any group of
patients, there will always be rule breakers, those who
resent authority, and those without the discipline to
adhere to the strict rehabilitation regimen demanded
after this injury. Psychological manipulation and more
time are the only direct means we have of improving
the results of these patients and it is debatable whether
we can change this factor more than a little. However,
among this group are some with low pain thresholds, B
poor social circumstances, or a low level of comprehen-
sion and we can, sometimes, help these individuals Figure 13(B)-2  Illustration of the current Billericay/
more, given adequate resources. Chelmsford variation of the Belfast splint with (A) the fingers
resting in extension, and (B) the fingers actively flexing.
Most ruptures in our study occurred with the splint
in place. These tendon repairs might have been pro-
tected from rupture by better mechanical obstruction of
the palm. Rubber bands across the palm have a definite
obstructing action, which was not present in the original we have not had time to research this fully and have
technique of early active motion.5 However, all of our only gone halfway from the original flexed position
patients at that time wore a modified Belfast splint, to a straight wrist splint. The actual therapy regimen
which included wide thermoplastic bars across the open has not changed since that described in 1994 (Box
side of the splint, running from the distal edge back to 13[B]-1).30 The time in the splint remains 5 weeks, fol-
the volar aspect of the wrist and known locally as “beer- lowed by 3 weeks weaning from the splint. Light activi-
can bars” (see Figure 13[B]-1).30 These provided a ties start at 8 weeks, with heavy lifting only after 12
similar obstruction to grasping to that of the rubber weeks. This 5-week period of total protection seems to
bands of the Kleinert splint. Attempts to increase this be in accord with our findings in respect of the timing
feature of splinting and/or attempts to make splints of rupture of repairs.4,28,46
impossible to remove might interfere with rehabilita-
RUPTURE RE-REPAIR
tion and would probably still fail in a proportion of
patients. They would certainly have little effect in those Our interest in the rupture of repairs was taken further
who remove the splint to use the hand for grasping. In in a more recent review of all ruptures of zone 1 and 2
the last five years, the ‘beer-can bars’ on our splints have primary flexor tendon repairs performed in our unit
given way to a sheath of lightly elasticated material between 1989 and 2003.46 Although concern about
which holds the fingers in extension against the dorsal tendon rupture had been one of the major determinants
splint for most of the time, with the sheath being rolled in the evolution of the various techniques of tendon
down into the palm for exercising of the fingers (Figure suture and early postoperative mobilization throughout
13[B]-2). the past 10 years of the twentieth century, there was still
almost no information in the literature about the etiol-
THE SPLINTED WRIST POSITION
ogy of tendon rupture.28,47 The intention of our 2006
While accepting the work of Savage that the best posi- report46 was to analyze in further detail (1) the reasons
tion for the wrist in respect of minimum firing of both for tendon rupture during the early mobilization period
the flexor and extensor muscles is in slight extension,45 and (2) the outcome of immediate re-repair, with a view

Box 13(B)-1  The St. Andrew’s Early
Active Mobilization Regimen (1994)
Week 1—Discharged from hospital when pain controlled
by simple oral analgesics, patient able to do dressings
and achieving full extension to splint and active flexion
to 25% of full flexion. Instructed to carry out 10 active
flexion and extension exercises per hour.
Week 2—Seen by surgeons and therapists. Full extension
to splint and active flexion to 50% of full flexion. Ten
exercise repetitions per hour. Passive flexion exercises
started.
Weeks 3 and 4—Seen weekly by therapists only. Full
extension to the splint and progression to full range of
active flexion as soon as possible (usually achieved by
the end of week 3). Ten exercise repetitions per hour.
Passive exercises. Ultrasound started if necessary in
week 3.
Week 5—Seen by surgeons and therapists. Splint removed,
except at night and when risk to the hand (e.g., in
crowds). Wrist extension started, with fingers relaxed at
first.
Weeks 6 and 7—Seen weekly by therapists. Progression
to full range of movements of wrist and fingers.
Week 8—Splint discarded completely. Passive extension
exercises and dynamic extension splinting started if nec-
essary. All but heavy activities allowed, including driving.
Return to work (except heavy manual workers).
Weeks 10 to 12—Progressive return to heavy work by
week 12.
to identifying whether this should be an invariable
policy, whenever possible. Discussion of our views on
the management of ruptures of primary repairs of flexor
tendons in zones 1 and 2 in the fingers are considered
further in Chapter 19.
VENTING THE PULLEYS
In retrospect, a factor in achieving these results that
received no attention at the time but was, possibly, of
significance was that, from the earliest of the studies in
which I was involved, it had been routine to “vent”
pulleys as necessary to allow repairs to travel through a
full range of excursion on passive movement of the
finger after repair without impinging on the A2 or A4
pulleys. The conviction that this “made sense” followed
a private conversation as a trainee in the mid-1980s at
the Derby Hand Course with Dr. Strickland. At the time,
Lister and others were quite adamant that these pulleys
should remain entirely intact. Dr. Strickland seemed
less certain and I, knowing the problems I personally
Chapter 13B:  The Chelmsford Experience 129
experienced in the emergency theater, was certain that
venting was correct and necessary in many cases. The
discussion of “venting” is taken further and, I believe,
to its logical conclusion in other chapters of this book
and in two review articles in the recent past.48,49 Analyz-
ing the sites along the tendon sheath were tendon injury
commonly occurs, Dr. Tang has described appropriate
pulley releases for each injury and accords this process
of pulley “venting” equal importance as the use of stron-
ger repairs in increasing the margin of safety of early
active mobilization.49 We believe the results of zone 1
primary flexor tendon surgery are equally dependent on
judicious venting of the A4 pulley.50
STRONGER REPAIRS
At that time, increasing the strength of our sutures
seemed likely to be the most effective preventative of
tendon rupture in this group of patients. The ability of
tendon sutures to withstand the forces of early move-
ment is, probably, the most fundamental limitation to
what can be achieved by early movement of primary
flexor tendon repairs by any technique. This has been
the second prong in the mechanical way forward since
Harmer, in Boston, in 1917, introduced a flexor tendon
core suture that he believed was sufficiently strong
to resist rupture and commenced immediate free
movement of the fingers postoperatively without any
splints,14 and, in the same year, Kirchmayr presented
his stronger suture, with the same purpose in mind.38
Our work on ruptures had convinced us, like others,
that we needed stronger sutures to continue aggressive
early active mobilization without this 5% rupture rate.
In the recent past, there had been numerous studies,
mostly experimental, describing a variety of means by
which this might be achieved. The suture changes can
be split, broadly, into those modifying the core suture
and those modifying the circumferential suture. Our
examination of the patients who had ruptured our
repairs simply confirmed what everyone had assumed
and highlighted a need to move toward clinical applica-
tion of the laboratory research into stronger sutures and
identify which of these suture modifications was suffi-
ciently practical to be used in clinical practice. Regret-
tably, few of the laboratory experiments of suture
configurations of the nineties have since been pro-
gressed to clinical studies by their authors.
ZONE 2 AS A BLACK BOX
Throughout the 1990s, we were not entirely happy with
the zone 2 model for investigation of the problem
further, although zone 2 had become the accepted
testing ground for mobilization techniques—and for
individual units! It was obvious that most studies
reported less than 50 cases and that it was difficult to
collect sufficient cases of zone 2 injuries alone in a
single unit to make a series. As a result, three things had
130 Section 2:  Primary Flexor Tendon Surgery
happened. The first was that the total number of studies
remained small. The second was that most studies were
small in themselves and, in many cases, too small to be
of scientific value. The third was that the available
numbers were too small to analyze exactly what was
going on in the “black box” we called zone 2, as all the
results had to be put together to achieve a publishable
total. Zone 2 is far from homogeneous: there are eight
permutations of tendon injury in what we call a zone 2
injury. We ignore the three partial injuries and put all
those with at least one complete tendon division into
the black box marked “zone 2 injury”: there are actually
five different injuries in this box. In the 1990s, we
looked at this briefly and it looked as if there might be
differences in results for different injuries, with a com-
plete flexor digitorum profundus (FDP) and partial FDS
division faring worse with our current mobilization
than any other combination of tendon lacerations.
Another fact that we ignore is that fingers with both
tendons cut with the finger flexed have two repair lines
that are a long way apart when the finger is extended
and only come together in flexion. By contrast, when
the finger is cut in extension, the tendon repairs remain
together all the time throughout flexion and extension.
It might reasonably be expected that the results would
differ between these two injuries. A third fact about
zone 2 that we ignore in putting all the results together
is that the sheath is not a cylinder of unchanging topog-
raphy along the length of the zone. This is equally true
of zone 1.50 So, the tendon environment is varying
quite dramatically along both zones. Unfortunately, the
circumstances in respect of analysis of zone 2 injuries
have not changed. The fact that it is difficult to collect
even 50 acute zone 2 finger flexor injuries in a single
unit makes for an ongoing problem for those research-
ing new suture configurations in this field: if only 2 or
3 in every 50 repairs rupture, then it takes a long time
before we can be sure that any innovation has achieved
anything.
THE FLEXOR POLLICIS LONGUS MODEL
The flexor pollicis longus (FPL) tendon had been
researched very little over the previous 30 years, but the
extensive literature of an earlier era (1937 to 1960)
clearly identified a much higher rupture rate after
primary repair than that of the finger flexors.51,52 Sur-
geons at that time recognized this and debated whether
to repair this tendon by insertion of a tendon graft or
by lengthening the proximal tendon.52 When we
reported our results of zone 1 and 2 finger flexors in
1994,30 we also looked at the FPL results and found a
rather horrific rupture rate of 17% in 30 thumbs when
mobilized in the Belfast regimen of active flexion/active
extension of the repairs. At that time, we recommended
that this technique of mobilization not be used in its
present form after repair of the long thumb flexor.
However, we realized that the higher rupture rate might
make the FPL a good clinical model to test new sutures
and suture techniques. Using this model, we were able
to examine some of the new suture configurations being
described in laboratory experiments in a series of
studies,52-54 which are described in Chapter 16. Although
these reports elaborate an increasingly safer technique
for dealing with division of the FPL tendon, they were
undertaken largely to examine possible ways forward in
respect of the finger flexors. Ultimately, these clinical
experiments with the divided FPL achieved zero rupture
rates using two different suture techniques (a combina-
tion of a four-strand core suture55 and a Silfverskiöld
circumferential suture56) and Tang’s three Tsuge suture
repair.57,58
To us, this confirmed the likelihood that increase
in suture complexity would successfully reduce the
rupture rate during early mobilization after repair of the
finger flexor tendons and, like most others, we have
gone the way of increasing suture complexity. After a
dalliance with more complex circumferential sutures,
we came to the conclusion that these were too compli-
cated for trainees, who are likely to operate on these
cases both in our own unit and worldwide. The combi-
nation of a four-strand core suture and a complex cir-
cumferential sutures also gave rise to concern about the
bulk of the repairs and possible problems of resistance
to movement of the repaired tendon.59 This was sug-
gested by a slight drop in the excellent and good results
in this group of FPL repairs compared with previous
results. However, this problem was small. Of more sig-
nificance was the fact that these complex sutures are
more difficult to use in clinical practice. In our FPL
studies, this led to the use of Tang’s triple Tsuge suture
technique57,58 for FPL repair, as this is a less complicated
suture technique.
STRONGER SUTURES—DILEMMAS
Four-strand repairs have become the order of the day
for zone 1 and 2 finger flexor repairs at present in
Chelmsford. However, there remain two causes for
concern as we all move to more complex suturing. Reex-
amination of the clinical series reported over the past
25 years identifies the study in 1989 by Savage and Risi-
tano,25 which introduced Savage’s six-strand suture and,
with it, the search for the ideal multistrand suture that
would have the strength of the Savage suture but be
simpler to put into the tendon, as the series with the
lowest rupture rate of one rupture in 31 zone 2 fingers
and 2 thumbs (3%). The next lowest rupture rate was
in our series from Chelmsford in 1999, which reported
17 ruptures after zone 1 and 2 primary flexor tendon
repairs in 397 fingers (4%).31 This much larger series of
cases were repaired with only two-strand Kirchmayr/
Kessler core sutures and simple running circumferential
suturing, making the hard evidence for improvement of

clinical results by more complex core suturing question-
able. A very interesting laboratory study from Manches-
ter may identify a further, previously unknown, factor
that is concerning.60 It showed that even a single suture
passed through a tendon significantly affected the teno-
cyte cell population of the tendon around it. The suture
foreign body caused the tenocytes to move away. So,
perhaps, we are unwittingly making tendon repair
breakdown more likely as we put in more sutures!
ECONOMIC FACTORS
It is possible that the current small but constant remnant
of repairs that rupture relates more closely to factors
such as the degree of cooperation of the individual
patient (discussed earlier) and the ability of surgical
units to maintain a continuing high quality of surgical
repair and rehabilitation. In the United Kingdom, as in
most parts of the world, the availability of a high level
of expertise to this patient group remains a medicopo-
litical battle over unit budgets, accommodation for
References
1. Verdan CE: Primary repair of flexor tendons, J Bone Joint Surg
(Am) 42:647–657, 1960.
2. Young RE, Harmon JM: Repair of tendon injuries of the hand,
Ann Surg 151:562–566, 1960.
3. Kleinert HE, Kutz JE, Ashbell T, et al: Primary repair of lacer-
ated flexor tendons in “no man’s land,” J Bone Joint Surg (Am)
49A:577, 1967.
4. Elliot D, Harris SB: The assessment of flexor tendon func-
tion after primary tendon repair, Hand Clin 19:495–503,
2003.
5. Small JO, Brennen MD, Colville J: Early active mobilisation
following flexor tendon repair in zone 2, J Hand Surg (Br)
14:383–391, 1989.
6. Becker H, Orak F, Duponselle E: Early active motion follow-
ing a bevelled technique of flexor tendon repair: Report on
fifty cases, J Hand Surg (Am) 4:454–460, 1979.
7. Brunelli G, Vigasio A, Brunelli F: Slip-knot flexor tendon
suture in zone 2 allowing immediate mobilisation, Hand
15:352–358, 1983.
8. Bunnell S: Repair of tendons in the fingers and description
of two new instruments, Surg Gynecol Obstet 126:103–110,
1918.
9. Emery FE: Immediate mobilization following flexor tendon
repair. A preliminary report, J Trauma 17:1–7, 1977.
10. Furlow LT: The role of tendon tissues in tendon healing, Plast
Reconstr Surg 57:39–49, 1976.
11. Garlock JH: The repair processes in wounds of tendons, and
in tendon grafts, Ann Surg 85:92–103, 1927.
12. Hernandez A, Velasco F, Rivas A, et al: Preliminary report on
early mobilization for the rehabilitation of flexor tendons,
Plast Reconstr Surg 40:354–358, 1967.
13. Hester TR, Hill L, Nahai F: Early mobilization of repaired
flexor tendons within digital sheath using an internal profun-
dus splint: Experimental and clinical data, Ann Plast Surg
12:187–198, 1984.
14. Harmer TW: Tendon suture, Boston Med Surg J 177:808–810,
1917.
15. Harmer TW: Cases of tendon and nerve injury, Boston Med
Surg J 194:739–747, 1926.
Chapter 13B:  The Chelmsford Experience 131
patients, the distribution of hand casualties, availability
of therapists, the training of more hand surgeons and
therapists, and so on. Regrettably, our government and
immediate administrators, in keeping with many others,
have reduced facilities for treatment of this group of
patients progressively over the past few years. Neverthe-
less, it is probably still true to say that, globally, the
number of good hand units continues to increase, with
the result that primary flexor surgery is being carried
out to higher standards in more places now than 20
years ago.
CONCLUSION
However, given that 10 of every 100 patients undergoing
surgery in a good unit will still either experience rupture
of the repair or require a tenolysis to free stuck tendons,
we should not be satisfied with current practice. While
we are still obliged to call results “excellent” when they
are only 85% of normal,37 the search for better treat-
ment should continue!
16. Harmer TW: Injuries to the hand, Am J Surg 42:638–658,
1938.
17. Lahey FH: A tendon suture which permits immediate motion,
Boston Med Surg J 188:851–852, 1923.
18. Lexer E: Die Verwerthung der freien Sehnentransplantation,
Archiv Klin Chir 98:818–825, 1912.
19. Kessler I, Nissim F: Primary repair without immobilisation of
flexor tendon division within the digital sheath, Acta Orthop
Scand 40:587–601, 1969.
20. Mangus DJ, Brown F, Byrnes W, et al: Tendon repairs with
nylon and a modified pullout technique, Plast Reconstr Surg
48:32–35, 1971.
21. Mantero R, Bertolotti P, Badoini C: II pull-out in “no man’s
land” e al canale digitale nelle lesioni dei flessori (metodo
personale), Riv Chir Mano 11:119–130, 1973/74.
22. Murray G: A method of tendon repair, Am J Surg 99:334–335,
1960.
23. Nigst H: Chirurgie der Beugesehnen, Handchir 8:225–236,
1976.
24. Pribaz JJ, Morrison WA, Macleod AM: Primary repair of flexor
tendons in no-man’s land using the Becker repair, J Hand Surg
(Br) 14:400–405, 1989.
25. Savage R, Risitano G: Flexor tendon repair using a “six strand”
method of repair and early active mobilisation, J Hand Surg
(Br) 14:396–399, 1989.
26. Bainbridge LC, Robertson C, Gillies D, et al: A comparison
of post-operative mobilization of flexor tendon repairs with
“passive flexion-active extension” and “controlled active
motion” techniques, J Hand Surg (Br) 19:517–521, 1994.
27. Cullen KW, Tolhurst P, Lang D, et al: Flexor tendon repair in
zone 2 followed by controlled active mobilisation, J Hand
Surg (Br) 14:392–395, 1989.
28. Elliot D, Moiemen NS, Flemming AFS, et al: The rupture rate
of acute flexor tendon repairs mobilized by the controlled
active motion regimen, J Hand Surg (Br) 19:607–612, 1994.
29. Harris SB, Harris D, Foster AJ, et al: The aetiology of acute
rupture of flexor tendon repairs in zones 1 and 2 of the fingers
during early mobilization, J Hand Surg (Br) 24:275–280,
1999.
132 Section 2:  Primary Flexor Tendon Surgery
30. Baktir A, Türk CY, Kabak S, et al: Flexor tendon repair in zone
2 followed by early active mobilization, J Hand Surg (Br)
21:624–628, 1996.
31. Lister GD, Kleinert HE, Kutz JE, et al: Primary flexor tendon
repair followed by immediate controlled mobilisation, J
Hand Surg (Am) 2:441–451, 1977.
32. Chow JA, Thomes LJ, Dovelle S, et al: A combined regimen
of controlled motion following flexor tendon repair in “no
man’s land,” Plast Reconstr Surg 79:447–455, 1987.
33. Chow JA, Thomes LJ, Dovelle S, et al: Controlled motion
rehabilitation after flexor tendon repair and grafting. A multi-
centre study, J Bone Joint Surg (Br) 70:591–595, 1988.
34. Gault DT: A review of repaired flexor tendons, J Hand Surg
(Br) 12:321–325, 1987.
35. Saldana MJ, Chow JA, Gerbino P 2nd, et al: Further experience
in rehabilitation of zone II flexor tendon repair with dynamic
traction splinting, Plast Reconstr Surg 87:543–546, 1991.
36. Duran RJ, Houser RG: Controlled passive motion following
flexor tendon repairs in zones II and III. In Hunter JM,
Schneider LH, editors: AAOS Symposium on Flexor Tendon
Surgery in the Hand, St Louis, 1975, CV Mosby, pp 105–114.
37. Strickland JW, Glogovac SV: Digital function following flexor
tendon repair in zone II: A comparison of immobilization
and controlled passive motion techniques, J Hand Surg (Am)
5:537–543, 1980.
38. Kirchmayr L: Zur Technik der Sehnennaht, Zentralbl Chir
40:906–907, 1917.
39. Amadio PC: Outcome assessment in hand surgery and hand
therapy: an update, J Hand Ther 14:63–67, 2001.
40. Jansen CW, Watson MG: Measurement of range of motion of
the finger after flexor tendon repair in zone II of the hand,
J Hand Surg (Am) 18:411–417, 1993.
41. So YC, Chow SP, Pun WK, et al: Evaluation of results in flexor
tendon surgery: A critical analysis of five methods in ninety-
five digits, J Hand Surg (Am) 15:258–264, 1990.
42. Tsuge K, Ikuta Y, Matsuishi Y: Intra-tendinous tendon suture
in the hand—a new technique, Hand 7:250–255, 1975.
43. Tsuge K, Ikuta Y, Matsuishi Y: Repair of flexor tendons by
intratendinous suture, J Hand Surg 2:436–440, 1977.
44. Silfverskiöld KL, May EJ: Flexor tendon repair in zone II with
a new suture technique and an early mobilization program
combining passive and active flexion, J Hand Surg (Am)
19:53–60, 1994.
45. Savage R: The influence of wrist position on the minimum
force required for active movement of the interphalangeal
joints, J Hand Surg (Br) 13:262–268, 1988.
46. Dowd MB, Figus A, Harris SB, et al: The results of immediate
re-repair of zone 1 and 2 primary flexor tendon repairs which
rupture, J Hand Surg (Br) 31:507–513, 2006.
47. Peck FH, Kennedy SM, Watson JS, et al: An evaluation of the
influence of practitioner-led hand clinics on rupture rates
following primary tendon repair in the hand, Br J Plast Surg
57:45–49, 2004.
48. Elliot D: Primary flexor tendon repair: operative repair,
pulley management and rehabilitation, J Hand Surg (Br)
27:507–513, 2002.
49. Tang JB: Indications, methods, postoperative motion and
outcome evaluation of primary flexor tendon repairs in Zone
2, J Hand Surg (Eur) 32:118–129, 2007.
50. Moiemen NS, Elliot D: Primary flexor tendon repairs in zone
1, J Hand Surg (Br) 25:78–84, 2000.
51. Murphy FG: Repair of laceration of flexor pollicis longus
tendon, J Bone Joint Surg (Am) 19:1121–1123, 1937.
52. Sirotakova M, Elliot D: Early active mobilization of primary
repairs of the flexor pollicis longus tendon, J Hand Surg (Br)
24:647–653, 1999.
53. Giesen T, Sirotakova M, Elliot D: Flexor pollicis longus
primary repair: further experience with the Tang technique
and controlled active mobilisation, J Hand Surg (Eur) 34:
758–761, 2009.
54. Sirotakova M, Elliot D: Early active mobilization of primary
repairs of the flexor pollicis longus tendon with two Kessler
two strand core sutures and a strengthened circumferential
suture, J Hand Surg (Br) 29:531–535, 2004.
55. Smith AM, Evans DM: Biomechanical assessment of a new
type of flexor tendon repair, J Hand Surg (Br) 26:217–219,
2001.
56. Silfverskiöld KL, Andersson CH: Two new methods of tendon
repair: an in vitro evaluation of tensile strength and gap for-
mation, J Hand Surg (Am) 18:58–65, 1993.
57. Tang JB, Shi D, Gu YQ, et al: Double and multiple looped
suture tendon repair, J Hand Surg (Br) 17:699–703, 1994.
58. Tang JB, Gu YT, Rice K, et al: Evaluation of four methods of
flexor tendon repair for postoperative active mobilisation,
Plast Reconstr Surg 107:742–749, 2001.
59. Kubota H, Aoki M, Pruitt DL, et al: Mechanical properties of
various circumferential tendon suture techniques, J Hand Surg
(Br) 21:474–480, 1996.
60. Wong JK, Cerovac S, Ferguson MW, et al: The cellular effect
of a single interrupted suture on tendon, J Hand Surg (Br)
31:358–367, 2006.
 C The Mayo Clinic Experience
Robert R.L. Gray, MD, and Peter C. Amadio, MD
OUTLINE
This chapter presents the indications, methods, and
postoperative care for flexor tendon repair that are
followed at the Mayo Clinic.
Flexor tendon injuries in the hand, especially in zone 2,
have proved to be a difficult clinical entity to manage,
with humbling results in many cases. Advances in repair
technique, suture material, and rehabilitation have
improved outcomes over historic controls, but the
typical result remains a finger with motion that is less
than normal.
Many basic science studies have looked at various
biomechanical aspects of tendon repair, as well as
biologic aspects of tendon healing and adhesion
formation.1-4 Manipulation of these biologic processes,
in an effort to speed healing, limit scarring, or both,
has come the fore of tendon repair research, as
biomechanical gains are providing relatively modest
clinical improvements in comparison with initial
breakthroughs.5
In our research in flexor tendon repair, we similarly
investigated methods of improving healing as well as
improving motion and lowering work of flexion. Pri-
marily, in our lab, we have focused on lowering gliding
resistance by improving repair methods and by the addi-
tion of bioactive compounds to limit scar formation
and decrease friction. The results are encouraging and
will direct future efforts by serving as benchmark and
model for comparison of new techniques.6-9
Examination of our clinical experience with flexor
tenorrhaphy reveals some emerging trends, but more
significantly, illuminates some limitations in our ability
to address these injuries. Without dedicated prospective
data collection, much of the outcome information is
not standardized. In addition, as part and parcel of
the patient population who experience these injuries,
frequently young men, not always steadily employed
and often, at our center, being referred from a great
distance for surgery, with aftercare provided closer to
home, compliance, and follow-up have been variable.
What follows is a resume of our current approach to
these problems.
INDICATIONS
Our indications for primary flexor tenorrhaphy are rela-
tively simple and inclusive. Any patient with an acute
traumatic tendon injury who desired surgery after an
explanation of the risks, benefits, and alternatives is
offered the procedure. In addition to the tendinous
injury, associated bony and neurovascular injuries are
repaired as indicated. Typically, this included primary
neurorrhaphy with or without a nerve conduit and arte-
rial repair if both proper digital arteries are injured. If
soft tissue coverage is lacking, this is addressed first,
though often recently through microsurgical techniques
that have allowed skin cover and tendon repair to be
accomplished simultaneously.
OPERATIVE TECHNIQUES
There are currently 12 hand surgeons at the Mayo Clinic.
Although there are some shared practices, each surgeon
manages his or her own patients. As time has progressed,
there has been a trend toward repair techniques with
greater numbers of core suture strands.2 Currently, for
flexor digitorum profundus (FDP) repairs in zone 2,
many surgeons use a double Tsuge repair of 3-0 Supra-
mid, with a running peripheral suture of 6-0 Prolene
(Figure 13[C]-1). Others prefer a double modified Pen-
nington repair of 3-0 or 4-0 Ticron, Supramid, or, more
recently, Fiberwire, again with a running suture of 6-0
Prolene in the epitenon (Figure 13[C]-2). Less com-
monly, some surgeons use the Strickland six-strand
technique, a Tajima modification of a Kessler two-strand
technique, or a cruciate four-strand technique.13 We find
the locking loops of the Pennington repair to be particu-
larly effective, especially when they are tightened sepa-
rately prior to tying the knot. For those who use it, the
speed of the Tsuge repair is an attraction, especially in
cases of polytrauma.
While a running simple epitendinous suture of 6-0
Prolene is most commonly used to tidy the FDP repair,
occasionally a running locked suture is used for this
purpose. In cases with transections of the FDP and both
slips of the flexor digitorum superficialis (FDS), we
seldom repair all three tendons. Most commonly, one
slip of FDS (the smaller or less easily repaired side, if
there is a difference) is excised to minimize bulk at the
repair site.10-12 When all three tendons are repaired, the
most common repair of the FDS slips is a single figure-
of-eight stitch.
In all repair techniques, efforts are made to keep any
surface knots and suture loops limited, especially on the
volar surface. If the knots and loops are not buried in
the repair site (modified Kessler), they are positioned
133
134 Section 2:  Primary Flexor Tendon Surgery

A B

C D

E F

G H
 Chapter 13C:  The Mayo Clinic Experience 135

Figure 13(C)-1  A, Nerve cutting box is used to freshen and prepare tendon edge. B, Tendon edges are opposed without
tension. Note the repaired FDS slip beneath and the Keith needle used to prevent the proximal FDP tendon stump from
retracting. C, The lateral third of the distal stump is grasped with the first stitch. D, The stitch is locked through the looped
end. E, The next throw is begun just distal to the grasping loop, taking care to center it within the tendon. The loop should
be pulled securely flat prior to completing the repair. F, The second Tusge stitch is placed in the same fashion. One side of
the suture loop is cut at this point. G, Approximately one-third of the tendon is grasped in the next throw. The two suture
ends are now tied for each suture loop to complete the repair. H, Completion of core suture repair. Note the absence of
gapping or bunching at the repair site. An epitendeninous repair is then performed at this point with fine (6-0)
nonabsorbable monofilament suture.

A B

C D

Figure 13(C)-2  A, Proximal stump is entered for modified

Kessler repair. Note that the tendon is grasped within
the stump so that the surface is not damaged by the
forceps—a “no-touch” technique. B, A grasping stitch is
completed and a transverse stitch is placed across the
midsubstance of the tendon. C, Another grasping stitch
exiting the proximal stump completes that side. The
grasping loop on the distal stump is thrown. D, The distal
stitch is completed. The strands are tied together so that
the knots are completely within the repair site. E, The
repair is completed and a running epitendinous repair is
E
completed with 6-0 nylon suture.
136 Section 2:  Primary Flexor Tendon Surgery
laterally (Tsuge) so that they do not interfere with
tendon gliding.14 Lateral position of the suture knots
has been shown to lower substantially the work of
flexion. Less frequently, knots of the Tsuge repair are
buried in slits made in the tendon substance.
Neurovascular injuries are quite common, occurring
in nearly two-thirds of our patients. Typically, all proper
digital nerves are repaired when feasible, but usually
isolated proper digital artery injuries are not repaired.
Mangled hands of course must be managed separately,
often with delayed repair or secondary reconstruction.
POSTOPERATIVE CARE
The postoperative protocol used nearly universally in
our historical series was the modified Duran protocol
as described in the Indiana Hand Center guide to hand
therapy.15 While this is still preferred by several in our
group, others now prefer early protected mobilization
with synergistic wrist motion flexor tendon rehabilita-
tion protocols.16 Some prefer the use of hinged dorsal
splints that, while effective, are expensive to fabricate.
Patients are usually seen for their initial visit 3 to 6
days postoperatively.17 The initial postoperative dressing
is usually a well-padded dorsal splint with the wrist in
30° of flexion and the metacarpophalangeal (MCP)
joints in flexion, with the interphalangeal (IP) joints
blocked at 0°extension. Using IP motion is allowed in
this splint, although some prefer full immobilization
for the first few days postoperatively. This initial dress-
ing is removed at the first postoperative visit, and the
wounds are examined. A protective dorsal-blocking
thermoplastic splint is then usually fabricated. Depend-
ing on the level of swelling present in the digits, the
standard Duran passive motion protocol is initiated at
this point or, if swelling is minimal, place-and-hold
exercises are begun immediately.18 Several surgeons
now use the modified Tanaka method, in which the
synergistic motion includes alternating wrist and MCP
References
1. Momose T, Amadio PC, Zhao C, et al: The effect of knot loca-
tion, suture material, and suture size on the gliding resistance
of flexor tendons, J Biomed Mater Res 53:806–811, 2000.
2. Momose T, Amadio PC, Zhao C, et al: Suture techniques
with high breaking strength and low gliding resistance: exper-
iments in the dog flexor digitorum profundus tendon, Acta
Orthop Scand 72:635–641, 2001.
3. Yang C, Zhao C, Amadio PC, et al: Total and intrasynovial
work of flexion of human cadaver flexor digitorum profundus
tendons after modified Kessler and MGH repair techniques,
J Hand Surg (Am) 30:466–470, 2005.
4. Tanaka T, Amadio PC, Zhao C, et al: Gliding characteristics
and gap formation for locking and grasping tendon repairs:
A biomechanical study in a human cadaver model, J Hand
Surg (Am) 29:6–14, 2004.
5. Zhao C, Sun YL, Ikeda J, et al: Improvement of flexor tendon
reconstruction with carbodiimide-derivatized hyaluronic acid
extension with IP flexion and wrist flexion, MCP exten-
sion, and IP extension. In this protocol, which allows
passive pull both proximally and distally in zone 2,
the MCP joints are separately mobilized by alternating
this modified synergistic pattern with the normal syner-
gistic motion of wrist extension with fist alternating
with wrist flexion and finger extension. For patients who
live close to the clinic, biweekly or every-other-day
therapy visits are scheduled in the first few weeks post-
operatively. The patient is seen by the surgeon at a
minimum of once weekly. Patients who live at a dis-
tance pose more problems, because it is difficult to
supervise their rehabilitation.
SUMMARY
The experience with primary flexor tendon repair at the
Mayo Clinic is probably typical of most institutions.
These are a challenging clinical entity in isolation and
more often than not are accompanied by a neurovascu-
lar injury that further hinders the results. Repair tech-
niques have tended to increase the number of core
suture strands over time, as well as those that use a
locking stitch as opposed to a grasping stitch. Most
surgeons are now choosing a four-strand technique with
a trend toward the Tsuge being the repair of choice.
Epitendinous stitches are nearly universally used with a
6-0 nonabsorbable monofilament suture. When both
slips of the FDS and the FDP are transected in zone 2,
one slip of the FDS is often, but not always, resected to
reduce bulk at the repair site.
Flexor tendon injuries remain an important clinical
problem due to their frequency and complex manage-
ment. As repair techniques and rehabilitation protocols
have improved, increasing attention is being placed on
biologic interventions to improve healing and decrease
adhesion formation. Improvements in results will likely
be seen once these adjunctive methods leave the labora-
tory and enter the clinical sphere.
and gelatin-modified intrasynovial allografts: study of a
primary repair failure model, J Bone Joint Surg (Am) 92:2817–
2828, 2010.
6. Akasaka T, Nishida J, Araki S, et al: Hyaluronic acid dimin-
ishes the resistance to excursion after flexor tendon repair: An
in vitro biomechanical study, J Biomech 38:503–507, 2005.
7. Sun Y, Chen MY, Zhao C, et al: The effect of hyaluronidase,
phospholipase, lipid solvent and trypsin on the lubrication
of canine flexor digitorum profundus tendon, J Orthop Res
26:1225–1229, 2008.
8. Zhao C, Sun YL, Kirk RL, et al: Effects of a lubricin-containing
compound on the results of flexor tendon repair in a canine
model in vivo, J Bone Joint Surg (Am) 92:1453–1461, 2010.
9. Yoshii Y, Villarraga HR, Henderson J, et al: Speckle tracking
ultrasound for assessment of the relative motion of flexor
tendon and subsynovial connective tissue in the human
carpal tunnel, Ultrasound Med Biol, 35:1973–1981, 2009.

10. Paillard PJ, Amadio PC, Zhao C, et al: Gliding resistance after
FDP and FDS tendon repair in zone II: An in vitro study, Acta
Orthop Scand 73:465–470, 2002.
11. Paillard PJ, Amadio PC, Zhao C, et al: Pulley plasty versus
resection of one slip of the flexor digitorum superficialis after
repair of both flexor tendons in zone II: A biomechanical
study, J Bone Joint Surg (Am) 84:2039–2045, 2002.
12. Zhao C, Amadio PC, Zobitz ME, et al: Resection of the flexor
digitorum superficialis reduces gliding resistance after zone II
flexor digitorum profundus repair in vitro, J Hand Surg (Am)
27:316–321, 2002.
13. Strickland JW: Flexor tendon injuries: II. Operative technique,
J Am Acad Orthop Surg 3:55–62, 1995.
14. Silva JM, Zhao C, An KN, et al: Gliding resistance and strength
of composite sutures in human flexor digitorum profundus
Chapter 13C:  The Mayo Clinic Experience 137
tendon repair: An in vitro biomechanical study, J Hand Surg
(Am) 34:87–92, 2009.
15. Cannon NM: Diagnosis and Treatment Manual for Physicians and
Therapists. Upper Extremity Rehabilitation, ed 4, Indianapolis,
Indiana, 2001, Hand Rehabilitation Center of Indiana, p 296.
16. Zhao C, Amadio PC, Zobitz ME, et al: Effect of synergistic
motion on flexor digitorum profundus tendon excursion,
Clin Orthop Relat Res 396:223–230, 2002.
17. Zhao C, Amadio PC, Tanaka T, et al: Short-term assessment
of optimal timing for postoperative rehabilitation after flexor
digitorum profundus tendon repair in a canine model, J Hand
Ther 18:322–329, 2005.
18. Boyer MI, Strickland JW, Engles D, et al: Flexor tendon repair
and rehabilitation: state of the art in 2002, Instr Course Lect
52:137–161, 2003.
 D The Nantong Experience
Jin Bo Tang, MD, Jun Tan, MD, and Ren Guo Xie, MD
OUTLINE
In this chapter, we review our experience and the
current methods of flexor tendon repair (in zone 2 in
particular) in our hand surgery service. We discuss
methods of tendon repair and postsurgical rehabilita-
tion, particularly procedures that may be critical to
optimal tendon function.
Our hand center is a part of the university hospital
system located in Nantong, serving about 7 million
people in the Yangtze River Delta area and neighboring
industrial and metropolitan cities, Suzhou and Shang-
hai. Injuries involving tendons that are seen at our clinic
vary from simple clean-cut injuries to major limb or
digital amputations. Three kinds of injuries—tendon
divisions in the digits and palm, tendon lacerations
in the wrist or forearm, and tendon injuries in digital
amputations—undergo primary, delayed primary, or
secondary repairs, respectively. Tendon transfer opera-
tions are performed for late functional reconstruction
following nerve injuries or neurological disorders. There
are 150 to 200 operations for these tendon injuries per-
formed annually, which constitutes 7% to 10% of the
total number of operations in our hand service. During
2011, the total number of operations for hospitalized
patients in our hand center was 2132 (day surgery cases
not included), of which tendon injuries in the digits and
palm, or dorsal hand, accounted for 68 cases (3.2%);
tendon injuries in the wrist, 44 cases (2.1%); and digital
(or limb) replantations, 84 cases (3.9%). Established as
an independent department with 100 beds devoted
solely to surgery of the hand and upper extremity, our
unit has the capacity to hospitalize patients for 10 days
to 2 weeks after tendon surgery. This system allows the
patients to be cared for and supervised within the hospi-
tal as they initiate early active digital motion exercises.
Our treatment of tendon injuries in wrist and distal
forearm and those associated with digital replantation
surgeries are discussed in other chapters. We presented
here our methods of flexor tendon repairs in the digits
and palm.
CLINICAL METHODS
Table 13(D)-1 summarizes the methods that we have
used over past decades, as well as the conceptual changes
138
underlying these methods. Our current methods are
illustrated in more detail next.
Anesthesia and Skin Incisions
We mostly use axillary regional block anesthesia when
performing flexor tendon repairs in the digits and palm.
General anesthesia is used in some patients with exten-
sive wounds or with injuries involving multiple sites. A
tourniquet is applied to the upper arm in all patients to
ensure a bloodless operation field. We prefer a Bruner’s
zigzag incision to expose the tendons (Figure 13[D]-1).
A midlateral incision is rarely used in primary or delayed
primary tendon repair. For a clean-cut injury, the inci-
sion usually does not exceed 3 cm longitudinally, a
length of a field just sufficient for surgical tendon repair.
We include the laceration in the skin as a part of this
incision in primary tendon repair. In delayed primary
repair, the skin wound is closed primarily and is healed
in 1 or 2 weeks, and we do not usually include the
original wound into the incision.
Lacerations through the skin and sheath are either
transverse or oblique and, in most cases, do not overlie
the site of tendon transection. The tendon ends can
mostly be brought into vision by passive flexion of the
digits. For zone 1 tendon injuries, the proximal flexor
digitorum profundus (FDP) tendon end does not
retracted far proximally and flexion of the metaphalan-
geal (MP) and proximal interphalangeal (PIP) joints
usually can bring the tendon end into the wound. In
some cases, a separate incision in the proximal part of
the digit or palm is necessary to find the retracted
tendon. For zone 2 tendon injuries, those in the proxi-
mal part of the fingers, in particular, often retract into
the palm (see Figure 13[D]-1). During surgery for
delayed primary repair, about half of our zone 2 repairs
require an additional incision to find the retracted prox-
imal tendon end; an incision at the distal palmar crease
usually reveals the tendon end (see Figure 13[D]-1).
Zone 2 Flexor Tendon Repairs
Incisions in the Sheath and Pulleys
By pulling the skin and subcutaneous flaps created by
the Bruner incision with retractors, the flexor sheath is
exposed. The major annular pulleys (the A1, A2, and A4
pulleys) are easily recognizable and are distinguished
from the remainder of the sheath by their thickness and
 Chapter 13D:  The Nantong Experience 139

Table 13(D)-1  Clinical Methods Used Over the Past Two Decades in Our Unit
1989–1994 The First Period
Tendon: repaired with two-strand modified Kessler, double, or six-strand looped suture methods.1,2
Sheath: closure, leave it open without repair, or interposing sheath graft reconstruction.2
New methods/concepts used: (1) Zone 2 subdivisions for recording sites of tendon lacerations and
analysis of treatment results; (2) stronger surgical repair methods.1-3
Investigations: (1) clinical results of double or multiple looped suture repairs;1 (2) analysis of clinical
outcomes in zone 2C;2,3 (3) results of sheath enlargement plasty.
Results: Zone 2C had the worst outcomes compared with other parts of zone 2, and 4% repair ruptures
occurred even with strong (six-strand) surgical repairs.1,3
1995–2002 The Second Period
Tendon: repaired with double or six-strand looped suture methods.
Sheath: closure, leave it open without repair, or interposing graft reconstruction.
New methods/concepts used: partial A2 pulley release or release of the entire A4 pulley.
Investigations: examination of finger movement after partial release of the A2 or A4 pulley.4
Results: release of a part of the A2 pulley or the A4 pulley, does not lead to clinically noticeable tendon
bowstringing, when other annular pulleys are intact.4
2003–2011 The Third Period
Tendon: repaired with a modified six-strand looped suture method (M-Tang repair).5
Sheath: leave it open without repair in most cases, but avoid opening sheath-pulley >2 cm.
Pulley: in cases when tendons are cut in or just distal to major pulleys, the A2 pulley is vented partially,
or the A4 pulley is vented entirely.5,6
New methods/concepts used: (1) a modified six-strand suture repair,5,6 (2) an early passive-active
motion regimen.6 and (3) definitions of length and limit of judicious pulley-sheath release.6
Subjects of interest: pulley-release may be a key to reducing resistance to tendon.
Loosely supervised early active motion may be feasible and safe clinically.
Investigations: examination of the cases treated with pulley-venting, strong core suture, and the new
passive-active motion regimen.
Results: Combination of stronger surgical repair, proper treatment (release) of the major pulley, and a
combined passive-active motion regimen favors near-ideal recovery.
Proper release of the constrictive part of the pulleys probably is most critical.

appearance as condensed, white fibrous structures. The
thin annular pulleys (the A3 and A5 pulleys) are not
seen clearly and, sometimes, appear indistinguishable
from the adjacent sheath. The cruciform pulleys are
usually not identifiable. However, the location of the A3
pulley has little variation and is almost always at the
level of the PIP joint. It is not necessary to identify the
A5 pulley or any of the cruciform pulleys.
The injured tendons are approached by incisions in
the sheath-pulleys at different sites according to the
level of the tendon laceration. When the level of tendon
laceration is judged to be in the vicinity of the PIP joint,
we incise the synovial sheath longitudinally, or even
excise a portion of it, to create a window in the sheath.
When the tendon is cut at the level of the A3 pulley, we
open the sheath between the A2 and the A3 pulleys. The
A3 pulley can be incised as well, but the incision should
not extend distally to the A4 pulley. A part of the syno-
vial sheath is kept intact distal to the PIP joint. When
the cut is between the PIP joint and the A4 pulley, we
frequently have to include the A3 pulley in the sheath
incision, but preserve the sheath proximal to the A3
pulley. In other words, some part of the sheath is pre-
served between the A2 and A3 pulleys.
In many other cases, the tendons are cut at the loca-
tion of one, or more, of the strong annular pulleys (e.g.,
a little distal to the A2 pulley, through the A2 and/or A1
pulleys and in the vicinity of the A4 pulley). We cut the
entire A4 pulley and a major part of the A2 pulley
around tendon repair sites, while leaving the synovial
part of the sheath and the other pulley structures intact.
When the tendons are cut slightly distal to the A2 pulley,
within zone 2B, we open the sheath longitudinally for
1 cm distal to the A2 pulley and also open the distal
half of the A2 pulley (see Figure 13[D]-3). When repair-
ing the tendon at the distal edge, or in the distal part,
of the A2 pulley, we cut open a part of the sheath distal
to the A2 pulley together with the distal two-thirds of
the A2 pulley.
When repairing a tendon under the middle or proxi-
mal part of the A2 pulley, we cut open the proximal
two-thirds of the A2 pulley. Because the excursion of the
FDP tendon within this part of zone 2 is usually about
2 cm, the lengths of release of the A2 pulley and the
140 Section 2:  Primary Flexor Tendon Surgery

C
A
Figure 13(D)-1  Skin incisions for primary or delayed primary repairs: A, skin incisions used in the hand to exposed the
injured tendons; B, Bruner’s zigzag incision is used to expose the wound in delayed primary repair; C, additional small
transverse incision proximal to the tendon cut level may be required if the proximal end of the tendon retracted proximally.
The retracted tendon end is lead through the synovial sheath tunnel by insertion of a silicone tube (or a catheter) to
approximate the distal tendon stump.

adjacent sheath referred to above are, in most cases, suf-
ficient to free the tendon repair from restriction by the
pulley, or catching on rims of the remaining parts of the
pulleys, during movement of the finger joints through
a full range of motion.
Tendons lacerated proximal to the A2 pulley are the
least difficult to access. They can be approached through
an incision in, or excision of, the sheath proximal to the
A1 pulley, or an incision over the A1 pulley. Extending
the skin incision proximally may help expose the
retracted tendon end.
Tendon Repair Techniques
After making the incisions in (or excisions of) the sheath
and pulleys, the tendon lacerations are exposed. The
distal tendon ends are brought into the operation field
by flexion of the distal interphalangeal (DIP) joint and
the proximal tendon ends are brought into the field
by, either flexion of the metacarpophalangeal and PIP
joints, or through a separate proximal incision (see
Figure 13[D]-1), as illustrated. The proximal tendon
ends are temporarily fixed using a needle proximal to
the laceration site, but the distal tendon ends do not
usually need temporary fixation because passive flexion
of the DIP joint during surgery by an assistant easily
brings the ends into the center of the operation field.
If the tendon ends are untidy, the tendon ends are
trimmed using a pair of scissors or a scalpel. In delayed
primary repairs, the tendon ends are usually covered by
granulation tissues or collagen clots. These are removed
to refresh the tendon ends. Then, the core sutures are
placed into the tendon when the two tendon ends pulled
together tightly, with the distal joints of the finger held
in flexion by an assistant. Looped sutures carried on a
single needle are used for the core suture. In repairing
the FDP tendons, we currently use a modified six-strand
repair, performed by passing two looped 4-0 sutures
through the tendons. A U-shaped repair is created first
to connect the tendon ends using one looped suture,
and the second looped suture is then placed at the
center of the tendon, making a six-strand M-shaped
core suture repair. For the flexor digitorum superficialis

B
C
D
F
Figure 13(D)-2  Summary of repair methods we use
in repairing flexor tendons: A, modified Kessler repair;
B, cruciate repair; C, U-shaped repair; D, cross-lock repair
(a four-strand repair made with one needle carrying two
separate double suture strands); E, Tang technique of three
Tsuge suture repairs; F, M-Tang repair; the two-strand
Kessler repair is now used in repairing tendons in zone 5. In
repairing the tendons, in zones 1 to 4, four- or six-strand
repairs are used. C, D, Two four-strand repairs developed in
our unit.
(FDS) tendons, and some parts of the FDP tendon (such
as in zone 1 or in the little fingers), we use only a four-
strand U-shaped repair using one looped suture.
Figure 13(D)-2 summarizes the methods we use in
repairing tendons in zones 2 to 5. A two-strand Kessler
repair is used only sometimes in repairing tendons cut
in zone 5. We currently do not use two-strand repairs
in zone 2 or 3. Figure 13(D)-3 details our method of
making a six-strand M-shaped repair. The method of
placing three Tsuge looped sutures is illustrated in Figure
13(D)-4. This technique was simplified to the M-shaped
repair (see Figure 13[D]-3) that we currently use.
Chapter 13D:  The Nantong Experience 141
A
B
C
D
E
Figure 13(D)-3  Illustrations of how to make a six-strand
core suture using a looped suture repair (M-Tang method),
which forms an M-shaped configuration within the tendon.
We complement the core repair with simple periph-
eral suturing, with a simple running peripheral suture
or a few interrupted sutures most often being used.
Peripheral sutures serve to smooth the junction site of
the two tendon ends. We are able to put six to eight
loops of the running stitch in tendons of larger diameter
using 6-0 monofilament nylon. However, adding even
the simplest peripheral suture to the dorsal aspect of the
tendon is difficult in some cases. Instead, we sometimes
add a few interrupted sutures on the palmar and dorso-
lateral aspects of the tendon. Nevertheless it also seems
reasonable not to supplement the repair with peripheral
sutures when a strong six-strand core suture is used.
Although we have no experience with “core-suture only”
142 Section 2:  Primary Flexor Tendon Surgery
A
B cient length of the core suture purchase ensures that the
Figure 13(D)-4  Two operative views showing the methods
of placing three looped sutures into the tendon (the Tang
method). The pictures show a case repaired by the authors
in 1989. This repair method was replaced by the M-shaped
repair in the early 2000s.
tendon repairs, this simplifies the surgery and does not
appear to decrease tendon strength.
In performing core sutures, we are careful to (1) use
multistrand (four- or six-strand), rather than conven-
tional two-strand, repairs; (2) ensure the length of core
suture purchase is greater than 0.7 cm (0.7 to 1.0 cm in
most cases); and (3) add some tension to the repair site
by tightening the core suture, producing a roughly 10%
shortening of the tendon segment encompassed by the
core suture (Box 13[D]-1). We avoid making a loose, or
tension-free, tendon repair. We no longer use conven-
tional two-strand repairs in repairing tendons in the
fingers or palms.
We believe that the above three points are crucial to
the strength of a surgical flexor tendon repair. These
three measures may be particularly necessary when one
considers that the tendon ends usually become softened
after injuries and tensioned during active tendon
motion, before biological healing is accomplished.
Increasing the number of strands across the repair site
Box 13(D)-1 Critical Technical Points
In Approaching the Tendon:
1. Small sheath incision and preservation of majority of the
sheath
2. A sheath incision less than 2 cm is allowed, which may
include a part of the A2 pulley (up to two-thirds) or
entire A4 pulley.
3. At least a portion of the A2 pulley should be maintained,
and loss of more than two annular pulleys should be
particularly avoided.
4. Additional small incisions in the sheath may be neces-
sary to find the retracted tendon ends. Avoid a lengthy
incision of the sheath, which will damage the pulley
function.
In Suturing the Tendon:
1. Use strong repairs: a four- or six-strand core suture
repair, or a strong suture material.
2. Ensure sufficient length of core suture—about 0.7 to
1.0 cm in either tendon stump.
3. Add some tension to the repair site by tightening the
core suture.
4. Only simple (or no) peripheral sutures are needed when
a strong core suture is used.
is the easiest and most effective way to provide the
tendon repair with greater strength. Maintaining suffi-
suture is anchored reliably in sufficient amount of the
tendon substance that will not soften during the early
period after repair. Otherwise, the core suture may slip
or be pulled out, particularly when the tendon ends
soften after repair.
Adding slight tension to the repair site can greatly
decrease the chances of gapping of the tendon repair.
The tendon repair site may look a little bulky when
proximal pull of the muscles is eased by temporary
needle fixation of the proximal tendon during surgery.
However, this is not the case after release of the tempo-
rary fixation. Adding such a baseline tension to the
repair sites produces appropriate tension after surgery,
as this counteracts the tension of the muscles proxi-
mally during active motion. If tension has not been
added to the repair site, the repair may overstretch and
gap after surgery during active digital mobilization. We
consider that adding a little tension is as important as
adding a peripheral suture to resisting gaps between
tendon ends. With appropriate pretension of the repair
site, the chance of gapping, or the size of the gap, can
be decreased, thereby lowering the risk of catching of
the repair sites on any edge of the sheath.
Treatment of the FDS Tendon
The FDS tendon bifurcates under the middle part of the
A2 pulley and only injury in the proximal part of the
finger can produce a complete FDS tendon laceration.

The FDS tendon does not always need repair. A partial
laceration of the FDS tendon does not need repair at all.
Complete laceration of the FDS tendon does not require
surgical repair if the FDP tendon is intact. For complete
FDS and FDP tendon lacerations, least problematic is
repair of the FDS tendon cut proximal to the bifurca-
tion. Injuries to this part of the FDS tendon can be
treated almost identically to those of the FDP tendon,
except that the FDS tendon is flatter and does not
accommodate more than four suture strands. The bifur-
cating part of the FDS tendon (the segment within zone
2C) is much more difficult to treat. We use two sepa-
rated Tsuge sutures (a two-strand repair in each FDS
slip) to repair FDS injuries in zone 2C. In repairing the
FDS tendon within zone 2B, we use a variety of tech-
niques, including repair with a tendon-to-bone junction
(as for reattachment of the FDP tendon to the distal
phalanx) if the residual distal stump is very short, or
repair with a two-strand core suture for each slip if the
distal stump is long enough. When one slip is com-
pletely cut, but the other is uninjured, repair may not
be necessary. Quite often, we find that one, or both, slips
of the bifurcated FDS tendon are partially severed. In
this situation, we make a judgment according to the
length of the distal stump and the extent of the tendon
division. The partial cut is left untreated, or one or two
stitches are placed, to prevent triggering of the FDS
tendon during tendon movement.
Repair of the FDS tendon together with the FDP
tendon may favor gain of the strength of finger flexion
and prevent hyperextension of the PIP joint. Neverthe-
less, observations indicate that these benefits may not
be substantial. Repair of only the FDP tendons in our
patients have not led to a significant loss of power of
finger flexion, and daily use of the hand has not been
affected after repair of only the FDP tendon. Develop-
ment of hyperextension of the finger joints usually is
not notable. During surgery, after FDS tendon repairs,
we noted that the repaired FDS tendon is sometimes
entrapped by the narrow pulleys and the repair decreases
motion of the FDP tendon. Therefore, in primary repairs,
we only repair the completely lacerated FDS tendon
when such repairs appear not to decrease or impair FDP
tendon gliding. Repair of both FDS and FDP tendons is
more difficult when the surgery is delayed by 1, or more,
weeks after injury. When the cut is at, or just distal to, the
A2 pulley (zones 2C and 2B), we find it almost impos-
sible to repair both tendons after such a delay. The FDS
tendon retracts far proximally, and it is hard to pass both
tendons under the A2 pulley, or even a residual part of
this pulley. We usually leave the FDS tendon unrepaired,
or excise it locally, in delayed primary tendon repair.
Figures 13(D)-5 and 13(D)-6 illustrate two cases of
delayed primary repair of the FDP tendon with the six-
strand repair method. The partially injured FDS tendon
was left unrepaired in one case (see Figure 13[D]-5)
Chapter 13D:  The Nantong Experience 143
and locally excised to accommodate tendon movement
in the other (see Figure 13[D]-6), which was an end-
to-end repair of the FDP tendon 3 weeks after rupture
of the primary repair of the tendon. In both cases, the
A2 pulley was either vented or partially excised.
Treatment of the FDP and FDS Tendons
in the Palm (Zone 3)
Injuries in zone 3 involve the flexor tendons to several
fingers in most cases, and are often complicated by
nerve and vascular injuries. However, the treatment of
the flexor tendons in the palm is not as difficult as in
zone 2, because no sheath or pulleys are present in this
region and the proximal tendon ends are not retracted
too proximally. In making core and epitendinous sutures
in the FDS and FDP tendons, we follow the principles
and methods that are described for zone 2 injuries.
Repair of both the FDP and FDS tendons is usually
possible and less difficult than in zone 2. We use either
a four- or a six-strand core suture, using looped sutures
together with a simple running peripheral suture. Both
the superficialis and profundus tendons are repaired in
almost all cases, when no soft tissue loss is present.
Nevertheless, it should be particularly noted that com-
pound injuries with nerve and vascular injuries, or soft
tissue loss are quite frequent, and repair of the nerves
and, in some cases, vascular anastomoses, are integral
to these surgeries.
Treatment of the FDP Tendon in Zone 1
In our clinic, we see patients with an injury to the FDP
tendon in the distal part of the digits (zone 1 injury)
much less frequently than injuries in zones 2 and 3.
Treatment of FDP tendon lacerated about 1 cm proxi-
mal to the insertion is the same as for the FDP tendon
in zones 2 or 3. For the tendon laceration in which end-
to-end repair is not possible, we advance the tendon to
anchor it to the distal phalanx with mini-anchors
(Figure 13[D]-7) or reinforced suture repairs (such as
placement of two cross-stitch repairs, one on each of the
two FDP tendon bundles, using Fiberwire, or, rarely,
passing sutures through a transverse drill hole through
the distal phalanx).
The conventional pull-out repair method was used in
our clinic for many years and had problems of trauma-
tizing the nail in a significant proportion of the cases.
The pull-out repair method is arguably not an ideal
method. Reattachment of the FDP tendon to the phalanx
using mini-anchors or to the residual distal stump with
reinforcement with two cross-stitches to create a strong
tendon junction appears as efficacious as the pull-out
repair. Because the distal end of the FDP tendon does
not glide, reinforcing suture repairs that might lead to
tendon bulkiness elsewhere cause no problem of tendon
function here. With currently available repair materials
(such as Fiberwire), we can easily achieve a strong repair
144 Section 2:  Primary Flexor Tendon Surgery

A B

C D

E F
Figure 13(D)-5  A case of delayed primary repair in zone 2C. A–D, The partially cut FDS tendon was left unrepaired. The FDP
tendon was repaired with the M-Tang method. The distal two-thirds of the A2 pulley was vented. E and F, Postoperative
digital extension and flexion.

that allows protected early active finger motion after
repairing the distal FDP tendon. The opened sheath is
not repaired in zone 1.
Treatment of the FPL Tendon
A number of facts should be considered in flexor pollicis
longus (FPL) tendon repairs within the thumb: (1) only
one flexor tendon is present; (2) the FPL tendon is
among the largest in diameter in the digits; (3) the
pulleys in the thumb are not as broad, narrow, and rigid
as in the fingers; and (4) the flexor sheath is relatively
short. Surgical repairs of this large flexor tendon are
perhaps the easiest. Nevertheless, its gliding path in the
hand is unique, and flexion force transmitted along this
 Chapter 13D:  The Nantong Experience 145

A B

C D

E F
Figure 13(D)-6  A to D, A case of repair of a ruptured tendon 3 weeks after rupture of the primary repair of this tendon. The
FDS tendon was excised locally during the repair and the A2 pulley was shortened. E and F, Postoperative digital extension
and flexion.

tendon is perhaps the highest, subjecting the repaired
FPL tendon to greater danger of rupture when moved
actively. Consequently, a strong surgical repair is par-
ticularly necessary. This tendon can easily accommodate
a six-strand repair, which we use regularly to repair it,
even in children (Figure 13[D]-8).
We preserve at least two pulleys in the thumb, and
most often we have to incise one annular pulley to
access the tendon. Keeping two pulleys amply maintains
tendon function.
It is common to find the proximal tendon end
retracted, under the thenar muscles or in the carpal
tunnel, particularly with delayed repair. Because there is
no sheath over the FPL tendon in the thenar muscles,
we usually attempt to find the retracted FPL end without
incising the muscles, but by retracting the thenar muscles
146 Section 2:  Primary Flexor Tendon Surgery

to expose the FPL tendon underneath. When the FPL

tendon retracts more proximally, sometimes a small
incision is made just distal to the transverse carpal liga-
ment to locate the FPL tendon.

Flexor Tendon Repairs in Children

Figure 13(D)-7  A mini-anchor was used to anchor the
tendon to the distal phalanx in distal zone 1. This method
has recently replaced the pull-out suture method in our
practice.
Flexor tendon injury in children (i.e., patients under 12
years of age) is less common than in adults. Among our
cases, flexor tendon injuries in children account for
about 15% of the acute tendon injuries treated. Func-
tional recovery of children with flexor tendon injuries is
usually satisfactory. In approaching the tendons, we take
particular care not to violate the annular pulleys, which
are usually not as rigid as in adults, and pulley venting
is usually not necessary. However, we do not usually
repair FDS tendons in children, as such repairs (particu-
larly in the bifurcated part of the FDS) are difficult, or
even impossible, in many cases. The FDP tendon is
repaired with either a four-strand repair using one
looped suture to make a U-shape repair, or two looped
sutures to make a double Tsuge repair. In patients over

A C

B D
Figure 13(D)-8  Repair of a lacerated FPL tendon in a 9-year-old child with a six-strand M-shaped repair.

7 or 8 years old, we sometimes use a six-strand repair;
4-0 looped nylon suture is used in all cases.
We perform primary repair of the tendon in children
whenever possible, or try to carry out the repairs within
2 or 3 days of injury, without a long delay, because their
wounds heal quickly. After a long delay, the tendon ends
may retract quite far proximally, due to inability to
prevent contraction of the flexors. We treat flexor tendon
injuries in young patients older than 12 years identically
to those in adults.
POSTOPERATIVE REHABILITATION
We currently adopt a combined active and passive finger
flexion regimen in postoperative care, except in (1) the
patients younger than 12 years old; (2) the patients with
flexor division(s) associated with fractures; and (3) in
rare instances, in which the patients are judged to be
unable to cooperate.
A few changes can be noted between our current
practice and those described by other surgeons: (1) we
do not use rubber band traction because we believe that
it contributes to extension deficits of the fingers; (2) we
emphasize that active motion should proceed after mul-
tiple cycles of passive motion in each session of exercise,
to reduce the resistance to the active movement; (3) we
do not encourage full active flexion in the early weeks
after surgery, as tendons with marked flexion are easiest
First 2.5 weeks
Wrist flexion
Full passive flexion Active finger flexion-limited range
Figure 13(D)-9  The protective position of the hand and methods of rehabilitation in the first 2 12 weeks after surgery. Full
finger extension is emphasized, but only partial active finger flexion is encouraged. Inclusion of thumb in the splint is not a
necessity, but it prevents unintentional pinch action of the hand.
Chapter 13D:  The Nantong Experience 147
to disrupt; (4) we start motion exercise 3 days (or as late
as 5 days in cases with remarkable edema in the hand
or with soft tissue repair as well) after surgery, and we
perform only four or five sessions of exercise each day,
rather than require patients to move hourly; and (5) we
emphasize full extension of the fingers in the early
weeks after surgery when tendon healing is still weak,
and then shift our emphasis to active flexion in later
weeks, when tendon healing is stronger.
At postoperative 2 1 2 weeks, we change the protective
position of the hand and shift the emphasis to active
flexion. We encourage partial active digital flexion first,
and then proceed to full active flexion of the fingers
when no resistance is perceptible. Regarding the timing
of change of the hand position, we consider that tendon
healing strength has only started to increase at that time
and that immobilization of a joint for 2 1 2 weeks would
not cause contracture of soft tissues of the joint. Never-
theless, we also believe that such a change in protective
hand position may be made any time between 2 1 2 weeks
and 3 weeks.
The details of our method is as follows: the hand
is protected in a dorsal thermoplastic splint, with the
wrist in slight flexion (20° to 30°), the MP joints in
slight flexion, and the interphalangeal joints in exten-
sion (or minimal flexion), for the first 2 1 2 weeks (Figure
13[D]-9). We do not encourage patients to move the
Exercise of full
finger extension
Active finger flexion-limited range
148 Section 2:  Primary Flexor Tendon Surgery

finger during the first few postoperative days, because

the hand is painful, edema is more prominent and, Second 2.5 weeks
more importantly, adhesions have not yet developed.
Decreasing the number of days of motion decreases the
chance of repair rupture.

The First Period (Surgery to

2 1 2 Weeks Postsurgery)
Exercise starts at 3 to 5 days after surgery. Before each
episode of active digital flexion, the finger is passively
flexed 10, or more, times to lessen the overall resistance
of the finger joints and soft tissues—a “warming up”
process—after which active flexion should encounter
lower resistance. The patient is then instructed to flex the
fingers actively with gentle force 20 to 30 times during
each morning, noon, evening and before sleep session,
up to the range with which the patients feels comfort-
able. The motion range is usually from full extension to
one-third, or half, of the full flexion range, although this
may even increase to two-thirds of the full range if this
can be achieved with ease. Active flexion over the full
range is not encouraged, unless it can be achieved very
easily. Patients may increase the number of motion epi-
sodes up to five or six per day, but we do not require
patients to move hourly. In this first period, full active
Figure 13(D)-10  The protective position of the hand and
extension is particularly encouraged and the fingers are
methods of rehabilitation in the second 2 12 weeks after
passively stretched against the splint if full extension is
surgery. Full active digital flexion is encouraged and
not achieved. Prevention of extension deficits rather emphasized.
than full active flexion is a major goal during this period.

The Second Period (2 1 2 to

5 Weeks Postsurgery)
At 2 1 2 weeks, a new thermoplastic splint is made, with
the wrist splinted at 30 degrees of extension (Figure
13[D]-10). Finger flexion, both passive and active,
is emphasized during this period. The patients are
instructed to actively flex after a passive warm-up, as
earlier. Active flexion up to the mid-range is required as
a minimum and is encouraged further, up to two-thirds,
or the full, range of flexion, depending on the patient’s
ability to perform resistance-free motion. Digital flexion
from the mid-range to the full range, in particular over
the final one-third of the flexion range, is usually carried
out passively if the fingers encounter resistance. Our
studies show that finger flexion over the final one-third
of the full range of motion range encounters 5 to 10
times more resistance than in the previous two-thirds of
the range of motion. Thus, ruptures are much more
likely in this final part of the flexion range. Ensuring full
passive flexion, to prevent dorsal ligament tightening
and extensor tethering, and encouraging finger flexion
actively, while avoiding flexing the finger forcefully over
the final flexion range, are guidelines during this second
period.
If both FDS and FDP tendons are repaired at the
same level, differential FDS and FDP motion exercise is
encouraged through the first 5 weeks, with separated
active flexion of the two interphalangeal joints.
After 5 weeks, full active finger flexion is encouraged.
This can be started earlier if flexion in the final part of
the flexion range is judged to have less resistance. After
5 to 6 weeks, the splint is discarded or used only at
night. Patients can return to normal use of the finger
from 8 weeks.
The mechanical basis of the protocol design is synergy
between wrist and finger actions: with the wrist flexed,
full finger extension is achieved with less tension on the
flexor tendons, while full finger flexion can be achieved
with less tension on the repairs with the wrist extended.7,8
Active finger flexion to full flexion encounters much less
resistance when the wrist is extended than when the
wrist is flexed. This, effectively, avoids overload of the
repaired tendons. However, we do not encourage
maximal active flexion of the finger when the exercise
meets remarkable resistance, but instead suggest incor-
porating active finger flexion up to the mid-range and
passive motion from mid- to maximal flexion into indi-
vidual motion cycles.
Our experience indicates that repair rupture can be
minimized using this exercise regimen, which is aimed
at avoiding placing high levels of tension on repairs

while achieving sufficient active motion, together with
release of the sheath and pulleys and an increase in
surgical repair strength.
For children, we immobilize both the wrist and the
MP joints in slight flexion after surgery for 3 weeks, and
a protective splint to immobilize the patient for an addi-
tional 1 week or 10 days is usually prescribed. Active
flexion exercise of the fingers starts in the fourth week.
For an incomplete tendon cut and repair, we immo-
bilize the hand in a protective position for 2 weeks, and
early active finger motion is initiated immediately after
surgery. Patients return to normal use of the hand 4 to
5 weeks after surgery.
For FPL tendon repair, we immobilize the thumb
with the MP joint flexed at about 45°, the interphalan-
geal joint slightly flexed, and the wrist in a resting posi-
tion (extension of about 20°). Active thumb flexion
starts 2 or 3 days after surgery. Full active flexion is
encouraged if no noticeable resistance is encountered.
The hand is brought out of the splint to assume wrist
flexion when active extension is ordered to ease the
tension. The splint is removed 5 weeks after surgery, and
normal thumb motion is initiated in week 6 or 7.
For tendon repairs with fixation of a fracture, we
prescribe early motion exercise of the fingers only when
the fixation is stable, and motion is initiated 10 days to
2 weeks after surgery. The protective splint is applied for
4 or 5 weeks. With screw fixation of bones, or placement
of mini-plates on the lateral aspect of the shafts of pha-
langes or metacarpus, early active finger flexion is pos-
sible after edema subsides and preliminary fracture
healing is achieved. In cases of simultaneous repair of
the vascular structures, we delay motion exercise for 7
to 10 days after surgery. In cases with tension-free nerve
repairs, we do not usually modify our motion regimen
or timing of exercise initiation.
OUTCOMES
Our results have been separately presented in several
reports.1-5 Of particular note, our first series of cases with
use of four- or six-strand repairs had a rupture rate of
4%. In 1994, we reported the results of using double
or multiple looped suture tendon repairs in 51 fingers
(46 patients).1 By the White criteria, 76.5% of cases had
the good or excellent results, with 4% of the finger
repairs rupturing. In an earlier report, we analyzed the
results of a series of 72 tendon injuries in 54 fingers in
43 patients by subdivisions. Tendon injuries in zone 2C
(16 fingers), which constituted one-third of the injuries
in zone 2, had only 69% good or excellent results by
Strickland criteria, compared with 84% good or excel-
lent results in the other three subzones of zone 2.2 The
tendons in this series of cases were repaired with one of
the four methods: two-strand modified Kessler, two-
strand Tsuge, four-strand double Tsuge, or six-strand
triple loop-suture method, without purposeful release
Chapter 13D:  The Nantong Experience 149
of the A2 pulley. The zone 2C tendon repairs were asso-
ciated with the worst recovery of function.
In a series of later cases, repaired with a six-strand
repair by experienced surgeons with venting of either a
part of the A2 or the entire A4 pulley when necessary,
91% of repairs in 36 fingers were given a Strickland
rating of good or excellent,5 and the results of zone 2C
repairs were no different from those in other parts of
zone 2. No tendon ruptures were noted. Since 2005, we
have used a modified six-strand repair (referred to as the
“M-Tang” method in our department because of its
M-shaped configuration inside the tendon) using looped
suture to repair the FDP tendon.6 The restricting part of
any annular pulley was released through either a midline
incision or partial excision, when necessary. For clean-
cut tendon injuries in the thumb, index, middle, and
ring finger, or those wounds that could be converted to
clean-cut wounds, the current authors—all experienced
in primary tendon surgery—have achieved good or
excellent results in almost all cases. We had less satisfac-
tory recovery of function (graded as “fair”) in some
tendon repairs in the little finger, and in fingers with
more extensive loss of soft tissues and untidy tendon
lacerations (occurring in the palm area). When injuries
in the palm involve tendon injuries to three or more
digits, not all digits are likely to achieve good or excel-
lent recovery. Good or excellent recovery of function was
achieved in 84% of primary and delayed primary repairs
in the thumb, fingers, and palm, including those with
borderline indications. We note that the expertise level
of the operator exerts a significant influence on the out-
comes. When treated primarily by junior surgeons (resi-
dents) who fail to consult with the senior attending
surgeons, the outcomes are hardly able to reach “excel-
lent.” However, when treated by experienced surgeons,
adhering to established principles of treatment, and
given a clean-cut wound (or a wound that can be con-
verted into a clean-cut wound after débridement and
trimming), good or excellent recovery is fairly predict-
able, and almost all the cases recover good or excellent
function, except in some little fingers. No repair rupture
was found in this period. Careful examination also
revealed no perceivable tendon bowstringing after the
venting or shortening of the A2 or the A4 pulley (Figure
13[D]-11).
Factors that worsen the results roughly by “one grade”
include (1) tendon repairs in a finger with a fracture;
(2) tendon repairs in the little finger; (3) crush injuries
in fingers or the palm causing extensive tissue damage;
and (4) tendon repairs by less experienced surgeons.
DISCUSSION
Mastery of anatomy and careful dissection. Repair of
flexor tendon injuries is a perfect test of the technical
and intellectual competence of a hand surgeon. To
achieve satisfactory functional recovery is a challenge for
150 Section 2:  Primary Flexor Tendon Surgery
A B
Figure 13(D)-11  Examination to confirm the absence of perceivable tendon bowstringing during active finger flexion (A and
B) and resisted finger flexion (C) in a patient following venting of the A2 pulley up to two-thirds of its entire length.
even an experienced hand surgeon. Detailed anatomical
knowledge and meticulous dissection and repairs are
essential to both the success of the surgery and later
functional recovery. Optimal surgical outcomes (rather
than just completed surgeries—“success of surgery”)
require us to master the anatomy of the flexor tendon
system with great precision. When we begin a flexor
tendon repair, we should have a clear mental picture of
the location of each of major pulleys and its length and
diameter, and which parts of the sheath and pulley are
the narrowest. Knowing the locations of the A2 and A4
pulleys is only the minimal requirement.
Most surgeons do know the nomenclature, number,
and rough distribution of the pulleys in the fingers, but
frequently do not master the anatomical details of these
pulleys to the extent of knowing their lengths and exact
locations. These details are imperative to appropriate
exposure of the tendon, release of the resistance to
tendon motion after repair and prevention of tendon
bowstringing. The two most essential anatomical points
are (1) the A2 pulley, of length about 1.5 to 1.7 cm in
the adult middle finger, spans the proximal two-thirds
of the proximal phalanx and the middle and distal part
of this pulley is the narrowest; and (2) the A4 pulley is
much shorter, of a length about 0.5 to 0.7 cm, and is
located in the middle part of the middle phalanx. It is
also narrow. We advise that surgeons, junior surgeons
in particular, take time to review relevant diagrams, or
textbooks, before surgery. During surgery, the A1, A2,
and A4 pulleys appear as easily recognizable white
dense bands.
Stronger surgical repair is always recommended. A
great number of repair techniques are available cur-
rently. Two-strand core suture repairs (using either 4-0
or 3-0 sutures) provide weak tendon repairs. Four- or
C
six-strand core suture repairs provide strong surgical
repair. Although a number of factors affect the strength
of surgical repairs, not all exert a clinically significant
influence. Among the factors that most notably influ-
ence strength are (1) adequate strength of the suture
materials, (2) increased number of repair strands, or
alternatively larger caliber sutures, and (3) secure anchor
of sutures to the tendon. Increasing the number of
stands across the repair site is the most straightforward
way to achieve stronger and safer repairs. Maintaining a
sufficient number of sutures passing through the repair
sites, ensuring adequate purchase length of all sutures,
and secure tendon-suture junction sites ensure a strong
repair. We recommend a strong surgical repair (four-
strand or beyond) be always used. Suture configuration
within the tendon does not alter the strength very drasti-
cally, given an equal number of suture strands passing
across the repair site. For this reason, given the available
four-, six-, or even eight-strand repairs described, sur-
geons actually have ample freedom to choose any one
when implementing a strong repair.
Currently, we use four- or six-strand repairs in repair-
ing the tendon, and believe that an eight-strand repair
is probably not necessary, although it is a valid option.
The FPL tendon and the FDP tendon in the adult index,
middle, and ring fingers can easily accommodate four-
or six-strands repairs. The FDP tendon in the little finger
and the FDS tendon in all fingers may easily accom-
modate a four-strand repair. All repairs using four-strand
(or greater) core sutures provide sufficient strength for
early active digital motion.
Release of the pulleys as a means to reduce “inter-
nal” resistance to tendon motion. Free tendon gliding
without repair rupture and restrictive adhesion remains
the ultimate goal of flexor tendon repair. Such free

tendon motion may be achievable through implemen-
tation of strong surgical repair, and decrease of tension
over the repaired tendon by decreasing the resistance to
tendon motion. Release of the narrow, constricting
pulleys that may present a “constricting band” during
tendon motion may be an effective way to release resis-
tance to tendon motion internally within the finger. A
pulley release takes only a few minutes, and multistrand
surgical repairs add only 10 to 15 minutes to the total
time of surgery, as compared to a conventional surgical
repair. Proper release of the pulleys and use of stronger
surgical repairs are much easier and more economical
than achieving increase in delicacy and expertise of
hand therapy. A pulley-release procedure or a multi-
strand repair cost less than 20 minutes of surgery, but
elaborate rehabilitation costs much greater efforts over
weeks.
We suggest consideration of such simple procedure
as releasing the critical parts of the pulley to decrease
the resistance to tendon gliding internally. We believe
that pulley release procedures and increasing repair
strength are two effective measures for achieving safe
postoperative active tendon motion, and releasing the
critical part of pulleys eventually allows tendon motion
free from major internal resistance during active tendon
motion.
Tendon repairs in the little fingers are worth par-
ticular attention. The little finger is shorter and smaller
than the other digits. Its tendons and sheath have a
much smaller diameter than those of the other fingers.
We have noted poorer outcomes of flexor tendon repairs
in the little finger. Not surprisingly, injuries in the little
finger are more difficult to treat, given that (1) the
cross-sectional area of the tendon is only 60% to 70%
that of the other fingers, (2) the diameters of the pulleys
are quite small, and (3) the tendons are bent in multi­
ple directions during finger flexion, gliding over paths
not only bent palmarly, but also bent medially. The
tendons in the little finger are subject to major bending
forces in at least two directions; the tendons in other
fingers are also subject to bending in two directions, but
not as extensively as the little finger. An additional
difficulty in carrying out repairs in the little finger is
the narrow space available in which to perform the
surgery. The distance between each pair of annular
pulleys is much shorter, and accessing the lacerated
tendon through an incision in the sheath is much more
demanding technically and requires precise dissection.
Openings of the sheath are frequently insufficient to
allow surgery, requiring extension of these windows in
the sheath.
In the little finger, we have adopted repair methods
similar to those used for other fingers thus far, but these
methods are often more difficult to use and are not
always adequate for the little finger. As we begin to
consider injuries in the little finger as qualitatively
Chapter 13D:  The Nantong Experience 151
distinct from those in the other fingers, the anatomical
features and biomechanics of the tendon system in the
little finger merit more thorough study, and different
approaches to treatment may be necessary. The anatomy
should be further investigated and treatment be further
documented, to provide repairs specifically designed for
the little finger.
Not repairing the FDS tendon facilitates return of
function in cases of delay or cases of unfavorable
conditions. Repairing both the FDS and FDP tendons
under favorable wound conditions may produce the
most ideal results—in terms of digital motion, strength,
and prevention of PIP joint hyperextension. However,
repairing all structures is not always possible and may
not be a necessity for ordinary use of the hand. In most
delayed repair cases, or with wounds that include some
degree of soft tissue loss, we suggest repairing the FDP
tendons alone. For injuries to both the FDS and FDP
tendons in the A2 pulley area, we recommend repair of
only one slip of the FDS, or removal of both slips of the
FDS tendon.
Repair of only the FDP tendon usually produces ade-
quate function for patients, restoring normal daily use
of the hand. A more complicated surgery sometimes
risks finger motion; adhesions formed between the
tendons and pulleys can render the tendons totally
immovable under unfavorable wound conditions.9,10
Loosely supervised hand rehabilitation—a future
direction? This is a topic we would like to raise, but,
thus far, have insufficient clinical data to recommend it
for widespread use. In recent years, in a number of cases,
we were confident that we had reduced resistance to
tendon gliding by venting critical parts of the pulleys,
and early active motion after surgery was only loosely
supervised. We prevented the patients from active finger
flexion against external resistance but did not instruct
patients to follow the number of exercise sessions and
sequence of passive-active motion in each session.
Rather, the patients were allowed rather large or nearly
full range of active finger flexion with greater freedom
if they could move their fingers actively with ease. These
patients experienced no repair rupture and returned to
normal function.
We cannot yet generally recommend this “loosely
supervised regimen,” but we do bring it to the attention
of surgeons and therapists with regard to an eventual
goal of simplifying rehabilitation regimens and allow-
ing more freely active motion in selected individuals in
whom surgeons have confidence. We urge surgeons and
therapists to expand our experience and explore the
usefulness of simplified motion regimens. Of course,
such a loosely supervised exercise program can only
be safely established when relatively resistance-free
tendon motion is ensured internally, no resistance to
finger flexion is applied externally, and the tendons have
undergone a strong surgical repair.
152 Section 2:  Primary Flexor Tendon Surgery
References
1. Tang JB, Shi D, Gu YQ, et al: Double and multiple looped
suture tendon repair, J Hand Surg (Br) 19:699–703, 1994.
2. Tang JB, Shi D: Subdivision of flexor tendon “no man’s land”
and different treatment methods in each sub-zone. A prelimi-
nary report, Chin Med J (Engl) 105:60–68, 1992.
3. Tang JB: Flexor tendon repair in zone 2C, J Hand Surg (Br)
19:72–75, 1994.
4. Tang JB, Shi D, Shen SQ, et al: An investigation of morphol-
ogy and function of flexor tendons in zone IIC in the hand
and treatment of flexor tendons, Chin J Surg (in Chinese)
37:639, 1999.
5. Tang JB: Clinical outcomes associated with flexor tendon
repair, Hand Clin 21:199–210, 2005.
6. Tang JB: Indications, methods, postoperative motion and
outcome evaluation of primary flexor tendon repairs in Zone
2, J Hand Surg (Eur) 32:118–129, 2007.
7. Tanaka T, Amadio PC, Zhao C, et al: Flexor digitorum pro-
fundus tendon tension during finger manipulation, J Hand
Ther 18:330–338, 2005.
8. Savage R: The influence of wrist position on the minimum
force required for active movement of the interphalangeal
joints, J Hand Surg (Br) 13:262–268, 1988.
9. Amadio P, An KN, Ejeskar A, et al: IFSSH Flexor Tendon Com-
mittee report, J Hand Surg (Br) 30:100–116, 2005.
10. Elliot D, Barbieri CH, Evans RB, et al: IFSSH Flexor Tendon
Committee Report 2007, J Hand Surg (Eur) 32:346–356, 2007.
 E The Singapore Experience
Alphonsus K.S. Chong, MBBS, MRCS (Ed), MMed (Orth), FAMS,
Beng-Hai Lim, MD, and Yeong-Pin Peng, FRCS
OUTLINE
We used looped sutures to make a six-strand core
suture repair supplemented with running epitendi-
nous suture in repairing the lacerated flexor digitorum
profundus tendon. After surgery, we performed passive
flexion and active extension exercise. In our initial
experience, in 32 fingers that underwent this tendon
repair, there were 41% excellent, 41% good, and 16%
fair results according to the revised Strickland criteria.
The rupture rate was 3% (1 of 32 digits). One case with
a fair result underwent tenolysis, with no improve-
ment after the procedure. Our results in more recent
case series with this technique are similar to our initial
results.
Flexor tendon injuries are common work injuries in
Singapore because there is a large manufacturing and
construction sector in our economy. Home accidents
and assault with sharp objects are other common mech-
anisms of injury. Singapore’s small physical size means
that our population has easy access to specialist care by
hand surgeons following the initial injury. In addition,
compliance with postoperative rehabilitation by hand
therapists is high because of this accessibility. As a result,
acute flexor tendon injuries that require primary flexor
tendon repairs form the bulk of our clinical experience
with flexor tendon injuries. Secondary or late repairs
requiring staged procedures are uncommon in our
practice.
Flexor tendon injuries occur in isolation or in asso-
ciation with other injuries like fractures, nerve, and
vessel injuries. In more serious injuries, such as amputa-
tion, a strong tendon repair is also critical to allow early
mobilization and return of digital function.1 Great
improvements in the results following primary flexor
tendon repairs have been obtained with better repair
techniques and rehabilitation protocols.2
Our community’s practice pattern for flexor tendon
repairs has closely paralleled the experience of estab-
lished hand centers worldwide. The practice of the
primary repairs started taking off in the 1970s, and Pro-
fessor Robert W.H. Pho published his experience in
1978 showing its efficacy in our setting.3 At that time,
the practice was to perform the Bunnell technique repair
using a 4-0 wire suture with a 6-0 epitendinous suture.
Rehabilitation consisted of a dynamic protocol using a
dorsal splint and rubber band traction. Currently, our
practice involves the use of a strong surgical repair fol-
lowed by early protective motion protocol. With special-
ist hand surgeons performing primary tendon repairs
and dedicated hand therapists supervising rehabilita-
tion, our clinical results are similar to results obtained
elsewhere.
Despite this, our results mirror that of other centers
in that there are still a significant proportion of patients
with poor clinical results. Beyond the ultimate result,
there is also a large socioeconomic burden in terms of
time off work and other opportune costs.4 This is due
to the long rehabilitation time required before the
patient returns to having function of the injured hand.
Improvement of the results following flexor tendon
injury has long been an important research focus in
Singapore. In 1974, Dr. Chacha described his results
with free composite autologous tendon grafts in pri-
mates and humans5 as a method to combat the problem
of adhesions following flexor tendon injuries and
primary repair. We have been trying to improve the
outcome of primary repair of the injured flexor tendon
and to reduce adhesion formations after primary or
secondary tendon surgery since then.
Our research strategy to address the limitations with
current repair and rehabilitation techniques has been
on two fronts: (1) improving the strength of the repair
to enable early active motion and shorter rehabilitation
and (2) research into biological methods to improve
the results of flexor tendon healing. One of our aims in
the primary repair is to enable a splint-free flexor tendon
repair and rehabilitation.6 A more robust repair will
allow splint free, unprotected use of the hand during
the rehabilitation phase. This will reduce the costs of
such an injury and possibly improve the ultimate
outcome. We collaborated with our Finnish colleagues
to evaluate different materials, such as nickel-titanium
alloy, to assess its suitability for use in flexor tendon
repairs.7
153
154 Section 2:  Primary Flexor Tendon Surgery
A variety of approaches have been taken to address
the biologic aspects of primary tendon healing. The
ability to increase the rate of healing or to improve
the ultimate quality of the healed tendon would be
extremely beneficial to patients. Our research in this
area has focused largely on the use of cells, primary
bone marrow–derived mesenchymal stem cells (bMSCs),
to enhance primary flexor tendon healing. Mesenchy-
mal stem cell marrow–based therapies show promise in
improving outcomes in a tendon injuries.4 Our interest
in this area began with the finding from our collabora-
tors that these bMSCs could be used to enhance the
histological and biomechanical properties of a tissue-
engineered tendon graft.8 We applied this strategy to a
primary tendon healing model in the rabbit Achilles
tendon with encouraging results.9 We are currently per-
forming the experiments using bMSCs to promote the
healing in a digital flexor tendon model.
The strength of a primarily repaired flexor tendon is
correlated with the number of core sutures. We favor six
core sutures in digital flexor tendon repairs. While this
may increase the bulk at the repair site, the gliding
characteristics are not compromised.10 Biomechanical
testing of six-strand repair techniques has also been
favorable. A human cadaveric tendon study demon-
strated that the six-strand repair technique using a loop
suture had a higher tensile strength compared to tech-
niques such as the modified Kessler (two-strand), the
Tsuge technique (two-strand), and the four-strand loop
suture technique.11
METHODS AND OUTCOMES
Operative Techniques
Our procedure for primary flexor tendon repairs is to
perform surgery with the patient under general or
regional anesthesia. The final choice depends on the
patient and the anesthetist.
We favor a six-strand core repair technique
co-developed by our senior author.12 This repair tech-
nique uses a looped suture made of nylon (Supramid
4/0; S. Jackson Inc., Alexandria, VA, USA) for the core
sutures. During the core suture repair, we add an epiten-
dinous repair using polypropylene (Prolene 5-0 or 6-0,
depending on tendon size).
The use of a loop suture brings three advantages: it
doubles the number of core sutures with each pass,
simplifies suture locking to the tendon, and reduces the
number of passes and tendon handling. Our clinical
and published experience involves using the commer-
cially available Supramid sutures. However, we realize
that these looped sutures may not be universally avail-
able, or the cost may be prohibitive in some countries.
We have described a technique to create a looped suture
using a straight 23-gauge hypodermic needle, pliers, and
available sutures such as polypropylene 4-0.13 Using this
technique, a 90-cm length of polypropylene can be used
to make three 15-cm strands of looped suture. This
allows the surgeon to capitalize on the advantages of a
loop suture with minimal effort.
In the original description of the technique,11 the
repair used two strands of looped suture for the repair.
We have since modified the technique to use only one
looped suture per repair. This results in a repair with
six-core sutures to readily allow for dynamic postopera-
tive rehabilitation. For larger flexor tendons in the wrist,
an 8- to 10-strand repair may be possible.
The technique needs all the usual requisites of a good
tension-free repair. The dorsal half of the epitendinous
repair can be done first to allow good approximation of
the tendon ends. The core suture repair itself is then
performed as shown (Figure 13[E]-1).
The flexor digitorum superficialis (FDS) tendon is
repaired with a simple Tsuge loop suture technique if it
is near the insertion or in zone 2C with the knot on the
dorsal side. If the FDS tendon is cut more proximally
(i.e., it lies on superficial to the deep flexor tendon), a
six-strand repair is made.
Postoperative Care
The patient is often discharged the same or next day if
the injury was uncomplicated. For more complicated
cases, such as microvascular repair or mutilating inju-
ries, the patient will remain as an inpatient as required.
The protective backslab and dressing is replaced with a
removable splint within 5 days of surgery by the hand
therapist. Protected dynamic rehabilitation is started
then. The splint is removed at about 4 weeks postinjury
by the therapist. Return to full activities occurs at about
12 weeks.
In the first 4 weeks, a dorsal blocking splint is applied
for the wrist and digits for continuous wear. The splint
places the wrist in a neutral position, with metacarpo-
phalangeal joints flexed 45°, and interphalangeal (IP)
joints in full extension (Figure 13[E]-2). The patient is
advised to strap the fingers in flexion during the day and
loosely in extension within the splint at night.
With the splint in place, the patient performs the fol-
lowing exercises hourly: (1) 20 repetitions of passive
flexion and extension of the distal IP (DIP) joint, (2) 20
repetitions of passive flexion and extension of the proxi-
mal IP (PIP) joint, and (3) passively bringing all fingers
into hook position (full IP joint flexion) and actively
holding down the finger lightly for 5 seconds, followed
by active extension of the fingers to fully straighten the
fingers against the splint for 5 repetitions. This last exer-
cise is done only when edema is resolved. Edema control
is achieved using Coban wrapping (a self-adherent tape)
or fingerstalls, in addition to limb elevation.
Therapy sessions are given three times a week. In
addition to supervision of the patient’s therapy, the
therapist manages the wound and scar and edema and

D performs passive tenodesis exercises to prevent joint
E At 6 to 8 weeks, the following activities are performed:
F lifting is allowed only after 12 weeks.
Figure 13(E)-1  A, Application of a superficial locking
suture in the proximal tendon 1.25 cm from the tendon
end. B, Placement of the first pair of core sutures, with the
needle inserted close to the locking suture and proceeding
parallel to the tendon fibers, from proximal to distal,
surfacing 1 cm from the distal tendon end. C, Application
of a superficial locking suture in the distal tendon 1.25 cm
from the tendon end. D, Placement of second pair of core
sutures across repair site in a similar fashion and locking
suture applied. E, Application of final pair of core sutures.
Note that one strand is divided at the repair site, while the
other strand crosses into the proximal end and is locked
before being passed into the repair site. The dorsal
epitendinous running suture is applied. F, The loop suture
repair is knotted in the repair site.
Chapter 13E:  The Singapore Experience 155
Figure 13(E)-2  The operated hand in a splint during the
first 4 weeks following tendon repair. The digital strap is
removed during exercises. Passive flexion of the digits is
done, followed by an active hold for 5 seconds.
stiffness.
At 4 to 6 weeks postsurgery, the dorsal block splint is
removed during the daytime. The patient wears the
splint at night and while going into crowded places. A
night gutter splint is worn if there is flexion contracture
of the PIP joints. The exercise program includes (1)
active flexion and extension of fingers (to initiate
blocked active hook, perform straight fist and full fist
exercises) and (2) blocking exercises to improve gliding
of the FDP and FDS tendons.
(1) light activities of daily living (e.g., writing, eating,
and combing hair are encouraged), (2) progressive
strengthening (e.g., putty, hand helper), (3) light resis-
tive exercises (e.g., light putty, light Velcro), (4) gentle
stretching of flexors to reduce tightness and adhesion,
and (5) gliding of flexor tendons and positioning at the
end of elastic limit.
At 8 to 12 weeks, work conditioning and hardening
may be initiated. Normal use of hand is allowed. Heavy
OUTCOMES
In our initial experience, we found that in 32 fingers that
underwent this tendon repair, there were 41% excellent,
41% good, and 16% fair results using the revised Strick-
land criteria.12 Twenty-one cases were repaired primarily
(within 24 hours), while 11 cases underwent delayed
primary repair. The rupture rate was 3% (1 of 32 digits).
One case with a fair result underwent tenolysis, with no
improvement after the procedure. Our results in more
recent case series with this technique are similar to our
initial results.
156 Section 2:  Primary Flexor Tendon Surgery
SUMMARY
In an independent study, Hoffman and his colleagues
compared this technique with the modified Kessler
repair, combined with a Kleinert/Duran mobilization
regimen.14 After a follow-up of 8 to 17 weeks, the loop
suture technique group had a better grip strength and a
significantly better total active motion of 141° com-
pared with 123°. In addition, the complication rate
was significantly lower and the average time of treat-
ment was significantly shorter using the loop suture
technique. The rupture rate was lower in the loop suture
technique (1 of 51 versus 3 of 26), although this did not
reach statistical significance. The results of Hoffman and
his colleagues are similar to results of our case series
using similar repair techniques.
The repair technique we describe using the looped
Supramid suture adheres well to well-established prin-
ciples and brings with it the advantages of using a loop
References
1. Lim BH, Tan BK, Peng YP: Digital replantations including
fingertip and ring avulsion, Hand Clin 17:419–431, 2001.
2. Boyer MI, Strickland JW, Engles D, et al: Flexor tendon repair
and rehabilitation: state of the art in 2002, Instr Course Lect
52:137–161, 2003.
3. Pho RWH, Sanguin R, Chacha PB: Primary repair of flexor
tendons within the digital theca of the hand, Hand 10:154–
160, 1978.
4. Chong AK, Chang J, Go JC: Mesenchymal stem cells and
tendon healing, Front Biosci 14:4598–4605, 2009.
5. Chacha P: Free autologous composite tendon grafts for divi-
sion of both flexor tendons within the digital theca of the
hand, J Bone Joint Surg (Am) 56:960–978, 1974.
6. Peng YP, Lim BH, Chou SM: Towards a splint-free repair for
flexor tendon injuries, Ann Acad Med Singapore 31:593–597,
2002.
7. Karjalainen T, He M, Chong AK, et al: Nickel-titanium wire
in circumferential suture of a flexor tendon repair: A compari-
son to polypropylene, J Hand Surg (Am) 35:1160–1164, 2010.
8. Ouyang HW, Goh JC, Thambyah A, et al: Knitted poly-lactide-
co-glycolide scaffold loaded with bone marrow stromal cells
in repair and regeneration of rabbit Achilles tendon, Tissue
Eng 9:431–439, 2003.
suture. The rehabilitation technique we use affords suf-
ficient protection of the repair, with the advantages of
early mobilization. Effective management of edema
and good communication between patient, surgeon,
and therapist enhance the rehabilitation process. There
remains much to be done to improve the clinical
outcome following these injuries, which typically occur
in the young and socioeconomically active. Efforts to
improve repair materials, techniques, rehabilitation,
and biologic methods to modulate healing will all con-
tribute to the improvement of flexor tendon healing
results in the future.
ACKNOWLEDGMENTS
Ms. Tan Lay Lay, principal hand therapist, and the Hand
Occupational Therapy Workgroup of National Univer-
sity Hospital, Singapore, are acknowledged for the flexor
tendon rehabilitation protocol.
9. Chong AK, Ang AD, Goh JC, et al: Bone marrow-derived
mesenchymal stem cells influence early tendon-healing in a
rabbit Achilles tendon model, J Bone Joint Surg (Am) 89:74–
81, 2007.
10. Sanders DW, Milne AD, Johnson JA, et al: The effect of flexor
tendon repair bulk on tendon gliding during simulated active
motion: An in vitro comparison of two-strand and six-strand
techniques, J Hand Surg (Am) 26:833–840, 2001.
11. Gill RS, Lim BH, Shatford RA, et al: A comparative analysis
of the six-strand double-loop flexor tendon repair and three
other techniques: A human cadaveric study, J Hand Surg (Am)
24:1315–1322, 1999.
12. Lim BH, Tsai TM: The six-strand technique for flexor tendon
repair, Atlas Hand Clin 65–76, 1996.
13. Wong M, Sebastin SJ, Lim BH: A simple technique of making
a looped suture for flexor tendon repair, J Hand Surg (Eur)
34:409–410, 2009.
14. Hoffmann GL, Büchler U, Vögelin E: Clinical results of flexor
tendon repair in zone II using a six-strand double-loop tech-
nique compared with a two-strand technique, J Hand Surg
(Eur) 33:418–423, 2008.
 F The Stanford Experience
Arash Momeni, MD, Emily Grauel, MS, and
James Chang, MD
OUTLINE
This chapter summarizes some of the important con-
siderations and current methods of primary repairs of
the injured flexor tendons in the authors’ unit. The
preferred postoperative rehabilitation protocols are
presented and discussed.
Management of flexor tendon injuries represents one of
the most demanding challenges in hand surgery. The
complexity of the task is reflected by the fact that despite
excellent technical execution numerous complications
may be experienced postoperatively.1 Particularly, repair
of zone 2 injuries has been an area of great controversy
since Bunnell’s proposal that “it is better to remove the
tendons entirely from the finger and graft in new tendon
throughout its length.”2
Flexor tendon repair confronts the surgeon with a task
that is two-fold, namely reestablishment of not only
tendon continuity but also the gliding mechanism of the
tendon and its surrounding structures. Achieving both
goals is equally important for a satisfactory functional
outcome.3 The various factors that affect functional
outcome can be classified into preoperative, intraopera-
tive, and postoperative factors (Table 13[F]-1), of which
the latter two can be influenced by the surgeon.
Particularly with regard to surgical technique, the
scientific literature is replete with technical modifica-
tions proposed for improved functional outcome.4
The multitude of available approaches along with the
nuances of flexor tendon repair make it particularly dif-
ficult for the trainee to identify and learn a reliable
technique, which allows for reproducible results with a
satisfactory functional outcome. In particular, zone 2
injuries are associated with poorer functional outcomes
and a higher complication rate compared with injuries
in other zones.5
Despite the myriad of reported techniques, several
principles of repair should be regarded as established.
These principles include early primary repair whenever
possible, performance of a multistrand repair (at least
four strands) combined with an epitendinous suture,
use of locking stitches, and adequate tendon purchase.
Furthermore, an early motion protocol should be used
in compliant patients to minimize extrinsic scarring and
adhesion formation and to promote intrinsic healing.6
Several studies have demonstrated the effect of the
following intraoperative factors on repair strength and
functional outcome:7
1. Number of core suture strands
An increase in the number of core sutures (at least
four strands) has been demonstrated to result in
an increased resistance to gap formation at the
repair site when compared with conventional two-
strand repairs.8-10 As a result of a stronger repair,
early active motion protocols may be instituted
postoperatively.
2. Caliber of core suture
Several authors have demonstrated that the use of
a larger caliber core suture (greater than 4-0) is
paralleled by an increased strength and stiffness of
the repair.11,12
3. Tendon purchase
Adequate tendon purchase when placing the core
suture is critical for a successful repair. The optimal
length of purchase has been shown to be between
0.7 and 1.0 cm.13 Similarly, placing the epitendi-
nous suture 2 mm from the cut end results in
increased repair strength compared with a 1-mm
purchase.
4. Locking of core suture
The superiority of a locking core suture with resul-
tant increased tensile strength and reduced risk of
suture pull-out was initially reported by Penning-
ton and has since been confirmed in numerous
reports.14,15
5. Epitendinous suture
Although it was initially assumed that the epiten-
dinous suture would merely contour the repair site,
it has been demonstrated that it contributes to the
strength of the repair as it bolsters repair strength
and prevents gap formation.16 Implementing an
epitenon-first technique further enhances repair
strength when compared with a modified Kessler
and epitendinous running suture.17
The complexity of flexor tendon repairs along with a
“no-error tolerance” environment in the operating room
represent significant challenges to resident training. As
such, surgical training is increasingly making use of
lessons learned from the aviation industry and has
157
158 Section 2:  Primary Flexor Tendon Surgery
Table 13(F)-1  Factors Affecting Outcome After
Primary Flexor Tendon Repair
Preoperative Intraoperative Postoperative
Factors Factors Factors
 Type/  Atraumatic  Postoperative
mechanism of tissue handling rehabilitation
trauma  Multistrand (i.e., early
 Degree of core suture active
wound  Locking stitch motion)
contamination  Epitendinous
 Associated suture
injuries (e.g.,  Tendon
concomitant purchase
fractures, etc.)  Suture material
endorsed simulator-based training models. Organiza-
tions such as the American College of Surgeons (ACS)
as well as the Accreditation Council for Graduate Medical
Education (ACGME) have underlined the importance of
such training models in surgical education.
Surprisingly, the challenges of flexor tendon repair
have not been met by appropriate simulation models.
Recently, colleagues in our unit introduced a curriculum-
based simulation model for teaching zone 2 flexor
tendon repairs. Combining a tutorial addressing con-
temporary literature along with providing a standard-
ized approach to flexor tendon repair incorporating
best evidence principles with hands-on experience
using human cadaver tendons resulted in significantly
improved flexor tendon repairs. Key aspects of this sim-
ulation model include inexpensive hands-on experi-
ence, review of the primary literature, and standardization
of the technique. This model is amenable to incorpora-
tion into training programs as part of a hand surgery
simulation curriculum.18
OPERATIVE TECHNIQUE
The authors’ preferred approach to flexor tendon inju-
ries, particularly those in zone 2, is early exploration and
repair via Bruner zigzag incisions. Every effort should be
made to repair each injured tendon, even in the setting
of combined flexor digitorum superficialis (FDS) and
flexor digitorum profundus (FDP) injuries. Although
some authors recommend repair of only the FDP tendon,
the authors believe that excessive scar formation origi-
nating from the free ends of an unrepaired FDS tendon
may result in functional compromise of the digit. Fur-
thermore, repair of both tendons will still allow proxi-
mal interphalangeal (PIP) joint flexion should the
repaired FDP tendon rupture during postoperative reha-
bilitation. During the repair, care should be taken to
preserve the A2 and A4 pulleys to prevent postoperative
bowstringing, which would result in loss of function.
The authors’ preferred method of flexor tendon repair
is illustrated in Figure 13(F)-1. The repair begins with
Epitendinous stitch Slit with #11 blade
A B
Modified Kessler Locking stitch
C D
0.7 to 1 cm
2 mm
E F
Horizontal mattress
G
Figure 13(F)-1  Authors’ preferred flexor tendon repair
using epitenon-first suture (A) followed by a modified
two-strand Kessler core suture (B–E) in locking configuration
and buried knot (F). Subsequently, two-strand horizontal
mattress suture is added (G), to complete a four-strand core
suture.
an epitendinous running suture using a 6-0 nonabsorb-
able monofilament suture on a tapered needle. The
tendon is purchased 2 mm from the cut end for place-
ment of this suture. This results in optimal tendon align-
ment and prevents the excessive bulging observed when
placing the core suture first. Next, a longitudinal slit is
made with a No. 11 blade at least 1 cm away from the
repaired edge. Using this slit as the entry point, a 3-0
nonabsorbable, braided suture is placed in a modified
Kessler technique with a locking loop. In the end, the
knot should lie in the depth of the previously created
slit, which will limit irritation of the tendon sheath.
Finally, a four-strand repair is obtained by placement of
a horizontal mattress stitch with a 3-0 nonabsorbable,
braided suture. The knot of this suture should be placed
away from the A2 and A4 pulleys. The repaired digit
should then be placed under passive range of motion
(ROM) intraoperatively to assess for triggering. If trig-
gering at one of the pulleys is observed, partial release
of the affected pulley is indicated. Postoperatively, early
active motion protocols are initiated.

POSTOPERATIVE REHABILITATION
Early mobilization protocols are now established com-
ponents of the comprehensive care provided to patients
following flexor tendon repair as they have been dem-
onstrated to result in superior functional outcomes
compared with prolonged immobilization. Among the
proposed benefits are improved tendon gliding in the
postoperative period with resultant decreased adhesion
formation and risk of joint stiffness.18 Early mobiliza-
tion also improves healing and revascularization leading
to an increased strength of the repair.19 Numerous
studies indicate that initiation of mobilization is most
successful in the first week; however, recommendations
for the specific day within that week vary.20,21 In vivo
animal studies suggest days 3 to 5 as the best choice to
begin a postoperative mobilization regimen based on
the strength of the repair and the resistance to digital
motion.21,22 Although the concept of early postoperative
mobilization represents a central dogma, a myriad of
rehabilitation protocols can be found in the literature.24
Standardization of protocols based on best available
evidence will lead to greater success of flexor tendon
repairs and allow comparative analyses of functional
outcomes.
There are two categories of early mobilization: early
passive motion and early active motion. Early passive
motion includes passive flexion (e.g., with rubber band
traction) with either active or passive extension. Early
active motion includes active flexion and extension of
the affected digit. A subtype of early active mobilization
includes “place and hold” techniques where the digit is
passively flexed and then held in place by the patient.23
Early controlled active finger flexion with place and
hold exercises is becoming a more popular treatment
compared to early passive flexion by rubber band
traction.24
Recently, Trumble et al conducted the first random-
ized prospective trial comparing active place-and-hold
therapy with passive motion therapy.6 A total of 103
patients (119 digits) were included in the study. The
authors demonstrated that active motion therapy pro-
vided significantly better range of motion, smaller
flexion contractures, and greater patient satisfaction.
This study provides strong scientific support for the
combination of multistrand tendon repairs and early
active motion protocols postoperatively.6
AUTHORS’ PREFERRED POSTOPERATIVE
REHABILITATION PROGRAM
Weeks 0 to 3
Postoperatively, the patient’s affected hand is placed in
a dorsal blocking splint (DBS) with the wrist neutral,
metacarpophalangeal (MCP) joints at 70° to 90°
flexion, and IP joints neutral. The DBS should be worn
Chapter 13F:  The Stanford Experience 159
at all times until its removal is recommended by the
therapist. Patient education about the proper way to
undergo active motion exercises is addressed in detail at
the first therapy visit.
Five therapeutic exercises are begun between days 3
and 7 postoperatively.
1. Passive range of motion composite wrist flexion.
2. Passive MCP flexion to 90° and active extension
of IP joints to neutral; Passive PIP/DIP extension
with MCP flexed.
3. Place and hold flexion of digits in palm with active
extension to DBS.
4. Passive wrist flexion with active extension to
neutral.
5. Active flexion and extension of unaffected digits
within the DBS while maintaining the affected
digit in passive flexion.
In clinic, the therapist performs retrograde massage, scar
massage, and skin care as needed. Precautions during
this stage of therapy include: no active flexion of the
affected digit, no active extension of MCP beyond 60°,
no active PIP extension unless MCP is flexed at 90°, and
no active wrist extension past neutral.
Weeks 4 to 5
The patient should continue to wear the DBS at all times
and is instructed in new therapeutic exercises:
1. Begin active digital flexion of affected digit within
the DBS with active extension to hood of splint;
the therapist may consider buddy taping affected
to adjacent digit within the splint for active flexion
if the affected digit is stiff.
2. Continue passive range of motion digital flexion.
3. During week 5 include full digital extension to
neutral.
4. Tenodesis of wrist out of DBS.
In clinic, the therapist performs edema management
techniques (retrograde massage, 3M Coban Self-
Adherent Wrap application), scar management tech-
niques (use of silicone gel sheet if needed), and skin
care. The main precaution during this stage of therapy
is avoidance of forceful flexion.
Week 6
At this point, the DBS can be removed except at night
and with lifting or higher risk activities. Therapeutic
exercises for week 6 include:
1. Begin active isolated joint blocking.
2. Active digital extension to neutral.
3. If lacking full PIP extension, a static PIP extension
splint can be fabricated.
4. Active wrist flexion and extension.
160 Section 2:  Primary Flexor Tendon Surgery
5. May begin ultrasound/neuromuscular electrical
stimulation as needed for scar management if not
obtaining tendon glide.
6. Encourage use of hand for light functional
activities.
7. Continue edema management techniques as
needed.
Week 8
The DBS can be fully discharged at this point. Strength-
ening exercises should be begun at this point and should
gradually increase as the patient can tolerate. Return to
sports activities should be discussed with the physician,
as full return is sports specific. Generally, full release for
sports is at 12 weeks.
References
1. Momeni A, Grauel E, Chang J: Complications after flexor
tendon injuries, Hand Clin 26:179–189, 2010.
2. Bunnell S: Repair of tendons in the fingers and description
of two new instruments, Surg Gyencol Obstet 26:103–110,
1918.
3. Beredjiklian PK: Biologic aspects of flexor tendon laceration
and repair, J Bone Joint Surg (Am) 85:539–550, 2003.
4. Strickland JW: Development of flexor tendon surgery: twenty-
five years of progress, J Hand Surg (Am) 25:214–235, 2000.
5. Karlander LE, Berggren M, Larsson M, et al: Improved results
in zone 2 flexor tendon injuries with a modified technique
of immediate controlled mobilization, J Hand Surg (Br)
18:26–30, 1993.
6. Trumble TE, Vedder NB, Seiler JG 3rd, et al: Zone-II flexor
tendon repair: A randomized prospective trial of active place-
and-hold therapy compared with passive motion therapy,
J Bone Joint Surg (Am) 92:1381–1389, 2010.
7. Kim HM, Nelson G, Thomopoulos S, et al: Technical and
biological modifications for enhanced flexor tendon repair,
J Hand Surg (Am) 35:1031–1037, 2010.
8. Savage R, Risitano G: Flexor tendon repair using a “six strand”
method of repair and early active mobilisation, J Hand Surg
(Br) 14:396–399, 1989.
9. Viinikainen A, Goransson H, Huovinen K, et al: A compara-
tive analysis of the biomechanical behaviour of five flexor
tendon core sutures, J Hand Surg (Br) 29:536–543, 2004.
10. Thurman RT, Trumble TE, Hanel DP, et al: Two-, four-, and
six-strand zone II flexor tendon repairs: An in situ biome-
chanical comparison using a cadaver model, J Hand Surg
(Am) 23:261–265, 1998.
11. Barrie KA, Tomak SL, Cholewicki J, et al: Effect of suture
locking and suture caliber on fatigue strength of flexor tendon
repairs, J Hand Surg (Am) 26:340–346, 2001.
12. Taras JS, Raphael JS, Marczyk SC, et al: Evaluation of suture
caliber in flexor tendon repair, J Hand Surg (Am) 26:1100–
1104, 2001.
SUMMARY
A growing body of evidence supports the combination
of multistrand (at least four strands) repairs and early
active motion rehabilitation protocols for management
of flexor tendon injuries. Incorporating simulation
modules into the hand surgery curriculum is an impor-
tant step in allowing the trainee to familiarize with the
technical complexity of flexor tendon repairs prior to
execution in the operating room. Standardization of
treatment protocols based on best available evidence
will lead to greater success of flexor tendon repairs and
also allow comparative analyses of functional outcomes
across various institutions.
13. Tang JB, Zhang Y, Cao Y, et al: Core suture purchase affects
strength of tendon repairs, J Hand Surg (Am) 30:1262–1266,
2005.
14. Pennington DG: The locking loop tendon suture, Plast Recon-
str Surg 63:648–652, 1979.
15. Hotokezaka S, Manske PR: Differences between locking loops
and grasping loops: effects on two-strand core suture, J Hand
Surg (Am) 22:995–1003, 1997.
16. Wade PJ, Muir IF, Hutcheon LL: Primary flexor tendon repair:
the mechanical limitations of the modified Kessler technique,
J Hand Surg (Br) 11:71–76, 1986.
17. Papandrea R, Seitz WH, Shapiro P, et al: Biomechanical and
clinical evaluation of the epitenon-first technique of flexor
tendon repair, J Hand Surg (Am) 20:261–266, 1995.
18. Amadio P, An KN, Ejeskar A, et al: IFSSH Flexor Tendon Com-
mittee report, J Hand Surg (Br) 30:100–116, 2005.
19. Strickland JW, Glogovac SV: Digital function following flexor
tendon repair in Zone II: A comparison of immobilization
and controlled passive motion techniques, J Hand Surg (Am)
5:537–543, 1980.
20. Tottenham VM, Wilton-Bennett K, Jeffrey J: Effects of delayed
therapeutic intervention following zone II flexor tendon
repair, J Hand Ther 8:23–26, 1995.
21. Zhao C, Amadio PC, Paillard P, et al: Digital resistance and
tendon strength during the first week after flexor digitorum
profundus tendon repair in a canine model in vivo, J Bone
Joint Surg (Am) 86:320–327, 2004.
22. Xie RG, Cao Y, Xu XF, et al: The gliding force and work of
flexion in the early days after primary repair of lacerated flexor
tendons: An experimental study, J Hand Surg (Eur) 33:192–
196, 2008.
23. Pettengill KM: The evolution of early mobilization of the
repaired flexor tendon, J Hand Ther 18:157–168, 2005.
24. Tang JB: Indications, methods, postoperative motion and
outcome evaluation of primary flexor tendon repairs in Zone
2, J Hand Surg (Eur) 32:118–129, 2007.
 G The Australian Experience
Michael A. Tonkin, MD, FRCS Ed Orth, FRACS, and
Richard D. Lawson, MBBS, FRACS
OUTLINE
This subchapter describes the contribution of Austra-
lian authors to the basic science and clinical manage-
ment of flexor tendon injuries. It then discusses the
current surgical management and rehabilitation of
flexor tendon injuries in Australia and ends with a
brief outline of our preferred approach to flexor
tendon repair.
In Australia, hand surgery developed in parallel with
and perhaps because of the necessity for hand surgery
services created by limb injuries sustained in World War
II. Sir Benjamin Rank, from Melbourne, though mostly
involved in secondary reparative surgery during and
immediately after the war years, established the place of
primary repair for hand injuries which became rife with
the mushrooming of light industry. Rank and Alan
Wakefield published Surgery of Repair as Applied to Hand
Injuries in 1953,1 being joined for the last two of five
editions by John Hueston. Their recommendations for
the place of primary and secondary flexor tendon recon-
struction and the techniques of the time are documented
in this text, which can best be summarized in the fol-
lowing: Primary repair in the digit was practiced for
flexor digitorum profundus (FDP) division only if the
repair did not interfere with the intact flexor digitorum
superficialis (FDS). If the primary repair of an FDP
tendon was likely to compromise FDS function, the FDP
was not repaired, relying on a tenodesis or an arthrod-
esis of the distal interphalangeal joint; alternatively, a
primary or delayed tendon graft from palm to terminal
interphalangeal joint was used. If both tendons were
divided, a graft was indicated. Results from primary
grafting did not compare favorably with those of sec-
ondary grafts. This became one of the exceptions to
the rule of primary repair in a tidy wound, which was
championed for all other soft tissue injuries. Primary
skin closure with delayed or secondary grafting was
favored. For primary repair, the suture used was a 5-0
polyester suture, inserted according to the method
described by Bunnell. The 6-0 sutures were used for
auxiliary apposition stitches, so as not to leave any open
tendon end exposed. Post-operative treatment main-
tained absolute immobilization until the third week,
followed by supervised active movement within the
inner range, once or twice a day. The splint was main-
tained for 5 weeks.
These methods of repair and rehabilitation were still
the mode of practice until the early 1970s. Since then,
flexor tendon surgery has evolved significantly and Aus-
tralian hand surgeons have made many contributions
to the development of the increasingly sophisticated
techniques currently practiced.
Perhaps one of the most important but basic contri-
butions was David Pennington’s recognition in 1979
that a locking loop tendon suture increased the tensile
strength of the repair and decreased gapping at the
repair site.2 He demonstrated that the alteration in the
relationship of the transverse and longitudinal intraten-
dinous parts of the suture technique of Mason and
Allen,3 modified by Kessler and Nissim,4 was vital to
prevent pullout of the suture under load. Now termed
the modified Kessler suture, the longitudinal compo-
nents of the suture configuration must pass deep to the
transverse limb. As tension is increased, the loops
tighten and lock. In fresh cadaveric flexor tendons, he
demonstrated that failure of the locking loop suture was
due to breakage of the suture, rather than suture pullout
that occurred with a nonlocking technique. Pennington
also performed some experimental repairs of cadaveric
tendons with wire and monofilament nylon, conclud-
ing that the stiffness of wire made it an unsuitable
material.2
The modified Kessler suture became the “work horse”
core suture for many years and is still favored by many,
although the use of monofilament nylon was largely
superseded by braided polyester sutures, and more
recently by other materials such as Fiberwire (Arthrex,
Naples, FL).
Pennington’s innovative approach to improving
flexor tendon surgical techniques included a discussion
of the use of a suction catheter technique to deliver the
retracted proximal end of a severed tendon to the repair
site when proximal digital milking of the tendon failed.5
Perhaps the most common technique in current practice
is that described by McGrouther and colleagues, from
the United Kingdom, in 1987, in which a fine Silastic
catheter is passed up the tendon sheath from a proximal
palmar wound and is sutured to the retracted tendon,
161
162 Section 2:  Primary Flexor Tendon Surgery

1
Pull to
advance
tendon

A 2
Secure
tendon
distally

B
3 4 5
Pull to Pull to Pull to
release undo remove
knot suture catheter
(distal (distal
catheter catheter
counter counter
traction) traction)

C D

Figure 13(G)-1  Diagram for tendon retrieval technique described by Michael J. Sandow. A, Loop release knot using 4-0
nylon is tied with a double throw first. B, Loop release knot: second throw. C, Loop release knot: completed securing catheter
to tendon. D, Catheter is pulled distally advancing tendon, the tendon is secured distally, the loop release knot is disengaged
by pulling on the trailing suture tail, the suture is removed, and the catheter is disengaged leaving the tendon in a good
position for repair. (From Sandow MJ: A further tendon retrieval trick, J Hand Surg [Br] 22[1]:125-127, 1997.)

which is then drawn into the repair site.6 Michael
Sandow, from Adelaide, suggested a modification of this
technique in his article “A Further Tendon Retrieval
Trick,” published in 1997.7 Instead of a simple knot to
secure the catheter to the tendon, a loop release knot is
used, which allows the tendon to be advanced with the
tube; once the tendon is delivered and stabilized dis-
tally, the knot can be released without the need to allow
the tendon to retract to the proximal wound. The loop
release knot is disengaged by pulling on the trailing tail
suture at the palmar wound (Figure 13[G]-1A–D).
Wayne Morrison, from Melbourne, has been another
major contributor to many aspects of flexor tendon
surgery in Australia. Writing with Pribaz and Macleod,
he reported satisfactory results using the Becker repair
and early active motion.8 Becker’s beveling and overlap-
ping of the tendon ends reduced the problem of gap
formation but did require profundus tendon shortening

of around 7 mm. Morrison’s ruptures (3 of 43) occurred
in those patients with crush injuries and stiff joints.
Morrison, in collaboration with Callan, described a
new and simple approach to gain access to the divided
flexor tendons within the flexor tendon sheath.9 They
recommended a transverse incision 1 cm distal to the
distal stump of the severed tendon. This allows delivery
of 1 cm of distal tendon through the sheath incision, be
it within the synovial sheath or within a pulley. The
proximal segment is retrieved and delivered through
the same incision by whatever technique is necessary,
including milking, flexion of proximal joints, and
catheter-assisted delivery, and is stabilized with a
23-gauge needle, allowing the core suture to embrace
1 cm of each end of the tendon, with ready access pro-
vided to the front and back walls for insertion of the
epitendinous suture. These authors claim that the lon-
gitudinal component of Lister’s L-shaped sheath inci-
sions created the possibility of narrowing the sheath
with repair, however many still prefer the increased
access gained by the L-shaped incisions. Tonkin and
Lister found no clinical evidence in their study to
support the necessity for closure of the synovial compo-
nent of the tendon sheath.10
Morrison, O’Brien, and co-authors investigated a
number of innovations designed to improve the results
of staged flexor tendon surgery. They developed a model
in which a flexor tendon was placed into bone prior to
using that tendon as a flexor tendon graft.11 Incorpora-
tion of the tendon into bone allowed the bone block to
be used as superior fixation into the digital phalanx at
the time of tendon grafting. This prefabricated bone-
tendon graft offered some theoretical advantages per-
taining to distal pullout strength but has not been
commonly adopted. Another fascinating study from the
same group compared the results of vascularized and
nonvascularized tendon grafts in a primate experimen-
tal model.12 The authors concluded that the concept of
vascularized tendon grafting may be advantageous in
scarred tendon beds. This work was developed during a
time of euphoria associated with the application of
microsurgical techniques to hand surgery but, although
it has some significant theoretical advantages, it has not
displaced the conventional approach of staged flexor
tendon grafting. Honner and Meares confirmed the reli-
ability of this technique in their review of 100 cases in
1977.13 The consistency of the results of flexor tendon
grafting performed with precise attention to detail was
also reported by Tonkin and Hagberg’s review of the
experience of Kleinert’s Louisville center, a fertile train-
ing ground for Australian hand surgeons.14
RECENT ADVANCES, 2000–2010
More recent Australian contributions relate to biome-
chanical testing of alternative suture configurations.
The search for optimal flexor tendon repair results has
Chapter 13G:  The Australian Experience 163
8000
6000
Strong
Force in grams
grip
6-strand
4000
4-strand
2000
Light 2-strand
active
Passive
0
Repair 1 week 3 weeks 6 weeks
Time in weeks
Figure 13(G)-2  A strength-versus-force graph showing
two-, four-, and six-strand repairs plotted against passive,
light active flexion, and strong grip. The data are adjusted for
friction, edema, and stress. (Data from Strickland JW: 25th
anniversary presentation: Development of flexor tendon
surgery: Twenty-five years of progress, J Hand Surg [Am]
25[2]:214-235, 2000.)
continued at a hectic pace. Most “improvements” have
centered on the development of stronger core and epi-
tendinous suture constructions which allow early post-
operative active mobilization. Savage, from the United
Kingdom, demonstrated the significantly improved
strength of repair gained by increasing the number of
strands within the core suture.15 Strickland’s graph is a
very helpful illustration of this concept comparing the
force generated by different postoperative rehabilitation
programs with the tensile strength of two-, four-, and
six-strand core sutures16 (Figure 13[G]-2). Descriptions
of modifications, all claiming some improvement in
one or more of the measured parameters, abound within
the current hand surgery literature. One is reminded of
the words of Guy Pulvertaft, in whose Derby hand unit
many Australian surgeons were trained: “it is not diffi-
cult to suture tendons and prepare the ground for sound
union; the real problem is to obtain a freely sliding
tendon capable of restoring good function.”17 Pulver-
taft’s point is pertinent. No tendon repair, regardless of
the number of strands in the core suture, technique of
epitendinous suture, or gauge of suture, will protect
against inappropriate postoperative activity against
resistance. Gelberman and others, from the United
States, have shown that the amount of movement
required to gain optimal promotion of tendon healing
and overcome adhesion formation is small.18,19 It would
seem logical to balance the determination to improve
the strength of repair against the increases in adhesion
formation, bulk, and resistance to glide, which may
164 Section 2:  Primary Flexor Tendon Surgery
follow excessive handling of the tendon when placing
more sophisticated suture configurations. Increased
adhesion formation was not found in the experimental
studies of Tonkin’s group in Sydney, which compared
adhesion formation in two- and four-strand configura-
tions with and without epitendinous sutures in a live
chicken model.20 However, this group concluded that
the expertise of the surgeon may play a substantial role
and suggested that complicated techniques in inexperi-
enced hands increased the potential for a less than sat-
isfactory result. It would seem appropriate to establish
surgical techniques that obtain reproducible results in
the hands of those who, although competent, may have
less experience than those who are able to confidently
perform more complex techniques.
Sandow found the 6-strand Savage configuration to
be too complex. His modification is similar to that
made by others and involves a 4-strand repair.21 This
“Adelaide” repair has been adopted by many Australian
hand surgeons. It provides four strands to the core
suture, is less likely to gap than a modified Kessler core
suture, is relatively easy to place in the tendon ends, and
may be combined with most of the currently preferred
epitendinous suture configurations. Its strength permits
protected active postoperative mobilization (Figure
13[G]-3).
Many Australian hand surgeons have collaborated
with William Walsh’s biomechanical laboratory at the
University of New South Wales in Sydney. Dona and
Gianoutsos, along with Walsh and others, investigated
the ideal size bite of locking loops for cruciate core
repairs, finding that each loop should optimally include
25% of the tendon’s width.22 In an earlier publication
they demonstrated the biomechanical superiority of an
interlocking horizontal mattress epitendinous suture
technique over that of an interlocking cross stitch, a
simple cross stitch, and a simple running repair.23 There
were statistically greater loads to failure, 2-mm gap for-
mation, and stiffness within those cadaveric tendons
repaired with the interlocking horizontal mattress
repair. Both studies used single progressive tensile
loading rather than cyclic loading when testing to
mechanical failure. Sandow and colleagues compared
the theoretical and actual repair strength of a multiple
strand repair in a single tension test with the strength
of a repair subjected to cyclic loading, finding a signifi-
cant decrease in ultimate tensile strength when the
repair was subjected to cyclical loading.24 This reduction
equated to the number of strands multiplied by the
strength of the knotted strand and was explained by the
change in stiffness of the knotted strand after cyclical
loading. They concluded that cyclic loading is more
representative of physiological loading after acute flexor
tendon repair and suggested that this should be the
testing model of choice in suture tenorrhaphy studies.
Matheson et al,25 again in collaboration with Walsh’s
A
B
C
Figure 13(G)-3  A, Modified Kessler core stitch. B, Inherent
gapping of modified Kessler under load. C, Adelaide
tenorrhaphy (four-strand single-cross grasp repair). (Adapted
from Sandow M, Kay S: Flexor tendon injuries. In Prosser R,
Conolly WB [eds]: Rehabilitation of the Hand & Upper Limb,
London, 2003, Elsevier Health Sciences, p. 47.)
laboratory, applied a cyclical testing protocol to a com-
parison of in vitro repairs using a modified Kessler core
suture or a four-strand modified Savage core suture,
with two different epitendinous techniques. They found
the modified Savage repair to be superior.
Vizesi and colleagues analyzed the stress relaxation
and creep properties of three materials used for flexor
tendon repair—Prolene (monofilament polypropyl-
ene), Ethilon (monofilament nylon), and Ticron
(braided polyester).26 Their study addressed the selec-
tion of suture material based on the temperature- and
time-dependent mechanical properties of a single-
strand suture. They reported that, based on static and
viscoelastic mechanical properties, Ticron was the most
suitable suture for flexor tendon repairs compared with
Prolene and Ethilon.
A number of studies from the same department have
investigated optimal methods of securing the FDP
tendon distally following avulsion. Schreuder et al
found that gap formation in such repairs was signifi-
cantly less when Ethibond (a braided polyester) was
used compared with Prolene or Supramid (a synthetic
polyfilament ensheathed by Caprolactin).27 Latendresse
et al28 compared the repair of FDP tendons using a
single micro-Mitek anchor with a modified Bunnell
two-strand pullout technique, using a monofilament or

a braided polyester suture. Load to failure in the modi-
fied Bunnell technique was superior to the micro-Mitek
anchor technique. Significant gap formation was present
when a monofilament suture was used but this problem
needed to be balanced against the difficulty of removal
of a braided polyester pullout suture. In the search for
alternatives to pullout sutures, with their potential for
creation of nail plate deformities, nail fold necrosis, and
infection, this group studied the influence of anchor
orientation when inserting the micro-Mitek anchor.29 In
an in vitro biomechanical study using 3-0 Ethibond
suture anchors in cadaver specimens, they did not find
any support for the theory that varying the angle of
anchor insertion improved the load to failure. However,
inserting the anchor in a retrograde fashion at 45°
appeared to result in fewer failures at the bone anchor
interface, with failure more likely to occur at the join
between suture and the eyelet of the anchor. Other sur-
geons in the same laboratory advised avoidance of nail
problems following reinsertion of FDP tendons distally
by placing the suture through two drill holes in the base
of the distal phalanx.30 They demonstrated that this
repair method was biomechanically sound with compa-
rable gap formation and load to failure to other com-
monly used repairs, was technically straightforward, and
did not impair the integrity of the distal phalanx.
In 2006, Dona and Walsh31 described a V-Y plasty
within pulleys to increase the cross-sectional area within
the pulley and thus decrease the friction of the repaired
tendon, allowing easier glide but maintaining a mechan-
ically sound pulley. They did not advocate this tech-
nique for routine use but as an alternative to venting or
resection in those circumstances in which gliding of the
repaired tendon was found to be unsatisfactory.
Much of the above experimental work relates to the
optimal types of suture material and techniques of core
and epitendinous sutures for flexor tendon repair. A
number of recent Australian studies have contributed to
an improved understanding of some other nuances of
flexor tendon surgery. Stewart and coauthors reminded
us of the ability of intact vincula to flex interphalangeal
joints despite tendon division.32 In an experimental
cadaveric model, they demonstrated that in the immedi-
ate postinjury period, the vinculum breve can hold a
divided tendon within a few millimeters of its insertion.
In these circumstances they quantified the motion
present at proximal and distal interphalangeal joints
as being 93% and 69% of normal, respectively. They
emphasized that testing of the injured digit against resis-
tance is important if one is to avoid missing the diag-
nosis of a tendon injury.
Lawson and coworkers addressed the difficulty of per-
forming a full circumferential epitendinous repair when
the tendon injury comes to lie beneath the A4 pulley
and access to the dorsal aspect of the tendon is com­
promised.33 They reported that a half-circumferential
Chapter 13G:  The Australian Experience 165
epitendinous repair applied to the palmar surface was
effective in improving the strength of repair compared
with a core suture alone and was effective in decreasing
gap formation. However, the load to failure was signifi-
cantly less than that of a core suture combined with a
full circumferential suture.
Hile and colleagues34 were concerned about the prev-
alence and consequences of piercing the thread of a
braided polyester suture with the needle during complex
multistrand repairs. They concluded that cutting needles
should not be used in tendon repairs because they can
damage or completely sever core sutures. They also
found that crushing of the suture between the teeth of
a needle holder significantly weakened the involved
segment.
The work of the investigators that was just outlined
is not inclusive of all such work that has been and is
being performed by Australian surgeons and their col-
leagues. However, the time and effort directed toward
obtaining optimal results from flexor tendon repair
within Australia and worldwide are indicative of the
importance of this pursuit. Although some thought
needs to be given to the worth of in vitro cadaveric
model experiments in which biology is removed from
the assessment, it is undeniable that such studies have
resulted in an improved understanding of the most
appropriate suture material, its gauge, and, importantly,
the surgical techniques and configurations of core and
epitendinous sutures that best prevent rupture, avoid
adhesions, and allow an optimal postoperative rehabili-
tation program. Despite these improvements, future
advances would appear to rely on our ability to modify
healing processes at a molecular level to increase early
strength of repair and to avoid adhesion formation.
CURRENT PRACTICE IN FLEXOR TENDON
REPAIR AND REHABILITATION
To understand the current state of primary flexor tendon
repair in Australia, we conducted a survey of the mem-
bership of the Australian Hand Surgery Society. Approx-
imately 40% of the active membership responded. A
very wide range of approaches was apparent, particu-
larly in the more controversial areas such as manage-
ment of the critical pulleys, and in methods of
postoperative rehabilitation.
In Australia, hand surgeons perform on average one
or two repairs a month (mean of 17 per year). Surgeons
with a large trauma practice perform substantially more.
Many other repairs are done by training residents and
by plastic, orthopedic, and general surgeons.
The most commonly used core suture material is
some form of braided polyester suture, typically Ticron
or Ethibond. For a large tendon, such as the FDP to the
middle finger, around two thirds prefer to use a 3-0 core
suture, but a significant minority prefer to use a 4-0 core
suture. Around 20% of the respondents who used a
166 Section 2:  Primary Flexor Tendon Surgery
braided suture as their core stitch preferred to use a
nonbraided suture for contaminated wounds.
There were two core suture configurations commonly
used: the four-strand modified Savage (often referred to
as an Adelaide repair) was used by 40% of the surveyed
surgeons and a four-strand modified Kessler was also
used by around 40%. Other favored techniques included
the six-strand Savage repair, and the Tsai-Lim six-strand
technique taught at Kleinert’s center in Louisville. Flex-
ibility in the choice of core suture is practiced by some,
depending on the ease of access to the cut ends of the
tendon around the pulley system.
The epitendinous suture of choice was polypropylene
(Prolene), with 60% of respondents preferring 6-0
Prolene and 25% favoring 5-0 Prolene. A simple running
epitendinous repair was performed by 70% of surgeons,
with the next most popular technique being the Silfver-
skiöld technique, used by around 20%.
Management of the A2 and A4 critical pulleys varied,
with forcefully held and disparate opinions; 12% of the
surveyed surgeons would not release any part of the
critical pulleys, while 88% would perform partial or full
releases. Of those who released the A4 pulley, 20%
would do so at the beginning of the repair as part of
their exposure; the remainder would do so if exposure
proved difficult during the repair or if the repaired
tendon did not glide adequately.
Two-thirds of respondents did not attempt to repair
divided pulleys, with some stating that they thought a
satisfactory repair was not possible; some of those who
would try to repair the pulley stated they would perform
a V-Y plasty to increase the diameter of the repaired
pulley. Closure of the synovial sheath/A3 pulley was
advocated by 55%.
Teaching of flexor tendon repair to trainees should
involve a sound grounding in basic principles, and 60%
of the surgeons surveyed believed, some very strongly,
that junior physicians should not be taught to release
the critical pulleys, believing they should first learn to
perform good repairs while working around the pulleys,
and perhaps when more expert would be able to make
an informed choice with respect to pulley release.
Rehabilitation protocols varied widely: 25% of
respondents used the same protocol for all of their
patients, while the other 75% tailored their approach to
the demands of each patient. The most popular regimen
was some form of immediate active motion, used by
65%. Passive flexion/active extension (Duran-Hauser)
was used by 19%, passive flexion/active hold (place and
hold) was used by 11%, and Kleinert traction was used
by 6%. Unrestricted use was allowed by 55% at 12
weeks, by 15% at 8 weeks and, by 15% at 6 weeks.
AUTHORS’ PREFERRED APPROACH
As shown, there is a considerable variety of approaches
to the management of flexor tendon injuries by
Australian hand surgeons. Our current practice is sum-
marized as follows:
1. The approach to the flexor sheath begins with
débridement of the existing wound, followed by
extension using a combination of Bruner, hemi-
Bruner, and midlateral incisions.
2. The A2 and A4 pulleys are preserved during the
approach, with access to the tendon achieved via
Lister’s L-shaped windows between these critical
pulleys. This technique acts to funnel the tendon
beneath the pulley and maximize the chance of
smooth running of the repair.
3. If access to the tendon ends is adequate, a modi-
fied Savage four-strand (Adelaide) repair is per-
formed, using 3-0 Ticron in larger tendons and 4-0
or 5-0 Ticron in smaller tendons (usually little
finger FDP and pediatric tendons, respectively).
A simple running or Silfverskiöld epitendinous
repair using 6-0 Prolene with a taper needle is
performed, depending on access. The back wall
repair is ideally done first to keep the tendon ends
snugly opposed. If access to the back wall is par-
ticularly difficult or not possible because of the
proximity of the A4 pulley, only the front half of
the tendon receives an epitendinous suture.
4. If the distal tendon ends lies beneath the A4 pulley,
combined proximal/distal repairs as described by
Lister are used. This technique precludes the use
of the modified Savage repair in our hands, and
instead a modified Kessler with a supplementary
horizontal mattress core suture is performed. This
technique permits retention of the A4 pulley while
allowing for a 10-mm purchase with the core suture.
5. If gliding of the repair is impeded, the pulleys can
be stretched with pediatric urethral dilators. Small
strands of tendon projecting from between the
epitendinous sutures can be carefully removed
with microscissors.
6. The incised sheath is laid over the tendons but no
formal repair is performed if there is any threat to
gliding.
7. Postoperative rehabilitation is tailored to the
quality of the repair, and the compliance of the
patient, with a tendency to err toward a less aggres-
sive form of mobilization. In cooperative patients
with high quality repairs an active range of motion
technique is used; in the less optimal repair or
patient a modified Duran regimen with passive
flexion and active extension is prescribed. A dorsal
extension blocking splint is used to protect the
repair. In all cases it is particularly important to
guard against the development of a proximal
interphalangeal joint flexion contracture.
8. The splint is typically removed at 6 to 8 weeks, at
which point a gentle strengthening program is

started. Full grip is prohibited until 3 months post
repair.
SUMMARY
Australian surgeons have made important contributions
in the field of flexor tendon repair, including key work
References
1. Rank BK, Wakefield AR: Surgery of Repair as Applied to Hand
Injuries, Edinburgh, 1953, E & S Livingstone.
2. Pennington DG: The locking loop tendon suture, Plast Recon-
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3. Mason ML, Allen HS: The rate of healing of tendons: An
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4. Kessler I, Nissim F: Primary repair without immobilization
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5. Pennington DG: Atraumatic retrieval of the proximal end of
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1990.
11. Singer D, Doi K, Morrison WA, et al: Comparative study of
the use of prefabricated bone tendon grafts and conventional
tendon grafts in flexor tendon reconstruction, J Hand Surg
(Am) 14:830–836, 1989.
12. Singer DI, Morrison WA, Gumley GJ, et al: Comparative study
of vascularized and nonvascularized tendon grafts for recon-
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in primates, J Hand Surg (Am) 14:55–63, 1989.
13. Honner R, Meares A: A review of 100 flexor tendon recon-
structions with prosthesis, Hand 9:226–231, 1977.
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ment of flexor tendon grafting, J Hand Surg (Br) 13:277–281,
1988.
15. Savage R: In vitro studies of a new method of flexor tendon
repair, J Hand Surg (Br) 10:135–141, 1985.
16. Strickland JW: Development of flexor tendon surgery: Twenty-
five years of progress, J Hand Surg (Am) 25:214–235, 2000.
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1948.
18. Boyer MI, Gelberman RH, Burns ME, et al: Intrasynovial
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canines, J Bone Joint Surg (Am) 83:891–899, 2001.
19. Silva MJ, Brodt MD, Boyer MI, et al: Effects of increased in
vivo excursion on digital range of motion and tendon strength
Chapter 13G:  The Australian Experience 167
by Rank, Morrison, and Pennington. The methods of
repair used by hand surgeons in Australia include use
of a four-strand core suture, careful consideration of
pulley management, and a trend toward active move-
ment in rehabilitation, but the precise methods vary
widely and are the subject of healthy debate.
following flexor tendon repair, J Orthop Res 17:777–783,
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cal performance of the 4-strand cruciate flexor tendon repair,
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23. Dona E, Turner AW, Gianoutsos MP, et al: Biomechanical
properties of four circumferential flexor tendon suture tech-
niques, J Hand Surg (Am) 28:824–831, 2003.
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vivo porcine study, Hand (NY) 4:113–118, 2009.
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2005.
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viscoelastic properties of common suture materials used
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2008.
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material on gap formation and failure in type 1 FDP avulsion
repairs in a cadaver model, Clin Biomech (Bristol, Avon)
21:481–484, 2006.
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pullout sutures and micro-mitek suture anchors in flexor digi-
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30:471–478, 2005.
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137, 2006.
32. Stewart DA, Smitham PJ, Gianoutsos MP, et al: Biomechani-
cal influence of the vincula tendinum on digital motion after
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(Am) 32:1190–1194, 2007.
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 H The Wellington Experience
Mark A. Rider, MBChB, FRCS, FRACS
OUTLINE
A series of prospective reviews is presented, showing
how stepwise changes in repair techniques lead to
dramatic improvements in outcomes. Our currently
preferred technique, and the rationale for it, is dis-
cussed. Some aspects of working as a hand surgeon in
New Zealand are mentioned. Finally, some guidelines
for preventing repair rupture are offered.
Multiple revolutions of the audit cycle are a power-
ful means of improving outcomes. The outcomes have
been improved drastically with progressive decreases
in the rupture rates of the tendons over the past 10
years with different surgical repair methods. Currently
the four-strand Adelaide repair with Fiberwire and
postoperative controlled active motion is a successful
combination in our practice.
“If you cannot measure it, you cannot improve it” is one
of many quotes attributed to Lord Kelvin. It is certainly
possible to measure the results of flexor tendon repair,
but this is not commonly done by surgeons. I submit
that measuring the results of our current practice, and
then making incremental changes based on the outcomes
and literature reviews, may yield great benefits for our
patients. Some surgeons rarely change their techniques,
ignoring important new developments; some change
constantly, following every fashion but having little idea
of their results. For me, a middle way has proved useful,
and I present a series of flexor tendon reviews to illus-
trate this.
THE AUDITS
The research method was the same for each period. All
adult patients presenting with completely divided flexor
tendons within zone 2 of the fingers were enrolled. The
study patients were treated in the same way as all other
patients with hand injuries who were admitted to the
unit; although the aim was to perform surgery on the day
of presentation, delays of up to 48 hours were common.
Both deep and superficial tendons were repaired. If
the flexor digitorum superficialis (FDS) was large enough
to accept a core suture, this was the same type as used
for the flexor digitorum profundus (FDP). Partial inju-
ries of critical pulleys were not repaired. The synovial
sheath was loosely repaired if this could be done without
168
impinging on the tendon repair. The A2 and A4 pulleys
were preserved during suturing of the tendons. However,
subsequent venting was allowed if there was impinge-
ment of the repaired tendon during passive on-table
testing. There was a varying degree of consultant super-
vision, with most of the work done by trainees. The
rehabilitation protocol was unchanged throughout all
periods (“modified Belfast” early active, commencing at
48 hours). The main outcome measures were rupture
rate and range of movement by original Strickland at 12
weeks, assessed by the hand therapists in a standard
manner. After review of each period’s results, one or two
aspects of the repairs were changed, and the process
repeated. The results of these are summarized in Table
13(H)-1.
The first review was conducted in September 2000
and was retrospective over the previous 6 months. No
protocols existed in the unit at that time, resulting in a
wide range of repair and suture types, modified Tajima
with 3-0 and 4-0 Prolene predominating. The data were
markedly incomplete, but of the 10 patients who were
followed, 2 had rupture. The initial recommendation
was to start a prospective audit.
An 18-month prospective review was completed in
October 2002. The repairs were mainly modified Tajima
with 3-0 and 4-0 Ticron or Ethibond, and a simple
running epitendinous, on 37 patients with 49 tendons.
The follow-up rate was low, but of the 21 patients fol-
lowed up, 7 had rupture! The obvious recommendation
was to move to a multistrand repair. We selected a cross-
locked cruciate repair (Figure 13[H]-1).
The next review covered a 2-year period to August
2005. The repairs were all Adelaide with 3-0 or 4-0
Ethibond, plus a variable epitendinous repair, most
usually Silfverskiöld. The rupture rate plunged to 1 of
23 patients, with 82% excellent or good.
For the next audit, the repair type was left unaltered
but the suture material was changed to 4-0 Fiberwire
(Arthrex Naples, FL). This final review covered an
18-month period. There were no ruptures, and 96% of
fingers achieved Strickland excellent or good results.
DISCUSSION
Benefits of Serial Audit
I hope the improvement in our (initially appalling)
results is a convincing demonstration of the benefits of
 Chapter 13H:  The Wellington Experience 169

Table 13(H)-1  The Results of Tendon Repairs for Each Period Reviewed
Ruptures
Patients Fingers
Lost to Fingers Good or Rate (%,
Year Patients Fingers Tendons Follow-Up Followed-Up Excellent (%) Patients Fingers Fingers)
2000 15 21 26 5 15 7 2 3 20
2002 37 42 49 16 23 43 7 7 33
2005 33 41 61 10 28 82 1 1 4
2007 32 39 43 10 28 96 0 0 0

serial audits. Much of the improvement was no doubt
due to the change to a four-strand repair. However, I
think there are other, less tangible benefits, particularly
the greater involvement by senior surgeons and the
general focus on quality and excellence by the whole
unit.
The Change to a Four-Strand Repair
We anticipated that the selection of the cross-locked
cruciate repair (known locally as the Adelaide repair)
would provide a good compromise between strength
and difficulty of insertion. Our unit is typical of many
large public hospital services in that many of the flexor
tendon repairs are performed by unsupervised, rela-
tively junior trainees. More complex repair patterns may
be stronger when performed by experts, but in our “real
world” situation are also more likely to be poorly
inserted. Studies confirming the favorable properties of
the Adelaide repair are now starting to appear.1
Fiberwire
As we completed our penultimate audit, we became
interested in Fiberwire. Some early reports attested to its
high strength compared to preexisting suture materials,
Fiberwire showing less gap formation at all loads and
the greatest load to failure. A subsequent study con-
firmed its strength with locking repairs.2 Some of the
benefit may be illusory due to its nonstandardized size:
a 4-0 Fiberwire may be much stronger than a 4-0 Ticron,
but it is also thicker.3 We remain happy to use Fiberwire,
but note some recent studies raising caveats, in particu-
lar poor knot holding requiring more throws (and
therefore greater bulk of suture material).4
Figure 13(H)-1  Four-strand locked cruciate repair method.
The Nature of Hand Injuries and Their
Management in New Zealand
New Zealand has in the past had a much higher
incidence of occupational injury than the safest of
the Northern European countries, although rates are
improving. The occupations with the highest rate of
hand injuries are machine operators, construction, for-
estry workers, and meat processing workers.5 The last
two occupations are relatively common in New Zealand
compared to more industrialized countries and may in
part explain the high numbers of hand injuries. Perhaps
surprisingly considering the high cost of these injuries,
etiological and preventable factors for work-related
hand injuries are poorly studied worldwide.6 In our
experience, meat processors were the group with the
highest work-related cause of flexor tendon injury. Pos-
sible risk factors include blunt knives, removing protec-
tive gloves, the cold environment, and the high turnover
rate of staff. From a surgeon’s point of view, the injuries
were usually sharp and tidy, although they carried a risk
of infection from raw meat.
Targets
An essential part of audit is to identify best practice from
the literature. Establishing a realistic target for rupture
rates is not a simple matter. During the 1990s, rates of
well over 4% were regularly reported. It is difficult to
judge these. On the one hand, they came from well-
known centers and could perhaps be presumed to be
best practice. On the other hand, many of the larger
series were from British public hospitals and undoubt-
edly included the results of unsupervised junior
surgeons.
In reviewing more recent publications, we can con-
clude that rupture rates from two-strand repairs are not
improving with time. However, there are a number of
reports of multistrand repairs with very low rupture
rates, although with small numbers of patients. One of
the largest recent reports of four-strand repairs gives a
headline rupture rate of 2%.7 If we extract from the
authors’ results only the zone 2 repairs, the rate rises
to 3.7%. Almost all the repairs were performed by
trainees.
170 Section 2:  Primary Flexor Tendon Surgery
It seems likely that ruptures will continue for the
foreseeable future, despite improvements in repair types
and ongoing research into biological factors. We cer-
tainly do not expect our rupture rate to remain at zero.
Patient irresponsibility is a factor in many ruptures.8 In
our series, we saw early ruptures in one patient playing
competitive rugby and another using a chainsaw having
first climbed a ladder. These incidents occurred despite
presumably adequate education from an expert and
well-staffed hand therapy service.
I suggest that a specialist hand unit, with some repairs
performed by trainees, should obtain a rupture rate in
References
1. Croog A, Goldstein R, Nasser P, et al: Comparative biome-
chanic performances of locked cruciate four-strand flexor
tendon repairs in an ex vivo porcine model, J Hand Surg (Am)
32:225–232, 2007.
2. Miller B, Dodds SD, deMars A, et al: Flexor tendon repairs:
the impact of fiberwire on grasping and locking core sutures,
J Hand Surg (Am) 32:591–596, 2007.
3. Scherman P, Haddad R, Scougall P, et al: Cross-sectional area
and strength differences of fiberwire, prolene, and ticron
sutures, J Hand Surg (Am) 35:780–784, 2010.
4. Waitayawinyu T, Martineau PA, Luria S, et al: Comparative
biomechanic study of flexor tendon repair using Fiberwire,
J Hand Surg (Am) 33:701–708, 2008.
5. Burridge JD, Marshall SW, Laing RM: Work-related hand
and lower-arm injuries in New Zealand, 1979 to 1988, Aust
N Z J Pub Health 21:451–454, 1997.
zone 2 of less than 4% and Strickland good/excellent
result of greater than 80%. An experienced hand surgeon,
reviewing his or her own repairs, should aim for a
rupture rate approaching zero and good/excellent results
in greater than 90%.
CONCLUSION
We have shown how multiple revolutions of the audit
cycle are a powerful means of improving outcomes. We
believe this should be a mandatory activity in every
hand unit. The Adelaide repair Fiberwire and controlled
active motion is, for us, a successful combination.
6. Sorock GS, Lombardi DA, Courtney TK, et al: Epidemiology
of occupational acute traumatic hand injuries: A literature
review, Saf Sci 38:241–256, 2001.
7. Caulfield RH, Maleki-Tabrizi A, Patel H, et al: Comparison of
zones 1 to 4 flexor tendon repairs using absorbable and
unabsorbable four-strand core sutures, J Hand Surg (Eur)
33:412–417, 2008.
8. Harris SB, Harris D, Foster AJ, et al: The aetiology of acute
rupture of flexor tendon repairs in zones 1 and 2 of the fingers
during early mobilization, J Hand Surg (Br) 24:275–280,
1999.
 CHAPTER
14  
PARTIAL TENDON
LACERATIONS
Morad Askari, MD, and Peter C. Amadio, MD
OUTLINE
Many patients with partial tendon laceration come
to the clinic several weeks after the injury due to
persistence of symptoms, by which time the cutane­
ous wound may be healed and closed. Evidence of
triggering or entrapment is adequate indication for
exploration of the wound. Partial tendon lacerations
can also be seen in a large wound together with com­
plete lacerations of other tendons, which are easy to
diagnose.
The degree of laceration directly impacts tensile
strength of the injured tendon. However, with even
larger degrees of laceration, the tendon retains enough
tensile strength to withstand most active motion. The
volar location of the laceration may lower a clinician’s
threshold for surgical repair. A lesser degree laceration
(<40% to 50%) may not need surgical repair. A tendon
laceration >50% to 60% usually needs surgical repair.
Repair of partial tendon lacerations decreases the
chance of tendon triggering and improves tendon
excursion. The partially lacerated tendon can be treated
with a circumferential suture with or without core
suture technique. Core sutures are used in large degree
(>60% to 75%) partial laceration. The lacerated parts
can be trimmed to reduce triggering in partial tendon
lacerations up to 75%. Complications of untreated
lacerations include triggering, entrapment, and rupture
of the tendons.
While little controversy exists today on necessity of
complete tendon laceration repair, the topic of treating
partial tendon laceration remains a subject of debate in
hand surgery. Opinions are divided on whether man­
agement of partial tendon laceration is best achieved
through surgical or nonsurgical approach.1 This con­
troversy, in part, stems from fewer in vivo studies of
partial as opposed to complete tendon laceration in the
literature many with conflicting results. In part, this
could also be due to fewer cases of partial tendon lacera­
tion properly diagnosed in clinical practice. Thus, major­
ity of studies have used in vitro cadaveric or animal
models. Additionally, a majority of these studies focus
on complete laceration of flexor tendons with much
smaller focus on partial tendon laceration.
The controversy centered on the repair of partial
tendon laceration was initiated by the work of Wray and
Weeks2 in a chicken model where nonrepaired partially
lacerated flexor tendons were deemed better than those
repaired. This result was similarly confirmed by Reyn­
olds et al3 in a similar model. Just a few years later, the
concept of not repairing partially lacerated tendons was
challenged by Kleinert and others.4 They advocated that
partially lacerated tendons should be treated similarly
to complete lacerations, emphasizing that this type of
injury required the same diligence in surgical repair and
postoperative care. In their series, they reported signifi­
cant rise in complications following nonrepair of partial
flexor tendon lacerations. Similarly, around the same
time, Janecki5 reported on two cases of entrapment fol­
lowing nonoperative treatment of partially lacerated
flexor tendons. The sentiment to repair this type of
tendon injury was further echoed by Schlenker and
coworkers,6 who reported a significant increase in trig­
gering, entrapment, and rupture among other complica­
tions when these lacerations were not repaired. They
recommended the repair of all lacerations greater than
25%. They favored modified Kessler core suture tech­
nique along with a running epitendinous suture for
lacerations greater than 50% while for those between
25% and 50%, a running braided polyester suture was
suggested. For laceration less than 25%, excision of the
distally based flap was recommended to avoid triggering
or entrapment in the pulley. However, since these
studies, a series of in vitro biomechanical studies along
with in vivo animal studies has resulted a better under­
standing of the properties of partially lacerated tendons
and a shift in paradigm of treatment of partial tendon
injury.
DIAGNOSIS AND PHYSICAL EXAMINATION
Clinically most patients have normal active motion, and
cutaneous wounds are either rather small or healed.
Identifying partial tendon laceration is a challenge.
Partial tendon laceration classically presents as painful
and weakened tendon excursion as opposed to absence
171
172 Section 2:  Primary Flexor Tendon Surgery
of active finger flexion or any excursion as would be
expected with complete laceration. However, without
direct visualization through an open wound or an
imaging modality, determining the degree of laceration
based on clinical exam is not possible. In majority of
cases, an opening in the skin at the site of trauma can
serve as a window for initial examiner to characterize
the degree of tendon laceration as a percentage of intact
tendon width. This measurement is commonly done
using a caliper. Interestingly, it has been showed that
neither caliper measurement nor estimation with naked-
eye provides consistent and reliable means of assessing
the degree of laceration when managing partial tendon
injuries.7 Yet, these are tools used by most in estimating
degree of tendon injury.
Many patients with partial tendon laceration may
present several weeks after the injury due to scheduling
or persistence of symptoms, by which time the wound
may be healed and closed. Evidence of triggering or
entrapment is adequate indication for exploration of the
wound. If a moderate index of suspicion exists for explo­
ration, an imaging study such as ultrasound or magnetic
resonance imaging is beneficial. Partial tendon lacera­
tion can also occur with other tendons lacerated com­
pletely in a larger wound, which is easy to diagnose.
PHYSIOLOGY OF TENDON HEALING
Through significant contribution early in the 20th
century by Mason, Allen, and Shearon8,9 an understand­
ing of various stages of tendon healing was developed.
Following injury, the tendons enter an exudative phase
of tendon healing (0 to 14 days) followed by a reparative
phase (15 to 35 days). An understanding of the phases
in tendon healing is important in choosing appropriate
time point for biomechanical and biological studies. The
healing tendon is strongest at day 1 with this strength
dropping by day 5. The lost strength is gradually restored
starting around day 15 and continues until the end of
the reparative phase. The exact length of time for the
tendon to reach maximum strength appears to extend
beyond the 5th week. The above authors also demon­
strated that the weakest sight on an undamaged tendon
corresponded to the musculotendinous junction and
the tendon–bone insertion. This group was among the
first to suggest that early motion resulted in increase in
strength and function of partially lacerated tendons. In
addition to tensile strength, the concepts of tendon
gliding and resistance against motion were emphasized
in the context of tendon repair. Many have shown the
deleterious effects of immobilization on tendons and
the subsequent change in substance constituents and
weakening of their insertion sites.10-12
The degree of laceration has an effect on tendon
healing. In an in vivo canine model of partial flexor
tendon injury, Cooney and others13 noted that the
greater lacerations had less evidence of healing. While
tendon with 30% laceration had histological evidence
of amorphous connective tissue in the tendon gap with
nascent collagen fibers bridging across the tendon edges,
the 60% and 90% lacerated tendons showed little evi­
dence of healing with no collagen present in the gap at
35 days.
BIOMECHANICAL PROPERTIES OF PARTIAL
TENDON INJURY
The majority of experimental data on partial tendon
injuries is the result of years of investigation using in
vitro cadaveric and animal tendons in addition to a
smaller number of in vivo studies in animal models.
The popular animal models for their proximity to
human tendon anatomy are the canine, chicken, sheep,
and pig models. Majority of effort in understanding
partial tendon injury has been associated with flexor
tendons specifically in zone 2.
Gap formation in the context of partial tendon injury
is an important point of clinical interest because its
increase is associated with higher gliding resistance, trig­
gering, and delay in healing.14,15 Gapping beyond 2 mm
is harmful to tendon healing.14
Tensile Strength and Cross-Sectional Area
Feared sequelae of improperly treated partial tendon
laceration include triggering, loss of entrapment, adhe­
sion formation, or late rupture. It is intuitive that partial
lacerated tendons would be weaker than intact tendons.
Additionally, some had suggested formation of a scar
mass at the laceration sites if a partial injury were to go
nonrepaired, thus adversely affecting tendon function.4
It is our presumption that many such tendons if they
were to be repaired would like be subjected to more
rigorous immobilization postrepair than if they were
left alone. In the following sections, the evidence that
has shaped our current approach to partial tendon
injury is reviewed. Of note, the great focus in study
partial tendon lacerated has involved mainly flexor
tendons and attention specifically to zone 2 injuries in
part due to the historical poor outcome of injury in this
area. Many times, the clinicians inadvertently extrapo­
late this information to treatment of flexor tendon in
other zones and to extensor tendon injuries.
In the recent decades, several studies have pointed
toward early active finger motion to decrease adhesion
formation and improve tendon gliding.16-18 While
rupture of partially lacerated tendons has been dis­
cussed as a complication of early motion and no repair,
many have shown this to be a more minimal concern
than previously thought. In a series of 34 partial tendon
lacerations ranging from 25% to 95% laceration of the
cross-sectional area of the tendon, no rupture occurred
following non surgical management even in the 11 cases
with more than 75% laceration. All but one case had
good to excellent function.19 Several studies have

characterized the strength of partially lacerated tendon.
While the tensile strength of the tendon decreases as the
cross-sectional area of laceration increase, these studies
support that a partially lacerated tendon in most cases
retains sufficient tensile strength to withstand motion
and loading. In chickens, Reynolds and others3 showed
the mean tensile strength of unsutured tendons to be
higher than the sutured repairs at both 2 and 4 weeks
of unrestricted motion after surgery. Dobyns and others20
demonstrated that 30% of lacerated tendons retain 80%
of their original strength, while 75% of lacerations
maintain 40% and 90% of lacerations have 25% of the
strength. Hariharan and others7 looked at the tensile
strength of 50% and 75% volarly lacerated flexor
tendons in cadavers and compared the failure loads to
in vivo forces measured in human flexor tendons during
unresisted active finger movement. Failure loads for
50% lacerated tendon were almost twice as much as
the failure load for 75% lacerated ones. However, the
failure values for both degrees of laceration far exceeded
the in vivo values required for unresisted active finger
movement.21
McCarthy and others7 noted a tendency for tendons
to fail at the site of partial laceration when the cross-
sectional area of laceration was equal or greater than
60% in an in vitro canine model. At this degree of lac­
eration, they noted a 22.8% decrease in stiffness, 41.5%
decrease in failure loads, 15.6% decrease in percent
elongation, and 56.2% decrease in energy absorbed
compared with intact tendons. The structural properties
change adversely with increasing degree of laceration.7
As inflicted lacerations through tendons are most
commonly not transverse, the effect of the direction of
laceration and its impact on tensile strength becomes
important. Tan and others22 have shown that obliquity
of tendon laceration affects the strength of partially lac­
erated tendons. Using pig tendons lacerated to 90% of
their diameter, they found that lacerations with 45° and
60° had significantly less ultimate tensile strength com­
pared with transverse, 15° or 30° oblique laceration.22
Tensile Strength and Repair
Several studies have investigated the effect of suture
repair and subsequent immobilization on tensile
strength of partially injured tendons. Suturing may
impair the vascularity of the tendon and damage tendon
cells.23 Ollinger and others24 found that sutured tendons
(Bunnell method) after partial laceration had less tensile
strength than nonrepaired controls. Similar results were
replicated by Bishop and others.25 In a canine model,
areas of tendon adjacent to the repair site had necrosis,
which explains the diminished tensile strength.25
Cooney and others12 showed in a similar model, that
for 30%, 60%, and 90% lacerated canine flexor tendons,
nonrepaired tendons had a greater mechanical strength
at 14 and 35 days compared with the repaired tendons.
Chapter 14:  Partial Tendon Lacerations 173
Early Mobilization and Tendon Remodeling
As hesitations to mobilize patients with partial tendon
lacerations due to risk of rupture are lessened through
the mentioned studies, early mobilization was advo­
cated to increase tensile strength and to improve mor­
phology of the nonrepaired partially lacerated tendons.
Wray and others26 showed that early motion accelerates
return of tensile strength to partially lacerated tendons.
Similarly, Reynolds and others3 showed that immobi­
lized repaired tendons were weaker than nonrepaired
partially lacerated tendon following unrestricted
motion. This finding may be due to a more pronounced
intrinsic healing with early motion.27 Using an in vivo
canine model, Bishop and others24 studied the relative
effects of immobilization, early protected mobilization,
tendon repair, and no repair by paired comparison to
contralateral side. Early motion improved stiffness and
excursion significantly. Under scanning electron micros­
copy, these tendons had more nearly normal morphol­
ogy compared with immobilized tendons. They also
found a decrease in breaking strength and stiffness in
tendons that had undergone repair compared with no
repair. They concluded that tendon lacerations up to
60% of the cross-sectional area of the tendon should be
treated with early protected mobilization with no
attempt to repair.24 Kubota and others,28 in their in vivo
chicken model, documented that early motion and
tension on partial tendon injuries resulted in superior
biological remodeling. Grewal and others29 compared
canine tendon healing 3 weeks after passive to active
rehabilitation following 60% tendon laceration. The
tendons were repaired with modified Kessler suture in
one and were left nonrepaired in the other group. In
each group, a subgroup underwent immediate active
mobilization while the other subgroup underwent
passive motion. No difference was found in tendon
excursion, stiffness, or load to failure between passive
versus active mobilization or repair versus nonrepair
groups. However, gapping was significantly increased
among the active rehabilitation group compared to the
passive rehabilitation group. The authors concluded
that active rehabilitation is safe in lacerations up to
60%, but gapping at 3 weeks raises the concern for
future complication in tendon healing.29
Tendon Gliding and Resistance
Unresisted gliding is important for normal tendon func­
tion. Proponents of surgical repair of partial tendon
laceration have argued that presence of flaps at the non­
repaired site may result in triggering, entrapment in the
pulley, and eventual rupture of the tendon.4-6 However,
following surgical repair, the bulk of surgical repair and
rough tendon surfaces can result in higher gliding resis­
tance. This in turn may adversely affect the rehabilita­
tion process.30,31 In an in vivo chicken study, Ollinger
and others24 showed not only a decrease in tensile
174 Section 2:  Primary Flexor Tendon Surgery
strength but also a decrease in tendon gliding following
exposure and tenorrhaphy of partial tendon lacerations.
Early postoperative motion can restore smooth tendon
surface and improve gliding.32 Al-Qattan and others33
studied triggering and tendon flap formation over an
8-week period in an in vivo sheep model with 50%
lacerated flexor tendons without surgical repair. Trigger­
ing occurred not due to bulbous scar formation but due
to “bunching” of the tendon fibers proximal and distal
to the area of laceration. With time and mobilization,
these fibers became incorporated into the healing
process resulting in spontaneous resolution of trigger­
ing in majority of tendons.33 Various suturing tech­
niques result in different degree of friction and resistance
at tendon–pulley interface. Zhao and others34 character­
ized gliding resistance with several suture techniques on
the 80% lacerated tendons using cadaveric tendons.
Modified Kessler repair had the least resistance com­
pared to Kessler, Savage, Tsuge, or Becker techniques.
Yet, on average, there was an average increase of 1.08 N
in gliding resistance of the tendon following repair,
which is sufficient to limit tendon gliding during passive
motion (average 0.49 N).34
Location as well as the degree of laceration of the
tendon also impacts the gliding resistance. Erhard and
others35 compared volar and laterally transected tendons
in an in vitro cadaver model. The degree of laceration
in two different groups was 50% and 75%. Increase in
laceration resulted in greater gliding resistance. More
interestingly, volar partial laceration resulted in greater
gliding resistance in comparison to lateral transections
for both 50% and 75% lacerations.35
Tendon Nutrition and Adhesion Formation
Formation of adhesion limits gliding ability of the
tendon. Aside from potentially creating large physical
mass that impedes proper excursion of the tendon at
the pulley, the act of tendon repair may result in more
inflammation and adhesion formation. Suture repair
and tendon immobilization contribute to adhesion
formation.36 Chow and Yu37 observed more extensive
adhesion and decrease in tendon gliding when unre­
paired incomplete tendon lacerations of greater than
50% were immediately moved, compared with those
repaired and immobilized.
SURGICAL REPAIR OF PARTIAL
TENDON INJURIES
Surgical Repair or Nonrepair
The exact extent of the lacerated tendon cross section
that warrants repair remains unknown. Schlenker and
others6 had recommended repairing laceration greater
than 50% with modified Kessler and running peripheral
suture. Balk and others38 recommended similar repair
for a slightly higher cutoff of 60% laceration. These
results have resulted in a general consensus among clini­
cians to repair tendon laceration of 50% and greater
based on a survey by McCarthy and others.1 Tendon
retains adequate tensile strength despite greater than
50% laceration of their cross section. Yet, structural
properties of the tendon are detrimentally affected with
greater laceration. Tan and others39 have found benefi­
cial effect to peripheral suture repair versus no repair of
60% to 90% lacerated pig tendons. They noted a signifi­
cant increase in load to failure and increase in gap for­
mation forces with this type of repair. On the other
hand, Boardman and others40 found no significant dif­
ference in repair versus nonrepair of a 70% canine
tendon laceration. Stahl and others41 found no signifi­
cant benefit to repair of the tendon lacerations up to
75% in children versus no repair.
Peripheral Suture or Core Suture Repair
Using an in vitro sheep model, Haddad and others42
studied the effect of repair versus nonrepair on 75%
lacerated flexor tendons. Repairs included a group with
only peripheral sutures and a group with peripheral
sutures plus a core sutures. After cyclic loading, the
nonrepaired group had 2mm or greater gap formation,
while either repair resulted in 1mm or smaller gap with
no significant difference between the two repair groups.
Load to failure values between the two repair groups
were also not different. Using cadaveric tendons with
75% laceration, Zobitz and others43 compared different
core sutures combined with a peripheral suture to
peripheral sutures alone (Figure 14-1). With static
testing, they did not find any difference in gap forma­
tion among the groups though an increase was recorded
in load to failure and stiffness among the repairs with
core sutures.43 Neither of these two studies found a
mechanical disadvantage to having a core suture on the
integrity of the tendon. This is in contrast to earlier
studies looking at lesser laceration injuries where core
suture weakened the tendon.24,25 Thus, it can be sug­
gested that high degree lacerations (>70%) benefit from
repair. We recommend surgical repair with a large degree
of partial laceration.
Another concern with repairing partial tendon lacera­
tion is its effect on gliding resistance. Presence of suture
was shown to increase tendon gliding resistance by four
times that of intact tendons in zone 2.34 In high-degree
laceration where a repair may be advocated, it is impor­
tant to use a suture technique that minimizes tendon
gliding resistance. As discussed previously, Zhao and
others34 had demonstrated in 80% lacerated tendons,
repair with modified Kessler technique plus a peripheral
suture results in least resistance compared with other
repairs in cadaveric tendons. Since adhesion formation
is related to gliding resistance, it is intuitive that the
suture techniques with lesser resistance will result in
fewer adhesions. In the same model, Zhao and others45

Kessler Modified Kessler
Augmented Becker Savage (modified)
Tsuge
Lee (modified)
Figure 14-1  Six popular core suture techniques for repair
of partially lacerated flexor tendons. Modified Kessler
technique was noted to have the lowest gliding resistance.
have shown at 3 and 6 weeks, the adhesion breaking
strength was significantly lower in tendon repaired with
modified Kessler core suture technique.
Direction of tendon laceration is an important factor
in consideration. Tan and others22 had shown that as
the direction of laceration becomes more oblique
(≥45°), the tensile strength of the tendon is decreased
for the same cross-sectional area of laceration. They
found a peripheral tenorrhaphy to significantly increase
gap formation forces and load to failure in such lacera­
tion. Therefore, this may lead one to consider surgical
repair for oblique laceration with smaller cross-sectional
area than a transverse laceration. The same group has
also shown that an oblique direction to the laceration
can weaken the conventional modified Kessler or cruci­
ate repair but their mechanical strength was strength­
ened by orientating the repair strands parallel to the
laceration.45 Thus, the orientation of the laceration
needs particular attention when choosing a core suture.
Trimming of the Partially Lacerated Tendons
An alternative to surgical repair of partial tendon lacera­
tions (≤75%) is trimming. The approach has been advo­
cated to be the more superior treatment even in light of
higher-degree laceration. Schlenker and others6 recom­
mended trimming beveled edges of tendons with less
than 25% of lacerations, while Al-Qattan and others33
Chapter 14:  Partial Tendon Lacerations 175
`V
Excursion
V
Figure 14-2  Trimming of partial tendon injury. In an effort
to prevent bulky scar formation and provide smooth gliding,
the lacerated edges of the tendon are trimmed as shown.
This technique is as effective as suture repair in reducing
gliding resistance of laceration up to 75%.
reported positive result from trimming partial lacera­
tions of some greater than 50%,. Erhard and others35
showed that in cadaveric tendons lacerated to 50%
and 75%, trimming tendon edges would result in less
gliding resistance than circumferential running repair
(Figure 14-2). Interestingly, both trimming and running
repair resulted in greater gliding resistance at 50% lac­
eration compared to no repair. This relationship changed
in fair of trimming or running repair at 75% volar lac­
erations compared to no repair. Trimming is indicated
for minor partial laceration as well, to reduce the chance
of triggering.
POSTOPERATIVE REHABILITATION
Protected early mobilization was shown to benefit
outcome of tendon repair including repair of partial
injuries. Zhao and others46 have pointed to the impor­
tance of the synergistic wrist motion in postoperative
rehabilitation following partial flexor tendon lacera­
tions. Following repair of 80% lacerated flexor tendons
in their in vivo canine model, gliding excursion of the
group that underwent synergistic wrist and finger motion
therapy was significantly greater than the group in which
the tendon were rehabilitated with wrist fixation (45°
flexion) and finger motion at 1, 3, and 6 weeks. Addi­
tionally, synergistic wrist motion has been shown to
result in significantly less severe adhesions and less
adhesion breaking strength at weeks 3 and 6.47
COMPLICATIONS
In management of partial tendon injuries, the incidence
of complications is related to the degree of laceration of
the cross-sectional area of the tendon. The prevalent
176 Section 2:  Primary Flexor Tendon Surgery

COMPLICATIONS

Tag or flap Tendon sheath

Entrapment
Rupture

Flapping

Figure 14-3  Complications of nonrepair of partial tendon A

laceration include entrapment, triggering or flapping, or
ultimately rupture of the tendon. This rate has been related
to the extent of laceration, direction, or location of the injury
on the tendon.

complications are triggering, entrapment, and rupture

(Figures 14-3 and 14-4). Interestingly, for lesser lacera­
tion, complications are more significant when repaired,
while for greater laceration, complications are more fre­
quent when no repair is performed. The exact cutoff in
the degree of the laceration between these groups again
is not exactly known. Cooney and others13 demon­
strated a higher complication rate with repair of 30%
and 60% lacerated flexor tendons but lower incidence
of complications with repair of 90% laceration flexor
tendons in a dog model at 35 days.
SUMMARY
Partially lacerated tendon has been shown to be stron­
ger than previously assumed. The degree of laceration
directly impacts tensile strength of the injured tendon.
Yet, with even large degrees of laceration (<75% lacera­
tion), the tendon retains enough tensile strength to
withstand most active motion. The degree of obliquity
and the volar location of the laceration are features that
may lower a clinician’s threshold for surgical repair of a
lesser degree laceration.
Many have pointed out the benefits of surgical repair
for large partial lacerations (>60% to 75%). Repair in
these cases will improve tendon excursion, lower the
resistance during rehabilitation, and protect the integrity
of intact tendon portion. Improving postoperative
smoother tendon gliding surface and avoiding triggers
are the major reasons for repair of the partially cut
tendon rather than restoring tensile strength, as the
tendon usually retains sufficient strength, but the cut
portion can be entrapped during tendon motion. The
entrapped partially cut tendon may be torn entirely
or resist tendon motion. Early active motion and syner­
gistic wrist motion are beneficial for proper healing
and remodeling of the tendon and lower the chance for
complications. Postoperative tendon gliding depends on
B
Figure 14-4  Triggering in a patient sustained a laceration
over his left thumb metacarpophalangeal joint crease  
3 weeks after he was treated with skin closure and
discharged from emergency department. He subsequently
had triggering and persistent pain at the A1 pulley site.  
A, Intraoperatively, tendon laceration was found smaller
than 50%, with a reactive scar mass at the site of injury.  
B, The mass along with lacerated edges of the tendon
were trimmed. Patient was asked to flex the thumb
intraoperatively to assure resolution of triggering at the
pulley. The pulley was left intact.
the method of tendon repair and the motion regimen.48
With or without core suture technique, adding circum­
ferential sutures results in equivalent results when the
laceration is less than 75%. We recommend core suture
repair of the greater degree of partial laceration. Trim­
ming can be as effective as suture repair in reducing
gliding resistance of laceration up to 75%. Early passive
or active motion is recommended after surgery.
Over the past 50 years, the paradigm of management
of partial tendon laceration has shifted thanks to the
active work, observations, and investigations of many
astute clinical scientists. We now have a wealth of infor­
mation regarding the biomechanical properties tendons
in the context of various degrees of laceration, different
modes of repair, and rehabilitation. Yet, many more
years of research is necessary to create a consensus in
different aspects of partial tendon injuries.

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management of partially lacerated digital flexor tendons: A
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2. Wray RC, Weeks PM: Experimental comparison of technics of
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3. Reynolds B, Wray RC Jr, Weeks PM: Should an incompletely
severed tendon be sutured? Plast Reconstr Surg 57:36–38,
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4. Kleinert HE: Should an incompletely severed tendon be
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9. Mason ML, Shearon CG: The process of tendon repair, Arch
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12. Woo SL, Gelberman RH, Cobb HG, et al: The importance
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13. Cooney WP, Weidman KA, Malo DS, et al: Partial flexor
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15. Gelberman RH, Boyer MI, Brodt MD, et al: The effect of gap
formation at the repair site on the strength and excursion of
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early stages of tendon healing in dogs, J Bone Joint Surg (Am)
81:975–982, 1999.
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mobilization on the vascularization of healing flexor tendons
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20. Dobyns RC, Cooney WP, Wood MB: Effect of partial lacera­
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21. Hariharan JS, Diao E, Soejima O, et al: Partial lacerations
of human digital flexor tendons: A biomechanial analysis,
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Chapter 14:  Partial Tendon Lacerations 177
22. Tan J, Ming L, Jia ZJ, et al: Repairs of partial oblique tendon
injuries: A biomechanical evaluation, J Hand Surg (Br) 29:
381–385, 2004.
23. Wong JK, Cerovac S, Ferguson MW, et al: The cellular effect
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24. Ollinger H, Wray RC Jr, Weeks PM: Effects of suture on tensile
strength gain of partially and completely severed tendons,
Surg Forum 26:63–64, 1975.
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27. Gelberman RH, Woo SL, Lothringer K, et al: Effects of early
intermittent passive mobilization on healing canine flexor
tendons, J Hand Surg (Am) 7:170–175, 1982.
28. Kubota H, Manske PR, Aoki M, et al: Effect of motion and
tension on injured flexor tendons in chickens, J Hand Surg
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29. Grewal R, Saw SSC, Varitimidus S, et al: Evaluation of passive
and active rehabilitation and of tendon repair for partial
tendon lacerations after three weeks of healing in canines,
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30. Coert JH, Uchiyama S, Amadio PC, et al: Flexor tendon-
pulley interaction after tendon repair: A biomechanical study,
J Hand Surg (Br) 20:573–577, 1995.
31. Lieber RL, Silva MJ, Amiel D, et al: Wrists and digital joint
motion produce unique flexor tendon force and excursion in
the canine forelimb, J Biomech 32:175–181, 1999.
32. Gelberman RH, Vande Berg JS, Lundborg GN, et al: Flexor
tendon healing and restoration of the gliding surface: An
ultrastructure study in dogs, J Bone Joint Surg (Am) 65:70–80,
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33. al-Qattan MM, Posnick JC, Lin KY: Triggering after partial
tendon laceration, J Hand Surg (Br) 18:241–246, 1993.
34. Zhao C, Amadio PC, Zobitz ME, et al: Gliding resistance
after repair of partially lacerated human flexor digitorum pro­
fundus tendon in vitro, Clin Biomech (Bristol, Avon) 16:696–
701, 2001.
35. Erhard L, Zobtiz ME, Zhao C, et al: Treatment of partial lac­
erations in flexor tendons by trimming. A biomechanical in
vitro study, J Bone Joint Surg (Am) 84:1006–1012, 2002.
36. de Klerk AJ, Jonck LM: Primary tendon healing. An experi­
mental study, S Afr Med J 62:276–281, 1982.
37. Chow SP, Yu OD: An experimental study on incompletely cut
chicken tendons—a comparison of two methods of manage­
ment, J Hand Surg (Br) 9:121–125, 1984.
38. Balk ML, Sotereanos DG: Partial flexor digitorum profundus
lacerations, Oper Tech Orthop 8:67–72, 1998.
39. Tan J, Wang B, Tan B, et al: Changes in tendon strength after
partial cut and effects of running peripheral sutures, J Hand
Surg (Br) 28:478–482, 2003.
40. Boardman ND 3rd, Morifusa S, Saw SS, et al: Effects of tenor­
raphy on the gliding function and tensile properties of par­
tially lacerated canine digital flexor tendons, J Hand Surg
(Am) 24:302–309, 1999.
41. Stahl S, Kaufman T, Bialik V: Partial lacerations of flexor
tendons in children: primary repair versus conservative treat­
ment, J Hand Surg (Br) 22:377–380, 1997.
42. Haddad R, Sherman P, Peltz T, et al: A biomechanical assess­
ment of repair versus nonrepair of sheep flexor tendons
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178 Section 2:  Primary Flexor Tendon Surgery
43. Zobitz ME, Zhao C, Erhard L, et al: Tensile properties of
sutures methods for repair of partially lacerated human flexor
tendons in vitro, J Hand Surg (Am) 26:821–827, 2001.
44. Zhao C, Amadio PC, Momose T, et al: The effect of suture
technique on adhesion formation after flexor tendon repair
for partial lacerations in a canine model, J Trauma 51:917–
921, 2001.
45. Tan J, Wang B, Xu Y, et al: Effects of direction of tendon lac­
erations on strength of tendon repairs, J Hand Surg (Am)
28:237–242, 2003.
46. Zhao C, Amadio PC, Zobitz ME, et al: Effect of synergistic
motion on flexor digitorum profundus tendon excursion,
Clin Orthop Relat Res 396:223–230, 2002.
47. Zhao C, Amadio PC, Momose T, et al: Effect of synergistic
wrist motion on adhesion formation after repair of partial
flexor digitorum profundus tendon lacerations in a canine
model in vivo, J Bone Joint Surg (Am) 84:78–84, 2002.
48. Zhao C, Amadio PC, Momose T, et al: Remodeling of the
gliding surface after flexor tendon repair in a canine model
in vivo, J Orthop Res 20:857–862, 2002.
 CHAPTER
15  
FLEXOR TENDON INJURIES
IN CHILDREN
Shian Chao Tay, PhD, and Steven L. Moran, MD
OUTLINE
Finger flexor tendon injury in the pediatric population
is less frequent than in adults and is often caused by
a sharp cut, requiring primary repair. Advances in
tendon repair techniques and the postoperative reha-
bilitation protocols are not always applicable to chil-
dren. The size of the tendon can be less than 4 mm in
young children, making the placement of multiple
core sutures difficult. Depending on the size of the
tendon, core suture size of 4-0 can be used, and a four-
strand repair should be attempted. Epitenon sutures
should be one size smaller than core sutures, and sizes
5-0 through to 7-0 can be used. In older children,
four-strand or even six-strand repairs can be per-
formed. The principle is to have as strong a repair as
possible without making the repair site too bulky. In
zone 2 injuries, both the flexor digitorum profundus
(FDP) and flexor digitorum superficialis (FDS) tendons
should be repaired. Repair of FDP alone and discard-
ing the lacerated FDS is not recommended. We recom-
mend that all children under 7 years of age or who are
not cooperative be immobilized in an above elbow
cast for 4 weeks after surgery. Children who are older
than 7 years and who are judged to be compliant can
be started on early mobilization regimens. Unre-
stricted exercises are started after 4 weeks. In delayed
cases with extensive scarring, tendon grafting will be
necessary. If the pulley system is excessively damaged,
a two-stage tendon grafting procedure is indicated.
Pediatric flexor tendon injuries remain a complicated
problem for the hand surgeon. The factors that contrib-
ute to the difficulties in treating these injuries in chil-
dren include difficulties in diagnosis, the technical
demands of the repair, and the child’s compliance with
postoperative therapy. Five decades ago, more than 90%
of flexor tendon injuries in children were missed at the
time of the initial injury and thus were treated late with
flexor tendon grafting.1 Unfortunately, within the
present day, a significant percentage of flexor tendon
injuries in children still present late making primary
repair more difficult. Reasons for continued delays in
identification of these injuries include difficulties or
inadequacy of physical examination. Many flexor
tendons injuries in children are due to lacerations with
broken glass, which may produce a small skin laceration
or puncture but is often associated with a high rate of
injury to underlying vital structure.2
Advances in flexor tendon repair techniques and the
introduction of early postoperative rehabilitation pro-
tocols have improved the results of flexor tendon surgery
in adults over the last two decades.3-7 Unfortunately,
these advances are not always applicable to children
with flexor tendon injuries due to the size of their
tendons and their compliance with therapy. The size of
the profundus tendon can be less than 4 mm in young
children, making the placement of multiple core sutures
difficult, particularly if larger suture material is used.
Finally, early motion protocols can result in flexor
tendon rupture if the child is noncompliant with splint-
ing or therapy. The purpose of this chapter is to review
the pertinent issues in the management of flexor tendon
injuries in children, including clinical pearls for identi-
fication, repair, and rehabilitation of these injuries in an
effort to improve outcomes of flexor tendon injuries in
this age group.
INCIDENCE
Finger flexor tendon injury in the pediatric population
is less frequent than in adults. In a report from Helsinki,
the annual incidence is 3.6 per 100,000 children (<16
years). Peak incidence is at 7 years of age. The ratio of
boys to girls was 3:1.8 Broken glass is the most common
mechanism of injury with some authors reporting
nearly 80% of such injuries being caused by it.9-12 As in
adults, zone 2 injuries are the most common injuries in
children with the little finger being the most commonly
injured.10,13,14 The rate of concurrent digital nerve injury
range from 36% to 58%.8,11,12,14-16
DIAGNOSIS
The assessment of flexor tendon injuries in the pediatric
population is difficult (Figure 15-1). Young children,
particularly those under 6 years of age, cannot be
expected to cooperate well with the examiner during the
179
180 Section 2:  Primary Flexor Tendon Surgery

A B

C D
Figure 15-1  A 2-year-old child suffered a laceration to
the small finger while playing on a slide. The laceration was
initially closed by the local emergency room physician 2
weeks prior to presentation to the hand surgeon for noted
lack of motion of the small finger. A, Note the lack of normal
cascade in repose. B, The lack of flexion of the small finger
with wrist extension tenodesis. C, Additional maneuvers to
identify flexor tendon injury include forearm compression
which should result in some flexion of the fingers, but none
is seen within the small finger of this child. D, The finger
was explored through a Bruner incision where a complete
laceration of the FDP and FDS tendons was noted in zone 2.
E, Tendon repair was performed with a four-strand core
repair using a modified Kessler technique followed by a
E
locked running epitendinous suture.

hand exam.1 Observation and additional techniques
must be used to determine the status of the flexor
tendon in children. Previous reports by Bell and Mason
have also noted the importance of observation of the
child’s hand at rest and during play to look for signs of
active flexion or a loss of the normal cascade within the
hand.1,9 Children with older injuries will learn to adapt
to their injury and can gasp the injured finger with a
normal adjacent finger during flexion, thereby giving
the impression that active motion is being performed.1
This trick maneuver, called “trapping,” may initially
mislead both parents and examiners into thinking that
there is no disability.13
Missed diagnosis resulting in a delayed diagnosis
still accounts for 15% to 30% of pediatric patients
with flexor tendon injuries.8,11,14 The risk of delayed diag-
nosis and treatment is particularly high in children who
are less than 6 years of age8 and, paradoxically, in chil-
dren who sustain injuries with small surface wounds
that bleed little.1 Wounds that bleed profusely often
compel parents to seek medical attention and the likeli-
hood of a missed flexor tendon injury is thus lower.
Regardless, a high index of suspicion should always be
adopted when faced with a child with a hand or finger
laceration.
Examination begins with simple observation of the
resting posture of the hand. In the normal situation, the
fingers of the hand lie in a cascade with some flexion
being present in all the finger joints. A finger that is
observed to be out of alignment from the normal finger
cascade may have a flexor tendon injury. If the joints in
that finger are carefully observed, it may be possible to
even determine which flexor tendon is injured. In com-
plete lacerations of both the flexor digitorum profundus
(FDP) and flexor digitorum superficialis (FDS) tendons,
both the proximal interphalangeal (PIP) joint and distal
interphalangeal (DIP) joint will be extended. In isolated
lacerations of the FDP tendon, only the DIP joint will
be in extension with residual flexion present in the PIP
joint. In isolated FDS injury, the finger will lie out of the
normal finger cascade but there will be residual flexion
present in both the PIP and DIP joints. If the child
permits, the tenodesis effect can be elicited by perform-
ing passive wrist flexion and extension to check for
integrity of the flexor tendons (Figure 15-2). In a normal
situation, one should observe increasing flexion of all
finger and thumb joints with passive wrist extension.
Assuming that the child is cooperative and is able to
relax, flexor tendon injury should be suspected if there
is either absence of flexion or decreased amount of
flexion in a finger joint. Passive flexor tendon excursion
can also be performed by compression of the flexor
tendons in the distal forearm. Again, if there is absent
flexion or decreased amount of flexion, this would
suggest a complete flexor tendon laceration (see Figure
15-1C).
Chapter 15:  Flexor Tendon Injuries in Children 181
Figure 15-2  Loss of tenodesis of the long finger with wrist
extension.
Radiographs of the injured finger or hand may be
useful in excluding a retained foreign body or underly-
ing fracture. Ultrasound has limited diagnostic accuracy
in an uncooperative child. Magnetic resonance imaging
(MRI) is expensive and requires a general anesthetic for
young children.13 Both modalities can be considered if
the child is sedated.
Concurrent injury to neurovascular structures should
always be assessed. Vascularity of the finger is assessed
in the usual manner by observation of color and contour
of the finger pulp. Capillary refill can be checked by
indenting the finger pulp and observing for the speed
of refill. In dark-skinned individuals, finger pulp color
may be difficult to assess. In such cases, the nail bed
is blanched by distal pressure on the nail and the
speed of refill of the nail bed is observed when the
pressure is released. Hand-held Doppler exam may be
used to aid in identification of unilateral digital arterial
injuries.
Examining for digital nerve injury in the child can be
virtually impossible if they are not able to understand
or cooperate with the examination. As such, the usual
methods employed in the adults such as comparative
light touch and two-point discrimination tests may not
work. Thus, in children, nerve injury should always
be suspected based on the location of the surface
wound. The loss of resistance to glide using a plastic pen
can help in diagnosing the loss of sweating in a nerve
injury. Alternatively, the hand may be immersed in
water at room temperature until skin wrinkling occurs.
As only innervated skin wrinkles, an area of unwrinkled
skin indicates a likely nerve injury.13 In older injuries,
dryness or trophic changes are clues to sensory nerve
disturbances.1 Surgical exploration under anesthesia
may be the only way to verify the condition of the
nerves.9,13
182 Section 2:  Primary Flexor Tendon Surgery
TREATMENT
In 1963, Entin stated that flexor tendon surgery in
children is more difficult and demanding than in
adults and requires meticulous attention to handling of
tissues as the structures are so delicate.9 Many authors
have also advocated that only surgeons trained in hand
surgery should perform such operations.3,4,9,10 Absorb-
able sutures should always be used for wound closure
so as to avoid another anesthetic exposure for suture
removal.13
The options for tendon repair in children are as
varied as they are in the adult patient. The literature is
scant with regard to comparative studies, but most series
favor some type of four-strand repair with an epitendi-
nous suture. Navali and Rouhani reported one rupture
in a group of children less than 4 years of age with a
two-strand repair while there were no ruptures in the
group with four-strand repairs.17 Nietosvaara et al
reported no ruptures in their group of children less
than 16 years of age who had multistrand repairs, but
three postoperative ruptures occurred in their group
with two-strand repairs.8 In both reports, other than the
ruptures, no difference in functional outcomes was
found between the two-strand and multistrand repair
groups. It appears that in children, multistrand repair
may protect against postrepair rupture but not have any
significant effect on functional outcomes.
ADJUNCTS TO SURGERY
Tuzuner et al20 reported on the adjunctive use of botu-
linum toxin type A for children less than 6 years with
zone 2 flexor tendon repairs. The principle was to tem-
porarily paralyze the muscle unit of the repaired flexor
tendon to avoid ruptures due to poor compliance. All
the patients received intramuscular injections into the
specific muscles of the repaired tendons. Postopera-
tively, all patients were started on Duran’s passive
motion program for 4 weeks, after which active motion
was allowed. The average duration of the botulinum
effect was 6 weeks and all seven patients achieved satis-
factory results with an average total active motion (TAM)
of 84%. There were no tendon ruptures. However, a few
concerns were noted. Forearm atrophy was noted in
three of the seven patients. Rehabilitation was pro-
longed when otherwise it would have taken only 4
weeks. Other potential concerns of this experimental
adjunctive therapy include allergic reactions. At this
point in time, the use of botulinum toxin A is experi-
mental and should be performed within the confines of
a clinical trial.
REHABILITATION
Young children cannot always be expected to cooperate
with a rehabilitation program. In this day and age when
early mobilization is the norm in adults with flexor
tendon injury, up to 46% of flexor tendon injuries in
children are still treated with plaster immobilization.8,14
Most authors now agree that no benefit can be found in
instituting early mobilization protocols in children.11,14-16
The Mayo Clinic group found that children started on
early mobilization had a TAM of 78%, whereas those in
the immobilized group, 82%, using the Strickland and
Glogovac formula.14 Fitoussi et al reported a mean TAM
of 87% for the group with early mobilization versus 86%
in the immobilized group.16 Berndtsson and Ejeskär
reported 79% mean TAM in the group with Kleinert
protocol versus 74% in the immobilized group.11 None
of these differences were statistically significant.
It is well known that flexor tendon healing is more
rapid in children.9,10 In children, the distances between
the vinculi are shorter so that the relative blood supply
per square centimeter of tendon substance is consider-
ably better than in the adult. The better vascularity of
the flexor tendon encourages healing and resultant
adhesions are less extensive and more pliable.9,19 As
such, prolonged immobilization beyond 4 weeks is
unnecessary in children. It is also documented that
immobilization for longer than 4 weeks significantly
deteriorates functional outcome.15,16
Fitoussi et al recommend that an above elbow cast
be routinely used for postoperative immobilization to
avoid tendon ruptures.16 In their study, five ruptures
occurred in 58 fingers reviewed. Of these, two of the
ruptures were attributed to noncompliance to splint.
The remaining three ruptures occurred in the group of
patients immobilized in a below elbow plaster cast. No
ruptures were found in the group immobilized in an
above elbow cast. Incidentally, four of the five ruptures
above occurred in children who were 5 years or younger.
The benefit of above elbow casting for postoperative
immobilization is corroborated by Kato et al’s report.
They looked at the long-term outcome of 12 children
less than 6 years of age with zone 2 flexor tendon lac­
erations repaired with a modified Kessler technique
and immobilized with an above elbow cast for 4 weeks.
They reported a mean TAM of 89% evaluated with the
Strickland formula, which was a very favorable result.12
OUTCOMES
As stated earlier, there are many factors that can affect
the outcome of flexor tendon repairs in children includ-
ing type of repair and zone of injury. Other variables are
more controversial; the effect of age on functional
outcome continues to be an area of debate. The Mayo
Clinic group reported that age was not a determinant of
outcome.14 On the other hand, Berndtsson et al reported
that older children tended to have better results.11
Fitoussi et al compared the outcomes between those
aged 0 to 5 years, 5 to 10 years, and 10 to 15 years.16
Although they did find that the youngest age group was
associated with higher rupture rates, they did not find

any significant difference in functional outcome among
the three age groups.
Concomitant injuries within the affected fingers may
also influence outcomes. The Mayo Clinic group
reported lower TAM in zone 2 for combined FDP/FDS
injuries compared with isolated FDP injuries. They also
reported that in patients with concomitant digital nerve
injury, the outcome was poorer.14 O’Connell et al also
reported poorer TAM in patients with concomitant
palmar plate or digital nerve injury.15 The one exception
to these findings was reported by Berndtsson and
Ejeskär, who evaluated their outcomes in zone 2 flexor
tendon repairs and found that concurrent superficialis
tendon injury did not appear to impact negatively on
functional outcome.11
Injuries within zone 2 are still presumed to produce
the poorest outcomes. Fitoussi et al reported that all
flexor tendon repairs in zones 1, 4, and 5 in children
achieved good or excellent outcomes.16 Outcomes in
zones 2 and 3 were good or excellent in 77% and 71%
of the digits in terms of TAM, respectively.16 The Mayo
Clinic group also reported better outcomes in zone 1
injuries compared to zone 2.14
Surprisingly, delayed repairs have not been shown to
consistently result in a poorer outcome in children. Ber-
ndtsson and Ejeskär found no significant difference in
outcome between children who had primary repair
versus those with delayed repairs (mean of 58 days after
injury, range 10 days to 1 year). In addition, none of
their patients with delayed treatment required tendon
grafting.11
Functional outcome in children following flexor
tendon repair appears to improve with time. This has
been attributed to better remodeling and continuing
digital growth, which contributes to the rupture of ten-
dinous adhesions.12,14,18 O’Connell et al reported con-
tinuing improvements in TAM beyond 18 months of
follow-up.15 In their report, a further 17% improvement
of TAM was noted in a subgroup of patients who were
available for extended reevaluation 18 to 120 months
later.
COMPLICATIONS
Grobbelaar and Hudson reported that complications
after flexor tendon repair in children were rare.10 In their
series of 38 patients, there were three cases of tendon
ruptures that they attributed to technical factors. All
underwent direct secondary repair and eventually
achieved excellent to good outcomes. None of their 38
cases required flexor tenolysis. However, they com-
mented that if tenolysis were required, they would prefer
to wait at least 18 months before contemplating it, as
adhesions in children are more pliable.10
In the Mayo Clinic group of 35 patients, complica-
tions were noted in only two patients.14 One had a
tendon rupture and the other had a stiff finger that
Chapter 15:  Flexor Tendon Injuries in Children 183
required tenolysis. Both achieved satisfactory outcomes
after secondary repairs and tenolysis, respectively.14 Kato
et al reported that only one of their 12 patients required
a tenolysis, which achieved excellent outcome at final
follow-up.12 Fitoussi et al reported a 9% rupture rate.16
They report that risk factors for rupture were a noncom-
pliant patient, age group less than 5 years, and immo-
bilization in a below elbow cast compared to an above
elbow cast.16 Two of the ruptures were treated by direct
secondary repair after lengthening at the musculotendi-
nous junction. Both achieved satisfactory outcomes at
final follow-up. The other 3 underwent two-stage flexor
tendon grafting with one achieving good outcome and
the other 2 fair outcomes. Navali and Rouhani had one
rupture in one child with a two-strand repair. In this
case, no further treatment was given as the parents
declined.17
Digital growth disturbances may occur after flexor
tendon injury during childhood. Kato et al reported that
there is a small risk of the finger being shorter at the
middle and distal phalanx as a result of previous flexor
tendon injury. The range of shortening was 2 to 4 mm
for each digit.12 A mean shortening of 3% of digit length
was also reported by Tuzuner et al.20
FLEXOR TENDON GRAFTING IN CHILDREN
Primary tendon repair has been shown to be superior
to tendon grafting and staged reconstruction.21-24 As
such, flexor tendon grafting should be done only when
direct repairs are not possible. Courvoisier et al recom-
mend that one-stage flexor tendon grafting can be per-
formed in a digit with moderate scarring with intact A2
and A4 pulleys and full passive mobility of the PIP and
DIP joints.25 Two-stage flexor tendon grafting should be
reserved for cases where scarring within the flexor sheath
is associated with extensive pulley damage with PIP or
DIP joint contractures. In his series, Courvoisier et al
reported 38% (3 of 8 children) satisfactory outcomes
for one-stage flexor tendon grafting and 42% (5 of 12
children) satisfactory outcomes for two-stage flexor
tendon grafting.25 Darlis et al painted a better picture in
a group of children who underwent two-stage flexor
tendon reconstruction with the modified Paneva-
Holevich technique.26 Eight of their 9 children achieved
satisfactory outcomes with a mean TAM of 75%.
However, they had one child who had a complication
of deep infection that required removal of the silicone
rod. They were able to reinsert the rod 3 months later
when the infection cleared.
Valenti and Gilbert reported satisfactory outcomes in
73% of the 27 children they treated with two-stage
flexor tendon grafting.27 They noted that they achieved
better outcomes in older children. The mean TAM for
children aged 10 to 15 years was 81.5%, whereas chil-
dren aged 1 to 3 years had a mean TAM of 53%. They
had a complication rate of 27%: there were 4 distal
184 Section 2:  Primary Flexor Tendon Surgery

ruptures occurring at the distal implant–tendon inter-

face, 2 silicone synovitis requiring synovectomy, and
one deep infection requiring removal of the silicone
rod. Four of these 7 cases with complications ended up
with unsatisfactory outcomes.27
CURRENT TREATMENT RECOMMENDATIONS
A high index of suspicion should always be adopted
when evaluating children for flexor tendon injury. If
there is any doubt, exploration under general anesthesia
should be performed to confirm the status of the flexor
tendon and digital neurovascular bundles.
Surgery should always be performed under general A
anesthesia, in a bloodless field using pneumatic tourni-
quet control, fine instruments, and magnification. If the
injury is more than 1 week old, the parents and the
patient should be informed of the possibility for graft-
ing of the flexor tendon. Direct tendon repairs should
be attempted even in delayed cases. Flexor tendon graft-
ing procedures should be reserved for salvage situations
where there is extensive injury to the flexor tendon
sheath or irreparable damage to the pulleys. Tenodesis
and arthrodesis should be avoided in children as they
may further affect finger growth adversely.
The flexor tendons should be approached through
a Bruner extension of skin laceration (Figure 15-3).
Windows in the flexor tendon sheath can be created B
using L-shaped incisions to expose the tendons. As far Figure 15-3  A, A Bruner incision is used to expose the
as possible, A2 and A4 pulleys should be preserved. If profundus and superfiicalis tendon injury of the middle
necessary not more than half the length of the A2 and finger in a 5-year-old child. B, Flexion cascade is restored
A4 pulleys can be released to aid in exposure of the following tendon repair.
flexor tendon for repair.
Depending on the size of the tendon, core suture size
of 4-0 can be used, and a four-strand repair should be For zone 1 repairs without sufficient distal tendon
attempted. Epitenon sutures should be one size smaller stump, the FDP tendon may be repaired directly to bone
than core sutures, and sizes 5-0 through to 7-0 can be using a nonabsorbable suture13 or a Bunnell pull-out
used. Cutting needles are preferred as they allow the repair using 4-0 monofilament suture.14 Care should be
needle to pass through the tendon with less trauma than taken not to damage the epiphysis if drill holes are
with round needles. made in the distal phalanx.
Whether a two-strand or multistrand repair is per- In zone 2 injuries, both the FDP and FDS tendons
formed will depend on the size of the tendon. In very should be repaired. Presently, repair of FDP alone and
small caliber tendons, a four-strand repair may not be discarding the lacerated FDS is not a recommended
possible. In older children, four-strand or even six- option. The tendons are repaired with nonabsorbable
strand repairs can be performed. The principle here is sutures. All skin wounds should be closed with absorb-
to have as strong a repair as possible without making able sutures so as to avoid suture removal, which may
the repair site too bulky. Tendon repair techniques be distressing for the child.
reported in children include Tajima,17 modified Kessler,14 Postoperatively, we recommend that all children
and Lim.8,28 under 7 years of age or children who are not cooperative
Once the repairs are complete, the finger should be be immobilized in an above elbow cast with the elbow
passively flexed and extended to make sure that the in flexion for 4 weeks. Children who are older than 7
repair can glide smoothly through the pulleys and the years and who are judged to be compliant and coopera-
flexor sheath. Occasionally, partial release of the unyield- tive can be started on early mobilization regimens. In
ing ends of the A4 or the A2 pulleys29 may be needed to both cases, unrestricted motion exercises are started
prevent the repair site from snagging on the pulley edges. after 4 weeks.
We prefer leaving the L-shaped windows of the flexor In delayed flexor tendon injuries with significant
sheath unrepaired to avoid constriction to the tendon. scarring making direct repair impossible, flexor tendon

grafting will be necessary. If the pulley system is intact
and there are no joint contractures, one-stage flexor
tendon graft using the palmaris longus or the plantaris
tendon should be performed with the proximal tendon
juncture sited in the palm.27 If the pulley system is exces-
sively damaged, a two-stage tendon grafting procedure
References
1. Bell JL, Mason ML, Koch SL, et al: Injuries to flexor tendons
of the hand in children, J Bone Joint Surg (Am) 40:1220–1230,
1958.
2. Provencher MT, Allen LR, Gladden MJ, et al: The underestima-
tion of a glass injury to the hand, Am J Orthop (Belle Mead
NJ) 35:91–94, 2006.
3. Kleinert HE, Kutz JE, Atasoy E, et al: Primary repair of flexor
tendons, Orthop Clin North Am 4:865–876, 1973.
4. Creekmore H, Bellinghausen H, Young VL, et al: Comparison
of early passive motion and immobilization after flexor
tendon repairs, Plast Reconstr Surg 75:75–79, 1985.
5. Savage R: In vitro studies of a new method of flexor tendon
repair, J Hand Surg (Br) 10:135–141, 1985.
6. Savage R, Risitano G: Flexor tendon repair using a “six strand”
method of repair and early active mobilisation, J Hand Surg
(Br) 14:396–399, 1989.
7. Small JO, Brennen MD, Colville J: Early active mobilisation
following flexor tendon repair in zone 2, J Hand Surg (Br)
14:383–391, 1989.
8. Nietosvaara Y, Lindfors NC, Palmu S, et al: Flexor tendon
injuries in pediatric patients, J Hand Surg (Am) 32:1549–
1557, 2007.
9. Entin MA: Flexor tendon repair and grafting in children, Am
J Surg 109:287–293, 1965.
10. Grobbelaar AO, Hudson DA: Flexor tendon injuries in chil-
dren, J Hand Surg (Br) 19:696–698, 1994.
11. Berndtsson L, Ejeskär A: Zone II flexor tendon repair in chil-
dren. A retrospective long term study, Scand J Plast Reconstr
Surg Hand Surg 29:59–64, 1995.
12. Kato H, Minami A, Suenaga N, et al: Long-term results after
primary repairs of zone 2 flexor tendon lacerations in chil-
dren younger than age 6 years, J Pediatr Orthop 22:732–735,
2002.
13. Havenhill TG, Birnie R: Pediatric flexor tendon injuries, Hand
Clin 21:253–256, 2005.
14. Elhassan B, Moran SL, Bravo C, et al: Factors that influence
the outcome of zone I and zone II flexor tendon repairs in
children, J Hand Surg (Am) 31:1661–1666, 2006.
15. O’Connell SJ, Moore MM, Strickland JW, et al: Results of zone
I and zone II flexor tendon repairs in children, J Hand Surg
(Am) 19:48–52, 1994.
Chapter 15:  Flexor Tendon Injuries in Children 185
will be necessary, which has been detailed by Valenti
and Gilbert.27 After stage 1 surgery, passive motion exer-
cises are started and continued for at least 3 months
before proceeding to stage 2 surgery. After stage 2, the
wrist and elbow are immobilized for 4 weeks before
beginning active motion exercises.27
16. Fitoussi F, Lebellec Y, Frajman JM, et al: Flexor tendon injuries
in children: factors influencing prognosis, J Pediatr Orthop
19:818–821, 1999.
17. Navali AM, Rouhani A: Zone 2 flexor tendon repair in young
children: a comparative study of four-strand versus two-
strand repair, J Hand Surg (Eur) 33:424–429, 2008.
18. Friedrich H, Baumel D: The treatment of flexor tendon injuries
in children, Handchir Mikrochir Plast Chir 35:347–352, 2003.
19. Arons MS: Purposeful delay of the primary repair of cut flexor
tendons in “some-man’s-land” in children, Plast Reconstr Surg
53:638–642, 1974.
20. Tüzüner S, Balci N, Ozkaynak S: Results of zone II flexor
tendon repair in children younger than age 6 years: botuli-
num toxin type A administration eased cooperation during
the rehabilitation and improved outcome, J Pediatr Orthop
24:629–633, 2004.
21. Boyes JH, Stark HH: Flexor-tendon grafts in the fingers and
thumb. A study of factors influencing results in 1000 cases,
J Bone Joint Surg (Am) 53:1332–1342, 1971.
22. Ejeskar A: Flexor tendon repair in no man’s land. II: Early
versus late secondary tendon repair ad modum Kleinert,
Scand J Plast Reconstr Surg 14:279–283, 1980.
23. Vahvanen V, Gripenberg L, Nuutinen P: Flexor tendon injury
of the hand in children. A long-term follow-up study of 84
patients, Scand J Plast Reconstr Surg 15:43–48, 1981.
24. Amadio PC, Wood MB, Cooney WP 3rd, et al: Staged flexor
tendon reconstruction in the fingers and hand, J Hand Surg
(Am) 13:559–562, 1988.
25. Courvoisier A, Pradel P, Dautel G: Surgical outcome of
one-stage and two-stage flexor tendon grafting in children,
J Pediatr Orthop 29:792–796, 2009.
26. Darlis NA, Beris AE, Korompilias AV, et al: Two-stage flexor
tendon reconstruction in zone 2 of the hand in children,
J Pediatr Orthop 25:382–386, 2005.
27. Valenti P, Gilbert A: Two-stage flexor tendon grafting in chil-
dren, Hand Clin 16:573–578, 2000.
28. Lim BH, Tsai TM: The six-strand technique for flexor tendon
repair, Atlas Hand Clin 1:65–76, 1996.
29. Amis AA, Jones MM: The interior of the flexor tendon sheath
of the finger. The functional significance of its structure, J Bone
Joint Surg (Br) 70:583–587, 1988.
 CHAPTER
16  
PRIMARY REPAIR OF
THE FLEXOR POLLICIS
LONGUS TENDON
David Elliot, MA, FRCS, BM, BCh
OUTLINE
A series of changes of primary treatment of divisions
of the flexor pollicis longus tendon were carried out
in the St. Andrew’s unit in a total of 216 thumbs over
18 years in an attempt to reduce the rupture rate
from the initial high level of 17%. It was possible,
eventually, by strengthening the sutures and including
the fingers in the splint, to reduce the rupture rate to
zero. A simplification was then made and others dis-
cussed, whereby elimination of mechanical ruptures
of the repairs could be achieved using simpler suture
methods that are more appropriate for use by the
training surgeons who normally perform these repairs
worldwide.
More difficulty is encountered in approximation of the
severed ends than in any other tendon of the hand.
Murphy, 1937
THE PROBLEM OF FLEXOR POLLICIS
LONGUS RETRACTION
It has been known that the flexor pollicis longus (FPL)
tendon is more difficult to repair than the finger flexors
for over 60 years. In 1937, Murphy identified this
problem and highlighted the fact that retraction of the
proximal end of the cut FPL tendon was almost always
greater than that of the proximal ends of cut finger flexor
tendons.1 Our clinical experience, and that of others
more recently, would agree that the greater retraction of
the cut FPL tendon is due to shortening of the FPL
muscle as there is often considerable difficulty pulling
the proximal tendon end out to length if FPL repair is
attempted after even a short delay beyond 48 hours. It
would seem likely that this increased tension is also the
cause of the higher rupture rate in the repaired FPL
tendon compared to that of finger flexor tendon repairs.
More recently, the presence of a retracted proximal end
of the FPL tendon at surgery has been shown to be det-
rimental to the outcome of the tendon repair.2 Whether
all FPL repairs, or only those with visible retraction of
the proximal tendon at surgery, are exposed to increased
186
tension as a result of the greater retraction of the FPL
muscle remains unknown. Murphy believed this
problem to be due to the fact that the FPL tendon is
completely separated from the other flexor tendons,
making retraction easier than where a tendon is
restrained by others. An alternative explanation may lie
in the difference of muscle configuration between the
FPL muscle and those of the finger flexors.
THE AVASCULAR ZONE 2 SITE OF THE FPL
Recently, we re-examined data from our earlier studies
and found that the rate of rupture after repair in zone
2 is twice as common as after zone 1 FPL repairs.3
Zone 1 FPL repairs had a rate of rupture similar to that
of primary finger flexor repairs.4 The increased rate of
rupture of zone 2 repairs largely explains the higher
rupture rate of the FPL tendon when compared with
finger flexor repairs in zones 1 and 2. A lack of extrin-
sic vascular supply of the FPL tendon immediately
palmar to the metacarpophalangeal joint was identi-
fied by Lundborg.5 Hergenroeder et al6 also found that
there is a zone of relative avascularity of the tendon at
the same point, and this was illustrated by Tubiana
et  al.7 This avascular point coincides with the zone
2 site of FPL repair and may explain the particular
susceptibility of zone 2 repairs to rupture, contributing
to the higher rupture rate of FPL tendon primary
repairs.
TREATMENT OF FPL DIVISION BEFORE 1989
Reports published in the 20 years after Murphy’s report,
when many repairs would now be classified as delayed
primary, or even secondary surgery, repeatedly high-
lighted the difficulty of direct repair of the FPL after any
delay and many recommended that primary repair be
avoided in most instances.8 To overcome this problem,
most authors favored tendon reconnection by interposi-
tion grafting,1,9-19 although some reported direct repairs
of the tendon, usually in cases seen within a few
hours.1,11,14-18,20-29 Tendon lengthening, either in the
muscle or in the tendon at the wrist, was also used
by several authors as an alternative to interposition
 Chapter 16:  Primary Repair of the Flexor Pollicis Longus Tendon
grafting.12,15,26,30,31 During this era, all cases were immo-
bilized postoperatively. Mobilization started at varying
intervals from surgery, in one instance as early as 12
days after operation but usually after a longer delay of
between 3 and 5 weeks. The results reported were often
impressive. Unfortunately, direct comparison with today
is difficult, if not impossible, as the methods of assess-
ment differ, not only between different reports but also
from all of the methods of assessment in current use.
Although a few very large studies were reported, many
contained very small numbers of cases, many being part
of much larger studies of treatment of finger flexor
tendon divisions. Rupture rates were rarely mentioned.
In 1973, Urbaniak and Goldner reported their own
experience32 and Urbaniak subsequently reviewed the
options of treatment.33 Like others before him, Urba-
niak favored direct repair when possible and used the
other techniques when the tendon gap was too wide.
The results of tendon lengthening in his unit were better
than those of interposition grafting in those cases in
which direct repair was not possible.
TREATMENT OF FPL DIVISION 1989–1999
Between the advent of primary direct repair and early
postoperative mobilization of flexor tendons in the late
1950s and the end of the 20th century, there were sur-
prisingly few reports published on the effectiveness of
primary repair of the FPL tendon in zones 1 and 2, this
being the common site of division of this tendon.34-37
These studies tended to confirm the high rupture rate
after primary repair compared to primary repair of
finger flexors. Various other studies of primary repair
and early mobilization of finger flexor tendons included
repairs of the FPL but usually in such small numbers
and/or with inclusion of divisions of the FPL in other
zones, as to make useful interpretation of the data
difficult.38-43 Few of the units that reported large series
of primary direct repairs of finger flexor tendons in zone
2 followed by early mobilization by any method have
published equivalent results for the FPL tendon. Three
studies of primary repair of the FPL tendon34,35,37 mobi-
lized the repairs postoperatively in variations of the
Kleinert technique of active extension-passive flexion
mobilization.44 The fourth compared this regimen with
immobilization of the repair for 4 weeks after surgery.36
Although Percival and Sykes reported an 8% rupture
rate of 50 repairs,36 we used the work of these authors
as a gold standard against which we compared our
results at that time because a variety of problems with
data presentation in the few other reports made direct
comparison with our work difficult.
FPL REPAIR WITH 8% RUPTURES:
ST. ANDREW’S 1994–1999
In an earlier report on primary repair of finger flexor
tendons followed by early active mobilization, we
187
included an assessment of 30 primary FPL repairs
repaired with a two-strand modified Kessler suture and
a simple running circumferential suture.45 These cases
were mobilized in the manner used to mobilize finger
flexor tendons but with the thumb only prevented from
free movement and had a rupture rate of 17%. We rec-
ommended that early active mobilization using the
technique we were using at that time was not appropri-
ate to FPL tendon primary repair. Subsequently, we
examined two additional groups of 39 and 49 patients
with divided FPL tendons.8 In the first of these, the FPL
tendons were repaired by the original method but
mobilization was carried out in a modified splint, which
included slight ulnar deviation of the wrist (intended to
allow the FPL tendon a straighter “run” into the thumb)
and inclusion of the fingers in the splint (Figure 16-1).
The second group underwent a modified repair that
included one of the more recent techniques of strength-
ening the circumferential repair46 (Figure 16-2) as well
as mobilization in the modified splint. The changes in
the splint alone made little difference to the rate of
ruptures, only reducing the rupture rate to 15%. We
retained the splint mainly because it included the
fingers: power gripping with the fingers is almost auto-
matically followed by movement of the thumb around
the dorsum of the index and middle fingers, which
brings the FPL into play and risks any primary FPL
repair. Preventing normal finger activities remains part
of our rehabilitation regimen. Despite achieving excel-
lent and good results and a rupture rate equal to those
in the Percival and Sykes study after addition of the
stronger circumferential suture technique, the 8% rate
of rupture in our study remained higher than the 4% to
5% reported from our unit for finger zone 1 and 2
primary flexor tendon repairs4 and was still a matter for
concern. Although the drop of rupture rate from 17%
to 8% was a definite improvement, the figures were not
statistically significant; it would have required a study
with 98 patients in each of the two groups for a reduc-
tion of this amount to attain a statistical significance of
p <.05. This would have required a study period of 15
years, or longer. This presents a dilemma to clinicians
reporting personal experiences in this field, even from
busy units.
FPL REPAIR WITH NO RUPTURES:
ST. ANDREW’S 1999–2004
The addition of a stronger core suture to the stronger
epitendinous suture was the most obvious way of trying
to further reduce the rupture rate of the FPL repair. In
2004, we reported another study in which a four-strand
Kessler suture with a Silfverskiöld circumferential suture
was used in the primary repair of 48 FPL tendons fol-
lowed by early active mobilization.3 Two Kessler two-
strand repairs in planes at 90° to each other were used
(Figure 16-3),47 which is, perhaps, the simplest means
188 Section 2:  Primary Flexor Tendon Surgery
A B
Figure 16-1  The modified splint with inclusion of the fingers used for early active mobilization in St Andrew’s of FPL repairs
since 1994. A, Mobilization of the fingers with the thumb resting. B, Early mobilization of the thumb using Kapandji’s
method. C, Later mobilization of the thumb to near-full flexion.
Figure 16-2  Diagram showing the technique of stronger
circumferential suturing described by Silfverskiöld and
Anderson (1993) and used in St. Andrew’s for FPL repair,
1996–2004.
Double Kessler core suture
Figure 16-3  Diagram showing the technique of four strand
repair using two Kessler core sutures described by Smith   SIMPLER FPL REPAIR WITH NO RUPTURES:
and Evans (2001) and used in St Andrew’s for FPL repair,
1999–2004.
of achieving a four-strand core suture. This combination
of sutures achieved a 0% rupture rate. However, the bulk
of a combination of a multistrand core suture and a
complex circumferential suture may increase the resis-
tance to movement of the repaired tendon.48 This may
C
have been the cause of the slight drop in the excellent
and good results in this group of patients compared
with our previous results.8 Possibly of more significance
is the fact that this technique is difficult to use in clinical
practice and may be too complicated for those routinely
doing these repairs worldwide.
FPL REPAIR WITH NO
RUPTURES: ELSEWHERE
In the early 2000s, an additional three studies of primary
repair of the FPL tendon were published,2,49,50 two of
which reported no mechanical ruptures of FPL repairs
using various conventional two-strand core sutures and
simple circumferential repair,2,49 albeit in small numbers
of patients (Table 16-1). These studies may identify a
factor that is currently given little attention because of
concentration on stronger sutures, namely the quality
of the rehabilitative service. At a time when stringent
financial pressures are being forced on clinicians
worldwide, this may be of political importance to the
well-being of this group of patients. Unfortunately,
strengthening of suture techniques is considerably easier
for most surgeons than achieving any increase in hand
therapy availability and expertise.
ST. ANDREW’S 2004–2009
Our most recent study51 reported the results of an addi-
tional 50 FPL primary tendon repairs performed since
January 2004 using Tang’s technique of three Tsuge
sutures as the “core” suture,52,53 with no circumferential
suture (Figure 16-4). The Tsuge system of suturing
flexor tendon repairs54,55 is as strong as the more con-
ventional core and circumferential suture combinations,
 Chapter 16:  Primary Repair of the Flexor Pollicis Longus Tendon 189

Table 16-1  Summary of Major Studies of Primary Repair of the FPL Tendon, 1989–2009
Study
Rehabilitation Number of Period Excellent and Good Mechanical
Authors Techniques Tendons Zones (Years) Results Rupture Rate (%)
Percival and Immobilized 25 1, 2, 3 4 44% (White76) 8
Sykes (1989) Kleinert 26 1, 2, 3 60% (White76) 8
mobilization
Noonan and Kleinert 30 1, 2, 3, 4, 5 6 71% Interphalangeal —
Blair (1991) mobilization joints normal
82% Metacarpophalangeal
joints normal
Nunley et al Kleinert 38 1, 2 2 Average IP 35% 3
(1992) mobilization
Thomazeau Immobilization 10 1, 2, 3, 4, 5
et al (1996)
Kleinert 3 1, 2, 3, 4, 5 5 85% (Tubiana7) 5
mobilization
Passive 7 1, 2, 3, 4, 5
mobilization
Sirotakova and Early Active 30 1, 2 8.5 70% (White76) 73% 17
Elliot (1999) Mobn (Group 1) (Buck-Gramcko77)
Early Active 39 1, 2 67% (White76) 72% 15
Mobn (Group 2) (Buck-Gramcko77)
(3) Early Active 49 1, 2 76% (White76) 80% 8
Mobn (Group 3) (Buck-Gramcko77)
Kasashima Immobilization 16 1, 2, 3 12 50% (JSSH 1994)* 0
et al (2002)
Kleinert 13 1, 2, 3 77% (JSSH 1994)* 0
mobilization
Peck et al Kleinert 23 1, 2 1.5 Not reported 4
(2003) mobilization
Baer et al Mantero Early 22 1, 2 6 91% (Buck-Gramcko)† 0
(2003) Active Mobn
Sirotakova and Early Active 48 1, 2 3.5 73% (White76) 77% 0
Elliot (2004) Mobn (Buck-Gramcko77)
Giessen et al Early Active 50 1, 2 2.75 78% (White76) 82% 0
(2009) Mobn (Buck-Gramcko77)
*JSSH, assessment of the Japanese Society for Surgery of the Hand (similar to the White Assessment, uses IP range of motion only).
†
This figure includes results of both finger and thumb flexor repairs. Although the authors indicate that the results were poorer in the
thumbs, they only give an overall result of excellent and good results for all cases.

which are commonly used in Europe and may be more
simple to insert.56 This group, again, had a 0% rupture
rate and showed that the three Tsuge suture technique
described by Tang and his colleagues is of adequate
strength to prevent rupture of primary repairs of the FPL
tendon during early active mobilization using the
“Belfast” regimen.57 It is also considerably easier to carry
out a repair by this technique. Although the results of
this latest cohort of repairs were better than those fol-
lowing repair with a combination of a four-strand
Kessler core suture and a Silfverskiöld circumferential
suture,3 this difference was not statistically significant.
More recently, Tang modified his technique of inserting
the three Tsuge sutures58 and, then, further modified
the technique to a four-strand Tsuge-type of repair to
make the repair easier and faster59 (Table 16-2). We
have no experience of these newer techniques and
cannot comment on them in a clinical setting, but
the results reported by these authors in their animal
studies would suggest that these variations are similar
in effectiveness to the original technique that was used
in our study.
190 Section 2:  Primary Flexor Tendon Surgery

beyond a 3-0 suture size. The Mantero technique,62

FPL REPAIR WITH NO RUPTURES: OTHER
SIMPLE ALTERNATIVES
Another method of simplifying the flexor repair while
adding to its strength is to use a larger caliber of core
suture.60,61 However, sutures become cumbersome to tie
and the knot is bulky at the flexor tendon junction
A alternative means of adding strength while simplifying
B experience that, even after short delays, apposition of
Figure 16-4  A, Illustration of the 1977 modification by
Tsuge of his own suture, which is used in B, the triple Tang
technique used in St. Andrew’s for FPL repair, 2004–2007.
probably based on a distal technique of flexor tendon
suture fixation first described by Brunelli 20 years
earlier,63 avoids the problem of suture knotting within
the flexor tendon sheath. It leaves less knotted suture
material in the repaired part of the tendon than do
Kessler repairs, so it is particularly suitable for use with
larger core sutures. This technique was, perhaps, the very
earliest attempt at early active mobilization without
rubber bands. It comprises a two-strand core suture with
suture fixation to the proximal part of the tendon using
half of a Kessler suture and distal fixation over a button
at the tip of the digit. Although the Mantero technique
has been used more recently with 3-0 sutures,49 the
original Mantero technique used a 2-0 suture.62 Both the
technique and this suture size are still used routinely in
many parts of southern Europe, including Mantero’s
unit.43,64-70 This technique is applicable to primary repair
of zone 1 and 2 divisions of the FPL, so it provides an
the FPL suture.
MANAGEMENT OF THE RETRACTED FPL
When retraction is obvious at surgery, proximal tendon
lengthening within the muscle31,71 or by “Z” lengthening
of the tendon at the musculotendinous junction30,72
may improve the results. It has certainly been our own
the FPL tendon ends is sometimes only possible by
considerable flexion of the interphalangeal (IP) joint of
the thumb. These repairs have then proved liable to

Table 16-2  Summary of the Five Groups of Primary FPL Tendon Repairs Carried Out in the St. Andrew’s Hand
Unit (1989–2007)
Number of Zones of Excellent and Rupture
Tendons Injuries Good Results (%)* Rate (%)
Group 1: Two-strand Kessler core suture, simple 30 1 and 2 70/73 17
circumferential suture, thumb only splint and early
active mobilization
Group 2: Two-strand Kessler core suture, simple 39 1 and 2 67/72 15
circumferential suture, thumb and finger splint and
early active mobilization
Group 3: Two-strand Kessler core suture, Silfverskiöld 49 1 and 2 76/80 8
circumferential suture, thumb and finger splint and
early active mobilization
Group 4: Four-strand Kessler core suture, Silfverskiöld 48 1 and 2 73/77 0
circumferential suture, thumb and finger splint and
early active mobilization
Group 5: Tang technique of triple Tsuge suture, no 50 1 and 2 78/82 0
circumferential suture, thumb and finger splint and
early active mobilization
*The first figures shown are the excellent or good results according to the White (1956) method and the second figures are the excellent or
good results according to the Buck-Gramcko et al (1976) method of assessment.
 Chapter 16:  Primary Repair of the Flexor Pollicis Longus Tendon 191

rupture during early postoperative mobilization, unless

one limited the speed and extent of rehabilitation and
accepted the possibility of an unsatisfactory result with
a very flexed IP joint. In these cases, we have used FPL
tendon lengthening within the muscle by simple trans-
verse division of the tendon in its intramuscular part at
one or two places as a tension relieving maneuver
(Figure 16-5), as described by Le Viet.71 Routine tendon
lengthening of all FPL repairs is another possible way of
reducing the FPL rupture rate. Rouhier described this in
1950 as an alternative to tendon grafting.31 The Rouhier
technique is well recognized and, occasionally, still used A
in France73 but is not commonly considered, or used,
elsewhere. The FPL tendon is detached from its muscle
along its intramuscular course and a tendon slide is
carried out within the muscle, allowing the FPL to act
as its own graft to close any gap without tension at the
site of tendon division. Once the repair has been com-
pleted, the tendon is sutured back to the muscle belly
more distally than its original attachment. Although we
have no experience of this technique, one would expect
it to allow considerable lengthening of the proximal FPL
tendon. It may be a useful means of tendon lengthening
B
for difficult cases when repair is delayed but it is pos-
sibly too elaborate for use in reducing the tension on Figure 16-5  Use of the technique of intramuscular division
an immediate repair. The Le Viet technique71 of making of the tendon described by Le Viet (1986) to overcome a
a complete transverse division of the tendon one or retracted FPL at primary repair. A, A single intramuscular cut
more times within the muscle belly is technically easier of the tendon. B, A double cut.
to carry out than intratendinous slide lengthening,
whether in the muscle or at the wrist. It only increases
the tendon length by 1 cm or so, but this can be suffi-
cient to reduce the active tension on the repair more additional 24 hours. Eleven achieved good results and
distally in the thumb during early mobilization. four achieved fair results using both methods of assess-
ment, suggesting that immediate re-repair, although not
THE SUCCESS OF FPL RUPTURE RE-REPAIR
easy, is the treatment of choice for most patients who
All 15 ruptures of the FPL in these studies presented present quickly after rupture of an FPL repair, as it is for
within 48 hours and were re-repaired within an finger flexor tendon repairs that rupture.4,57,74,75

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 CHAPTER
17  
TREATMENT OF FLEXOR
TENDON INJURIES AT OR
PROXIMAL TO THE WRIST
A Zone 5 Flexor Tendon Repairs
David Elliot, MA, FRCS, BM, BCh
OUTLINE
Recent reports concerning management of zone 5
flexor tendon injuries have identified this injury as
more significant in terms of digital motor dysfunction
than previously thought. Recent research has shown
that, despite a small risk of losing differential tendon
gliding when the superficialis tendons are repaired,
repair of both sets of tendons is beneficial and to be
recommended.
Arguably, flexor tendons are more commonly injured in
the flexor aspect of the distal forearm (zone 5) than in
any other zone, yet less is written about the manage-
ment after tendon divisions in this zone than in any
other. This may relate directly to a comment by Kleinert
and his colleagues over 30 years ago that “tendon gliding
in this area should not be a problem.”1
CLINICAL FEATURES
These cases are an everyday feature of upper limb trauma
units. The mechanisms of injury include laceration by
broken glass (alcohol-related in many instances), sharp
machinery at work, knives, and self-inflicted injuries.
The flexor aspect of the distal forearm transmits eigh-
teen longitudinal structures superficial to the wrist and
carpal joints, with the pronator quadratus lying trans-
versely across the wrist area between the skeleton and
these longitudinal structures. Any, or all, of these struc-
tures can be injured. Most emergency surgery is con-
cerned with the (longitudinal) running flexor tendons,
radial and ulnar arteries, and the median and ulnar
nerves. A “spaghetti” wrist is defined as one with a flexor
laceration in which at least 10 of the 15 longitudinal
structures (11 tendons, 2 arteries, and 2 nerves, exclud-
ing the palmaris longus) have been transected.2 Often
forgotten are the palmar branches of the median and
194
the ulnar nerves, division of which is almost inevitable
if the main longitudinal structures are divided. These
can, occasionally, cause significant problems of end-
neuroma pain if ignored at primary surgery.3-5
The wounds are generally transverse, or nearly so,
across the wrist. Access is easiest by converting the
wound to an “H” or “Z.” Whatever is done with the skin,
it is unusual to have healing problems with the skin as
whatever extension incisions of the primary laceration
are made surgically to aid access, the flaps so designed
(without thought) will be broad-based, short fasciocu-
taneous flaps with the radial and ulnar arteries feeding
directly into their bases. It is rare to be unable to achieve
safe primary wound closure for this reason.
The tendon repairs are carried out largely using the
techniques used in zone 2, so this will not be discussed
further, except to say that the anatomy mostly allows for
larger core and circumferential sutures than in zones 1
and 2. The tendon repairs are, theoretically, easier than
in the fingers because the tendons are not confined
within a tendon sheath. However, the multitude of
structures and the associated nerve and, sometimes,
arterial injuries make flexor wrist injuries daunting and
long operations for junior training surgeons and these
injuries should not be dismissed by seniors as “good
training cases,” to be left without help to junior sur-
geons. The many structures to be repaired can turn these
operations into marathons in inexperienced hands! It
is, also, often the case that the individual tendons are
not cut transversely but obliquely, with different tendons
cut at different levels relative to the carpal canal or, even,
within the carpal tunnel by shards of glass. The tendons
may be “shredded” longitudinally, making textbook
repairs difficult. Where multiple structures are divided
or surgery is lengthy and, particularly, when the tendon
repairs approximate to the proximal edge of the carpal
ligament on full digital extension, the carpal tunnel

should be decompressed to avoid both the development
of secondary carpal tunnel syndrome6 and loss of exten-
sion as a result of the tendon repairs impinging on the
carpal ligament on full extension of the wrist and digital
joints.
Following surgery, these injuries are mobilized using
the same regimes as zone 2 injuries and these are not
discussed further. When the carpal ligament has been
divided, the fingers are mobilized with the wrist splinted
in the neutral position or slight extension. In other cir-
cumstances, a straight wrist or only slightly flexed wrist
position may be preferred, but it should be remembered
that the 30° flexed wrist position originally advocated
for rehabilitation is little different from the Phalen test
we use to irritate the median nerve when diagnosing
carpal tunnel syndrome and may precipitate this
problem postoperatively if the carpal ligament remains
intact.
One point about rehabilitation of zone 5 flexor
tendon repairs that is unique to this zone is that there
will be no intrinsic proximal interphalangeal (PIP) joint
extensors of the ulnar fingers if the ulnar nerve has also
been divided. This requires that the metacarpophalan-
geal (MCP) joints of these fingers be held in flexion
during the 4-week postoperative splinting period to acti-
vate PIP extension by the long extensor tendons, if PIP
joint contractures are to be avoided.7
It is also frequently forgotten by surgeons what may
be being asked of a patient with a spaghetti, or near-
spaghetti, wrist. At 1 to 3 days after surgery, the patient
is being expected to move a large number of swollen
tendons, possibly bristling with unabsorbable suture
ends and tightly bound down by swollen fasciocutane-
ous flaps across repaired median and/or ulnar nerves.
This is painful! Mobilization may be hindered by lack
of adequate analgesia, making the therapist’s job impos-
sible and the ultimate result less than perfect.
THE FLEXOR DIGITORUM SUPERFICIALIS
TENDONS: TO REPAIR OR NOT
Until the introduction of early mobilization of flexor
tendon repairs in the latter half of the twentieth century,
it was believed that repair of divided flexor digitorum
superficialis (FDS) tendons following wrist lacerations
in which both the superficial and deep digital flexor
tendons had been divided caused adhesions with limi-
tation of excursion of the associated fingers.8,9 However,
the superficial digital flexors increase the grip of the
hand and make pinch and flexion of the PIP joint more
stable, in addition to providing superior individual
finger flexion.10 For these reasons and, possibly, reas-
sured by the comment that “tendon gliding in this area
should not be a problem,”1 repair of the superficial
digital flexors became routine with the advent of early
mobilization.1,10-12 The possibility of PIP hyperextension
Chapter 17A:  Zone 5 Flexor Tendon Repairs 195
following failure to repair the FDS tendon in zone 5,
although of less significance, is suggested by a single
case report.13 The possibility of adhesions causing limi-
tation of finger excursion and/or loss of independent
FDS action, despite early mobilization, was not
researched at that time.
The literature on injuries to the flexor aspect of the
distal forearm immediately prior to 2000 is scant.11,13-16
Two of these reports were small and concentrated their
reviews mainly on the injuries to the median and ulnar
nerves and not on the outcome of the finger flexor
tendon injuries.11,16 In 1985, Puckett and Meyer reviewed
37 patients who suffered a minimum of three and an
average of eight completely transected longitudinal
structures at the wrist.15 One-third of their patients had
“spaghetti” wrists. The hands were mobilized postop-
eratively using a Kleinert regimen. Tendon function was
considered to be excellent when digital range of motion
was 85% to 100% of normal or finger flexion brought
the fingertip within 1.0 cm of the distal palmar crease;
good with 70% to 84% of normal digital range of
motion or the fingertip within 2.0 cm of the distal
palmar crease; fair with 50% to 60% of normal digital
range of motion; or poor with fixed contractures or
adhesions. Thirty-three (97%) of 34 wrists available for
assessment were reported to have good or excellent
ranges of digital motion and one patient to have a fair
range of motion. The method by which the overall
results were derived from the assessment of the indi-
vidual fingers was not given. No tendon ruptures
occurred in their series.
In 1992, Stefanich et al13 reported independent FDS
action in only 30% of a retrospective series of 23 patients
who underwent zone 5 flexor tendon repairs that were
mobilized using Kleinert’s early mobilization (active
extension-passive flexion) regimen. In this series, five
patients had transection of a single digital (finger or
thumb) flexor tendon and 18 patients had transections
of multiple digital flexor tendons. The total active
motion (TAM) of the associated digits as well as for the
corresponding unaffected digits was calculated, as sug-
gested by the American Society for Surgery of the Hand,
but, unfortunately, the associated scoring system of
excellent/good/fair/poor was not recorded. Instead the
average TAM (as a percentage of the uninjured contra-
lateral digit) was given for the whole group of 23 patients
for each of the five digits. Sixteen of the 23 patients
regained full digital flexion of all digits but the number
of digits in these patients that had not suffered flexor
tendon injury was not stated. There was an average PIP
extension deficit of 8° and distal interphalangeal exten-
sion deficit of 4°. Two patients (9%) had extremely
limited motion. Rupture of one flexor pollicis longus in
one patient and rupture of one ring finger flexor digito-
rum profundus (FDP) in an additional patient occurred
196 Section 2:  Primary Flexor Tendon Surgery
in their series. This report reintroduced the question of
adhesion of the flexor tendons after repair of both
tendon groups in zone 5 and the possibility that loss of
digital excursion and/or independent FDS action is
more common than had been assumed.
Subsequent to this small study,13 we carried out a
larger prospective study17 over a 2-year period to examine
the results of routine repair of both finger flexor tendons
in zone 5 followed by early postoperative mobilization
using the variant of the controlled active mobilization
(active extension-active flexion) regimen described pre-
viously and used routinely in our unit.14 In this study,
after mobilizing the injured hands using an early active
motion regimen, good or excellent results were achieved
in 90% of fingers that had repair of completely divided
flexor tendons in zone 5 and independent FDS action
was achieved in 66% of the fingers. No tendon ruptures
occurred in this series. The group of patients with “FDS
injuries only” fared better than those with ‘“FDS and
FDP” injuries in terms of independent FDS action, the
difference being statistically significant. This most prob-
ably reflects the difference in magnitude of the total
injury to the wrist between those with more superficial
injuries and deeper injuries, rather than simply a differ-
ence between division of one or two tendon groups.
Multivariate analysis showed that the presence of a “spa-
ghetti” wrist injury had a significant adverse effect on
the overall hand recovery in terms of independent FDS
action but had no significant adverse effect on the
overall hand recovery in terms of digital range of motion.
While the extensive scar tissue likely to follow a “spa-
ghetti” wrist injury might be expected to eliminate dif-
ferential gliding of the tendons, the resultant tendon
mass appeared to be capable of moving the fingers
through a full, or near full, range of motion in most
cases. Age was not a significant factor in determining
recovery of either independent FDS action or range of
digital motion. A statistically significant association
between recovery of independent FDS action and recov-
ery of the digital range of motion appears to confirm
that wrists that do well with respect to one modality will
do well with respect to the other. Those fingers with FDS
tendons lying close to the FDP tendons at the wrist—
namely, the index and little—are more likely to lose
independent FDS action after division and repair of
their tendons at the wrist. The little finger had the lowest
incidence of independent FDS action in this study.
However, those little fingers without independent FDS
References
1. Kleinert HE, Kutz JE, Atasoy E, et al: Primary repair of flexor
tendons, Orthop Clin North Am 4:865–876, 1973.
2. Katz RG: Discussion. Results of treatment of extensive volar
wrist lacerations; the spaghetti wrist, Plast Reconstr Surg
75:720–721, 1985.
action after repair of the FDS at the wrist in this study
may include fewer failures of mobilization than is sug-
gested by our figures as it has been shown that the
superficialis tendon of the little finger, although present
at the wrist, cannot achieve flexion of this finger in one-
third of normal individuals.18,19
For the first time, an analysis was presented to math-
ematically to analyze these injuries in terms of the effect
on overall hand function rather than by consideration
of the individual fingers that had sustained division of
flexor tendons at the wrist. This showed that there was
a statistically significant interdependence of the flexor
systems of the different fingers in those wrists with inju-
ries to the flexors of all four fingers. This indicates that
the consequences of this injury in respect of hand func-
tion are more complex than the mere sum of its con-
stituent tendon injuries and future attempts to assess
the zone 5 injury need to change to reflect this
complexity.
Since our study, few reports on zone 5 have been
written.20-24 Two of these studies lend support to the
benefit of active, as opposed to passive, mobilization of
zone 5 flexor repairs.22,23 In 2005, Wilhelmi et al reviewed
168 zone 5 tendon flexor divisions24 repaired using their
own core suture technique and mobilized early using a
technique of protected active motion similar to that
reported by Silfverskiöld and his colleagues from Göte-
borg in Sweden25 in 29 patients treated over 4 years.
Despite the emphasis of the authors on the strength and
benefits of their particular suture technique, three rup-
tured tendons occurred in one patient. Of more interest
was the use of a technique of mobilization that opti-
mized differential gliding between the FDS and FDP
tendons. This allowed these authors to achieve good or
excellent results in 97 (99%) of 103 fingers and inde-
pendent FDS action in 88 (91%) of 103 fingers. These
authors stressed loss of extension in patients with con-
comitant ulnar nerve injuries as responsible for their
few less than perfect results.
The benefits of FDS function favor repair of the FDS
tendons in zone 5 flexor tendon injuries. There would
appear to be no logical basis for not repairing the FDS
tendons at the wrist as the use of a supervised active
mobilization regimen in the early postoperative period
is likely to achieve a high proportion of good and excel-
lent results in terms of finger movement and a good
chance of retaining independent action of the superfi-
cial finger flexors.
3. Atherton DD, Leong JCS, Anand P, et al: Relocation of painful
end neuromas and scarred nerves from the zone II territory
of the hand, J Hand Surg (Eur) 32:38–44, 2007.
4. Evans GRD, Dellon AL: Implantation of the palmar cutane-
ous branch the median nerve into the pronator quadratus for

treatment of painful neuroma, J Hand Surg (Am) 19:203–206,
1994.
5. Sood MK, Elliot D: Treatment of painful neuromas of the
hand and wrist by relocation into the pronator quadratus
muscle, J Hand Surg (Br) 23:214–219, 1998.
6. Figus A, Iwuagwu FC, Elliot D: Subacute nerve compressions
after trauma and surgery of the hand, Plast Reconstr Surg
120:705–712, 2007.
7. Elliot D: Primary flexor tendon repair: operative repair, pulley
management and rehabilitation, J Hand Surg (Br) 27:507–
513, 2002.
8. Carroll RE, Match RM: Common errors in the management
of wrist lacerations, J Trauma 14:553–562, 1974.
9. Verdan C: Practical considerations for primary and secondary
repair in flexor tendon injuries, Surg Clin North Am 44:951–
970, 1964.
10. Kleinert HE, Meares A: In quest of the solution to severed
flexor tendons, Clin Orthop Relat Res 104:23–29, 1974.
11. Hudson DA, de Jager LT: The spaghetti wrist. Simultaneous
laceration of the median and ulnar nerves with flexor tendons
at the wrist, J Hand Surg (Br) 18:171–173, 1993.
12. Strickland JW: Flexor tendon repair, Hand Clin 1:55–68,
1985.
13. Stefanich RJ, Putnam MD, Peimer CA, et al: Flexor tendon
lacerations in zone V, J Hand Surg (Am) 17:284–291,
1992.
14. Elliot D, Moiemen NS, Flemming AFS, et al: The rupture
rate of acute flexor tendon repairs mobilised by the con-
trolled active motion regimen, J Hand Surg (Br) 198:607–
612, 1994.
15. Puckett CL, Meyer VH: Results of treatment of extensive volar
wrist lacerations; the spaghetti wrist, Plast Reconstr Surg 75:
714–721, 1985.
Chapter 17A:  Zone 5 Flexor Tendon Repairs 197
16. Rogers GD, Henshall AL, Sach RP, et al: Simultaneous lacera-
tion of the median and ulnar nerves with flexor tendons at
the wrist, J Hand Surg (Am) 15:990–995, 1990.
17. Yii NW, Urban M, Elliot D: A prospective study of flexor
tendon repair in zone 5, J Hand Surg (Br) 23:642–648, 1998.
18. Austin GJ, Leslie BM, Ruby LK: Variations of the flexor digi-
torum superficialis of the small finger, J Hand Surg (Am)
14:262–267, 1989.
19. Baker DS, Gaul JS, Williams VK, et al: The little finger
superficialis–clinical investigation of its anatomic and func-
tional shortcomings, J Hand Surg (Am) 6:374–378, 1981.
20. Bircan C, El O, Akalin E, et al: Functional outcome in patients
with zone V flexor tendon injuries, Arch Orthop Trauma Surg
125:405–409, 2005.
21. Gibson TW, Schnall SB, Ashley EM, et al: Accuracy of the
preoperative examination in zone 5 wrist lacerations, Clin
Orthop Relat Res 365:104–110, 1999.
22. Korstanje JW, Schreuders TR, van der Sijde J, et al: Ultrasono-
graphic assessment of long finger tendon excursion in zone
V during passive and active tendon gliding exercises, J Hand
Surg (Am) 35:559–565, 2010.
23. Panchal J, Mehdi S, Donoghue JO, et al: The range of excur-
sion of flexor tendons in zone V; a comparison of active and
passive flexion mobilisation regimes, Br J Plast Surg 50:517–
522, 1997.
24. Wilhelmi BJ, Kang RH, Wages DJ, et al: Optimizing indepen-
dent finger flexion with zone V flexor repairs using the Mas-
sachusetts General Hospital flexor tenorraphy and early
protected motion, J Hand Surg (Am) 30:230–236, 2005.
25. Silverskiöld K, May E: Flexor tendon repair in zone II with a
new suture technique and an early mobilization program
combining passive and active flexion, J Hand Surg (Am)
19:53–60, 1994.
 B Methods and Outcomes of Zone 5
Flexor Tendon Repairs
Jun Tan, MD, and Jin Bo Tang, MD
OUTLINE
Flexor tendons in zone 5 are located in the distal and
middle parts of the forearm. A severe injury can
produce “spaghetti wrist,” namely, lacerations of 10 or
more structures, including tendons, nerves, and vessels.
In this chapter, we present our current methods for
repair of zone 5 flexor tendon injuries and follow-up
of 52 patients. Recovery of active digital motion and
grip strength are generally good, but functional loss
caused by accompanying nerve injuries is a concern.
Repairs by experienced surgeons produce better recov-
ery. Outcomes of “spaghetti” injury are worse than
those of less severe injuries.
The region of the distal and middle forearm, which
extends from the proximal border of the transverse
carpal ligament to the musculotendinous junctions of
the forearm flexors, contains zone 5 flexor tendons. In
the forearm, the flexor digitorum profundus (FDP) has
a single muscle belly and travels distally to separate into
a radial bundle and an ulnar bundle. The radial bundle
forms the FDP tendon to the index finger, and the ulnar
bundle forms the FDP tendons of the middle, ring, and
small fingers. The flexor digitorum superficialis (FDS)
separates into individual tendon units and muscle
bellies. No synovial sheath covers the tendons in this
region.
Tendon lacerations in this zone are easy to diagnose;
with rare exceptions, all the injuries are repaired primar-
ily. Secondary surgeries are reserved for tenolysis or
nerve grafting. Wound contamination can be a serious
concern if the patients are injured by dirty tools or oily
machines. Thorough irrigation of the wounds and
débridement of wounds are particularly necessary,
together with intravenous administration of antibiotics
to prevent wound infection.
We perform primary, rather than “delayed” primary
repairs, for tendons injured in zone 5, because these
wounds are open and in many cases are extensive. The
tendon ends are easily found during surgery. The
proximal tendon ends may retract, but not over a
long distance. Additional incisions are in most cases
not required to locate the retracted tendon ends. If
proximal tendon ends retract too proximally, a single
198
longitudinal incision suffices. The distal tendon ends
are easily brought into the operative field after wrist
flexion and the wrist is held in flexion by an assistant
during surgery. Because of frequent lacerations in nerve
trunks, particular care must be taken to identify the
tendons and nerves and to suture the corresponding
ends correctly. Careful attention to their locations in the
wound, diameters and the shape of the lacerated struc-
tures, and the oblique angle of their cross sections help
produce a proper match of the tendon ends.
Adhesion formations between tendon injuries and
overlying skin and fascia are frequent, but subsequent
limitations to active finger motion vary. In a majority of
cases, adhesions between the tendons and loose
paratenon are not problematic, because the adhesions
are not as restrictive as those between the tendon and
fibroosseous sheath or the firm flexor retinaculum.
Severe adhesions can arise between multiple tendons
and affect the motion of multiple digits, subsequently
requiring secondary tenolysis.
The median and ulnar nerves and the radial and ulnar
arteries are frequently involved. The median nerve is
more frequently cut than the ulnar nerve, and the lacera-
tions to the ulnar artery are more frequent than those
to the radial artery. Because the ulnar nerve and artery
are located so close together in the distal forearm, injury
to the artery is almost always accompanied by injury to
the nerve. In the presence of intact radial artery and
positive Allen’s test, the severed ulnar artery may not
require anastomosis, but the ulnar nerve should always
be repaired primarily if no lengthy defect presents.
We reviewed the records of 52 patients (52 wrists)
treated in our clinic and found that 43 wrists (83%) had
complete lacerations to median or ulnar nerves, with
median nerve cut in 31 (59%) and ulnar nerve cut in 21
(40%). Both median and ulnar nerves were lacerated in
nine wrists (17%). Twenty-nine (56%) had complete
or major severance of ulnar (40%) artery, radial (26%)
artery, or both (10%). Lacerations in anterior cutaneous
branches of median or ulnar nerves (which need no
repair) were seen in almost all cases. We repaired all
severed median and ulnar nerves primarily with direct
end-to-end suture along with tendon repairs.
We should emphasize that cases necessitating second-
ary tenolysis and secondary surgery are not rare. We
 Chapter 17B:  Methods and Outcomes of Zone 5 Flexor Tendon Repairs 199

perform 10 to 15 cases of secondary surgeries for zone 5

flexor tendons (and their accompanying nerve repairs)
annually. Around three-fourths of the patients are
referred from local hospitals where primary repair is
done. The secondary surgeries are indicated in one of
the following situations: (1) adhesions form between
multiple tendons, (2) tendon adhesion with skin
wounds, (3) nerves are not sutured during primary
surgery, or (4) infrequently, loss of proper finger flexion,
due to improper match of the tendon ends (e.g., wrong
tendon-to-tendon match, or tendon is sutured to a
nerve). Among the zone 5 injures that are treated primar-
ily in our unit, 7% of the wrists need secondary tenolysis
due to formation of adhesions among multiple tendons.
In our unit, we routinely repair lacerated nerve trunks Figure 17(B)-1  The distal part of the left forearm of a
primarily, and tendons are carefully identified to ensure 36-year-old patient was cut with a knife, presenting a
proper match, but this is not always the case in the “spaghetti” injury involving complete cut of 11 tendons, two
nerves (median and ulnar), and ulnar artery.
hospitals when injuries are handled by surgeons with
inadequate training. In such cases, the complications
rate of zone 5 tendon repairs can be higher, including
(1) improper primary treatment of the tendons, such as
mismatching of the tendon ends or suturing nerves to
tendons, (2) failure to repair the lacerated nerves, and
(3) extensive adhesion formations involving multiple
tendons.

PATIENTS AND OUTCOMES

Patients
In 2010, we reviewed the medical charts of the patients
admitted after surgery for primary repairs of zone 5
tendon injuries over the previous 6 years. We were
unable to include a small number of patients who had
lacerations to a single tendon in forearms because they
were discharged immediately after surgery. Cases of
massive soft tissue loss, extensor tendon injuries, hand
fractures, or replantation surgery were excluded, as were
patients younger than 12 years. A total of 69 patients
with intact medical records were reviewed. Follow-up
was available for 52 patients. The average follow-up
period was 2 years 8 months (range, 11 to 78 months).
There were 41 males and 11 females, with a mean age
of 35 years (range, 15 to 57 years).
The flexor tendons to 163 digits (14 thumbs, 35 index,
44 middle, 42 ring, and 28 small fingers) were involved.
There were 14 flexor pollicis longus (FPL) tendon cuts,
82 FDP tendon cuts, and 147 FDS tendon cuts.
Of the 52 patients, 16 (30.7%) had “spaghetti”
wrists (i.e., at least 10 structures lacerated, involving
tendons, nerves, and arteries, not including cutaneous
nerve branches and palmaris longus tendon) (Figure
17[B]-1).
Surgical Methods
All patients were treated with primary surgery within 12
hours after trauma by staff hand surgeons in our
Figure 17(B)-2  A thermoplastic splint is applied with the
wrist in flexion of 20° to 30° and the fingers in slightly
flexed position after surgery.
department, including the current authors. We repaired
flexor tendons using one of three methods: a two-strand
modified Kessler method (with either 4-0 or 3-0 sutures),
a four-strand cruciate method (with either 4-0 or 3-0
sutures), or a six-strand Tang (or M-Tang) method1,2
(with 4-0 looped nylon sutures), supplemented with a
simple running or locking circumferential suture (with
a 5-0 or 6-0 nylon suture). Choice of repair methods
remains a personal preference; over the last a few years,
we have tended to use four- or six-strand repairs, and
two-strand Kessler repairs were used only sometimes.
When multiple tendons were repaired in a single patient,
a mixture of simple or more complicated methods were
used, which reduces the total operation time.
Postoperative Care
After surgery, a cast or a thermoplastic splint with the
wrist in flexion of 20° to 30° and the fingers in slightly
flexed position is used to protect the hand (Figure
17[B]-2). We used a motion protocol similar to that
used for zone 2 tendon repair1 but under less stringent
200 Section 2:  Primary Flexor Tendon Surgery
supervision. Typically, patients begin the early passive-
active motion on postsurgical day 3 or 4 under the
supervision of surgeons and therapists while they are
still hospitalized. During the first 3 weeks, in each exer-
cise session, passively placing the fingers into flexion
and extension position is initiated first, followed by
active motion over the amplitude at which the motion
does not encounter marked resistance.
Within the first 3 weeks, when multiple tendons are
lacerated or the tendon repairs are accompanied by
direct nerve approximation, we do not encourage
patients to move actively through the full range of finger
motion. Instead, we encourage them to move in a rela-
tively small range, just enough to move the tendons in
the forearm, avoiding pain, potential bunching of the
repaired tendons, or disturbance to the nerves by
tendons. The patients move to the extent they feel com-
fortable. Flexion of the wrist is a component of the
motion protocol.
At the end of week 3, a dorsal extension block splint
is applied to keep the wrist at 30° extension. From the
third to fifth weeks, the dorsal splint is discontinued
gradually and further active and passive finger flexion is
emphasized. After 5 weeks, the splint is discarded. After
6 to 7 weeks, the patients return to normal activities.
Differential FDS and FDP motion exercise can be started
from the second or third weeks, and continue for 3 to
4 weeks.
Exercise can be controlled more loosely than zone 2
repairs. The number of exercise sessions each day varies
among patients. Generally, at least four or five sessions
are encouraged daily, but it is not necessary to perform
exercise hourly. Each session consists of about 20 to 30
repetitions of motion; active motion precedes passive
motion.
Outcomes
Consistent with the results reported previously, we
found that tendon repairs in zone 5 generally yield quite
satisfactory results, but we also noted that patients with
severe injuries or whose repairs were carried out by
junior surgeons had a higher percentage of digits func-
tionally ranked as “fair” or “poor.”
Graded using Strickland and Glogovac criteria3 for
the range of active digital motion among 163 digits of
52 patients, excellent results were achieved in 123 digits
(75.5%), good in 23 (14.1%), fair in 12 (7.4%), and
poor in 5 (3%). The good and excellent rate was 89.6%.
No repairs ruptured. Independent FDS action was dem-
onstrated in 103 (70.1%) of the 147 fingers with FDS
injuries. Grip strength recovered to an average of 68%
and tip pinch strength to 65% of the uninjured hand,
respectively. Mean DASH (Disabilities of the Arm,
Shoulder and Hand) score was 11.9 (SD 11.0, range 1.7
to 40).
IV 31 3
Level of expertise
III 66 11 5
II 22 10 7 2 *
I 2 1 3 **
0 10 20 30 40 50 60 70 80 90 100
% Functional recovery
Excellent Good Fair Poor
Figure 17(B)-3  The graph showing correlation between
expertise levels of surgeons and functional outcomes. The
outcomes in terms of active range of digital motion treated
by more experienced surgeons (Levels 3 and 4) are better
than junior surgeons (Level 2)* or residents (Level 1).** The
numbers shown in the bars are number of fingers evaluated.
Patients under 35 years of age were more likely to
have satisfactory outcomes than were patients over 35
years of age (p < 0.01). Outcomes in the nondominant
hand were significantly worse than when the dominant
hand was involved (p < 0.01). Outcomes in the fingers
with a mixture of FDS and FDP injuries were worse than
those of only FDS injuries (p < 0.01). Gender and
follow-up time (from 11 months to 6.5 years) were not
associated with any significant differences in the out-
comes of digital range of motion and independent FDS
action.
Worse outcomes were significantly associated with
repairs performed by surgeons with lower levels of
expertise4 (Figure 17[B]-3).
Sixteen cases had “spaghetti” wrists. Grip and pinch
strength, DASH, active range of digital motion, and
independent FDS motion of the spaghetti wrists were
significantly worse as compared with non-spaghetti
wrists (p < 0.01). Grip and pinch strength of spaghetti
wrists recovered to only about one-third of the unin-
volved side (Table 17[B]-1).
SUMMARY
We were able to perform primary tendon repairs in all
the cases brought to us. Over the past 6 years, no cases
were unsuitable for primary repair, which would have
necessitated delayed or secondary tendon repairs. None
of the cases developed serious wound infection. Patients
with an extensive wound were given intravenous anti­
biotics, and particular care was taken to irrigate the
wound. We consider that thorough wound irrigation
and débridement are an important part of treatment.
 Chapter 17B:  Methods and Outcomes of Zone 5 Flexor Tendon Repairs
Table 17(B)-1  Comparison of Outcomes Between the Wrists With “Spaghetti” and “Non-Spaghetti” Zone 5
Tendon Injuries
Digital Range of Motion*
No. of
Injuries Patients Excellent Good Fair Poor
Spaghetti 16 42   15 8 2
(62.7) (22.4) (11.9) (3.0)
Non- 36 81   8 4 3
spaghetti (84.4) (8.3) (4.2) (3.1)
Grip and pinch strengths of the injured side were recorded as percentage of the contralateral side. Numbers in parentheses are percentages.
Digital range of motion was examined by the nonparametric Mann-Whitney U test; other comparisons were done with student t test.
*Of significant difference between two types of injuries.
Proper identification of nerves and tendons during
surgery is important to ensure correct surgical repair.
Particularly, junior surgeons can confuse two different
structures.
Our follow-up findings indicate that it is not abso-
lutely necessary to use four- or six-strand repairs for
zone 5 tendon injuries, but this has become a preference
in our unit in recent years. We suggest that stronger
repair methods be used, rather than the weaker conven-
tional Kessler repairs. Alternatively, it is also proper to
use 3-0 suture rather than 4-0 suture to enhance repair
strength. We do not have recommendations about the
particular one or two methods that should be used in
zone 5; methods vary. In our unit, we use a cruciate
repair or a six-strand M-Tang repair. At a hand surgery
center in a neighboring city, surgeons use a four-strand
U-shaped method (another method developed by the
senior author5) with 4-0 looped suture together with a
running peripheral suture. The surgeons achieved gener-
ally good and excellent results in more than 25 cases
without repair ruptures over the past 3 years (Zun Shan
Ke, MD, personal communication, 2011). We have not
used the U-shaped method in zone 5 repairs; a six-
strand M-Tang method has been adopted.
In our cases, 89% of the digits have good or excellent
active range of digital motion, and 70% fingers exhib-
ited independent FDS action. An overall good and excel-
lent rate of 90% was reported by Yii et al,6 though they
used American Society for Surgery of the Hand (ASSH)
criteria; those are in fact different from the criteria in
our follow-up. The thumb was not included into the
grading by Yii et al. Our cases appeared to have more
severe vascular injuries. In the past reports, the propor-
tion of independent FDS action varied from 30% to
85% of the fingers after zone 5 tendon repairs.7-14
Regarding the number of tendons to repair, all the
wrist flexors except the palmaris longus tendon should
be repaired. While FDP and FPL tendon repairs are nec-
essary, it may not be necessary to repair all the FDS
tendons, particularly if the wounds are untidy and
201
Independent Grip Pinch
Total FDS Action Strength Strength DASH
Digits (Digits)* (%)* (%)* Scores
67 36 (59.0) 50 ± 26 47 ± 25 21 ± 12
96 67 (77.9) 75 ± 18 75 ± 20 8±8
tendon ends are crushed. We consider repairs to the FDS
tendon a positive option, favoring gain in grip strength.
Nevertheless, no clinical data indicate whether lacerated
FDS tendon repairs are absolutely necessary or whether
only a part of the lacerated FDS tendons need to be
repaired. If the FDS tendons are to be selectively repaired
to reduce operation time or reduce the chance of adhe-
sions, we usually repair the FDS to the index and middle
fingers.
One of us (the senior author) proposed classification
and documentation of the level of expertise of sur-
geons4; we considered zone 5 injuries a perfect test
ground in which to apply such criteria to analyze pos-
sible associations between expertise levels and treat-
ment outcomes. In fact, outcomes were correlated
positively with expertise levels. While the results of zone
5 tendon repairs are generally considered favorable, we
found that this injury is more likely to have a better
outcome in more experienced hands within our unit.
When treated by experienced surgeons, patient out-
comes were rated as good or excellent in nearly all cases;
the few cases with poor results were all treated by junior
staff members.
Accompanying nerve injuries in this area present a
greater concern than tendon lacerations. Loss of hand
function is mostly due to incomplete recovery of associ-
ated nerve injuries (Figure 17[B]-4). Inadequate active
finger extension is not infrequently, caused by incom-
plete functioning of the intrinsic muscles.
The “spaghetti” wrist consists of severe trauma to
the soft tissues of the wrist.8 Previous studies indicated
that a spaghetti wrist was associated with poor indepen-
dent FDS action.1,3-6 Our results are consistent with pre-
vious findings. Spaghetti wrist trauma produces a severe
adverse effect on overall hand function. Grip and pinch
strength of such wrists recovered to only about one-
third that of the contralateral side. After median or ulnar
nerve injuries, intrinsic muscles do not function nor-
mally, which contributes to decreased grip strength and
the inability to perform fine hand actions.
202 Section 2:  Primary Flexor Tendon Surgery

A B
Figure 17(B)-4  Findings of a patient with spaghetti wrist injury 2 years 8 months after primary tendon and ulnar nerve
repair. The patient recovered full digital extension (A), and full flexion (B). Note the patient was unable to abduct the little
finger (A [arrow]) due to incomplete recovery of ulnar nerve function. There were mild hypotrophy of intrinsic muscles and
flattened hypothenar area (A). Incomplete function of intrinsic muscles presented as a prominent problem. Recovery of grip
strength was also incomplete.

References
1. Tang JB: Indications, methods, postoperative motion and
outcome evaluation of primary flexor tendon repairs in Zone
2, J Hand Surg (Eur) 32:118–129, 2007.
2. Tang JB: Clinical outcomes associated with flexor tendon
repair, Hand Clin 21:199–210, 2005.
3. Strickland JW, Glogovac SV: Digital function following flexor
tendon repair in Zone II: A comparison of immobilization
and controlled passive motion techniques, J Hand Surg (Am)
5:537–543, 1980.
4. Tang JB: Re: Levels of experience of surgeons in clinical
studies, J Hand Surg (Eur) 34:137–138, 2009.
5. Cao Y, Tang JB: Biomechanical evaluation of a four-strand
modification of the Tang method of tendon repair, J Hand
Surg (Br) 30:374–378, 2005.
6. Yii NW, Urban M, Elliot D: A prospective study of flexor
tendon repair in zone 5, J Hand Surg (Br) 23:642–648, 1998.
7. Bircan C, EI O, Akalin E, et al: Functional outcome in patients
with zone V flexor tendon injuries, Arch Orthop Trauma Surg
125:405–409, 2005.
8. Puckett CL, Meyer VH: Results of treatment of extensive volar
wrist lacerations: the spaghetti wrist, Plast Reconstr Surg
75:714–721, 1985.
9. Noaman HH: Management and functional outcomes of com-
bined injuries of flexor tendons, nerves, and vessels at the
wrist, Microsurg 27:536–543, 2007.
10. Weinzweig N, Chin G, Mead M, et al: “Spaghetti wrist”:
management and results, Plast Reconstr Surg 102:96–102,
1998.
11. Jaquet JB, van der Jagt I, Kuypers PD, et al: Spaghetti wrist
trauma: functional recovery, return to work, and psychologi-
cal effects, Plast Reconstr Surg 115:1609–1617, 2005.
12. Stefanich RJ, Putnam MD, Premier CA, et al: Flexor tendon
lacerations in zone V, J Hand Surg (Am) 17:284–291, 1992.
13. Wilhelmi BJ, Kang RH, Wages DJ, et al: Optimizing indepen-
dent finger flexion with zone V flexor repairs using the
Massachusetts General Hospital flexor tenorrhaphy and early
protected active motion, J Hand Surg (Am) 30:230–236,
2005.
14. Katz RG: Discussion. Results of treatment of extensive volar
wrist lacerations: the spaghetti wrist, Plast Reconstr Surgt 75:
720–721, 1985.
 CHAPTER
18  
FLEXOR TENDON REPAIRS
WITH NOVEL SUTURES
AND DEVICES
A Mantero’s Technique for
Tendon Repair
Ombretta Spingardi, MD, Mario Igor Rossello, MD,
and Renzo Mantero, MD
OUTLINE
We present our experience with pull-out repairs of
flexor digitorum profundus (FDP) tendon injuries in
zone 2. Since 1973, we have repaired zone 1 and 2
tendon injuries with the Bunnell technique of pull-out
suture through the fingertip, together with immediate
active digital mobilization of patients. We followed a
sample of patients with zone 2 FDP tendon lacerations
treated between 2005 and 2008, and no patients had
rupture of the repairs. We assessed the outcomes of
one group of 46 patients (46 digits) by evaluating
subjective and objective function; 33 digits (72%) had
good or excellent results. We also compared the results
in 22 digits treated with the pull-out method to those
in 22 digits after two-strand surgical repairs. We noted
faster recovery of active finger flexion and grip strength
after the pull-out method. Poor results were seen only
when tendon mobilization was begun too late or was
insufficient.
Flexor tendon surgery has made much progress since
the 1970s due to accrued knowledge of the biology of
tendon tissue repair and great improvement in suture
techniques and postoperative mobilization concepts.
However, tendon repair in zone 2 still is a problem due
to the high risk of adherence and consequent limitation
of range of active motion, even when early postopera-
tive protected motion is adopted.
The pull-out technique was described by Bunnell in
the beginning of the 20th century for tendon repair.
Mantero and colleagues1-3 started using the technique
in 1973 in association with immediate postoperative
active motion. With this regimen, the occurrence of
tendon adherence and an hypertrophic cutaneous scar
with consequent acquired and permanent deformity
and stiffness of the joints was remarkably decreased.
INDICATIONS
Any clean-cut injury of the flexor digitorum profundus
(FDP) tendon in zone 2 or the flexor pollicis longus
(FPL) tendon in zone 2 can be repaired with this tech-
nique. This method is also indicated for FDP tendon
injuries in proximal zone 1, where direct end-to-end
tendon repair is necessary.1,4-6 However, we do not use
this method in the case of complex trauma (e.g., ampu-
tation or tendon injury associated with exposed frac-
ture), because early motion is not possible, and the
button on the top of the finger carries a risk of causing
ischemia in situations in which digital circulation is
already poor.
When both the FDS and FDP tendons are injured,
the FDS tendon can be repaired with any end-to-end
repair method in association with FDP repair by our
method.
SURGICAL TECHNIQUES
Under regional anaesthesia, two cut tendon ends are
exposed through a Bruner’s skin incision. A needle (size:
20G) used for spinal anesthesia is inserted from the
fingertip and passed through the distal FDP tendon
stump, from distal to proximal. Then, a 2-0 nylon thread
is passed in the proximal tendon stump for 1 to 1.5 cm
from the cut creating an Ω-shaped loop. The needle is
then cut and the two ends of the suture are passed in
the distal tendon stump by the previously inserted
needle. The thread is pulled out from the tip of the
finger and its two ends are secured over a mother-of-
pearl button with multiple knots (Figures 18[A]-1 to
18[A]-6). For all repairs, ensuring correct coaptation of
203
204 Section 2:  Primary Flexor Tendon Surgery

Distal
tendon
stump

Proximal
tendon Figure 18(A)-3  A case of zone 2B flexor tendon injury in a
stump child and skin incisions to expose the tendons.

Figure 18(A)-1  Illustration of the pull-out technique. The

needle is passed through the distal part of the tendon after
an Ω-shaped loop is made in the proximal tendon stump.

Distal
tendon
Figure 18(A)-4  The retracted proximal tendon stump was
stump exposed and pulled distally under the A2 pulley.

Proximal
tendon
stump

Figure 18(A)-2  Passing the thread through the distal Figure 18(A)-5  The Ω-shaped suture was placed in the
tendon stump. proximal stump of the tendon.

Figure 18(A)-6  The thread was passed through the distal
stump of the tendon and tired over a mother-of-pearl button
on the fingertip.
the two tendon ends with good tension is very impor-
tant and depends on the surgeon’s experience. A running
suture with 4-0 suture is added to tighten the tendon
edges. Previously, we used a 4-0 Prolene suture and
noted some foreign body reactions caused by sutures
during long-term follow-up, and suture remnants had
to be removed. We prefer to use absorbable (such as
PDS) sutures presently.
Tendons cut distal to the A2 pulley (in zones 2A
and 2B) can be more easily repaired with this method,
because the distal tendon is shorter and has fewer con-
strictive pulleys. Therefore, it is easier to insert the needle
from the fingertip through the entire distal tendon
stump. For tendons cut at or proximal to the A2 pulley,
the needle will pierce a greater length of the distal tendon
stump with both DIP and PIP joints slightly flexed. After
piercing, the internal guide of a spinal needle is retracted
so that the passage of the 2-0 nylon thread is allowed. We
prefer to use two different passages through the tendon
stump for the thread; it ensures greater tightness of the
system as the suture tension is more evenly spread along
all parts of the tendon during motion.
Whenever possible, the pulley system is respected.
When the A2 or A3 pulley is partially or totally damaged
or when the pulleys must be partially incised to avoid
any impingement of the tendon repair site on the edge
of the pulley, these pulleys are not repaired. When more
pulleys are injured, reconstruction is strongly recom-
mended, especially for A2 and A4 pulleys, to avoid
tendon bowstringing. We prefer to use a flap of extensor
retinaculum (Lister technique) or one of the FDS tendon
slips (when the FDS tendon is not repaired), sutured to
the pulley remnants. A suction drain is placed and the
skin is sutured with absorbable sutures. The drain is
removed 1 day later, and a thinner dressing is made so
that a wider range of active digital motion is allowed.
Chapter 18A:  Mantero’s Technique for Tendon Repair 205
B
Figure 18(A)-7  Seventeen days after pull-out suture repair
of the FDP tendons in the ring and little fingers. Active
flexion and extension exercise are shown.
POSTOPERATIVE CARE
Immediate active motion is the keystone to success with
this technique and it has to start as soon as possible.1-4
In particular, full extension of the proximal interphalan-
geal (PIP) joint must be achieved in the first few days
after surgery. On the first day, the dressing is reduced
and the patient can start active digital motion with the
wrist in a protected position (wrist in flexion). Daily
homework is given to the patient, so that he or she can
be autonomous, not only in moving but also in clean-
ing and renewing the dressings if necessary. One week
later, the wound is checked and any remaining swelling
is controlled. If possible, a smaller dressing is placed to
allow a wider range of motion. The range of active
digital flexion is increased gradually (Figure 18[A]-7).
At about 21 days, it is important to observe whether
there are any early clinical signs of block of tendon
gliding or joint motion. If nothing abnormal is found,
more vigorous and full active digital flexion exercises are
performed.
The patient returns every 6 to 8 days to have the dress-
ing changed and for a wound check. In more recent
206 Section 2:  Primary Flexor Tendon Surgery

years, we have preferred to use absorbable sutures for

skin closure to avoid the need for removal of suture
stitches, which can be painful or quite unpleasant, espe-
cially for young patients. From 30 to 35 days after surgery,
the pull-out suture is cut and the button is removed. The
scab on the tip of the finger, where the button has created
a small bedsore, will fall off within 2 to 3 days with daily
antiseptic cleaning. A rehabilitation program is started
after pull-out removal, with progressive strengthening
active digital flexion from 8 weeks. The average time to
return to work is 10 weeks after injury.
OUTCOMES
We conducted two studies on patients who were treated
with the pull-out technique. Both studies contained
only a portion of the patients who were treated in this
period. The patients included in the two studies were
those living in close proximity to our city, so they could
come to our department for regular follow-up. In the
first study, we followed 46 patients with injuries to 46
FDP or FPL tendons in zone 2 treated with this method
between 2005 and 2008. At postoperative weeks 3, 6,
and 12, we evaluated the total active range of motion
of the distal inter­phalangeal (DIP), PIP, and metacarpo-
phalangeal (MCP) joints; visual analog scale;7 DASH
(Disabilities of the Arm, Shoulder, and Hand) score;
grip strength; and Kapandji test8 (for thumb motion
evaluation during opposition to long fingers). Being
impossible to equally compare all these data, as all the
tests have different numerical ranges, we decided to
make them homogeneous by calibrating their minimum
and maximum values from 0 to 30. According to all the
data provided from the different evaluation systems, we
could obtain poor, fair, good, and excellent results—
“poor” for mean values between 0 and 7, “fair” for
values between 7 and 15, “good” for values between 16
and 21, and “excellent” for values between 22 and 30.
We recorded poor results in 13 patients (28%), fair
results in none, good results in 28 patients (61%), and
excellent results in 5 patients (11%) (Figure 18[A]-8).
Similar to literature data,5 tendon injuries in the ring
and little fingers led to the worst recovery of range of
motion of the hand. No repairs ruptured.
The second study that we carried out between 2005
and 2008 compared two different treatments: (1) 22
patients (22 FDP tendons injured in zone 2) treated by
pull-out technique followed by active digital flexion and
extension exercise and (2) 22 patients (22 FDP tendons
in zone 2) treated with two-strand repair methods
(Tsuge, Kleinert, Kessler, or Kessler-Tajima) followed by
either Kleinert or Duran early motion programs. Our
referring hand therapist evaluated all the patients at 4,
6, 8, and 12 weeks after surgery. We recorded impres-
sively superior results for the patients treated with the
pull-out method: (1) faster recovery of the active range
of digital motion, (2) lower number of rehabilitative
Figure 18(A)-8  Complete recovery of active finger flexion
after surgical repair of FDP tendon of the little finger with
the pull-out method.
sessions, (3) less pain and disability, and (4) earlier
recovery in grip strength. The ultimate total range of
active digital motion was not significantly different, and
repair ruptures were not recorded in either group.
We had no case of deep infection or tendon rupture.
A few patients had superficial infection on the fingertip,
due to prolonged contact of the button on the skin.
The wound healed within a few days after use of local
and oral antibiotics and daily careful disinfection. An
infrequent but serious complication is a permanent
residual loss of extension of the PIP joint, due to late
start of active mobilization. This often occurred in low-
compliant patients. However, they seldom requested
surgical treatment (tenolysis) because the extension
deficits were often only mild and were not bothersome,
creating no serious limitation of function.
DISCUSSION
Because the pull-out technique is not popular outside
of southern Europe, it is difficult to compare our results
with reports in the literature. However, we agree with
Wulle5 that the best results of the pull-out repair method
are achieved in young patients with early tendon motion
exercise, even when injuries of the arteries and/or nerves
coexist. Elder patients have a worse prognosis.
Except for cases involving bone injuries, to which
early motion cannot be applied, all zone 2 tendon cuts
deserve to be treated with this easy, reliable, and fast
method. This pull-out repair method can be used for
FDP tendon injuries in zones 1 and for FPL tendon
injuries in the thumb.1-6,9,10 Owing to reliable strength,

this method also allows use of early motion of the
repaired finger in children. Nevertheless, this method
has not been used popularly so far, possibly because
putting a button on the top of a finger is not considered
“smart” or, more simply, because it is an old technique
and hence “out of fashion.” We believe that these
ideas are prejudicial. Although this method is rarely
included in descriptions of currently prioritized surgical
techniques of repair of flexor tendons, it should be
considered.
References
1. Mantero R, Bertolotti P, Badoino C: Il pull-out in “no man’s
land” e al canale digitale nelle lesioni dei flessori (metodo
personale), Riv Chir Mano 11:119–130, 1973–1974.
2. Mantero R, Bertolotti P: La mobilizzazione precoce nel trat-
tamento dei tendini flessori al canale digitale, Revista Esp Chir
Mano 5:35–43, 1975.
3. Mantero R, Bertolotti P: La mobilisation précoce dans le trait-
ement del lesions des tendons fléchisseurs au canal digital,
Ann Chir Main 30:889–896, 1976.
4. Grandis C, Rossello MI: Dieci anni di esperienza con il pull-
out intertendineo nella chirurgia dei tendini flessori al canale
digitale (zona 1–2), Riv Chir Mano 25:43–49, 1988.
5. Wulle C: Flexor tendon suture in zone 1 and distal zone 2 by
the Mantero technique, Ann Hand Upper Limb Surg 11:200–
206, 1992.
Chapter 18A:  Mantero’s Technique for Tendon Repair 207
The advantages of this technique are easy technical
execution, cheap (and easy to find) surgical materials,
reliability of repair strength, and no need to wear a
splint. The pull-out system is of particular merit in the
case of tendon injuries in multiple fingers because it
allows active motion of these fingers. Rupture of the
suture or infection of the tip of the finger is rare, even
if the patient is not quite compliant. Postoperatively few
dressings are needed; at 30 to 35 days, the thread passing
though the fingertip is cut and the button is removed.
6. Guinard D, Montanier F, Thomas D, et al: The Mantero
flexor tendon repair in zone 1, J Hand Surg (Br) 24:148–151,
1999.
7. Ohnhaus EE, Adler R: Methodological problems in the mea-
surement of pain: a comparison between verbal rating scale
and the visual analogue scale, Pain 1:379–384, 1975.
8. Kapandji A: Clinical test of apposition and counter-apposition
of the thumb, Ann Chir Main 5:67–73, 1986.
9. Elliot D, Southgate CM: New concepts in managing the long
tendons of the thumb after primary repair, J Hand Ther 18:
141–156, 2005.
10. Schaller P: Repair of the flexor pollicis longus tendon with
the motion-stable Mantero technique, Scand J Plast Reconstr
Surg Hand Surg 44:163–166, 2010.
 B Teno Fix for Tendon Repair
Antonio Merolli, MD, FBSE, Lorenzo Rocchi, MD, and
Francesco Catalano, MD
OUTLINE
We present our experience with the Teno Fix Tendon
Repair System (Ortheon Medical, Winter Park, Florida)
device for primary flexor tendon repair in digits. We
treated 22 patients presenting with laceration of a
single flexor digitorum profundus or superficialis
tendon or flexor pollicis longus tendon within the
digital sheath in zone 2; the mean follow-up was 16
(range, 6 to 26) months. Of the 22 patients, the results
according to the Strickland’s total active motion crite-
ria were excellent in 12, good in 6, and fair in 4.
Radiography revealed rather smooth gliding of the
repaired tendon after surgical implantation of the
device. However, in our series, the results of four
patients were not satisfactory, and the device was
removed from three of them. The other patients did
not complain of discomfort, nor have they required
secondary surgery for removal of the device after
tendon healing, with the longest follow-up being 7
years. This device is practical clinically and can produce
strong tendon repairs that withstand early active finger
motion. Use of this device may ensure a quicker recov-
ery and return to work after surgery. However, we also
present possible reasons for unsatisfactory recovery in
four cases in our series.
Our main motivation for testing the Teno Fix Tendon
Repair System device (Ortheon Medical, Winter Park,
Florida) in the clinic is the way it interfaces with the
fibers of the tendon. Specifically, Teno Fix does not
apply tractional force to a small number of fibers con-
stricted inside a knot; instead, it distributes traction
more evenly along a greater number of fibers. Despite
being compressed into the small volume of the anchor-
ing system, those fibers maintain their physiological axis
of elongation.
The Teno Fix device has been marketed as a practical
clinical tool, able to produce strong tendon repairs that
withstand early active finger motion.1-6 It is advisable to
mobilize the tendon with either passive or active flexion
as soon as possible, to prevent adhesions. Late initiation
of finger mobilization would increase the risk of an
incomplete functional recovery.7-10
*Conflict of interest: The authors have no financial relation-
ship with the manufacturer or the distributors of the device.
208
We present clinical findings on our early patients
treated with Teno Fix, including detailed follow-up. We
also performed mechanical tests of two devices from our
hospital inventory.
A BIOMECHANICAL STUDY
The Teno Fix is a stainless steel device (ASTM F138-00)
composed of two intratendinous spindle–coil com-
plexes (the “anchor”) joined by a multifilament 2-0
stainless steel suture (the “wire”). The anchor is
composed of a spiralling cork-screw-like coil around
a hollow spindle core (Figure 18[B]-1A). The early
anchor that we used was 2.0 mm in diameter and
4.0 mm in length; a smaller anchor is now available.
Two stop-beads are used for tensioning the wire. One is
secured by the manufacturer, while the other must be
crimped intraoperatively by the surgeon (with the help
of a dedicated instrument). This latter step seemed to
us to be the weak point of the device, since in clinical
practice the strength of the stop grain is crucial for the
mechanical performance of the device. For this reason,
we tested two devices randomly chosen from the stan-
dard inventory of the hand clinic.
To evaluate the load needed to pull out the lower and
upper stop grains from the wire and the load at which
the wire itself starts rupturing, a metal plate with a suit-
able hole was used to constrain each grain, allowing us
to test the effective strength of the grain-wire assembly.
A wire length of 15 mm (common in clinical practice)
was chosen. Two grips were used to hold the plate con-
straining the grain and the end of the wire. The tests
were performed in a tensile mode at 1 mm/min, using
a material testing machine (Model 5566; Instron Corp,
Norwood, Massachusetts) with a load cell of 100 N
(Figure 18[B]-1B).
Results showed a typical load-displacement curve
that was linear until a maximum load value was reached
(Figure 18[B]-1C). Maximum load values of 56.7 and
58.9 N were recorded (greater than the mean stated by
the manufacturer). Although the wires became damaged
in tests, it was notable that the stop grains were not
pulled out (Figure 18[B]-1D).
We believe these data support the conclusion that the
device withstands loads in excess of those likely to be
encountered in clinical practice. They also support the
conclusion that crimping the grain intraoperatively is a
suitable procedure.
 Chapter 18B:  Teno Fix for Tendon Repair 209

CLINICAL TECHNIQUES AND OUTCOMES

We report on treating 22 patients presenting primary
flexor tendon injuries within the digital sheath in zone
2. Results were assessed after a mean of 16 (6 to 26)
months of follow-up.
Clinical end points assessed included a comparison
in range of active motion according to the Strickland
and Glogovac method9,10 of the distal and proximal
A interphalangeal (DIP and PIP, respectively) joints of the
finger as well as a recording of the linear measurement
of pulp–to–distal palmar crease distance.11 We adopted
the Strickland criteria in the documentation of out-
comes of flexor tendon repair in zones 1 and 2, because
we find these criteria more practical than the total active
motion (TAM) method advocated by the American
Society for Surgery of the Hand (ASSH). In fact, some
degree of joint stiffness is always present after tendon
repair, making patients with normal TAM rare. With the
Strickland method, excellent functional status requires
a sufficiently large total range of active digital motion
but not necessarily the same range as on the contralat-
eral side.12

Patients
There were 14 men and 8 women, with a mean age of
32 (range, 18-46) years, presenting with a complete
B tendon transsection caused by a sharp blade injury, in
flexor digital sheath zone 2 (the subdivision zones
60
defined by Tang12-14 were followed). Lesions were treated
50 on the thumb (3 patients) and index (12 patients),
middle (3 patients), ring (1 patient), and little (3
40 patients) fingers. The study reports the complete experi-
Load (N)

ence of the authors, and no patient was lost to follow-up

30 before end results were determined.
20 Inclusion Criteria
10 All patients were treated within 12 hours of injury, and
the injured flexor tendons were treated primarily. Four
0 kinds of lesions were included in this case series: (1)
0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 complete transsection of the flexor digitorum profundus
C Displacement (mm) (FDP) tendon without or with only minor negligible
lesion of the flexor digitorum superficialis (FDS) tendon
at zones 2B or 2C; (2) complete transsection of the FDP
tendon without concomitant lesion of the FDS tendon,
at zone 2A; (3) complete transsection of the FDS alone,
at zone 2D (the authors propose surgical intervention
in young and active patients; the reason is that even if
D
finger motion remains normal when only the FDP is
Figure 18(B)-1  A, The spindle–coil complex (the “anchor”) present, cumulative grip strength is reduced); and (4)
positioned on the needle of its delivery tube. B, The second complete transsection of the flexor pollicis longus (FPL)
stop-bead, with the multifilament wire already in place,   tendon at zone 2.
held by the dedicated crimping instrument. C, A load-
displacement curve shows a linear trend, with a sawtooth Exclusion Criteria
denoting the partial breaking of wire filaments. D, At the In the interest of simplification, patients with injuries
time of failure under load, the wires were broken, but stop
of both flexor tendons or accompanying injuries (of the
grains were not pulled away from the wire.
210 Section 2:  Primary Flexor Tendon Surgery

vessels or joints) or fractures were excluded. Because of
the diameter of the anchors, children were excluded
from the study as well as some adult patients presenting
lesions in comparably small fingers (most often, the
little finger).
Operative Techniques
Under brachial plexus block anesthesia, after the skin
has been incised according to Bruner, the injured tendon
stumps are exposed. A longitudinal palmar split is made
about 10 mm from the cut edge, to accommodate the
obturator and the delivery tube, which contains the
anchor–coil complex. The tendon sheath at this level is
often disrupted by the trauma; however, a limited lon-
gitudinal incision can be made if necessary. Either proxi-
mal or distal stumps can be chosen as the first point of
entry, according to clinical need (Figure 18[B]-2A).
Once the complex has been gently twisted into place,
the straight needle with the stainless steel suture and the
built-in stop-bead (the “wire”) is passed through the
hole in the core, until the bead comes into contact with
the complex. After the wire has passed through the
second anchor and the second stop-bead (allocated into
the preloaded crimping instrument), the stumps are
gently redirected into the tendon sheath and under the
pulleys, to be held together under proper tension. The
second stop-bead is crimped and the excess wire is cut
away. A continuous epitendinous 6-0 nylon suture com-
pletes the repair, while the longitudinal tenotomies are
sutured by buried knots. We never found it necessary to
close the sheath, although we repaired the pulleys
whenever necessary.
Postoperative Care
The most attainable active digital flexion to the palm
was allowed beginning on the first postoperative day.
Extension was limited by placing the hand in a plaster
cast with both the wrist and metacarpophalangeal
(MCP) joints flexed at 30° until the 14th postoperative
day. Afterward, the plaster cast and the skin suture were

A B

D
Figure 18(B)-2  A, FDP tendon cut in the index finger in a patient. We chose the proximal stump as the first point of entry.
B and C, Despite an initial effort at early active and passive motion, after 20 days, rehabilitation was discontinued and rigidity
of the index finger ensued. D, We removed the device after 5 months and performed a cruciate repair.

removed. A dorsal splint in neutral wrist position was
applied until the 28th day for limiting wrist extension.
Complete active motion of all the fingers was allowed
(apart from flexion against resistance and forced passive
extension).
The patients were monitored on outpatient visits
weekly during the first month and then at 2, 6, 12, and
24 months. Anterior and lateral x-ray films in flexion
and extension were taken on the 14th and 60th postop-
erative days.
Outcomes
Of the 22 patients, function was excellent in 12, good
in 6, and fair in 4 by the Strickland criteria 12 months
after surgery. The four patients who scored a “fair” had
an unsatisfactory outcome, and in three of them the
device was removed; the details are given below. The first
patient fell accidentally after surgery, provoking a forced
hyperextension and the eventual tendon rupture around
the anchors; the device did not rupture but was removed.
The second patient required the removal of the device
because of a low-grade sepsis that gave persistent pain;
the use of Teno Fix was probably a poor choice for this
patient, who presented with a torn and poorly vascular-
ized wound at the time of surgery. The third patient was
extremely noncompliant and did not follow any reha-
bilitation instructions. The fourth patient, despite an
initial effort at early active motion (Figure 18[B]-2B
and C), failed to continue a rehabilitation program, and
ended up with a rigidly extended finger. The device was
removed (Figure 18[B]-2D). As with all other removals
of the device, we performed a traditional cruciate repair
for the tendon. However, failure to comply with a reha-
bilitation regimen resulted in novel rigidity.
In the remaining 18 patients (i.e., six FDP cuts at
zones 2B or 2C, 5 FDP cuts at the border of zone
2A, 4 FDS cuts at zone 2D, and 3 FPL cuts), we found
notable that patients returned to work after a mean
of 34 (±12) days, a comparatively short period. We
extended use of this device in treating disruption of the
FPL tendon of the thumb and outcomes were excellent
(Figure 18[B]-3A and B).
Dynamic x-ray films in full flexion and full extension
showed that the device did not interfere with the
pulleys, since no blockage of the repaired tendon
occurred under them. This proved true with a critical
pulley like the A4 in distal zone 2A lesions (Figure
18[B]-3C) and with another critical pulley like the A2
(Figure 18[B]-3D).
In 14 cases of the series, radiographs taken 2 months
after surgery showed that the anchors had slid closer to
the junction site (see Figure 18[B]-3C). This has been
interpreted as a sign of effective tendon scarring, which
involves a physiological contracture of the stump tissue.
However, in the other cases anchors were not displaced,
even in the long term (see Figure 18[B]-3D).
Chapter 18B:  Teno Fix for Tendon Repair 211
DISCUSSION
Advantages
An ideal tendon repair should be simple and reproduc-
ible in execution, of immediately high strength, take up
only a small amount of space within the sheath, produce
negligible gaps, allow vascularization, and tolerate early
active tendon mobilization. Many proposed techniques
are adequate in tensile strength but are technically
demanding, requiring excessive tendon manipulation
and possibly increasing the tendon bulk.14-17 Teno Fix
respects the vascular perfusion provided by the vincula
vessels. Tendon repairs with this device do not directly
involve the surfaces of the tendon cut and do not require
knots to be placed between tendon cut surfaces. This
characteristic facilitates the closure of the epitenon,
favoring reestablishment of tendon continuity.19,20
We noted that this device has a unique feature: the
intratendinous complex inserted in the tendon belly
allows the tendon collagen fibers, caught between the
coil and the core, to maintain their physiological elon-
gation. This happens without excessive twisting and/or
constriction of the tendon fibers, which is more likely
in repairs using ordinary surgical sutures. Surgical suture
repairs may interfere with vasculature of the tendon
and produce a well-demarcated acellular zone in tied
knots.21
We compared results in the literature from clinical
series of traditional treatment of flexor tendon injuries
in zone 2 with our results with Teno Fix. They are in the
same range when the Strickland criteria and percentage
of rupture are considered.22 However, Teno Fix appears
to have faster functional recovery and return to work. In
our series, the average time needed to return to work
was only 34 days.
We did not receive any complaints or requests for
removal of the device in the long term, and our oldest
case now dates back 7 years. We believe it is not neces-
sary to remove the device after successful healing because
of the possible damage to healed tendons, presenting a
risk that far outweighs the benefits of not having an
artificial device in place.
Disadvantages
Because of the diameter of the anchors, use of the Teno
Fix is not indicated in children or some adult patients
presenting with lesions in comparably small fingers, like
the little finger. Regarding possible risk of infection due
to the presence of a metallic device, in our opinion the
Teno Fix is not indicated in treatment of dirty lesions or
generally in complex multiple lesions. Because it requires
good-quality tissue in the stumps receiving the anchors,
the device is not indicated in case of fraying cut tendons.
Finally, the need for full patient compliance with the
rehabilitation program suggests that the device should
not be used with uncooperative patients. All these are
212 Section 2:  Primary Flexor Tendon Surgery

A B

AP LL

sb

a
sb

D
Figure 18(B)-3  A and B, Good results were obtained in the thumb, as shown in this patient 22 months after surgery.
C, Dynamic x-ray films taken after 2 months showed that the anchors (a, anchor; sb, stop-beads) had slid toward the junction
site in the majority of patients. This is interpreted as a sign of effective tendon healing and scarring, which involves a
physiological contracture of the stump tissue. D, In the other cases, anchors were not displaced, even after 2 years.

clear disadvantages that argue against the use of Teno
Fix in these clinical settings. In our series, this treatment
was not the right choice for four patients, giving us fair
results and a reoperation rate no lower than in recent
reports of primary flexor tendon repairs in zone 2.
We should acknowledge that in our case series, only
a single flexor tendon was injured, which calls for a
relatively simple clinical response. We do not know
whether this device would work well for patients with
simultaneous injuries of both FDS and FDP tendons. In
addition, four of our cases did not recover satisfactory
function. Three of those four required removal of the
device, and we then performed a traditional four-strand
cruciate repair to provide some kind of treatment.
However, we must also note that two of the four patients
with unsatisfactory outcomes were unable to comply
with a rehabilitation regimen, a requirement in recovery
from tendon surgery. In the other two patients with
unsatisfactory outcomes, we stress that the reasons for
removal (forced hyperextension and low-grade sepsis)
were not directly associated with the device itself. The
drawbacks and limitations revealed in our case series
should be taken into consideration when this device is
used in future cases.
Acknowledgments
We would like to thank Professor Luigi Ambrosio and
Dr. Antonio Gloria from the Institute of Biomedical
Composite Materials (Naples, Italy) for their coopera-
tion in performing mechanical tests. Figures 18-1A and
18-3, A–D, are used with permission from Springer
Verlag, Heidelberg-New York.

References
1. Lewis N, Quitkin HM: Strength analysis and comparison of
the Teno Fix Tendon Repair System with the two-strand modi-
fied Kessler repair in the Achilles tendon, Foot Ankle Int
24:857–860, 2003.
2. Su BW, Protopsaltis TS, Koff MF, et al: The biomechanical
analysis of a tendon fixation device for flexor tendon repair,
J Hand Surg (Am) 30:237–245, 2005.
3. Su BW, Solomons M, Barrow A, et al: Device for zone-II flexor
tendon repair. A multicenter, randomized, blinded, clinical
trial, J Bone Joint Surg (Am) 87:923–935, 2005.
4. Su BW, Raia FJ, Quitkin HM, et al: Gross and histological
analysis of healing after dog flexor tendon repair with the
Teno Fix device, J Hand Surg (Br) 31:524–529, 2006.
5. Su BW, Solomons M, Barrow A, et al: A device for zone-II
flexor tendon repair. Surgical technique, J Bone Joint Surg
(Am) 88(Suppl 1 Pt 1):37–49, 2006.
6. Wolfe SW, Willis AA, Campbell D, et al: Biomechanic com-
parison of the Teno Fix tendon repair device with the cruciate
and modified Kessler techniques, J Hand Surg (Am) 32:356–
366, 2007.
7. Kitsis CK, Wade PJ, Krikler SJ: Controlled active motion fol-
lowing primary flexor tendon repair: a prospective study over
9 years, J Hand Surg (Br) 23:344–349, 1998.
8. Peck FH, Bucher CA, Watson JS: A comparative study of two
methods of controlled mobilization of flexor tendon repairs
in zone 2, J Hand Surg (Br) 23:41–45, 1998.
9. Strickland JW, Glogovac SV: Digital function following flexor
tendon repair in Zone II: A comparison of immobilization
and controlled passive motion techniques, J Hand Surg (Am)
5:537–543, 1980.
10. Strickland JW: Flexor tendon surgery. Part 1: primary flexor
tendon repair, J Hand Surg (Br) 14:261–272, 1989.
Chapter 18B:  Teno Fix for Tendon Repair 213
11. Boyes JH: Flexor tendon grafts in the fingers and thumb: an
evaluation of end results, J Bone Joint Surg (Am) 32:489–499,
1950.
12. Tang JB: Clinical outcomes associated with flexor tendon
repair, Hand Clin 21:199–210, 2005.
13. Tang JB, Shi D: Subdivision of flexor tendon “no man’s land”
and different treatment methods in each sub-zone. A prelimi-
nary report, Chin Med J 105:60–68, 1992.
14. Tang JB, Shi D, Gu YQ, et al: Double and multiple looped
suture tendon repair, J Hand Surg (Br) 19:699–703, 1994.
15. Wade PJ, Wetherell RG, Amis AA: Flexor tendon repair: sig-
nificant gain in strength from the Halsted peripheral suture
technique, J Hand Surg (Br) 14:232–235, 1989.
16. Trail IA, Powell ES, Noble J: The mechanical strength of
various suture techniques, J Hand Surg (Br) 17:89–91,
1992.
17. Barrie KA, Tomak SL, Cholewicki J: Effect of suture locking
and suture calibre on fatigue strength of flexor tendon repairs,
J Hand Surg (Am) 26:340–346, 2001.
18. Strickland JW: Flexor tendon repair, Hand Clin 1:55–68,
1985.
19. Strickland JW: Development of flexor tendon surgery:
twenty-five years of progress, J Hand Surg (Am) 25:214–235,
2000.
20. Ketchum LD: Suture materials and suture techniques used in
tendon repair, Hand Clin 1:43–53, 1985.
21. Wong JKF, Cerovac S, Ferguson MWJ, et al: The cellular effect
of a single interrupted suture on tendon, J Hand Surg (Br)
31:358–367, 2006.
22. Rocchi L, Merolli A, Genzini A, et al: Flexor tendon injuries
of the hand treated with Teno FixTM: mid-term results,
J Orthop Traumatol 9:201–208, 2008.
 CHAPTER

19  
TREATMENT OF RUPTURE
OF PRIMARY FLEXOR
TENDON REPAIRS
David Elliot, MA, FRCS, BM, BCh

strength. Two curious facts should make us wary of

OUTLINE
Clinical series of primary flexor tendon repairs world-
wide, using a variety of suture materials and suture
configurations, all include a small, but ever present,
rupture rate. That the assumption that stronger sutures
will “cure” the problem may be false is discussed and
the role of the sheath and of the patient considered.
Immediate re-repair of ruptures has been carried out
for many years without analysis of the success of this
procedure. This chapter discusses a study of the effec-
tiveness of immediate re-repair of ruptures of the
primary repair. It identifies that this works adequately
for all digits but the little finger. Possible modifica-
tions of the method of re-repair used in this study
which might improve the results are discussed and an
alternative management plan for the little finger is
considered.
Rupture of the tendon repair, or detachment of the rein-
serted tendon, if recognised immediately, should be treated
with prompt re-exploration and repair.
Leddy, 19821
With a few exceptions, most studies published during
the past 25 years discussing acute flexor tendon repair
and early mobilization report a rupture rate of between
3% and 9%. In studies of less than 100 patients, which
are the norm for this field, these figures indicate negli-
gible differences in the number of patients with rup-
tured tendon repairs in different units using a multitude
of core and circumferential suture techniques and many
variations of the three basic regimes of early postopera-
tive mobilization.
THE SUTURE
Survey of the many new suture techniques used through-
out the past 20 years confirms that the Savage six-strand
suture2,3 is still the strongest suture, although it is diffi-
cult to use. One could argue that 20 years have been
spent trying to achieve a simpler suture with equal
this search for the perfect suture configuration. Savage
reported one rupture in 20 fingers and 3 thumbs with
zone 2 complete flexor divisions repaired with a six-
strand suture, a rupture rate in the fingers of 5% or
a rupture rate of 3% overall.2 Harris et al,4 reporting
results from my own unit from June 1989 to December
1996, recorded 17 ruptures in a series of 397 fingers
(4%) with zone 2 complete flexor divisions using a two
strand modified Kessler core suture. So simply putting
in more complex sutures is possibly not the answer, or
not the only answer.
A very interesting laboratory study from Professor
McGrouther’s laboratory in Manchester5 showed that
even a single suture passed through a tendon signifi-
cantly affects the cell population of the tendon around
it: the suture foreign body causes the tenocytes to move
away. So, perhaps, we are, unwittingly, making tendon
repair breakdown more likely as we put more foreign
suture material into the tendon.
THE PATIENT
This may be the reason why we cannot get past an inevi-
table rupture rate, although it is probably more likely
that it is simply human nature that is defeating us. In
1999, we highlighted the role of patient irresponsibility
in the etiology of rupture of primary flexor tendon
repairs.4 This study included 526 fingers in 440 patients
with primary flexor tendon repairs in zones 1 and 2 who
underwent surgery and postoperative mobilization in a
controlled or early active motion. Twenty-three patients
ruptured 28 tendon repair(s) in 23 fingers, an overall
rupture rate of 4%. Eleven of these, just less than half,
occurred as a result of patients using the hand, in or out
of their splint, against therapy advice. It is likely than
this figure is an underestimate of this problem of patient
noncompliance in this population worldwide.
THE SHEATH
In a laboratory study, Tang et al6 identified a further
possible factor in the etiology of these ruptures. These

214
 Chapter 19:  Treatment of Rupture of Primary Flexor Tendon Repairs
Table 19-1  Timing of Ruptures of Primary Finger
Flexor Tendon Repair in a Total of 62 Fingers
Mechanical Infective
Time After Primary Ruptures Ruptures
Repair (Wk) (n = 57) (n = 5)
<1 6 2
1-2 23 0 cumstances of the 62 fingers in 61 patients who ruptured
2-3 9 2
3-4 7 1
4-5 6 0
5-6 2 0
6-7 2 0
7-8 1 0
8-9 1 0
authors suggested that repair rupture is most likely to
occur at sites where tendons glide over a rim of a major
pulley or over gliding curves of a small diameter, char-
acteristics found typically in zone 2B repairs and repairs
of tendons in little fingers. In our study, described later,
32 of a total of 42 fingers (77%) requiring re-repair of
the flexor tendons occurred in zone 2B and/or in little
fingers.7
TIMING OF OCCURENCE OF THE RUPTURE
The times after primary repair at which the ruptures
occurred are shown in Table 19-1, which contains infor-
mation from our unit in 62 fingers in 61 patients who
ruptured primary zone 1 and 2 finger flexor tendon
repairs. The average time to rupture of the primary
repairs was 18 days (range, 3 to 61 days). The highest
incidence of rupture of primary finger flexor tendon
repairs was seen in the second week after surgery. The
incidence of rupture was higher in the first 5 weeks after
surgery than in the later 4 weeks (weeks 6 to 9).
IMMEDIATE RE-REPAIR OF RUPTURES
Little has been published specifically about the manage-
ment of ruptured primary flexor tendon repairs. For 20
years, the quotation at the beginning of this chapter has
been the teaching on the management of rupture of
primary flexor tendon repairs of the fingers in zones 1
and 2 during the early part of the rehabilitation program.
While most experienced clinicians would agree with this
opinion, this statement was made without published
evidence to support it. The available literature in the
period immediately following Leddy’s statement sug-
gested that he was correct.4,8-11 However, the numbers of
ruptures and re-repairs in these studies, which were pri-
marily concerned with the surgical management and
215
rehabilitation of the initial tendon division, were rela-
tively small and the studies were not focused on the
results of re-repair.
THE RESULTS OF RUPTURE RE-REPAIR
In view of the paucity of data on the results of immedi-
ate re-repair, we carried out a study to examine the cir-
primary zone 1 and 2 finger flexor tendon repairs in
our unit over a 14-year period, from 1989 to 2003, and
reported the outcome of immediate re-repair of the rup-
tured tendons in those fingers in which re-repair was
undertaken.7 This study remains the major work on this
subject to date.
There are some absolute contraindications to attempt-
ing re-repair after rupture, such as poor general health
precluding either regional or general anesthesia, infec-
tion of the involved finger, and a mental status of the
patient incompatible with cooperation with therapy.
Most other contraindications are relative but may
constitute logical reasons not to attempt to re-repair a
rupture of a primary finger flexor tendon repair in a
particular individual or in a particular finger. These
include advanced or very young age, the general medical
status of the patient, the suitability and compliance of
the patient, other pathologies or injuries of the affected
hand or digit, rupture of the flexor digitorum profundus
(FDP) tendon in the presence of a functioning flexor
digitorum superficialis (FDS) tendon with a good range
of motion of the proximal interphalangeal joint, palmar
skin loss of the affected digit or excessive stiffness, and/
or swelling of the digit. It is commonly thought that
re-repair should be performed no more than 48 to 72
hours from rupture, although there are no data to
support this cut-off time. After 5 weeks from the primary
repair, the digit is often at that stage of the healing
process when it is hard and “wooden” and re-repair is
difficult and may endanger other structures in the opera-
tive field. The re-repair is also very likely to stick post-
operatively. In our study, the average time to rupture of
the primary repairs was 18 days (range, 3 to 61 days),
so most ruptures fall within the time when this factor
does not prevent re-repair. Patients may also decline
further surgery for various reasons. In our study, two
patients in whom only the FDP repair had ruptured,
leaving an “FDS-only” finger with full proximal inter-
phalangeal (PIP) joint flexion, declined to undergo
re-repair. A third patient, who ruptured both tendon
repairs, declined re-repair for business reasons. He, sub-
sequently, underwent a two-stage tendon graft proce-
dure at a more convenient time with a good result.
Although it is usually possible to re-repair the rup-
tured tendon(s) if correct decisions have been made
preoperatively, it can become obvious at surgery that
this will be difficult, impossible or unwise. It is impor-
tant that the patient be informed of this possibility
216 Section 2:  Primary Flexor Tendon Surgery

preoperatively. The tendons may be too swollen,
although this can often be overcome by single tendon
repair and excision of the whole, or half, of the FDS
tendon. The proximal end of the tendon may have
retracted too far. This is most commonly a problem of
the long flexor tendon of the thumb but can occur with
finger flexor tendons. It can often be overcome by
lengthening the proximal tendon, using either the Le
Viet technique12 or conventional tendon lengthening at
the wrist, although this was not necessary in our series.
The alternatives to immediate re-repair should be
discussed carefully with the patient preoperatively both
to allow informed consent and in case re-repair proves
impossible. Making a discussion intraoperatively will be
impossible if general anesthesia has been used initially
or after failure of regional anesthesia. Where immediate
re-repair is clearly impossible preoperatively, or it
becomes apparent during surgery that re-repair is impos-
sible, the options include (1) doing nothing further; (2)
single-stage tendon grafting; (3) the first stage of two-
stage tendon grafting, i.e., insertion of a silicone rod;
and (4) tendon transfer. Doing one of these may convert
the failure of the primary intention to re-repair the
flexor tendon(s) into a useful operation.
In our series, it was not possible to carry out immedi-
ate re-repair in 18 fingers (29%) in 18 (30%) patients,
approximately one-third of cases. The reasons for not
re-repairing the ruptured tendon repairs in these cases
included infection in five cases, poor previous compli-
ance with therapy in four cases, patient choice in three
cases, general medical problems in two cases, dense
scarring in the flexor sheath and frayed tendon ends in
two cases, a large gap between the tendon ends preclud-
ing direct suture of the tendon without undue tension
in one case, and an overly long delay of 9 days between
tendon rupture and presentation in one case. This list
emphasizes some of the more common considerations
of management.
Immediate re-repair of the flexor tendons was per-
formed in 44 fingers (71%) in 43 (70%) patients. All
were carried out within 48 hours from the rupture. Two
fingers in two patients were excluded from analysis of
the effectiveness of immediate re-repair because the sub-
sequent poor results were considered an unfair repre-
sentation of the result of the immediate re-repair
procedure. One patient developed chronic regional pain
syndrome (CRPS) type 1 postoperatively and one had
severe osteoarthritis of multiple joints in all of his
fingers. Five patients re-ruptured their re-repairs in five
fingers and so were excluded from analysis of the effec-
tiveness of immediate re-repair.
In the remaining 37 fingers in 36 patients, the results
were assessed using the original Strickland method13
(Table 19-2). This group of patients included 31 men
(average age, 36 years; range, 30 to 58 years) and five
women (average age, 23 years; range, 16 to 32 years).
Eighteen fingers had primary repair of both the profun-
dus and superficialis flexor tendons (FDP, FDS). In nine
of these fingers, both tendon repairs had ruptured. In
eight of these, both tendons were re-repaired, while only

Table 19-2  Results of Immediate Re-Repair of Ruptures of Primary Flexor Tendon Repairs and Distribution of
Ruptures of Primarily Repaired Tendons Among Different Fingers at the St Andrew’s Centre for Plastic Surgery,
Chelmsford, UK
Locations Excellent Good Fair Poor Second Rupture Total
Results by fingers
All fingers 9 (24%)* 10 (27%) 5 (14%) 13 (35%) 5 42
Index 2 4 1 1 0 8
Middle 4 3 0 4 1 12
Ring 1 0 0 1 0 2
Little 2 3 4 7 4 20
Results by locations in fingers
Zone 1 1 (20%) 2 (40%) 0 (0%) 2 (40%) — 5
Zone 2 8 (25%) 8 (25%) 5 (16%) 11 (34%) — 32
Zone 2A 0 1 0 0 — 1
Zone 2B 5 5 4 7 — 21
Zone 2C 2 2 1 3 — 8
Zone 2D 1 0 0 1 — 2
*The percentages shown are only for the 37 fingers which were rehabilitated successfully.
 Chapter 19:  Treatment of Rupture of Primary Flexor Tendon Repairs
FDP was re-repaired in one finger, with no reason being
given by the operating surgeon as to why FDS was not
re-repaired. In the other nine of these fingers, rupture of
the FDP repair only occurred and immediate re-repair of
the FDP was performed. Nineteen fingers, including five
zone 1 injuries, had primary repair of FDP only, so only
this tendon repair ruptured. All nineteen underwent
re-repair of this tendon alone. Of the 37 re-repairs, nine
(24%) had excellent, 10 (27%) had good, 5 (14%) had
fair, and 13 (35%) had poor results (see Table 19-2).
Earlier studies mentioning the results of immediate
re-repair of zone 1 and 2 finger flexor tendon injuries
after rupture of primary repairs during rehabilitation
suggest that immediate re-repair can achieve an excel-
lent or good result in just over 60% of cases. This study,
specifically examining this option of treatment in a
larger number of fingers, does confirm that immediate
re-repair is feasible in cases which present within 48
hours of rupture but only achieved excellent or good
results in just over 50% of the fingers. While flexor
tendon grafting may achieve better results in the hands
of some surgeons and in some patients, it should be
remembered that these patients include many who are
unlikely to achieve excellent or good results by any
method of treatment.4
RUPTURE OF THE RE-REPAIR
In this study, second rupture was also associated with a
high incidence of noncompliance. That only 50% of the
patients in this series achieved excellent or good results
after immediate re-repair of ruptures of previous tendon
repairs may be a realistic expectation for this subgroup
of patients. Nevertheless, this, and the fact that 5 of the
41 patients in this study ruptured the re-repairs again
(see Table 19-2), is a poor result that brings into ques-
tion a universal policy of immediate re-repair of all
ruptured primary finger flexor tendon repairs and alter-
natives should be considered.
POSSIBLE MODIFICATIONS OF THE RE-REPAIR
In our study, all of the tendons were re-repaired using
the same technique, which had been used in the primary
repair, namely the modification of the two-strand
Kirchmayr/Kessler core suture14,15 in which the suture is
tied with a single intratendinous knot, and a continuous
circumferential suture. Core sutures of 3-0 or 4-0 poly-
propylene (Prolene) and a continuous circumferential
suture of 5-0 or 6-0 nylon (Ethilon) or polypropylene
were used in all tendons, with the suture sizes being
chosen according to tendon size. The repairs were mobi-
lized postoperatively using the same technique as used
after the primary repair, namely a variation of the
controlled, or early, active motion regimen previously
described in 1989 in Belfast,9,11 for a minimum of 8
weeks. Use of stronger suturing techniques might seem
appropriate to withstanding the forces of rehabilitation
217
and/or additional unadvised use of the hand after
re-repair, provided the resulting repair is not so thick as
to preclude free gliding within the sheath. However, the
size of the re-repair is more likely to be a problem in
this respect than at the time of primary repair as the
fingers involved are already edematous from the primary
injury and repair. This limitation was initially identified
in primary repair when increasingly complicated cir-
cumferential repairs were used,16 and our clinical experi-
ence supports this finding. For reasons discussed
previously, simply putting in more complex sutures may
not be the answer, or not the only answer.
Given the above, single tendon re-repair may also be
more appropriate after double tendon rupture. In this
study, both previously repaired tendons ruptured in
nine fingers. Both were re- repaired in eight fingers. This
policy may be one of perfection that should be modi-
fied. However, five (62.5%) of these eight fingers had
excellent or good results. It is certainly easier to repair
one tendon only as the tendons are swollen and the
tendon ends are more frayed and less easily handled at
re-repair than primary repair. Removing the FDS tendon
from the finger to reduce the likelihood of the tendons
sticking under the A2 pulley is a further step to reducing
the possibility of tendon adhesion. This is unlikely to
result in PIP swan-necking as these fingers mostly have
shortened PIP palmar plate ligaments as a result of their
postinjury/operative state. The extensibility of this joint
can easily be tested intraoperatively and appropriate
tenodesis of the distal part of the superficialis tendon
across the proximal interphalangeal joint carried out, if
necessary.
THE LITTLE FINGER
In previous studies, we have found difficulty achieving
good results in the little finger after primary repair.17
This experience is repeated in this series of re-repair of
ruptures of the primary repairs. The percentage of rup-
tures of primary repairs was very much greater in the
little finger (46%) than in the other fingers and second
rupture was almost exclusively a problem of the little
finger, with four of the five re-ruptures occurring in the
little finger (see Table 19-2). The number of excellent
or good results after immediate re-repair of ruptured
primary repairs in the index and middle fingers was
higher than in the ring and little fingers and only 5 of
20 re-repairs in the little finger achieved excellent or
good results. Certainly, there are technical difficulties to
repairing the small tendons and to rehabilitation of this
finger and, possibly, higher risks to the repair in the
border digit.
As mentioned earlier, Tang et al6 suggested that repair
rupture is most likely to occur at sites where tendons
glide over gliding curves of a small diameter, a charac-
teristic found typically in repairs of tendons in little
fingers. These figures support a policy of no re-repair in
218 Section 2:  Primary Flexor Tendon Surgery
patients who rupture primary flexor tendon repairs of
the little finger. Unfortunately, even when only the FDP
tendon of the little finger has ruptured, doing nothing
may not be an option as the FDS tendon may be absent,
or too weak, to provide sufficient PIP joint flexion for
useful function. In this difficult finger, particularly in a
less than ideal patient, we would not contemplate single
stage tendon grafting. In making a decision to insert
a rod when the patient presents with a rupture of a
primary repair in a little finger, it is often possible to
identify those patients who are most likely to do badly
if they are known to the therapy department, having
spent time—or not—mobilizing the primary repair.
CONCLUSION
Most ruptures outside of the little finger should be
re-repaired if possible. Little finger ruptures with a strong
intact FDS tendon can provide adequate little finger
flexion and usually do not have significant hooking of
References
1. Leddy JP: Flexor tendons: acute Injuries. In Green DP,
editor: Operative Hand Surgery, New York, 1982, Churchill
Livingstone, p 1359.
2. Savage R: In vitro studies of a new method of flexor tendon
repair, J Hand Surg (Br) 10:135–141, 1985.
3. Savage R, Risitano G: Flexor tendon repair using a “six strand”
method of repair and early active mobilisation, J Hand Surg
(Br) 14:396–399, 1989.
4. Harris SB, Harris D, Foster AJ, et al: The aetiology of acute
rupture of flexor tendon repairs in zones 1 and 2 of the fingers
during early mobilization, J Hand Surg (Br) 24:275–280,
1999.
5. Wong JK, Cerovac S, Ferguson MW, et al: The cellular effect
of a single interrupted suture on tendon, J Hand Surg (Br)
31:358–367, 2006.
6. Tang JB, Xu Y, Wang B: Repair strength of tendons of varying
gliding curvature: a study in a curvilinear model, J Hand Surg
(Am) 28:243–249, 2003.
7. Dowd MB, Figus A, Harris SB, et al: The results of immediate
re-repair of zone 1 and 2 primary flexor tendon repairs which
rupture, J Hand Surg (Br) 31:507–513, 2006.
8. Allen BN, Frykman GK, Unsell RS, et al: Ruptured flexor
tendon tenorrhaphies in zone 2: repair and rehabilitation,
J Hand Surg (Am) 12:18–21, 1987.
9. Elliot D, Moiemen NS, Flemming AFS, et al: The rupture
rate of acute flexor tendon repairs mobilized by the con-
the finger. Review at 6 months will identify functional
problems requiring tendon grafting in individual cases
but these are likely to be rare. Where the little finger has
no means of flexing after rupture of a primary repair, we
would advise that a rod be inserted into the finger and
secondary grafting scheduled when the finger is soft and
supple, as the alternative of re-repair has a 4 : 20 (20%)
chance of a second rupture, necessitating further treat-
ment within a few weeks, and a 7 : 20 (35%) chance of
creating a little finger that is a hindrance because of loss
of sufficient extension and hooking and/or insufficient
flexion ability to provide good grip function and prevent
objects dropping out of the ulnar side of the hand.
Although these conclusions are empirical, they are no
less worthwhile and useful in formulating a treatment
strategy for the management of primary flexor tendon
repairs which rupture. When evidence that stronger
re-repairs give better results in the little finger is avail-
able, this policy may require modification.
trolled active motion regimen, J Hand Surg (Br) 19:607–612,
1994.
10. Moiemen NS, Elliot D: Primary flexor tendon repair in zone
1, J Hand Surg (Br) 25:78–84, 2000.
11. Small JO, Brennen MD, Colville J: Early active mobilisation
following flexor tendon repair in zone 2, J Hand Surg (Br)
14:383–391, 1989.
12. Le Viet D: Flexor tendon lengthening by tenotomy at the
musculotendinous junction, Ann Plast Surg 17:239–246,
1986.
13. Strickland JW, Glogovac SV: Digital function following flexor
tendon repair in Zone II: a comparison of immobilization
and controlled passive motion techniques, J Hand Surg (Am)
5:537–543, 1980.
14. Kessler I, Nissim, F: Primary repair without immobilization
of flexor tendon division within the digital sheath, Acta
Orthop Scand 40:587–601, 1969.
15. Kirchmayr L: Zur Technik der Sehnennaht, Z Chir 40:906–
907, 1917.
16. Kubota H, Aoki M, Pruitt DL, et al: Mechanical properties of
various circumferential tendon suture techniques, J Hand Surg
(Br) 21:474–480, 1996.
17. Elliot D: Invited personal view. Primary flexor tendon repair:
operative repair, pulley management and rehabilitation,
J Hand Surg (Br) 27:507–513, 2002.
 CHAPTER
20  
CLOSED AVULSION OR
RUPTURE OF FLEXOR TENDONS
A Traumatic Avulsion of
Flexor Tendons
Pierre Mansat, MD, PhD, and Michel Mansat, MD
OUTLINE
Traumatic avulsion of flexor tendons is not uncom-
mon. Often observed in athletes, this lesion concerns
mainly an avulsion of the flexor digitorum profundus
tendon on the distal phalanx of the ring finger.
Although clinically typical, diagnosis is often missed.
Prognosis factors identified are the level of retraction
of the tendon, the status of the vinculae, the delay
between injury and treatment, and the presence
and size of a phalangeal bony fragment. Acutely,
direct reinsertion of the profundus tendon on the
distal phalanx gives satisfactory results. Long-standing
lesions with tendon retraction and impaired tendon
vascular supply should not be treated by reinsertion
to avoid finger stiffness. No surgery is recommended
when impairment of function is slight, the proximal
interphalangeal (PIP) joint perfectly mobile, and the
distal interphalangeal (DIP) joint stable. If the PIP
joint is stiff, the retracted flexor digitorum profundus
tendon is resected, followed by tenodesis or capsu-
lodesis of the DIP joint. One-stage tendon graft is
reserved for cases in which the loss of strength and
range of active finger flexion are not acceptable, but
the PIP and DIP joints have normal passive motion.
Closed traumatic avulsion of the insertion of flexor
tendons is a relatively common injury, particularly in
athletes. The majority of injuries involve the profundus
tendon at its insertion1-4 and, less frequently, the super-
ficialis5,6 or both tendons.7-10 Avulsion of the flexor digi-
torum superficialis (FDS) tendon can be directly from
the middle phalanx5 or can be associated with a middle
phalangeal cortical bone avulsion.6 Avulsion of the
flexor digitorum profundus (FDP) tendon occurs most
commonly at the bony insertion on the distal phalanx,
with or without bone fracture.1,2 The injury has been
reported to occur in all fingers, but the ring finger is
involved in more than 75% of cases.1,2,4 Satisfactory
results of surgical repair are usually obtained in most
cases if the diagnosis is made quickly. However, impair-
ment of the function of the finger can result from a late
diagnosis. In these chronic cases, the results of surgical
treatments are often unpredictable.
BACKGROUND
In 1960, Gunter11 reported avulsion of the FDP tendon
occurring in eight rugby players. In 1970, Carroll and
March12 reviewed 35 cases and emphasized the particu-
lar involvement of the ring finger and the irreversibility
of the injury once the tendon had retracted into the
palm. The “grasping jersey” mechanism of this trauma
was specified by Folmar et al13 and Chang et al.14 A clas-
sification into three types according to the amount of
tendon retraction has been proposed initially by Leddy
and Packer in 19771 and then in France by Mansat and
Bonnevialle in 19852 after review of a series of 19 cases.
In 1981, Smith15 described a fourth type, with avulsion
of the profundus tendon in association with a bone frac-
ture of the distal phalanx. Al-Qattan, in 2001,16 added a
type V with tendon and bony avulsion and transverse
fracture of the distal phalanx. Only case reports have
been published of traumatic rupture of the FDS.5,6,13,17
MECHANISM OF INJURY
Many of these injuries occur in rugby or American
football, when the finger is forcibly extended during a
maximum contraction of the profundus flexor muscle.
The injury occurs when a player is attempting to make
a tackle and the little finger slips off the opposite player’s
pants or jersey (Figure 20[A]-1). As this occurs, the ring
finger is caught in the pants or jersey. Because of the
mechanism of injury, the lesion has been termed “jersey
finger” or “rugby finger.”2,18-20 Other etiologies have
been reported, including blast injury21 and closed blunt
trauma.22
219
220 Section 2:  Primary Flexor Tendon Surgery
Figure 20(A)-1  Mechanism of injury of a “rugby finger.”
The ring finger is most susceptible to avulsion of the
FDP tendon.1 Several studies have shown that the inser-
tion of the profundus tendon is anatomically weaker in
the ring finger than in the middle finger.19,23 The FDP of
the ring finger is tethered in the palm by a bipennate
lumbrical muscle,19 and the anatomic arrangement of
the extensor tendons in the ring finger may also relate
to the susceptibility of the ring finger to rupture.1
When the four long fingers are grasping an object with
force, they bear strong traction, which causes acute hyper-
extension of the distal interphalangeal (DIP) joints. The
index, whose muscular belly is independent, can release
its grip before the others. Because the muscular part of
the profundus is united to the surrounding structures
and because of the existence of tendinous connections,
the ring finger is submitted to the constraint along with
the middle and little fingers. Because of the shorter size
of the little finger, it closes up before the others. This
leaves the middle and ring fingers to oppose this strong
hyperextension force. The distal insertion of the ring
finger, being weaker than that of the middle finger, gives
away first.2
CLASSIFICATION
The amount of injury to the extrinsic vascular supply of
the distal flexor tendon is proportional to the degree of
retraction of the avulsed tendon. The short vinculum,
located at the neck of the middle phalanx and at the
DIP joint, is injured when the FDP tendon is avulsed
from the distal phalanx. However, the tendon may be
still supplied by the long vinculum located on the FDS
tendon closed to its chiasma, which extends to the FDP
tendon. The intactness of this long vinculum determines
the severity of the injury.24-26
Leddy and Packer classified the FDP tendon avulsion
injury in the finger into three types1 (Figure 20[A]-2):
 Type I, the avulsed FDP tendon is retracted into the
palm. The vincular system has been completely
Type I Type II Type III
Figure 20(A)-2  Leddy and Packer’s classification.1
disrupted, resulting in loss of blood supply to the
tendon.
 Type II, the tendon retracts back to the level of the
proximal interphalangeal (PIP) joint, being held
there by the intact long vinculum.
 Type III, there is usually a large bony fragment that
is avulsed from distal phalanx and holds the
tendon from proximal retraction by catching on
the A4 pulley. The tendon and vinculae remain
intact.
Mansat and Bonnevialle2 have found it more logical
to classify this injury according to the extent of retrac-
tion of the avulsed FDP tendon from a more benign
form to a more severe form:
 Type I, proximal retraction of the avulsed FDP
tendon to the level of the bifurcation of the FDS
tendon, but the long vinculum remains intact.
 Type II, marked retraction of the avulsed FDP
tendon into the palm, with avulsion of the vincu-
lae and loss of the tendon vascular support.
 Type III, Intraarticular fracture of the distal phalanx
and dorsal subluxation of the DIP joint; the
tendon still attaches to the bony fragment and
proximal retraction of the FDP tendon is very
limited. The bony fragment is entrapped in the
distal part the digital sheath tunnel.
 Type IV, the tendon is avulsed from the fractured
fragment of the distal phalanx and retracts; the frac­
ture is intraarticular, involving articular surface.15
 Type V, avulsion of an osseous fragment connect-
ing to the insertion of the FDP tendon. There is a
 Chapter 20A:  Traumatic Avulsion of Flexor Tendons 221

concomitant fracture of the distal phalanx beside tendon.27 The only differential diagnosis is a torn volar
the avulsion.16 plate of the DIP joint as described by Bowers and
Fatjgenbaum.28
In some rare cases, both flexor tendons can be avulsed Isolated, closed avulsion of the FDS tendon at its
on the same finger.7-10 insertion can present diagnostic and therapeutic chal-
lenges. The injury is often associated with flexion defor-
DIAGNOSIS
mity and diminished extension of the involved digit.
The problem of this injury is that it is often missed This presentation is readily explained by the anatomy
initially. In the Mansat and Bonnevialle series, only 50% of the digital flexor tendon and annular pulley system.
of the cases had been diagnosed within the first 3 weeks.2 Once torn from its insertion on the middle phalanx, the
The history of the mechanism of injury is typical. While superficialis tendon retracts proximally. It stops at the
playing rugby, American football, or other sports, the level of the A1 pulley where Camper’s chiasma acts as
patient feels a searing pain in the ring finger when grasp- noose to ensnare the FDP tendon. If diagnosis is delayed,
ing the opposite player’s jersey, sometimes with ecchy-
mosis (Figure 20[A]-3). The patient may notice loss of
active DIP joint flexion (or PIP joint flexion for an FDS
tendon avulsion) (Figure 20[A]-4). Pain localization
may give an indication of the amount of retraction of
the avulsed tendon. According to Mansat and Bonnevi-
alle’s classification,2 in type I, patients have pain, swell-
ing, and loss of motion of the PIP joint as well as no
active flexion of the DIP joint. In type II, the patient may
have tenderness over the insertion area of the FDP
tendon on the distal phalanx, and there also may be
tenderness and swelling in the palm where the tendon
has retracted. In type III, the patient has marked swell-
ing, ecchymosis, and pain over the distal aspect of the
middle phalanx just proximal to the DIP joint, as well
as no active flexion at the DIP joint. Radiographs are
often negative in type I and II lesions. However, in types Figure 20(A)-4  Loss of active flexion of the DIP joint after
rupture of the FDP tendon in a ring finger.
III, IV, and V, a lateral radiograph shows a large bony
fragment just proximal to the DIP joint with or without
distal phalanx fracture (Figure 20[A]-5). The use of
ultrasound has been proposed to localize the avulsed

Figure 20(A)-5  A lateral x-ray film showing a bony

Figure 20(A)-3  Ecchymosis along the finger. fragment avulsed from the base of the distal phalanx.
222 Section 2:  Primary Flexor Tendon Surgery
inflammation and adhesion formation further entrap
the profundus tendon.5 Lateral radiograph can show a
bony fragment at the middle phalanx.6
TREATMENT
Several factors have been identified which influence the
prognosis and treatment of injury of the FDP tendon:
(1) the level of retraction of the tendon, (2) the status
of the vinculae, (3) the delay between injury and treat-
ment, and (4) the presence and size of a phalangeal
bony fragment.2,18
The definition of “acute” cases varies from one sur­
geon to another. For Mansat and Bonnevialle,2 a delay
of 3 weeks is the limit, whereas for Tropet et al,3 10 days
is the maximum. For Leddy and Packer,1 the delay is not
the major factor but more the level of tendon retraction
at diagnosis. If the tendon is not retracted, a direct repair
can be performed up to 3 months after injury; on the
other hand, if the tendon is retracted into the palm,
direct repair may not be possible after 10 days have
elapsed. Usually, final decision is made during surgery.
The treatment of an acute injury, according to Mansat
and Bonnevialle’s classification,2 is described below. The
decision to repair or reattach the tendon to the distal
phalanx depends on the degree of retraction.
In type I, the optimal treatment for this injury is early
reinsertion of the tendon to the distal phalanx. The
exposure is through a zigzag incision on the finger,
exposing the flexor sheath from the area of the insertion
to just proximal to the PIP joint. An opening is created
in the sheath just distal to the A2 pulley to identify the
retracted tendon (Figure 20[A]-6). The tendon is found
and threaded beneath the flexor tendon sheath to the
level of the distal phalanx in a nontraumatic manner.
A raised osteoperiosteal flap is then created at the
insertion site on the distal phalanx, and the profundus
tendon is reinserted. If some tendon materials remain
on the distal phalanx direct tendon-to-tendon suture
must be avoided because of a high risk of secondary
Figure 20(A)-6  Surgical exposure for a type I lesion.
rupture.4 Transosseous suture repair is preferred, using
a standard pull-out wire and button technique,1,2 a
double-arm reinsertion technique,29 or micro-anchors4,30
(Figure 20[A]-7). In the Brustein et al study,31 the
micro-bone suture anchor provided a stronger tendon-
to-bone repair compared to pull-out wire and button
or a mini-anchor. However, McCallister et al32 have
shown no difference between pull-out wire and button
technique and mini-anchors for zone 1 flexor tendon
repair in respect of clinical outcome, although signifi-
cant improvement was found in the time to return to
work following repairs using suture anchor technique.
There was less potential morbidity associated with the
anchor technique compared to the pull-out wire and
button technique. The main problems reported with the
pull-out technique were discomfort, pain, suture wire
rupture, difficulty in daily care of the bolster, infection,
skin necrosis, and nail bed injury.33 The use of a braided
polyester suture instead of a monofilament suture is
recommended, as it is more resistant to cyclic testing.34
Care should be taken not to injure the volar plate of the
DIP joint when reinserting the tendon.
In type II, the exposure is identical to that for a type
I injury. If the tendon is not identified just distal to the
A2 pulley, it must have retracted into the palm. Then, a
slightly curved incision is made just proximal to the
distal palmar crease; this allows exposure of the flexor
sheath proximal to the A1 pulley. A small incision is
made in the sheath, and the distal end of the profundus
tendon is identified. Next, a small catheter is inserted
into the sheath through the incision in the distal finger
and passed to the level of the A1 pulley. The profundus
B
Figure 20(A)-7  Repair of the FDP tendon by means of
pull-out or barb-wire suture (A), or micro-anchors (B).
 Chapter 20A:  Traumatic Avulsion of Flexor Tendons 223

tendon is then sutured to the catheter, which is pulled

distally, threading the profundus tendon back beneath
the pulleys and through the superficialis chiasma to the
level of the PIP joint. The tendon is then passed in a
similar fashion beneath the C1, A3, C2, A4, and C3
pulleys to the level of the distal phalanx. The tendon is
reattached to the phalanx with the methods for a type I
injury. However, if reinsertion on the phalanx is difficult
and under tension, resection of the tendon with stabi-
lization of the DIP joint in slight flexion is preferred. A
Using the distal remnant of the profundus tendon may
help to create a simple tenodesis protected by a tempo-
rary K-wire. Fusion is an alternative to tenodesis.2
In type III, treatment consists of open reduction and
internal fixation of the bone fragment. Correct reduc-
tion of the joint line is necessary to obtain good motion
without pain. Internal fixation can be performed with
K-wires,2,4,15,35,36 micro-screws,20,37,38 or a micro-plate39,40
(Figure 20[A]-8).
In types IV and V, the bony fragment is openly
reduced and fixed followed by repair of the avulsed B
profundus tendon, as described for type I and II injuries,
depending on the level of retraction.15,16
For old injuries, management is variable and indi-
vidualized for each case. Decision-making is based on
functional impairment (PIP joint stiffness, loss of
strength), patient’s needs and expectation, and total
ranges of active and passive motion of the PIP and DIP
joints. Those patients who are asymptomatic should be C
left alone. Rarely do patients have limitation of motion
at the PIP joint 6 months after injury; however, if there
is instability of the DIP joint with weakness of pinch
or recurrent dorsal dislocation, arthrodesis or tenodesis
of the joint should be considered18 (Figure 20[A]-9).
Fusion provides joint stability and does not interfere
with the function of the superficialis tendon. If there is
a tender lump in the palm, the retracted tendon end can
be excised at the time of fusion. Generally, Mansat and
Bonnevialle2 advocated (1) no surgery when impair-
ment is slight (non-manual workers), the PIP joint is
perfectly mobile, and the DIP joint is stable; and (2) D
simple resection of the retracted FDP tendon if the PIP
joint is stiff, in association with tenodesis of the DIP
joint. There is a risk of PIP and DIP joint stiffness if
reinsertion is performed, even in type I injury. One-stage
tendon graft with palmaris longus tendon should be
reserved for patients for whom strength and function
impairment of the ring finger are not acceptable but who
have normal passive motion of PIP and DIP joints
(Table 20[A]-1).
FDS tendon avulsion can be reinserted or sutured
totally or partially with repair of one slip through a
palmar zigzag incision centered on the PIP joint if diag-
nosed early. However, for long-standing cases, the inci- E
sion must be extended into the palm. The retracted end Figure 20(A)-8  Treatment of a type III lesion. A, Osteosyn-
of the tendon is found at the level of the A1 pulley. thesis of the fracture with a screw. B and C, Tendon repair
with a micro-anchor. D and E, Clinical results at follow-up.
224 Section 2:  Primary Flexor Tendon Surgery

Table 20(A)-1  Operative Methods for Avulsion of the

FDP Tendon
Operative Treatment: Operative Treatment:
Type* Acute (<3 Wk) Late (>3 Wk)
I Direct repair   FDP resection + DIP
(+micro-anchors) joint capsulodesis or
tenodesis
FDP resection + DIP FDP resection + DIP
joint capsulodesis or joint arthrodesis
tenodesis

A FDP resection + DIP Tendon graft

joint arthrodesis
II Direct repair   Direct repair  
(+micro-anchors) (+micro-anchors)
FDP resection + DIP
joint capsulodesis or
tenodesis
FDP resection + DIP
joint arthrodesis
Tendon graft
III Osteosynthesis   Osteosynthesis  
(±suture of the (±suture of the
tendon) tendon)
*Classifications by Leddy and Packer.1

B
Figure 20(A)-9  Type I lesion treated by resection of the
FDP tendon (A), and tenodesis of the remnant of the FDP
tendon at the DIP joint (B).

Peritendinous adhesions and scar tissue were excised

along with the FDS tendon.5 If a bony fragment is
attached to the tendon, it is removed with the tendon.6
POSTOPERATIVE CARE
Postoperatively, in type I and II lesions after reinsertion
of the FDP tendon to the distal phalanx, a dorsal splint
is used to hold the wrist in slight flexion, the MCP joints
in 75° of flexion, and the PIP and DIP joints in relative
extension (Figure 20[A]-10). Passive flexion exercises
are started early in the postoperative course. Active exer-
cises are begun at 3 weeks when the splint is removed.
The pull-out wire and button are removed 3 to 4 weeks
postoperatively, and the remaining rehabilitation is
similar to that for other flexor tendon injuries.
Figure 20(A)-10  Dorsal splinting to place the MCP joint in
In type III, IV, and V lesions, immobilization of the
flexion and PIP and DIP joints in extension.
DIP joint of 45 days is necessary for consolidation of the
fracture. Then passive and active mobilization is begun.
et al.3 For type II lesions according to Mansat and Bonn-
OUTCOMES
evialle’s classification, reinsertion of the FDP tendon on
For acute lesions of the FDP tendon, surgical repair is the distal phalanx must be performed without tension
always indicated, and satisfactory results varied from to obtain satisfactory results.2 If not, the finger becomes
70% for Gaston et al4 to 80% for Mansat and Bonne­ stiff with limitation of active motion of the DIP and PIP
vialle2 and 100% for Leddy and Packer1 and Tropet joints. For type III, IV, and V lesions, the prognosis
 Chapter 20A:  Traumatic Avulsion of Flexor Tendons 225

depends on the quality of articular surface reduction, For patients seen more than 3 weeks after injury, the
often with loss of few degrees of active motion of the FDP tendon was resected in one case, the FDP tendon
DIP joint.4 was resected with a DIP joint capsulodesis in 4 cases,
For chronic lesions, if the patient has no or slight and tendon grafting using the palmaris longus was per-
impairment, conservative management is the best formed in one case.
option. If the patient complains of digital pain, with Patients were reviewed at an average of 7 years
flexion deficit of the PIP joint, resection of the avulsed (3 months to 13 years) from treatment (Table 20[A]-2).
tendon must be proposed. If there is instability of the Four of the 10 patients had a complete recovery (range
DIP joint, capsulodesis, or arthrodesis of the DIP joint of motion and strength), 3 had an incomplete recovery
can be added. Tendon grafting should be limited to (range of motion of the DIP joint between 60° and 80°
young and active patients with specific needs. Preopera- of flexion, normal strength), and one had an unsatisfac-
tive normal passive motion of the PIP and DIP joints is tory result (range of motion of the DIP joint of 20° and
a prerequisite to a good result. The patient must be loss of strength). Two ruptures were observed within the
aware that a tendon graft usually does not allow com- first month postoperatively: one type I lesion with
plete recovery of DIP active flexion. McClinton et al,41 tendon reinsertion using a barb-wire suture, and one type
reviewing 100 cases of tendon graft for isolated FDP II lesion with direct tendon suture. In the 3 patients with
tendon laceration, obtained 48° of average DIP active type III lesion, one was lost to follow-up, one had a
flexion. Liu and Yang,42 reviewing 15 cases of tendon complete recovery, and one developed osteoarthritis of
graft for isolated FDP tendon rupture, obtained an the DIP joint (Figure 20[A]-11).
average of 33° of DIP active flexion. Main complica-
tions were loss of PIP joint extension (more than 30°
in 27% of the cases of Liu et al,42 less than 10° in 55%
of the cases, and more than 10° in 9% of the cases of
McClinton et al41).
OUR PERSONAL EXPERIENCE
We recently reviewed our experience of treating avulsion
of the FDP tendon in 20 patients.4 These included 17
men and 3 women (average age, 31 years; range, 20 to
52 years). In 12 cases, the injury was related to sports
injury (football or rugby), and in 8 cases, to domestic or
work-related trauma. The ring finger was involved in 14
cases, the middle finger in 3 cases, and the little finger A
in 3 cases. In 14 cases the patients were seen within 3
weeks from the injury. According to Leddy and Packer’s
classification,1 the lesion was staged as type I in 5 patients,
type II in 6, and type III in 3. In 6 cases, the patient was
seen more than 3 weeks from the initial trauma. These
lesions were classified as type I in 5 and type II in 1.
For the 14 patients seen acutely (within 3 weeks), all
type I and II injuries except one were treated surgically.
The FDP tendon was reattached to the distal phalanx B
using a micro-anchor in 4 cases, a pull-out suture in 4,
and barb-wire fixation in one case. In one case, a direct
tendon-to-tendon suture was performed with a distal
remnant of the FDP on the distal phalanx. In one case
of type I lesion, the FDP tendon was resected. Postop-
eratively, early mobilization was proposed using a dorsal
splint with the MCP joint in flexion and the PIP and
DIP joints in extension. Passive flexion exercises were
started immediately in 6 patients and after 2 weeks in
4 patients. Active exercises were begun at 4 weeks when
the splint was removed. An osteosynthesis of the distal
phalanx was performed in type III lesions, using K-wire C
to fix the avulsed bone in all 3 cases, along with a pull- Figure 20(A)-11  A, Another example of type III lesion.
out suture of the FDP tendon in one case. The fingers B, Subsequent development of malunion of the avulsed
were immobilized with a splint for 4 weeks. bone fragment. C, Secondary arthritis of the DIP joint.
226 Section 2:  Primary Flexor Tendon Surgery

Table 20(A)-2  Treatment Results of Avulsion of the FDP Tendon in Our Unit
Number of Patients
Methods of Treatment and Types Results* Complications
Surgery: <3 wk after injury
  Transosseous reinsertion (micro-anchors) 3, Type I 2 Excellent 0
1, Type II 1 Good
1 Poor
  Transosseous reinsertion (pull-out) 4, Type II 2 Excellent 0
2 Good
  Transosseous reinsertion (barb-wire) 1, Type I 1 Poor Rupture
  Direct FDP repair 1, Type II 1 Poor Rupture
  FDP resection 1, Type I Lost to follow-up —
  Osteosynthesis (K-wire) 2, Type III 1 Excellent 0
1 Lost to follow-up
  Osteosynthesis (K-wire + pull-out) 1, Type III 1 Poor DIP joint osteoarthritis
Surgery: >3 wk after injury
  FDP resection + capsulodesis 4, Type I 3 Good Capsule lengthening and
1 Fair Loss of strength
  FDP resection 1, Type I 1 Fair Loss of strength
  Tendon graft 1, Type II 1 Poor PIP/DIP joint stiffness
*Assessed with Strickland and Glogovac criteria.

Of the 5 patients seen lately with resection of the
FDP tendon, 3 of 5 were satisfied with their surgery
despite an ongoing loss of strength. The patient with a
tendon graft had poor results, with 10° of extension
deficit and 60° of flexion of the PIP joint, and had a
stiff DIP joint.
SUMMARY
Diagnosis of the closed FDP tendon can often be missed.
History of the mechanism of injury as well as the clinical
presentation is typical; tracing pain along the finger,
ecchymosis, and loss of active DIP joint flexion can be
helpful in making a diagnosis. Radiographs are essential
to diagnose a fracture of the distal phalanx. The level of
retraction of the tendon, the status of the vinculae, the
delay between injury and treatment, and the presence
and size of a phalangeal bony fragment affect the final
results of treatment. In acute cases (less than 3 weeks
after injury), direct reinsertion of the FDP tendon on the
distal phalanx gives satisfactory results. Long-standing
lesions with tendon retraction and impaired tendon
vascular supply should not be treated by reinsertion, to
avoid finger stiffness. No surgery is recommended when
function loss is slight, the PIP joint is mobile, and the
DIP joint is stable. If the PIP joint is stiff, the retracted
FDP tendon should be resected, followed by tenodesis
or capsulodesis of the DIP joint. One-stage tendon graft
should be reserved for patients whose strength and range
of active finger flexion are not acceptable but passive
motion of the PIP and DIP joints are normal.

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23. Manske PR, Lesker PA: Avulsion of the ring finger flexor digi-
torum profundus tendon: An experimental study, Hand 10:
52–55, 1987.
24. Edwards EA: Organisation of the small arteries of the hand
and digits, Am J Surg 99:837–846, 1960.
25. Smith JW: Blood supplies of tendons, Am J Surg 109:272–276,
1965.
26. Leffert RD, Weiss C, Athanasoulis CA: The vincula; with par-
ticular reference to their vessels and nerves, J Bone Joint Surg
(Am) 56:1191–1198, 1974.
27. Cohen SB, Chabbra AB, Anderson MW, et al: Used of ultra-
sound in determining treatment for avulsion of the flexor
digitorum profundus (rugger jersey finger): A case report, Am
J Orthop (Belle Mead, NJ) 33:546–549, 2004.
Chapter 20A:  Traumatic Avulsion of Flexor Tendons 227
28. Bowers WH, Fajgenbaum DM: Closed rupture of the volar
plate of the distal interphalangeal joint, J Bone Joint Surg (Am)
61:146, 1979.
29. Messina A, Messina JC: Double armed reinsertion suture
(DARS) of the profundus flexor tendon with immediate
active mobilization of the finger. 63 cases, Ann Chir Main
Memb Super 16:245–251, 1997.
30. Bonin N, Obert L, Jeynet L, et al: Réinsertion du tendon
fléchisseur par ancre de suture: Etude prospective continue
avec mobilisation active précoce, Chir Main 22:305–311,
2003.
31. Brustein M, Pellegrini J, Choueka J, et al: Bone suture anchors
versus the pullout button for repair of distal profundus
tendon injuries: A comparison of strength in human cadav-
eric hands, J Hand Surg (Am) 26:489–496, 2001.
32. McCallister WV, Ambrose HC, Katolik LI, et al: Comparison
of pullout button versus suture anchor for zone I flexor
tendon repair, J Hand Surg (Am) 31:246–251, 2006.
33. Kang N, Marsh D, Dewar D: The morbidity of the button-
over-nail technique for zone 1 flexor tendon repairs. Should
we still be using this technique? J Hand Surg (Eur) 33:566–
570, 2008.
34. Latendresse K, Dona E, Scougall PJ, et al: Cyclic testing of
pullout sutures and Micro-Mitek suture anchors in flexor digi-
torum profundus tendon distal fixation, J Hand Surg (Am)
30:471–478, 2005.
35. Buscemi MJ Jr, Page BJ 2nd: Flexor digitorum profundus avul-
sions with associated distal phalanx fractures, Am J Sports Med
15:366–370, 1987.
36. Boussouga M, Jaafar A, Bousselmane N, et al: Avulsion of
flexor digitorum profundus combined with articular fracture
of distal phalanx: A case report, Chir Main 26:250–252, 2007.
37. Eglseder WA, Russell JM: Type IV flexor digitorum profundus
avulsion, J Hand Surg (Am) 15:735–739, 1990.
38. Trumble TE, Vedder NB, Benirschke SK: Misleading fractures
after profondus tendon avulsions: A report of 6 cases, J Hand
Surg (Am) 17:902–906, 1992.
39. Chen CY, Li TS, Liu YT, et al: Miniplate hooking method for
repair of type III flexor digitorum profundus avulsion injury
with a small bone fragment: Case report, J Hand Surg (Am)
34:1449–1453, 2009.
40. Kang N, Pratt A, Burr N: Miniplate fixation for avulsion inju-
ries of the flexor digitorum profundus insertion, J Hand Surg
(Br) 28:363–368, 2003.
41. McClinton MA, Curtis RM, Wilgis EF: One hundred tendon
grafts for isolated flexor digitorum profundus injuries, J Hand
Surg (Am) 7:224–229, 1982.
42. Liu TK, Yang RS: Flexor tendon graft for late management of
isolated rupture of the profundus tendon, J Trauma 43:103–
106, 1997.
 B Tendon Rupture After Fractures
or Carpal Disorders
Hiroshi Yamazaki, MD, PhD, Hiroyuki Kato, MD, PhD,
and Shigeharu Uchiyama, MD
OUTLINE
Closed flexor tendon ruptures can be caused by some
pathologies of the carpal bones and joints, such as
fracture of the hook of the hamate, Kienböck’s disease,
scaphoid nonunion, and pisotriquetral disorders. We
analyzed 21 patients with closed rupture of the flexor
tendons caused by carpal bone and joint disorders. In
most patients the closed flexor tendon rupture occurred
when mild resistance forces were applied to the finger
or spontaneously. The mechanism of the tendon rup-
tures is attrition from passage back and forth over a
rough bone surface. We found it difficult to identify
the causes of these tendon ruptures using plain radio-
graphs, especially in the elderly or in manual laborers
who have preexisting abnormal lesions, such as osteo-
arthritis, instability of the carpus, and radiographic
evidence of previous trauma. Radiocarpal arthrogra-
phy was useful in identifying the site of the lesion
responsible for the flexor tendon ruptures. The radio-
graphic signs of lesions from which contrast medium
leaked subsequently corresponded to the disruption
site of the periosteum or joint capsule at surgery. Our
preferred management is free tendon graft reconstruc-
tions followed by early controlled mobilization, and
we suggest that the projected bony parts be resected
and the capsule/periosteum repaired to prevent recur-
rence of tendon rupture.
Most flexor tendon ruptures result from avulsion of the
flexor digitorum profundus (FDP) tendon at its inser-
tion. Although not common in contrast to rheumatoid
arthritis, closed flexor tendon ruptures caused by hidden
pathologies of the carpal bones and joints have been
reported, namely fracture of the hook of the hamate,1-4
Kienböck’s disease,5 scaphoid nonunion,6,7 pisotrique-
tral osteoarthritis,8,9 pisotriquetral instability,10 lunate
fracture,11 and chronic lunate dislocations.12 Boyes et al13
reported that 10 of 80 flexor tendon ruptures (12.8%)
had occurred in the carpal tunnel and that 2 of the
10 had associated abnormalities of the carpal bones.
Folmar et al14 reported the flexor pollicis longus (FPL)
228
tendon and the FDP tendon of the little finger were
most frequently affected in 10 patients with flexor
tendon ruptures. Yamazaki et al15 reported 21 patients
with closed rupture of the flexor tendons caused by
carpal bone and joint disorders and described useful-
ness of radiocarpal arthrography as a diagnostic tool.
In this section, characteristic clinical and roentgeno-
graphic features of closed rupture of the flexor tendon
secondary to fractures or carpal disorders are reviewed.
Pathophysiology and reconstruction are discussed.
METHODS AND OUTCOMES
Patients
We analyzed 21 patients with closed rupture of the
flexor tendons caused by carpal bone and joint disor-
ders.15 The mean patient age was 68 (range, 35 to 89)
years. Fourteen patients were men and seven were
women. Fifteen of the 21 patients were manual laborers.
The pathological conditions included nonunion of the
hook of the hamate in six patients, pisotriquetral joint
arthritis in seven patients, nonunion of the scaphoid in
four patients, the presence of a rough surface of the
hook of the hamate in two patients, Kienböck disease
in one patient, and the presence of an intraosseous
ganglion of the lunate in one patient. Affected digit was
the thumb in four patients, index finger in one patient,
ring and little fingers together in one patient, and little
finger in fifteen patients. Patients with tendon rupture
caused by direct invasion by synovitis associated with
rheumatoid arthritis or infection were excluded. Radio-
carpal arthrography was performed in 14 of the 21
patients and capsular perforation demonstrated by con-
trast medium leakage into the carpal canal in 11 patients
(Figure 20[B]-1). A free palmaris longus tendon or
plantaris tendon graft was interposed between the prox-
imal and distal stumps of the ruptured tendon in 17
patients. Tendon transfer of the flexor digitorum super-
ficialis (FDS) tendon of the ring finger to the FDP
tendon of the little finger was performed in two patients.
End-to-side tendon transfer using the FDP tendon of the
long finger with interposition of the palmaris longus
 Chapter 20B:  Tendon Rupture After Fractures or Carpal Disorders
Figure 20(B)-1  Radiocarpal arthrogram showing leakage
(arrow) of contrast medium into the flexor tendon sheath in
pisotriquetral joint arthritis.
tendon to the FDP tendons of the little and ring finger
was performed in one patient.
Operative Techniques
During operation, a curved and zigzag incision was
made on the palm between distal palmar crease and
proximal crease. The patients underwent release of the
carpal tunnel for exposure of carpal pathologies and the
ruptured tendon stumps. We used this method to check
the neighboring tendon, which often frayed. The volar
capsule/periosteum of the carpus was perforated at the
site of the tendon ruptures. The free or sharp bone frag-
ment was excised. At the site of mobile nonunion and
osteoarthritis, sclerotic cortical surface of the bone was
curetted and filled with cancellous bone graft. The edges
of the palmar capsule defect were approximated and
sutured. In free tendon grafting, the palmaris longus or
the plantaris tendon was harvested. The proximal stump
was well pulled until myostatic contracture was released.
The FDP tendon was reconstructed only in the finger in
which both the FDP and FDS tendons were ruptured.
The remnant tendon was trimmed out, and the inter­
positional or transferred tendon was sutured to the
refreshed stump with interlacing or Pulvertaft weave
suture. The junction of the graft with the stump was
placed away from the carpal area for preventing adhe-
sion of the tendon stump within the carpal tunnel. The
tourniquet was then deflated, and correct tension was
achieved by observation of the resting position of the
finger and the interphalangeal (IP) joint during passive
flexion and extension of the wrist. One patient in whom
229
the transverse carpal ligament was sutured developed
carpal tunnel syndrome subsequent to surgery and we
now do not recommend repairing this ligament.
Postoperative Care
After tendon reconstruction, early controlled mobiliza-
tion with a modified Kleinert elastic band technique was
used for 3 to 4 weeks. The Duran method was also per-
formed to prevent contracture of IP joint. Thereafter, the
hand was protected by a dorsal splint only and active
flexion exercise was encouraged. Active finger use was
permitted at 12 weeks postoperatively. Dorsal blocking
splint with rubber band was not used in the thumb. The
affected thumb was immobilized for 3 weeks, and active
exercise was started after that.
Outcomes
Postoperative total active range of motion (TAM) in the
finger after 13 free tendon graft reconstructions averaged
213° (range, 170° to 265°) (Table 20[B]-1). The TAM
of the thumb IP joint after free tendon graft reconstruc-
tion in three cases improved from 0° to 33° on average
(range, 10° to 40°). In nine patients, the postoperative
grip strength ratio averaged 84% (range, 57% to 126%).
Illustrative Case
A 73-year-old woman noticed the distal IP (DIP) joint
of the little finger gradually became incapable of active
flexion. Radiography in an oblique lateral view in supi-
nation and computed tomography (CT) imaging (Figure
20[B]-2) showed pisotriquetral joint arthritis. In the
operation, the FDP tendon of the little finger was seen
to be ruptured and adherent to the FDS tendon of that
finger. The pisiform was removed (Figure 20[B]-3), and
a free tendon graft from the palmaris longus tendon was
interposed between the stumps. Modified Kleinert early
mobilization was carried out. One year after the opera-
tion, percent TAM was 92% and outcome according to
the American Society for Surgery of the Hand criteria
was good. No pain was present at the wrist. The grip
strength ratio was 89%.
DISCUSSION
A detailed history and clinical examination allow diag-
nosis of rupture of the flexor tendon to be made.
However, especially in chronic cases, diagnosis of
rupture of the flexor tendon is often delayed or missed.
In most patients, the closed flexor tendon rupture occurs
when mild resistance forces applied to the finger or
spontaneously. In some cases, flexor tendon attrition
and rupture cause discomfort within the region of the
synovial sheath of the digit.
Some patients have past history of trauma to the wrist,
and others have no recollection of obvious injury. The
symptoms at the wrist resulting from fractures or carpal
bone disorders are often free or mild, and disability is
230 Section 2:  Primary Flexor Tendon Surgery

Table 20(B)-1  Patient Data, Tendon(s) Ruptured, Findings of Arthrography, and Recovery of TAM After
Treatment
Involved Site of Contrast
Finger(s)/ Medium Leakage Functional
Age Ruptured on Radiocarpal Recovery* (% TAM
(Yr)/Sex Disorder/Hand Tendon(s) Arthrography Treatment and Grade)
35/M Hamate hook Little/FDP Not examined Tendon graft 100%, Excellent
nonunion/R
51/M Hamate hook Little/FDP Not examined Tendon graft 71%, Fair
nonunion/R
55/M Hamate hook Little/FDP, FDS Not examined Tendon graft 88%, Good
nonunion/R
58/M Hamate hook Little/FDP Not examined Tendon graft 75%, Fair
nonunion/R
63/M Hamate hook Little/FDP, FDS Triquetrohamate Tendon transfer 83%, Good
nonunion/L joint
73/M Hamate hook Little/FDP, FDS Not examined Tendon graft, tenolysis 85%, Good
nonunion/L
50/F Hamate hook Little/FDP, FDS Not examined Tendon graft Not available
projection/R
76/M Hamate hook Little/FDP, FDS No leakage Tendon graft 85%, Good
projection/L
67/F Pisotriquetral OA/R Little/FDP Pisotriquetral joint Tendon graft 75%, Fair
70/F Pisotriquetral OA/L Little/FDP Pisotriquetral joint Tendon graft 81%, Good
70/M Pisotriquetral OA/L Little/FDP Pisotriquetral joint Tendon graft 83%, Good
73/F Pisotriquetral OA/R Little/FDP Pisotriquetral joint Tendon graft, tenolysis 83%, Good
73/F Pisotriquetral OA/L Little/FDP Pisotriquetral joint Tendon transfer 92%, Good
80/F Pisotriquetral OA/L Little/FDP, FDS Pisotriquetral joint Tendon graft 77%, Good
89/M Pisotriquetral OA/R Little/FDP Pisotriquetral joint Tendon graft 85%, Good
65/M Scaphoid nonunion/R Thumb/FPL Not examined Tendon graft Good†
72/M Scaphoid nonunion/L Thumb/FPL Nonunion site no operation Not available
72/M Scaphoid nonunion/R Thumb/FPL Nonunion site Tendon graft Fair†
83/M Scaphoid nonunion/R Thumb/FPL Nonunion site Tendon graft Good†
76/F Kienböck disease/R Little, ring/FDP Radiolunate joint End-to-side, tenolysis 87%, Good; 75%,
fair
71/F Intraosseous ganglion Index/FDP, FDS Radiolunate joint Tendon graft, 65%, Fair
of the lunate/R arthrodesis
M, male; F, female; OA, osteoarthritis. R, right; L, left.
*Evaluated by the TAM method advocated by ASSH, except †by Buck-Gramcko method.

sometimes minimal. These disorders are often neglected
until the closed flexor tendon rupture occurs, because
routine anteroposterior and lateral roentgenograms of
the wrist fail to detect them.3,16 In approximately 14%
of hamate hook fracture, nonunion of the hook may
escape discovery, until it eventually causes closed rupture
of the flexor tendon of the little or ring finger.17 When
these historical and physical features exist, closed flexor
tendon rupture should raise suspicion of concealed dis-
orders of the carpal bones and joints. Other nonosseous
causes include anomalous tendon,18 nonspecific synovi-
tis,19 and crystal-induced tenosynovitis.20
The mechanism of these tendon ruptures is attrition
from gliding back and forth over a rough bone surface,
the latter having perforated the dorsal wall of the carpal
tunnel.14,21 The tendon that ruptured depended on the
 Chapter 20B:  Tendon Rupture After Fractures or Carpal Disorders
Figure 20(B)-2  A CT scan of the wrist showing
pisotriquetral joint arthritis.
Figure 20(B)-3  Intraoperative findings. The rough surface
of the pisiform is apparent. The FDP of the little finger is
ruptured at the lesion.
location of the bone perforation into the carpal tunnel.
The affected digit provides useful information about the
location of the carpal disorders. Disorders with an ulnar
location, such as fracture of the hook of the hamate and
arthritis involving the pisotriquetral joint, may abrade
the FDP tendon of the little finger, particularly. The
neighboring FDS tendon of the little finger and the FDP
tendon of the ring finger may subsequently be affected.
The FPL tendon lies over the ulnar surface of the scaph-
oid, and nonunion of the scaphoid may cause FPL
tendon rupture. The lunate forms the dorsal wall of the
carpal tunnel and contacts the FDP tendon of the index
finger, the tendon located most dorsally in the carpal
tunnel. Therefore, a lunate abnormality in which bone
penetrates the volar capsule is most likely to cause attri-
tion of flexor tendons of the index finger.
Ultrasound, magnetic resonance imaging (MRI),20,22
and three-dimensional CT imaging23 have been reported
to be useful tools for diagnosing flexor tendon injury
and pinpointing the site of rupture, which is crucial for
preoperative planning and thus avoiding unnecessary
surgical exploration. In patients with flexor tendon
231
rupture caused by carpal bone and joint disorders,
detection of the underlying pathological lesion before
surgery is also extremely important for the treatment,
because the surgical approach to the lesion is needed to
prevent flexor tendon re-rupture. To prevent recurrence
of tendon rupture, the sharp bone must be resected and
the capsule/periosteum repaired. The nonunion and
osteoarthritis with instability often require bone graft-
ing. Plain radiography of the wrist is often unhelpful,
unless special views are taken. Radiography in a carpal
tunnel view, radiography in an oblique lateral view
in supination, conventional tomography,16 and CT
imaging3 can help make diagnosis of the pathologies.
MRI was also useful to the diagnosis. However, it is
often difficult to differentiate the causative lesion of
the tendon rupture from the other abnormal lesions
by these diagnostic imaging studies, especially in the
elderly or in manual laborers who have preexisting
carpal abnormalities, including osteoarthritis, instabil-
ity of the carpus, and radiographic evidence of previous
trauma. Radiocarpal arthrography was very useful in
identifying the site of the lesion responsible for the
flexor tendon rupture. Similarly, using arthrography, we
identified extensor tendon rupture as a result of osteo-
arthritis of the distal radioulnar joint.24 Radiocarpal
arthrography was performed in 13 patients of flexor
tendon rupture in our series, and capsular perforation
demonstrated by contrast medium leakage into the
carpal tunnel in 11 patients. A high percentage of cases
in our investigation displayed contrast medium leakage
(see Figure 20[B]-1), and the radiographic lesions from
which contrast medium leaked corresponded to the
site of disruption of the periosteum or capsule seen at
surgery. Their adjacent tendons were disrupted. Gener-
ally, the lesion from which contrast medium leaks will
indicate location of the tear in the soft tissues and,
hence, the bony cause of the tendon rupture.
The goals of surgery are to reconstruct flexor tendon
function and to prevent flexor tendon re-rupture. The
affected tendon(s) invariably have frayed stumps, with
a long defect between the ends. Thus, direct suture
is impossible. The options of tendon reconstruction
include DIP joint arthrodesis, tenodesis, cross transfer of
flexor tendons from adjacent fingers, buddying to adja-
cent flexors, and free tendon graft. Milek and Boulas25
reported surgical results in four patients, three of whom
were treated by tendon transfer and one by tendon graft.
They attributed variation in the results largely to differ-
ences of the patients’ ages and recommended side-to-
side tendon suture. We prefer an interposition tendon
graft, since use of the tendon of another finger for a
tendon transfer may compromise function of that finger.
Motion of the DIP joint is reconstructed only by means
of free tendon grafting. We obtained mean digital TAM
of 213° after 13 free tendon graft reconstructions fol-
lowed by early controlled mobilization.15 In our series,
232 Section 2:  Primary Flexor Tendon Surgery
the mean patient age was 68 years. Although most
patients were older adults, results were satisfactory after
tendon grafting and outcome did not depend on patient
age or the interval between tendon rupture and recon-
struction. We believe that free tendon grafting is reason-
able, though this technique has the risk of adhesion and
re-rupture, and the postoperative early controlled mobi-
lization could be complicated.
Tendon graft should be done early to prevent myo-
static contracture in the affected digit. If the tendon
rupture was neglected, myostatic contracture may result
in undue tension of the tendon graft at surgery and
References
1. Clayton ML: Rupture of the flexor tendons in carpal tunnel
(non-rheumatoid) with specific reference to fracture of the
hook of the hamate, J Bone Joint Surg (Am) 51:798–799, 1969.
2. Minami A, Ogino T, Usui M, et al: Finger tendon rupture
secondary to fracture of the hamate. A case report, Acta Orthop
Scand 56:96–97, 1985.
3. Stark HH, Chao EK, Zemel NP, et al: Fracture of the hook of
the hamate, J Bone Joint Surg (Am) 71:1202–1207, 1989.
4. Yamazaki H, Kato H, Nakatsuchi Y, et al: Closed rupture of
the flexor tendons of the little finger secondary to non-union
of fractures of the hook of the hamate, J Hand Surg (Br)
31:337–341, 2006.
5. Niwa T, Uchiyama S, Yamazaki H, et al: Closed tendon
rupture as a result of Kienböck disease, Scand J Plast Reconstr
Surg Hand Surg 44:59–63, 2010.
6. McLain RF, Steyers CM: Tendon ruptures with scaphoid
nonunion. A case report, Clin Orthop Relat Res 117–120,
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7. Saitoh S, Hata Y, Murakami N, et al: Scaphoid nonunion and
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24:1211–1219, 1999.
8. Lutz RA, Monsivais JJ: Piso-triquetral arthrosis as a cause of
rupture of the profundus tendon of the little finger, J Hand
Surg (Br) 13:102–103, 1988.
9. Saitoh S, Kitagawa E, Hosaka M: Rupture of flexor tendons
due to pisotriquetral osteoarthritis, Arch Orthop Trauma Surg
116:303–306, 1997.
10. Corten EM, van den Broecke DG, Kon M, et al: Pisotriquetral
instability causing an unusual flexor tendon rupture, J Hand
Surg (Am) 29:236–239, 2004.
11. Minami A, Ogino T, Usui M: Delayed rupture of a flexor
tendon secondary to fracture of the lunate, Ital J Orthop Trau-
matol 11:233–236, 1985.
12. Stern PJ: Multiple flexor tendon ruptures following an old
anterior dislocation of the lunate. A case report, J Bone Joint
Surg (Am) 63:489–490, 1981.
reduce grip strength. In our series, tendon reconstruc-
tion does not improve grip strength.
Postoperative management following free tendon
grafting is, therefore, important. Free tendon grafting for
FDP reconstruction incurs the risk of postoperative con-
tracture in the interphalangeal joint. It is our belief that
postoperative immobilization after free tendon grafting
may lead to adhesion that compromises function, so we
adopted immediate early controlled mobilization with
a modified Kleinert elastic band technique. Early mobi-
lization after FDP reconstruction ensures larger gliding
excursion of the grafted tendon.
13. Boyes JH, Wilson JN, Smith JW: Flexor-tendon ruptures in the
forearm and hand, J Bone Joint Surg (Am) 42:637–646, 1960.
14. Folmar RC, Nelson CL, Phalen GS: Ruptures of the flexor
tendons in hands of non-rheumatoid patients, J Bone Joint
Surg (Am) 54:579–584, 1972.
15. Yamazaki H, Kato H, Hata Y, et al: Closed rupture of the flexor
tendons caused by carpal bone and joint disorders, J Hand
Surg (Eur) 32:649–653, 2007.
16. Murray WT, Meuller PR, Rosenthal DI, et al: Fracture of the
hook of the hamate, Am J Roentgenol 133:899–903, 1979.
17. Boulas HJ, Milek MA: Hook of the hamate fractures. Diagnosis,
treatment, and complications, Orthop Rev 19:518–529, 1990.
18. Bois AJ, Johnston G, Classen D: Spontaneous flexor tendon
ruptures of the hand: Case series and review of the literature,
J Hand Surg (Am) 32:1061–1071, 2007.
19. Prosser GH, Sterne GD, Nancarrow JD: Intratendinous
rupture of flexor digitorum profundus caused by non-specific
synovitis, Br J Plast Surg 55:77–79, 2002.
20. Matloub HS, Dzwierzynski WW, Erickson S, et al: Magnetic
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22. Kumar BA, Tolat AR, Threepuraneni G, et al: The role of
magnetic resonance imaging in late presentation of isolated
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 C Rupture of the Pulleys
Rohit Arora, MD, and Markus Gabl, MD
OUTLINE
We present our experience with a total of 23 patients
with closed traumatic lesions of the flexor pulleys that
required surgical reconstruction. The A2 pulleys were
reconstructed with use of one of the two methods. In
extensor retinaculum grafting, a strip of extensor reti-
naculum together with the periosteum from the floor
of the extensor tunnel is harvested. After bilateral
holes are drilled in the palmar aspect of the phalanx
at the distal and proximal ends of the A2 pulley, the
graft is fixed by the periosteum to the bone of the
phalanx. The ligamentous portion of the graft is
sutured to the remnants of the pulley system. It is
important to fix the graft adequately to the remnants
of the sheath. In palmaris longus tendon grafting, a slip
of the tendon is passed through holes created in the
remnants of the A2 pulley, and the graft is sutured to
itself or to the fibrous rim at each end of the pulley.
Postoperatively, the fingers were immobilized with a
palmar splint extending from the distal interphalan-
geal to the proximal palmar crease for 4 weeks. The
range of active digital motion, pinch strength, and grip
power of the hand improved to the levels close to
those of the contralateral uninjured hand with both
methods. Extensor retinaculum as an intrasynovial
tissue may have less resistance to tendon gliding than
a palmaris longus graft.
Detailed anatomic and mechanical investigations of the
finger flexor tendon sheath and pulley system have
allowed better understanding of biomechanical impor-
tance of the cruciate and annular pulleys.1 Pulleys main-
tain the digital flexor tendons close to the axes of the
joints and secure efficiency in finger flexion by provid-
ing the most efficient use of flexor tendon excursion.2 If
the pulleys are injured, the tendons are displaced volarly
(bowstringing), leading to a decreased maximum range
of active joint flexion and power and to an increased
risk of developing fixed flexion contractures.3
In acute cut injuries, flexor tendons are frequently cut
through a laceration in the pulley system; partial or
complete injuries of the pulleys are common. Closed
ruptures of the flexor tendon pulleys are rare injuries
and most of them are reported to occur during rock
climbing.4-6
Biomechanical studies demonstrated that the mech­
anical load between finger flexor tendons and the distal
edge of the A2 pulley is especially high in rock climbers
using the “crimp grip.”5,7,8 In this position, the proximal
interphalangeal (PIP) joints are flexed 90° and the
distal interphalangeal (DIP) joints are hyperextended
(Figure 20[C]-1). The superficial and profundus flexor
tendons are at maximum possible contractile ability
in order to maintain the finger position under the
climbers’ body weight load.9 Pulley injuries (“climber’s
finger”) mostly occur as a result of grim grip when sud-
denly the climber slips off with the hand holding rock
niches, and the load to the finger is increased. Closed
flexor tendon pulley ruptures can also occur in other
situations in which a flexed finger is subjected to high
and rapidly applied forces, causing a sudden finger
extension3—for example, while lifting a heavy object or
while opening a door or drawer as seen in our patients.
The ring and middle fingers are usually injured while
the index and little fingers are less exposed.10 Generally,
reconstruction of both the A2 and A4 pulleys, the most
essential pulleys, is recommended.11
A number of surgeons reported various surgical
methods of pulley reconstruction, using various sources
of graft material like autogenous tendons,12,13 the exten-
sor retinaculum,6,14 the palmar plate of the PIP joint,14
or synthetic materials.15,16 Loop techniques are believed
to be stronger than nonencircling methods of pulley
reconstruction.16 The encircling procedures are believed
to interfere with the function of the extensor tendon
system.16
We present a retrospective review of 23 patients with
closed traumatic rupture of the flexor pulleys treated
with two techniques of nonencircling pulley reconstruc-
tion in our unit, with special reference to the long-term
functional outcome after pulley reconstruction.
METHODS AND OUTCOMES
Patients
Between 1996 and 2003, a total of 56 patients with
closed traumatic lesions of the finger pulleys were
treated in our unit. Patients with partial pulley ruptures
were treated conservatively. Twenty-three patients,
including 3 women and 20 men, with a mean age of 40
(range, 24 to 59) years, with a complete A2 pulley
rupture or with a combined A2 and A3 pulley rupture
were reviewed. Of the 23 patients, 14 had isolated rup-
tures of the A2 pulley and 9 had combined ruptures of
the A2 and A3 pulleys. The C1 pulley was ruptured in
233
234 Section 2:  Primary Flexor Tendon Surgery
Figure 20(C)-1  Crimp grip used by rock climbers to make
the best use of small niches in the rocks for safe support.
* sisted of 13 patients who had pulley reconstruction
Figure 20(C)-2  Intraoperative findings of complete
ruptures of the A2 (*) and C1 pulleys in a rock climber.
all patients (Figure 20[C]-2). Fifteen injuries were
caused by rock climbing and all of these patients
described inability to perform their sports at their previ-
ous level. Three injuries occurred while lifting a heavy
object and five occurred while opening a door or drawer.
Figure 20(C)-3  Significant bowstringing in a patient with
ruptures of A2, A3, and A4 pulleys.
These patients complained of reduced finger dexterity
while performing their daily activities and work. The
persisting impairment of finger function and strength
in these patients was the indication for surgery. Bow-
stringing was noted in all patients (Figure 20[C]-3).
Additionally, magnetic resonance imaging (MRI) and
ultrasound were performed and the diagnosis of closed
rupture of annular pulleys was verified at surgery in all
patients. Ultrasound is very useful in diagnosis.17,18
Rupture of the pulley system was indicated by tendon
bowstringing, assessed using high-resolution ultraso-
nography (Acuson Sequoia 512, 15L8W; Siemens
Medical Solutions, Erlangen, Germany) (Figure 20[C]-
4). MRI was performed in the sagittal and coronal
planes with a 1.5-T superconductive Magnetom (Vision,
Siemens Medical Solutions) to assess the bowstringing
(Figure 20[C]-5).19
Operative Techniques
We used two methods of nonencircling pulley recon-
struction in the patients. The age, sex, affected fingers,
and ruptured pulleys of the patients with two treatment
methods are shown in Table 20[C]-1. One group con-
using a graft from the extensor retinaculum of the wrist
(Figure 20[C]-6). As described by Gabl et al,6 a strip of
extensor retinaculum approximately 10 mm in width
together with the periosteum from the floor of the
extensor tunnel was used for reconstruction of the A2
pulley (Figure 20[C]-7). After drilling bilateral burr
holes in the palmar aspect of the phalanx at the distal
and proximal ends of the A2 pulley, the graft was fixed
by the periosteum to the bone of the phalanx, placing
the synovial layer innermost (Figure 20[C]-8). Addi-
tionally, the ligamentous portion of the graft was sutured
to the remnants of the pulley system. The other group
consisted of 10 patients who were treated with a free
tendon graft of the palmaris longus tendon for recon-
struction of the A2 pulley (Figure 20[C]-9). The pulley

was made by passing a slender slip of tendon graft
through perforations made in the remnants of the origi-
nal A2 pulley, and the tendon graft was sutured to itself,
or to the fibrous rim at each end, with two sutures,
resulting in a shoelace-like reconstruction, as described
by Kleinert and Bennett13 (Figure 20[C]-10).
Postoperative Care
Postoperatively, patients of both treatment groups were
immobilized with a palmar splint extended from the
DIP to the proximal palmar crease for 4 weeks. The
metacarpophalangeal (MCP) joint and the PIP joint
A
B tive PIP joint flexion was 80° (75° to 90°). After surgery,
Figure 20(C)-4  A, Preoperative longitudinal
ultrasonography scans showing pulley injury (A2, C1, A3)
with bowstringing of tendon and increased distance (arrow)
between phalanx and tendon. B, Postoperative longitudinal
ultrasonography scans after pulley reconstruction (A2) using
an extensor retinaculum graft showing decreased distance
(arrow) between phalanx and tendon.
Table 20(C)-1  Patient Demographics for Two Groups of Patients
Graft Materials Total Patients Sex (M/F)
Extensor retinaculum 13 11 : 2
Palmaris longus 10 9 : 1
Chapter 20C:  Rupture of the Pulleys 235
were kept in full extension. Physiotherapy was started
after splint removal. Manual work, full load-bearing,
and sport activities were not permitted for 3 months.
The time from injury to surgery was 9 (range, 6 to 13)
weeks for patients treated with extensor retinaculum
graft and 7 (range, 5 to 9) weeks for patients treated with
palmaris longus tendon graft.
Evaluations
The mean follow-up was 48 (range, 18 to 43) months
after extensor retinaculum graft and 57 (range, 16 to 48)
months after palmaris longus tendon graft. Evaluations
included measurement of the ranges of motion of all
joints of involved fingers using a goniometer. Pinch
strength and the power grip strength were measured.
The circumference of the finger was measured at the
distal end of the A2 pulley. The outcome was also
assessed using the Buck-Gramcko score.19 Patients were
asked if they would undergo the treatment again in the
event of the same injury occurring to another finger.
Results
The MCP and the DIP joints of all patients had almost
normal active movement at preoperative and postopera-
tive examination. The PIP joint extension was also unre-
stricted at preoperative and postoperative examination.
Before surgery, grip strength of the injured hand was
reduced to 42 kg (range, 29 to 57 kg) and pinch grip
reduced to 6 kg (range, 3 to 9 kg), due to pain in all
patients.
In the patients with extensor retinaculum graft, pre-
operative PIP joint flexion was 82° (70° to 90°). After
surgery, the PIP joint flexion improved to 91° (85° to
100°) (i.e., 97% of the uninjured side). Postoperative
power grip strength was 48 kg (34 to 60 kg) (96% unin-
jured side). Postoperative pinch grip strength was 8 kg
(4 to 11 kg), which was equal to that of the uninjured
side. The circumference of the finger was 76 mm (60 to
90 mm) before surgery and 70 mm (58 to 88 mm) after
surgery (94% uninjured side).
In the patients with palmaris longus graft, preopera-
PIP joint flexion was 91° (80° to 100°) (94% uninjured
side). Postoperative power grip strength was 48 kg (32
to 68 kg) (98% uninjured side); the pinch grip was 7 kg
(3 to 10 kg), equal to that of the uninjured side. The
circumference of the finger was 66 mm (58 to 80 mm)
before surgery and 62 mm (54 to 82 mm) after surgery
(94% uninjured side).
Age (Yr) Fingers Pulleys Ruptured
41 (26–51) 10 Middle, 3 ring A2 in 8, A2 + A3 in 5
38 (24–59) 7 Middle, 3 ring A2 in 8, A2 + A3 in 4
236 Section 2:  Primary Flexor Tendon Surgery

Figure 20(C)-5  A, Preoperative MRI

demonstrating bowstringing as increased
distance between bone and tendon
(arrow) after rupture of A2, C1, and A3
pulleys. B, Postoperative MRI after pulley
reconstruction (A2) using an extensor
retinaculum graft showing decreased
distance (arrow) between phalanx and
tendon.

A B

P
Graft

FDP

R ET

Figure 20(C)-6  Fixation of the extensor retinaculum graft to

the fibro-osseous floor. P, Periosteum; FDP, flexor digitorum G
profundus tendon; R, remnants of the normal pulley.

Using the Buck-Gramcko score, 10 had excellent

result, 2 had good results, and 1 had fair results after
extensor retinaculum grafting, and there were 7 excel-
lent, 2 good, and 1 fair after palmaris longus tendon
grafting. All 15 climbers returned to their previous stan-
dard of climbing. In 13 of these climbers, the pulleys
were reconstructed using extensor retinaculum. All non-
climbers returned to their previous work and described
no restrictions of finger dexterity. All patients said that
they would want similar surgery if they had the same
injury. No significant difference was noted in active
range of digital motion, finger circumference, power,
and pinch grip strength between the two methods of
reconstruction.
Figure 20(C)-7  Graft of extensor retinaculum 10 mm in
width, together with the periosteum from the floor of the
extensor tunnel. G, Extensor retinaculum graft; EPL, extensor
pollicis longus tendon.
DISCUSSION
Partial ruptures and isolated single pulley ruptures can
be treated conservatively by immobilization of all finger
motion in the acute phase and taping the injured finger
above the pulley after pain had been reduced.5 In

Figure 20(C)-8  Photograph showing reconstruction of the
A2 pulley with the extensor retinaculum graft sutured to the
remnants of the original A2 pulley, without encircling the
phalanx.
G parallel incisions in the palmar plates of each joint.21
R the phalanx for pulley reconstruction.12 Kleinert and
Figure 20(C)-9  Nonencircling technique using a free
tendon graft. A tendon weave using the fibrous rims of the
original tendon sheath, which are always present. G, Free
tendon graft; R, fibrous rim.
patients with multiple pulley ruptures, surgical repair is
recommended in the patients who have been primarily
treated conservatively, but the patients have ongoing
pain, decreased range of finger motion, and tendon
bowstringing.20 These patients are not able to resume
their previous sports and daily activities.
A number of techniques are available to reconstruct
the ruptured pulleys. The strength of belt loop pulley
reconstructions roughly correlates with the number of
loops passing around the phalanx.21 The reconstructed
pulley of triple loops resists as much load to failure as
a normal annular pulley.11 Okutsu et al22 reported the
results of six fingers with A2 pulley reconstructions using
the triple loop technique in six patients. At follow-up of
9 months to 3 years, active range of motion of MCP, PIP,
Chapter 20C:  Rupture of the Pulleys 237
Figure 20(C)-10  Photograph showing reconstruction
of the A2 pulley with a free tendon graft sutured to the
fibrous rims.
and DIP joints improved and satisfactory grip function
was achieved in all six patients. Karev made “belt pulleys”
at the MCP and PIP joint levels by making transverse
The FDP tendon was re-routed through these palmar
plate incisions as pulleys. Bunnell and Böhler harvested
a free tendon graft and encircled it several times around
Bennett used free tendon graft technique for nonencircl-
ing pulley reconstruction,13 which we have used in the
patients. Lister used the extensor retinaculum graft to
surround the phalanx as a belt loop.14 Gabl et al6
reported a combination of the technique described by
Kleinert and Bennett and Lister, using an extensor reti-
naculum that did not encircle the phalanx.
It is reported that the encircling techniques interfere
with extensor mechanism and may lead to an extension
block.16 Gabl et al6 reported on A2 pulley reconstruc-
tion in five patients using the free tendon graft tech-
nique described by Kleinert and Bennett.13 At mean
follow-up of 31 months, active range of motion of the
PIP joint was reduced by 4°, relative to the contralateral
side. The circumference of the finger at the reconstruc-
tion region was increased by 4.8 mm. All patients had
satisfactory grip function. Bowstringing was reduced in
all patients.
In our cases with reconstruction of pulleys in fingers,
both nonencircling techniques had quite satisfactory
outcomes with the benefit of not interfering with the
extensor mechanism. We assume that the remaining
limitation of PIP flexion of the fingers of our patients
was caused by scarring and/or soft tissue swelling. In
addition, intrasynovial tissue, such as extensor retinacu-
lum, may be more appropriate than extrasynovial grafts,
such as palmaris longus, because the former produces
238 Section 2:  Primary Flexor Tendon Surgery
less frictional resistance to tendon gliding.23 We know
nothing about the fate of free tendon grafts in recon-
structed pulleys. The grafted tendons likely remain avas-
cular and probably are embedded in scar.
At surgery, it is very important to fix the graft ade-
quately to withstand high loads. Interweaving the
tendon graft to the remnants of the sheath is difficult if
the site of pulley rupture is at the side and close to the
attachments of the sheath. We harvested a periosteal
strip connecting with the extensor retinaculum to
References
1. Doyle JR: Anatomy of the finger flexor tendon sheath and
pulley system, J Hand Surg (Am) 13:473–484, 1988.
2. Peterson WW, Manske PR, Bollinger BA, et al: Effect of pulley
excision on flexor tendon biomechanics, J Orthop Res 4:96–
101, 1986.
3. Bowers WH, Kuzma GR, Bynum DK: Closed traumatic
rupture of finger flexor pulleys, J Hand Surg (Am) 19:782–
787, 1994.
4. Arora R, Fritz D, Zimmermann R, et al: Reconstruction of the
digital flexor pulley system: A retrospective comparison of
two methods of treatment, J Hand Surg (Eur) 32:60–66, 2007.
5. Bollen SR: Injury to the A2 pulley in rock climbers, J Hand
Surg (Br) 15:268–270, 1990.
6. Gabl M, Reinhart C, Lutz M, et al: The use of a graft from the
second extensor compartment to reconstruct the A2 flexor
pulley in the long finger, J Hand Surg (Br) 25:98–101, 2000.
7. Schweizer A: Biomechanical properties of the crimp grip posi-
tion in rock climbers, J Biomech 34:217–223, 2001.
8. Vigouroux L, Quaine F, Labarre-Vila A, et al: Estimation of
finger muscle tendon tensions and pulley forces during spe-
cific sport-climbing grip techniques, J Biomech 39:2583–2592,
2006.
9. Marco RA, Sharkey NA, Smith TS, et al: Pathomechanics of
closed rupture of the flexor tendon pulleys in rock climbers,
J Bone Joint Surg (Am) 80:1012–1019, 1998.
10. Vigouroux L, Quaine F, Paclet F, et al: Middle and ring fingers
are more exposed to pulley rupture than index and little
during sport-climbing: A biomechanical explanation, Clin
Biomech (Bristol, Avon) 23:562–570, 2008.
11. Lin GT, Amadio PC, An KN, et al: Biomechanical analysis of
finger flexor pulley reconstruction, J Hand Surg (Br) 14:278–
282, 1989.
12. Bunnell S, Böhler J: Die Chirurgie der Hand, Wein, Wilhlem
Maudrich Verlag, Teil 1:533–643, 1958.
increase the contact area of fixation and to allow bio-
logical healing of the periosteum to the phalanx. The
extensor retinaculum graft is fixed to the floor of the
sheath with both sutures passing through the perios-
teum and sutures to the rims of the sheath, so that the
load can be distributed over a greater area of fixation.
Although this method is more demanding technically
and the donor site of the extensor retinaculum is aes-
thetically less ideal, we obtained good functional out-
comes of the fingers and high patient satisfaction.
13. Kleinert HE, Bennett JB: Digital pulley reconstruction employ-
ing the always present rim of the previous pulley, J Hand Surg
(Am) 3:297–298, 1978.
14. Lister GD: Reconstruction of pulleys employing extensor reti-
naculum, J Hand Surg (Am) 4:461–464, 1979.
15. Bader KF, Sethi G, Curtin JW: Silicone pulleys and underlays
in tendon surgery, Plast Reconstr Surg 41:157–164, 1968.
16. Widstrom CJ, Johnson G, Doyle JR, et al: A mechanical
study of six digital pulley reconstruction techniques: Part I.
Mechanical effectiveness, J Hand Surg (Am) 14:821–825,
1989.
17. Klauser A, Bodner G, Frauscher F, et al: Finger injuries in
extreme rock climbers. Assessment of high-resolution ultra-
sonography, Am J Sports Med 27:733–737, 1999.
18. Bodner G, Rudisch A, Gabl M, et al: Diagnosis of digital flexor
tendon annular pulley disruption: Comparison of high fre-
quency ultrasound and MRI, Ultraschall Med 20:131–136,
1999.
19. Buck-Gramcko D, Dietrich FE, Gogge S: Evaluation criteria in
follow-up studies of flexor tendon therapy, Handchirurgie
8:65–69, 1976.
20. Moutet F: Flexor tendon pulley system: Anatomy, pathology,
treatment, Chir Main 22:1–12, 2003.
21. Karev A: The “belt loop” technique for the reconstruction of
pulleys in the first stage of flexor tendon grafting, J Hand Surg
(Am) 9:923–924, 1984.
22. Okutsu I, Ninomiya S, Hiraki S, et al: Three-loop technique
for A2 pulley reconstruction, J Hand Surg (Am) 12:790–794,
1987.
23. Nishida J, Amadio PC, Bettinger PC, et al: Flexor tendon-
pulley interaction after pulley reconstruction: A biomechani-
cal study in a human model in vitro, J Hand Surg (Am)
23:665–672, 1998.
 CHAPTER
21  
THE EVOLUTION OF
END-TO-END SURGICAL
TENDON REPAIRS
Robert Savage, MB, FRCS, FRCS Ed Orth, MS
OUTLINE
Approximately 100 years ago, tendon repair for acute
division was performed with silk sutures using two-
strand repair methods, and although it is a gross
simplification, mediocre results with resultant poor
movement and function were attributed to tissue
adhesion and poor capacity for tendons to heal. The
problem was countered by strategies such as tendon
grafting or excision of the tendon sheath, but ulti-
mately better methods of direct repair have evolved. It
has been realized that mobilization of the finger and
the injured tendon prevents adhesion of the tendon
to tendon sheath and to bone and that the necessary
post repair mobilization can most safely be carried out
using multistrand tendon repair techniques. Current
practice divides the tendon repair into core sutures
and peripheral sutures, which together contribute
greatly to repair strength and gap resistance. Tough
synthetic suture materials that have low tissue reactiv-
ity and that retain their initial strength are now
standard. Such a strategy of robust repair and active
protected postsurgery mobilization ensures a high
chance of obtaining clinically excellent movement and
function. In addition, the worst results that follow
partial repair failure with gap formation, and total
failure with repair rupture, are infrequent.
There have been many influences on tendon repair over
the past century related to the history of repair methods,
to our understanding of the biology and healing of
tendons, to laboratory studies on repair techniques, to
availability of suture materials, and to the practice of
post surgical mobilization. There is a mountain of sci-
entific and clinical literature on this fascinating subject,
but I have drawn on a small part of it that appears most
relevant.
My impression when I commenced tendon surgery
as an orthopedic trainee in 1983 was to relate what I
saw of tendon repair as instructed, compared to other
aspects of surgery that I had learned, mainly as a general
surgery trainee in the United Kingdom. In the closure
of various important tissues, for example, intestine,
bladder, abdominal wall, artery and vein graft, etc., I was
taught that the more suture material that crossed the
repair site, the greater was the repair strength and distri-
bution of load (and prevention of leakage) and the
more assured would be the subsequent result.
I was taught tendon repair by using a two-strand
Bunnell or Kessler type repair and was told the outcome
of repair was likely to be complicated by a high inci-
dence of repair dehiscence, tendon adhesions, and stiff-
ness. I remember thinking that the repair did not match
the general closure principles I had learned.
Tendon repair has changed significantly since then
and I would say that now it is accepted in many hand
centers that a multistrand repair is required to allow
protected movement during the early stages of healing,
so critical for preventing adhesions, and that in most
circumstances this will result in satisfactory movement,
a low incidence of rupture, and a good functional
outcome.
EARLY REPAIRS AND SURGICAL STRATEGY
In 1922, Bunnell1 described the principles of tendon
repair that we would find it hard to disagree with now.
His details and materials then were slightly different to
ours now, but the idea then was similar. He described a
robust criss-cross suture, in the anterior half of the
tendon to protect the tendon blood supply, sufficiently
strong to allow early movement, with little exterior
exposure of suture material to reduce adhesion, a splint
with the wrist flexed but the fingers free so that “the
muscles that pull the tendons are thus robbed of their
power of too much traction and still they can keep the
tendon actively moving.” Cooperation by the patient
was essential.
Just a year later in 1923, Lahey2 reported a method
of tendon repair that used a grasping technique where
the suture material encircled some of the tendon fibers,
gripping them tightly to prevent slippage. Three addi-
tional interrupted sutures at the tendon junction were
added to promote accurate apposition. The sutures were
overtightened sufficient to allow the suture to settle in
239
240 Section 2:  Primary Flexor Tendon Surgery
when the tendon was moved and active postoperative
finger mobilization was commenced. The suture mate-
rial was either silk or linen. Regrettably this work did
not contain clinical results but it would be fascinating
to try out this method today, for it seems not dissimilar
to some current methods and it used active mobiliza-
tion prior to a very long period where immobilization
or passive mobilization was used.
In 1944, Bunnell3 advocated overtightening the
sutures slightly to counteract the tendency for tendon
ends to separate and now he also immobilized the
finger for 3 weeks after surgery. He also popularized the
use of stainless steel for its low biological reaction and
high tensile strength. To counteract the tendency of wire
to break when repeatedly bent, he developed the pull-
out wire system. Bunnell had named zone 2 of the
fingers “no man’s land” for primary tendon repair. It is
not clear exactly what caused poor results in Bunnell’s
cases, although from the discussion that follows we
might assume it was a subtle mix of repair quality and
postsurgical immobilization. Tissue adhesion at the
repair site was recognized, and he popularized primary
tendon grafting, thus taking the site of surgical repair
away from zone 2 and placing it at the end of the finger
and within the palm or forearm.
In 1941, Mason and Allen4 devised a technique that
was quite similar to the subsequent original Kessler
repair in 1973.5 After the creation of an anchor point
on each side of the tendon the suture was passed trans-
versely across the tendon but proximal to the anchor
point and then tied to the corresponding suture from
the opposite tendon end. Additional sutures were placed
at the tendon margin. Animal studies showed that the
external sutures were soon covered by a thin sheet of
tissue, countering the argument that sutures on the
tendon surface should be avoided because they caused
adhesions. Again, reactive silk was used and there were
multiple knots, giving potential for weakness.
In 1960, Verdan6 described primary repair in zone 2
using a completely different strategy to counteract fre-
quently observed poor results from tendon grafting and
from the adhesions that followed attempts at primary
repair. His repair comprised two pins that transfixed the
tendon at a distance from the cut end and a fine arterial
type epitendinous suture. The sheath at the repair site
was excised for 1 inch so that the adhesions necessary
for healing were not attached to firm tissue. Results were
not particularly good by current standards but one of
his principles has stood the test of time, for the marginal
peripheral suture is widely used now.
In 1973, Kleinert et al7 described a simplified short
criss-cross core suture, a variant of the Bunnell longer
criss-cross suture, and a peripheral marginal running
suture. The principle was to produce a neat repair with
no gaps and then to apply the now well-known elastic
band dynamic mobilization system. They used synthetic
suture materials of fine caliber, 5-0 for the core repair
and 6-0 or 7-0 for the peripheral running suture. The
sheath was opened sufficiently to complete the repair
but was retained enough to prevent bowstringing.
Results from primary repair were improved but signifi-
cant numbers of tenolysis were required. It would be
interesting to speculate whether there would have been
advantage if they had used the probably superior Mason-
Allen or original Kessler core repair.
By 1981, Kleinert et al8 had changed to a modified
Kessler core suture of 3-0 or 4-0 braided polyester
together with a 6-0 nylon epitendon suture. Both these
repair elements persisted for most of the next 25 years
mainly for the good, and there was widespread develop-
ment of hand therapy services that were an essential part
of Kleinert’s method.
PATHOLOGY OF TENDON HEALING
Our understanding of tendon healing capability has
strongly influenced clinical practice over the decades,
sometimes for the better and sometimes for the worse.
In 1932, Mason and Shearon,9 studying dog tendons,
found that sheath tissues proliferated, that tendon ends
frequently separated, and that the resultant gap became
filled with blood and healing tissue that grew out from
the tendon ends. This suggested that the sheath should
be repaired and that the tendon should be moved.
Although this was practiced by Bunnell in 1922 and
Garlock in 1926,10 this practice did not seem to persist.
Other studies demonstrated that mobilized animal
tendons regained strength more quickly than immobi-
lized tendons.
The views of Peacock (1965)11 and Potenza (1969)12
dominated for a couple of decades. The widely held
view on tendon healing was that finger and sheath
tendons had very little capacity for healing. Peacock
popularized the “one wound” concept in which healing
to all tissues from skin down to bone was in the general
process of inflammation, granulation, and scar forma-
tion, such that expecting the tendon to move within the
scar appeared impractical.
Potenza’s view was possibly more negative than this,
for he concluded that tendon had no repair potential
itself and that healing only occurred when granulation
tissue grew from the neighboring tissues and tendon
sheath into the tendon, although following subsequent
work it seems their conclusions were misinterpreted. He
found that surgical pricking of the tendon induced
adhesions and that worse damage to the tendons pro-
duced more adhesion. Excision of the tendon sheath
caused no delay of healing and this practice was advo-
cated by Verdan.6
Matthews and Richards (1976)13 and Lundborg
(1976)14 showed that tendon proliferation was seen
in parts of rabbit tendon devoid of blood supply,
apparently as a result of nutrition by synovial fluid.
 Chapter 21:  The Evolution of End-to-End Surgical Tendon Repairs
In addition, Matthews and Richards (1974, 1976)15
designed a very clever biological model for tendon
healing experimentation. This followed a clinical obser-
vation by Harold Richards (personal communication)
that sometimes when a clinical case of tendon division
presented late, on exploring the tendon sheath, little by
way of adhesion and scarring was found around the
tendon end. They postulated that it was the factors that
surgeons apply to the finger that caused poor healing
and adhesion formation. The laboratory experiments
were carried out in rabbit flexor tendons. The ingenious
part of the methodical analysis was to partly divide the
tendon so that it could be observed within the tendon
sheath in an unsutured, non–sheath-injured, and non-
immobilized paw. This setup served as the control for
subsequent addition of surgical factors, namely sutur-
ing, sheath injury, and immobilization.
The control tendons showed evidence of healing
within the partial tendon gap and no sign of adhesions.
The three surgeon-induced factors each produced
modest adhesions between the tendon and the tendon
sheath, but these resolved with time. When two factors
were applied together, there were moderate adhesions
that eventually resolved. But when all three factors
were applied, the adhesions were dense, restrictive, and
unresolving.
These very important studies certainly changed the
view on tendon healing, although the authors did not
suggest how the surgical dilemma could be resolved. As
I see it, that came gradually with surgeons carrying on
doing what they thought should work clinically. I argue
in retrospect that these and many other laboratory
studies support the notion that if surgical repair can be
done neatly but with sufficient strength for immobiliza-
tion to be avoided, then healing can occur without
dense adhesions forming.
FURTHER DEVELOPMENT OF SURGICAL
REPAIR TECHNIQUE
In the 1970s and 1980s, most surgeons were using a
two-strand tendon repair technique. Various ways of
making the tendon suture weave into or grip onto the
tendon fibers were devised and published. It appears
that the principle laid down by Bunnell and Kessler, that
the suture gripped firmly onto tendon fibers, was partly
lost in Kleinert’s method of the foreshortened Bunnell
core suture and the modified Kessler-type core suture,
which appears to have less gripping power onto the
tendon than the original methods.
In 1991, Mashadi and Amis16 studied the modified
Kessler technique described by Pennington in 1979,17 in
which the transverse part of the suture passed superficial
to the longitudinal part, apparently creating a locked
arrangement of suture against tendon. This was com-
pared with Verdan’s technique, which had two of the
lock arrangements, and the Ketchum repair, which had
241
three such lock points (effectively producing a blanket
stitch down each side of the tendon). The study used
stainless steel sutures and sequential radiography to
produce photographs of the suture unraveling: under
very light tension (3 N) the curly lock points began to
unravel, at 9 N the lock points were nearly untwisted,
and at 15 N the lock points had straightened completely
and the suture migrated progressively to the cut tendon
end. The study showed no strength advantage to the
extra lock points and a stretch disadvantage to the mul-
tiple lock points, because there was more suture to
unravel and to create a wider gap. The authors con-
cluded that the “locking loop” should not be included
in designs for load-bearing tendon repair.
However, Kleinert popularized the very important
epitendon or peripheral suture, previously described by
Verdan, with the principal aim of creating a smooth,
neat repair. Wade et al (1989)18 investigated the mechan-
ical properties of the peripheral suture. Using a simpli-
fied Kessler core repair without locking loops, they
added a running “over and over” peripheral stitch
(Kleinert) using 5-0 braided polyester; and they studied
a Halsted-type peripheral repair using 5-0 polypropyl-
ene. Their values for initial gap forming under a load
test were core stitch alone, 3.4 N; core stitch with
running peripheral suture, 22 N; core stitch with Halsted
peripheral suture, 39 N.
Kitsis et al19 subsequently used the Halsted periph-
eral repair clinically and reported a large series with very
good results and a very low rupture rate. The Halsted
repair is easy to perform and the suture lies mainly
beneath the tendon surface.
Silfverskiöld and Andersson20 taught us that a periph-
eral cross-stitch repair (Figure 21-1) gave similar loads
and gap resistance to Wade’s Halsted-type repair (namely
about 50 N at a 2-mm gap and 60 N ultimate failure).
A minimum of 14 strands is necessary for best effect
according to the report of Kubota et al in 1996,21 but
Figure 21-1  A 14-strand Silfverskiöld peripheral suture.
(Modified from Silfverskiöld KL, Andersson CH: Two new
methods of tendon repair: An in vitro evaluation of tensile
strength, and gap formation, J Hand Surg [Am] 18:58–65,
1993, Figure 1b.)
242 Section 2:  Primary Flexor Tendon Surgery
Anchor
point
Anchor Anchor
point point
A Dorsal
Tendon Tendon
1 2
3 4
5 6
B rupture rate.23 Interestingly, Sandow and McMahon’s
Figure 21-2  A six-strand Savage repair. A, Position of
anchor points. B, Six type 3 anchor points: six strands.
(Modified from Savage R: In vitro studies of a new method of
flexor tendon repair, J Hand Surg [Br] 10:135–141, 1985,
Figure 6a, b.)
this is easy to achieve with seven suture bites on each
side of the tendon: their repair was combined with a
two-strand modified Kessler core suture. Suture material
in Silfverskiöld’s cross-stitch was left on the outside of
the tendon, something that has worried many surgeons,
but many recent studies have used the repair without
apparent extra adhesion.
In 1985 I published a laboratory study on the deriva-
tion of a new technique of core suture.22 The principle
was to use the most effective suture material, to find the
most effective junction of suture onto tendon (then
called “grasp” but which I now call “anchor point”), and
to use multiple strands of suture material. In addition,
the three anchor points were positioned on the radial
lateral, ulnar lateral, and volar sectors of the tendon to
avoid the dorsal vascular supply to the tendon (Figure
21-2A). I tested three patterns/types of anchor point:
type 1 (least intricate) had the lowest strength and the
greatest slippage under tension, and type 3, the most
complex anchor point, gripped the tendon fibers reli-
ably with little slippage, such that in the test on pig
extensor tendon, at the point of ultimate failure either
the suture snapped or a piece of tendon was stripped
out from the tendon substance. The type 2 anchor point
characteristics were between those of types 1 and 3. A
six-strand repair created by using the “type 3” anchor
Figure 21-3  A six-strand Sandow single-cross grasp:
modified Savage technique. (Modified from Sandow MJ,
McMahon MM: Single-cross grasp six-strand repair for acute
flexor tenorrhaphy: Modified Savage technique, Atlas Hand
Clin 1:65–76, 1996, Figure 16.)
points (Figure 21-2B) without an epitendon suture,
showed a 2-mm gap force of about 4 kg and a maximum
strength of about 6 kg. These values were about three
times greater than two-strand core repairs without a
peripheral suture and quite similar in strength to Wade’s
peripheral type repair. Both the Wade and the Savage
studies indicated the very powerful effect of multistrand
repairs whether the sutures be peripherally or centrally
placed. I used my method clinically and without formal
physiotherapy produced excellent outcomes with a low
(1996) anchor point in their modified six-strand Savage
repair24 and Xie and Tang’s (2005) type B “embedded
cross-lock” anchor point25 were the same as my type 2
anchor point in the 1985 study.
Other simpler methods of creating six-strand core
repairs have evolved. In 1996, Sandow and McMahon24
published a simpler anchor point (as noted earlier)
(Figure 21-3) with reduced needle passes, now known
as the Adelaide repair in four-strand form, also has a
simple epitendon suture. In 1994, Tang et al26 com-
bined the principles of Savage’s six-strand repair with
Tsuge et al’s (1975)27 two-strand technique, thus creat-
ing a six-strand Tsuge-type repair. A simple peripheral
epitendon suture was added to prevent gapping.
A way of inserting two strands easily emerged with
Gill et al’s (1999)28 use of a looped suture; being a
single needle swaged onto two ends of a nylon suture,
it could be easily anchored into the tendon by a single
transverse pass of the needle through tendon, with the
needle hooking through the loop. Then it was run down
to the cut end and into the other tendon end where the
suture was inserted about 1 cm; one thread was cut and
the other was passed transversely to create an anchor
point and was knotted at the correct length: an epiten-
don suture was added to prevent gapping. Critics will
notice that although there are six suture strands, there
are only two anchor points on each side, so the repair
is potentially weaker than a repair with three anchor
points.
Four-strand core repairs have proliferated, as a com-
promise to the complexity of six-strand repairs, where
smaller tendons do not accommodate six strands and
three anchor points, and for those who fear, with some
 Chapter 21:  The Evolution of End-to-End Surgical Tendon Repairs
Tang method
M -Tang method
Figure 21-4  A six-strand Tang method—three Tsuge
sutures and six-strand M-Tang method. (Modified from
Wang B, Xie RG, Tang JB: Biomechanical analysis of a
modification of Tang method of tendon repair, J Hand Surg
[Br] 28:347–350, 2003, Figure 2.)
justification, that extra damage to the tendon may result
from more needle insertions. Patterns used include
combinations of modified Kessler, in line, at right
angles, and side by side, and looped sutures have been
paired, tripled, or looped at one end, the “M Tang”
described by Wang et al29 in 2003 and Cao and Tang30
in 2005 (Figure 21-4).
Optimum anchor point position is about 1 cm from
the cut end, according to Cao et al (2006)31 and Tang
et al (2005),32 and optimum anchor point diameter is
about 2 mm, according to Xie et al (2005).33 Despite
much research, it is not clear exactly what style of anchor
point is best; indeed, it may be emerging from Xie and
Tang’s (2005) studies25 and Viinikainen et al (2004)34
that perhaps the anchor point pattern is not as impor-
tant as the multiplication of anchor points and strand
numbers. At least this may be true for repairs treated by
the current favored controlled semiactive mobilization
regimen, but it might not be true, for example, if the
repair was not protected after surgery, although this has
not been tried formally.
It is a possibility that anchor point type cannot be
tested adequately in pig flexor tendons, for Hausmann
et al35 and Peltz et al36 showed there was more resistance
to suture pull-out in pig flexors than sheep or human
flexor tendons in 2009 and 2010. Similarly, a single pull
test could be insufficiently sensitive to distinguish one
anchor point type from another and cyclic load tests
would better mimic real life: In 2005, Matheson et al37
showed minor differences and poor survivorship for
both simple and Silfverskiöld peripheral repairs but
marked differences comparing these repairs to the Savage
repair, which showed 100% survivorship under cyclic
tests. In 1998, Thurman et al,38 in cyclic load tests
in human tendons, showed less gapping with four-
strand Strickland repairs and six-strand Savage repairs
compared to two-strand original Kessler repairs and
243
A F
F F
F
B F
Figure 21-5  A, Effective anchor points with no slack to
allow lengthening in a four-strand repair. B, Ineffective grip
of tendon by suture allowing lengthening in a two-strand
repair. (Modified from Xie RG, Xue HG, Gu JH, et al: Effects
of locking area on strength of 2- and 4-strand locking
tendon repairs, J Hand Surg [Am] 30:455–460, 2005,
Figure 4.)
a proportionate increase in ultimate strength related
to core strand number. Load sharing between suture
strands appears to be an important part of the repair
and it has been argued that a less complex anchor point
contributes to equal load sharing between suture strands
and thus overall improved strength across the whole
repair.
An important element of repair design is that sutures
should pass from the cut end to the anchor point, and
then back to the cut end immediately, then to the
opposite cut end to make another anchor point, and
then return to the cut end, etc., so that the sutures cross-
ing the tendon gap are multiplied (Figure 21-5A),
according to Xie et al.33 In the modified Kessler repair,
the suture crosses from the first to the second anchor
point by crossing to the opposite side of the same
tendon end, losing the mechanical effect of suture cross-
ing the tendon gap, halving the number of strands in
the repair and creating coils to lengthen under tension
(Figure 21-5B).
Studies have demonstrated the very clear mechanical
advantage of increasing the suture caliber from size 4-0
to 3-0 but, again, in smaller tendons, larger sutures
may not sit comfortably within the tendon. More con-
troversial is the choice of suture material, weighing
the advantage of tougher materials (fiberwire, braided
polyester) with a rough surface against more flexible
materials (polyethylene, polypropylene), which are
slightly weaker but have a with a smooth surface. There
244 Section 2:  Primary Flexor Tendon Surgery
is no advantage to absorbable materials, which may
weaken and cause tissue reaction.
RELATION OF POSTSURGICAL MOBILIZATION
METHODS TO SURGICAL REPAIR TECHNIQUE
Once it became clear that postsurgical mobilization of
fingers could result in excellent outcomes, varying forms
of postsurgical mobilization have evolved and, I believe,
have influenced the way in which surgical repair is
carried out.
In 1973, Kleinert et al, using “dynamic passive mobi-
lization,” showed us that with a relative weak tendon
repair, good mobility could be achieved. However, some
of the poor results with repair rupture39 and repair
stretching and subsequent scar formation40 suggested
that with a stronger tendon repair technique, these poor
outcomes could be improved.
What we now call “controlled active mobilization”
(CAM), initially described by Small et al41 in 1989, dis-
carded the elastic band of Kleinert, replacing gentle
active movement within a tendon splint, and the authors
showed good results in the majority of cases but a 10%
rupture rate. Interestingly, they used the original Kessler/
Mason-Allen core suture with the epitendon part of
Kleinert’s repair technique but not the modified Kessler
core suture, which arguably is weaker.
Following the good results of Small et al, CAM has
been used widely (with variations in exact technique),
although in the United Kingdom at least, it did not yield
the good results in all centers. For example in 1998,
Peck et al,39 in Manchester, reported a 46% rupture rate,
References
1. Bunnell S: Repair of tendons in the fingers, Surg Gynec Obstet
35:88–97, 1922.
2. Lahey FH: A tendon suture which permits immediate motion,
Boston Med Surg J 188:851–852, 1923.
3. Bunnell S: Surgery of the Hand, Philadelphia/London/
Montreal, 1944, JB Lippincott.
4. Mason ML, Allen HS: The rate of healing of tendons: An
experimental study of tensile strength, Ann Surg 113:424–
459, 1941.
5. Kessler I: The “grasping” technique for tendon repair, Hand
5:253–255, 1973.
6. Verdan CE: Primary repair of flexor tendons, J Bone Joint Surg
(Am) 42:647–657, 1960.
7. Kleinert HE, Kutz JE, Atasoy E, et al: Primary repair of flexor
tendons, Orthop Clin North Am 4:865–876, 1973.
8. Kleinert HE, Schepels S, Gill T: Flexor tendon injuries, Surg
Clin North Am 61:267–286, 1981.
9. Mason ML, Shearon CG: The process of tendon repair: An
experimental study of tendon suture and tendon graft, Arch
Surg 25:615–692, 1932.
10. Garlock JH: Repair of wounds of the flexor tendons of the
hand, Ann Surg 83:111–122, 1926.
11. Peacock EE: Biological principles in the healing of long
tendons, Surg Clin North Am 45:461–476, 1965.
12. Potenza AD: Mechanisms of healing of digital flexor tendons,
Hand 1:40–41, 1969.
while in 1994, Elliot et al42 reported a 4% rupture rate,
again raising the possibility that the surgical repair was
not sufficiently strong for CAM. Among other possible
differences between the two series, the repair techniques
were slightly different: even though both used a two-
strand core suture together with the simple over-and-
over epitendon suture, the 46% rupture rate was
associated with the probably weaker modified Kessler
core suture popularized by Kleinert, and the 4% rupture
rate was associated with a more original version of
Kessler’s, which Elliot describes as Kessler/Kirchmayer
(personal communication). The Manchester group now
uses four or six strand core sutures with much improved
results with CAM. There are other examples of this real-
ization around the globe.
SUMMARY
It does appear that 90 years later we have more or less
met Bunnell’s goal. Robust suture repairs have evolved
by multistrand design, both in core sutures and in
peripheral sutures. These are in the main sufficiently
strong to allow early movement but within the restric-
tions of a careful program of exercises and curtailed
activity to protect the repair during healing, and the
results are mainly good. It has taken this time to advance
gradually, learning from use of synthetic low reactivity
sutures, correcting errors in the principles of repair
and mobilization, resolving misunderstandings of the
pathology of healing, and applying simple mechanics
to suture design.
13. Matthews P, Richards H: Factors in the adherence of flexor
tendon after repair: An experimental study in the rabbit,
J Bone Joint Surg (Br) 58:230–236, 1976.
14. Lundborg G: Experimental flexor tendon healing without
adhesion formation: A new concept of tendon nutrition and
intrinsic healing mechanisms. A preliminary report, Hand
8:235–238, 1976.
15. Matthews P, Richards H: The repair potential of digital flexor
tendons: An experimental study, J Bone Joint Surg (Br)
56:618–625, 1974.
16. Mashadi ZB, Amis AA: The effect of locking loops on the
strength of tendon repair, J Hand Surg (Br) 16:35–39, 1991.
17. Pennington DG: The locking loop tendon suture, Plast Recon-
str Surg 63:648–652, 1979.
18. Wade PJF, Wetherell RG, Amis AA: Flexor tendon repair: Sig-
nificant gain in strength from the Halsted peripheral suture
technique, J Hand Surg (Br) 14:232–235, 1989.
19. Kitsis CK, Wade PJF, Krikler SJ, et al: Controlled active motion
following primary flexor tendon repair: A prospective study
over 9 years, J Hand Surg (Br) 23:344–349, 1998.
20. Silfverskiöld KL, Andersson CH: Two new methods of tendon
repair: An in vitro evaluation of tensile strength and gap for-
mation, J Hand Surg (Am) 18:58–65, 1993.
21. Kubota H, Aoki M, Pruitt DL, et al: Mechanical properties of
various circumferential tendon suture techniques, J Hand Surg
(Br) 21:474–480, 1996.
 Chapter 21:  The Evolution of End-to-End Surgical Tendon Repairs
22. Savage R: In vitro studies of a new method of flexor tendon
repair, J Hand Surg (Br) 10:135–141, 1985.
23. Savage R, Risitano G: Flexor tendon repair using a “six-strand”
method of repair and early active mobilisation, J Hand Surg
(Br) 14:396–399, 1989.
24. Sandow MJ, McMahon MM: Single-cross grasp six-strand
repair for acute flexor tenorrhaphy: Modified Savage tech-
nique, Atlas Hand Clin 1:41–64, 1996.
25. Xie RG, Tang JB: Investigation of locking configurations for
tendon repair, J Hand Surg (Am) 30:461–465, 2005.
26. Tang JB, Shi D, Gu YQ, et al: Double and multiple looped
suture tendon repair, J Hand Surg (Br) 19:699–703, 1994.
27. Tsuge K, Ikuta Y, Matshuishi Y: Intra-tendinous tendon suture
in the hand: A new technique, Hand 7:250–255, 1975.
28. Gill RS, Lim BH, Shatford RA, et al: A comparative analysis
of the six strand double loop flexor tendon repair and three
other techniques: A human cadaveric study, J Hand Surg (Am)
24:1315–1322, 1999.
29. Wang B, Xie RG, Tang JB: Biomechanical analysis of a modi-
fication of Tang method of tendon repair, J Hand Surg (Br)
28:347–350, 2003.
30. Cao Y, Tang JB: Biomechanical evaluation of a four-strand
modification of the Tang method of tendon repair, J Hand
Surg (Br) 30:374–378, 2005.
31. Cao Y, Zhu B, Xie RG, et al: Influence of core suture purchase
length on strength of four-strand tendon repairs, J Hand Surg
(Am) 31:107–112, 2006.
32. Tang JB, Zhang Y, Cao Y, et al: Core suture purchase affects
strength of tendon repairs, J Hand Surg (Am) 30:1262–1266,
2005.
33. Xie RG, Xue HG, Gu JH, et al: Effects of locking area on
strength of 2- and 4-strand locking tendon repairs, J Hand
Surg (Am) 30:455–460, 2005.
245
34. Viinikainen A, Göransson H, Huovinen K, et al: A com­
parative analysis of the biomechanical behaviour of five
flexor tendon core sutures, J Hand Surg (Br) 29:536–543,
2004.
35. Hausmann JT, Vekszler G, Bijak M, et al: Biomechanical com-
parison of modified Kessler and running suture repair in 3
different animal tendons and in human flexor tendons,
J Hand Surg (Am) 34:93–101, 2009.
36. Peltz T, Haddad R, Savage R, et al: A comparison of human,
porcine and ovine deep flexor tendons. What is the ideal
animal model for in vitro flexor tendon studies? Proceedings
of 15th Congress of the FESSH. June 23–26, 2010. Bucharest,
Romania.
37. Matheson G, Nicklin S, Gianoutsous MP, et al: Comparison
of zone II flexor tendon repairs using an in vitro linear cyclic
testing protocol, Clin Biomech 20:718–722, 2005.
38. Thurman RT, Trumble TE, Hanel DP, et al: Two-, four- and
six-strand zone II flexor tendon repairs: an in situ biome-
chanical comparison using a cadaver model, J Hand Surg
(Am) 23:261–265, 1998.
39. Peck FH, Bucher CA, Watson JS, et al: A comparative study of
two methods of controlled mobilization of flexor tendon
repairs in zone 2, J Hand Surg (Br) 23:41–45, 1998.
40. Ejeskar A: Finger flexion force and hand grip strength after
tendon repair, J Hand Surg (Am) 7:61–65, 1982.
41. Small JO, Brennen MD, Colville J: Early active mobilisation
following flexor tendon repair in zone 2, J Hand Surg (Br)
14:383–391, 1989.
42. Elliot D, Moiemen NS, Flemming AF, et al: The rupture
rate of acute flexor tendon repairs mobilized by the con-
trolled active motion regimen, J Hand Surg (Br) 19:607–612,
1994.
 CHAPTER
22  
OUTCOMES OF FLEXOR
TENDON REPAIRS AND
METHODS OF EVALUATION
Jin Bo Tang, MD
OUTLINE
Reports of clinical flexor tendon repairs over the past
20 years have documented good or excellent recovery
of function in three-fourths of patients treated in the
finest hand centers worldwide. The most significant
changes in conception and technique regarding flexor
tendon repairs are (1) use of stronger surgical repair
techniques (either multistrand core suture or stronger
peripheral suture) and (2) inception and development
of active finger flexion exercise regimens. Over the past
two decades, rupture rates of the flexor tendon repair
in the fingers gradually declined from around 10% to
less than 2% to 4%, and rupture rates of thumb flexor
tendon repair declined from 10% to 17% to 0%. The
original Strickland and Glogovac criteria are most
popularly used to evaluate the recovery of total active
motion of the fingers. A few novel evaluation methods
emerged, including Moiemen-Elliot’s distal interpha-
langeal joint–only method for zone 1 repair outcomes,
and the author’s method, which incorporates modifi-
cations in grading the total active motion, measure-
ment of grip strength, and assessments regarding the
nature of finger motion. In the final part of this chapter,
I discuss a few issues relating to functional evaluation,
such as a framework of comprehensive assessment of
outcomes, the need for separate evaluation of recovery
of the tendon repair in the little fingers, and grading
the expertise of physicians in clinical reports regarding
outcomes.
The well-recognized importance and challenges in flexor
tendon repair in the hand are reflected in the number
of the past investigations (publications) relating to this
subject. The inaugural issue of the widely read Hand
Clinics was devoted to flexor tendon repair. Twenty years
later, in the preface of the second issue of Hand Clinics
for flexor tendon repair in 2005, Daniel Mass and Craig
Phillips wrote that this controversial complex topic “has
produced more articles in the peer-reviewed hand litera-
ture than any other single topic.” It is true that flexor
tendon repairs have been and remain one of the hottest
246
topics in hand surgery. The reports of outcomes of
primary repair of the injured flexor tendons were spo-
radic before the 1980s, because this practice had not
become the mainstay of surgical repair of the injury in
the early and middle of the last century. From the 1980s
up to the recent years of this century, we have seen a
great number of reports1-31 that document the outcomes
of primary, or delayed primary, tendon repair, end-to-
end surgical tendon repair methods and evolving post-
surgical rehabilitation methods.
OUTCOMES OVER THE PAST 20 YEARS
I reviewed the outcomes of primary tendon repair in
a 2005 article in Hand Clinics.1 An updated review of
the outcomes of flexor tendon repairs in fingers and
thumb over the past 20 years (1989–2009) is provided
in Table 22-1.
A few important observations can be summarized
from an analysis of outcomes over this period (as well
as the results presented in Chapter 13):
1. Good or excellent recovery of function from the
centers involved (which are among the leading
hand surgery units treating flexor tendon inju-
ries) were in around three-fourths, or 75% of the
cases.
2. The most common method of quantifying out-
comes is the original Strickland and Glogovac
method.
3. Primary or delayed primary tendon repairs were
prioritized over secondary repair by all surgeons.
4. Early tendon motion, either passive or active (or
combined), was advocated in all cases by sur-
geons and participating therapists, except for
children.
5. Early active motion regimens were adopted in
the late 1980s, initially producing a high rate of
repair rupture (around 10%) with conventional
(weaker) two-strand repairs, which has been a
great concern.
6. There has been a gradual but clear shift from
using two-strand core suture repairs to stronger
 Chapter 22:  Outcomes of Flexor Tendon Repairs and Methods of Evaluation 247

Table 22-1  Some Major Reports of Function of Primary Flexor Tendon Repairs Over the Past 20 Years
Number of Excellent/ Rupture
Years Authors Digits Zones Repair Methods Good* Rate
Finger flexor tendons
1989 Small et al 138 2 2-strand Kessler 77% (TAM) 9.4%
1989 Cullen et al 38 2 2-strand Kessler 78% 6.4%
1989 Savage and Risitano 23 2 6-strand Savage 69% (Buck- 4%
Gramcko)
1989 Pribaz et al 43 2 Becker 70% (White) 7%
1992 Tang and Shi 54 2 2-, 4-, and 81% …
6-strand repairs
1994 O’Connell et al 95 (children) 1, 2 2-strand methods 69%† 0%
†
1994 Silfverskiöld and May 55 2 Silfverskiöld 90% 3.7%
1994 Grobbelaar and 38 (children) 1–5 2-strand Kessler 82% (Lister) 7.9%
Hudson
1994 Elliot et al 244 1, 2 2-strand Kessler 79% 5.8%
1994 Tang et al 51 2 4- or 6-strand 77% (White) 4%
Tang
1996 Sandow and McMahon 23 2 4-strand Savage 78% 0%
1998 Kitsis et al 208 1–5 2-strand Kessler 92% 2.9%
87 2 88% 5.7%
1999 Fitoussi et al 58 (children) 1–5 2-strand Kessler 89% 0%
1999 Harris et al 626 1, 2 2-strand Kessler … 4.3%
129 1 … 5.0%
397 2 … 4.0%
†
2006 Elhassan et al 16 (children) 1 Bunnell pull-out 89% 0%
†
25 (children) 2 2- and 4-strand 71% 0%
Kessler
2008 Caulfield et al 416 1–4 4-strand 74% 2%
Strickland
2008 Haffmann et al 51 2 6-strand Lim/Tsai 78% 2%
26 2 2-strand Kessler 43% 11%
2008 Novali and Rouhani 16 (children) 2 6-strand 94% 0%
Strickland
16 (children) 2 2-strand Kessler 88% 6%
Thumb FPL tendon
1989 Percival and Sykes 51 1–3 2-strand Kessler 53% (White) 8%
1992 Nunlev et al 38 1, 2 2-strand Tajima or …‡ 3%
2-strand Kessler
*The results were evaluated with Strickland and Glogovac criteria unless specified.
†
These percentages are percent return of TAM judged by Strickland and Glogovac criteria.
‡
Excellent and good rates were not reported. The active IP joint motion was, on average, 35°.
Continued
248 Section 2:  Primary Flexor Tendon Surgery

Table 22-1  Some Major Reports of Function of Primary Flexor Tendon Repairs Over the Past 20 Years—cont’d
Number of Excellent/ Rupture
Years Authors Digits Zones Repair Methods Good* Rate
1999 Sirotakova and Elliot 30 (1st period) 1, 2 2-strand Kessler 70% (White) 17%
73% (Buck-
Gramcko)
39 (2nd period) 1, 2 2-strand Kessler 67% (White) 15%
72% (Buck-
Gramcko)
49 (3rd period) 1, 2 2-strand Kessler 76% (White) 8%
80% (Buck-
Gramcko)
2004 Sirotakova and Elliot 48 1, 2 Silfverskiöld 73% (White) 0%
77% (Buck-
Gramcko)
2009 Giesen and Elliot et al 50 1, 2 6-strand Tang 78% (White) 0%
82% (Buck-
Gramcko)

four- or six-strand surgical repairs, or to use
stronger peripheral repair since 1990s.
7. Use of stronger surgical repairs has lowered
rupture rates, but in most reports, ruptures have
not been eliminated, with 2% to 4% rupture rates
frequently recorded.
8. Over the past decade, more surgeons have
adopted (and reported) some type of early active
motion regimen, together with use of stronger
surgical tendon repairs.
9. New tendon repair materials (such as fiberwire)
emerged, and surgeons have reported good func-
tional outcomes and fewer repair ruptures with
fiberwire repair.
10. Multiple methods are currently used to evaluate
and record the outcomes of tendon repair. Some
worldwide consensus on methods of recording
outcomes is necessary to facilitate comparisons
of results.
MAJOR REPORTS AND
IMPORTANT INFORMATION
Over the past 20 years, a number of excellent clinical
reports have highlighted some important facts regarding
primary flexor tendon repairs. In 1989, The Journal of
Hand Surgery (British Volume) simultaneously published
clinical reports of primary tendon repairs with con-
trolled early active tendon motion by Small et al,2 Cullen
et al,3 and Savage and Risitano.4 Small et al2 presented
114 patients with 138 zone 2 flexor tendon injuries
treated over a 3-year period. Ninety-eight patients were
followed and graded using the total active range of
motion (TAM) method of the American Society for
Surgery of the Hand (ASSH). The active range of motion
was graded excellent or good in 77% of the digits, fair
in 14%, and poor in 9%. Repair rupture occurred in
9.4% of the fingers (11 digits). The ruptured tendons
were re-repaired immediately and a similar early motion
program was applied. Cullen et al3 treated 34 adult
patients with 70 zone 2 flexor tendon injuries in 38
fingers; 78% fingers were rated excellent or good by the
original Strickland criteria after a mean follow-up of 10
months. Two tendons ruptured during active finger
flexion exercise. Savage and Risitano4 used their six-
strand method of repairs to treat flexor tendon lacera-
tions in 36 fingers followed by protective active finger
flexion exercise; 63% of lacerations were zone 2 and
27% were zone 1, and 69% and 100% (respectively)
achieved an excellent or good result using Buck-
Gramcko’s assessment method.
Silfverskiöld and May5 reported outcomes of use of
an innovative strong peripheral suture (cross-stitch epi-
tendinous suture) combined with a modified Kessler
core suture in treatment of flexor tendon injuries in
zone 2 in 55 digits among 46 patients. For the first 4
weeks after surgery, fingers were mobilized with a com-
bination of active extension and passive and active
flexion. Repair ruptures occurred in two tendons. Six
months after surgery, the mean TAM of the distal and
proximal interphalangeal (DIP and PIP, respectively)
 Chapter 22:  Outcomes of Flexor Tendon Repairs and Methods of Evaluation
joints in the remaining fingers was 63° and 94°, respec-
tively. Elliot et al11 reported 233 patients with complete
divisions of the flexor tendons in zones 1 and 2. Their
cases included 203 patients with 224 finger injuries (317
divided flexor tendons) and 20 patients with 30 com-
plete divisions of the flexor pollicis longus (FPL) tendon.
The patients were treated with a controlled active motion
regimen postoperatively. Repaired tendons ruptured in
13 (5.8%) fingers and 5 (16.6%) thumbs. In follow-up
of the patients treated during the last year of the study,
10 (62.5%) of 16 fingers with zone 1 repairs and 50
(79.4%) of the 63 fingers with zone 2 repairs were
rated good or excellent using the original Strickland and
Glogovac criteria.
Emphasis on the need and application of strong
(four- or six-strand) core repairs in clinical tendon
repairs appeared first in Savage and Risitano’s report4 in
the late 1980s, followed by the report of Tang and Shi7
and Tang et al7,12 in 1992 and 1994 and then a series of
reports in Atlas of the Hand Clinics by Taras et al,13
Sandow and McMahon,14 and Lim and Tsai15 in 1996.
In 1992, Tang and Shi7 reported the results of treatment
of 72 flexor tendon injuries in zone 2 in primary
or delayed primary stages; 80.4% of the fingers were
rated good or excellent results on assessment by the
Strickland and Glogovac criteria. Among 72 tendons, 32
tendons were repaired with four- or six-strand core
sutures using looped sutures, together with simple
peripheral stitches. In 1994, Tang et al12 reported 51
fingers from 46 patients with zone 2 flexor tendon lac-
erations. Doubled threads of the looped suture were
placed to repair injured flexor digitorum profundus
(FDP) or superficialis (FDS) tendons, or three threads
of the looped suture to repair the FDP tendons. The
results were good or excellent in 76.5% using White’s
criteria. They reported two repair ruptures (4%) during
the postoperative motion program. Taras et al13 used
double-grasping Kessler-type core and cross-stitch peri­
pheral sutures in repairing 21 flexor tendons (three
FPL, four FDP in zone 1, and 14 FDS or FDP in zone
2) of 14 digits. The patients underwent active finger
flexion motion initiated on the first postoperative day,
including place-and-hold exercise three times weekly
under supervision. Between therapy sessions, a standard
elastic-thread traction passive flexion and active exten-
sion program was maintained. Overall recovery of
digital motion was graded as excellent in 12 and good
in 2. The seven fingers with FDP and FDS repairs in zone
2 averaged 83% recovery of motion. Sandow and
McMahon14 reported 37 FDP tendons in zones 1 to 5
using a modified single-cross six-strand repair based on
the original Savage method followed by early active
tendon motion. Of 23 zone 2 tendon injuries in 18
patients, 78% were rated as good or excellent using the
Strickland and Glogovac criteria, with no ruptures or
need of secondary surgery. Lim and Tsai15 used six-strand
249
tendon repairs with looped suture to repair the tendon
injuries in zone 2 with good functional outcomes.
Several other reports also provide interesting and
important information about tendon repairs. Kitsis
et al16 reported results of treatment of 339 flexor tendon
repaired with two-strand modified Kessler core suture
and a Halsted peripheral suture in zones 1 to 4 of 208
fingers. The important message from this large case
series is that among 6 ruptures of the repaired tendons,
5 occurred in zone 2 and one in zone 5. Repair rupture
was most frequent in zone 2 and the rupture rate was
5.7%. Harris et al18 reviewed the results of 728 primary
zone 1 and zone 2 flexor two-strand modified Kessler
core suture tendon repairs in 526 fingers of 440
patients. A total of 23 fingers (6 in zone 1 and 17 in
zone 2) ruptured 28 tendon repairs. One hundred
twenty-nine fingers with zone 1 injuries had a rupture
rate of 5% (6 fingers) and 397 fingers with zone 2 inju-
ries had a rupture rate of 4% (17 fingers). The ruptures
occurred in 6 tendons within the first week, 5 in the
second week, 6 in the third week, 5 in the fourth week,
3 in the fifth week, and 1 in the tenth week. An impor-
tant message from this case series is that rupture can
occur anytime from the first week to the tenth week
after surgery. The “dangerous period” is postsurgical
weeks 1 to 6, and postoperative week 2 is not associ-
ated with a higher incidence of repair ruptures than
week 1 or weeks 3 to 6. More recently, Dowd et al19
analyzed the results of immediate re-repair of zones 1
and 2 flexor tendon repairs that rupture during postop-
erative early motion exercise. The outcomes of the
re-repair of the ruptured tendons were generally poorer
than the primary repairs, but function of re-repaired
tendons were still clinically acceptable, with 9 (24%)
excellent, 10 (27%) good, 5 (14%) fair, and 13 (35%)
poor when assessed by the Strickland and Glogovac
criteria out of a total of 37 fingers with re-repair of the
tendon.
In 2008, The Journal of Hand Surgery (European Volume)
published a series of reports on flexor tendon repairs
using stronger core tendon sutures (multistrand core
sutures) combined with early active flexion exercise.20-22
These reports indicate lower rupture rates among
tendons with strong core tendon repairs but also illus-
trate that it is not always possible to avoid repair rup-
tures. Caulfield et al20 reported 416 tendon repairs in
zones 1 to 4 repaired with a four-strand Strickland core
suture in 272 patients. The results were 74% good or
excellent graded by the Strickland criteria, with only 2%
repair ruptures. They had identical outcomes using
absorbable and nonabsorbable sutures. Hoffmann
et al21 reported 51 fingers of 46 patients undergoing
zone 2 flexor tendon repair using the Lim/Tsai repair
method combined with a Kleinert and Duran early
motion regimen and place-and-hold exercises. Repair
rupture occurred in 1 (2%) of 51 repaired fingers. Two
250 Section 2:  Primary Flexor Tendon Surgery
(4%) fingers required tenolysis. In the cases they treated
with the two-strand modified Kessler repair and the
Kleinert and Duran motion regimen alone, they had
repair ruptures in three fingers (11%) and tendon adhe-
sions, or dehiscence, in three fingers (11%), which
required secondary surgery. The good or excellent
outcome rate was 78% with the Lim/Tsai method and
43% with the two-strand Kessler method. Navali and
Rouhani22 reported on 32 flexor tendon repairs in zone
2 of 29 children using either the two-strand modified
Kessler method (16 tendons) or the four-strand Strick-
land method (16 tendons). They achieved good or
excellent outcomes in all fingers, except one rupture and
one fair outcome among the tendons with the two-
strand repair and one fair outcome in the tendons with
the four-strand repair.
In children, repairs of flexor tendons produced gener-
ally good or excellent results. Early motion exercise is
not essential for a tendon to regain a good range of
active motion. These observations were validated in
reports by Elhassan et al23 in 2006 and by Navali and
Rouhani22 in 2008.
Repair of the FPL tendons is usually discussed sepa-
rately from flexor tendon repair in the fingers.24-31 Siro-
takova and Elliot27,30 analyzed the results of primary
repairs of the FPL tendon followed by early active
motion with only the thumb splinted. The first 30
patients were repaired with a Kessler suture and simple
epitendinous suture. The later 49 patients underwent
repair with a Kessler suture and a reinforced epitendi-
nous suture but in a splint with the thumb position
altered and the fingers also splinted. Other reports
include those from Percival and Sykes,24 Noonan and
Blair,25 Nunley et al,26 Fitoussi et al,28 and Kasashima
et al.29 Most recently, Giesen et al31 published the latest
results of repair of the FPL tendon. They analyzed 50
FPL tendon repairs using a six-strand core repair method,
without peripheral sutures. Excellent or good results
were recorded in 78% and 82% of cases (White and
Buck-Gramcko criteria, respectively). No patients rup-
tured repairs as a result of early active mobilization.
None developed tendon dehiscence postoperatively.
The important message from this report is perhaps that
a strong core suture can adequately tolerate early active
tendon motion without the incorporation of peripheral
sutures, which is a conceptual evolution in the treat-
ment of flexor tendon injuries and may lead to signifi-
cant simplification of surgery.
The case series presented by Elliot and his col-
leagues27,30,31 over the past 20 years reflects some unique
findings relating to repair of FPL injury. Their outcomes
were increasingly improved from a rupture rate of 17%
to the present 0% rate. Their methods of tendon repair
and rehabilitation evolved greatly. The thumb flexor
tendon appears capable of returning to near-ideal func-
tion after proper repair and rehabilitation.
The use of stronger surgical repairs improved out-
comes compared with the earlier reports using weaker
repair methods but has not entirely eliminated postop-
erative repair rupture.20-22 It is the combination of strong
surgical repair, proper venting of the pulleys, and early
active motion, which reported recently,31,39,41 that has
produced more consistently good or excellent outcomes
without postoperative repair ruptures.
The above reports indicate that clinical flexor tendon
repairs had excellent or good functional return in about
three-quarters of primary tendon repairs. Nevertheless,
it should be noted that most of these reports came from
the finest hand surgery centers and that these teams
were supervised by at least one expert hand surgeon
with experience in treating flexor tendon injuries. We
may reasonably assume that outcomes in a general hos-
pital setting might achieve a lower level of success. In
other words, flexor tendon repairs might have been
unsatisfactory in a larger proportion of patients when
treated in a general hospital setting.
Over the past 20 years, the conceptual evolution in
tendon repair has been remarkable and the technical
innovations have been numerous. The most significant
changes are (1) use of stronger surgical repairs (includ-
ing core and peripheral sutures), (2) incorporation of a
variety of early active motion regimens in postsurgical
exercise, and (3) a redefinition of the management of
the pulleys (see Chapters 9 and 10). Compared to those
in earlier reports, the incidence of repair ruptures in
the most recent series has declined, typically being less
than 2% to 4%. Initiation of early active motion in the
late 1980s, use of stronger surgical repair methods and
active motion regimens in the 1990s, and incorporation
of strong surgical repairs and venting the critical pulleys
with delicate early active motion in the past decade
represent three steps in the pursuit of optimal tendon
repair and ideal recovery of function. These efforts have
transformed the outcomes of flexor tendon repairs from
being very unpredictable to their current state: fairly
predictable. My feeling is that when treated by ade-
quately trained hand surgeons, using updated concepts
and thorough knowledge of flexor tendon repairs, the
outcomes of zone 2 repairs are likely to be comparable
with repairs in the other areas of the hand.
METHODS OF EVALUATIONS
The most common method of recording outcomes is
the original Strickland and Glogovac method intro-
duced in 1980 (Table 22-2).32 This grading system is a
simplification of the method postulated by the ASSH
(Table 22-3).33 The Strickland criteria include TAM of
only the DIP and PIP joints, without inclusion of the
metacarpophalangeal (MCP) joint motion as in the
ASSH method. Strickland pointed out that inclusion of
the MCP joint in assessment of zone 2 repairs artificially
biased the results to be better as the MCP joint was
 Chapter 22:  Outcomes of Flexor Tendon Repairs and Methods of Evaluation 251

Table 22-2  Criteria of Assessment of Functional Outcomes of Flexor Tendon Repairs

% Return of Motion* Grip Strength† Quality of Motion‡ Function Grade
Strickland criteria (1980) 85–100 (>150°)
70–84 (125°-149°) Excellent
50–69 (90°-124°) Good
0-49 (<90°) Fair
Moiemen-Elliot criteria (2000)—for Poor
zone 1 injuries, the DIP joint only
85–100 (>62°) Excellent
70–84 (51°-61°) Good
50–69 (37°-50°) Fair
0–49 (<36°) Poor
Tang criteria (2007)
90–100 + Excellent or good Excellent +
− Poor Excellent −
70–89 + Excellent or good Good +
− Poor Good −
50–69 Fair
30–49 Poor
<30 Failure
*Percent return of a theoretical normal value or contralateral hand. Strickland and Tang criteria use the sum of active range of motion of the
DIP and PIP joints. The theoretical normal is 175°. Moiemen-Elliot criteria use motion of the DIP joint only compared with 74°.
†
Grip strength is recorded as (+) when it is greater than that of the contralateral hand (the nondominant hand) or over 70% of that of the
contralateral hand (dominant hand). Otherwise, grip strength is considered abnormal and recorded as (−).
‡
Quality of motion is rated on a basis of direct observation of finger motion by the evaluators. It is recorded as “Excellent” when all three
aspects—motion arc, coordination and speed—are normal; as “good” when any two are normal; as “poor” when only one, or none, is
normal.
Function is graded as excellent − or good − when either the grip strength is (−) or quality of motion is “poor.”

Table 22-3  ASSH Method of Evaluation requires the injured fingers to recover a normal active
range of motion. In reality, excellent functional status
Grade TAM*
requires a sufficiently ample TAM, but it does not neces-
Excellent 100%, Normal sarily demand that the active range of motion returns
Good >75% of the normal side to normal. In addition, flexion of the MCP joint does
not relate only to function of the FDS and FDP tendons;
Fiar >50% of the normal side
exclusion of the MCP joint from measurement yields
Poor <50% of the normal side more accurate documentation of TAM of the PIP and
Worse worse than before surgery DIP joints. Strickland modified the original criteria in
1985,34 but the modified criteria have not gained popu-
*Sum of the active range motion of the MCP, PIP, and DIP joints. larity and are considered very lenient.
The Buck-Gramcko method consists of TAM (the sum
of angles formed by the MCP, PIP, and DIP joints in
always nearly normal.32 Most subsequent authors maximal active flexion minus active flexion deficit at
adopted Strickland criteria but have not actually stated each joint) and the distance between fingertip and distal
why they preferred the Strickland criteria to the ASSH palmar crease (Table 22-4).35 This method is mainly
method. However, my experience indicates that the used by members of the German-speaking societies for
ASSH method is very strict in its “excellent” grade, which surgery of the hand. The Tubiana method is used mostly
252 Section 2:  Primary Flexor Tendon Surgery

Table 22-4  Buck-Gramcko Method Elliot38 in 2000, and my suggestion39 in 2007 of a

Item Measurement Points
method that includes modified criteria to redefine the
grades of TAM of the DIP and PIP joints and incorpora-
Distance finger pulp to 0–2.5 cm/>200° 6 tion of grip strength and quality of finger motion into
distal crease
the criteria (see Table 22-2).
Composite flexion 2.5–4 cm/>180° 4 Admittedly, my suggested method initially appears
4–6 cm/>150° 2 more complex. However, one can easily break it down
into components that can be used separately. For
>6 cm/<150° 0 example, the simplest method is to measure TAM of the
Extension deficit 0°-30° 3 DIP and PIP joints, and then use the redefined grades
to record outcomes, the essential function of the criteria.
31°–50° 2
The results can be classified into “excellent,” “good,”
51°–70° 1 “fair,” “poor,” and “failure,” without a tag of “+” or “−.”
>70° 0 It is noteworthy that I have set a more stringent bar for
grading the results as “excellent,” requiring recovery of
TAM* >160° 6 TAM to 90% of the contralateral side. Additionally, I
>140° 4 added the grade “failure” to designate cases that defi-
nitely require further surgery to restore essential digital
>120° 2
function. Nevertheless, the active range of motion
<120° 0 required for grading as good or excellent (i.e., overall
*Sum of the active range of motion of the MCP, PIP, and DIP good and excellent rate) remains the same as in the
joints. Strickland method. In this way, reports regarding total
good or excellent rates using the new method are made
comparable to those in the past using the Strickland and
Table 22-5  The White Method Glogovac method.
By adding measurement of grip strength and assess-
Grade TAM* ment of quality of finger motion, the functional status
Excellent 70%–100% of the normal side of digits can be further indicated with “+” or “−” to
provide supplementary information about hand func-
Good 60%–69% of the normal side
tion. The information relates to fine functional status of
Fair 40%–59% of the normal side the repaired tendon and indicates the degree of perfec-
Poor <40% of the normal side tion of hand function attained.

*Active range of motion of the interphalageal (IP) joint only.

FACTORS AFFECTING OUTCOMES
Adhesion Formation
Table 22-6  Finger-to-Palm Distance Method
(Boyes-Lister) Adhesion is a frequent cause of incomplete recovery of
active range of digital motion after tendon repairs
Finger-to-Palm
(Figure 22-1). Adhesions arise because trauma to the
Grade Distance* (cm) Extension Deficit (°)
tendon surface, inappropriate surgical maneuvers, and
I 0–1 0–15 lack of sufficient innate healing capacity of the tendon.
II 1–1.5 16–30 The amount and density of the adhesions are decided
by the severity of the trauma to the tendon and periten-
III 1.5–3 31–50
dinous tissues and the originating tissues. The influ-
IV >3 >50 ences of adhesions on tendon function vary according
to both the amount and density of adhesions. Repair of
*Distance between the finger pulp and the distal palmar crease in
full finger flexion.
clean-cut tendon injuries, when sufficiently moved after
surgery, may not develop adhesion or only develop
filmy adhesions. The filmy adhesions do not affect
in France. Among the less popular methods in current tendon gliding. The formation of restrictive adhesions
use are White’s method (Table 22-5)36 and the linear are seen after extensive trauma to the tendon or its sur-
measurement method introduced by Boyes and then rounding structures and jeopardize the gliding of
Lister et al (Table 22-6).37 repaired tendons. During postoperative tendon motion,
Two more recent methods introduced to record out- loose adhesions can be disrupted, or modified, to avoid
comes include the “DIP motion-only” method for the reducing the amplitude of tendon motion. However,
zone 1 tendon repairs advocated by Moiemen and moderate or dense adhesions are difficult to alter and
 Chapter 22:  Outcomes of Flexor Tendon Repairs and Methods of Evaluation 253

Trauma factors Surgical factors Postoperative factors (rehabilitation)

Trauma to tendons Surgical skills Strength of repair methods Hand position in splint
Peritendinous injuries Treatment options Healing strength of tendon Motion range of finger joints
Friction of tendon on sheath Synergistic motion of joints
Gap formation, edema Incorporation of particular
protocols for joint stiffness

Adhesion formations Repair rupture Joint stiffness

Outcome of tendon repairs

Figure 22-1  Factors that affect the outcomes of the flexor tendon repairs in the hand.

should, instead, be prevented through careful surgery
and well-supervised postoperative treatments. Tenolysis
is indicated when postoperative treatments cannot sub-
stantially improve tendon motion.
Repair Rupture
Among all the consequences of flexor tendon surgery,
repair ruptures are the worst and are of prime concern
to hand surgeons, because they require secondary oper-
ations. If ruptures occur soon after primary repair, direct
re-suture of the ruptured tendons may be attempted; if
ruptures occur at the late period, a secondary tendon
graft is indicated.40 The following factors trigger the rup-
tures of repaired tendons (see Figure 22-1):
1. Overload of the repaired tendons. Forceful or resisted
active flexion or extension of the fingers may
subject the repaired tendons to a load exceeding
the limit of the tensile resistance of the repairs.
2. Tendon edema or bulky tendons. Edema of the
tendons is inevitable after surgery, although its
severity varies among patients. Severely trauma-
tized wounds, extensive soft tissue injuries, long
duration of surgery, and poor surgical repair
maneuvers all contribute to postsurgical edema.
Edema makes the tendon bulky. In addition,
excessive suture materials also contribute to bulki-
ness. A bulky tendon increases the pressure of the
tendon on the surrounding tissues and its friction
against the sheath and pulleys during tendon
mobilization after surgery. A greater force must be
applied to the finger to move the bulky tendons
within the sheath, increasing the likelihood of
ruptures.
3. Triggering in pulleys or edges of opened sheath and
increased resistance of the repaired tendons by presence
of narrow pulleys. Annular pulleys, particularly the
A2 and A4, are narrow and restrict tendon gliding.
Edematous, or bulky, tendons are easily entrapped
by these pulleys. Edematous and bulky tendons
can trigger on the edge of the sheath or pulley
openings as well. The narrow part of the annular
pulley constricts the gliding tendons and increases
the resistance to tendon movement, which lead to
gapping or elongation of the tendon repair site.
Catching of the tendon on the edges of narrow
pulleys, halting finger flexion or extension, and
causing patients to feel a sudden increase in resis-
tance to finger motion, is a major cause of rupture
of tendon repairs. After surgery, a forceful pull to
overcome the resistance frequently leads to rupture
of the repairs.
4. Unexpected finger motion. During the period of
wearing protective splints or casts, patients may
sustain unexpected finger actions, such as when
falling down on the outstretched hand or sud-
denly gripping. These actions impose a sudden
increase in the force transmitting through the
repaired tendons with a higher risk of ruptures.
5. Misuses of the fingers. Misuses of the repaired
fingers, such as using the hand to lift a heavy
object, may exceed the repair strength of the
tendon and cause rupture.11,18
6. Unprotected active motion. Unprotected active
flexion of the finger can cause the repaired tendon
to disrupt due to great tension in the tendon.
Joint Stiffness
Stiffness of the DIP and PIP joints is frequently observed
during the rehabilitation after primary flexor tendon
repair. Stiffness of finger joints is troublesome. The
postoperative protective finger position may cause
254 Section 2:  Primary Flexor Tendon Surgery
contracture of soft tissue structures of finger joints, par-
ticularly the palmar ligaments of the PIP joints. Because
active finger motion requires both an ample gliding
amplitude of the tendons and a normal passive range
of motion of the joints, to improve the outcomes of
tendon repairs, emphasis should be placed upon pre-
venting stiffness of these joints. Rubber band traction to
the fingertip holds the PIP joint in a flexed position for
long periods, which may lead to development of palmar
ligament contracture and joint stiffness. Modifications
have been suggested to improve the finger motion and
reduce the risk of finger stiffness. In recent years, we
have begun to see fewer cases of finger stiffness after the
use of more delicate active and passive finger motion
regimens, without rubber band traction.20,21,41
Extent of Injuries
Extensive destruction of the peritendinous structures,
the presence of tendon defects, and epitendinous abra-
sion of the tendon are frequently associated with
poorer recovery of function. It is sometimes difficult to
judge whether primary tendon repairs are justified for
wounds that do not involve clean cuts but where direct
approximation of the severed stumps is still possible.
These wounds, which are typified by loss of soft tissues
(sometimes with a short segment of flexor tendons
and a portion of pulleys) over a limited area of the
fingers or palm and defects of soft tissues, are border-
line contraindications to primary tendon repair. Repair
of tendon injuries in severely traumatized wounds
may exacerbate adhesion formation and increases the
likelihood of requiring secondary tenolysis or tendon
reconstruction.
Surgical Skill
Surgical skill affects the outcomes greatly. The flexor
tendon system is composed of anatomic structures
with an intricate biomechanical relationship. Satisfac-
tory repairs of the tendons and associated structures,
particularly those in the intrasynovial regions, remain a
challenge even to an experienced surgeon. In practice,
these difficult injuries are frequently treated by residents
or general orthopedic (or plastic) surgeons without suf-
ficient expertise of flexor tendon surgery. With currently
available knowledge and technical advances, favorable
outcomes may be achieved by an experienced surgeon,
but an individual who lacks expertise may affect repairs
no better than those seen decades ago. It should be
emphasized that when no surgeons experienced in
tendon surgery are readily available, patients should
be referred to hand centers with more experience in
dealing with flexor tendon injuries. Alternatively, after
primary closure of the skin wounds, tendon injuries are
repaired at a delayed primary stage by an experienced
surgeon.
DEVELOPMENT OF COMPREHENSIVE,
UNIVERSALLY ACCEPTABLE CRITERIA
Currently, functional recovery after tendon surgery is
assessed by recording TAM of the digits or distance from
the fingertip to the palm. Grip strength and other factors
relating to tendon function have recently been inte-
grated into new criteria.39 Assessment of motion of a
specific joint relating closely to the repaired tendon,
such as assessment of only the DIP joint after zone 1
tendon repairs, has gained popularity.42 For both the
Strickland and the Moiemen-Elliot methods, issues
remain regarding standardizing the criteria of each
grade in terms of joint angles. Whether to use a fixed
degree of finger motion or the motion range of the
contralateral hand as the baseline has not yet been
agreed. In my experience, contralateral hand motion is
always more reliable than a fixed degree of finger motion
as the baseline for grading. I record angles of the affected
fingers and compute a percentile recovery of TAM com-
pared with the contralateral hand.
There are no universal criteria for documenting the
outcomes of flexor tendon repairs. I suggest that the
authors consider reporting the outcomes at different
levels (i.e., details) (Box 22-1). My preliminary sugges-
tions about such a framework are as follows:
 Level 1. The basic level (essential and relating to
active hand motion only) chiefly includes TAM of
the related joints. Ranges of motion are graded
more stringently. Requirements should be more
rigorous for grading the function as “excellent,”
and a separate grade for failure is necessary. Other
grades of the currently popular Strickland criteria
can be unchanged.
The criteria can be used independently as the
basic level criteria; grip strength and items describ-
ing the nature of motion can be integrated to con-
struct the expanded basic level criteria.
 Level 2. The intermediate level (more comprehen-
sive, but limited to hand function). Criteria incor-
porate TAM, grip strength, other components
reflecting hand motion, sensibility, and assess-
ment of vascular circulation. Multiple aspects of
hand function are reflected at this level.
 Level 3. The advanced, or comprehensive, level (com-
prehensive, relating to entire body function, and
incorporating social environmental impacts). Cur-
rently, the World Health Organization (WHO) is
developing universally adaptable sets of criteria to
reflect the functional status of the hand. This set
of criteria takes into consideration whole body
function, activities, and both environmental and
personal factors. One study has utilized this
concept to evaluate function after flexor tendon
 Chapter 22:  Outcomes of Flexor Tendon Repairs and Methods of Evaluation 255

Box 22-1 Suggestion About Three Levels in Recording Outcomes of Tendon Repairs in the Hand

Level 1—Basic: Relating to Motion of the Finger/Hand Only

My suggested 5 grades according to the criteria:
Excellent: 90% to 100% TAM* of the contralateral side
Good: 70% to 89%
Fair: 50% to 69%
Poor: 30% to 49%
Failure: <30%
Basic expanded: Relating to hand motion and force
Add: Grip strength and quality of finger motion (detailed in Table 22-2)
Level 2—Intermediate: Relating to Hand Motion, Force, Sensation, Circulation, and Cosmetics
Add: Sensation of the hand, blood circulation, and cosmetic appearance
Level 3—Comprehensive: Relating to Hand Function and Cosmetics; Impact on Whole Body; Personal, Social,
and Environmental
Add:
 Whole body function
 Activities
 Environmental and personal factors

*Include the MCP joint when injuries are proximal to this joint (i.e., zone 3 and proximal); otherwise, exclude the MCP joint.

repairs.43 The criteria will reflect entire body func-
tion after flexor tendon repairs.
I expect that, in the future, surgeons and therapists will
record in medical charts, report to social welfare offices,
and publish in the medical literature using criteria with
different details, according to the needs of individual
patients and different levels of academic rigor. Basic
Level criteria may meet the essential requirement. If the
impact of tendon injuries (recovery) on the whole hand
or entire human being is a matter of concern, the record-
ing should move up to Levels 2 and 3.
CONSIDERATIONS RELATING TO OUTCOMES
At the closing of this section on primary flexor tendon
repair, I bring to the attention two issues relating to
outcomes that are likely to receive more attention in the
future.
Repair of the Flexor Tendons in the
Little Fingers
It is now a well-accepted practice to analyze tendon
repairs in the thumb separately from other digits. In
contrast, another issue gaining little specific attention is
repair of the flexor tendons in the little finger. The flexor
tendons in the little finger have a few special character-
istics. The flexor tendons (Figure 22-2) (1) are the
smallest in diameter, (2) move along a multidirection-
ally and significantly curved path, not only flexing but
also curving laterally during finger flexion, (3) are
subject to large structural variations of the sheath and
pulleys, with the A2 pulley being especially narrow, and
(4) have a greater gliding curvature of the tendon, which
predisposes the tendon to a greater bending force.
Repairs in this finger are easier to disrupt.19,44,45 Dowd
et al19 identified a much higher rupture rate and
re-rupture rate and poorer results in the little finger. I
have found it difficult to pass the repaired FDP tendon
under the A2 pulley. Another practical difficulty is that
it is hard to accommodate repairs of over four strands;
although I can put in a six-strand repair, it makes the
tendon gliding surface remarkable rough.
I would bring repair of the flexor tendon injuries in
the little finger to the attention of hand surgeons. I
suggest that this injury be discussed as a separate injury
and its repair outcomes be reported separately, as we do
for tendon repairs in the thumb. The anatomical fea-
tures and biomechanics of the tendon in the little finger
are very different from those of other fingers, and treat-
ment of injuries in the little fingers might also have to
be different from those in the index, middle, and ring
fingers. Unsatisfactory return of function and repair
failure plausibly are more frequent in the little finger.19
Repair of flexor tendon injuries in the little finger
produce less satisfactory function compared with the
other fingers, which remains a concern.
Report Levels of Expertise of Physicians
in Clinical Studies
It is well known and has been popularly written that
outcomes of flexor tendon repairs are expertise depen-
dent. However, currently we do not have any objective
method to scale the expertise of caregivers. Thus far, the
256 Section 2:  Primary Flexor Tendon Surgery
A B
reports, including those of flexor tendon repairs, have
rarely contained information about the degree of profi-
ciency of the caregivers.
This is a topic that does not limit to the reports of
outcomes of flexor tendon repairs. However, flexor
tendon repairs are a perfect example of such needs. To
varying extents in all medical practices, treatment out-
comes are influenced—and biased—by the skill with
which medical personnel perform procedures. In clini-
cal studies, because experience with implemented tech-
niques is not paralleled by job position, simply
categorizing caregivers as residents, attending surgeons,
or consultants, etc., provides little, if any, scientific infor-
mation regarding their expertise in specific techniques
adopted. Individuals grouped into one such category
often differ in their abilities to perform treatment
techniques.
On account of such differences, in reports of treat-
ments that rely heavily on methodology, the use of
technique-performance evaluation criteria is critical for
clear, objective interpretation of treatment outcomes.
Figure 22-2  A, The little finger is much smaller in size
and its flexion arc is much smaller than that of the other
finger. B and C, The pulleys are very narrow and tendons
are much smaller in the little finger, and the repaired FDP
tendon is relatively unsmooth with multi-strand core
suture. The treatment of the tendon injuries in this finger
should be separately discussed; different principles or
methods may be required.
This concept holds particular importance in comparable
studies conducted in different institutions or geographi-
cal areas—which exhibit divergences in prevalence of,
and consequently physicians’ exposure to, the study
condition.
To date, no report of clinical outcomes of flexor
tendon repair has documented the level of expertise of
the surgeon(s). We cannot be certain whether worse
outcomes of a specific surgical method relate to the level
of mastery of the surgeon or to the techniques
themselves.
I suggest that expertise levels of the caregivers who
conduct the treatment be reported, perhaps, under
“Methods.” An example of such criteria is detailed in
Table 22-7.46 In reporting the expertise, we should note
that the documented expertise levels are those of the
caregivers performing the treatment, rather than the
expertise of the senior authors of the report. The exper-
tise levels should also relate to specific techniques (or
disorders) under investigation, not to the caregivers’
overall expertise in practice.
 Chapter 22:  Outcomes of Flexor Tendon Repairs and Methods of Evaluation 257

Table 22-7  Levels and Criteria Suggested to Document Expertise of the Physicians in Reporting
Clinical Outcomes
Level Category Criteria
I Nonspecialist A physician who is under training, or is a general practitioner of medicine or surgery.
II Specialist—less A physician who has completed training and is a specialist in a subspecialty of
experienced medical or surgical techniques involved, but who has not yet acquired in-depth
knowledge or high-volume experience in the use of the techniques pertinent to the
report.
His or her less degree of experience can be judged by his or her shorter duration of
practice (for example, less than five years) as a specialist, or limited exposure to the
investigated disorder.
III Specialist—experienced A physician who has obtained sufficient experience in the use of the techniques
pertinent to the report.
He or she has practiced as a specialist over a longer period (five years or beyond),
with reasonably extensive exposure to the disorder.
IV Specialist—highly A specialist who possesses in-depth knowledge/treatment experience with use of
experienced the techniques being investigated.
This experience is best indicated by having performed, or having been involved as a
leading participant in, scholastic studies relevant to the disorder or techniques being
investigated.
V Expert A highly experienced specialist who has made recognized contribution to
advancements of knowledge/treatments related to the disorder being investigated.
Or, a physician who has pioneered the technique in the report.
This category is distinct in that the physician need not first be a specialist if fulfilling
the criteria.

References
1. Tang JB: Clinical outcomes associated with flexor tendon
repair, Hand Clin 21:199–210, 2005.
2. Small JO, Brennen MD, Colville J: Early active mobilization
following flexor tendon repair in zone 2, J Hand Surg (Br)
14:383–391, 1989.
3. Cullen KW, Tolhurst P, Lang D, et al: Flexor tendon repair in
zone 2 followed by controlled active mobilization, J Hand
Surg (Br) 14:392–395, 1989.
4. Savage R, Risitano G: Flexor tendon repair using a “six strand”
method of repair and early active mobilization, J Hand Surg
(Br) 14:396–399, 1989.
5. Pribaz JJ, Morrison WA, Macleod AM: Primary repair of flexor
tendons in no man’s land using the Becker repair, J Hand Surg
(Br) 14:400–405, 1989.
6. May EJ, Silfverskiöld KL, Sollerman CJ: The correlation
between controlled range of motion with dynamic traction
and results after flexor tendon repair in zone II, J Hand Surg
(Am) 17:1133–1139, 1992.
7. Tang JB, Shi D: Subdivision of flexor tendon “no man’s land”
and different treatment methods in each sub-zone. A prelimi-
nary report, Chin Med J 105:60–68, 1992.
8. O’Connell SJ, Moore MM, Strickland JW, et al: Results of zone
I and zone II flexor tendon repairs in children, J Hand Surg
(Am) 19:48–52, 1994.
9. Silfverskiöld KL, May EJ: Flexor tendon repair in zone II with
a new suture technique and an early mobilization program
combining passive and active flexion, J Hand Surg (Am)
19:53–60, 1994.
10. Grobbelaar AO, Hudson DA: Flexor tendon injuries in chil-
dren, J Hand Surg (Br) 19:696–698, 1994.
11. Elliot D, Moiemen NS, Flemming AFS, et al: The rupture
rate of acute flexor tendon repairs mobilized by the con-
trolled active motion regimen, J Hand Surg (Br) 19:607–612,
1994.
12. Tang JB, Shi D, Gu YQ, et al: Double and multiple looped
suture tendon repair, J Hand Surg (Br) 19:699–703, 1994.
13. Taras JS, Skahen JR, Raphael JS, et al: The double-grasping
and cross-stitch for acute flexor tendon repair, Atlas Hand Clin
1:13–28, 1996.
14. Sandow MJ, McMahon MM: Single-cross grasp six-strand
repair for acute flexor tendon tenorrhaphy, Atlas Hand Clin
1:41–64, 1996.
15. Lim BH, Tsai TM: The six-strand techniques for flexor tendon
repair, Atlas Hand Clin 1:65–76, 1996.
16. Kitsis CK, Wade PJF, Krikler SJ, et al: Controlled active motion
following primary flexor tendon repair: a prospective study
over 9 years, J Hand Surg (Br) 23:344–349, 1998.
17. Yii NW, Urban M, Elliot D: A prospective study of flexor
tendon repair in zone 5, J Hand Surg (Br) 23:642–648, 1998.
18. Harris SB, Harris D, Foster AJ, et al: The aetiology of acute
rupture of flexor tendon repairs in zones 1 and 2 of the fingers
during early mobilization, J Hand Surg (Br) 24:275–280,
1999.
19. Dowd MB, Figus A, Harris SB, et al: The results of immediate
re-repair of zone 1 and 2 primary flexor tendon repairs which
rupture, J Hand Surg (Br) 31:507–513, 2006.
20. Caulfield RH, Maleki-Tabrizi A, Patel H, et al: Comparison of
zones 1 to 4 flexor tendon repairs using absorbable and
unabsorbable four-strand core sutures, J Hand Surg (Eur)
33:412–417, 2008.
258 Section 2:  Primary Flexor Tendon Surgery
21. Hoffmann GL, Büchler U, Vögelin E: Clinical results of flexor
tendon repair in zone II using a six-strand double-loop tech-
nique compared with a two-strand technique, J Hand Surg
(Eur) 33:418–423, 2008.
22. Navali AM, Rouhani A: Zone 2 flexor tendon repair in young
children: a comparative study of four-strand versus two-
strand repair, J Hand Surg (Eur) 33:424–429, 2008.
23. Elhassan B, Moran SL, Bravo C, et al: Factors that influence
the outcome of zone I and zone II flexor tendon repairs in
children, J Hand Surg (Am) 31:1661–1666, 2006.
24. Percival NJ, Sykes PJ: Flexor pollicis longus tendon repair: a
comparison between dynamic and static splintage, J Hand
Surg (Br) 14:412–415, 1989.
25. Noonan KJ, Blair WF: Long-term follow-up of primary flexor
pollicis longus tenorrhaphies, J Hand Surg (Am) 16:653–662,
1991.
26. Nunley JA, Levin LS, Devito D, et al: Direct end-to-end repair
of flexor pollicis longus tendon lacerations, J Hand Surg (Am)
17:118–121, 1992.
27. Sirotakova M, Elliot D: Early active mobilization of primary
repairs of the flexor pollicis longus tendon, J Hand Surg (Br)
24:647–653, 1999.
28. Fitoussi F, Mazda K, Frajman JM, et al: Repair of the flexor
pollicis longus tendon in children, J Bone Joint Surg (Br)
82:1177–1180, 2000.
29. Kasashima T, Kato H, Minami A: Factors influencing prognosis
after direct repair of the flexor pollicis longus tendon: multi-
variate regression model analysis, Hand Surg 7:171–176, 2002.
30. Sirotakova M, Elliot D: Early active mobilization of primary
repairs of the flexor pollicis longus tendon with two Kessler
two-strand core sutures and a strengthened circumferential
suture, J Hand Surg (Br) 29:531–535, 2004.
31. Giesen T, Sirotakova M, Copsey AJ, et al: Flexor pollicis
longus primary repair: further experience with the Tang tech-
nique and controlled active mobilisation, J Hand Surg (Eur)
34:758–761, 2009.
32. Strickland JW, Glogovac SV: Digital function following flexor
tendon repair in zone II: a comparison of immobilization
and controlled passive motion techniques, J Hand Surg (Am)
5:537–543, 1980.
33. Kleinert HE, Verdan C: Report of the committee on tendon
injuries, J Hand Surg (Am) 8(Suppl):794–798, 1983.
34. Strickland JW: Results of flexor tendon surgery in zone II,
Hand Clin 1:167–179, 1985.
35. Buck-Gramcko D, Dietrich FE, Gogge S: Evaluation criteria
in follow-up studies of flexor tendon therapy, Handchirurgie
8:65–69, 1976.
36. White WL: Secondary restoration of finger flexion by digital
tendon grafts an evaluation of seventy-six cases, Am J Surg
91:662–668, 1956.
37. Lister GD, Kleinert HE, Kutz JE, et al: Primary flexor tendon
repair followed by immediate controlled mobilization, J
Hand Surg 2:441–451, 1977.
38. Moiemen NS, Elliot D: Primary flexor tendon repair in zone
1, J Hand Surg (Br) 25:78–84, 2000.
39. Tang JB: Indications, methods, postoperative motion and
outcome evaluation of primary flexor tendon repairs in Zone
2, J Hand Surg (Eur) 32:118–129, 2007.
40. Liu TK, Yang RS: Flexor tendon graft for late management of
isolated rupture of the profundus tendon, J Trauma 43:103–
106, 1997.
41. Al-Qattan MM, Al-Turaiki TM: Flexor tendon repair in zone
2 using a six-strand ‘figure of eight’ suture, J Hand Surg (Eur)
34:322–328, 2009.
42. Schaller P, Baer W: Motion-stable flexor tendon repair with
the Mantero technique in the distal part of the fingers, J Hand
Surg (Eur) 35:51–55, 2010.
43. Oltman R, Neises G, Scheible D, et al: ICF components
of corresponding outcome measures in flexor tendon
rehabilitation—A systematic review, BMC Musculoskelet Disord
9:139, 2008.
44. Tang JB, Cao Y, Xie RG: Effects of tension direction on
strength of tendon repair, J Hand Surg (Am) 26:1105–1110,
2001.
45. Tang JB, Xu Y, Wang B: Repair strength of tendons of varying
gliding curvature: A study in a curvilinear model, J Hand Surg
(Am) 28:243–249, 2003.
46. Tang JB: Re: Levels of experience of surgeons in clinical
studies, J Hand Surg (Eur) 34:137–138, 2009.
 CHAPTER
23  
TENOLYSIS
Nada Berry, MD, and Peter C. Amadio, MD
OUTLINE
Tenolysis is often necessary when adhesions develop
and seriously affect tendon movement. Tenolysis is
indicated for a supple finger with insufficient active
motion in a cooperative patient after plateau in therapy
has been reached. Ideally, tenolysis is done in an
awake patient under local anesthesia, so that active
motion can be assessed continuously. Special knives
may help free the tendons from beneath intact pulleys.
Any patient being consented for tenolysis should also
be consented for tendon grafting, since it is impossible
to be sure preoperatively that adequate tendon integ-
rity will be present postoperatively. Most commonly,
two-stage grafting is appropriate to salvage a failed
attempt at tenolysis. Early active motion is critical to
the success of tenolysis. Special protocols may be nec-
essary if the tendons are noted to be frayed at the
completion of the tenolysis.
Tendon adhesions form frequently after tendon repairs
and reconstructions, phalangeal fractures, and deep
tissue (e.g., flexor sheath) infections.1 Multiple postop-
erative modalities including early active range of motion
protocols have been developed to optimize tendon
gliding. Aggressive therapy may be sufficient to restore
full range of motion for mild adhesions.2 Alternatively,
tenolysis can be a beneficial procedure for patients who
have provided sufficient effort during vigorous therapy
and have plateaued in their range of motion progress.3-8
One must approach these surgeries with caution, as
additional surgery on a less than supremely compliant
patient can lead to further edema, scaring, and worsen-
ing stiffness. Patient and physician expectations should
be thoroughly discussed as it may be difficult to gain
back the hand function, even if the adhesion is not
extensive. Patients with severe trauma requiring multiple
secondary procedures, including nerve repair, tendon
grafting, capsulotomies and osteotomies, those older
than 40 years, tenolysis delayed by a year, and diffuse
adhesions have worse prognosis than those with isolated
tendon injuries and short segments of adhesions.9
INDICATIONS
The indications for tenolysis are a supple digit, a plateau
in motion following a well-supervised therapy program,
insufficient active motion, a cooperative patient, and
access to postoperative therapy. Only when all these
conditions are met should the surgeon consider pro-
ceeding with tenolysis.
A supple digit is important. Releasing contractures
and freeing adhesions at the same time make therapy
unnecessarily complex. Where possible, correcting con-
tractures by serial casting or dynamic splinting should
be performed. Tenolysis must be performed through
supple skin. Skin grafts may be replaced with flaps
beforehand. It is of course logical to require a plateau
in therapy prior to tenolysis; if the patient is still making
progress nonoperatively, an intervention might reverse
rather than accelerate progress. A cooperative patient is
also essential. A patient who, for example, is not willing
to manage their own therapy every day for 6 weeks or
longer, defer vacations and other personal gratification,
and otherwise demonstrate a strong desire to assume
responsibility for their own recovery is unlikely to
benefit from tenolysis. Finally, patients need to have
access to therapy supervision postoperatively. A patient
who lives at a long distance from the surgeon and thera-
pist, or who is prevented from access due to financial or
insurance constraints, will similarly fail to achieve the
maximum benefit from tenolysis surgery.
TIMING OF SURGERY
Tenolysis should be carried out after therapy has been
exhausted and the patient does not show improvement
despite conscientious effort. All scars and affected sur-
rounding tissues should be supple, without evidence of
inflammation. Scar erythema and firmness indicate cor-
ollary deep tissue reaction and should advise the surgeon
against additional surgery.
All fractures and wounds should be healed, and
chronic infections cleared. Joint contractures must be
mobilized. Patient-dependent passive joint motion
should be near normal prior to tenolysis.9 Occasionally,
serial casting or a dynamic external fixator may be useful
prior to the procedure to correct stubborn joint contrac-
tures, especially of the proximal interphalangeal joint.10
Some authors have previously recommended waiting
6 months prior to secondary tendon surgery, as strip-
ping of the tissues surrounding the tendon may devas-
cularize the healing tendon scar and can lead to late
tendon rupture.5 Other studies show that delayed
261
262 Section 3:  Secondary Flexor Tendon Surgery

tenolysis after a year results in a decreased postoperative especially in longer standing cases. Only “wide awake”
improvement, possibly due to a developing joint con- surgery can detect such adhesions.
tracture.11 It has been our practice to perform tenolysis The incision for tenolysis is usually placed over the
when all of the following conditions have been met: the previous scar and extended proximally and distally so
digit and soft tissues are supple and well perfused; active that the tendon and other vital structures can be
motion is unacceptable to the patient; a plateau in approached from virgin tissue. If there is a choice, a
therapy progress has been reached, with no improve- mid-lateral incision may have an advantage of providing
ment in motion over at least 4 weeks, and the patient easy access to both flexors and extensors, such as in cases
has been cooperative with the therapy regimen. It is rare of fractures or known extensor tendon injury (Figure
for these conditions to be met in less than 3 or even 4 23-2). This approach is also useful when resistant joint
months from the time of initial tendon injury or repair, contractures need to be released.17
but it is our opinion that tenolysis can be safely per- In addition to the preservation of the crucial A2 and
formed as soon as 3 months after the injury, providing A4 pulleys, the flexor tendon sheath should be mini-
that previously mentioned criteria have been met. mally traumatized. Releasing any of the pulleys exposes
the tendon to the surrounding tissues and predisposes
SURGICAL TECHNIQUE
it to further scarring. In addition, active grip applies
Patient involvement during the tenolysis procedure is additional force to the remaining pulleys, leading to
considered important by many surgeons and is advis- potential pulley rupture and bow stringing of the tendon.
able whenever possible. Use of local anesthesia, with or A transverse opening is made into the tendon sheath.
without limited sedation, allows the patient to aid in Tenotomes (Figure 23-3) or Freer elevator can be passed
confirmation of release of all the motion-limiting adhe-
sions.7,12-14 Intraoperative active range of motion is the
best predictor of adequate release. In addition, visual-
izing the expected outcome may motivate the patient to
work through the tenderness of the fresh incision and
new edema. While a sterile forearm tourniquet may be
better tolerated than an upper arm tourniquet during
the procedure, it is our preference to eschew all tourni-
quet use, in favor of the “wide-awake” technique advo-
cated by Lalonde and others.13,15
If “wide-awake” surgery is not feasible, a traction test
can be used.16 The involved tendon is exposed proximal
to the area of injury and retracted until digit flexion is
visualized (Figure 23-1). Restrictions in movement
indicate incomplete adhesion release. However, this test
is not infallible; adhesions between muscle bellies may
be well proximal to the zone of initial injury and surgery, Figure 23-2  Extensor tenolysis is performed through an
additional incision in this patient with a healed proximal
phalanx fracture and limited active range of digital motion.

Figure 23-1  Traction test is performed on a patient after Figure 23-3  Tenolysis knives are very useful in releasing
tenolysis. Complete finger flexion is noted in this patient dense adhesions between the tendon and the flexor sheath.
under general anesthesia, indicating adequate tenolysis. She Meals tenolysis knives shown are available from George
had previously undergone flexor tendon repair in zone 2. Tiemann & Co, Hauppauge, NY.

A3
A B
Figure 23-4  A, MR image shows normal relationship between the flexor tendon (T), overlying bone, and the A3 pulley. B,
MR image shows increased distance between the tendon and the bone, as well as the attenuated pulley.
under the pulley system to separate the tendon from the
sheath. Active finger flexion can aid in lysis of distal
adhesions. If the critical A2 pulley is not intact, it can
be reconstructed, but this is likely to compromise the
result of the tenolysis, since vigorous active postopera-
tive motion will be contraindicated in the face of a
pulley reconstruction.18 In such cases, a staged recon-
struction may be an alternative consideration.19,20 Pre-
operative magnetic resonance imaging (MRI) (Figure
23-4) or ultrasound may aid in determining pulley
status.21 In contrast, the A4 pulley may not be so critical;
if it is not intact and the profundus is also compromised
but the superficialis is intact, then the distal interpha-
langeal joint can be stabilized and the profundus
excised. A superficialis finger can be superior to both a
staged reconstruction and even a heroic attempt at
tenolysis of the profundus and A4 reconstruction.
The tendon quality should be examined. Pseudo-
tendon formation in the gap between the tendon
ends can mislead the surgeon into thinking that the
tendon healing is complete and result in surgical failure.
Hunter has advised that a tendon defect involving
more than 30% of the tendon is grounds to consider a
staged tendon reconstruction,20 and we agree with this
approach. Such a defect may be obvious initially or at
the completion of tenolysis. An additional advantage of
the “wide-awake” approach is that the patient can be
asked to make a strong fist at the end of the procedure.
It is far better that a compromised tendon rupture intra-
operatively, where a staged procedure can then be done
Chapter 23:  Tenolysis 263
immediately, than to have this happen in the postopera-
tive period.
In some cases the profundus is intact but the
superficialis is not. In such cases, the superficialis can
be resected, always with care not to compromise the
blood supply or integrity of the profundus tendon
or the pulley status. A similar approach can be taken
if the superficialis tendon is intact and the profundus
is not.
We prefer early active range of motion and aggressive
postoperative therapy to prevent further adhesion for-
mation. New studies involving absorbable mechanical
barriers and lubricants to prevent adhesion formation
and substances to improve tendon gliding show pro­
mising results both experimentally22-24 and clinically.25
Antimetabolites such as 5-fluorouracil may also be of
benefit.26 We tend to use these adjunctive agents on a
second tenolysis but not usually with initial procedures,
because usually the result of a first tenolysis is satisfac-
tory without these agents, which may compromise
wound healing.
REHABILITATION
Early active motion is a key factor in the success of any
tenolysis procedure and should be instituted as soon as
possible.27-32 If hemostasis is not a concern and the pain
is tolerable, we prefer to begin rehabilitation in the
operating room, taking advantage of the “wide-awake”
method, and continue in the recovery room. In general,
we prefer light dressings and regular active motions—if
264 Section 3:  Secondary Flexor Tendon Surgery
possible, 10 repetitions every hour while awake or at
least two sessions per day. Splinting is usually not neces-
sary unless the tendon is frayed, in which case the wrist
and metacarpophalangeal joints can be splinted in
flexion, especially while the patient sleeps. Formal
therapy continues until the patient has reached a plateau
in recovery, with no improvement in active range of
motion over 3 weeks. In general, patients will maintain
their gains in the long term if they improve during the
first postoperative week and maintain the gains for the
following 2 to 3 weeks.5
Indwelling catheters for administration of local anes-
thetic can be useful postoperatively.33-37 Painful, rigor-
ous activity may lead to additional swelling and an
overall setback.
Wound dehiscence may require a halt in therapy,
especially if the tendon is exposed. To minimize the risk
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10. Kawakatsu M, Ishikawa K, Terai T, et al: Distraction arthrolysis
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12. Hunter JM, Schneider LH, Dumont J, et al: A dynamic
approach to problems of hand function using local anesthe-
sia supplemented by intravenous fentanyl-droperidol, Clin
Orthop Relat Res 104:112–115, 1974.
13. Lalonde DH: Wide-awake flexor tendon repair, Plast Reconstr
Surg 123:623–625, 2009.
14. Whitaker JH, Strickland JW, Ellis RK: The role of flexor teno­
lysis in the palm and digits, J Hand Surg (Am) 2:462–470,
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15. Higgins A, Lalonde DH, Bell M, et al: Avoiding flexor tendon
repair rupture with intraoperative total active movement
examination, Plast Reconstr Surg 126:941–945, 2010.
16. Strickland JW: Flexor tendon injuries. Part 5. Flexor tenolysis,
rehabilitation and results, Orthop Rev 16:137–153, 1987.
17. Saffar P: Total anterior teno-arthrolysis. Report of 72 cases,
Ann Chir Main 2:345–350, 1983.
of dehiscence, it is important to use a very careful tech-
nique when elevating skin flaps, in ensuring hemostasis
at the time of closure, and in establishing a secure skin
closure.
RESULTS
Overall, larger reviews in the literature suggest that 80%
of patients show improvement with tenolysis proce-
dures, 10% remain mostly unchanged, and 10% worsen
their range of motion or sustain a rupture of the tenoly-
sis.4,5,14,25 It is unusual for a patient to regain active
control of the full passive range that is present preopera-
tively, however. These statistics and expectations should
be discussed with the patient preoperatively. Tenolysis
requires a combination of patient cooperation, skillful
therapy, and careful surgery to achieve a satisfactory
outcome.
18. Foucher G, Lenoble E, Ben Youssef K, et al: A post-operative
regime after digital flexor tenolysis. A series of 72 patients,
J Hand Surg (Br) 18:35–40, 1993.
19. Amadio PC, Wood MB, Cooney WP 3rd, et al: Staged flexor
tendon reconstruction in the fingers and hand, J Hand Surg
(Am) 13:559–562, 1988.
20. Hunter JM: Staged flexor tendon reconstruction, J Hand Surg
(Am) 8:789–793, 1983.
21. Drape JL, Silbermann-Hoffman O, Houvet P, et al: Complica-
tions of flexor tendon repair in the hand: MR imaging assess-
ment, Radiology 198:219–224, 1996.
22. Zhao C, Sun YL, Amadio PC, et al: Surface treatment of flexor
tendon autografts with carbodiimide-derivatized hyaluronic
acid. An in vivo canine model, J Bone Joint Surg (Am) 88:2181–
2191, 2006.
23. Zhao C, Sun YL, Kirk RL, et al: Effects of a lubricin-containing
compound on the results of flexor tendon repair in a canine
model in vivo, J Bone Joint Surg (Am) 92:1453–1461, 2010.
24. Karakurum G, Buyukbebeci O, Kalender M, et al: Seprafilm
interposition for preventing adhesion formation after tenoly-
sis. An experimental study on the chicken flexor tendons,
J Surg Res 113:195–200, 2003.
25. Riccio M, Battiston B, Pajardi G, et al: Efficiency of Hyaloglide
in the prevention of the recurrence of adhesions after tenoly-
sis of flexor tendons in zone II: A randomized, controlled,
multicentre clinical trial, J Hand Surg (Eur) 35:130–138,
2010.
26. Zhao C, Zobitz ME, Sun YL, et al: Surface treatment with
5-fluorouracil after flexor tendon repair in a canine in vivo
model, J Bone Joint Surg (Am) 91:2673–2682, 2009.
27. Alba CD, LaStayo P: Postoperative management of function-
ally restrictive muscular adherence, A corollary to surgical
tenolysis: A case report, J Hand Ther 14:43–50, 2001.
28. de Soras X, Thomas D, Guinard D, et al: Use of an implanted
electrode for rehabilitation after tenolysis of the flexor
tendons, Ann Chir Main Memb Super 13:317–327, 1994.
29. Feldscher SB, Schneider LH: Flexor tenolysis, Hand Surg 7:61–
74, 2002.
30. Foucher G, Marin Braun FM: An original mobilization technic
after tenolysis of zone II flexor tendons, Ann Chir Main 8:
252–253, 1989.
31. Goloborod’ko SA: Postoperative management of flexor tenol-
ysis, J Hand Ther 12:330–332, 1999.

32. McCarthy JA, Lesker PA, Peterson WW, et al: Continuous
passive motion as an adjunct therapy for tenolysis, J Hand
Surg (Br) 11:88–90, 1986.
33. Braun C, Bauer M, Bühren V: Experiences with continuous
nerve block of the wrist, Handchir Mikrochir Plast Chir 23:
207–209, 1991.
34. Jablecki J, Syrko M: The application of nerve block in early
post-operative rehabilitation after tenolysis of the flexor
tendon, Orthop Traumatol Rehabil 7:646–650, 2005.
Chapter 23:  Tenolysis 265
35. Kirchhoff R, Jensen PB, Nielsen NS, et al: Repeated digital
nerve block for pain control after tenolysis, Scand J Plast
Reconstr Hand Surg 34:257–258, 2000.
36. Kulkarni M, Elliot D: Local anaesthetic infusion for postop-
erative pain, J Hand Surg (Br) 28:300–306, 2003.
37. Lurf M, Leixnering M: Ultrasound-guided ulnar nerve
catheter placement in the forearm for postoperative pain
relief and physiotherapy, Acta Anaesthesiol Scand 53:261–263,
2009.
 CHAPTER

24  
SINGLE-STAGE FREE TENDON
GRAFTING FOR FLEXOR
TENDON INJURY IN FINGERS
Pierre-Yves Barthel, MD, and Pierre Mansat, MD, PhD

 Delayed presentation of closed FDP avulsion inju-

OUTLINE
Successful primary flexor tendon repair has limited the
indications for flexor tendon grafting. Tendon grafting
is an alternative treatment for patients with neglected
digital flexor tendon lacerations and after failure of
primary flexor tendon repair. Tendon grafting can be
considered if the local conditions of the hand are
favorable. However, the outcomes after flexor tendon
grafting are inferior to those of primary flexor tendon
repair. A decision must be made after careful discus-
sion with the patient of the risks and benefits of this
procedure and specific needs of the patient.
Single-stage free tendon grafting is a common secondary
procedure for tendons not suitable for or not treated by
primary repair. The surgery must be carefully discussed
between the surgeon and the patient to evaluate the risk
and benefits of the procedure. This operation is usually
indicated for injury of both flexor digitorum profundus
(FDP) and flexor digitorum superficialis (FDS) tendons
in zone 2 in the presence of a good pulley system and
without serious scarring. The decision as to the need for
staged reconstruction is often made during surgery
depending on the state of the pulleys and the extent of
adhesions. The injured tendons are excised and replaced
by a harvested tendon graft sutured to the base of the
distal phalanx at the FDP insertion and to a proximal
motor in the palm or distal forearm.
INDICATIONS
Single-stage free tendon graft is carried out as an initial
procedure in selective cases including:
ries from the insertion associated with significant
tendon retraction.
 Closed rupture of the flexor tendons at any level
from zone 1 to zone 3, with retraction of the
proximal tendon that does not permit a direct
end-to-end repair.
Preoperative prerequisites include the following:
 The wound should be healed, the joints should be
free of contracture, and maximum passive motion
should have been obtained.
 There is no extensive scarring.
 Passive movements are full, or nearly full.
 The circulation is satisfactory.
 At least one digital nerve in the affected digit is
intact.
Contraindications to single-stage free tendon grafting
are:
 Extensive scarring, pulley incompetence, or joint
contracture.
 Insensate or poorly vascularized digits.
The best indication for single-stage free tendon graft for
flexor tendon injury is the grade 1 hand according to
Boyes’ classification (Table 24-1)1 or according to Merle
and Dautel’s classification (Table 24-2).2 For grade 2 or
3 hands, staged tendon grafting is preferred.
In cases of disruption of both the FDP and FDS
tendons, general surgical principles for this procedure
include:
 Place only one graft in each finger.
 Use a graft of a suitable caliber to fit into the finger.
 Place the proximal junction outside the tendon


sheath.
Flexor tendon injuries with segmental tendon loss.
 Avoid damage to the fingernail or fingertip, in
 Severe damage to peritendinous tissues, or obvious
making the distal junction.
risk of wound infection that prevented primary
 Ensure adequate graft tension.
repair.
 Delay in repair of more than 3 weeks that com- In cases with an intact or functioning FDS tendon, the
promises primary repair. following additional principles apply:

266
 Chapter 24:  Single-Stage Free Tendon Grafting for Flexor Tendon Injury in Fingers
Table 24-1  Boyes’ Preoperative Classification1
Grade Preoperative Condition
1 Good: Minimal scar with mobile joints and no
trophic changes
2 Cicatrix: Heavy skin scarring because of injury
or prior surgery; deep scarring because of failed
primary repair or infection
3 Joint damage: Injury to joint with restricted
range of motion
4 Nerve damage: Injury to digital nerves resulting
in trophic changes in finger
5 Multiple damages: Involvement of multiple
fingers with combination of above problems
Table 24-2  Preoperative Classification Based on
Modified Grading of Merle and Dautel2
Grade Preoperative Condition
1 Minimal or mild scar without major damages to
digital vascular bundles and nerves
2 Extensive scar in the digit causing or together
with:
 Destruction to multiple annular pulleys
 Joint stiffness
 Damage of one digital neurovascular
bundle
3 Serious scar in the digit with:
 Injury of bilateral digital neurovascular
bundles
 Injury of main vascular supplies to the hand
 Carefully explain the risk of no or limited recovery
of digital function before surgery.
 FDS-only fingers may have sufficient function
without using free tendon grafting to reconstruct
the FDP tendon.
 Never sacrifice an intact FDS or damage the surface
of the FDS tendon during surgery.
OPERATIVE METHODS
Injuries to Both FDP and FDS Tendons
Incision
Surgery is usually performed under local or regional
anesthesia with tourniquet control. A Bruner-type or
mid-lateral incision is used to expose the tendon system.
The lower limb must be prepared if the surgeon intends
to harvest a graft from there.
Dissection of the Flexor Tendons
The neurovascular bundles are preserved throughout
the dissection. The tendon sheath is explored and pro-
tected as much as possible. Approximately 1 cm of the
267
distal FDP tendon is preserved. The remainder of the
damaged FDP tendon is excised distal to the lumbrical
origin in the palm. The FDS tendon is resected, leaving
1 or 2 cm of the insertion of the FDS tendon to provide
stability and avoid hyperextension deformity of the
interphalangeal joint (Figure 24-1).
Graft
The most frequent donors are the palmaris longus and
the plantaris tendons. The palmaris longus tendon is
preferred for palm-to-fingertip reconstruction, and the
plantaris for forearm-to-fingertip reconstruction. Other
possibilities include the long extensors of the three
middle toes, the toe flexors, the extensor indicis pro-
prius, and the extensor digiti minimi (Figure 24-2).
Placement of the Graft
A suture is placed at the end of the graft, and the graft
is passed atraumatically under the pulleys using a flex-
ible catheter or a Silastic Hunter rod in a distal-to-prox-
imal direction. Care must be taken to minimize trauma
to the intact sheath to limit the risk of adhesion and
secondary stiffness (see Figure 24-1).
Sequence of Attachment of the Graft Ends
Creating the distal juncture first may allow easy judg-
ment of tension and determination of the graft length
in the palm. The proximal suture is accomplished after
the distal juncture has been completed.3 The alternative
is to create the proximal juncture first, with adjustment
of the graft length at the fingertip. In our opinion, the
latter is more difficult and less reliable for restoring
proper tension to the graft.
Distal End Attachment
Several techniques are available to anchor the tendon
graft to the distal phalanx, depending primarily on the
length and condition of the distal FDP tendon. (1) If
enough FDP tendon is available, the graft can be sutured
to this tendon or through it. (2) When the length of
distal FDP tendon is not sufficient, the tendon is attached
to the distal phalanx using a tendon-to-bone pull-out
technique. A drill hole is made in the palmar cortex
of the distal phalanx into which straight needles are
passed through the nail plate. A sterile button is usually
used to tie over the surface on top of the nail plate. This
conventional method has been criticized for damaging
the fingernail and risking infection.4 Although surgeons
still use this method, many have started using other
methods for distal juncture that have no interference
with the nail complex (see Figure 24-1).
More recent alternatives to the conventional method
include (1) drilling a transverse drill hole across the
base of the distal phalanx with the graft passed through
and sutured to itself. This technique allows for easy
judgment of graft tension, but the graft must be thin
268 Section 3:  Secondary Flexor Tendon Surgery

B Two methods of distal tendon junction

A Preservation of pulleys and passing the graft within the sheath C Pulvertaft repair for proximal junction

Figure 24-1  A, Incision and methods of insertion of a grafted tendon into preserved tendon sheath. B, Two methods of
distal tendon juncture. C, Pulvertaft method of proximal tendon juncture.

to pass through the bony tunnel. Risk of fracture must
be known (Figure 24-3). (2) For patients with good
bone quality, some authors have proposed distal fixation
with metallic suture anchors (Figure 24-4) and non­
absorbable sutures. Biomechanical studies have shown
that metallic anchors are sufficient to provide stable
fixation of the graft to the distal phalanx, avoiding the
complications of pull-out techniques.5-8 Metallic anchors
are preferred to avoid possible complications of auto­
lysis associated with bioabsorbable anchors.9 Surgeons
in some units have virtually abandoned the conven-
tional pull-out suture, replacing it with these metallic
anchors for distal juncture. For patients with poor bone
quality, a pull-out suture method is preferred to avoid
 Chapter 24:  Single-Stage Free Tendon Grafting for Flexor Tendon Injury in Fingers
Palmaris longus
Plantaris tendon Tendon stripper
C Achilles tendon
Figure 24-2  Methods of harvesting tendons from donor sites in forearm or lower extremity.
Gauze
Profundus
stump
Figure 24-3  Distal tendon juncture method: passing the
tendon through a drill hole in the distal phalanx.
migration of the anchor.10,11 (3) Taras and Kaufmann
describe their method of passing the suture around the
distal phalanx and tying it over the nail.3 The sutures are
threaded onto the end of the grafted tendon with straight
needles. The tendon graft is woven through distal stump
of the FDP tendon. The needles are then passed around
both sides of the distal phalanx and through the middle
third of the nail plate, avoiding the germinal nail matrix;
the ideal point to exit through the nail plate should be
3 to 4 mm distal to the lunula and approximately 2 mm
from the midline. The ends of the suture are tied directly
over the nail plate. At least two reinforcing sutures on
each side are used to reinforce the FDP–graft juncture
(Figure 24-5).
269
Extensor
digitorum
longus
B
After using the pull-out suture technique for many
years, we now use metallic anchor sutures to gain imme-
diate strength of the junction and also to avoid the
complications of a pull-out suture, such as nail dys­
trophy, pulp ulceration, and infection. Furthermore,
because of the strong tendon anchor, immediate mobi-
lization of the finger can be allowed with fewer risks of
anchor site rupture. After preparation of the distal
phalanx by removing the remnant of the distal FDP
tendon, one or two mini-anchors are placed into the
distal phalanx. The tendon graft is guided into position
and secured to the distal phalanx with the sutures
carried by the anchor. Additional sutures of 3-0 PDS
ensure the graft stays well coapted to the distal phalanx
and to the surrounding tissues, including the palmar
plate of the DIP joint. Strength of the distal fixation are
assessed by adding a traction force on the graft. A radio-
graphic examination is always performed to verify that
the metallic anchors are well seated in the distal phalanx.
Proximal Juncture Suture
In the palm, the proximal end of the graft is attached to
the FDP tendon just distal to the lumbrical origin. The
end of the motor (proximal) tendon is opened with a
blade, and the graft is then passed into the split. The
graft is passed transversely in different planes according
to the Pulvertaft technique. Then 3-0 PDS sutures are
used to suture the tendons at the interconnection points,
and the distal split is closed over the graft to obtain a
perfect continuity between the motor tendon and the
graft (see Figure 24-1).
270 Section 3:  Secondary Flexor Tendon Surgery
A Figure 24-5  Method of distal tendon attachment to the
B
C extension of the MCP joint and the wrist. At 2 weeks,
Figure 24-4  A, The tools for inserting a mini-anchor into
the distal phalanx. The upper, a drill, is used to drill a hole
on the proximal palmar surface of the bone if necessary, and
the lower, the anchor will be inserted into the bone by the
inserter. The mini-anchor, carrying two sets of suture lines,
is attached to the tip of the inserter. B, Drilling a hole on the
palmar surface of the distal phalanx. C, The mini-anchor is
securely placed into the bone. After that, the tendon is
sutured with the suture lines carried by the anchor.
(Courtesy of Jun Tan, MD, and Jin Bo Tang, MD.)
distal phalanx. The suture is anchored over the nail surface.
Graft Tensioning
Graft tensioning is estimated by the relaxed position of
the fingers with the wrist in the neutral position. Each
finger should fall into semiflexion, slightly less flexed
than its ulnar neighbor and more flexed than its radial
neighbor. The Pulvertaft technique is especially amen­
able to adjusting tension; if the posture of the hand is
satisfactory with one suture in place, the juncture is
completed by adding additional sutures (Figure 24-6).
Postoperative Care
Postoperatively, the hand is immobilized with a static
dorsal blocking splint with the wrist positioned in
neutral to mild flexion, the metacarpophalangeal (MCP)
joints in 45° of flexion, and the splint distal to the MCP
joint in 0° of extension to allow the finger proximal
and distal interphalangeal (PIP and DIP) joints to rest
in the neutral position. The position of splinting is
changed after 3 to 4 weeks to place the wrist and hand
in the functional position. This splint is retained until
6 weeks after surgery. Passive range of motion exercise
can be instituted 2 or 3 days after surgery, but avoid
slight active short-arc digital flexion and extension exer-
cises can be added, with the MCP joint in flexion if
strong distal suturing is obtained. However, if the distal
sutures are less robust because of poor bone quality or
loss of the distal flexor tendon stump, active mobiliza-
tion is delayed until 4 weeks. At 4 weeks, blocked flexion
exercises of the MCP or PIP joint are started. Usually the
splint is discarded at 6 weeks and resistance exercises
can be started. Passive stretching splint can then be used
if flexion contracture remains.
FDP Tendon Disruption with
FDS Tendon Intact
Surgeons have mixed recommendations regarding
surgery for the patient with complete disruption of the
FDP tendon but an intact FDS tendon. FDS-tendon
 Chapter 24:  Single-Stage Free Tendon Grafting for Flexor Tendon Injury in Fingers
A
B
Figure 24-6  The fingers’ cascade for deciding tension placed on the graft in different fingers.
fingers may function very well without surgical recon-
struction of the FDP tendon. There is also a risk to
damage to the FDS function during surgery. The sur-
geons should carefully evaluate the patient and explain
to the patient about the degree of improvement of func-
tion and possible risk of reconstructing the FDP tendon
with a tendon graft in the presence of an intact FDS
tendon.
First, function of the FDS tendon must be examined
thoroughly. When the FDS tendon is fully functional,
caution must be observed before proposing a free tendon
graft to restore distal joint function. Because most useful
motion is maintained when the FDS tendon is fully
functional, patients may have adapted perfectly, even
with an injured or retracted FDP tendon. The problem
for the patient is mostly about the DIP joint position.
If there is no hyperextension of the joint, functional
adaptation is usual. However, if there is hyperextension
of the joint with instability, procedures for stabilization
can be discussed with the patient. Simple yet effective
procedures, like distal tenodesis or arthrodesis of the
DIP joint, can be proposed. Indications for tendon graft-
ing are discussed in selected cases, especially young
patients with mobile joints and a reasonable need for
active DIP joint function. A graft is probably more fre-
quently justified on the ulnar side of the hand than on
the radial side because of the need to obtain a total arc
of flexion to be able to perform power gripping.
The method of tendon grafting is the same as the
technique described earlier for patients with injuries to
both. In performing grafting for such patients, we take
great care in passing the graft through the intact FDS
tendon decussation. The graft can be laid anterior to the
271
FDS tendon if the tendon decussation is tight for the
grafted tendon, but we found this rarely necessary, as the
grafted tendon is usually thinner than the FDP tendon,
though the collapse of the pulleys and sheath occurs
after delay of the surgery. Fitting the grafted tendon and
intact FDS into the sheath or pulley may be difficult. In
such cases, surgeons may consider partial removal of
narrow parts of the sheath or pulley, but obviously the
sheath and pulley should be preserved segmentally to
maintain function of the tendons. Avoiding damage to
an intact, fully functioning FDS tendon is an important
principle. Incision or removal of the FDS tendon is pro-
hibited under any conditions. In some cases, one slip of
the FDS tendon can be removed for graft passage and to
allow gliding of the grafted tendon. However, removal
of a slip of FDS tendon can be risky, which the authors
do not recommend. If extensive scarring in the FDS, or
the flexor tendon bed, or pulleys, is found during surgery,
staged tendon grafting is preferable.
OUTCOMES AND COMPLICATIONS—
PROGNOSIS FACTORS
Outcomes
In general, the outcomes after flexor tendon grafting
are inferior to those of primary flexor tendon repair. In
Boyes and Stark’s study,12 reviewing 1000 flexor-tendon
grafting, 607 at the fingers, the preoperative condition
of the digit was found to be the most important factor
affecting the result of flexor-tendon grafting. In good
cases (grade 1), regardless of age, time since surgery,
specific digit, or tendon used as a graft, 23% of the
fingers flexed the pulp to the palmar crease; only 9%
272 Section 3:  Secondary Flexor Tendon Surgery

Table 24-3  Results of Single-Stage Free Tendon Grafting for Flexor Tendon Reconstruction in the Hand
Authors Digits Type of Graft Results Complications
Boyes and 607 PL 413 Full flexion obtained in: Secondary rupture:
Starks12 PL+ paratenon 11   23% in grade 1 fingers 15 in the palm, 7
FDS 128   12% in grade 2 fingers at distal insertions
Plantaris 21   10% failures (ppd = 5 cm) PIP recurvatum 13
Toe extensor 29 Failure (i.e., ppd > 5 cm): Hematoma 6
Others 5 32 fingers Ulcer of the pulp 2
McClinton 100 PL 80 ppd: Not stated
et al13 Isolated FDP injury EDC 10 0 cm: 55
EIP 4 0-1.3 cm: 24
Toe extensor 4 1.4-2.5 cm: 15
Plantaris 1 2.6-5 cm: 6
FDS 1 AROM DIP joint: 48° on average
Failure:* 13
Leversedge 4 FDL 2nd toe Excellent 1, good 1, fair 1, poor 1 Rupture 1
et al14 64% TAM recovery Tenolysis 1
Kotwal and 264 PL Excellent 18.5% Infection 7
Gupta15 Plantaris Good: 70.5% Secondary rupture 3
Poor: 11%
EDC, Extensor digitorum communis; EIP, extensor index proprius; FDL, flexor digitorum longus; PIP, proximal interphalangeal joint;
DIP, distal interphalangeal joint; AROM, active range of motion; TAM, total active motion; PL, palmaris longus; ppd, pulp–palm distance.
*Failure was defined in this study as loss >20° from preoperative PIP joint flexion or DIP joint flexion less than 20°.

achieved this in the scar (grade 2) and nerve injury
groups (grade 4), while in the joint and salvage groups
(grades 3 and 5), none could flex to make the finger nostic factors—scarring from injury, additional scarring
tip touch the distal palmar crease. McClinton et al13
reviewed 100 tendon grafts for isolated FDP injuries procedures compromised the results of secondary
and reported that 55 digits could be flexed to touch tendon grafting; fingers in which joints had been
the distal palmar crease postoperatively. Twenty-four
digits were flexed to bring the fingertip within 1.3 cm,
15 between 1.3 and 2.5 cm, and 6 between 2.5 and
5 cm of the distal palmar crease. Using intrasynovial
tendon grafts and early mobilization, Leversedge et al14
reported that recovery of active motion was 64% for
single-stage reconstruction and 55% for multiple-stage
reconstruction. Single digit reconstruction had the best
outcome, with recovery of total active motion of 73%.
Kotwal and Gupta15 reviewed the results of one-stage
free tendon grafting in 240 patients (264 digits) and
found excellent results in 18.5% of the cases, good
results in 70.5%, and poor results in 11% (Table 24-3).
Complications
The major complications seen after flexor-tendon graft-
ing are hyperextension at the PIP joint, rupture of the
graft in the palm, rupture at the distal juncture, and
trophic ulcers of the finger pulp. A tendon graft may also
become adherent and fail to move the finger through a
functional range of motion. The digit itself may become
so scarred in a flexed position that extension is limited
and total range of the motion is very small, which requires
tenolysis.12-15
Prognosis Factors
In their series, Boyes and Stark12 outlined different prog-
from inept previous surgery, or failed primary reparative
damaged or in which the IP joints had become stiffened
from neglect did not respond well to tendon grafting,
even though the joints were mobilized well before
surgery. In fingers with minimum scarring and only
one nerve injured, the results were not impaired, but
fingers with both nerves damaged had much less motion.
The level of tendon injury, whether in the proximal,
middle, or distal part of no-man’s land, was not a deter-
mining factor on the result, nor was the time from
injury to operation. Injury of the tendon of more than
one digit in itself was not important. They found that
the condition of the individual digit determined the
outcome for that finger. Patients over 40 years of age
did not regain as much motion from tendon grafting
as did the patients in younger age groups. The palmaris
longus tendon was the best donor tendon, but there was
little difference noted when a good superficialis tendon
was used.
SUMMARY
Single-stage free tendon grafting is a valuable secondary
reconstructive procedure of the injured deep flexor
tendons of the fingers. It is mainly used after injury to
both flexor tendons in zone 2. The preoperative status
 Chapter 24:  Single-Stage Free Tendon Grafting for Flexor Tendon Injury in Fingers
of the digit is of paramount importance. Secondary
single-stage flexor tendon grafting is only considered
when the wound is healed, the joints are free of con-
tracture with maximum passive motion, there is not
extensive scarring, and the patient has good circulation
and soft tissue coverage of the hand. With rigorous because the patient may have adapted his/her hand
surgical technique, appropriate tensioning of the graft,
and postoperative therapy, patients can recover their
hand function quite remarkably. However, the results
References
1. Boyes JH: Flexor-tendon grafts in the fingers and thumb: An
evaluation of end results, J Bone Joint Surg (Am) 32:489–499,
1950.
2. Merle M, Dautel G: Chirurgie secondaires des tendons fléchis-
seurs. In Michel M, Gilles D, editors: La Main Traumatique–
Tome 2–Chirurgie Secondaire/Le Poignet Traumatique, Paris,
1995, Masson, pp 55–92.
3. Taras JS, Kaufmann RA: Flexor tendon reconstruction. In
Wolfe SW, Hotchkiss RN, Pederson WC, et al, editors: Green’s
Operative Hand Surgery, ed 6, Philadelphia, 2011, Elsevier, pp
207–238.
4. Kang N, Marsh D, Dewar D: The morbidity of the button-over-
nail technique for zone 1 flexor tendon repairs. Should we still
be using this technique? J Hand Surg (Eur) 33:566–570, 2008.
5. Bonin N, Obert L, Jeunet L, et al: Réinsertion du tendon flé-
chisseur par ancre de suture: etude prospective continue avec
mobilisation active précoce, Chir Main 22:305–311, 2003.
6. Brustein M, Pellegrini J, Choueka J, et al: Bone suture anchors
versus the pullout button for repair of distal profundus
tendon injuries: a comparison of strength in human cadaveric
hands, J Hand Surg (Am) 26:489–496, 2001.
7. McCallister WV, Ambrose HC, Katolik LI, et al: Comparison
of pullout button versus suture anchor for zone I flexor
tendon repair, J Hand Surg (Am) 31:246–251, 2006.
8. Latendresse K, Dona E, Scougall PJ, et al: Cyclic testing the hand, Clin Orthop Relat Res 431:66–71, 2005.
of pullout sutures and Micro-Mitek suture anchors in flexor
273
after flexor tendon grafting are generally inferior to the
results of primary flexor tendon repair. When only the
FDP tendon has been injured with an intact FDS
tendon, caution must be observed before carrying out a
free tendon graft reconstruction of the FDP tendon,
function. Alternative options, such as distal tenodesis
or arthrodesis of the DIP joint, must be discussed with
the patient.
digitorum profundus tendon distal fixation, J Hand Surg (Am)
30:471–478, 2005.
9. Galano GJ, Jiang KN, Strauch RJ, et al: Inflammatory response
with osteolysis related to a bioabsorbable anchor in the
finger: A case report, Hand (NY) 5:307–312, 2010.
10. Matsuzaki H, Zaegel MA, Gelberman RH, et al: Effect of
suture material and bone quality on the mechanical proper-
ties of zone I flexor tendon-bone reattachment with bone
anchors, J Hand Surg (Am) 33:709–717, 2008.
11. Giannikas D, Athanaselis E, Matzaroglou C, et al: An unusual
complication of Mitek suture anchor use in primary treat-
ment of flexor digitorum profundus tendon laceration: A case
report, Cases J 14:9319, 2009.
12. Boyes JH, Stark HH: Flexor-tendon grafts in the fingers and
thumb. A study of factors influencing results in 1000 cases,
J Bone Joint Surg (Am) 53:1332–1342, 1971.
13. McClinton MA, Curtis RM, Wilgis EF: One hundred tendon
grafts for isolated flexor digitorum profundus injuries, J Hand
Surg (Am) 7:224–229, 1982.
14. Leversedge FJ, Zelouf D, Williams C, et al: Flexor tendon
grafting to the hand: an assessment of the intrasynovial donor
tendon—A preliminary single-cohort study, J Hand Surg (Am)
25:721–730, 2000.
15. Kotwal PP, Gupta V: Neglected tendon and nerve injuries of
 CHAPTER
25  
A HISTORICAL PERSPECTIVE
ON FLEXOR TENDON
RECONSTRUCTION AND
SURGICAL PROCEDURES
Andrew E. Farber, DO, and Daniel P. Mass, MD
OUTLINE
Flexor tendon reconstruction is a spectrum of
challenging treatment options ranging from non-
operative treatment to tenolysis to single-stage
and multistage reconstructive surgical procedures. Sec-
ondary tendon reconstruction is indicated in the
patients whose tendon injuries are not treated at the
primary or delayed primary stages, whose injuries
to the tendon are too serious, or where destruction of
the flexor pulleys are too extensive, which prevents
primary repair of the tendon. In the presence of
severe scar in the tendon gliding bed or extensive
pulley damages, both patient and surgeon are to be
prepared for multiple surgical procedures. This chapter
starts with a concise review of the development of
secondary flexor tendon reconstruction, followed by
descriptions of surgical procedures and postoperative
rehabilitation of tendon grafting and staged tendon
reconstructions.
In the tenth century, Avicenna, an Arabian surgeon, was
credited with performing the first tendon repair surgery.
In Europe, however, Galen teachings resulted in infre-
quent tendon repair. Galen did not differentiate between
nerves and tendons, noting that nerves entered muscles
and muscles ended with whitish cords. Accordingly,
teaching at that time (circa 150 AD) involved an intimate
relationship between tendons and nerves, so much so
that physicians feared severe consequences from damag-
ing or even touching a nerve or a tendon. They further
believed that suturing of a nerve or a tendon would
result in pain, convulsions, and gangrene.1
In 1752, Galen’s concept that complications are asso-
ciated with tendon damage was finally refuted by the
work of Albrecht von Haller,1 who demonstrated the
insensibility of tendons. In England around 1850, Syme
reported success with several cases of tendon repair
274
paving the way for modern tendon repair and
reconstruction.
DEVELOPMENT OF TENDON
RECONSTRUCTION
Until the 1960s, tendon lacerations in zone 2, or “no
man’s land,” were treated with removal of the tendon
with grafting of new tendons. Sterling Bunnell taught “it
is better to remove the tendons entirely from the finger
and graft in new tendons smooth throughout its
length.”2,3 Based on Bunnell’s classic work in the early
twentieth century, repair of tendon lacerations in zone
2, “no man’s land,” involved removal of the tendon and
grafting new tendons.3 The techniques of single-stage free
tendon grafting were later refined by a number of master
hand surgeons, including Pulvertaft, Graham, Littler,
Boyes, and Stark.5-17 Boyes’ large series of tendon grafts
popularized the procedure in 1950s and 1960s.13,14,17
In 1963, Bassett and Carroll subsequently first
described this type of two-stage flexor tendon recon-
struction using a silicone implant.18 In 1965, Hunter
first published his experience with tendon implants for
tendon reconstruction.19 As is widely reported, Hunter
further refined this process in the early 1970s, resulting
in the naming of the Hunter silicone rod and staged
tendon reconstruction techniques currently used.19,20 An
alternative method was described by Paneva-Holevich
in 1969,21 who sutured the proximal cut end of the
flexor digitorum superficialis (FDS) tendon to the proxi-
mal cut end of the profundus tendon in the palm. At
the second stage, the FDS tendon was severed as far
proximal as possible and this end was brought out to
be inserted at the distal phalanx as a pedicle graft. In
1982, Paneva-Holevich reported secondary repair of
324 flexor tendon injuries using pedicle FDS tendon
grafting. In 39 fingers, this technique was combined
with silicone rod implantation at the first stage to
prepare a smooth bed for the graft.22
 Chapter 25:  A Historical Perspective on Flexor Tendon Reconstruction and Surgical Procedures
SURGICAL PROCEDURES
It is helpful to think of flexor tendon reconstruction as
a spectrum of challenging treatment options ranging
from nonoperative treatment to tenolysis to single-stage
and multistage reconstructive surgical procedures. Both
patient and surgeon need to be prepared for multiple
surgical procedures and strict compliance with postop-
erative rehabilitation protocols. It is therefore impera-
tive to carefully consider surgical and nonsurgical
indications when selecting the best treatment protocol.
Additionally, it is essential to discuss the range of out-
comes with the patient including the likelihood of stiff-
ness and the possible need for amputation. In some
cases, doing nothing or performing a primary amputa-
tion or arthrodesis may avoid a series of painful proce-
dures that may ultimately provide or restore minimal
function.
Bunnell’s extensive work on flexor tendon injury and
reconstruction resulted in the widely accepted belief
that injured tendons should be removed and replaced
with new tendon graft.2,3 Bassett, Carroll, and Hunter
refined this recommendation with their works on the
silicone rod, which was designed to create a smooth bed
for tendon grafting. These developments led to the
widespread acceptance and use of the two-stage tendon
reconstruction.
Over the four decades that followed, however, signifi-
cant advancements in flexor tendon repair and recon-
struction led to revised indications for both primary
repair and secondary reconstruction. When considering
secondary repair, the decision needs to be made whether
to graft and reconstruct the tendons in a single stage or
to perform a two-stage repair. This decision requires
careful preoperative and intraoperative examinations.
Regardless of the surgical technique chosen, patients
should be counseled and should be prepared to partici-
pate in a complex rehabilitation program. This may
preclude performing the procedure on children younger
than 3 years of age.
Single-Stage Reconstruction
Preoperatively, patients considered for single-stage
reconstruction with tendon grafting must display a well-
healed, neurovascularly intact digit without excessive
scarring. Intraoperatively, an intact, smooth tendon bed
should be present with an adequate pulley system.
Patients with inadequate soft tissue coverage, those
with significant, dense scarring, or an inadequate pulley
system generally benefit from a two-stage reconstruc-
tion. Additional indications and limitations are described
next.
Although primary flexor tendon repair has become
increasingly popular, select patients can still benefit from
single-stage flexor tendon reconstruction.4-10 Careful
patient selection and intraoperative evaluation are
275
critical to maximize the chance for a successful outcome.
Boyes and others have described indications for single-
stage grafting including: (1) injuries with segmental
tendon loss and (2) delayed presentation resulting in the
inability to perform a primary end-to-end repair. This
may include injuries older than 3 to 6 weeks.4,11-17
The hand and finger should also demonstrate at least
one intact digital nerve in the affected finger, a well-
healed wound without extensive scarring, adequate cir-
culation; and near full-passive motion of all joints.
Insufficient passive range of motion should be addressed
with a course of hand therapy prior to considering surgi-
cal intervention. Patients should also be prepared to
participate in a rigorous and complex postoperative
rehabilitation program. This requirement generally
excludes growing children and some elderly patients.19
Excellent surgical technique is imperative and should
be carried out under loupe magnification and tourni-
quet control.
Except in the case of preexisting scar, choice of surgi-
cal incision is generally a matter of surgeon preference.
Options include the Bruner zigzag or mid-lateral inci-
sions. During dissection, neurovascular structures are
identified and protected. Damaged sheath is excised
and effort is made to protect the sheath and pulley
system.23-26 Missing pulleys, in particular the A2 and A4
pulleys, need to be reconstructed.
While several donor tendon options exist, the ipsilat-
eral palmaris longus or plantaris tendons remain the
most common choices. Since these tendons are both
nonsynovial tendons, some surgeons prefer to use toe
extensors from beneath the ankle retinaculum within
the sheath. Toe flexors are also intrasynovial; however,
their sheaths tend to be much shorter than those of
the fingers. In the event of harvesting the tendon from
the lower extremity, the incision in the hand is at
this point covered with moistened sponges and the
tourniquet deflated. Additionally, although vascularized
tendon grafts have been described and investigated, they
are rarely used and little is written about their use in the
English literature.
The FDP insertion site is next identified distally. In
the case of an intact distal FDP, the stump is reflected
and the graft is secured in the method of Bunnell. Spe-
cifically, a 3-0 Prolene or similar suture is placed at the
end of the graft and criss-crossed twice. In an adequate
FDP stump, the graft may be woven to reinforce fixation.
Otherwise, the FDP stump is split and the suture ends
are threaded onto a Keith needle. The needles are then
passed around both sides of the distal phalanx or, alter-
natively, drilled obliquely from the proximal aspect of
the volar distal phalanx, exiting through the middle-
third of the nail plate, approximately 3 to 4 mm distal
to the lunula and approximately 2 mm from the midline.
Whenever possible, avoid letting them exit through the
germinal nail matrix. The sutures are then passed
276 Section 3:  Secondary Flexor Tendon Surgery
Figure 25-1  Demonstration of a suture anchor for distal
fixation of the grafted tendon.
through the holes and tied over a padded button.4 If
available, a suture anchor can be used for fixation to the
distal phalanx (Figure 25-1).
The proximal aspect of the graft is then secured to the
FDP tendon just distal to the lumbrical origin. Any
remaining scar or frayed tissue is removed from the
native FDP tendon and a Brand tendon braider or a fine
scalpel is used to pass the graft. The graft should be
passed through several planes in the native tendon and
the tendon junctures are sutured in place.
Estimating proper tension is often difficult, especially
in the anesthetized patient; however, this remains
among the most important aspects of this procedure.
Placing the wrist in a neutral position allows for evalu-
ation of the relaxed position of the fingers.24,27-30 Each
semiflexed finger should be slightly more flexed than
the next radial finger and slightly less flexed than the
next ulnar finger (Figure 25-2). The Pulvertaft weave
technique is commonly used for securing the tendon
graft to the proximal tendon stump in the palm or distal
forearm. This technique is particularly useful in that it
allows for adjustment of graft tension.
Postoperative protocols typically included 3 weeks of
immobilization. More recently, however, active motion
protocols have become prevalent in primary flexor
tendon repairs,31,32
Two-Stage Reconstruction
Despite significant improvements in primary repair
and single-stage tendon reconstruction, two-stage recon-
struction remains a valuable option for some patients,
including patients who suffer severe trauma, those with
Figure 25-2  Position of the fingers and tension set during
operation.
Figure 25-3  Hand demonstrating adequate passive range
of motion.
extensive destruction of flexor pulleys, those with crush-
ing injuries with extensive soft tissue damage or under-
lying fractures, and patients with extensive scarring of
the flexor tendon bed. Adequate passive range of digital
motion and pliable skin are essential for the patients as
candidates of the staged reconstruction (Figures 25-3
and 25-4).
Hunter, among others, is credited with describing
and refining these techniques with the goal of creating
a new flexor tendon bed allowing for gliding of the
implanted tendon graft. As mentioned earlier, it is
imperative to maintain or recreate a sufficient and func-
tional pulley system. Traditional teaching has said that
at a minimum, the A2 and A4 pulleys at the proximal
and middle phalangeal levels respectively must be in
place. However, more recent data suggest that a four-
pulley system may be superior whenever possible.4 At
the same time, however, tight pulleys can inhibit tendon
graft gliding; accordingly, constricted pulleys can be
dilated. Damaged but intact pulleys should be repaired
 Chapter 25:  A Historical Perspective on Flexor Tendon Reconstruction and Surgical Procedures
Figure 25-4  Hand demonstrating pliable skin.
Figure 25-5  Reconstruction of flexor pulley at the middle
of the proximal phalanx.
and missing or irreparable pulleys must be reconstructed
(Figure 25-5). A variety of options exists for pulley
reconstruction, including grafting of extensor retinacu-
lum, remnant of free tendon, or synthetic materials.33,34
Bunnell originally recommended reconstructing the
pulley with placement of the tendon graft deep to the
extensor mechanism at the A2 level and superficial at
the A4 level;35 however, Taras and others more recently
suggested placing the tendon graft deep at all levels.36
As in other flexor tendon procedures, volar Bruner
incisions are ideal and should incorporate previous
scars where possible. Flexor tendons are then excised
leaving a 1-cm FDP stump attached to the distal phalanx.
A 1-cm FDS stump should also be maintained at the
middle phalanx. If necessary, collateral ligaments and
the volar plate can be released freeing remaining joint
contractures.
With a sufficient pulley system in place, the silicone
or Hunter rod is placed. A smooth forceps is used to
277
Figure 25-6  At the first stage, with a Bruner incision in
the middle of the finger and two incisions at the fingertip
and the palm, the Hunter rod is placed to replace the FDP
tendon and to stimulate formation of tendon gliding bed.
avoid damage to the rod and talc-free gloves should be
used as talc contamination is known to cause implant
adherence.
A tendon passer is used to pass the implant from
proximal to distal or from distal to proximal (Figure
25-6).37-39 The implant is then secured distally below the
FDP stump, taking care to pass sutures through the
Dacron tape in the implant since the silicone itself offers
little holding strength. Hunter rods are also available
fitted with a metal eyelet that can accommodate a
2.0-mm screw for fixation into the distal phalanx. When
using this technique, it is important to avoid penetrating
the dorsal cortex, inuring the nail bed. Additionally, the
screw must be distal enough in the distal phalanx to
avoid blocking DIP motion.
Next, range of motion is performed and observed to
ensure an adequate pulley system and free passage of
the graft with no bowstringing. Revision or additional
pulley reconstructions may be indicated at this point in
the procedure.
Wounds are then irrigated and closed. A bulky dress-
ing is applied, supporting the wrist in approximately
35° of flexion, metacarpophalangeal joints in 60° to
70° of flexion, and the interphalangeal joints relaxed in
extension. Passive motion may be started 2 to 3 days
postoperatively.
To allow for adequate wound healing and develop-
ment of a gliding tendon sheath in response to the
implant, typically 3 months is allowed between stages
of reconstruction. The criteria for proceeding with the
278 Section 3:  Secondary Flexor Tendon Surgery
second stage of reconstruction are similar to those
mentioned for the first stage and include a soft scar, near
full passive range of motion, and intact protective
sensation.
In the second stage of flexor tendon reconstruction,
the implant is removed and a tendon graft is placed.
Previous surgical scars are opened and distally, the
implant is identified and removed from the FDP stump.
Depending on the site of injury, the proximal incision
in the hand or forearm is reopened and the implant is
carefully exposed to avoid injuring the tendon sheath.
Typically, the adjacent profundus motor unit is selected.4
References
1. Adamson JE, Wilson JN: The history of flexor tendon grafting,
J Bone Joint Surg (Am) 43:709–716, 1961.
2. Strickland JW: Development of flexor tendon surgery: twenty-
five years of progress, J Hand Surg (Am) 25:214–235, 2000.
3. Bunnell S: Repair of tendons in the fingers and description
of two new instruments, Surg Gynecol Obstret 26:103–110,
1918.
4. Pulvertaft RG: Indications for tendon grafting. In Hunter JM,
Schneider LH, Mackin EJ, et al, editors: Rehabilitation of the
Hand, St Louis, 1984, CV Mosby, pp 277–279.
5. Colville J: Tendon graft function, Hand 5:152–154, 1973.
6. Mason ML, Allen HS: The rate of healing of tendons, Ann Surg
113:424–459, 1941.
7. Pulvertaft RG: Problems of flexor tendon surgery of the hand,
J Bone Joint Surg (Am) 47:123–132, 1965.
8. Pulvertaft RG: Indications for tendon grafting. In AAOS Sym-
posium on Tendon Surgery in the Hand, St Louis, 1975, CV
Mosby, pp 123.
9. Pulvertaft RG: Indications for tendon grafting. In Hunter JM,
Schneider LH, Mackin EJ, et al, editors: Rehabilitation of the
Hand, St Louis, 1984, CV Mosby, pp 277–279.
10. Schneider LH: Treatment of isolated flexor digitorum profun-
dus injuries by tendon grafting. In Hunter JM, Schneider LH,
Mackin EJ, editors: Flexor Tendon Surgery in the Hand, St Louis,
1986, CV Mosby, pp 518–525.
11. Adamson JE, Wilson JN: The history of flexor tendon grafting,
J Bone Joint Surg (Am) 43:709–716, 1961.
12. Allen HS: Flexor tendon grafting to the hand, Arch Surg
63:362–369, 1951.
13. Boyes JH: Evaluation of results of digital flexor tendon graft,
Am J Surg 89:1116–1119, 1955.
14. Boyes JH: Why tendon repair? J Bone Joint Surg (Am) 41:577–
579, 1959.
15. Boyes JH: Bunnell’s Surgery of the Hand, ed 4, Philadelphia,
1964, JB Lippincott.
16. Boyes JH: The philosophy of tendon surgery. In AAOS Sym-
posium on Tendon Surgery in the Hand, St Louis, 1975, CV
Mosby, pp 1–5.
17. Boyes JH, Stark HH: Flexor tendon grafts in the fingers and
thumb: A study of factors influencing results in 1000 cases,
J Bone Joint Surg (Am) 53:1332–1342, 1971.
18. Bassett CAL, Carroll RE: Formation of tendon sheaths by
silicone rod implants, J Bone Joint Surg (Am) 45:884–885,
1963.
19. Hunter JM. Artificial tendons. Early development and appli-
cation, Am J Surg 109:325–338, 1965.
20. Hunter JM, Salisbury RE: Flexor-tendon reconstruction in
severely damaged hands. A two-stage procedure using a sili-
cone Dacron reinforced gliding prosthesis prior to tendon
grafting, J Bone Joint Surg (Am) 53:829–852, 1971.
The graft is harvested, the silicone implant is detached
from its distal insertion site, and the graft is sutured to
the proximal end of the implant for passage through the
sheath. The graft is passed from proximal to distal as the
implant is removed.
As previously described, the graft is secured distally.
The incisions are washed and closed and a short-arm
dorsal blocking splint is applied. Typically, the wrist is
placed in neutral, the metacarpophalangeal joints in
45° of flexion and the interphalangeal joints in neutral.
Protected passive range of motion with early controlled
active motion is employed postoperatively.39-41
21. Paneva-Holevich E: Two-stage tenoplasty in injury of the flexor
tendons of the hand, J Bone Joint Surg (Am) 51:21–32, 1969.
22. Paneva-Holevich E: Two-stage reconstruction of the flexor
tendons, Int Orthop 6:133–138, 1982.
23. Wilson RL: Flexor tendon grafting. Flexor tendon surgery,
Hand Clin 1:97–107, 1985.
24. Watson AB: Some remarks on the repair of flexor tendons in
the hand, with particular reference to the technique of free
grafting, Br J Surg 43:35–42, 1955.
25. Bunnell S: Repair of tendons in the fingers, Surg Gynecol Obstet
35:88–97, 1922.
26. Strickland JW: Delayed treatment of flexor tendon injuries
including grafting, Hand Clin 21:219–243, 2005.
27. Peljovich A, Ratner JA, Marino J: Update of the physiology
and biomechanics of tendon transfer surgery, J Hand Surg
(Am) 35:1365–1369, 2010.
28. Kim SH: A loop-tendon suture for tendon transfer or graft
surgery, J Hand Surg (Am) 32:367–372, 2007.
29. Boyes JH: Operative technique of digital flexor tendon grafts,
Instr Course Lect 10:263–268, 1953.
30. Littler JW: Free tendon grafts in secondary flexor tendon
repair, Am J Surg 74:315–321, 1947.
31. Stenstrom SJ: Functional determination of the flexor tendon
graft length, Plast Reconstr Surg 43:633–634, 1969.
32. Strauch B, de Moura W: Digital flexor tendon sheath: an
anatomic study, J Hand Surg (Am) 10:785–789, 1985.
33. Freilich AM, Chhabra AB. Secondary flexor tendon recon-
struction, a review, J Hand Surg (Am) 32:1436–1442, 2007.
34. Lin GT, Amadio PC, An KN, et al: Biomechanical analysis of
finger flexor pulley reconstruction, J Hand Surg (Br) 14:278–
282, 1989.
35. Bunnell S: Surgery of the Hand, Philadelphia, 1944, JB
Lippincott.
36. Taras JS, Kaufmann RA: Flexor tendon injury. B. Flexor tendon
reconstruction. In Wolfe SW, Hotchkiss RN, Pederson WC,
et al, editors: Green’s Operative Hand Surgery, ed 6, Philadel-
phia, 2011, Churchill Livingstone-Elsevier, pp 207–238.
37. Seradge H, Homan ES, Spiegel PG: Tendon passer, Clin Orthop
Relat Res 155:307–308, 1981.
38. Sourmelis SG, McGrouther DA: Retrieval of the retracted
flexor tendon, J Hand Surg (Br) 12:109–111, 1987.
39. Hunter JM, Blackmore S, Callahan AD: Flexor tendon salvage
using the Hunter tendon implant, J Hand Ther 2:107–113,
1989.
40. Mackin EJ: Physical therapy and the staged tendon graft: pre-
operative and postoperative management. In AAOS Sympo-
sium on Tendon Surgery in the Hand, St Louis, 1975, CV Mosby,
pp 283–291.
41. Stanley BG: Flexor tendon injuries: late solution. Therapist’s
management, Hand Clin 2:139–147, 1986.
 CHAPTER
26  
EXPERIENCE WITH SECONDARY
FLEXOR TENDON REPAIRS
Peter C. Amadio, MD, and Chunfeng Zhao, MD
OUTLINE
Between roughly 1920 and 1960, secondary repair was
the preferred choice when dealing with flexor tendon
injuries in zone 2. Subsequent advances in primary
repair, especially with newer suture designs and reha-
bilitation techniques, have made primary repair the
preferred option for the most zone 2 flexor tendon
injuries. Currently, secondary repair options remain
viable in a number of circumstances. Secondary repair
in zone 2 include neglected injuries, in which retrac-
tion and adhesion of the tendon ends preclude reap-
proximation, or only permit reapproximation with
extreme positioning of the finger and wrist in flexion,
and segmental injuries, especially with segmental
tendon loss. In such cases primary repair is not techni-
cally possible. A good tendon bed is an indication for
one-stage grafting, such as when there is no or very
little scar, the pulleys (or at least the major pulleys A2
and A4) are intact, and there are no or minimal associ-
ated joint contractures. In addition, soft tissue nutri-
tion must be adequate, with preservation of at least
one neurovascular bundle. Finally, soft tissue coverage
must be normal or nearly normal: tendon grafts do
not thrive under scar or skin grafts. When tendon graft-
ing is indicated to restore tendon function and a one-
stage graft is relatively contraindicated because of
excessive scar, joint contracture, pulley loss, or a need
for better soft tissue cover, a two-stage reconstruction
can be considered. The patient should be fully informed
as to the time commitment to the staged surgery: the
initial stage, to address the scar, contracture, pulley and
soft tissue issues that contraindicate a one-stage graft;
an interval for soft tissue healing, which is usually 3
months or longer; a second stage, a “one-stage” graft;
and interval for graft healing; and the potential need
for a third stage, namely tenolysis or some sort of
salvage if the two-stage graft fails. Current research
efforts indicate improvement of the gliding character-
istics of extrasynovial autografts after tendon surface
modification with carbodiimide-derivatized hyalu­
ronic acid mixture and possibility of using tendon
allografts, which point to future promise of changes
in secondary tendon repair or reconstruction.
Between roughly 1920 and 1960, secondary repair was
the preferred choice when dealing with flexor tendon
injuries in zone 2.1-4 Subsequent advances in primary
repair, especially with newer suture designs and reha-
bilitation techniques, have made primary repair the pre-
ferred option for the vast majority of zone 2 injuries.
Nonetheless, secondary repair options remain viable in
many circumstances. Newer research may also expand
the role of secondary reconstruction, as described in the
final section of this chapter.
ONE-STAGE GRAFT
Indications
The classic one-stage tendon graft was described and
popularized by Bunnell,1 with definitive descriptions of
outcomes reported by Boyes, Stark, and others in the
middle years of the twentieth century.2,5,6 These descrip-
tions have not been bettered and serve as the reference
point here for a description of the classic indications,
technique, and results of one-stage grafting.
The classic indications for a one-stage graft are a zone
2 injury for which repair is not appropriate, with an
otherwise good tendon bed, in a cooperative patient.
These criteria remain valid; indeed, the only difference
between the 1950 and 2010 indications at all is the
assessment of which zone 2 injuries might not be appro-
priate for primary repair.
Another feature that has not changed over the years
is that it is often difficult to be certain beforehand
whether a tenolysis, one-stage graft, or two-stage graft
will be needed preoperatively; a procedure that begins
as a tenolysis may easily end with a shredded tendon,
damaged pulleys, and a two-stage reconstruction. The
surgical consent should include consideration of each
of these options, whenever tendon reconstruction is
discussed.
Currently, tendon injuries not suitable for primary
repair in zone 2 include neglected injuries, in which
retraction and adhesion of the tendon ends preclude
reapproximation, or only permit reapproximation
with extreme positioning of the finger and wrist in
flexion, and segmental injuries, especially with segmen-
tal tendon loss. In such cases primary repair is not
279
280 Section 3:  Secondary Flexor Tendon Surgery
Figure 26-1  A finger suitable for one-stage tendon graft:
tendon bed is good; scarring is minimal; the pulleys are
intact; and the soft tissues are supple.
technically possible. Even so, one-stage grafting might
not be indicated—in the presence of an intact and
functioning flexor digitorum superficialis (FDS) tendon,
grafting to restore flexor digitorum profundus (FDP)
function might cause more harm than good.6 It is always
important to recall that in the presence of a normal
FDS, the FDP contributes only to distal interphalangeal
joint (DIP) motion. Due to inevitable adhesions, the
amount of restored DIP motion is often limited, and
the amount of incremental grip strength may also be
limited. These limited gains must be counterbalanced by
the risks of infection and contracture, the time and effort
required for a successful tendon graft procedure, includ-
ing the possible need for a tenolysis, and the impact of
these on the patient’s life and livelihood. Except in
special circumstances, such as a musician who plays a
stringed instrument, serious consideration should be
given to simpler alternatives, such as DIP tenodesis, with
FDS tenolysis and lumbrical release as needed.
Certainly, the criterion of a good tendon bed has not
changed as an indication for one-stage grafting (Figure
26-1). A good bed is one in which there is no or very
little scar, the pulleys (or at least the major pulleys A2
and A4) are intact, and there are no or minimal associ-
ated joint contractures. In addition, soft tissue nutrition
must be adequate, with preservation of at least one
neurovascular bundle.5 Finally, soft tissue coverage must
be normal or nearly so: Tendon grafts do not thrive
under scar or skin grafts.
Finally, the patient must be capable of cooperating
with the grafting procedure. Sufficient voluntary motor
control must be available to power the graft motor, and
the patient must be able to cooperate with the rehabili-
tation program, which will include typically several
months of protected mobilization. Children, especially
under the age of 10, may not be fully capable of coop-
eration; reconstruction should be undertaken with
caution in such patients.7
METHODS
The technique of one-stage tendon grafting has not
changed over the years. Timing is dependent on the
Figure 26-2  The Pulvertaft weave is useful, especially to
join tendons of dissimilar sizes.
quality of the soft tissues. The wound should be clini-
cally stable; the skin soft and pliable. If good soft tissues
are not present, the procedure is almost certain to
fail. Indeed, poor soft tissues are an indication for an
alternate procedure, such as a staged tendon graft, as
described next.
The finger can be approached through either a volar
Bruner or midaxial incision. The key decision is whether
to put the proximal juncture in the palm or the distal
forearm. This decision should be based on the quality
of the soft tissue bed; the palm is preferred provided
that the soft tissues there are soft and supple. Otherwise,
a longer graft, repaired proximal to the carpal tunnel, is
preferred.
At least under the pulleys, the old tendon should be
excised. If the pulleys are not intact, especially the key
A2 pulley, pulley reconstruction as a two-stage proce-
dure should be strongly considered.
The tendon graft donor should be considered care-
fully. Ideally, in an intrasynovial location, an intrasyno-
vial graft should be used, but these are rarely available.
In addition, to minimize bowstringing, a graft that fits
the pulley should be used, but again, a good diameter
match is rarely on offer. When such tendons are avail-
able, they should be considered. Some creativity can
sometimes fashion a better choice: an index extensor is
intrasynovial at the extensor retinaculum; such a tendon,
harvested and then reversed, so that the distal end is
proximal and vice versa, can serve as a good alternative
to a palmaris longus, when a short graft is needed.8
When a long graft is needed for a juncture in the distal
forearm, usually only a plantaris or toe extensor have
the required length. Alternatively, tendon allografts can
be used, but without some modification (see later) the
results may be suboptimal.
The proximal juncture is classically made with a Pul-
vertaft weave (Figure 26-2), but other weaving tech-
niques can provide similar or even superior holding
strength, with less bulk.9 There is little question, though,
 Chapter 26:  Experience With Secondary Flexor Tendon Repairs
Figure 26-3  Tendon cascade after repair; tension should
be set slightly tighter than normal.
that when joining tendons of grossly dissimilar diam-
eter, a weaving method is superior in strength to a direct
repair. The choice of donor motor depends to some
extent on what is available, but usually either the pro-
fundus or superficialis tendon of the affected digit is
chosen.
Distally, the graft is usually fixed with a pullout
suture. There is some controversy as to whether the
tendon graft should be drilled into bone or fixed to
the bony surface of the distal phalanx; recent research
suggests that surface fixation may result in better
healing.10 Tension may be adjusted proximally or dis-
tally; the operated finger should usually be slightly
more flexed than the normal cascade would suggest
(Figure 26-3).
Postoperatively, the patient is managed usually with
early passive mobilization, to reduce the risk of joint
contracture. The role of active motion is somewhat con-
troversial in tendon grafting; unlike a direct repair, the
graft is avascular, and must have its nutrition restored
somehow. Thin grafts may be able to survive on synovial
nutrition, but thicker grafts will almost certainly require
some adhesions to deliver a vascular source. The balance
that results is extremely delicate and likely explains the
usually mediocre results of tendon grafting—moving
too much and too soon disrupts adhesions and may
jeopardize long-term graft viability; protecting too long
will result in too many, short adhesions that unaccept-
ably limit function of a better vascularized graft. Our
compromise has been to use passive mobilization in the
281
first few weeks, to provide a limited range of graft
gliding, and then progressing along a rehabilitation
pathway similar to that for tendon repairs.
RESULTS
The results of one-stage grafting are best summarized in
the classic 1971 report by Boyes and Stark,5 which
reviewed their results in 1000 cases. It is unlikely that
anyone will ever duplicate this experience, so it is worth
reviewing. They classified the digits as being either good,
scarred, with joint contractures, as one of multiple
injured digits in the same hand, and as salvage cases, in
which there were associated skin, bone, or nerve inju-
ries. Results were graded based on active flexion; resid-
ual flexion contractures were not considered unless they
were more than 40° in the index and middle fingers and
60° in the ring and little fingers. According to this
scheme, the good digits did best, with two of three
flexing to within 0.5 inch to the palm, and 85% flexing
within 1 inch. The corresponding figures for the mul-
tiple and scar categories were a little worse: 30% and
60%, respectively. The digits with joint contractures
were worse again: 10% and 50%, respectively, while the
salvage cases did extremely poorly: no digits in this
group could flex with 0.5 inch and only 20% could flex
within 1 inch. Patients over age 30 did worse, and
patients over age 40 did much worse, for similar grades
of digit. So long as the digit remained supple, delay to
surgery did not seem to matter.
TWO-STAGE GRAFT
Indications
When tendon grafting is indicated to restore tendon
function and a one-stage graft is relatively contraindi-
cated because of excessive scar, joint contracture, pulley
loss, or a need for better soft tissue cover, then a two-
stage reconstruction can be considered. One aspect of
the indications that does not change between the one-
and two-stage procedure is the absolute need for a coop-
erative patient, who is fully informed as to the time
commitment that is likely to be necessary: the initial
stage, to address the scar, contracture, pulley and soft
tissue issues that contraindicate a one-stage graft; an
interval for soft tissue healing, which is usually 3 months
or longer; a second stage, which is a “one-stage” graft as
described earlier; and interval for graft healing, again as
described earlier; and then consideration of the need for
a possible third stage, namely tenolysis or some sort of
salvage if the two-stage graft fails. Only a patient willing
and able to travel this long road with the surgeon should
be considered for surgery; only a need great enough to
justify such an arduous journey should prompt the
surgeon to suggest it. Thus, for example, such proce-
dures are rarely indicated in young children7 or in those
who live at such a distance from the surgeon that close
282 Section 3:  Secondary Flexor Tendon Surgery
follow-up becomes impossible.11 Reconstruction of a
profundus tendon in the presence of a normally func-
tioning superficialis must be carefully considered—Will
the potential benefit outweigh the considerable risks6?
Even reconstruction of the thumb flexor should be care-
fully thought through—How does the risk/benefit ratio
compare, for example, with a much simpler interpha-
langeal arthrodesis?
METHOD
The first-stage procedure involves addressing the soft
tissue issues outlined earlier and then using a silicone
rubber spacer to maintain a place for the second-stage
tendon graft (Figure 26-4). Thus, each operation is
unique. Nevertheless, some basic principles are useful
to note. Joint contractures should be released prior to
soft tissue reconstruction, so that the full length of
needed tissue can be ascertained. When releasing con-
tractures in the presence of pulley loss, it is especially
important to excise all scar anterior to the bone; often
a hard triangle of scar will feel like bone and may deceive
the unwary surgeon, who then reconstructs a pulley that
does not hold the graft close enough to the bone to
prevent postoperative bowstringing.
As with one-stage grafting, a key decision is where
to put the proximal junction—in the palm or forearm.
In the case of one-stage grafts, which ought to have
good surrounding tissues, usually the palm is appropri-
ate. In the case of two-stage grafts, usually it is the
opposite—the palm and the finger are scarred, and the
most hospitable location is often the distal forearm.
Regardless, the tendon implant should be inserted and
fixed distally to bone, with either screw or suture. It is
threaded through any intact pulleys and pulleys are then
reconstructed around the graft where needed. When
completed, the graft should fit snugly within the new
sheath but should piston smoothly, without any ten-
dency for buckling with passive flexion. Any buckling at
this stage will simply become synovitis and infection
postoperatively.
We do not use active implants.12 The literature sug-
gests that their results are no better than passive ones,
Figure 26-4  Stage 1 surgery with a silicone implant in
place. Note pulley reconstruction at the middle part of the
proximal phalanx.
and when they break they are difficult to reconstruct.
Proximal failure typically leaves a destroyed muscle–
tendon junction, which is hard to salvage.
After stage 1, the finger is passively mobilized as the
wound conditions permit. Stage 2 is performed when
the incisions are soft and supple and passive finger
motion has reached a maximum. Stage 2 surgery is a
tendon graft, repaired and rehabilitated as for one-stage
grafts. The main difference is that often longer grafts are
needed, such as plantaris or a toe extensor.
RESULTS
The results of two-stage grafts are certainly better than
those of a one-stage graft performed for similar indica-
tions but remain unexciting in many cases.13-19 Flexion
contractures and limited flexion remain common; the
recovery period is long, and patient satisfaction is often
low, with expectations incompletely met. Among the
more common complications are graft rupture and late
contracture, especially of the DIP joint. This latter com-
plication can be avoided if the graft is used to recon-
struct the flexor superficialis, and the distal joint is
fused.
SECONDARY REPAIR IN THE FUTURE
Improving the gliding characteristics of extrasynovial
autografts may lead to improved clinical results
after tendon graft surgery. Recent studies have shown
that extrasynovial graft surface modification with
carbodiimide-derivatized hyaluronic acid mixture
decreased gliding resistance of the tendon and
increased the durability after repetitive motion in the
in vitro studies.20,21 Zhao et al conducted an in vivo
flexor tendon graft in canine model using autologous
peroneus longus tendon. They demonstrated that the
surface of an extrasynovial tendon autograft with
a carbodiimide-derivatized hyaluronic acid gelatin
decreases adhesions and increases tendon gliding.22
These encouraging experimental results potentially
provide surgeons with a new and useful method to
improve the quality of tendon graft surgery.
Although intrasynovial tendon autologous grafts
are rarely obtained without compromising the donor
site morbidity, allograft-matched intrasynovial flexor
tendons are possibly available. Allograft tendon grafts
are frequently used for anterior cruciate ligament recon-
struction,23-27 but flexor tendon reconstruction with
allograft tendon has been rarely reported.28 The use
of allografts for tendon reconstruction merits serious
consideration for the following reasons: intrasynovial
allograft tendon sources are abundant, which permits
easy clinical application; allograft use limits surgical
morbidity, as no graft harvest is necessary; allograft use
reduces the surgical time required by eliminating the
graft harvesting procedure, which directly translates into
a cost reduction29; and better size matching. A major
 Chapter 26:  Experience With Secondary Flexor Tendon Repairs 283

Figure 26-6  Scarred digit after initial surgery in an animal

Figure 26-5  Lubricated tendon graft after chemical model of tendon grafting.
modification of tendon surface.

disadvantage is the potential for an immune reaction,

but this can reduced by processing the allograft prior to
use. A lyophilized, decellularized allograft is less immu-
nogenic, better tolerated, and as effective as autograft.30-32
Preserved allografts also maintain their mechanical
properties with the convenience of availability at any
desired time.25,33,34
In addition to the needs of mechanical strength and
appropriate tendon/bone healing, the flexor tendon
allograft also requires a smooth gliding surface. However,
Ikeda et al found that the procedures used to prepare
allografts damage the tendon surfaces leading to greater
frictional force in canines.35 This adverse effect can
be reversed by surface treatment with carbodiimide-
derivatized hyaluronic acid and gelatin (Figure 26-5).35 Figure 26-7  Treated (top) and untreated (bottom) grafts in
A flexor tendon reconstruction with surface modified a canine model. Adhesions were markedly reduced in the
treated graft.
allografts has been studied in a canine in vivo model of
failed primary repair.36 In this experiment, the flexor
tendons were lacerated and repaired, and the animals
were allowed free active motion postoperatively. The function, reduced adhesions, and decreased gliding
repaired tendons were all ruptured within 2 weeks. After resistance compared with allografts without such modi-
6 weeks, a scarred digit with a uniform failure pattern fication (Figure 26-7).36 We believe that treated allografts
was routinely produced (Figure 26-6). Subsequent may similarly improve the results after flexor tendon
grafting with surface-treated allografts improved digital reconstruction in humans.

References
1. Bunnell S: Hand surgery, J Bone Joint Surg (Am) 29:824,
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2. Boyes JH: Evaluation of results of digital flexor tendon grafts,
J Surg (Am) 89:1116–1119, 1955.
3. Hauge MF: The results of tendon suture of the hand: A review
of 500 patients, Acta Orthop Scand 24:258–270, 1955.
4. Kelly AP Jr: Primary tendon repairs: A study of 789 consecu-
tive tendon severances, J Bone Joint Surg (Am) 41:581–598,
1959.
5. Boyes JH, Stark HH: Flexor-tendon grafts in the fingers and
thumb. A study of factors influencing results in 1000 cases,
J Bone Joint Surg (Am) 53:1332–1342, 1971.
6. Stark HH, Zemel NP, Boyes JH, et al: Flexor tendon graft
through intact superficialis tendon, J Hand Surg (Am) 2:456–
461, 1977.
7. Amadio PC: Staged flexor tendon reconstruction in children,
Ann Chir Main Memb Super 11:194–199, 1992.
8. Nishida J, Amadio PC, Bettinger PC, et al: Excursion
properties of tendon graft sources: interaction between
tendon and A2 pulley, J Hand Surg (Am) 23:274–278,
1998.
9. Tanaka T, Zhao C, Ettema AM, et al: Tensile strength of a new
suture for fixation of tendon grafts when using a weave
technique, J Hand Surg (Am) 31:982–986, 2006.
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10. Silva MJ, Thomopoulos S, Kusano N, et al: Early healing of
flexor tendon insertion site injuries: Tunnel repair is mechan-
ically and histologically inferior to surface repair in a canine
model, J Orthop Res 24:990–1000, 2006.
11. Amadio PC, Wood MB, Cooney WP 3rd, et al: Staged flexor
tendon reconstruction in the fingers and hand, J Hand Surg
(Am) 13:559–562, 1988.
12. Hunter JM, Singer DI, Jaeger SH, et al: Active tendon implants
in flexor tendon reconstruction, J Hand Surg (Am) 13:849–
859, 1988.
13. Sun S, Ding Y, Ma B, et al: Two-stage flexor tendon reconstruc-
tion in zone II using Hunter’s technique, Orthopedics 33:880,
2010.
14. Alnot JY, Masmejean EH: The two-stage flexor tendon graft,
Tech Hand Up Extrem Surg 5:49–56, 2001.
15. Smith P, Jones M, Grobbelaar A: Two-stage grafting of flexor
tendons: results after mobilisation by controlled early active
movement, Scand J Plast Reconstr Surg Hand Surg 38:220–227,
2004.
16. Amadio PC, Wood MB, Cooney WP 3rd, et al: Staged flexor
tendon reconstruction in the fingers and hand, J Hand Surg
(Am) 13:559–562, 1988.
17. Wehbé MA, Mawr B, Hunter JM, et al: Two-stage flexor-
tendon reconstruction. Ten-year experience, J Bone Joint Surg
(Am) 68:752–763, 1986.
18. Schneider LH: Staged flexor tendon reconstruction using the
method of Hunter, Clin Orthop Relat Res 171:164–171, 1982.
19. Paneva-Holevich E: Two-stage reconstruction of the flexor
tendons, Int Orthop 6:133–138, 1982.
20. Momose T, Amadio PC, Sun YL, et al: Surface modification
of extrasynovial tendon by chemically modified hyaluronic
acid coating, J Biomed Mater Res 59:219–224, 2002.
21. Sun YL, Yang C, Amadio PC, et al: Reducing friction by chemi-
cally modifying the surface of extrasynovial tendon grafts,
J Orthop Res 22:984–989, 2004.
22. Zhao C, Sun YL, Amadio PC, et al: Surface treatment of flexor
tendon autografts with carbodiimide-derivatized hyaluronic
acid. An in vivo canine model, J Bone Joint Surg (Am) 88:2181–
2191, 2006.
23. Jackson DW, Grood ES, Goldstein JD, et al: A comparison
of patellar tendon autograft and allograft used for anterior
cruciate ligament reconstruction in the goat model, J Sports
Med (Am) 21:176–185, 1993.
24. Kustos T, Bálint L, Than P, et al: Comparative study of auto-
graft or allograft in primary anterior cruciate ligament recon-
struction, Int Orthop 28:290–293, 2004.
25. Tejwani SG, Shen W, Fu FH: Soft tissue allograft and
double-bundle reconstruction, Clin Sports Med 26:639–660,
2007.
26. Dustmann M, Schmidt T, Gangey I, et al: The extracellular
remodeling of free-soft-tissue autografts and allografts for
reconstruction of the anterior cruciate ligament: A compari-
son study in a sheep model, Knee Surg Sports Traumatol
Arthrosc 16:360–369, 2008.
27. Scheffler SU, Schmidt T, Gangéy I, et al: Fresh-frozen
free-tendon allografts versus autografts in anterior cruciate
ligament reconstruction: delayed remodeling and inferior
mechanical function during long-term healing in sheep,
Arthroscopy 24:448–458, 2008.
28. Liu TK: Clinical use of refrigerated flexor tendon allografts to
replace a silicone rubber rod, J Hand Surg (Am) 8:881–887,
1983.
29. Cole DW, Ginn TA, Chen GJ, et al: Cost comparison of
anterior cruciate ligament reconstruction: Autograft versus
allograft, Arthroscopy 21:786–790, 2005.
30. Webster DA, Werner FW: Mechanical and functional proper-
ties of implanted freeze-dried flexor tendons, Clin Orthop
Relat Res 180:301–309, 1983.
31. Gulati AK, Cole GP: Nerve graft immunogenicity as a factor
determining axonal regeneration in the rat, J Neurosurg
72:114–122, 1990.
32. Fromm B, Schäfer B, Parsch D, et al: Reconstruction of the
anterior cruciate ligament with a cyropreserved ACL allograft.
A microangiographic and immunohistochemical study in
rabbits, Int Orthop 20:378–382, 1996.
33. Goertzen MJ, Clahsen H, Schulitz KP: Anterior cruciate liga-
ment reconstruction using cryopreserved irradiated bone-
ACL-bone-allograft transplants, Knee Surg Sports Traumatol
Arthrosc 2:150–157, 1994.
34. Mahirogullari M, Ferguson CM, Whitlock PW, et al: Freeze-
dried allografts for anterior cruciate ligament reconstruction,
Clin Sports Med 26:625–637, 2007.
35. Ikeda J, Zhao C, Sun YL, et al: Carbodiimide-derivatized hyal-
uronic acid surface modification of lyophilized flexor tendon:
A biomechanical study in a canine in vitro model, J Bone Joint
Surg (Am) 92:388–395, 2010.
36. Zhao C, Sun YL, Ikeda J, et al: Improvement of flexor tendon
reconstruction with carbodiimide-derivatized hyaluronic
acid and gelatin-modified intrasynovial allografts: Study of
a primary repair failure model, J Bone Joint Surg (Am) 92:
2817–2828, 2010.
 CHAPTER
27  
SECONDARY RECONSTRUCTION
OF THE FLEXOR POLLICIS
LONGUS TENDON
David Elliot, MA, FRCS, BM, BCh
OUTLINE
Primary repair of the flexor pollicis longus tendon is
generally recommended, except in zone 3 or 4 injuries,
when primary grafting can be advisable. Techniques
are discussed that allow primary repair under circum-
stances that might otherwise require tendon grafting.
Circumstances in which no secondary repair is accept-
able are also discussed. The requisites for function that
must be met if the flexor pollicis longus muscle is to
be used as the motor for a tendon graft are examined.
Some technical aspects of tendon grafting are dis-
cussed and the usefulness of two-stage grafting under
certain circumstances is considered.
The technical execution of the various surgical maneu-
vers used in secondary reconstruction of the flexor pol-
licis longus (FPL) (Box 27-1) are relatively straight
forward to any hand surgeon versed in the techniques
of flexor tendon surgery. However, decision making as
to what is done in any particular circumstance is com-
plicated by various anatomical peculiarities of the FPL
tendon compared to the flexor system of the finger, the
timing of presentation, the plethora of treatment
options, and, in some instances, by the differing flexion
needs of the thumb in different individuals.
PRIMARY REPAIR OF FLEXOR POLLICIS
LONGUS BY PREFERENCE
Recent practice (see Chapter 16) has established that
primary repair of the FPL tendon is desirable where pos-
sible and 70% to 80% of the results will be within the
excellent or good range, although it should be noted
that “excellent” in our current classifications does not
imply return to normal function. Nevertheless, these
results are better than the 30° to 40° degrees of move-
ment previously perceived as necessary to good function
of the interphalangeal (IP) joint of the thumb.1,2 With
various modern suturing techniques of primary repair,
early mobilization can also be progressed safely to com-
pletion without rupture of the repair.3,4 Direct repair
may be possible as late as 3 to 4 weeks after injury but,
more frequently, in my experience, there is sufficient
shortening of the muscle within a few days as to make
direct primary repair without proximal tendon length-
ening impossible without the IP being flexed to a degree
from which it never recovers extension.
PRIMARY GRAFTING OF ZONE 3 AND
4 INJURIES
The FPL is rarely divided in zone 3, within the thenar
muscles, where it is deeply placed. However, surgical
repair is difficult in zone 3 as access is past the digital
nerves of the thumb and through the thenar muscles,
with risk to the motor branches of the median nerve.
That loss of thumb sensation or opposition are greater
disabilities than loss of terminal flexion should be con-
sidered before extending an already extensive injury in
this zone to repair the tendon directly.5 Any direct
tendon repair in zone 3 will also be surrounded by
edematous and swollen muscle during rehabilitation.
Except where the injury is a small puncture wound of
the thenar eminence and dissection to the site of divi-
sion can be precise and small, there is justification for
the approach recommended by Matev (1983) of replac-
ing the tendon from the wrist to its distal attachment
with a tendon graft, even if seen immediately.6 In these
injuries, the proximal end of the tendon is frequently
found retracted to the wrist. When presentation is even
only slightly delayed, the distal end of the tendon may
be adherent within the muscle tunnel and require
careful release from adhesions through the digital expo-
sure, if necessary leaving the end itself within the muscles
by division of the tendon just proximal to the metacar-
pophalangeal joint.
Isolated division of FPL in the carpal tunnel (zone 4)
is even rarer. Direct tendon repair in the carpal tunnel
may snag on the relatively narrow opening from the
carpal tunnel into the tunnel through the thenar muscles
or on the proximal edge of the carpal ligament. Under
these circumstances, the Matev approach of grafting the
FPL from the wrist to the distal phalanx of the thumb
285
286 Section 3:  Secondary Flexor Tendon Surgery
Box 27-1  Treatment Options for the Divided
FPL Tendon
Primary and Delayed Primary Repair
1. End-to-end suture of the cut tendon
(Advised in all but zone 3)
2. Reattachment of the distal tendon to the distal phalanx
(a) After tendon avulsion
(b) After division close to the distal insertion
Extended Primary Repair
Primary repair with proximal tendon lengthening
Secondary Reconstruction
1. No surgery
2. Distal tenodesis of the FPL or IP joint fusion
3. Tendon grafting in one stage
4. Tendon grafting in two stages
5. Tendon transfer
also has some merit. With multiple tendon injuries
within the carpal tunnel, swelling of the tendons makes
tethering of the multiple repairs within the tunnel likely.
With this rare injury, we have previously provided suf-
ficient space to avoid the problem of tethering of the
swollen tendons and impeded movement by repairing
only the finger profundus tendons and have repaired
the FPL tendon primarily. To achieve the necessary
repairs in the carpal tunnel requires division of the
carpal ligament. To allow for swelling and avoid possi-
ble compression of the median nerve, we have not
reconstructed the carpal ligament but have mobilized
the tendons repairs in a neutral, or slightly hyperex-
tended, wrist position.
TECHNIQUES TO EXTEND PRIMARY REPAIR
In general, the use of primary flexor surgery can be
extended and secondary surgery avoided by (1) using
techniques that allow one to do more primary repairs,
such as undertaking delayed primary repairs, using
proximal tendon lengthening, and using techniques
such as splitting swollen tendons distally to allow their
passage through the pulleys7; (2) by using techniques
that reduce the failures of primary repair, such as
improved rehabilitation; and (3) by re-repairing rup-
tures.8 Many of these techniques are applicable to the
divided FPL tendon. Occasionally, the FPL may be too
swollen to pass through the A1 and A2 pulleys. The
technique of halving the distal end of the tendon that
we described to pass a swollen flexor digitorum profun-
dus (FDP) tendon through the A4 pulley7 can also be
used in FPL surgery (Figure 27-1). However, the most
significant problem preventing primary FPL repair is
the propensity of the FPL muscle to contract after divi-
sion of the tendon,9 and proximal tendon lengthening
to deal with this eventuality can be considered an
extension of primary repair or a technique of secondary
reconstruction. This has been discussed in some detail
in Chapter 16 but more from the point of view of avoid-
ing a tightly flexed interphalangeal (IP) joint of the
thumb and/or tendon rupture by primary suture under
tension.
The considerable literature of the 1940–1960 period,
when most presentations and repairs were delayed,
presents a conflict of opinion as to whether the FPL
should be repaired by interpositional grafting or by
proximal tendon lengthening, either in the muscle or
in the tendon at the wrist, with direct repair being
entirely avoided by many authors, or exceptional, except
after very early presentation for others. Urbaniak and
Goldner favored direct repair when possible and used
the other techniques when the tendon gap was too
wide.10,11 They found the results of tendon lengthening
in their unit to be better than those of interposition
grafting in those cases in which direct repair was not
possible. In their writings, others are more circumspect
as to whether tendon lengthening gives better results
than tendon grafting.5,6 This debate as to the relative
merits of extending primary repair by proximal length-
ening or moving on to grafting continued through the
period after 1970 and remains in the literature with
Schneider (1999), in Green’s Operative Hand Surgery,
confessing to little experience with tendon lengthen-
ing,12 while Matev (1983) considered Z lengthening in
the musculotendinous part of the tendon as a logical
extension of primary suturing and preferable to grafting
when the muscle has retracted but not undergone
degeneration and fibrosis.6 Our experience has largely
been after only slight delay of presentation, with muscle
shortening sufficient for primary suture to be under
tension, or significantly flex the IP joint, but before
muscle degeneration. Proximal tendon lengthening
within the muscle by the Le Viet technique13 has usually
achieved the lengthening of up to 1 cm required in
these circumstances. My experience of “Z” lengthening
of the FPL tendon at the musculotendinous junction14,15
is limited and usually as an adjunct to lengthening
within the muscle where this alone is not adequate
(Figure 27-2). Pulvertaft (1966) wrote that a gap of 11 2
to 2 inches (3.8 to 5 cm) could be closed by this tech-
nique alone.5 The long length of FPL tendon—3 to
4 cm—at the wrist with no muscle fibers attached aids
this degree of lengthening without impingement of the
tendon sutures on the carpal ligament on full extension
of the thumb with the wrist dorsiflexed, if the lengthen-
ing is carried out at the musculotendinous junction.10
The adjacent muscle can also be tacked around the
lengthening to make it more smooth. I have no experi-
ence of Rouhier lengthening within muscle, still said to
be used in France.16,17
The practice of advancing the proximal end of the
FPL to allow direct reattachment to the distal phalanx
A B

C D

E F
Figure 27-1  The right thumb of a 54-year-old woman
who lacerated her thumb and required skin suturing only.
Six weeks later, the partially divided FPL tendon snapped
during use. A, The swollen FPL tendon held at the base
of the thumb. B, The FPL tendon is too swollen to pass
under the A1 pulley. C, The tendon is narrowed by distal
splitting. D, Repair with two Kessler sutures at 90° and
a simple running circumferential suture, with the repair
allowing full IP extension without snagging of the repair
on the A2 pulley or the junction of the tendon split
snagging on the A1 pulley. E, IP flexion limited by
G snagging on the oblique pulley. F, Fuller flexion after
venting of the oblique pulley. G, The final position of
the thumb is a little tight, presumably due to muscle
shortening as the tendon length has not been unchanged.
288 Section 3:  Secondary Flexor Tendon Surgery

A B

C D

E F
Figure 27-2  A, Exploration of the thumb of a 45-year-
old man after primary repair of the FPL ruptured through
infection, with the arrows showing a considerable length
of the tendon replaced by scar. B, The arrow on the
thumb indicates the position of the distal end of the FPL
tendon when pulled distally. C, Showing the additional
length achieved by one Le Viet cut of the tendon in
muscle. D, Tendon suture indicates that the tendon is still
too short. E, Two Le Viet cuts still not providing sufficient
tendon lengthening. F, Further advance of the tendon by
Z lengthening at the wrist. G, Achieving adequate position
G of the IP joint.
 Chapter 27:  Secondary Reconstruction of the Flexor Pollicis Longus Tendon 289

after very distal division is frequently mentioned in the

literature. This can be considered as a means of dealing
with a gap in the tendon, albeit one created by the
surgeon by removing the distal segment of the FPL. A
warning is often given that such an advancement can
only be done without significant flexion contracture of
the IP joint if the division is within 1 cm of the inser-
tion. I believe this practice to be unwise and likely to
give rise to IP flexion contracture if an advancement of
even 1 cm is carried out. When the distal part of the
tendon is 3 4 to 1 cm in length, it is quite possible to
insert a core suture into the distal end of the tendon.
With divisions closer to the insertion than 3 4 cm, it is A
possible to leave the distal segment of tendon in place
and anchor the suture into the distal phalanx by one of
the various described techniques, after passage of the
sutures through the distal segment of the tendon. While
the small attached segment of tendon could be excised
and any IP contracture subsequent to advancement of
the proximal tendon corrected by lengthening of the
proximal tendon, this seems a complicated way of
achieving the same end.
B
NO FPL REPAIR
In respect of patients presenting after significant delay,
management by doing nothing, particularly if the car-
pometacarpal (CMC) and metacarpophalangeal (MCP)
joints are functioning normally, is generally only sug-
gested as suitable for the elderly.12 It has been my experi-
ence with several younger-than-elderly patients who
have presented late with inability to flex the IP joint that
they have been quite happy with the function of the C
thumb for their needs and, when the option of a com-
plicated operation and a lengthy rehabilitation period Figure 27-3  A 50-year-old woman who presented several
months after division of the FPL and declined surgery as she
is explained as the logical treatment of their problem,
thought that her disability was minimal. A, Full thumb
have declined any treatment (Figure 27-3). Doing
extension. B, Pinch to the index. C, Pinch to the little finger.
nothing or a (relatively simple) distal fixation procedure
to prevent hyperextension of the IP joint, if this is
causing problems of pinching, is definitely an option to
be discussed with all patients. As the variable hyperex- grafting or tendon transfer reconstruction, presumably
tension of this joint commonly seen, particularly in because the excursion of the new tendon is largely
supple hands, appears to have no useful function,18 such taken up by movement of the MCP and the segment
fixation causes no obvious deficit of thumb function. of new tendon beyond the MCP moves little during
When fixation of the IP joint is necessary, general obser- rehabilitation. I have tried passing a K-wire across
vation suggests that plastic surgeons prefer distal tendon the MCP for 4 to 6 weeks to prevent this failure to
tenodesis and orthopedic surgeons prefer joint fusions. achieve IP joint flexion,19 but with no greater success, as
Either, performed correctly, works well, but both require the patients reverted to MCP flexion on removal of the
1 to 2 months of protection before being used for force- K-wire. Tubiana (1988) warns that satisfactory flexion
ful pinching. A small but definite group of patients who of the distal phalanx will only be achieved by grafting
may be best advised to choose this option of manage- in the absence of hyperextension of the MCP joint.20 I
ment are patients with very mobile MCP joints who have no experience of this alternative problem of MCP
routinely flex the MCP joint through 40° to 50° degrees extension hypermobility affecting FPL surgery.
when pinching. This variation of thumb flexion can be
THE IDEAL OF INTERPHALANGEAL MOTION
ascertained by examining the contralateral thumb. In
my experience, these patients will continue to flex the With these exceptions, it is generally advisable in respect
MCP joint alone, with no, or little, IP flexion after either of best function of the thumb to try to achieve some
290 Section 3:  Secondary Flexor Tendon Surgery
movement of the thumb IP joint. Our experience of
primary repair of the extensor pollicis longus tendon18
identified a group of patients who developed extensor
tendon adherence by scar tissue to the underlying bone
and overlying skin, with loss of IP joint movement that
caused functional problems. In this study, eight patients
complained of difficulties with fine pinch functions
such as the handling small screws, when the IP joint of
the thumb has to flick back and forth rapidly over a
small range of motion within its flexion range. This is
most likely to be a problem to those in whom fine
degrees of movement of this joint are critical, such as
musicians, surgeons, craftsmen, mechanics, and electri-
cians. The same problem arises if the FPL is not intact,
or the IP joint imperfect, and it is the loss of rapid move-
ment over a small range, rather than the loss of the fuller
range of motion of this joint, that we record with a
goniometer, which is the problem. The stated goal of a
previous generation of surgeons of achieving only 30°
to 40° of IP movement to provide good function of the
thumb is in keeping with the above observations.1,2
TENDON GRAFTING—THE FPL MUSCLE
Where there is a delay of presentation and a significant
gap between the tendon ends, it is usually recommended
that a tendon graft be interposed. A sine qua non for
this to be successful is that the FPL muscle is still func-
tional and has not fibrosed after shortening. This is a
particular concern after a delay of years between tendon
division and reconstruction. Pulvertaft (1988) addressed
this subject by examination of 77 tendon grafts per-
formed more than 2 years after tendon division, of
which 11 were divisions of the FPL.1 This study recorded
an average joint range of the IP joint of the thumb of
64° in a population of patients of average age of 18
years at operation, after an average delay of 51 2 years.
This study showed that muscle shortening does not
occur as often, or as severely, as might be expected.
Tendons retract only as far as natural structures attached
to them permit, provided these do not rupture at the
time of injury, or immediately after. The FPL only very
rarely has a lumbrical.21 The distal vinculum brevis is
present in 90% of thumbs and is strong.22 If intact after
injury at the level of the IP joint, it may transmit some
amount of flexion of the IP joint and it will retain the
FPL within the thumb. The existence of a true vinculum
longus is debated.10 Pulvertaft thought that local adhe-
sions played a part in maintaining the tendon in the
thumb. A partial division of a tendon that ruptures later
may have the same effect, as a result of edema in the
tendon preventing retraction (see Figure 27-1). There-
fore, the muscle may still be functional, albeit partially,
and its integrity preserved, after a considerable period
of time. More recently, Urbaniak and Goldner (1973)
recorded retraction of the proximal tendon to the thenar
area or wrist after laceration distal to the MCP joint in
21 of 35 tendons.11 Matev (1983) warned that the FPL
muscle was particularly liable to lose its contractile
qualities quickly after tendon division at the wrist,
giving poor results from grafting.6 He recommended
that another motor be used more readily after tendon
division at this level. This observation in itself appears
inexplicable until considered in the light of Pulvertaft’s
observations as mentioned earlier. Of all FPL divisions,
those at the wrist are the most likely to suffer complete
retraction of the proximal tendon and muscle as there
is little to hold the tendon to length, or partial length,
and complete retraction probably occurs immediately
after tendon division.
Pulvertaft usually found the tendon and sheath distal
to the division to be in good condition but warned that,
in children, there was no stimulus to develop and the
tendon and sheath remained as they had been at the
time of injury, necessitating reconstruction of an entirely
new set of pulleys to retain any tendon graft.1 Once in
situ and working, the graft grows with the child’s hand
and late contracture due to relative shortening of the
graft is not seen.
There is no way of determining the quality of
the muscle before exposing the proximal tendon, so
the possible need for another motor should always be
explained before surgery to the patient. The FPL has a
functional amplitude of excursion of 5.5 to 6 cm23: if the
amplitude of excursion of the cut end of the proximal
tendon is far short of this, then it is unlikely that using
it as a motor for reconstruction will achieve much in
respect of IP joint flexion. Matev provided a useful rule
of thumb in this respect: if the passive stretch of the
muscle fibers, measured at the wrist, is 3 to 4 cm, full
restoration of function may be expected.6 Even with 1.0
to 1.5 cm of passive stretch, the result is likely to be ade-
quate. If less than this, he advised using another motor.
TENDON GRAFTING—BRIDGE GRAFTS
Although some authors recommend and illustrate inter-
position of short segments of graft to bridge gaps,20,24 I
believe that it is more logical in most situations to use
long grafts that take the suture lines to the wrist and the
distal insertion of the FPL tendon, as short segment
grafting most commonly creates a suture line within the
narrow confines of the digital sheath or in the thenar
muscles, or both. Because of the other tendon, artery,
and nerve injuries, it is rare for a division of the FPL
tendon at the wrist not to be repaired primarily. Where
it is not, a short segment of graft will reestablish contact
between the distal tendon and the retracted proximal
tendon and can be used, provided the muscle has not
lost its contractility early, as discussed above. Care is
necessary to avoid impingement of the distal suture line
on the proximal edge of the carpal ligament on full
thumb extension and this part of the ligament may have
to be resected.
 Chapter 27:  Secondary Reconstruction of the Flexor Pollicis Longus Tendon 291

TENDON GRAFTING—WRIST–TO–DISTAL
PHALANX GRAFTS
A length of tendon graft of 13 to 14 cm is sufficient to
replace the FPL from the wrist to the distal phalanx.
Palmaris longus (PL) is usually of suitable length, always
of suitable diameter and conveniently near to hand. It
is also present in a very high percentage of the popula-
tion. Plantaris is probably the next choice although it is
often very thin and difficulty to suture well with convic-
tion. It remains a matter of wonder to me that it usually
retains its distal attachment throughout rehabilitation.
My third option is the extensor indicis tendon as this
tendon is of adequate length, is sufficiently thick as to
be easy to sew, is near to hand, can be harvested through A
small dorsal incisions, is almost always present, and is
seldom missed, as we know from our various other
uses of it.
TENDON GRAFTING—DISTAL AND
PROXIMAL ATTACHMENT
Grafting of the FPL is generally carried out using various
techniques of distal attachment to the distal phalanx of
the thumb and a Pulvertaft weave proximally. I routinely
suture the Pulvertaft weave with a continuous 4-0
Prolene suture (Figure 27-4), which starts at one end of
the weave and returns to the same end to be knotted
with a single knot. I prefer this technique to leaving
multiple knots along the weave, which are more likely
to snag. It is seldom that the passage of the needle cuts B
a previous pass of the suture. Even if it does and a
second knot is required, this technique is still faster and Figure 27-4  A 48-year-old man who ruptured a primary
neater than the conventional use of multiple suture and repair of the FPL. Reconstruction at immediate exploration
with a one-stage PL graft from the wrist to the distal
knots.
phalanx of the thumb. A, The technique of suturing the
TENDON GRAFTING—THE THENAR TUNNEL Pulvertaft weave at the wrist using a single continuous
suture is illustrated in close-up (B).
The most difficult technical activity in secondary recon-
struction of the FPL is passing the new tendon, or the
silicon rod if a two-stage procedure is carried out,
through the thenar muscles, particularly if the tunnel is
scarred and closed. Good exposure of the entry to the the tension of the graft is set by placing the hand flat on
tunnel at the base of the thenar muscles includes fully the table with the thumb in a position of slightly
opening the carpal tunnel and identifying the motor increased flexion over its normal resting position, then
branch of the median nerve and the sensory branches using the wrist tenodesis action to check that the IP joint
to the thumb more distally. Where the tunnel is present, of the thumb is fully extended when the wrist is held in
the tendon can be pulled through to the base of the full flexion and is partially flexed and opposed when the
thumb with a fine tendon passer or attached by a suture wrist is extended to the functional position.24 Schneider
to a small-bore stiff plastic tube. Where necessary, the (1999) detailed a more precise setting of the wrist at 0°,
tunnel is recreated with McKindoe scissors and, mostly, the thumb abducted in front of the index finger meta-
blunt dissection. Under these circumstances, we would carpal, and the IP joint of the thumb in 30° of flexion.12
use a two-stage tendon graft reconstruction. Matev suggested the IP joint be set at 20° to 30°.6 All
of these recommendations are very similar in practice
TENDON GRAFTING—THE TENSION
and can all be used in combination. In general, the
OF SETTING IN THE GRAFT
tension should be a little greater than normal, allowing
The tension at which the graft is set is important. Camp- for the fact that the contracted muscle will extend
bell Reid and McGrouther (1986) recommended that slightly towards normal with subsequent use.1 A graft
292 Section 3:  Secondary Flexor Tendon Surgery
A B
that is too tight is more likely to gain extension than
one that is too slack to regain flexion.
TENDON TRANSFER
Where there is doubt as to the function of the FPL
muscle at exploration (Figure 27-5), it is necessary to
use a tendon transfer to provide another motor for
thumb flexion. While the flexor digitorum superficialis
of the ring finger, the PL, the brachioradialis, and the
flexor carpi radialis have all been suggested as suitable
for this transfer, the first is that normally used. The PL
is an antagonist to the FPL, making re-education more
difficult. Dissection of the brachioradialis is unnecessar-
ily extensive, compared with that necessary to harvest
the flexor digitorum superficialis (FDS) of the ring
finger, and leaves a long and visible forearm scar to no
particular advantage. The FDS of the ring finger can be
harvested without difficulty through small incisions that
fade to be inconspicuous at the base of the finger and
in the palm, if a palmar incision is needed. The length
of the tendon is such that it will always replace the FPL
Figure 27-5  Exploration of a nonfunctioning FPL in a
48-year-old woman 4 months after removal of a plate
elsewhere that had been used to treat a radial fracture 5
years earlier. The plate was perceived to be the cause of
difficulties of finger and thumb movement. A, View after
extensive tenoneurolysis (with the appearance of the
median nerve as an indicator of the degree of scarring
prior to tenoneurolysis). The FPL muscle was completely
bound in scar tissue and nonfunctional. B, The FPL
tendon had snapped or been divided at removal of the
plate, with the distal end resting at the MCP level of the
thumb. C, Insertion of a silicone rod with a view to
performing a secondary FDS tendon transfer from the
ring finger.
entirely without supplement by a tendon graft. This
transfer also needs little re-education. Little has been
written in recent years about this transfer but what has
been written is favorable.25,26
While some authors suggest transfer of the FDS
tendon of the ring finger as an alternative to grafting of
the FPL,27 I do not agree with this for various reasons.
Use of this tendon transfer introduces a further com-
plexity to the situation. Weakening the ring finger may
have little functional significance, but it has been my
experience, even with a very experienced and large
therapy department looking after these patients after
surgery, that the subsequent mobility of the ring finger
is not always normal. In particular, in a white popula-
tion, loss of extension of the proximal interphalangeal
(PIP) joint as a result of palmar plate contracture is
possible. Those with more mobile joints are more
likely to suffer swan-necking unless the distal end of the
FDS tendon is carefully sutured to the sheath or A2
pulley proximal to the PIP joint. More significant inter-
ference with normal flexion and extension movements
 Chapter 27:  Secondary Reconstruction of the Flexor Pollicis Longus Tendon 293

of the remaining flexor tendon may occasionally arise

as a result of adhesion formation. Ebelin et al also
reported problems with this reconstruction, including a
problem of cortical integration in two cases.16 Therefore,
I believe this transfer, although a relatively simple pro-
cedure, should only be used if the FPL muscle is not
functional or has been badly damaged in a complex
forearm injury. This view is supported by most previous
authors. Without knowledge of the mentioned possible
problems, many patients also see this as an unneces­
sarily complex alternative to reconnecting the original
system.
TWO-STAGE TENDON GRAFTING
Most authors recommend single stage reconstruction of A
the FPL and this would seem reasonable where the
suture lines are placed at the wrist and the distal phalanx
and not within the digital tendon sheath or the thenar
muscles. However, there are circumstances in which two
stage reconstruction28-32 can be useful, or advisable,
whether the actual reconstruction is by grafting or
tendon transfer. Some cases in my unit requiring sec-
ondary FPL reconstruction have already had a primary
repair that has stuck and is found at tenolysis to have a
gapped tendon. Removal of the tendon may leave a
badly scarred sheath (see Figure 27-5) and/or damage
of the pulleys (Figure 27-6) to an extent that reconstruc-
tion of new pulleys is necessary. A few more primary
repairs rupture and, for a variety of reasons (see Chapter
19), cannot be re-repaired, although they generally B
re-present to us early. In all of these cases, we insert a
silicone rod, with reconstruction of new pulleys over the Figure 27-6  Immediate exploration of the FPL in a
rod if need be. This is a convenient means of both creat- 32-year-old woman after rupture of a primary repair.
A, Pulley reconstruction using the discarded distal FPL over
ing a better tendon “tunnel” and recreating pulleys that
a tendon rod as the first stage of a two-stage reconstruction.
will not be expected to withstand the forces of a func- B, The completed pulleys.
tioning tendon for a few months. Many of these failures
of primary surgery are known better to us and our thera-
pists than cases presenting acutely; a human factor also
comes into our choice of two-stage grafting. These recent reports33,34 of two-stage FPL grafting achieved the
patients have already had primary surgery fail, so they 30° to 40° of IP motion required for fine pinch func-
may be at least as likely to have secondary surgery fail tion but their results are disappointing compared to the
for reasons as diverse as that they are noncompliant extraordinary results mentioned earlier of Pulvertaft1 in
with therapy, they live too far away to attend therapy, patients presenting after long delays. However, many
other home circumstances militate against their attend- hidden factors may be at play here, not the least being
ing therapy, they have a very low pain tolerance, the the difference between the average age of Pulvertaft’s
initial injury was more severe and likely to have laid group of 18 years and that of the patients in these
down considerable scar in the thumb, etc. Under such studies. I also believe that the delay between the stages
circumstances, we believe that the two-stage process in one study34 of 8 weeks is too short.
gives them the best chance of avoiding adherence of the The presence of an annular pulley at the base of the
tendon and further tenolysis surgery. In other circum- thumb is essential to FPL function. In most circum-
stances, where presentation is delayed and the sheath is stances where pulleys need to be reconstructed, the
found to be badly scarred, such as after tendon sheath clinical situation includes a need for secondary recon-
infection, or complex thumb injuries that include major struction of the FPL tendon and we prefer to reconstruct
loss of the palmar surface soft tissues, including the the pulleys over a silicone rod at a first stage and recon-
palmar face of the sheath and/or the pulleys, two-stage struct the flexor tendon later (see Figure 27-5). This
secondary reconstruction has the same benefits. Two allows the use of a pulley reconstruction in which the
294 Section 3:  Secondary Flexor Tendon Surgery

new pulley, typically made from discarded tendon,
which has been split longitudinally, is simply sutured
to the remnants of the sheath on either side of the sili-
cone rod. By the time of replacing the rod with a func-
tioning tendon, the bond of the pulley at its lateral
margins is strong. This reconstruction also avoids enter-
ing the extensor space of the thumb, with the inherent
risk of extensor adhesion and loss of passive flexion of
the thumb joints. However, the situation does arise
where the patient presents with an intact FPL with bow-
stringing from previous loss of the A1 and oblique
pulleys alone (see Figure 27-6). The need to re-create a
pulley at the base of the thumb, which must immedi-
ately withstand the forces of a functional FPL, also arises
if a decision is made to reconstruct both the pulley and
the FPL at a single stage (Figure 27-7). These cases
require a new pulley with immediate strength. Invasion
of the extensor space with the risk of extensor tethering
is surrendered here to achieve strength.35 We prefer to
reconstruct the pulley by use of a tendon, as described
in 1944 by Bunnell,36 rather than using the extensor
retinaculum, as described by Lister,37 the harvesting of
which leaves a prominent scar on the dorsum of the
wrist.
Many secondary reconstructions of the FPL tendon
will be carried out within a few weeks of the primary
injury and the need to consider use of the techniques
of tendon reconnection described in this chapter only
become apparent at surgery, when it is seen that a simple
primary repair cannot be carried out. Other cases will be
undertaken as a one-stage reconstruction after a greater
delay, or will undergo a two-stage reconstruction. In
these cases, where there has been an injury but no imme-
diate surgery or a first stage tendon operation, it is advis-
able to delay the second operation and have the patient
undertake preoperative therapy with passive forced
flexion exercises and ultrasound to mobilize the extensor
tendon. The thumb is no stranger to tethering of the long
extensor tendon and tightening of the dorsal capsules of
the MCP and IP joints with loss of passive flexion of
these joints.18,35 The result of the subsequent FPL recon-
struction can only be as good as the maximum passive
flexion of these joints. I agree with Pulvertaft’s policy of
allowing a minimum of 6 months between injury and

A B

C D
Figure 27-7  A, Six-year bowstringing in a 44-year-old woman. B–D Reconstruction of a pulley at the base of the thumb
over an intact FPL tendon using PL tendon passed around the phalanx and under EPL.
 Chapter 27:  Secondary Reconstruction of the Flexor Pollicis Longus Tendon
reconstruction whenever possible, particularly as the
lack of an FPL tendon does not negate use of the thumb.1
We use a similar gap in time between the stages of a
two-stage procedure. This advice applies to the Northern
European hand, and hands of Northern European origin,
and may not be necessary in other parts of the world.
TENDON GRAFTING—REHABILITATION
Our splinting regimen and rehabilitation after all sec-
ondary FPL reconstructions are exactly as for primary
repair of this tendon, i.e., early active mobilization in a
protective dorsal splint (see Chapter 16), although one
could argue reasonably for a more relaxed regimen as
the both tendon sutures are much stronger than an end-
to-end primary repair. It is necessary to include a dorsal
splint behind the fingers as well as behind the thumb
and prevent finger gripping activities, as these are fol-
lowed by movement of the thumb into tight flexion over
the dorsum of the index finger, which may rupture any
suture of the FPL.
OUTCOMES AND PROGNOSIS
It is my impression, from accumulated experience of
these secondary operations over twenty years, that the
results of the various procedure in which the FPL tendon
is reconstructed secondarily are mostly functionally
better than before reconstruction, although they are
subjected to the same problems as all flexor tendon
surgery, namely loss of IP joint flexion as a result of
extensor tendon tethering and joint dorsal capsule tight-
ening, repair rupture, and flexor tendon tethering.
Rupture is uncommon as the repair techniques are
References
1. Pulvertaft RG: Flexor tendon grafting after long delays. In
Tubiana R, editor: The Hand, Vol 3, Philadelphia, 1988, WB
Saunders, pp 244–254.
2. Schneider LH, Wiltshire D: Restoration of flexor pollicis
longus function by flexor digitorum superficialis transfer,
J Hand Surg 8:98–101, 1983.
3. Giesen T, Sirotakova M, Elliot D: Flexor pollicis longus
primary repair: further experience with the Tang technique
and controlled active mobilisation, J Hand Surg (Eur) 34:
758–761, 2009.
4. Sirotakova M, Elliot D: Early active mobilization of primary
repairs of the flexor pollicis longus tendon with two Kessler
two strand core sutures and a strengthened circumferential
suture, J Hand Surg (Br) 29:531–535, 2004.
5. Pulvertaft RG: Flexor tendon grafting. In Flynn JE, editor: Hand
Surgery, Baltimore, 1966, Williams and Wilkins, pp 297–314.
6. Matev IB: Reconstructive Surgery of the Thumb, Brentwood,
1983, Pilgrim’s Press, pp 50–56.
7. Elliot D, Khandwala AR, Ragoowansi R: The flexor digitorum
profundus “demi-tendon”: a new technique for passage of
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Surg (Br) 26:422–426, 2001.
8. Dowd MB, Figus A, Harris SB, et al: The results of immediate
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295
strong, but the other two problems, particularly those
on the dorsal surface of the thumb, are common enough
that full free and fast movements of the IP joint, which
are the long-term goals of FPL surgery, are often less
than perfect, even if better than preoperatively. Patients
should be advised of this accordingly and consideration
given seriously to the option described regarding no FPL
repair, even if only to delay the secondary surgery for
sufficient time for the patient to assess whether recon-
struction is necessary.
CONCLUSION
In writing this paragraph, I make no apology for repeat-
ing the opinions of some of the experts of old in this
field so freely. My generation of surgeons were brought
up to carry out primary flexor tendon repairs for most
patients, as witness the 215 patients with primary repair
of divisions of the FPL over the 20 years of my consul-
tant practice who are the basis of the research described
in Chapter 16. This leaves only a few who got through
the primary catchment net during this period, or failed
to complete rehabilitation, and required secondary
reconstruction, subsequently. I perform these secondary
reconstructions of the flexor pollicis longus now much
less than primary repairs. By comparison, the authors of
the past carried out many more secondary reconstruc-
tions. Given that the techniques of reconstruction are
entirely unchanged, their experience is invaluable for us
and it is my impression that the uses to which they were
put by the masters of an earlier era were well thought
out, logical, and improved on the preoperative thumb
function.
9. Murphy FG: Repair of laceration of flexor pollicis longus
tendon, J Bone Joint Surg (Am) 9:1121–1123, 1937.
10. Urbaniak JR: Repair of the flexor pollicis longus, Hand Clin
1:69–76, 1985.
11. Urbaniak JR, Goldner LJ: Laceration of the flexor pollicis
longus tendon: delayed repair by advancement, free graft or
direct suture, J Bone Joint Surg (Am) 55:1123–1148, 1973.
12. Schneider LH: Flexor tendons—late reconstruction. In Green
DP, Hotchkiss RN, Pederson WC, editors: Green’s Operative
Hand Surgery, Vol 2, ed 4, New York, 1999, Churchill Living-
stone, pp 1915–1918.
13. Le Viet D: Flexor tendon lengthening by tenotomy at the
musculotendinous junction, Ann Plast Surg 17:239–246,
1986.
14. Nigst H, Megevand RP: La réparation du long fléchisseur du
pouce. Technique de l’élongation du tendon, Helv Chir Acta
4/5:456–459, 1956.
15. Vigliani F, Martinelli B: Repair of rupture of flexor pollicis
longus by “Z” lengthening at the wrist, Ital J Orthop Trauma
2:171–179, 1981.
16. Ebelin M, Le Viet D, Lemerle JP, et al: Chirurgie secondaire
du long fléchisseur du pouce, Ann Chir Main 4:111–119, 1985.
17. Rouhier G: La restauration du tendon du long fléchisseur du
pouce sans sacrifice du tendon primitif, J Chir 66:537–542,
1950.
296 Section 3:  Secondary Flexor Tendon Surgery
18. Khandwala AR, Blair J, Harris SB, et al: Immediate repair and
early mobilisation of the extensor pollicis longus tendon in
zones 1-4, J Hand Surg (Br) 29:250–258, 2004.
19. Brown CP, McGrouther DA: The excursion of the tendon of
flexor pollicis longus and its relation to dynamic splintage,
J Hand Surg (Am) 9:787–791, 1984.
20. Tubiana R: Flexor tendon grafts in the hand. In Tubiana R,
editor: The Hand, Vol 3, Philadelphia, 1988, WB Saunders,
p 237.
21. Hollinshead WH: Back and limbs. In Anatomy for Surgeons,
Vol 3, ed 2, New York, 1969, Harper, p 410.
22. Armenta E, Fisher J: Anatomy of flexor pollicis longus vincu-
lum system, J Hand Surg (Am) 9:210–212, 1984.
23. Kaplan EB: Functional and Surgical Anatomy of the Hand, ed 2,
Philadelphia, 1965, Lippincott, p 12.
24. Campbell Reid DA, McGrouther DA: Surgery of the Thumb,
London, 1986, Butterworth, pp 30–36.
25. Posner MA: Flexor superficialis tendon transfers to the
thumb—an alternative to the free tendon graft for treatment
of chronic injuries within the digital sheath, J Hand Surg
8:876–881, 1983.
26. Schneider LH, Wiltshire D: Restoration of flexor pollicis
longus by flexor digitorum superficialis transfer, J Hand Surg
(Am) 8:98–101, 1983.
27. Razemon JP, El Hassar S, Meresse B: Les réparations
secondaires du long fléchisseur du pouce par transposition
du fléchisseur superficial du IV, Lille Chir 26:198–205,
1971.
28. Bassett AL, Carroll RE: Formation of tendon sheaths by sili-
cone rod implants. In Proceeding of the American Society for
Surgery of the Hand, J Bone Joint Surg (Am) 45:884, 1963.
29. Hunter JM: Artificial tendons: Early development and
application, Am J Surg 109:325–338, 1965.
30. Hunter JM: Staged flexor tendon reconstruction, J Hand Surg
8:789–793, 1983.
31. Hunter JM, Salisbury RE: Flexor tendon reconstruction in
severely damaged hands. A two stage procedure using a sili-
cone Dacron reinforced gliding prosthesis prior to tendon
grafting, J Bone Joint Surg (Am) 53:829–858, 1971.
32. Mayer L, Ransohoff N: Reconstruction of the digital tendon
sheath: a contribution to the physiological method of repair
of damaged finger tendons, J Bone Joint Surg (Am) 18:607–
616, 1936.
33. Frakking TG, Depuydt KP, Kon M, et al: Retrospective outcome
analysis of staged flexor tendon reconstruction, J Hand Surg
(Br) 25:168–174, 2000.
34. Unglaub F, Bultmann C, Reiter A, et al: Two-staged recon-
struction of the flexor pollicis longus tendon, J Hand Surg (Br)
31:432–435, 2006.
35. Kulkarni M, Harris SB, Elliot D: The significance of extensor
tendon tethering and dorsal joint capsule tightening after
injury to the hand, J Hand Surg (Br) 31:52–60, 2006.
36. Bunnell S: Surgery of the Hand, Philadelphia, 1944, Lippin-
cott, p 315.
37. Lister GD: Reconstruction of pulleys employing extensor reti-
naculum, J Hand Surg (Am) 4:461–464, 1979.
 CHAPTER
28  
STAGED TENDON GRAFTS AND
SOFT TISSUE COVERAGE
David Elliot, MA, FRCS, BM, BCh
OUTLINE
The following quotation clearly identifies the intended
benefit of two-stage tendon grafting. The evolution of
the technique is recorded and its benefits discussed,
including the use of the technique to deal with
problems requiring pulley and skin reconstruction
simultaneously with reconstituting the flexor tendon
system.
The objective of the two-staged flexor tendon method is
to improve the predictability of final results in difficult
problems dealing with tendon reconstruction.
Hunter, 19901
The ideal treatment of flexor tendon injuries under
almost every circumstance is primary repair. I believe
this to be true whether the injury is a simple laceration
of the finger or a replantation, as it is easier to rehabili-
tate a finger over the several months following injury
with the finger flexing actively than being flexed pas-
sively. However, this is not always possible. A percentage
of primary repairs may also either become adherent to
their surrounds, gap, and become secondarily adherent
to their surrounds, or rupture. All of these circumstances
may lead to “secondary flexor tendon surgery,” which is
a broad description of a variety of procedures, including
tenolysis, tendon grafting, pulley reconstruction, and
skin replacement over the tendons. Although tendon
grafting may give comparable results to primary flexor
tendon repair in the hands of some experts, general
opinion would support the view that primary repair is
less difficult for most surgeons and more likely to be
more successful, even if this has never been proved by
comparative trial. For most of us, tendon grafting is
more difficult, therapy is more vital to success and the
results are usually less near to normal. The reported
results of secondary flexor tendon surgery are generally
worse than those of primary surgery. Undoubtedly, this
relates, not only to surgical technique, but also to the
fact that we collect and report all secondary flexor
surgery cases together. We are bundling together the
complex cases who also, and incidentally, need a tendon
graft with fingers that simply need a graft instead of a
primary repair to reconnect the tendons.
Wherever one practices, the patients included in the
group “secondary flexor tendon surgery” will include
some of your “worst” injuries and “worst” patients.
These cases are more likely to do badly whatever one
does and may do no better after secondary surgery than
they did the first time, if they have already undergone
primary surgery. Unfortunately, conventional one-stage
secondary flexor tendon surgery is not always followed
by satisfactory return of flexor function. Two-stage flexor
tendon grafting was introduced with the intention of
achieving better results under circumstances where the
likelihood of poor results can be identified. The per-
ceived advantage over single-stage grafting is that mobi-
lization of the tendon graft following the second
operation is started with the graft moving in a smooth-
walled pseudo-sheath, created by the silicone rod over
several months after insertion at a first operation, and
in a less traumatized, less painful, and more supple
hand. Despite a very small incidence of reaction to sili-
cone rods and a small incidence of infection and/or
extrusion of the rods, the two-stage procedure appears
at least to reduce the influence of the “scarring” factors
on the result.
The primary, and most significant, problem of flexor
tendon surgery is the formation of adhesions between
injured tendons and their surrounds, particularly the
tendon sheath within the digits and distal palm. Over-
coming adhesion of repairs to the sheath has been
the driving force for most research in this field over the
past 100 years. Mayer and Ransohoff (1936), writing in
the era when delayed flexor tendon grafting was the
routine,2 described how “these adhesions extend from
the point of division of the tendons down to the distal
end of the digital theca (tendon sheath)… . It is obvious
that the normal gliding mechanism of the tendon has
been completely destroyed and that, consequently, the
conditions for re-establishing free gliding of a trans-
planted tendon are so unfavorable that only in excep-
tional instances can an implanted tendon perform its
normal function.” Mayer was the first surgeon to try to
297
298 Section 3:  Secondary Flexor Tendon Surgery
reestablish the milieu required for free gliding of the
tendon within the sheath by insertion of an inert rod,
then, at a later stage, replace this with a tendon graft.
He used celloidin tubes but had to abandon his experi-
ment to create a “pseudo-synovial” sheath as these were
too rigid. Twenty-five years later, Bassett and Carroll
(1963) repeated the work using silicone rods.3 James
Hunter carried this work forward through the 1960s and
1970s to establish the technique clinically.1,4-10 The suc-
cessors to the rods of woven Dacron covered by silicon
developed by him for use in staged flexor tendon graft-
ing are known to us all today simply as “Hunter” rods.
Curiously, Hunter’s first use of a silicone rod was to
replace an extensor tendon. The rod was sutured to the
extensor tendon with fine wire. It became clear that the
rod was being stretched and acting as an elastic band to
pull the flexed finger back into extension when the
flexor tendon relaxed. Had the wire suture not pro-
truded through the skin, there would have been no
second stage. On exploration of the protruding wire, it
was clear to Hunter that a shiny mesothelium-lined
membrane had formed around the rod. The rod was
replaced by a tendon graft and the finger went through
rehabilitation to achieve acceptable function. Hunter’s
initial intention was to design an artificial tendon for
permanent use and he pursued both the concept of the
pseudo-sheath and the idea of a permanent artificial
tendon replacement in his research. While the former
has become part of the armamentarium of most hand
surgeons, a permanent artificial tendon remains “experi-
mental,” largely because of the problems of achieving a
permanent bond between the rod and the biological
tissues to which it must be attached proximally and
distally.
THE PSEUDO-SHEATH
After implantation, the silicone rod holds the adjacent
tissues apart. Microscopic studies show that the pseudo-
sheath is not simply a tube of scar.11 The tissues adjacent
to the rod organize over a few days into a mesothelium-
like layer. In the chicken experiments described by
Salisbury and his colleagues, this intima consisted pre-
dominantly of one layer of flattened fibroblasts with
a surface made irregular by pleats and pores, whereas
the normal tendon sheath has an intima of several
layers of thicker, cuboidal cells. The intima also con-
tained macrophages, intermediate cells, mast cells, and
Schwann cells. By 4 to 6 weeks, the deeper tissues have
formed a second layer of loose, well-vascularized con-
nective tissue and the pseudo-sheath has a basic appear-
ance similar to normal synovial sheath. The collagen in
the outer layer was of variable thickness and contained
collagen, reticulum, and elastic and unmyelinated nerve
fibers. The collagen was orientated along the axis of the
implant much as it is orientated along the lines of stress
in a tendon sheath.
CHOICE BETWEEN SINGLE-STAGE AND
TWO-STAGE GRAFTING
Although much of the flexor tendon surgery performed
in western Europe is primary surgery, we do have to
undertake a surprising amount of secondary flexor
surgery, some of which is because of delayed presenta-
tion and some of which is because the flexor tendon
injury quite frequently does not come as an isolated and
simple one but rather in association with injuries to
other tissues. Nevertheless, secondary surgery for us is
mostly that of the complications of primary repair,
namely ruptured and adherent primary repairs, as the
results of the initial surgery are not universally good. In
the best units, the failures constitute about 10% of all
primary repairs, not a small number and something of
an indictment of our present techniques of primary
flexor tendon surgery. The cases that come to secondary
surgery are mostly either the result of more severe inju-
ries or have occurred in patients who make excessive
amounts of scar tissue or have not cooperated with
therapy because of low pain thresholds, social circum-
stances, or lack of judgment.12 Therefore, the cases
needing secondary surgery can be considered under the
headings of either “bad injuries” or “bad patients.” Else-
where in the world, many patients will only get to an
appropriate surgeon at a time when secondary repair of
the tendon using grafts is the only option because of
proximal tendon retraction. This, by definition, becomes
“secondary flexor surgery,” although the problem is
simply an extended finger with good passive but no
active flexion but now no longer amenable to direct
repair. However, among the patients presenting after
delay, and also defined as undergoing “secondary flexor
surgery,” are a group with much more complicated
problems, sometimes as a result of injuries to the other
structures of the digits and, sometimes, as a result of the
unaided healing process within a digit in the presence
of an inactive flexor system. The problems in these cases
are not simply those of being unable to get the tendon
ends together. So, in terms of the pathologies in the
digits themselves, the problems we all face in the rather
heterogeneous mix of cases that we call “secondary
flexor tendon surgery” are not so different—namely,
flexor tendons that are not intact and flexor tendons that
are stuck in scar tissue, variably associated with divided
pulleys, skin deficit on the flexor aspect of palm and
digits, stiff fingers, and injuries to other, adjacent struc-
tures in the fingers, hand, or forearm.
Whether we should be carrying out single-stage or
two-stage tendon grafting, or a mixture of both, depend-
ing on the individual case, is a matter of opinion with
little hard fact to support either side of the debate. It is,
perhaps, worth remembering that the two-stage graft
was introduced because of dissatisfaction with the
results of the one-stage procedure, albeit in North
 Chapter 28:  Staged Tendon Grafts and Soft Tissue Coverage
America, which has a largely white population of
Northern European origin. When the scar tissue between
the tendon and sheath is fine and diaphanous, we talk
of “adhesions” and two-stage grafting seems to be
overkill. When the scar is more dense, we talk not of
adhesions but of scarring! This is an inconsistency of
surgical thought as either can prevent movement and,
perhaps, it might be better to stage the grafting in all
cases, because a failure of secondary flexor tendon
surgery is usually a handicap for life and can even lead
the patient to demand amputation.
I almost always use two-stage grafting as I was brought
up at a time and place where this was believed to give
the best results. Sometimes, it seems that this is overkill,
particularly when the sheath is not badly scarred.
However, most of my cases for tendon grafting are
patients for whom primary surgery failed and, as a
group, are “bad patients,” as defined earlier. Although
not the reason for doing two-stage grafting when I
started, I have come to realize that this technique may,
particularly, suit these cases and my practice. More gen-
erally, it is also the case that no one has worked out how
to identify the “bad patient,” whether in northern
Europe, or elsewhere.
Two-stage graft surgery can be unrealistic to the eco-
nomic needs of many patients in many parts of the
world and the circumstances of hand practice elsewhere
push surgeons more toward single-stage grafting. Prag-
matism in this respect, and one’s early teaching and
experience, is probably the major determinant of the
preferences of different surgeons for single or two-stage
grafting! Despite the preference for single-stage grafting
of many senior surgeons, who may have great skill in
this, and the supportive feeling that the particular sup-
pleness of the hands of certain peoples, compared to the
hand of those of northern European origin, allows
single-stage grafting to be effective more often, there will
be circumstances where this expedient may be so
unlikely to give a good result that the two-stage graft
should be considered by even the most ardent supporter
of the one-stage graft.
Previously unemphasized reasons for staging grafting
have become evident in my practice over the past 20
years. Some patients present with ruptures of primary
repairs and undergo immediate exploration with a view
to re-repair.13 If it is found at surgery that re-repair is not
possible, we routinely put a tendon rod into the finger,
with the rod being replaced by a graft when the finger
has settled. At this point in time, the finger is often
unsuited to a single-stage tendon graft procedure
because of its swollen condition, this being the third
traumatic episode for this finger (exploration of the
rupture following after the causative incident and the
primary repair) in a short period of time. Others who
rupture a primary repair and cannot undergo immediate
re-repair for reasons such as skin breakdown and
299
infection and those who re-rupture the re-repair will
present at a later stage for tendon grafting but also may
be unsuitable for single-stage grafting, for a variety of
reasons, including those grouped together above under
“bad injury” and “bad patient.”
A small group of patients presenting with severe and/
or contaminated injuries, sometimes with missing seg-
ments of the flexor tendons, are deemed unsuitable for
primary repair. This subject is discussed in Chapter 9 by
Professor Tang. While we endeavor to carry out primary
repairs now in most of these patients while carrying out
the other procedures necessary to their overall hand
reconstruction, then mobilize them as early as possible,
there are some cases where primary repair is impossible.
Whenever possible in such cases, we insert tendon rods
into the flexor sheaths to maintain these until the flexor
tendons can be reconstituted at a later date.
Most other situations in which the surgeon has to
consider the need to graft arise in clinic in preparation
for exploration of digits with various deficits of move-
ment on elective surgical lists, whether after delayed
presentation or after problems following primary
surgery. In clinic, the latter group of patients have to be
told that the surgeon cannot predict whether the need
at surgery will simply be to free the (intact) tendon from
scarring and then move it as early as possible to prevent
readhesion, with 2 to 4 weeks off work, or the tendon
will be found to have gapped or be so scarred that
releasing it intact from the scarring will prove impossi-
ble. If grafted immediately, this will require a 2- to
3-month period without use of this hand while the graft
heals fully at each end. The dilemma for the patient,
given this information and, often, having just had a long
period off work, is that he or she cannot tell his, or her,
employer how long the period off work after surgery will
be until after the event. Under these circumstances,
many, if given the option of staged grafting, will prefer
to have a rod inserted, buddy strap the finger to the
adjacent one for use for a few months, and choose
an opportune time from the point of view of his or
her employment to have a graft inserted and the subse-
quent 2 to 3 months of one-handed life. The second
stage can be carried out at any time after the hand has
become supple, giving the patient a wide choice of the
timing of the second operation. That the second stage
is inevitably being planned with a minimum of 3 to 4
months’ notice is often convenient to the work situation
in Europe.
Where it is obvious in clinic that there is either a pulley
or skin deficit on the palmar aspect of the finger, or both,
I also advise two-stage grafting because (1) I believe it is
easier to deal with the deficit(s) surgically without having
the reconstructions of pulleys and/or skin mobilized
aggressively in the early postoperative period, as is neces-
sary to maintain movement of a tendon graft, and (2) it
is easier to rehabilitate the tendon graft after the second
300 Section 3:  Secondary Flexor Tendon Surgery
operation without restrictions to protect reconstructions
of pulley and/or skin deficiencies.
THE CLINICAL PRINCIPLES OF TWO-STAGE
TENDON GRAFTING
Detail of the First Stage
This often begins as the exploration of a digit with a
deficit(s) of movement on an elective surgical list.
Simple statements, such as “tenolysis” and “tendon
graft” that we put on our operating lists are often a gross
simplification of the surgery needed and reinforce an
underestimation of the problem. Whether secondary
surgery is being carried out after delayed primary pre-
sentation or for failed primary surgery, all of the tissues
on the palmar side of the finger may be scarred to some
degree and each layer may require treatment. In respect
of the management of the sheath and tendon, the sepa-
ration of sheath and tendons by surgical dissection
requires meticulous technique, time, and considerable
concentration, and can be tediously slow. Great care is
required to try to achieve an end point of intact tendons
and intact pulleys whenever possible. Where this dissec-
tion ends otherwise, both tendons are usually removed
in preparation for tendon grafting. If the flexor digito-
rum superficialis (FDS) tendon is intact and functional,
this is normally left in situ with a view to replacing
the profundus tendon with a graft passed through the
chiasma of the FDS, or a decision is made to leave the
finger with proximal interphalangeal (PIP) flexion only,
in which case a hyperextending distal interphalangeal
(DIP) joint may need distal flexor tendon tenodesis or
joint fusion.
Two situations will make tendon grafting inevitable.
The first is where the tendon is found to be so severely
scarred to the sheath that achieving an end point of
Figure 28-1  A flexor tenolysis showing such dense
scarring that excision of the flexor tendons leaving a
functional pulley system is impossible.
intact tendons and intact pulleys after surgical dissec-
tion is impossible (Figure 28-1). The second is finding
a gapped tendon with scar in the tendon gap after a
previous primary repair. The tendon is now several mil-
limeters too long, and tenolysis is likely to be followed
by re-adhesion as the tendon will be moving less than
optimally during rehabilitation. It is usually the case
that these tendons are considerably scarred within the
tendon sheath, possibly because the gapped tendon has
moved inadequately for most of period of rehabilitation
after the primary surgery.
If a tendon is so frayed after tenolysis that I do not
think it will survive rehabilitation, I replace it with a
rod, with a view to two-stage tendon grafting. In this
circumstance, I do not use special regimens, such as the
Strickland frayed tendon regimen, as this places thera-
pists in the uncomfortable position of using a regimen
with which they are less familiar with tendons that may
snap under their care. This may make their rehabilita-
tion too cautious in a group of patients in whom this is
likely to be counterproductive and lead to further stuck
tendons.
Under all three of these circumstances, I insert a
tendon rod. The distal end of the tendon of the FDS or
flexor digitorum profundus (FDP) that will motor the
graft is held to physiological length by suturing it, with
a nonabsorbable 2-0 or 3-0 suture, to either the deep
transverse ligament in the palm or the ligamentous
structures of the flexor aspect of the wrist. My preference
is to use the palmaris longus whenever possible as the
graft, as it is easier to suture than the smaller plantaris,
and to graft from the distal phalanx back to the palm,
as this only requires harvest of the palmaris tendon in
its extramuscular part. Only occasionally have I found
it necessary to graft back to the wrist. A silicone rod of
approximately the diameter of one of the patient’s flexor
tendons is passed through the sheath from the distal
end of the proximal motor tendon to the distal phalanx.
These rods are manufactured in round and oval shape:
either works equally well. We use sizes 3 or 4 most com-
monly. A new and useful alternative is the “Universal
Tendon Spacer,” which is a flexible silicon rod whose
diameter changes along its length. This rod is moved
through the tendon sheath until the part of appropriate
diameter fits comfortably within the sheath; then the
two ends are cut off (Figure 28-2). The distal end of
the rod is cut obliquely and passed behind the FDP
stump distally, to maintain a pocket to aid attachment
of the distal end of the tendon graft to the distal phalanx
at the second operation. The rod is then sutured with
4-0 nylon to the FDP stump, and to the A4 pulley if
suture to the FDP stump is thought to be too weak
to hold the rod in position during subsequent finger
movements until the second stage. The free proximal
end of the rod is not sutured and should reach slightly
proximal to the sutured distal end of the motor tendon
 Chapter 28:  Staged Tendon Grafts and Soft Tissue Coverage 301

Subcutaneous scarring

Sheath scarring

Figure 28-2  A Universal Tendon Spacer passed through Figure 28-3  The undersurface of the skin and
the tendon sheath until the part of appropriate diameter fits subcutaneous fat of a typical case of flexor tenolysis,
comfortably within the sheath, then the two ends will be   showing the scarring of the subcutaneous fat which causes
cut off. a longitudinal skin deficiency.

in the palm or wrist. The hand is then closed. The first

stage of a staged tendon graft procedure requires no
protection postoperatively. The hand is mobilized early
without protective splinting and the patient usually
returns to work within 2 to 3 weeks. Adjunctive proce-
dures, such as pulley reconstructions and skin replace-
ment, are also carried out at this stage (see later).
Usually between 3 and 6 months is an adequate
delay before carrying out the second-stage tendon graft-
ing procedure. Impatience to complete the second stage
by the patient or the surgeon is counterproductive as the
final result is generally much better if the healing process
of the first, and larger, operation is completely over.

Correction of Skin Deficiencies at the A

First Stage
Scarring of the skin and subcutaneous soft tissues at the
time of primary injury may cause longitudinal skin
shortening in the finger or thumb. In fact, during dis-
section of the digit to reach the tendon sheath, if one
examines the undersurface of the subcutaneous fat, one
will see that this almost never escapes some scar deposi-
tion with resultant tightening of the overlying skin
(Figure 28-3). I routinely open these cases using a mid-
lateral incision to allow this incision to be extended
into the distal palm as a V (Figure 28-4). This allows
one to advance the V of skin from the palm into the
finger to compensate for the subcutaneous scarring B
in the finger. We first reported use of this technique
Figure 28-4  A, Marking of the typical skin excisions used
for reconstruction of skin deficits of the palmar aspect
by the author for secondary exploration of the digital flexors.
of the fingers.14 This advancement of palmar skin is
These include distal palmar V incisions. B, These allow
usually sufficient to deal with skin shortage where the advancement of the distal palmar skin into the digits to
skin injury has been a simple cut. We usually do not counter the typical skin shortage due to the subcutaneous
close the V as a Y but allow it to epithelialize under a scarring shown in Figure 28-3, with the palmar wounds
moist antiseptic dressing done twice daily by the patient being allowed to heal by secondary intention under moist
during the first few postoperative weeks of mobilization antiseptic dressings during early postoperative mobilization.
302 Section 3:  Secondary Flexor Tendon Surgery
A B
C
in the manner described after the McCash open palm
technique in Dupuytren’s surgery. Preoperatively, it is
usually obvious from the nature of the primary injury
and/or the appearance of the finger whether more sig-
nificant skin shortage is present and more skin will have
to be incorporated onto the palmar aspect of the finger
to achieve full extension (Figure 28-5A). Use of a cross
finger flap is a simple way of incorporating more skin
onto the palmar aspect of the finger for moderate cases
D
Figure 28-5  A, A case with more extensive shortage of
skin, for which the palmar V incision is inadequate. B, The
same incision was made initially, then the flap was split
at the PIP joint level (shown by the white line). C, A cross
finger flap was inset into the split. D and E, The finger
was mobilized normally postoperatively after the cross
finger flap pedicle was divided.
of skin deficiency. The finger is opened through a mid-
lateral incision on the same side as the intended donor
finger for the cross finger flap (Figure 28-5B). The mobi-
lized skin is split at the PIP level, and a cross finger flap
is incorporated into the gap (Figure 28-5C–E).
Cases with greater skin deficiency need more exten-
sive flap reconstruction. There are many options of free
and distant pedicled flaps available. Most will swell sig-
nificantly and require secondary thinning of the flap
 Chapter 28:  Staged Tendon Grafts and Soft Tissue Coverage 303

later. Guimberteau (2001) described a simple means of 4 pulley reconstructions Design of two
resurfacing the whole palmar aspect of a finger using a over a rod bipedicle flaps
distal ulnar artery pedicled fasciocutaneous flap from
the distal part of the ulnar aspect of the flexor surface
of the forearm.15 Unlike distally based radial artery–
based forearm flaps, the ulnar artery can be dissected
free into the middle of the palm, so the flap reaches the
tip of the finger comfortably.
Skin deficit in the palm with flexor tendon exposure
can often be reconstructed using local flaps, which have Excision of unstable skin
the advantage of avoiding the swelling and subsequent A (recurrent breakdown)
unnatural wobbling mobility which is common after
distant flap reconstruction of the palm. A longitudinal
exposure of a flexor tendon in the palm can be closed
quickly and simply using local bipedicled flaps. We first
reported this technique as a means of closing the gap in
the palm after harvesting a Zancolli reverse digital artery
flap for finger tip reconstruction.16 Two bipedicle flaps
are designed, one on either side of the defect (Figure
28-6A). The common digital neurovascular structures
are retained in the flaps by dissecting under the skin
bridges at a deep level, immediately adjacent to the
tendons and their sheaths. At the lateral margin of each
palmar flap, only the skin is incised and the fibers in
the subcutaneous fat broken by blunt scissor dissection B
to create a much more superficial wound. The palmar
flaps then slide in to close the deep defect (Figure
28-6B) and the superficial lateral wounds epithelialize
under moist antiseptic dressings done by the patient
during the first few postoperative weeks of mobiliza-
tion, as in the McCash Open Palm Technique for
Dupuytren’s surgery (Figure 28-6C). We have used the
same principle to close longitudinal skin defects on the
palmar surface of the fingers exposing the flexor tendons
and their sheath.17
For round, or near-round, defects of the palm, large
triangular flaps are useful. This technique was first
described by Mathes and his colleagues in 1988 for
closure of defects on the sole of the foot.18 One, or more,
skin triangles are designed and incised adjacent to the C
defect (Figure 28-7A). The fibers immediately below
the skin incisions are released by pressing down on the Figure 28-6  A, A patient presenting for secondary flexor
subcutaneous fat with a scalpel, then the deeper fat is surgery with a longitudinal defect of the palm and exposure
mobilized by blunt scissor dissection. The blood supply of the flexor tendons in the mid-palm. The poor quality
palmar skin has been excised. B, Bipedicle flaps have been
of each flap is from small arterial branches coming up
advanced centrally to close the mid-palmar defect. C, Late
through the underlying pulp from the underlying neu- view showing excellent healing of the palm with palmar skin.
rovascular bundles. While a very small flap may have This case also illustrates multiple pulley reconstructions over
insufficient blood supply beneath the triangle of skin, a silicone rod.
big flaps are entirely safe. These flaps will slide freely in
any direction after being released in this way (Figure
28-7B). Several flaps may be designed, each sliding in a
different direction, or a very big one right across the technique,19-21 or using fascial flaps with skin graft, or
palm may be used. fascial flaps carrying a skin island vascularized by the
Skin deficiency exposing flexor tendons in zone 5 underlying fascia.22-24 These reconstructions may be
can be easily reconstructed in most cases with local based on either the radial or the ulnar artery in the distal
flaps from the forearm, using the V-Y fasciocutaneous forearm.
304 Section 3:  Secondary Flexor Tendon Surgery
A B
Figure 28-7  A, A patient presenting for secondary flexor surgery with a near-round skin deficiency in the distal palm. A
palmar triangle flap has been designed and dissected prior to movement laterally into the defect. B, Late view showing
excellent healing of the palm with palmar skin.
Correction of Pulley Deficiencies at the
First Stage
Single-stage tendon grafting in conjunction with pulley
reconstruction requires that the pulleys be strong
enough to resist the tendon forces when mobilization
is started immediately. The most important pulley defi-
cits requiring reconstruction are those of the A2 at the
base of the finger and the A1 at the base of the thumb.
By careful preservation of the sheath in the middle part
of the digit to avoid distal digital bowstringing, it is
usually unnecessary to reconstruct an A4 pulley (see
Chapter 10 regarding distal bowstringing). Commonly,
palmaris longus tendon, the proximal tendon of which-
ever of the flexor muscles will not be used to motor the
tendon graft, or the extensor retinaculum, is used as the
new pulley at the base of the digit. Whichever material
is used, it is passed around the repaired flexor tendons,
or flexor tendon graft, and the proximal phalanx, and
under the extensor tendon two or three times, then
sutured to itself. Bearing in mind that many cases under-
going flexor surgery have poor results because the exten-
sor tendons, bathed in fibrin in the edema of the injury,
tether to the underlying skeleton and overlying skin to
a greater degree than do the flexor tendons in their
sheaths, and are restricting even passive finger flexion,25
I have reservations about use of techniques of pulley
reconstruction that require passage of tendon, or exten-
sor retinaculum, around the phalanges and through the
extensor compartment. Attachment of new pulleys to
the sides of the phalanx avoids invading the extensor
space but leaves concerns in respect of their strength,
unless elaborate bone fixation techniques are used. We
mostly have a need for pulley reconstruction when we
explore a flexor secondarily and come across a severe
“mess” of scarring (see Figure 28-1). Sometimes, the
last cut of the tenolysis, or the removal of a completely
welded-in flexor, destroys what was left of a weakened
pulley and, sometimes, it is simply impossible to undo
the scar tissue. For us, this is a situation that demands
use of a two-stage tendon graft. The tendons being
removed from the finger or, if these are too poor, the
more proximal part of the tendon of the muscle not
intended for use later as the motor for the graft can be
used to reconstruct the pulleys. The tendon is split lon-
gitudinally and opened out, then turned through 90°
(Figure 28-8A). This provides enough material to make
as many pulleys as one wants (Figure 28-8B). Because
there will be no force on them for 3 to 6 months, the
new pulleys can be simply sutured to the remnant edges
of the sheath, to which they will be strongly bound by
the time they have to hold a tendon against the skele-
ton. This technique avoids harvesting of tendons that
may be required for the second stage or the use of exten-
sor retinaculum, which leaves an obvious scar on the
very visible dorsum of the wrist.
Correction of Joint Deficiencies at
the First Stage
The deepest problems at exploration of these fingers,
and the most likely to give rise to a recurrence of loss
 Chapter 28:  Staged Tendon Grafts and Soft Tissue Coverage
Rod under Split FDS
preserved
A3 and A4
pulleys
New pulley
A
B
Figure 28-8  A, A pulley reconstruction over a silicone rod
using the proximal (FDS) tendon, which will not be the
eventual motor of the tendon graft. B, Another case using
the same material to entirely replace the pulley system of a
finger.
of extension, are the ligaments of the underlying joints.
In general, this has little bearing on whether one grafts
in a single stage or two stages, except that the degree of
dissection of the interphalangeal joints usually reflects
the degree of general scarring of the fingers. A consider-
able dissection of the PIP joint, particularly, will also
give rise to more inflammation and scarring in the post-
operative period and increase the likelihood of failure
of the one-stage procedure.
Details of the Second Stage
At the second operation, it is only necessary to expose
the rod at its two ends through small skin incisions to
allow removal of the 4-0 nylon sutures attaching the rod
to the stump of the profundus tendon distally, then
remove the rod and attach the graft distally and proxi-
mally. The harvested tendon graft is sutured to the proxi-
mal end of the rod and pulled distally through the new
pseudo-sheath. Before working distally to attach the graft
305
to the distal phalanx, it is advisable to pass a temporary
suture through the proximal end of the graft and attach
it to the tissues in the palmar, or wrist, incision to prevent
the tendon graft being pulled out of the sheath repeat-
edly during the distal suturing activities. Numerous
methods of attachment of the distal end of the graft to
the distal phalanx have been described: we mostly use
the technique we described in 1996, which dispenses
with the use of a button on the nail of the digit26 and is
simple, effective, and cheap. The proximal end of the
graft is woven into the tendon of the motor using Pul-
vertaft’s technique, with the tension of the new muscu-
lotendinous unit being set in the conventional manner
by reference to the finger cascade when the hand is
resting on the operating table with the wrist in the neutral
position. After the second stage, the graft is mobilized
by the modification of the early active mobilization
technique we use for primary flexor tendon repairs.27,28
We use exactly the same regimen of immediate mobi-
lization after tendon grafting as we do after primary
repair (see Chapter 13B, Box 13[B]-1), which simplifies
things for everyone in the unit. Mobilization is started
the day after the second stage and continues for the
same period, although it could be argued that this
regimen could be relaxed as the suture techniques are
stronger than those of primary flexor tendon surgery.
OUTCOMES AND PROGNOSIS
It is my impression, after using two-stage tendon graft-
ing for many years, that the results are better than previ-
ously with a one-stage procedure. The inclusion of the
extra step of insertion of the rod converts the situation
normally found in secondary surgery in respect of
moving a repair in a scarred environment to one that is
more like that found in primary flexor tendon surgery,
as intended by the pioneers of this technique. Conse-
quently, these cases are assessed by us using the more
rigorous methods of assessing primary flexor tendon
surgery, rather than those of earlier times, which accepted
a much poorer expectation from secondary surgery. It is
my belief that all flexor tendon grafting should now be
assessed in this way to identify any difference from
primary surgery and emphasize the disparity, should
such exist. Where disparity exists, it should be inter-
preted as a need to improve on surgery and rehabilita-
tion and not an acceptance, as in the past, that the cases
are more “difficult.”
Failure of staged flexor tendon grafting may occur at
either of the two stages. Protrusion of the rod, always
through the skin of the distal part of the finger and
not the palm, where it is better covered, is a very rare
experience in our practice, except where there has been
an infection, which has also been a rare occurrence,
perhaps because all are given 5 days of antibiotic cover-
age after insertion of the rod. More common, but also
uncommon, has been movement of the rod from the
306 Section 3:  Secondary Flexor Tendon Surgery
finger proximally into the forearm. This has occurred in
three patients, each of whom required secondary flexor
tendon grafting after rupture of a primary repair. All
three patients were of slightly “manic” personality, with
the fault of overactivity rather than underactivity in the
pursuit of their rehabilitation. One presumes that, in
pursuit of either their daily activities or their therapy,
the rod was, in some way, pulled proximally and the
suture attachment distally in the finger gave way. Why
all three rods were coiled in the forearm and the mecha-
nism of this occurring are mysteries.
Failures after the second stage are exactly like failure
of one-stage flexor tendon grafting and include (1) poor
References
1. Hunter JM, Singer DI, Macklin EJ: Staged flexor tendon recon-
struction using passive and active tendon implants. In Hunter
JM, Schneider LH, Mackin EJ, et al, editors: Rehabilitation of
the Hand: Surgery and Therapy, ed 3, St Louis, 1990, CY Mosby,
Ch 34:427.
2. Mayer L, Ransohoff N: Reconstruction of the digital tendon
sheath: A contribution to the physiological method of repair
of damaged finger tendons, J Bone Joint Surg (Am) 18:607–
616, 1936.
3. Bassett CAL, Carroll RE: Formation of a tendon sheath by
silicone-rod implants, J Bone Joint Surg (Am) 45:884–885,
1963.
4. Hunter JM: Artificial tendons. Early development and appli-
cation, Am J Surg 109:325–338, 1965.
5. Hunter JM, Aulicino PL: Salvage of the scarred tendon systems
utilizing the Hunter tendon implant. In Flynn JE, editor:
Tendon Surgery in the Hand, ed 3, Baltimore, 1981, Williams
and Wilkins.
6. Hunter JM, Blackmore S, Callahan AD: Flexor tendon salvage
and functional redemption using the Hunter tendon implant
and the superficialis finger operation, J Hand Ther 2:107–113,
1989.
7. Hunter JM, Jaeger SH: Tendon implants. In AAOS Symposium
on Tendon Surgery of the Hand, St Louis, 1975, CV Mosby.
8. Hunter JM, Jaeger SH: Tendon implants: primary and second-
ary usage, Orthop Clin North Am 8:473–489, 1977.
9. Hunter JM, Jaeger SH: Flexor tendon implants and prosthe-
ses. In Rubin LR, editor: Biomaterials in Reconstructive Surgery,
St Louis, 1983, CV Mosby.
10. Hunter JM, Jaeger SH, Singer DI, et al: Tendon reconstruction
with implants. In Tubiana R, editor: The Hand, Vol 3,
Philadelphia, 1988, WB Saunders, pp 255–279.
11. Salisbury RE, Levine NS, McKeel DW, et al: Tendon sheath
reconstruction with artificial implants: A study of ultrastruc-
ture. In Hunter JM, Schneider LH, editors: AAOS Symposium
in Tendon Surgery in the Hand, St Louis, 1975, CV Mosby,
Chapter 6:59–65.
12. Harris SB, Harris D, Foster AJ, et al: The aetiology of acute
rupture of flexor tendon repairs in zones 1 and 2 of the fingers
during early mobilization, J Hand Surg (Br) 24:275–280,
1999.
13. Dowd MB, Figus A, Harris SB, et al: The results of immediate
re-repair of zone 1 and 2 primary flexor tendon repairs which
rupture, J Hand Surg (Br) 31:507–513, 2006.
ranges of movement due to extensor tendon tethering
and joint dorsal capsule tightening, (2) rupture of the
repairs (which is rare as they are stronger than those
after primary surgery), and (3) adhesion of the graft to
its surrounds, which is not common but more likely
than rupture of one of the two repairs. The management
of each of these crises is exactly as after their occurrence
following primary surgery or one-stage grafting, except
that the patient may be influenced to choose options of
treatment more accepting of the disability and less
inclined to further surgery because of the passage of
time with adaptation of the hand to his, or her, needs
and the repeated failure of one’s surgery.
14. Moiemen NS, Elliot D: Palmar V-Y reconstruction of proxi-
mal defects of the volar aspect of the digits, Br J Plast Surg
47:35–41, 1994.
15. Guimberteau JC: New Ideas in Hand Flexor Tendon Surgery,
Aquitaine, 2001, Domaine Forestier, pp 135–143.
16. Moiemen NS, Elliot D: A modification of the Zancolli reverse
digital artery flap, J Hand Surg (Br) 19:142–146, 1994.
17. Yii NW, Elliot D: Bipedicle flap reconstruction of longitudinal
palmar skin and soft tissue defects of the digits, J Hand Surg
(Br) 27:122–128, 2002.
18. Colen LB, Replogle SL, Mathes SJ: The V-Y plantar flap for
reconstruction of the forefoot, Plast Reconstr Surg 81:220–228,
1988.
19. Bardsley AF, Soutar DS, Elliot D, et al: Reducing morbidity in
the radial forearm flap donor site, Plast Reconstr Surg 86:287–
292, 1990.
20. Elliot D, Bainbridge LC: Ulnar fasciocutaneous flap of the
wrist, J Hand Surg (Br) 13:311–312, 1988.
21. Elliot D, Bardsley AF, Batchelor AG, et al: Direct closure of
the radial forearm flap donor defect, Br J Plast Surg 41:358–
360, 1988.
22. Becker C, Gilbert A: Le lambeau cubital, Ann Chir Main
7:136–142, 1988.
23. Elliot D, Lloyd M, Hazari A, et al: Relief of the pain of
neuromas-in-continuity and scarred median and ulnar nerves
in the distal forearm and wrist by neurolysis, wrapping in
vascularized forearm fascial flaps and adjunctive procedures,
J Hand Surg (Br) 35:575–582, 2010.
24. Yii NW, Niranjan NS: Fascial flaps based on perforators for
reconstruction of defects in the distal forearm, Br J Plast Surg
52:534–540, 1999.
25. Kulkarni M, Harris SB, Elliot D: The significance of extensor
tendon tethering and dorsal joint capsule tightening after
injury to the hand, J Hand Surg (Br) 31:52–60, 2006.
26. Sood MK, Elliot D: A new technique of attachment of flexor
tendons to the distal phalanx without a button tie-over,
J Hand Surg (Br) 21:629–632, 1996.
27. Elliot D, Moiemen NC, Flemming AFS, et al: The rupture
rate of acute flexor tendon repairs mobilised by a controlled
active motion regimen, J Hand Surg (Br) 19:607–612,
1994.
28. Elliot D: Primary flexor tendon repair: operative repair, pulley
management and rehabilitation, J Hand Surg (Br) 27:507–
513, 2002.
 CHAPTER
29  
TWO-STAGE RECONSTRUCTION
WITH THE MODIFIED
PANEVA-HOLEVICH TECHNIQUE
Alexandros E. Beris, MD, Marios G. Lykissas, MD, and
Ioannis Kostas-Agnantis, MD
OUTLINE
Flexor tendon reconstruction in zone 2 with the
Hunter technique is an established approach to restore
digital flexion and to overcome adhesions in the fibro-
osseous canal. Paneva-Holevich modification of the
Hunter technique refers to forming a pseudo-sheath
around a silicone rod and a loop between the flexor
digitorum profundus and the flexor digitorum super-
ficialis in the first stage, and the use of the formed
pedicle graft through the pseudo-sheath in the second
stage. This combination presents several technical
advantages and resolves problems emerging from the
Hunter technique. We describe the indications, opera-
tive technique, postoperative care, outcomes, and
complications of this method for the flexor tendon
reconstruction in zone 2 based on our clinical experi-
ence over the past decades.
In 1965, Paneva-Holevich1 published a small series of
flexor tendon injuries in which the proximal part of the
flexor digitorum superficialis (FDS) was used as a pedicle
graft for flexor digitorum profundus (FDP) tendon
reconstruction. In 1969, Paneva-Holevich reported two-
stage tendon reconstruction using this method in 34
digits.2 She called her new method “two-stage teno-
plasty.” This surgery was later known as the “Paneva-
Holevich procedure.” James Hunter,3 the pioneer of
staged tendon reconstruction, first described the use of
a silicone rod as a “space saver” followed by free tendon
grafting for the management of patients with poor prog-
nosis (Boyes grades 2 to 5) in 1971. The philosophy was
simple: a flexible silicone-Dacron–reinforced gliding
implant for the formation of a pseudo-sheath as the first
stage of profundus tendon reconstruction, followed by
grafting an autogenous tendon into the pseudo-sheath
in the second stage. This method was used rather popu-
larly in later years.5-9
In 1972, Kessler4 reported a combination of these
techniques using the pedicle tendon transfer to replace
the rod. This method was later known as “modified
Paneva-Holevich method.” This combination presents
several technical advantages and resolves some prob-
lems emerging from the Hunter technique.11 The graft
used (FDS) is an intrasynovial donor tendon and has
better morphological, functional, and healing character-
istics than extrasynovial tendons.12-14 In the past two
decades, we used modified Paneva-Holevich method in
the patients who were indicated for staged tendon
reconstruction in the digits. We found that this tech-
nique has some unique advantages. The size of the FDS
is similar to the silicone rod that is used in the first stage
for stimulation of pseudo-sheath formation. In addi-
tion, during the second stage we found it very easy to
locate the loop between FDP and FDS that is usually
situated at the level of the lumbrical muscles. There have
been no donor site morbidity. This operation is associ-
ated with a lower rate of post-reconstruction tendon
ruptures, because there is only one suture site at the
second stage instead of two for a free tendon graft as
with the Hunter technique.
INDICATIONS
The indications for the modified Paneva-Holevich are
the same as for the Hunter technique. Candidates
for a modified Paneva-Holevich technique must have
suffered injuries of both flexor tendons to the affected
digit with serious scarring and a nonfunctional flexor
apparatus. More specifically, indications include (1)
flexor tendon reconstruction in Boyes 2 to 5 injuries
in zone 2 with considerable scarring of the tendon
bed; (2) finger replantation with damage to the fibro­
osseous canal; and (3) failed previous flexor tendon
reconstruction.11
In cases where FDS of the injured finger is intact this
technique cannot be used, since a distal interphalangeal
307
308 Section 3:  Secondary Flexor Tendon Surgery
(DIP) tenodesis or arthrodesis is the treatment of
choice.11 A relative contraindication is scarring in the
palm that may compromise the anatomic integrity of
the FDS.
This procedure greatly facilitates staged flexor tendon
reconstruction in children with minor modifications in
the rehabilitation program.15 Indications and contrain-
dications of a modified Paneva-Holevich in children are
the same as in adults.
OPERATIVE TECHNIQUE
The surgical technique includes two stages with a
minimum of a 3-month time interval.11 In both stages,
the use of magnifying loupes is mandatory.
Stage 1
The flexor tendons are exposed through a Bruner inci-
sion, which gives excellent access. Complete removal of
the cicatrix follows and special care is taken to preserve
as many pulleys as possible. The injured FDP tendon is
excised proximally at the level of the lumbrical muscles.
Distally, a 1-cm FDP stump at the base of the distal
phalanx is preserved for anchoring of the silicone rod
during the first stage and the tendon graft during the
second stage.
A second incision is made in the palm (inverted L)
and is center near thenar for index and middle finger
and near hypothenar for the ring and small finger
(Figure 29-1). The FDS and FDP tendon ends of the
injured finger are retrieved, freed of adhesions, and
sutured together with a loop at the lumbrical level in
an end-to-end fashion (Figure 29-2). A silicone rod
Figure 29-1  A Bruner incision in the digit and an L incision
in the palm for the FDS-FDP loop junction.
is chosen corresponding to the diameter of the FDS
tendon (usually No. 3 to 5). The implant is inserted
and its distal insertion is secured with direct sutures to
the profundus stump and is reinforced with pull-out
suture to the distal phalanx. The proximal part of
the silicone rod is cut to the lumbrical level and is left
free underneath the FDS-FDP loop after checking its
free motion.
We usually reconstruct at least A1, A2, and A4 pulleys
using pieces of the removed tendons (see Figure 29-2).
The technique used for pulley reconstruction is suturing
these pieces of flexors to the lateral sides of the fibro-
osseous canal. Pulley reconstruction should follow
silicone rod insertion in order to accurately match the
selected implant. Any necessary secondary procedures,
such as nerve repair, interphalangeal (IP) or metacarpo-
phalangeal (MCP) joint arthrolysis, and web space
plasty, are performed at this point, and the skin is closed
without tension.
Stage 2
The stage 2 surgery is done after an interval of 3 months
and consists of three steps: (1) a mid-palmar inverted L
incision for loop retrieval; (2) an antebrachial incision
for transsection of the FDS at the musculotendinous
junction; and (3) an angular incision over the DIP joint
for graft retraction and anchoring the graft (FDS) to the
distal phalanx (Figures 29-3 to 29-5).
Silicone rod
Reconstructed
A1, A2, and A4
pulleys
Flexor Flexor
digitorum digitorum
profundus superficialis
(FDP) (FDS)
Figure 29-2  Formation of a loop between FDS and FDP
tendon, reconstruction of A1, A2, and A4 pulleys, and
silicone rod placement in stage 1.
 Chapter 29:  Two-Stage Reconstruction With the Modified Paneva-Holevich Technique 309

Figure 29-3  An L incision in the palm for retrieval of

the loop and rod. A longitudinal incision is made in the
antebrachium for proximal transection of the FDS, and an Figure 29-5  The FDS tendon is retrieved from the wrist.
angular incision made at the DIP joint level for rod removal The area of the healed FDS-FDP junction is indicated with an
and advancement of the grafted FDS tendon. arrow.

A mid-palmar incision is used to identify the proxi-

mal end of the silicone rod and to retrieve the FDS-FDP
loop. The loop is identified easily because of its volume.
Flexor Trimming of the loop may be necessary in rare cases.
digitorum
A longitudinal antebrachial incision is used to iden-
superficialis
(FDS) tify the FDS tendon to the same finger. The tendon is
cut at the musculotendinous junction after a measure-
ment is done for the needed length. The cut FDS is then
pulled out to the palmar incision through the carpal
tunnel (see Figure 29-5). The FDS stump is sutured to
the proximal end of the silicone rod.
A third angular incision is made over the DIP joint
and the silicone rod with the graft sutured to its end is
gently retracted through the pseudo-sheath (Figure
29-6). The silicone rod is then discharged and the
tension of the graft is estimated by temporary stabiliza-
tion with a hypodermic needle through the skin of the
Flexor distal phalanx. The desired tension is adjusted so that
digitorum
profundus the reconstructed finger is kept in slightly more flexion
(FDP) than the adjacent fingers in flexion and extension of the
wrist. Then, the graft is secured to the profundus stump
in the distal phalanx with three or four interrupted 3-0
Figure 29-4  The loop site between FDS and FDP has nonabsorbable sutures. To avoid nail deformities, pull-
healed. The distal end of the FDS tendon is sutured to the out sutures should exit proximal to the nail matrix on
distal stump of the FDP tendon. the dorsum of the phalanx. In the recent years, we used
310 Section 3:  Secondary Flexor Tendon Surgery
Figure 29-6  An angular incision is made over DIP joint and
the silicone rod with the FDS graft sutured to its distal end is
retracted through this incision.
a small anchor inserted in the palmar aspect of the distal
phalanx, securing the distal part of the graft.
POSTOPERATIVE CARE
A part of the preoperative passive physiotherapy program
to overcome stiffness and achieve maximum joint
motion, a postoperative rehabilitation program is also
of paramount importance to maintain maximum finger
joint flexion. Intensive postoperative physiotherapy
should follow both stages.
Stage 1
At the end of the first stage, the hand should be immo-
bilized with a bulky dressing for 48 hours. An intensive
rehabilitation program consisting of passive MCP and
IP joints flexion is initiated 3 days after surgery. The goal
is to achieve and preserve full passive joint flexion and
extension of the reconstructed finger until the second
stage is undertaken.
Stage 2
After the second stage operation, a dorsal splint is
applied to hold the wrist in 30° flexion, the MCP joint
in 70° flexion, and the IP joints in a slightly flexed posi-
tion. An early controlled motion program comprising
passive flexion and active extension is started at day 3.16
The splint is removed by 5 weeks and active motion
and blocking exercises are initiated to avoid flexion
contractures.
OUTCOMES
Between 1992 and 2011, we treated 46 patients (55
digits) with zone 2 injuries using modified Paneva-
Holevich reconstruction. Between 1992 and 2000, we
had 20 patients (22 digits); they were followed for at least
1 year. The mean age of the patients was 24 years (range,
3 to 54 years). The mean total active motion recorded
was 189° of 219° of total passive motion (71% of the
contralateral respective finger) (Figure 29-7).11 Accord-
ing to the Buck-Gramcko scale, overall, an excellent
score was achieved in 50%, good in 32%, fair in 9%, and
poor in 9% of the digits. Using the revised Strickland
scale, 73% of the digits had good or excellent results.
Complications included pulley rupture in 4, nail defor-
mity in 8 (cosmetically unacceptable in one only), trig-
gering at the MCP joint in one, sensitive scar in one, and
deep infection in 2 digits in stage 1. These results are
slightly better than those achieved by Wehbe and others8
with the Hunter method of reconstruction. They reported
a total active range of digital motion of 176°. Superior
results were also noted when our findings were com-
pared with those of the two of the largest series using the
Hunter method.9,10 The good and excellent results in
these reports were 40% and 42% (La Salle-Strickland
scale), respectively, for zone 2 injuries, compared with
72% in our series (revised Strickland scale).
Since 1970s, many authors have reported good and
excellent results in the majority of their patients by
using the modified Paneva-Holevich technique (Table
29-1). Kessler4 had good and excellent results in 83%
of his patients by using the Strickland scale. Winspur
and colleagues17 obtained good and excellent results in
80% of their patients, by using the Buck-Gramcko scale.
Similarly, in our patients, good and excellent results
were recorded in 82% of the digits after surgery using
the Buck-Gramcko scale and 73% using the modified
Strickland scale.11
We used the modified Paneva-Holevich technique in
9 children (nine digits) with zone 2 injuries between
1992 and 2005 and recorded good and excellent results
in 8 children (89%) after a mean follow-up of 40
months.15 The mean total active motion achieved was
196° (75% of the contralateral finger) of 237° of total
passive motion.
COMPLICATIONS
The staged flexor tendon reconstruction is a demanding
technique with risks and complications. The complica-
tions can appear in both stages of surgery.25
In stage 1 of the two-stage flexor tendon reconstruc-
tion, complications include (1) rod buckling, (2) necro-
sis of the skin, (3) rod migration, (4) rupture of the distal
end of silicone rod, (5) synovitis, and (6) infection.
At the second stage, the following complications can
be noticed: (1) bowstringing, (2) impingement of the
 Chapter 29:  Two-Stage Reconstruction With the Modified Paneva-Holevich Technique 311

Figure 29-7  Flexion (A) and extension

(B) of a ring finger 3.5 years after tendon
reconstruction with the modified
Paneva-Holevich method.

A B

Table 29-1  Outcomes of the Modified Paneva- Flexion contracture of the DIP joint is one of the most
Holevich Technique commonly described complications that can be treated
Criteria* and with night extension splints.10,11,15,17-24 Silicone rod
Authors Digits Good-Excellent Rate rupture, bowstringing, and rupture of the distal graft
suture are other common complications.
Kessler et al4 6 83%†, Strickland
In stage 1, rod buckling can be prevented by avoiding
Winspur et al17 10 80%† suturing the pulleys under tension, so that silicone rod
Brug et al18 27 52% moves freely. Skin necrosis can be avoided by using a
Bruner incision with angles no less than 45°. We could
Chuinard et al19 16 62.5%, Boyes (modified) prevent rupture of the distal end of the silicone rod by
Paneva-Holevich 39 56%, Boyes (modified) suturing the rod to the distal stump of the FDP and a
et al20 pull-out suture of the silicone rod. In case of rupture of
Alnot et al21 19 73%, total active motion the silicone rod, the volar aspect of the distal phalanx
is opened and the implant is fished out with a retriever.
22
Naam 21 52.4%, Strickland Silicone rod synovitis can be treated effectively with
Brug et al 23
76 55% antibiotics and splinting. In stage 2, bowstringing can
11
be prevented by meticulous and secure reconstructions
Beris et al 22 82%
of A1, A2, and A4 pulleys in stage 1. If the distal graft
15
Darlis et al 9 89% junction is disrupted, the graft should be reattached
Abdul-Kader and 12 75% methods are same for silicone rod rupture. Flexion
Amir24 deformity of the DIP joint can be prevented by placing
less tension of the graft during surgery and dynamic
*Buck-Gramcko method was used unless specified. night splints after stage 2.
†
Calculated based on data provided in the articles.
Infection is an uncommon complication but can be
a serious one that may affect considerably the outcome.
The percentage of infection varies from 2.3% to 25.6%
proximal suture in the fibro-osseous canal, (3) tendon in both stage 1 and 2.8,9,15,25-28 Inadequate treatment may
grafts loose or tight, (4) disruption at the distal or proxi- require removal of the rod and reoperation with the
mal junctions, (5) flexion deformity of the proximal two-stage technique after 5 months. Infection is more
interphalangeal (PIP) and/or DIP joints, which is con- common in stage 1 than in stage 2; this fact may be
sidered to be the most common complication at this attributed to extensive surgical exposure of the digit and
stage, and (6) infection. silicone rod synovitis or both. In our series infection was
Complications after the modified Paneva-Holevich recorded in 2 digits (9%) during stage 1.29 In one
technique occur in 0% to 27% of the digits.10,11,15,17-24 case infection was resolved by closed irrigation and
312 Section 3:  Secondary Flexor Tendon Surgery
intravenous antibiotics, while in another case rod
removal was necessary.
DISCUSSION
In 1971, Hunter and Salisbury2 presented the prelimi-
nary results after two-stage flexor tendon reconstruction
addressing the problem of functional compromise after
flexor tendon injuries in zone 2. Since then, two-stage
flexor tendon reconstruction has been widely accepted,
presenting different rates of success and complica-
tions.26,30,31 In the first stage, the silicone rod is inserted
to stimulate pseudo-sheath formation with a smooth
and gliding surface that allows the passage of a free
tendon graft through it at a second stage.32,33 In further
studies Hunter showed that the fibroosseous canal
reconstruction in zone 2 allows an unrestricted gliding
without adhesions formation.34
In 1982, Paneva-Holevich reported 324 digital flexor
tendon reconstruction with her method of pedicle FDS
tendon grafting, among which in 39 digits with exten-
sive scar, she combined her technique (loop between
the FDP and the FDS in the first stage and the use
of the formed pedicle graft in the second stage) with
the Hunter silicone rod technique.20 Compared to
the Hunter technique, the modified Paneva-Holevich
method is advantageous because (1) there is no need of
identifying the motor during the first stage; (2) the
FDS-FDP loop can be identified easily in the palm
during the second stage; (3) there is no donor site mor-
bidity, since no free grafts are harvested; (4) it can be
performed easily in children15; (5) it comprises a pedi-
cled tendon graft with a strong proximal junction that
has already healed by stage 2; (6) it uses a tendon graft
(FDS) that is consistent compared with palmaris longus
(PL) and plantaris, which are reported to be absent in
20% and 25% of healthy individuals, respectively35; (7)
the FDS tendon graft is three times larger than conven-
tional grafts used in the Hunter technique (mean cross-
sectional area of 10.6 mm compared with the 3.1 mm,
1.6 mm, and 3.2 mm of PL, plantaris, and toe extensors,
respectively)3,36; and (8) it uses an intrasynovial graft,
which has better morphological, functional, and healing
characteristics than extrasynovial grafts.12-14
We have found only two disadvantages with the
Paneva-Holevich technique: (1) the difficulty in ten-
sioning the graft at the distal anchoring site of the graft.
The proximal tendon junction presents no problem
References
1. Paneva-Holevich E: Two stage plasty in flexor tendon injuries
of the fingers within digital synovial sheath, Acta Chir Plast
7:112–124, 1965.
2. Paneva-Holevich E: Two-stage tenoplasty in injury of the flexor
tendons of the hand, J Bone Joint Surg (Am) 51:21–32, 1969.
3. Hunter JM, Salisbury RE: Flexor-tendon reconstruction in
severely damaged hands. A two-stage procedure using a
because it has already healed by stage 2; and (2) the FDS
of the little finger sometimes is thin in the wrist area
and cannot be used. This problem can be overcome by
reinforcement of the tendon with a PL graft or by using
the FDS of an adjacent finger.18
We started using the modified Paneva-Holevich tech-
nique from 1992. Since 1999, this method has been
used for all patients who required staged tendon recon-
struction. The modified technique has several advan-
tages over the Hunter’s staged reconstruction and is now
more familiar to us. Some modifications regarding the
methods of tendon junction have been described in the
literature, where a Kessler suture or a fish-mouth tech-
nique was used for the loop junction between the FDS
and the FDP in stage 1 operation,22,23 but three or four
simple sutures are considered more than enough for the
loop. The lumbrical muscle belly can be folded over the
FDS-FDP loop, but this may increase the risk for a lum-
brical plus finger.18,23 Pulley reconstruction can be
achieved by using the excised tendon material and not
using the PL19 or extensor retinaculum.21
Many authors recommended that the distal anchor of
the graft during stage 2 should include attachment to
both the FDP tendon stump and a pull-out suture. Addi-
tional strength can be achieved by passing the graft
through an osseous tunnel in the distal phalanx.3,5 We
currently prefer to pass the graft underneath the distal end
of the profundus stump and suture to it with transverse
sutures on both sides and an additional suture through
an absorbable anchor to the distal phalanx without a
pull-out suture through the nail. If the A5 pulley has been
preserved, the proximal end of the profundus stump can
also be sutured to the distal edge of the A5 pulley.37
In most cases, the proximal part of the FDP to the
injured finger is used as a motor. When power of this
FDP muscle is absent or questionable, the FDS of the
same or adjacent finger can be used as a motor.8 During
operation, care should be taken to making proper judge-
ment about which proximal motor tendon is the best
motor, and either a FDP or a FDS tendon can be the
motor source.18
Two-stage flexor tendon reconstruction with combi-
nation of a silicone rod and a pedicle FDS tendon graft
is an efficient method of restoration of function of the
flexor tendons in zone 2. The combination presents
several technical advantages and resolves some prob-
lems emerging from the Hunter technique.
silicone-Dacron reinforced gliding prosthesis prior to tendon
grafting, J Bone Joint Surg (Am) 53:829–858, 1971.
4. Kessler FB: Use of a pedicled tendon transfer with a silicone
rod in complicated secondary flexor tendon repairs, Plast
Reconstr Surg 49:439–443, 1972.
5. Schneider LH: Flexor tendons-late reconstruction. In Green
DP, Hotchkiss RN, Pederson WC, editors: Green’s Operative
 Chapter 29:  Two-Stage Reconstruction With the Modified Paneva-Holevich Technique
Hand Surgery, ed 4, New York, 1999, Churchill Livingstone,
pp 1898–1941.
6. Soucacos PN: Two-stage flexor tendon reconstruction using
silicone rods. In Vastamaki M, editor: Current Trends in Hand
Surgery, Amsterdam, 1995, Elsevier, pp 353–357.
7. Soucacos PN: Secondary flexor tendon reconstruction. In
Duparc S, editor: Textbook on Techniques in Orthopaedic Surgery
and Traumatology, Paris, 2000, Elsevier SAS, pp 55–340.
8. Wehbé MA, Mawr B, Hunter JM, et al: Two stage flexor-tendon
reconstruction, Ten-year experience. J Bone Joint Surg (Am)
68:752–763, 1986.
9. LaSalle WB, Strickland JW: An evaluation of the two-stage
flexor tendon reconstruction technique, J Hand Surg (Am)
8:263–267, 1983.
10. Amadio PC, Wood MB, Cooney WP 3rd, et al: Staged flexor
tendon reconstruction in the fingers and hand, J Hand Surg
(Am) 13:559–562, 1988.
11. Beris AE, Darlis NA, Korompilias AV, et al: Two-stage flexor
tendon reconstruction in zone II using a silicone rod and a
pedicled intrasynovial graft, J Hand Surg (Am) 28:652–660,
2003.
12. Abrahamsson SO, Gelberman RH, Lohmander SL: Variations
in cellular proliferation and matrix synthesis in intrasynovial
and extrasynovial tendons: An in vitro study in dogs, J Hand
Surg (Am) 19:259–265, 1994.
13. Seiler JG 3rd, Chu CR, Amiel D, et al: Autogenous flexor
tendon grafts. Biologic mechanisms for incorporation, Clin
Orthop Relat Res 345:239–247, 1997.
14. Leversedge FJ, Zelouf D, Williams C, et al: Flexor tendon
grafting to the hand: An assessment of the intrasynovial
donor tendon—a preliminary single-cohort study, J Hand
Surg (Am) 25:721–730, 2000.
15. Darlis NA, Beris AE, Korompilias AV, et al: Two-stage flexor
tendon reconstruction in zone 2 of the hand in children,
J Pediatr Orthop 25:382–386, 2005.
16. Kleinert HE, Kutz JE, Atasoy E, et al: Primary repair of flexor
tendons, Orthop Clin North Am 4:865–876, 1973.
17. Winspur I, Phelps DB, Boswick JA Jr: Staged reconstruction
of flexor tendons with a silicone rod and a “pedicled” subli-
mis transfer, Plast Reconstr Surg 61:756–761, 1978.
18. Brug E, Stedtfeld HW: Experience with a two-staged pedicled
flexor tendon graft, Hand 11:198–205, 1979.
19. Chuinard RG, Dabezies EJ, Mathews RE: Two-stage superficia-
lis tendon reconstruction in severely damaged fingers, J Hand
Surg (Am) 5:135–143, 1980.
20. Paneva-Holevich E: Two-stage reconstruction of the flexor
tendons, Int Orthop 6:133–138, 1982.
313
21. Alnot JY, Mouton P, Bisson P: Longstanding flexor tendon
lesions treated by two-stage tendon graft, Ann Chir Main
Memb Super 15:25–35, 1996.
22. Naam NH: Staged flexor tendon reconstruction using pedi-
cled tendon graft from the flexor digitorum superficialis,
J Hand Surg (Am) 22:323–327, 1997.
23. Brug E, Wetterkamp D, Neuber M, et al: Secondary recon-
struction of flexor tendon function of the fingers, Unfallchirurg
101:415–425, 1998.
24. Abdul-Kader MH, Amin MA: Two-stage reconstruction for
flexor tendon injuries in zone II using a silicone rod and ped-
icled sublimis tendon graft, Indian J Plast Surg 43:14–20, 2010.
25. Soucacos PN, Beris AE, Malizos KN, et al: Two-stage treatment
of flexor tendon ruptures: Silicone rod complications analyzed
in 109 digits, Acta Orthop Scand (Suppl) 275:48–51, 1997.
26. Weinstein SL, Sprague BL, Flatt AE: Evaluation of the two-
stage flexor-tendon reconstruction in severely damaged digits,
J Bone Joint Surg (Am) 58:786–791, 1976.
27. Frakking TG, Depuydt KP, Kon M, et al: Retrospective outcome
analysis of staged flexor tendon reconstruction, J Hand Surg
(Br) 25:168–174, 2000.
28. Finsen V: Two-stage grafting of digital flexor tendons: A
review of 43 patients after 3 to 15 years, Scand J Plast Reconstr
Surg Hand Surg 37:159–162, 2003.
29. Beris AE, Korompilias AV, Lykissas MG, et al: Management
of infection in 2-stage flexor tendon reconstruction. In
Malizos KN, Soucacos PN, editors: Infections of the Hand and
Upper Limb, Athens, 2007, Paschalidis Medical Publications,
pp 271–276.
30. Honner R, Meares A: A review of 100 flexor tendon recon-
structions with prosthesis, Hand 9:226–231, 1977.
31. Reill P: Die zweizeitige beugesehnentransplantation, Hand-
chirurgie 10:215–221, 1978.
32. Schneider LH: Staged tendon reconstruction, Hand Clin
1:109–120, 1985.
33. Schneider LH: Complications in tendon injury and surgery,
Hand Clin 2:361–371, 1986.
34. Hunter JM: Staged flexor tendon reconstruction. In Hunter
JM, Schneider LH, Mackin EJ, et al, editors: Rehabilitation of
the Hand, St Louis, 1984, CV Mosby, pp 288–313.
35. Wehbé MA: Tendon graft anatomy and harvesting, Orthop Rev
23:253–256, 1994.
36. Carlson GD, Botte MJ, Josephs MS, et al: Morphologic and
biomechanical comparison of tendons used as free grafts,
J Hand Surg (Am) 18:76–82, 1993.
37. Viegas SF: A new modification of two-stage flexor tendon
reconstruction, Tech Hand Up Extrem Surg 10:177–180, 2006.
 CHAPTER
30  
OUTCOMES OF THE MODIFIED
PANEVA-HOLEVICH
PROCEDURES AND
EARLY POSTOPERATIVE
MOBILIZATION
Nash H. Naam, MD, FACS, and Lori Niemerg, OTR/L, CHT
OUTLINE
Patients with severe flexor tendon injuries associated
with scarred digital tendon sheath may require tendon
grafting. Single-stage flexor tendon reconstruction may
be unfeasible because of the scarred tendon bed; there-
fore, staged flexor tendon reconstruction is recom-
mended. The Paneva-Holevich technique uses the
pedicled flexor digitorum superficialis (FDS) as the
donor graft thereby avoiding harvesting a free tendon
graft. The modified technique incorporates the use of
a Silastic rod in the first stage to promote the formation
of a new tendon sheath and the use of a pedicled FDS
as the tendon graft in the second stage. This technique
combines the benefits of the Hunter rod and the use
of a pedicled intrasynovial tendon, which may create
less adhesion than extrasynovial tendons. This modi-
fied technique is ideal for the implementation of an
early active range of motion (AROM) program since
the proximal repair is already healed by the time the
second stage is performed, but the distal graft repair
to the bony distal phalanx should be strong enough
to withstand the stresses of the AROM program. The
incorporation of an early AROM program with this
technique provides a significant advantage in improv-
ing the ultimate outcome of the procedure.
Flexor tendon reconstruction in the presence of a
damaged flexor tendon sheath with destruction of
majority of pulley system or serious scar formation is
very challenging to the hand surgeon. The fibrotic
tendon gliding bed does not allow smooth excursion of
the tendon graft, which results in significant adhesions
and limited range of motion. In these circumstances
single-stage flexor tendon reconstruction would not be
appropriate and staged tendon reconstruction should
be considered.
314
In 1965, Paneva-Holevich suggested the use of pedi-
cled flexor digitorum superficialis (FDS) tendon as a
graft by creating a loop of the flexor digitorum profun-
dus (FDP) and flexor digitorum superficialis (FDS) then
reflecting the latter in the second stage as a pedicled
tendon graft.1,2 In 1971, Hunter and Salisbury intro-
duced the concept of using a silicone-Dacron reinforced
tendon rod to stimulate formation of a new tendon
sheath before tendon grafting.3 This transforms the
scarred tendon bed into a gliding pliable functional
system. In 1972, Kessler reported on the combined use
of Hunter rod and pedicled FDS for staged flexor tendon
reconstruction.4 Since then, several reports of the com-
bined method have been published.5-9
We started performing this procedure in 1983. In
1997, we published our experience with the use of this
technique in 33 patients.8 Up to 2009, we applied this
technique in 116 patients. Candidates for this type of
tendon reconstruction included patients who did not
have their flexor tendon repaired or those who had their
repairs failed secondary to rupture or adhesions (Figure
30-1). Most of these procedures are performed in
patients with zone 2 flexor tendon injuries. However,
zone 1 injuries are also amenable to this type of recon-
struction. Zone 3 and 4 injures can usually be treated
with conventional single-stage interposition tendon
grafts unless there is a concomitant damage to the flexor
tendon sheath in zone 2. This procedure is particularly
useful in tendon injuries associated with severe crushing
injuries when there are associated fractures, nerve inju-
ries, and skin defects.5,7,8
This technique has become our standard technique
for flexor tendon reconstruction when the tendon bed
does not allow one-stage flexor tendon grafting. A dis-
tinct advantage of this procedure is to allow earlier
active range of motion (AROM), since the proximal
repair should be completely healed by the time the
 Chapter 30:  Outcomes of the Modified Paneva-Holevich Procedures and Early Postoperative Mobilization
Figure 30-1  Loss of active flexion of the index finger after
an old injury of both flexor tendons.
Figure 30-2  Stage 1: severely scarred flexor tendon
sheath. Some of the pulleys are still intact.
second stage is performed if a tendon graft, instead of
tendon transfer, is used. A strong distal repair, preferably
attaching the tendon to the bony distal phalanx, would
allow the graft to withstand the forces of early AROM
without fears of rupture. Actually, Paneva-Holevich rec-
ommended starting active motion of the involved digit
in the first postoperative week and reported no increase
in the incidence of rupture in her early report of second-
ary reconstruction of the FDP tendon by FDS transfer
from the same finger.7
SURGICAL TECHNIQUE
Stage 1
Through a Bruner zigzag incision, the flexor tendon
sheath is exposed. The remnants of the flexor tendons
are excised (Figures 30-2 to 30-4). Special care should
be taken to preserve all the normal pulleys as much as
possible. If the important pulleys or majority of the
flexor pulley system are destroyed, pulley reconstruction
315
Figure 30-3  The FDS and FDP tendons are seen at the
base of the finger. Note the scarring of the flexor tendon
sheath.
Figure 30-4  The flexor tendons remnants have been
excised. Note the proximal ends of FDS and FDP tendon are
ready for the repair.
should be performed at this stage utilizing pieces of the
excised flexor tendons. Any nerve grafting or flexion
contracture release can be done at this stage. The largest
possible Hunter rod is then inserted. The Hunter rod
should not touch the gloves as this may produce inflam-
matory reaction secondary to the contact with the talc
powder. The distal end of the rod is sutured to the distal
stump of the FDP with horizontal mattress sutures of
4-0 Prolene or 4-0 fiberwire. It is important to be sure
that the sutures include the Dacron tape within the
Hunter rod since the silicone alone has very little
holding power. The proximal stump of the rod is left
free in the palm. The FDS and FDP tendons of the
injured finger are exposed at the mid palm level. Their
ends are freshened to healthy margins and then sutured
to each other with an end-to-end method (Figures 30-5
and 30-6).
In making the end-to-end suture, the dorsal epiten-
dinous layer is performed first with a running interlock-
ing 6-0 Prolene suture followed by core suture of 4-0
316 Section 3:  Secondary Flexor Tendon Surgery
Figure 30-5  The proximal ends of the FDS and FDP
tendons have been repaired end-to-end.
Figure 30-6  A Hunter rod has been inserted. The A2 pulley
has been reconstructed using part of the excised flexor
tendons.
Prolene or 4-0 fiberwire in a modified Kessler technique.
The volar epitendinous layer is then completed using
the 6-0 Prolene. The Prolene suture is left long to facili-
tate easier identification of the site of the tendon repair
during the second stage. The wounds are closed and the
patient is put in a dorsal splint with the wrist flexed 45°.
This technique is used mostly for flexor tendon inju-
ries in zones 1 and 2. If the tendon laceration is in zone
3 or 4 and the digital sheath is compromised, because
of either a concomitant injury or extension of scarring
that limits tendon excursion, this technique can be used
as well. This will require placing the end-to-end suturing
of the FDS and FDP either distal to the carpal tunnel in
zone 3 injuries or proximal to the carpal tunnel in zone
4 injuries. The FDS tendon may be divided proximal to
the musculotendinous junction and stripped of any
muscle tissue.
Box 30-1 Clinical Pearls—Stage 1
 Flexor tendon remnants are excised.
 Pulleys are preserved or reconstructed using the excised
flexor tendons.
 The proximal ends of the FDS and FDP are repaired end-
to-end in the palm.
 Leave the Prolene suture long to facilitate identification
in stage 2.
 The largest possible Hunter rod is inserted. The distal
end is repaired to the FDP stump and the proximal end
is left free in the palm.
 PROM is started 3 to 5 days postoperatively.
Figure 30-7  Stage 2: the site of FDS and FDP tendon
repair and the proximal end of the Hunter rod are exposed in
the palm.
Patients are started on passive range of motion
(PROM) of the operated digits 3 to 5 days postopera-
tively, which lasts as long as required to ensure adequate
passive range of finger motion. PROM is performed to
keep the joints flexible. The patient is instructed to
perform PROM of each joint of the involved digit for 10
repetitions 6 to 8 times a day. Unrestricted active motion
exercises of the uninvolved digits are emphasized as well
(Box 30-1).
Stage 2
We recommend allowing at least 12 weeks before pro-
ceeding with the second stage. The scar should be
supple. Excellent PROM is a prerequisite before pro-
ceeding to stage 2. Through a zigzag incision in the
palm, the site of FDS-to-FDP tenorrhaphy in the palm
is exposed and freed of the scar tissue (Figure 30-7). A
zigzag incision is made over the distal forearm and the
FDS tendon of the involved digit is isolated. The tendon
is divided at the musculotendinous junction and then
retrieved in the palm incision as a pedicled graft (Figures
30-8 and 30-9). The Hunter rod is exposed and the new
sheath is opened at its proximal end in the palm.
 Chapter 30:  Outcomes of the Modified Paneva-Holevich Procedures and Early Postoperative Mobilization 317

Figure 30-8  The FDS tendon is exposed at the distal

forearm and divided at the musculotendinous junction.
Figure 30-10  The end of the FDS is guided by the Hunter
rod through the new sheath.

Figure 30-9  The FDS tendon is retrieved in the palm Figure 30-11  The FDS pedicled graft has been delivered to
incision. the distal attachment site guided by the Hunter rod.

A distal incision is made at the level of the distal

interphalangeal (DIP) joint. The distal end of the new
sheath is opened and the Hunter rod is exposed and
freed. The proximal end of the rod is sutured to the
proximal end of the FDS graft (Figure 30-10). As the
rod is pulled distally, it guides the FDS graft through
the new sheath (Figure 30-11). After the distal end of
the FDS tendon is pulled beyond the fingertip, tension
of the graft is adjusted. Optimal tension on the graft is
set to allow extension of the finger with the wrist flexed
and flexion of the finger with wrist extension. The
tension should flex the finger should be slightly more
than the normal flexion cascade. The distal end of
the graft is anchored to the volar aspect of the base
of the distal phalanx using 4-0 stainless steel pullout
wire that is tied over a button (Figure 30-12). Extra Figure 30-12  The position of the digit after repair of
horizontal mattress sutures of 4-0 Prolene are inserted the distal end of the graft to the distal phalanx with a
attaching the graft to the distal stump of the FDP. pullout wire.
318 Section 3:  Secondary Flexor Tendon Surgery
Box 30-2 Clinical Pearls—Stage 2
 Allow at least 12 weeks before proceeding with the
second stage.
 The second stage should not be performed unless the
patient gains excellent passive range of motion.
 The site of the tenorrhaphy is exposed in the palm.
 An incision is made at the distal forearm and the FDS
of the involved digit is isolated and divided at the   importance of this rehabilitation program and its impact
musculotendinous junction.
 The tendon graft is retrieved in the palm.
 The tendon graft is threaded through the new sheath
guided by the Hunter rod.
 Optimum tension should be adjusted then the tendon
graft is anchored to the bony distal phalanx with 4-0
stainless steel wire. Extra sutures of 4-0 Prolene can be
placed between the FDP and the tendon graft.
 Early active motion starts 3 to 5 days postoperatively.
Postoperatively, the patients are instructed to perform
early AROM exercise 3 to 5 days after surgery, as detailed
in the paragraphs that follow (Box 30-2).
EARLY MOBILIZATION
In the past four decades, significant advances in basic
and clinical research have improved our understanding
of tendon function, physiology, and tendon healing.10-13
These advancements triggered an evolution in the post-
operative rehabilitation after flexor tendon repairs. Suc-
cessful rehabilitation after flexor tendon repairs has to
provide both protection of the repair and prevention of
adhesions from limiting the tendon excursion. Studies
have documented improved tendon function with early
controlled mobilization as the forces applied to flexor
tendon repairs provide more rapid recovery of tensile
strength with improved tendon excursion and fewer
adhesions.14,15 Several studies have documented the
superior results of early AROM following flexor tendon
repair and reconstruction.13,16-20
This technique of flexor tendon reconstruction using
the pedicled FDS is ideal for implementation of an
AROM program. The site of the proximal repair is
already healed by the time the second-stage procedure
is performed. The strong bony fixation of the graft to the
bony distal phalanx provides a strong construct allowing
AROM. In our experience we have found that the results
of the more recent procedures were significantly better
than the older ones essentially because of the AROM
program that we adopted in the last 15 years. Smith and
colleagues17 used early AROM following staged flexor
tendon reconstruction. In 26 digits in 22 patients, 20
digits (77%) achieved good to excellent results.
Our Protocol
Early AROM requires a cooperative, focused, and under-
standing patient. We found that preoperative teaching
by the hand therapist to be of an immense value. Patients
tended to understand the details of the program better
and their compliance with the therapy program to be
also better. Patients are seen preoperatively by our certi-
fied hand therapist. The therapist discusses with the
patient the postoperative rehabilitation program to
allow the patient to participate in understanding the
on the eventual result of the staged flexor tendon recon-
struction. Sometimes splints are prefabricated preopera-
tively to decrease the time and the difficulty of making
custom splints postoperatively. Since virtually all these
patients are scheduled on an elective basis, preoperative
teaching by the therapist can be easily incorporated in
the protocol.
At the first postoperative visit, 3 to 5 days postopera-
tively, the compression dressing is removed and a light
compression dressing is applied along with fingersocks
or 1-inch Coban. A dorsal blocking splint is applied.
The wrist is kept in neutral or 20° flexion and the meta-
carpophalangeal joints (MP) in 60° flexion with the IP
joints kept extended. Patients are taught first the place-
and-hold exercise program as well as wrist tenodesis
exercises. The patient is advanced gradually to AROM
exercises within the middle arc of motion and within
the restraints of the dorsal blocking splint. The extremes
of the arc of motion in extension and flexion are to be
avoided in this early phase. Exercises are performed 4
times a day.
At 2 weeks, scar mobilization is started. Scar mobili-
zation is a manual therapeutic technique that uses
massage to break down scar tissue. It is performed 4
times a day by applying gentle firm pressure over the
scar and massaging it in a horizontal, vertical and circu-
lar motion. A self adhesive Silicone gel sheet is used at
night. The sheet is cut appropriate to the size of the scar
and applied directly over the scar. It may be wrapped
with Coban or stockinet. It helps to reduce, flatten, and
smooth the scar.
At 2 weeks, the AROM is increased. Gentle blocking
exercises may be started. Exercises are repeated 6 to 8
times a day. Sometimes ultrasound is used if adhesions
are excessive.
At 4 to 5 weeks, the dorsal blocking splint is dis­
continued. A clamshell splint is fabricated supporting
the MP joint at 0°, allowing full AROM of the PIP and
the DIP joints to promote excursion of the flexor
tendons. The splint is a hand-based, volar/dorsal splint
maintained with Velcro straps on the ulnar and radial
aspects of the hand (Figure 30-13). All the fingers are
included in the splint, but the thumb is excluded to
allow full range of motion of the thumb. The splint
may be used all the time or just during exercises. Neu-
romuscular electrical stimulation may be used. The
patient is advised to avoid any lifting or heavy use of
the hand.
 Chapter 30:  Outcomes of the Modified Paneva-Holevich Procedures and Early Postoperative Mobilization 319

Figure 30-13  Clamshell splint.

A B
Figure 30-14  Postoperative function at 1 year after surgery. A, Flexion. B, Extension.

At 8 weeks, progressive strengthening exercises with
the use of putty and/or hand gripper are started. Patients
are gradually weaned from the clamshell splint after
obtaining satisfactory AROM. Unrestricted activities are
allowed at 8 weeks (Figure 30-14).
PERSONAL EXPERIENCE AND OUTCOMES
From 1983 to 2009, we treated 116 patients with this
technique; 94 patients were available for review. The 68
male and 26 female patients ranged in age from 14 to
71 years with an average of 34 years. The index finger
was involved in 21 patients; long finger in 37; ring finger
in 17; and little finger in 19 patients. Twelve patients
had injuries in zone 1; 63 patients in zone 2; 13 patients
in zone 3; and 6 patients in zone 4. Preoperatively,
patients were evaluated according to modified Boyes
classification.21,22 There were no patients in grade 1; 32
patients in grade 2; 14 patients in grade 3; 19 patients
in grade 4; and 29 patients in grade 5. Sixty-six patients
had previous surgery: 36 patients had tendon repairs;
25 were primary and 11 were secondary repairs. Eleven
patients had single staged flexor tendon grafts and 19
had flexor tenolysis.
During the first stage of the tendon reconstruction,
42 patients underwent pulley reconstruction. Pulley
reconstruction was performed using Kleinert and
Bennett’s method in which the tendon graft is sutured
to the remaining rim of tissue at the site of the pulley.23
Twelve patients had nerve grafting, 5 patients had nerve
conduits using polyglycolic acid neurotubes, and 26
patients had release of flexion contractures of the PIP
joint by excision of the check-rein ligaments.
320 Section 3:  Secondary Flexor Tendon Surgery

Table 30-1  Results According to Zone of Injury

Functional Recovery
Zone No. of Patients Excellent Good Fair Poor Excellent + Good, %
1 12 2 9 0 1 92
2 63 20 24 10 9 70
3 13 3 8 0 2 85
4 6 2 2 1 1 67
Total 94 27 43 11 13 74

Table 30-2  Results According to Preoperative Status With the Modified Boyes Grading Method
Functional Recovery
Grade No. of Patients Excellent Good Fair Poor Excellent + Good, %
II 32 9 16 4 3 78
III 14 4 7 1 2 79
IV 19 6 9 2 2 79
V 29 8 11 4 6 66

The postoperative follow-up ranged from 2 to 27
years with an average of 9.5 years. The results were
evaluated using the grading system reported by Strick-
land and Glogovac.24 This method measures the active
degree of PIP and DIP joint flexion minus any extension
lag. Patients who have more than 150° are rated as
excellent, 125° to 149° as good, 90° to 124° as fair,
and less than 90° as poor. According to this evaluation,
27 of our patients were rated as excellent, 43 as good,
11 as fair, and 13 as poor. The results by zone of injury
are listed in Table 30-1. The results according to the
preoperative status of the finger according to the modi-
fied Boyes grading system are listed in Table 30-2.
Patient satisfaction was very high; 78% of the patients
were satisfied or very satisfied with the procedure. Of the
94 patients, 64 were manual laborers; 59 of them
returned to their original work activities, 3 retired, and
2 had to change their job.
Persistent flexion contractures of the PIP or the
DIP joints or both were present in 57 patients. The
flexion contracture ranged from 5° to 57° with an
average of 14°.
There were no infections or tendon ruptures in this
group of patients. Fourteen patients required tenolysis;
10 improved, but 4 did not improve and 2 of them
underwent arthrodesis of the PIP joint because of per-
sistent flexion deformities.
CHOICE OF PROCEDURE
Whenever the FDS is available, this technique has proved
to be simple and reliable, and the results are reproduc-
ible. This technique avoids harvesting a donor graft,
thereby reducing the morbidity of the site of the donor
graft. The FDS being an intrasynovial tendon has advan-
tages over the use of an extrasynovial tendon. There have
been several studies that found improved function in
animal models following tendon grafting using an
intrasynovial tendon such as the FDS compared to
extrasynovial tendons such as the palmaris longus or
plantaris.25-28 Gelberman and colleagues25 compared the
morphological and functional characteristics of intrasy-
novial tendons with the extrasynovial tendon grafts in
dogs. They found that the intrasynovial tendon grafts
heal with minimal adhesions with normal cellularity
and collagen organization. This provided a smooth
gliding surface. The extrasynovial grafts, on the other
hand, healed with ingrowth of connective tissue from
the digital sheath that obliterated the gliding surface
and occupied the space between the tendon surface and
surrounding tissues. They concluded that intrasynovial
tendon grafts had significantly improved morphological
and functional characteristics compared with the extra-
synovial tendon grafts.
An added advantage of this technique is proximity of
the size of the FDS tendon to that of the FDP compared
 Chapter 30:  Outcomes of the Modified Paneva-Holevich Procedures and Early Postoperative Mobilization
with the size of the palmaris longus or plantaris, which
is much smaller. Carlson and colleagues29 studied the
morphological and biomechanical characteristics of the
free tendon grafts, comparing palmaris longus, plan-
taris, and extensor digitorum longus of the toe with the
FDP. They found that the average cross-sectional area of
the FDP was 10.6 mm2 and the cross-sectional areas of
the palmaris longus, plantaris, and the toe extensors
were 3.1 mm2, 1.6 mm2, and 3.2 mm2, respectively.29
The FDS tendon has a cross-sectional area much closer
to the FDP tendon. That is why we recommend using
the largest possible size of Hunter rods during the first
stage. We used size 6 Hunter rods in 76%, size 5 in 14%,
and size 4 in 10% of the patients.
From the technical standpoint this procedure is
straightforward. Even identification of the site of the
References
1. Paneva-Holevich E: Two-stage plasty in flexor tendon injuries
of fingers within the digital synovial sheath, Acta Chir Plast
7:112–124, 1965.
2. Paneva-Holevich E: Two-stage tenoplasty in injury of the
flexor tendons of the hand, J Bone Joint Surg (Am) 51:21–32,
1969.
3. Hunter JM, Salisbury RE: Flexor tendon reconstruction in
severely damaged hands: a two-stage procedure using a
silicone-Dacron reinforced gliding prosthesis prior to tendon
grafting, J Bone Joint Surg (Am) 53:829–858, 1971.
4. Kessler FB: Use of a pedicled tendon transfer with a silicone
rod in complicated secondary flexor tendon repairs, Plast
Reconstr Surg 49:439–443, 1972.
5. Chong JK, Cramer LM, Culf NK: Combined two-stage teno-
plasty with silicone rods for multiple flexor tendon injuries
in “no-man’s land,” J Trauma 12:104–121, 1972.
6. Winspur I, Phelps DB, Boswick JA: Staged reconstruction of
flexor tendons with a silicone rod and a “pedicled” sublimis
transfer, Plast Reconstr Surg 61:756–761, 1978.
7. Paneva-Holevich E: Two-stage tenoplasty: results. In Hunter
JM, Schneider LH, Mackin EJ, editors: Tendon Surgery in the
Hand, St Louis, 1987, CV Mosby, pp 272–281.
8. Naam NH: Staged flexor tendon reconstruction using pedi-
cled tendon graft from the flexor digitorum superficialis,
J Hand Surg (Am) 22:323–327, 1997.
9. Beris AE, Darlis NA, Korompilias AV, et al: Two-stage flexor
tendon reconstruction in zone II using a silicone rod and a
pedicled intrasynovial graft, J Hand Surg (Am) 28:652–660,
2003.
10. Lundborg G: Experimental flexor tendon healing without
adhesion formation—a new concept of tendon nutrition and
intrinsic healing mechanisms. A preliminary report, Hand
8:235–238, 1976.
11. Gelberman RH, Vande Berg JS, Lundborg GN, et al: Flexor
tendon healing and restoration of the gliding surface: An
ultrastructural study in dogs, J Bone Joint Surg (Am) 65:70–80,
1983.
12. Boyer MI, Strickland JW, Engles D, et al: Flexor tendon repair
and rehabilitation: state of the art in 2002, Instr Course Lect
52:137–161, 2003.
13. Tang JB: Indications, methods, postoperative motion and
outcome evaluation of primary flexor tendon repairs in Zone
2, J Hand Surg (Eur) 32:118–129, 2007.
321
FDS-to-FDP repair in the second stage is much easier
than trying to isolate the profundus tendon of that digit.
The addition of a long Prolene suture at the site of the
repair actually makes identification of the repair site
much easier. The use of the largest possible size of
Hunter rod takes away the uncertainty of whether the
FDS tendon graft will fit in the new tendon sheath. We
have not had any difficulty with passing the FDS in the
tendon sheath. This combined approach of using Hunter
rod to stimulate the production of a new sheath and the
use of the pedicled FDS as a graft takes advantage of the
benefits of the two techniques. This method of flexor
tendon reconstruction provides certain advantages over
the classic use of Hunter rod and an extrasynovial
tendon graft such as the palmaris longus, plantaris, or
toe extensors.30-33
14. Chesney A, Chauhan A, Kattan A, et al: Systematic review of
flexor tendon rehabilitation protocols in zone II of the hand,
Plast Reconstr Surg 127:1583–1592, 2011.
15. Gelberman RH, Woo SL, Lothringer K, et al: Effects of early
intermittent passive mobilization on healing canine flexor
tendons, J Hand Surg (Am) 7:170–175, 1982.
16. Khan K, Riaz M, Murison MS, et al: Early active mobilization
after second stage flexor tendon grafts, J Hand Surg (Br)
22:372–374, 1997.
17. Smith P, Jones M, Grobbelaar A: Two-stage grafting of flexor
tendons: results after mobilization by controlled early active
movement, Scand J Plast Reconstr Surg Hand Surg 38:220–227,
2004.
18. Braga-Silva J, Kuyven CR: Early active mobilization after
flexor tendon repairs in zone two, Chir Main 24:165–168,
2005.
19. Pettengill KM: The evolution of early mobilization of the
repaired flexor tendon, J Hand Ther 18:157–168, 2005.
20. Yamazaki H, Kato H, Uchiyama S, et al: Long term results of
early active extension and passive flexion mobilization fol-
lowing one-stage tendon grafting for neglected injuries of the
flexor digitorum profundus in children, J Hand Surg (Eur)
36:303–307, 2011.
21. Boyes JH: Flexor tendon grafts in the fingers and thumb: an
evaluation of end results, J Bone Joint Surg (Am) 32:489–499,
1950.
22. Boyes JH, Stark HH: Flexor tendon grafts in the fingers and
thumb: a study of factors influencing results in 1000 cases,
J Bone Joint Surg (Am) 53:1332–1342, 1971.
23. Kleinert HE, Bennett JB: Digital pulley reconstruction employ-
ing the always present rim of the previous pulley, J Hand Surg
(Am) 3:297–298, 1978.
24. Strickland JW, Glogovac SV: Digital function following flexor
tendon repair in Zone II: A comparison of immobilization
and controlled passive motion techniques, J Hand Surg (Am)
5:537–543, 1980.
25. Gelberman RH, Seiler JG III, Rosenberg AE, et al: Intercalary
flexor tendon grafts: A morphological study of intrasynovial
and extrasynovial donor tendons, Scand J Plast Reconstr Surg
Hand Surg 26:257–264, 1992.
26. Seiler JG III, Gelberman RH, Williams CS, et al: Autogenous
flexor-tendon grafts: A biomechanical and morphological
study in dogs, J Bone Joint Surg (Am) 75:1004–1014, 1993.
322 Section 3:  Secondary Flexor Tendon Surgery
27. Abrahamsson SO, Gelberman RH, Lohmander SL: Variations
in cellular proliferation and matrix synthesis in intrasynovial
and extrasynovial tendons: An in vitro study in dogs, J Hand
Surg (Am) 19:259–265, 1994.
28. Leversedge FJ, Zelouf D, Williams C, et al: Flexor tendon
grafting to the hand: an assessment of the intrasynovial donor
tendon: A preliminary single-cohort study, J Hand Surg (Am)
25:721–730, 2000.
29. Carlson GD, Botte MJ, Josephs MS, et al: Morphologic and
biomechanical comparison of tendons used as free grafts,
J Hand Surg (Am) 18:76–82, 1993.
30. Brug E, Stedtfeld HW: Experience with a two-stage pedicled
flexor tendon graft, Hand 11:198–205, 1979.
31. LaSalle WB, Strickland JW: An evaluation of the two-stage
flexor tendon reconstruction technique, J Hand Surg (Am)
8:263–267, 1983.
32. Amadio PC, Wood MB, Cooney WP 3rd, et al: Staged flexor
tendon reconstruction in the fingers and hand, J Hand Surg
(Am) 13:559–562, 1988.
33. Wehbe MA, Mawr B, Hunter JM, et al: Two-stage flexor-
tendon reconstruction. Ten-year experience, J Bone Joint Surg
(Am) 68:752–763, 1986.
 CHAPTER
31  
VASCULARIZED TENDON
TRANSFERS FOR
RECONSTRUCTION
A Tendon Vascularity and
Gliding, Island and Free
Vascularized Transfers
Jean Claude Guimberteau, MD
OUTLINE
This chapter presents several new approaches to flexor
tendon reconstruction for salvage tendon surgery. The
use of an island tendon, vascularized by the mesoten-
don, with all its gliding surfaces intact, provides new
methods to deal with adhesions and has the added
merit of being a one-stage procedure. The procedure
can be done as a local pedicled flap, as a free vascular-
ized composite tissue transfer from the foot, or as a
vascularized transplant from a cadaver donor. These
types of vascularized tendon, or tendon and flap, trans-
fers had multiple applications; the author achieved
rather favorable functional results in the patients.
These procedures are expected to offer reconstructive
options for the cases involving damages to multiple
structures together with flexor tendons.
From the outset, surgical principles concerning the
reconstruction of finger flexor tendons have centered on
the tendon as a simple force transmission belt connect-
ing the muscular structure. Muscles create the forces that
move articulated structures of bones, and the tendon is
bent by this force around the joints during motion of
the extremities. Consequently, this very mechanical
concept led to the development of techniques mainly
aiming at rebuilding this “transmission belt” as solidly
as possible. The tendon is considered as mostly avascu-
lar; mechanically, the tendon simulates a transmission
belt.
From the 1940s, many researchers have accumulated
evidence of poor tendon healing capacity. The major
reason for poor tendon healing is believed to
be insufficient collagen production. Instead, vascular
connections develop through adhesion between the
tendon and peripheral tissues. The adhesion diminishes
the sliding capacity of the tendons and limits functional
recovery of the tendon.
Potenza introduced the essential roles of adhesions
for tendon healing in early 1960s.1 Since then, investiga-
tors sought to lessen functional impact of adhesion
formation and optimize the sliding capacities of the
tendon. Few attempts were made to understand why
tendons need vascular or pseudo-vascular connections.
Indeed, some researchers tended to minimize the role
of vascularization. The efforts have led to less research
aimed at providing vascular supplies to the tendon for
many years because it seemed pointless to carry out
research on this subject if tendons are very slightly vas-
cularized and receive sufficient nourishment from the
synovial fluid.2
Major past effort was done to diminish adhesion by
limiting the contact between the grafted tendon and the
recipient site. Catgut, polyester, and silicone interposi-
tions were introduced and showed their efficacy but to
the detriment of tendon solidity; rupture due to insuf-
ficient healing or necrosis is a major complication. The
fact that some damaged tendons need adhesions in
order to heal was acknowledged, as was its detrimental
effect on sliding and functional outcome. For decades,
research was aimed at decreasing the adhesion. Yet two
antagonistic aspects have to be reconciled: healing with
poor sliding and with the risk of rupture.
Different avascular tendon grafts, such as the pal-
maris longus, the plantaris, and others, have been used
thus far.3 The two-stage techniques became popular to
323
324 Section 3:  Secondary Flexor Tendon Surgery
treat the cases with serious scar during secondary
repairs or reconstruction. Two-stage tenoplasty by James
Hunter4 and Paneva Holevitch5 needs to be completed
with multiple operations. In these operations, a silicone
rod capable of recreating the conditions of a synovial
sheath is inserted first. A tendon is then grafted or trans-
ferred in a second stage. Despite all the precautions,
functional results were sometimes mediocre because,
apart from Hunter’s series, which found 80% good
results, other teams only approached 50% success rates.
A good skin condition is required before surgery. The
two-stage technique necessitates at least 6 months, thus
discouraging patients and surgeons owing to the time
factor and to the difficulty in obtaining good functional
result. Moreover, in the mid to long term, the outcome
becomes even less satisfactory sometimes, with some
fingers in flexion deformities.
In fact, these techniques obey a certain mechanical
logic. The tendon acts as a force transmission cord; its
motion should require optimization of smooth gliding
surface in the first stage of the operation. An attempt
was made to solve the biological problem by trying to
create sliding conditions with a synovial pseudo-sheath.
Although this principle may represent enormous prog-
ress compared to the past, the biological realities and
requirements are not respected. The results of the pro-
cedures and the difficulties encountered led some sur-
geons to question very foundations of avascular nature
and believed mechanical role of the tendon.
In the staged tendon reconstruction, the tendon is
not vascularized and placed in a more or less sclerotic
recipient site. It is not always possible to achieve both
healing and gliding of the repaired tendon at the same
time. Past investigations demonstrated that the tendon
is a vascularized structure and has vascularity distribut-
ing both inside and outside the tendon, as well as
having a very specific lymphatic drainage system.6-9 The
current techniques remain completely alien to these
biological realities and ignore, or at least exclude, neces-
sity of vascular supplies to the grafted tendon during
surgical reconstruction. Therefore, better knowledge of
the intricate physiology of the tendon and the condi-
tions favoring optimum function are necessary to obtain
better outcome of the surgery.
For many decades, terms such as hierarchical tissue
distribution, stratification, and virtual space between struc-
tures have been taken for granted, yet the real basis for
them needs to be questioned. Their scientific under­
pinnings were limited to the notion of virtual space
or the existence of loose connective tissue, but their
biomechanical foundations were more than vague. In
the past 50 years, research focused on the microscopic
findings of these structures while the global concept of
the structures has not been addressed. As we have exam-
ined these tissues more closely, new hypotheses and
findings have emerged concerning the organization of
the subcutaneous tissues and led to new concepts and
to new surgical procedures.10
ANATOMICAL STUDIES AND SURGICAL BASIS
Microvideo Observations of Tendon
Structures in Zones 3, 4, and 5
We have performed 95 video observations in vivo with
functional analysis, either directly under the skin or
close to tendons, muscle, and nerve sheaths during
human surgical dissection using light microscopy (at
magnification ×25).
This gliding or sliding tissue structure, traditionally
called “connective,” “areolar,” or “loose tissue and
paratenon around the tendons,” has for long been con-
sidered to be packing tissue that fills spaces. In fact, this
tissue plays a mechanical role, allowing movements
between the structures it connects, preserving mobility
and independence between organs, in particular,
between tendons and skin. This tissue is important
for the nutrition of the structures embedded in it
and acts as a frame for blood and lymph vessels
(Figure 31[A]-1).
Mechanically, it diminishes friction while facilitating
deformability and adaptability. The fibrous tissue,
known as the paratendon, surrounds the tendon. It is
composed of multidirectional filaments, intertwining
and creating partitions that enclose microvacuolar
shapes (Figure 31[A]-2). We term this the Multimicro-
vacuolar Collagenous Dynamic Absorbing System
(MVCAS) to emphasize its function. This system is situ-
ated between the tendon and its neighboring tissue and
favors optimal sliding. The tendon is able to travel far
and fast without any hindrance, and without inducing
movement in any other neighboring tissue, thus account-
ing for the absence of any dynamic repercussions of
movement on the skin surface. When the flexor tendon
moves, its movement is barely discernible in the palm.
In the light of above new information obtained, the
time has come to confirm some anatomical truths
about this tissue. The notion of multilayered sliding
between completely anatomically separate tissues—
sliding thanks to what many believe to be an elastic
process—is likely to be revised in the light of these
observations. Continuous matter and microvacuolar
framework should be noted between the tendon and
surrounding structures.11,12 Scanning electron micro­
scopy demolished the existence of different super­
imposed layers because they were never observed.
Furthermore, the elementary laws of mechanics and rhe-
ology presented the problem in terms of global dynam-
ics where continuous matter composed of millions of
vacuoles, each measuring a few microns to a few milli-
meters in size, is organized in dispersed branching
fractal patterns (Figure 31[A]-3). The sides of the vacu-
oles, which are intertwined, are composed of collagen
 Chapter 31A:  Tendon Vascularity and Gliding, Island and Free Vascularized Transfers 325

A A

B B

Figure 31(A)-1  A, Traction on the paratenon that shows Figure 31(A)-3  Multifibrillar framework, microvacuoles
tendon surface and fibrous tissue. B, Fiber networks inside inside the sliding system. Illustrates the microvacuole filled
the sliding system between the tendons. with components (e.g., glycosaminoglycan and framed by
collagen types I and III).

fibers. This approach to tendon physiology also sup-

Figure 31(A)-2  Histological and collagenous continuity
between the epitenon and sliding system.
poses a completely different way of perceiving the
problem of reconstruction. These observations demon-
strating the real histological continuity between the
paratenon, the common carpal sheath, and the flexor
tendons illustrate the perfect vascularization of this
functional ensemble. The observations introduce a new
concept: the sliding unit, composed of the tendon and
its surrounding sheaths. Further functional detail of this
sliding unit includes (1) a tendon only has optimal
functional value when it is surrounded by its original
sliding sheath and its vascular heritage; (2) a tendon is
adherent only when it is artificially separated from its
own sliding sheath, or when the harmony between the
tendon and the sheath has been interrupted; and (3) a
tendon is only one of the elements involved in the
transmission of force through the sliding unit.
326 Section 3:  Secondary Flexor Tendon Surgery

A B

C D
Figure 31(A)-4  A and B, Sliding unit composed of flexor tendon, common carpal sheath (zone 3), and mesotendon
(branches of the ulnar artery inside). C and D, Movement of the MCVAS during tendon gliding.

For zones 3, 4, and 5, the author set out to define a
different role for the tendon in the production and
transmission of a force. The tendon is not purely a
transmission belt acting in the carpal sheath surrounded
by a virtual space, nor is it a tissue that is avascular or
only very slightly vascularized. The tendon is nourished
by its own vascular system. Due to existence of the
MVCAS, the tendon is extensively linked to its sur-
rounding structures in these areas, including sheath in
zone 4. The MVCAS lies above the tendon and exerts a
major role of tendon vascularization with peritendinous
tissues.
Basic Principles for Our Methods
of Tendon Reconstruction
The idea is to transfer en bloc a digital flexion unit
composed of the flexor tendon with the sheaths from
zones 3, 4, and 5 to zones 1 and 2 at a single stage. The
author uses this technique for the reconstruction of
finger flexor tendons with Boyes grade 3 and 4 presenta-
tions.13,14 These patients include those with restricted
passive motion in the proximal interphalangeal (PIP)
or distal interphalangeal (DIP) joints even after a period
of elastic traction (grade 3) and those with all possible
complicating factors such as major soft-tissue damage,
joint stiffness, poor vascularization, and trophic changes
(grade 4).
The theoretical bases for this technique are that the
tendon can be conceived as vascularized and that the
tendon is an element of a highly complex sliding and
functional unit in association with its surrounding
sheaths (Figure 31[A]-4).
In developing this technique, the author sought to
answer following basic questions: (1) Which sliding
structures should be used to replace zone 1 and 2
tendons? The mesotendon and its vascular branches
provide good vascularization of the flexor tendon and
the sliding carpal sheath both extrinsically and intrinsi-
cally. The structure thus transferred is a real sliding struc-
ture which already exists naturally in zones 3, 4, and 5.
(2) How will the replacement flexion structure be vas-
cularized? Vascularization is ensured by a preretinacular
mesotendon with branches arising from the ulnar artery.
At the inferior third of the wrist, just before the flexor
retinaculum or the annular ligament, the latter has
two or three branches of around 1 mm in diameter.
 Chapter 31A:  Tendon Vascularity and Gliding, Island and Free Vascularized Transfers
These branches pass through the common carpal sheath
toward the superficial flexor tendons, especially those
of the middle, the ring, and the little fingers, through a
fine transparent mesotendon acting as a mesentery con-
necting the tendons. This vascular supply to the flexor
system and the common carpal sheath is distal to the
tendon–muscle junction, thus allowing harvesting of
retrograde island transfers of purely tendinous struc-
tures without muscles. (3) How will the sliding unit be
positioned in zone 2? For reversed vascularized tendon
transfer, only the ulnar artery–based pedicle is suitable
owing to its distally based palmar point of rotation and
to its branch transmission at the level of the tendon.
Since there are many clinical circumstances and forms
of tissue destruction, this surgical technique has been
developed over time to include a wide range of variants
(Figure 31[A]-5).
Anatomical Features of the Ulnar
Artery–Based Pedicle Flap
In the distal forearm, the ulnar artery runs parallel to
the nerve between the flexor carpi ulnaris (FCU) tendon
laterally and the flexor digitorum superficialis (FDS)
tendons of the fourth and fifth fingers medially. Covered
only by skin, subcutaneous fat, and the superficial fascia,
this artery is relatively superficial in the lower and
middle compartments. However, in the upper compart-
ment, the cutaneovascular relationships are less clear
and the raising of a reverse island flap is thus more
problematic. Cutaneous vascularization is ensured by a
series of two to four small pedicles linked to the main
pedicle through the fascia. The vessels are about 1 cm
long and 1 to 3 mm in diameter. Since the small pedi-
cles lie 15 to 25 mm apart, each flap usually contains at
least two pedicles of good quality. In all our patients,
the anatomic presentation was constant, both topo-
graphically and with regard to vascular distribution
(Figure 31[A]-6). The anterior compartment of the
forearm is drained by two venous systems, the venae
comitantes of the ulnar artery and the superficial system,
whose veins are of larger diameter. Both systems have
abundant anastomotic networks, which make it easy to
raise both free and pedicle flaps.
OPERATIVE PROCEDURES
Vascularized FDS Tendon Graft Based on the
Ulnar Artery: Essential Procedures
The basic procedure consists of the transfer of the FDS
tendon of the ring finger to repair tendon defects of the
other fingers. Preoperative evaluation includes Allen and
Doppler tests to ascertain that the radial artery provides
adequate blood supply to the hand. Angiography of the
arm is also advisable. A bayonet-shaped incision is first
traced and then made on the medial side of the forearm,
the axis of the incision overlying the lateral border of
327
the FCU tendon. The ulnar artery is dissected, and all
its branches are carefully separated and divided. First,
the cutaneous branches between the ulnar artery and the
skin are carefully isolated. The branches emerge from
the volar aspect of the pedicle and are major compo-
nents of the ulnar forearm flap. These branches should
be divided only when skin transfer is not required. The
ulnar pedicle is then separated from the ulnar nerve on
its dorsal aspect along its whole length from the lower
third of the forearm to Guyon’s canal. On the posterior
aspect of the artery, the branches to the ulna are then
identified. The branches on the anterolateral side emerg-
ing just proximal to the Guyon’s canal are those supply-
ing the common carpal sheath and the flexor sliding
system. These small branches emerge from the ulnar
artery and go into the common carpal sheath and the
multi-microvacuolar absorbing system. The vascular
branches and fibrous tissues act as a mesentery, i.e.,
mesotendon, a mobile structure 2 cm long.
A mesotendinous structure composed of the FDS
tendon of the ring finger is then raised with the carpal
sheath and its vascular connections from the ulnar
artery (Figure 31[A]-7). These connections, usually
comprising two or three small branches on the antero-
lateral side and measuring on average 0.2 to 0.5 mm
in diameter, are found just proximal to the proximal
edge of the flexor retinaculum. At the level of the A1
pulley, the FDS tendon is transected proximal to the
decussation after forceful traction on the tendon, avoid-
ing laceration of the vinculum longum of the flexor
digitorum profundus (FDP) tendon. The ulnar artery is
then ligated proximally. All the other branches of the
ulnar artery to the deep arch division are ligated to
obtain a rotation point at the level of the deep branch.
The MVCAS surrounding the tendon is kept in place,
thus ensuring a real vascular connective link around the
tendon. A composite mesotendinous unit of 20 cm long
is then raised.
The sliding unit is transferred to the distal part of the
hand to provide a complete flexor tendon unit from the
finger tip to the wrist. The transferred tendon unit is laid
into the zone 2 and is passed under the A2 and A3
pulleys. These pulleys must be carefully preserved or
reconstructed if necessary, since the tendon transfer
exposes them to much greater force than a simple
tendon graft does. The pulley system often presents a
difficult problem. We prefer to use the remaining parts
of pulleys. Sometimes, the preserved pulleys are too
narrow and require careful dilatation. It is better to
rebuild a pulley than to keep one if the transfer and its
blood supply are compromised.
The distal junction of the grafted tendon is achieved
by inserting the graft tendon into the distal phalanx
with a “barbed wire” suture. The proximal junction with
the distal stump of the relevant FDP tendon is per-
formed using Pulvertaft repair. The tension on the suture
328 Section 3:  Secondary Flexor Tendon Surgery

Middle Ring

Flexor
digitorum
superficialis
(FDS)
tendon

Ulnar
artery
Ulnar
Flexor digitorum artery
superficialis (FDS)
of the ring finger
A B

Flexor digitorum
superficialis (FDS)
tendon

Ulnar
artery

C D
Figure 31(A)-5  Transfer of a sliding flexion unit composed of a flexor tendon and surrounding sheath as a reverse island
pedicle graft. A, Identification of mesotendon around the FDS tendon of the ring finger. B, Section of FDS tendon of the ring
finger and ulnar artery. C, Insertion of the grafted tendon into the middle finger. D, Completion of the transfer and tendon
junction placed outside zone 2.
 Chapter 31A:  Tendon Vascularity and Gliding, Island and Free Vascularized Transfers 329

Radial rotation
Flexor digitorum point
superficialis

6 cm

Skin

Ulnar Ulna
artery Ulnar rotation Ulnar straight
A B point line continuity

C D
Figure 31(A)-6  A, Various vascular branches emerging from the ulnar artery proximal to entrance to Guyon’s canal. B, The
ulnar artery forearm flap has a very distal rotation point, the graft can be used to repair the distal part of the hand. Radial
forearm flap does not have a distal rotation point, not fitting distal finger repair. C, Vascular branches running from the ulnar
artery to the FDS tendon. D, Mesotendon and its vascular connections to the ulnar artery act as a mesentery.

should be slightly overcorrected in comparison with the
other fingers. The whole procedure takes about 3 hours:
1 hour for finger dissection and preparation, 1 hour
for raising the transfer and 1 hour for insertion and
closure.
On completion of the procedure, a dynamic Kleinert
splint is applied to allow early movement, which is
indicated in the cases with flexor tendons or pulleys
reconstruction but without skin problems and where
mobilization can intervene early.
FDS Tendon Transfer to Reconstruct the FDP
Tendon With an Intact FDS in Another Finger
This procedure was first attempted after much reflection
and with good experience of the basic procedure
obtained in 30 cases. There is no fundamental difference
in the dissection and the donor elevation. The most
difficult part is to respect the FDS tendon in the recipi-
ent site and the chiasma of Camper. Because the two
tendons are squeezed together, the presence of the A1
and A2 pulleys sometimes make the procedure difficult.
Delay between injury and reconstruction seems to cause
progressive narrowing of the pulleys. The pulleys may
be widened by mechanical manipulations, avoiding
rupture, but this maneuver is not easy. Otherwise, surgi-
cal pulley reconstruction is mandatory. Our functional
results obtained to date have been good and very often
excellent. Under good patient conditions, the results are
much better than with a tenodesis or an arthrodesis.
Combined Island FDS Tendon and Palmaris
Longus Tendon Transfer for Tendon and
Pulley Reconstruction
For a long time we used the Weilby procedure for pulley
reconstruction. However, the idea arose of using the
palmaris longus as another vascularized tendon on the
same mesotendon as the FDS. The palmaris longus is
transferred together with the FDS. Like the Weilby pro-
cedure, we use this method with a periosteum wedge
suture as cross lacing from A1 to A4 pulleys. Before
suturing, the smooth sliding of the transferred tendon
has to be checked.
330 Section 3:  Secondary Flexor Tendon Surgery

C
D
Figure 31(A)-7  A, The mesotendon and branches of the ulnar artery to the FDS tendon and sectioning the FDS proximal to
the Camper’s chiasma. B, After tendinomuscular section and before ulnar artery section. C, The flexion sliding unit is created.
D, The unit is moved distally and the sliding unit is grafted to the recipient finger.

Composite Flexor Tendon and Skin
Flap Transfer
Combined transfer of vascularized flexor tendon and
skin flap allows surgeons to treat skin problem and to
reconstruct the tendon at the same time (Figure 31[A]-
8). In the lower third of the forearm, the ulnar artery
sends branches not only to the FDS tendons but also to
the skin. These branches are easily identified, being
close to the mesotendon branches and constantly of
excellent caliber, allowing simultaneous composite
transfer of the skin and tendon.13-15 Slight upward trac-
tion on the internal edge of the flap reveals the small
vertical vessels arising from the ulnar artery to the skin.
After identifying the skin flap pedicle, the flap is dis-
sected (Figure 31[A]-9).
The second step is dissection of the ulnar artery and
identifying the mesotendon branches. Generally, the
skin flap lies proximal to the mesotendon. However,
thanks to the flexibility of these cutaneous branches, the
flap can be rotated for 180° and positioned on the
digital surface, but the tendon can be placed at its physi-
ological orientation due to flexibility of mesotendon.
The skin is closed tension free, providing good healing
without skin disunion or necrosis. This is of fundamen-
tal importance for achieving a good functional result.
Based on author’s experience, the operation is reli-
able, with almost complete absence of complications.
The anatomy of ulnar artery is constant, with at least
one good-sized artery found in all the patients. The flap
has 360° mobility around a rotation point in the palm,
which makes the entire skin surface of the hand acces-
sible. This is not the case with the radial forearm flap.
Tissue quality is excellent, being fine, fat free, and virtu-
ally hairless. There are no serious consequences at the
donor site. The scar on the forearm is usually very fine
and not hypertrophic. The technique allows for further
developments such as sensory innervation by means of
the medial cutaneous branches of the ulnar nerve.
 Chapter 31A:  Tendon Vascularity and Gliding, Island and Free Vascularized Transfers 331

Figure 31(A)-8  Transfer of a sliding flexion unit composed of a flexor tendon and a skin flap. A, Mesotendon and skin
branches identification. B, Section of FDS tendon to the ring finger and ulnar artery. The tendon and ulnar artery flap are
isolated. C, Tendon junction outside of the zone 2 and digital skin coverage with the flap.

This procedure is indicated in cases with significant
contracture of the skin on the palmar aspect of the digits
after multiple surgical procedures. A plain skin graft
cannot solve this problem. In some cases where the
overlying skin is extremely scarred and of poor quality,
it would be impossible to replace the flexor tendon
underneath and achieve early motion. Skin of this sort
inevitably breaks down or necroses, compromising
the functional result, so it should be replaced (Figure
31[A]-10). The solution is to perform a safe skin flap
transfer together with tendon reconstruction, thereby
making early motion possible.
332 Section 3:  Secondary Flexor Tendon Surgery

A B

C D
Figure 31(A)-9  Rising of the composite flexor tendon and skin flap island transfer for tendon repair and digital palmar
resurfacing. A, Outline of the skin flap incision based on the lateral edge of the FCU tendon. B, Identification of the fascia
connection to the tendon before cutting the ulnar pedicle. C, Owing to plasticity and distal rotation point of the ulnar pedicle,
the graft can be easily placed to the finger. D, Skin resurfacing is completed in the same time of the tendon reconstruction.

The wide variety of composite flap transfer is made
possible by the ulnar artery at the lower third of the
forearm, which offer a solution to a large number of
clinical cases and meet varied surgical reconstructive
requirements. For example, it is possible to perform a
double skin flap with one or two flexor tendon transfers,
or a skin flap with a flexor tendon for reconstruction
and a palmaris longus as an island transfer for pulley
repair. It is also possible to add a bone transfer at the
same time (Figure 31[A]-11).
RESULTS AND DISCUSSION
It is almost impossible to evaluate the results of tendon
reconstruction operations by any statistical method. There
are so many variables; e.g., the type and extent of the
injury, the age of the patient, the accompanying injuries
of nerves and vascular structures and the procedures
used—that only general conceptions, based on experience,
can be used. Tendons in the fingers are the most difficult
to repair.
Joseph H. Boyes16
This statement remains true. The influences of aspects
of the patient’s life such as their psychological profile,
smoking, socioeconomic status, and desire for future
employability have an impact on functional outcome.
All of these factors must be taken into consideration in
determining the aim of reconstruction, in choosing
these procedures and result evaluation.
Many systems of evaluation have been proposed. We
use the modified Strickland’s criteria.17 Nevertheless,
the arithmetical addition of degrees between extension
and flexion compared with the hypothetical maximum
amplitude, while not distinguishing between metacar-
pophalangeal (MCP) joint and PIP or DIP joints, would
seem debatable for this sort of salvage situation. A
significant alteration of MCP joint movement only
rarely occurs. Clearly in such cases, the principal aim
is to restore effective and useful function, including
grip, and especially to achieve recovery of good PIP
joint movement. For heavily damaged fingers, too many
unfavorable factors are present and it is not possible
achieve a full recovery. The patient should be informed
of incapability of full recovery preoperatively. More
 Chapter 31A:  Tendon Vascularity and Gliding, Island and Free Vascularized Transfers 333

A B

C D
Figure 31(A)-10  A and C, Results of two cases of palmar skin contracture and loss of flexor tendon function. B and D, Skin
resurfacing with a composite flexor transfer and skin flap.

importance should also be given to preoperative skin
condition.
We treated 75 patients with Boyes grade 3 and 4
injuries, all previously operated on at least twice. Our
strategy was determined by the skin quality primarily.
Since mobilization is early (3 days postoperatively), it
is mandatory to avoid skin dehiscence or necrosis. In
these circumstances, we use a composite skin and flexor
tendon transfer.
Our patients were divided into three groups: (1) 18
patients, including 13 grade 3 and 5 grade 4 patients in
whom FDS tendon transfers were used; (2) 17 patients
in whom only the FDP tendon was injured with intact
FDS tendon were repaired by islanded FDS transfer; and
(3) 40 grade 4 patients, needing flap transfers due to
either major skin retraction, due to presence of a skin
defect or skin stiffness together with vascular or nerve
problems.
Group 1
There were 5 excellent (4 grade 3, 1 grade 4, 27.8%); 7
good (6 grade 3, 1 grade 4, 38.9%); 4 medium (2 grade
3, 2 grade 4, 22.3%); and 2 poor (1 grade 3, 1 grade 4,
11.1%) results (Figure 31[A]-12). Improvement was
achieved in 66.5% of patients. The fair and poor results
were mainly due to healing problems during early
mobilization inducing pain and inflammation and
requiring dressing. We now prefer to add a skin flap in
order to reinforce cicatrization, even if slight revision
under local anesthesia may be required several months
later.
Group 2
We began to have this group of patient 10 years after
group 1. With the experience gained, the technique was
extended, to be indicated in young subjects, such as
rugby players. Nevertheless, the technique is extremely
intricate and is indicated only in young subjects capable
of following stringent rehabilitation. We had 17 cases:
7 excellent (41%), 7 good (41%) and 3 poor, including
2 who preferred not to have joint arthrodesis after inter-
vention. A useful range of motion was obtained in 80%
of cases (Figure 31[A]-13).
Four cases (23. 5%) required tenolysis, which revealed
the excellent state of the transferred tendon. Any adher-
ences found were always located around the tendinous
anastomoses. After tenolysis, 4 fingers obtained 2 excel-
lent and 2 good results.
Group 3
Forty patients were analyzed. There were 1 excellent
(2.5%), 26 good (65%), 5 fair (12.5%), and 8 poor
334 Section 3:  Secondary Flexor Tendon Surgery

Figure 31(A)-11  Several types of combined

transfers of multiple tissues. A, Transfer of multiple
flexor tendons. B, Transfer of double flexor tendons
and double skin flaps. C, Combined skin flap,
island FDS tendon transfer, and grafting palmaris
longus (PL) tendon for flexor pulley reconstruction.
D, Composite skin flap, flexor tendon, and bone
transfer. We called above types of combined transfer
as “ulnar trail.”

Two flexor tendons Skin flap

Flexor digitorum
superficialis (FDS)
tendon Skin flap
Palmaris
longus (PL)
tendon

Skin flap
Bone

(20%) results (Figure 31[A]-14). The results show that
67.5% of these extreme salvage flexor tendon situations
were greatly improved. The technique also produces
favorable trophic changes. Finger skin becomes more
supple and sensitive, joints are less stiff and are mechan-
ically active, and flexion is improved.
Overall, 42 patients (66.6%) achieved an excellent,
good result compared to an average of 55% in series
where similar cases are operated using the two-stage
procedure with or without a silicone rod. However, in
this particular field, precise evaluation of results is a real
challenge, and in many previous publications results
 Chapter 31A:  Tendon Vascularity and Gliding, Island and Free Vascularized Transfers 335

GROUP 1: 18 CASES

Poor
11.1%

Excellent
Fair 27.75%
22.25%

Good
38.9%

B
A
Figure 31(A)-12  Functional results of the flexion system transfer.

GROUP 2: 17 CASES

Excellent
41%

Poor
18%

Good
41%

B
A
Figure 31(A)-13  Results of the flexion system transfers for cases of the FDP tendon disruption with an intact FDS.

GROUP 3: 40 CASES

Excellent
2.5%

Poor
20%

Fair Good
12.5% 65%

B
A
Figure 31(A)-14  Results of combined flexor tendon–pulley and skin flap transfer.
336 Section 3:  Secondary Flexor Tendon Surgery
have been evaluated by different methods, rendering
true comparison difficult, if not misleading. What is
sure is this new technique seems to give better func-
tional performance and reduces time lost from work.
The new technique using a mesovascular tendon
transfer unit, which is now our standard procedure for
Boyes grade 3 or 4 cases, is likely to set the trend for
flexor tendon surgery because the requisite tendon
reconstruction can be carried out in one operation.
Compared with other techniques, the advantages of this
technique are as follows. It makes use of a living tendon
islanded on a thin mesotendon with vascular branches,
providing a perfect blood supply to all areas both extrin-
sic and intrinsic. It thus avoids adhesions and improves
the vascularity of the surrounding tissues. Since the graft
is a vascularized flexor tendon, rather than a simple
avascular graft, it retains its flexibility, pliability, and
resistance and allows the correct tension to be achieved.
The MVCAS and the carpal sheath retain the unrestricted
gliding movement of the tendon. The grafted tendon is
approximately 18 to 20 cm, which can be used to recon-
struct flexor tendon defect from the pulp to the carpal
area. All the damaged pulleys have to be reconstructed
because the traction exerted by this type of tendon is
greater. The vascular supplies to the tendon are anatomi-
cally constant. Because of the very distal rotation point
and the plasticity and versatility of the mesotendon, the
flap transfer is performed in the same way as a classic
reverse-flow radial or ulnar forearm flap.
It should be noted that the radial forearm flap does
not allow transfer of the common carpal sheath and the
flexor tendon because the radial artery supplies them
only at the myotendinous level and its point of rotation
is too proximal. The composite flap and tendon transfer
described here are confined to the ulnar vascular system.
The main disadvantage is the need to transect the
ulnar artery. However, in our experience of 629 cases of
a variety of ulnar artery–based flaps, no serious long-
term effects such as paresthesia or functional deficits
have been encountered.
These procedures described in this chapter have now
become routine practice in the author’s unit. Our experi-
ence indicates that they are safe, technically feasible, and
above all provide practical solutions to problems that
often led to amputations or arthrodesis in the past. Only
one patient requested an amputation since he was
unable to carry plasterboard panels owing to a problem
with his index finger.
Nevertheless, the functional outcome of our patients
has not improved in the past 15 years. The good or
excellent rates are still the same as they were then.
Factors influencing the outcome go far beyond the
purely technical or surgical. Such concerns exist as to
skin tissue quality of the patient, whether pain or edema
is present, and the duration of the postoperative edema-
tous phase. Other factors affecting the outcomes are
the patient’s own will and the skills of the therapist.
Smoking appeared to be a major factor to worsen the
outcomes.
Regrettably, in the earlier years, we did not perform
vascularized flexor tendon grafting during a tenolysis,
when the tendons were found continuous but of poor
quality. Some tendons ruptured one day after surgery.
It is also regrettable that such procedures were not
performed in patients with poor tendon conditions
such as dehiscence. From 1996, the author changed
the approach, and now performs composite skin and
tendon transfers more often. It led to good results. The
composite skin flap allows surgery to be done under
good conditions and facilitates immediate rehabilita-
tion, which is a major advantage. Sometimes a later
tenolysis may still be required. However, the psychologi-
cal impact is very positive in our patients. Rehabilitation
can be begun immediately after surgery.
FUTURE CHALLENGES: PROCEDURES
USING OTHER GRAFT SOURCES
Our experience in the more recent years using vascular-
ized flexor tendon autotransplants from the toes and
homotransplants (allografts) suggests some applicable
procedures. In the author’s unit, the transfer of flexor
mechanism of the second toe was performed in six patients
to repair the digital flexor tendons, sheath, and palmar
plates in a single operation. On the donor site, the
tendon is approached through a plantar incision from
the medial side of the second toe to the mid plantar
area. The plantar fat is retracted and the plantar aponeu-
rosis is transected, exposing the second toe flexor system
and its vascular network. Attention should be paid to
several anatomical points: (1) The flexor sheath of the
second toe is shorter than the second, third and fourth
digital flexor sheaths in the hand by 15% on average,
while it is longer than the fifth digital flexor sheath (by
5%); (2) the metatarsophalangeal (MTP) plate is wider
and thicker than the MCP joint plate; and (3) the A3
pulley is more developed in the toe flexor sheath.
The vascular type is identified and the composite
tendon flap is harvested from distal to proximal. The
vascular supply of the toe flexor system depends on the
medial collateral digital artery, which is a terminal
branch of the first common plantar digital artery, a
branch of the medial plantar artery. Venous drainage is
from its comitantes veins.
There are two different anatomic types. In type I,
which is present in 50% of the cases, the second toe
medial collateral artery arises directly from the first
common plantar digital artery, giving a long vascular
pedicle. In type II (i.e., the other 50% of cases), the
second toe medial collateral artery arises from the
medial branch of the medial plantar artery beneath
the big toe flexor tendon and has a short vascular
pedicle. Dissection is performed under the periosteum,
 Chapter 31A:  Tendon Vascularity and Gliding, Island and Free Vascularized Transfers 337

FDS

Vascular pedicle
Type I FDP

A B

C D
Figure 31(A)-15  Free vascularized transfer of flexor tendon system from the big toe. A, Lack of flexion of the index finger.
B, Flexor tendons and pulleys harvested from the toe. C, Flexor tendons and pulleys transferred into the index finger.
D, Flexion of the finger 1 year after surgery.

elevating the whole flexor toe system with the two
tendons, flexor pulleys and the three plantar plates with
their vascular supply. The flexor tendons are transected
as far as required for the tendon defect in the hand and
the vascular pedicle is freed as far as possible depending
on the anatomical type. Finally, the skin of the donor
site is closed directly.
The freed tendon flap is then deployed over the recip-
ient digit. Some surgical adjustments may be required
to adapt the flap to its recipient site. For example, lateral
resection of the MTP plate may be needed to narrow it,
or full circumferential incision of the flexor tube on the
cruciform pulleys to lengthen it and to fix the A2 and
A4 pulleys exactly in their most functional positions.
The digital sheath is secured laterally to the fibrous
bundles by two continuous non-absorbable sutures. The
annular pulleys should be fixed in their anatomical
position. The distal stump of the FDP tendon is secured
with a Kleinert suture and protected with a barbed
wire for 4 weeks. Meanwhile, the proximal FDS and
FDP tendon stumps are repaired with the Pulvertaft
technique. The tendons are sutured with adequate
tension, the digits in a cascade position. The second toe
free flexor tendon flap is the only one-step procedure
for reconstructing complex digital flexor tendon defects
anatomically, dynamically, and functionally.
Six patients underwent above operations. All started
physiotherapy the day after the operation with the
Duran protocol. Four had recovery to good (2 grade 3,
2 grade 4, 66.6%), 1 fair (1 grade 4, 16.6%), and 1 poor
(1 grade 4, 16.6%). No patients complained about the
foot scar (Figure 31[A]-15).
Vascularized tendon homograft (allograft) provides
another source of donor tendon.18,19 Introduction of
cyclosporine in 1980 changed the indications and
improved success rates in tissue allograft with the use of
low, nontoxic maintenance doses for the relatively weak
antigenic response organs. The author’s team performed
a vascularized tendon allograft in patients based on the
previous experience of vascularized tissue transfers.20
To harvest the tendon, the arm is placed in abduction
to facilitate cooperation with other surgical teams. A
338 Section 3:  Secondary Flexor Tendon Surgery

tourniquet is applied to the upper arm just before aorta

clamping. While the heart, liver, and kidney are removed
by other surgical teams, the author’s team harvested the
flexor tendon from the forearm. Above procedures may
take more than 2 hours.
The ulnar artery and its branches nourishing the
tendon are identified in the forearm. The FDS of the ring
finger is dissected at the tendon–muscle junction. All
the branches of the ulnar artery nourishing the tendon
as well as adjacent mesotendon are carefully preserved. A
The superficial palmar arcade is then clamped and tran-
sected distally to the third common palmar digital artery,
preserving the two collateral arteries inside the donor.
The functional unit composed of the FDS and FDP
tendons and all the pulleys is then separated from the
phalanges through a medial approach. Dissection is per-
formed under the periosteum over the phalanges, but
the flexor sheath is not opened. The radial side of the
ring finger is similarly dissected. Upon completion of
above dissections, the only remaining link between the
structure to be transplanted and the donor’s hand is the
ulnar artery. The tourniquet is then released. The super- B
ficial veins of the forearm are used for venous drainage.
The ulnar artery is ligated proximal to its branches sup-
plying the harvested skin. The transplant is placed in a
sterile plastic container filled with serum at 4°C.
The donor tendon is brought to the recipient patient
to repair tendon defects in the digits. The proximal parts
of the grafted FDS and FDP tendons are passed under
the superficial palmar arch of the recipient hand and is
sutured to the distal end of the recipient tendons with C
a Pulvertaft method. The ulnar artery of the donor is
connected to that of the recipient with an end-to-side Figure 31(A)-16  Free vascularized flexor tendon
anastomosis. The superficial veins of the donor are also allografting. A, Loss of flexion of the ring finger before surgery.
B, Harvested allograft. C, Finger flexion 1 year postoperatively.
anastomosed with recipient anterior forearm veins.
Total ischemia time is 3 hours.
SUMMARY
In these patients, the swelling abated little by little
after surgery, and good functional results were obtained The use of vascularized tendon grafts nourished by ulnar
4 months later. One patient had a passive flexion of 80° artery through mesotendon, with all gliding surfaces
in the PIP joint without extension defect, and passive intact, provides new methods to reduce adhesions and
flexion of 55° in the DIP joint with an extension deficit has the added merit of being a one-stage procedure.
of 35° (Figure 31[A]-16). The average total active These types of vascularized tendons or tendon and flap
flexion almost equaled the range of passive motion. This transfers are indicated in secondary reconstruction and
finger is now very functional and fully adapted. The can be expected to offer effective options for tendon
merit of the procedures is to reconstruct all the pulleys, reconstruction. Transfer of vascularized flexor tendon
to keep the digital sheath intact, and to avoid adhesion system from the toes or homotransplants of the digital
formation. flexor tendon are additional sources of tendon grafts.

References
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 B Physiotherapy After Vascularized
Tendon Transfers
Serge Rouzaud
OUTLINE
As is the case with all physiotherapy following repair
of the flexor tendon, the return of satisfactory active
motion amplitudes, in flexion as well as in extension,
requires a specific physiotherapy program. The therapy
must be modified in different postoperative periods
with emphasis of different exercises. This chapter
describes specific day-by-day therapy regimens that are
used in the cases of vascularised tendon transfer. Such
therapy must respect not only the recipient digit and
its vascular anastomoses, but also the donor digit, so
that function of the donor and recipient digits is
restored as much as possible.
Physiotherapists are confronted with new surgical
methods of flexor tendon reconstruction with vascular-
ized tendon transfers.1 This technique provides a last
resort solution to salvage a nonfunctional finger. At this
stage, the patient has had a long history of time-
consuming treatment, which has often not only kept the
patient from professional activities but also greatly
reduced the ability to perform day-to-day tasks. This last
resort solution is proposed at the end of a long treat-
ment, often after amputation of the finger has been
evoked; therefore, it can represent hope for the patient.
Nevertheless, the risk of lassitude and diminished will-
ingness to participate in the treatment is great. The
medical team should therefore encourage and support
the patient in this ultimate stage of the treatment.
PREOPERATIVE PHYSIOTHERAPY
Physiotherapy starts before surgery for the patients with
complex hand trauma. The therapy is usually applied to
a finger with serious limitation in passive extension and
flexion. The presurgery phase is important to improve
the quality of local tissues and restore passive joint
motion as much as possible. The improvement in the
quality of tissues and joint suppleness obtained in this
phase will reduce “surgical aggression” and create a
proper local status, which would favor improvement of
hand motion and therefore outcomes of the surgery.
340
PHYSIOTHERAPY AFTER SURGERY
Timing
Postoperative physiotherapy starts early after surgery, so
as to limit or at least modulate tendon adhesions due
to scar healing. Physiotherapy must be careful and effi-
cient. This requires perfect knowledge of the kind of
surgery, the methods of tendon repair, and the pulleys
that may have been rebuilt. The physiotherapist must
have a thorough knowledge of physiopathology of the
tendon so as to ensure the quality of the work.2 The
physiotherapist should ensure sufficient therapy to
improve the results but avoid being too aggressive,
which could cause disruption or diastasis at tendon
junctions that hampers the result.
Three Phases of Physiotherapy After Surgery
The surgical technique consists of the transfer of a vas-
cularized sliding unit to favor intrinsic healing. The
proximal and distal tendon junctions are situated in
zones 1, 3, or 4, which are deemed “safe” and may
shorten the period of putting the tendon in rest position
and favor active flexion exercise. The protocol that we
have made for vascularized tendon transfer comprises
three stages: days 0 to 21, days 21 to 45, and after day
45, governed by the periods of tendon healing. Days 0
to 21 represent the most important stage. In this stage,
the therapy determines the final result by limiting adhe-
sions arising from extrinsic healing and favoring intrin-
sic healing.
Splinting and Joint Positions
Within the first 72 hours after surgery, a modified Klein-
ert splint is applied (Figure 31[B]-1). The wrist is set at
the neutral position, metacarpophalangeal (MCP) joints
are set in 60° flexion, and the interphalangeal (IP)
joints are set at flexion between 0° and 10°.3 The trac-
tion is anchored in distal part of the nail distally and
runs under a pulley, which allows a flexion of three
digital joints (MCP and proximal and distal [PIP and
DIP] joints). The friction forces against the pulley are
limited by a nylon thread tethered to a rubber band
below the pulley. The tension of the rubber band must
 Chapter 31B:  Physiotherapy After Vascularized Tendon Transfers
60°
0°
Figure 31(B)-1  Modified Kleinert splint with a palmar
pulley.
Figure 31(B)-2  Active extension against the rubber band.
be as weak as possible, yet still able to bring the finger
into full flexion (see Figure 31[B]-1). The wrist at
neutral position allows the proximal tendon junction
site to move and glide, favoring forming gliding surfaces
between the tendon and surrounding tissues.
Once the splint is applied, the patient carries out 10
active extensions an hour, with a passive return to
flexion by tension of the rubber band, and 10 active
flexions of the wrist with return to extension as far as
the splint allows, so as to favor gliding of the different
tissues and to disrupt adhesions (Figure 31[B]-2 and
31[B]-3). The active extension should not be forcefully
against the splint.4 The patient relaxes during active
extension to reduce resistance. Edema and dressings are
reduced to lower resistance to extension.
341
Figure 31(B)-3  Passive flexion with the rubber band force.
Methods of Physiotherapy
In the first phase we aim to reach following goals at day
21: (1) passive flexion of the MCP, PIP, and DIP joints
back to normal, (2) normal extension of the IP joints
or at least limited to a 20° flexion, and (3) active flexion
from 0° to 60° on the PIP joint and from 0° to 20° on
the DIP joint.
In this phase, we perform daily physiotherapy: (1)
Prevention of edema. Edema is a factor favoring tendon
adhesions and articular ligament retractions. Measures
to prevent edema must start as soon as possible after
surgery, such as elevation of the upper limb and mobi-
lization of adjacent digits.5,6 (2) Passive mobilization.
Passive mobilization keeps the joints mobile, and these
exercises also allow differential FDS and FDP tendon
motion in case the FDP is rebuilt with an intact FDS
tendon. It is important to maintain the MCP joints in
extension while the IP joints are flexed (Figure 31[B]-4).
(3) Active mobilization. Surgeons and physiotherapists
should decide together whether to undertake active
motion according to strength and quality of tendon
junctions. The Pulvertaft method of proximal junction
and distal reinsertion by pull-out technique appear to
be reliable in strength. Protected active flexion was
advocated by Rouvillois7 and Bellemère.8 The place-and-
hold is exercised and the amplitude of active digital
flexion is gradually increased. Place-and-hold exercises
are less aggressive and are often easily achieved by the
patient. This exercise may avoid resistance during move-
ment. When a tendon is transferred to a finger with an
intact FDS, differential motion of two tendons needs to
be practiced (Figure 31[B]-5). Between day 8 and day
15, the tendon is weak and the exercises are fewer.
342 Section 3:  Secondary Flexor Tendon Surgery
Figure 31(B)-4  Passive PIP joint flexion of the finger with
the transferred tendon.
Figure 31(B)-5  Place-and-hold IP joint flexion with MP
joint extension.
Reconstructed pulleys must be protected during
active finger flexion by positioning the fingers of the
physiotherapist correctly over these pulleys to reduce
the tension.9 The protection with Elastoplast rings is
risky because of precarious skin healing. Their tourni-
quet effect may damage vascular supply of the flap.
The donor finger, usually the ring finger, must be
included into active flexion exercises. Removal of the
FDS may cause adhesions of the intact FDP tendon of
this finger, which should be avoided. If extension deficit
of the donor finger is present, a Velcro strap is installed
to place the finger in intrinsic plus position to correct
the extension deficit.
The tendon motion by means of tenodesis effect is a
useful method.10 Active wrist extension favors passive
flexion of the fingers and vice versa. The patient should
be relaxed to reach maximum efficiency during exercise.
This exercise does not stimulate FDP tendon gliding on
the FDS, but the FDS tendon is not present in most
instances of this type of tendon reconstruction. The dif-
ferential motion should be exercised every day.
It is noteworthy that development of flexion contrac-
ture of the joint after these surgical reconstructions,
especially at the DIP joint, is very likely under rubber
band traction. Lack of extension of the finger up to
about 60° may be observed very early, which is difficult
to correct if not taken care of. When a flexion contrac-
ture of more than 20° is present in the PIP and/or the
DIP joints, we modify the splint as early as day 15 after
surgery. The rubber band is temporarily withdrawn and
a Velcro strap is made setting the finger in an intrinsic
plus position. The strap is gradually tightened by the
patient to increase joint extension. The rubber band is
re-positioned every hour to achieve a series of 10 active
extensions with passive return to flexion. Between day
21 and day 45, the splint is removed during the day time
and the joint is gradually allowed to actively move, but
the splint is kept at night. If active flexion of the finger
can be easily achieved by day 21, we apply the splint
only for 8 more days, but the pull-out suture is kept for
another 10 days.
During the therapy period, passive motion is per-
formed every day. Ample passive motion amplitudes are
always emphasized. The finger extension is also sought,
and usually increases at week 5 or 6 after surgery. Intrin-
sic muscle weakness or contracture may develop and
electric stimulation helps prevent such problems.
After removal of the splinting, exercise of active finger
flexion should be increased. The place-and-hold exercise
is gradually given way and active movement, with no
resistance, is encouraged. During active movement, the
rebuilt pulleys are to be protected. Elastoplast strapping
can be used to protect the pulley with no risk to the
vascularization. Protection to the pulleys is required
until the end of 2 months after surgery. The active flexion
of the donor finger is exercised. Electrical stimulation to
the FDP tendon of the donor finger help build the
strength of digital flexion, we do so as early as week 5.
After day 45, active exercises are increased and the
patient is urged to start all daily activities. To favor the
recruitment of neuromuscular activity, electrical stimu-
lation to the FDP muscle to which the grafted tendon
is sutured is added if there are difficulties in active
flexion of the repaired finger. The site of electrical stimu-
lation must be as specific as possible, entailing adequate
setting of skin electrodes. Exercises that enhance func-
tion of wrist and hand as a whole also begin at this time.
Late Therapy of Extension Deficits
Development of extension deficits is not uncommon,
despite all the measures used in the earlier periods to
prevent finger flexion contractures. In the late stage, it is
often necessary to apply a dynamic extension splint
 Chapter 31B:  Physiotherapy After Vascularized Tendon Transfers
Figure 31(B)-6  The strap is gradually tightened by the
patient as the tissues allow more extension.
(Figure 31[B]-6). Such a splint should be adapted to
the affected joints (usually the IP joints). The splint is
mainly worn at night, as well as during day periods of
two hours in the morning and two hours in the after-
noon if the flexion contracture is difficult to correct. The
splint is kept till obtaining a good-quality extension.
Frequently, this splint should be worn for 4 to 6 months.
However, the splint must not be worn continuously
during the daytime (which some patients are inclined
to do because the splint is better tolerated when they
move than at night when they are at rest). Instead, active
References
1. Guimberteau JC, Panconi B, Boileau R: Mesovascularized
island flexor tendon: new concepts and techniques for flexor
tendon salvage surgery, Plast Reconstr Surg 92:888–903,
1993.
2. Caffinière JY, Simmons BP: Physiologie de la flexion des
doigts. In Tubiana R, editor: Traité de Chirurgie de la Main.
Tome 1, Paris, 1980, Masson, pp 339–411.
3. Kleinert HE: Réparations primitives des tendons fléchisseurs.
In Tubiana R, editor: Traité de Chirurgie de la Main. Tome 3,
Paris, 1986, Masson, pp 198–205.
4. Van Alphen JC, Oepkes CT, Bos KE: Activity of the extrinsic
finger flexors during mobilization in the Kleinert splint,
J Hand Surg (Am) 21:77–84, 1996.
5. Thomas D, Moutet F, Guinard D, et al: Mobilisation posto-
pératoire immédiate des tendons fléchisseurs, Ann Kinésithér
27:338–347, 2000.
343
use of the hand should be encouraged in the intervals
when the splint is removed, so as to render function and
use of the hand, which has already been insufficiently
used for several months or even several years.
In some cases, above measures may not effectively
correct the deficit in extension of the PIP and/or DIP
joints. We then use a series of plaster casts between
physiotherapy sessions. Tubular splint may also be
applied. This technique was originally developed for the
treatment of irreducible flexion contracture accompany-
ing untreated PIP joint sprains. It is extended to the
treatment of irreducible flexion contracture, regardless
of the cause.
Additional Methods
During physiotherapy, classic techniques of circulatory
massages and scar softening must be an integral part
of our work to fight edema and pain, which favor pre-
venting adhesions and joint stiffness. Deep pressure
massage is an excellent adjuvant for the treatment of
skin adhesions and scarring. Silicone gels are advised
when scars are hypertrophic.
It should also be emphasized that during the process
of physiotherapy, we, physiotherapist and patient, must
be patient, and active and regular physiotherapy must
not be limited to the sessions directed by the
therapist.
6. Aoki M, Manske PR, Pruitt DL, et al: Work of flexion after
tendon repair with various suture methods, J Hand Surg (Br)
20:310–313, 1995.
7. Tubiana R: Considerations anatomo-pathologiques et
biologiques. In Tubiana R, editor: Traité de Chirurgie de la
Main. Tome 3, Paris, 1986, Masson, pp 49–61.
8. Rouvillois A, Sifre G, Hu W, et al: Mobilisation en flexion
active protégée associée à la technique de Kleinert, Ann
Kinésithér 19:123–138, 1992.
9. Bellemère P, Chaise F, Friol JP, et al: Résultats de la mobilisa-
tion active précoce après réparation premiers des tendons
fléchisseurs, La Main 3:221–234, 1998.
10. Zhao C, Amadio PC, Momose T, et al: Effect of synergistic
wrist motion on adhesion formation after repair of partial
flexor digitorum profondus tendon lacerations in a canine
model, J Bone Joint Surg (Am) 80:78–84, 2002.
 CHAPTER
32  
EXTENSOR TENDON INJURIES—
PRIMARY MANAGEMENT
Brandon E. Earp, MD, and Philip E. Blazar, MD
OUTLINE
Acute extensor tendon injuries to the hand and wrist
have typically received less attention than their flexor
counterparts. The anatomy of the extensors is para­
doxically more complex and the management of inju­
ries is more varied and corresponds to the anatomical
zone of injury. In this chapter, the anatomy, identifica­
tion, and management of injury based on anatomical
zone are reviewed. Surgical and nonsurgical treatment
of these injuries is discussed, including the indica­
tions. The role of early mobilization after injury and
repair is described.
The extensor tendon system of the wrist, hand, and
fingers is surprisingly complex. The six extensor com­
partments of the wrist and the intrinsic muscles of the
hand comprise 23 musculotendinous units. Open and
closed injuries to these structures are more common
than injuries to the flexor structures and range from very
subtle, seemingly minor traumas to overt complex inju­
ries with failure and/or loss of multiple tissue types.
Failure to diagnose and treat these injuries, including
those in the superficially subtle categories, can lead to
significant loss of motion and function.
The zones of injury have been assigned beginning
distally with odd numbered zones located over the
respective distal interphalangeal (DIP), proximal inter­
phalangeal (PIP), metacarpophalangeal (MCP), and
wrist joints, while the even numbered zones are located
over the underlying intervening osseous structures (see
Chapter 1, Figure 1-7). The detailed anatomy of these
tendons is discussed in Chapter 1.
A few general anatomical points are critical to be
aware of when evaluating patients with potential inju­
ries to the extensor mechanism. (1) Variations in exten­
sor anatomy are common, such as extensor digiti minimi
(EDM) duplication, absence of extensor digitorum com­
munis (EDC) to the small finger. (2) The juncturae
tendinum (see Chapter 1, Figure 1-7) connect the EDC
tendons of the ulnar four digits and are more common
and more substantial (tendon like) on the ulnar part
of the hand. An injury to the extensor mechanism
proximal to a juncturae can be masked on examination
by the ability to extend the injured digit at the MCP
joint through an intact juncturae to an adjacent tendon.
(3) Because of the superficial location of the extensors
partial and complete injuries can and do occur with
seemingly minor lacerations. (4) Injuries may be ini­
tially compensated for by the duplications and intercon­
nections of the extensor mechanism but a clinically
significant deformity can develop with time. (5) A high
percentage of these injuries have associated bone, skin,
or joint injury.1
A major component of the care of tendon injuries is
rehabilitation with controlled early motion. While
exceptions exist, the vast majority of flexor tendon inju­
ries are currently treated with early motion. In the exten­
sor system, the biomechanical characteristics of repair
do not as routinely allow for the same degree of early
mobilization. In general, the biomechanical strength of
utilized repairs is dependent on the zone of injury.
Hence the most important factors in determining the
treatment of extensor tendon injuries include the ana­
tomical zone, the chronicity of the injury, and any
pathology of the adjacent tissues (principally skin,
bone, and joints).
The remainder of this chapter will discuss extensor
tendon injuries, repair, and rehabilitation based on ana­
tomical zone.
ZONE 1—DIP JOINT
The relatively complex anatomy of the extensor hood
becomes much simpler distally as the terminal tendon
is the only structure that extends the distal joint. In
addition, the terminal tendon is a surprisingly delicate
structure when handled surgically, particularly after
trauma. Disruption of the terminal tendon at this level
is commonly referred to as a “mallet” finger because
of the characteristic flexion deformity (Figure 32-1).
Closed injuries are the most routinely seen variant and
occur from multiple mechanisms ranging from injury
in sports with a ball striking the tip of the digit to
“trivial” injuries such as tucking in bed sheets. The ulnar
digits are more commonly affected and males with this
injury tend to have it a younger age than women. Injury
347
348 Section 4:  Extensor Tendon Repair and Reconstruction
Figure 32-1  Clinical presentation of mallet injury with
flexion deformity at the DIP joint.
Figure 32-2  Radiograph of bony mallet injury with distal
phalangeal intra-articular fracture.
is thought to occur from any activity that results in
forced flexion of the tip of a digit. Variations include
closed, open with or without tissue loss, and mallet
fractures (Figure 32-2); it is not infrequent for these
injuries to present late after trauma. Mallet fractures
involving large portions of the articular surface can lead
to joint subluxation.2 Injuries older than 4 weeks have
been classified as “chronic.”3
The resulting deformity ranges from a small extensor
lag to a lag equivalent to full passive DIP flexion. In
some patients the deformity seems to progress over a
few hours or days, suggesting that partial injuries may
become worse with further trauma or with routine use.
Mallet finger injuries may lead to a swan-neck deformity
(flexion of the DIP and PIP hyperextension) through
overpull of the extensors at the PIP joint. This is more
common in individuals with PIP joint volar plate laxity
and illustrates the concept that a tendon imbalance at
one interphalangeal (IP) joint may lead to an opposite
deformity in the adjacent IP joint.4
Diagnosis and categorization of a mallet injury
are based on the posture of the digit and typically
straightforward. Radiographs of the injured digit are
recommended to asses for fracture and joint sub­
luxation. Management of the injury is based on the
category of injury (i.e., closed versus open, acute versus
chronic, etc.).
Closed mallet injuries without a fracture are managed
by observation, immobilization, or surgery. Nonsurgical
treatment is most commonly used in the treatment of
closed mallet injuries and is used for the vast majority,
including those with fractures that involve one third of
the articular surface or less. Joint subluxation is typically
not seen until approximately 50% of the articular surface
is involved. Controversy exists over the type of immobi­
lization, length of immobilization, and the need to
include the PIP joint. The principle of immobilization
is to maintain the DIP joint in extension to approximate
the injured structures and allow for healing. Constant
immobilization is maintained for 6 to 8 weeks but care
must be exercised as dorsal skin compromise occurs,
particularly if the DIP joint is positioned in hyperexten­
sion. A recent randomized trial suggests that digit-based
cast treatment leads to a lower rate of skin problems and
improved patient compliance.5 Some authors advocate
restarting the period of immobilization if the DIP
becomes flexed at any point during the treatment cycle.
The same protocol is typically recommended for patients
who present subacutely up to at least 8 weeks from
injury.
Some residual deformity (extensor lag) in the inter­
mediate and long term is common but rarely function­
ally limiting.6,7 Furthermore, the apparent extensor lag
may improve over an extended period of time of up to
1 year.8
Mallet fractures are also typically managed with a
similar protocol of closed treatment. The most accepted
indication for surgery is joint subluxation; however,
some advocate surgical treatment for large fragments in
the absence of subluxation. Techniques include open
reduction and internal fixation with small screws,
K-wires, or a pull-out suture/wire. Pinning of the DIP
joint in extension is commonly considered, particularly
in the situation where the fixation is not rigid. A closed
technique of extension block pinning, where the DIP
joint is brought into full flexion and a K-wire is intro­
duced into the middle phalanx and then the joint is
extended. The previously inserted K-wire serves to block
extension of the fractured fragment while allowing
extension of the remainder of the distal phalanx, reduc­
ing the fracture. The two distal phalangeal fragments are
then pinned to each other and/or the DIP joint is pinned
in a neutral position. The K-wires are left in about 6
weeks, until clinical union.9
Open mallet injuries are commonly associated with
loss of skin and/or tendon substance as well as a trau­
matic arthrotomy requiring débridement. Even if there
is no loss of tissue, the soft tissue injury can be expected
to be more severe than with a closed injury. While many
 Chapter 32:  Extensor Tendon Injuries—Primary Management
A B
Figure 32-3  A, Open mallet injury with soft tissue loss including skin and tendon. Note the transarticular K-wire. B, Local
advancement flap coverage of the defect.
open extensor injuries are treated with suture repair of
the tendon, the nature of the tendon at this level makes
a biomechanically strong repair challenging. Many sur­
geons choose to add K-wire fixation as an internal splint
or to incorporate the skin in a tenodermodesis repair.
With a tenodermodesis repair a suture or sutures are
placed through the dorsal skin and tendon and the
repair includes both skin and tendon with the same
suture. The tenodermodesis stitch is left in for 6 weeks
in contrast to standard skin sutures so a less reactive
nonabsorbable material such as polypropylene suture is
used.10
In open injuries with tendon or skin loss, wound
management needs to be considered. Local advance­
ment flaps can make up for small defects and skin grafts
can also be helpful in select situations (Figure 32-3).
There are also indications for heterodigital flaps for loss
of larger amounts of skin. Free tendon grafts are also
occasionally needed to reconstruct the extensor mecha­
nism. While these more severe injuries are likely to
include more loss of motion at the DIP joint due to their
more severe trauma, it is important to maintain PIP
joint mobility so the overall impact on the total digital
motion is minimized.
Rehabilitation for all mallet injuries focuses on main­
taining DIP joint extension without even momentary
exception for the first 6 weeks in the vast majority of
cases, regardless of treatment. During that time PIP and
MCP joints and adjacent digit mobilization as well as
techniques to prevent skin complications are encour­
aged. If a splint is used, the skin is inspected daily; the
thumb and countertops or other external aids are used
to maintain the DIP joint in extension when the ortho­
sis is removed. Cast treatment obviates the need for skin
inspection except at the intervals of cast change. After
the period of absolute immobilization most protocols
typically require an additional period of approximately
the same length of night-time extension splinting.
349
ZONE 2—MIDDLE PHALANX
In contrast to zone 1 injuries, zone 2 injuries typically
occur from a laceration. Injuries at this anatomical level
are more likely to be partial with some intact tendon
and therefore some active extension. Despite the differ­
ence of only a few millimeters distance anatomically
from zone 1, these injuries are seen much less frequently.
In the scenario where only one lateral band is lacerated
(50% of the tendon or more is intact), the injury can be
treated with a short course of immobilization. Injuries
with an apparent extensor lag or loss of DIP joint exten­
sion strength should be treated with a longer period of
immobilization or with primary repair. Primary repair
is the preferred treatment for complete lacerations of the
extensor in this area (Figure 32-4). As these injuries
are less common there are no studies that specifically
compare the surgical techniques for repair at this level.
The options used range from technically simple sutures
(figure-of-eight or horizontal mattress) to more complex
such as the Silfverskiöld or an interlocking horizontal
mattress. Tenodermodesis has also been used in this
zone. Many authors chose to use a supplemental K-wire
across the DIP joint with the joint in extension to protect
the repair, particularly if there is loss of skin or tendon
substance.
Immobilization and rehabilitation are largely similar
to the more common zone 1 injuries. Six weeks of
immobilization of the DIP joint in extension with
mobilization of the PIP joint is maintained. Typically
this is in a splint or cast. Active flexion is permitted at
6 weeks but part time splinting at night is continued for
an additional 4 to 6 weeks.
ZONE 3—PIP JOINT
Zone 3 injuries occur in both open and closed manners.
However, closed injuries are frequently underappre­
ciated by patients and medical professionals. The
350 Section 4:  Extensor Tendon Repair and Reconstruction
A flexion is performed throughout the treatment to mobi­
B
Figure 32-4  A, Complete zone 2 tendon injury of the
middle finger in a patient who sustained a laceration on
glass to the dorsum of two fingers. B, Zone 3 injury with
open PIP joint of the index finger in the same patient.
functional morbidity of the resultant boutonniere
deformity is more limiting than the deformity of a
neglected mallet finger in most cases. Therefore, vigi­
lance is necessary to prevent the sequelae of this type of
injury. With closed injuries, patients present with swell­
ing at the PIP joint, decreased PIP joint extension
strength against resistance and a subtle PIP joint exten­
sion lag. The Elson test is the physical examination
maneuver that is felt to be the most specific for an early
closed central slip injury.11 The test is performed with
the PIP joint flexed 90° and the patient extends the IP
joints against resistance. A positive test shows increased
DIP extension than the contralateral or adjacent DIP
joint.
With an acute presentation, treatment depends on
whether the injury is open or closed. For open injuries,
an arthrotomy and irrigation and débridement of the
joint are indicated (see Figure 32-4). These injuries
occur from a variety of mechanisms and while human
mouth injuries are more common at the MCP joint,
they also occur at the PIP joint so vigilance is necessary.
In the absence of purulence or overt signs of infection,
surgical repair of the central slip is indicated. For inju­
ries without adequate distal tendon for direct repair,
suture anchor repairs are described. Biomechanically
suture anchor repair appears similar to suture repairs.12
Acute closed isolated central slip injuries are managed
nonoperatively. Extension splinting or casting of the PIP
joint is prescribed with the PIP joint in full extension
and the DIP “free” or capable of full flexion. Immobili­
zation is maintained for 6 weeks and is followed by a
period of night-time splinting in extension typically of
an additional 6 weeks. Active and passive DIP joint
lize the lateral bands dorsally or at least prevent them
from subluxating volarly. The goal of treatment is to
prevent the secondary deformity (volar subluxation of
the lateral bands and DIP joint hyperextension) from
developing. For closed injuries with displaced avulsion
fractures and/or PIP joint subluxation/dislocation, open
treatment is indicated. Reconstruction of the central slip
insertion into the dorsal base of the middle phalanx is
performed. Depending on the fragment size and quality,
constructs using screws, K-wires, suture anchors or
tension band may be used. Joint instability may require
pinning the PIP joint in extension.
Subacute presentations are a frequent problem. This
occurs as the injuries are commonly underappreciated
and because attenuation of the central slip and the
resultant boutonniere deformity can develop over
weeks. In this situation, the goal of treatment is to
prevent development or worsening of the deformity.
Splinting of the PIP joint in extension while leaving the
DIP joint free to move is therefore indicated when an
injury to the central slip is suspected. Failure of initial
management of a central slip injury with development
of a boutonniere deformity is a controversial area. Many
authors will consider splinting in the subacute period
but surgical reconstruction is indicated in select cases
where nonsurgical treatment fails. Favored reconstruc­
tive techniques are more complex than reattaching the
retracted central tendon such as mobilization of a com­
ponent of the lateral band or a tendon graft such as a
slip of flexor digitorum superficialis (FDS) left attached
to the base of the middle phalanx. Boutonniere recon­
struction is discussed in more detail in Chapter 36.
Rehabilitation after central slip injury has tradition­
ally included immobilization of the PIP joint for 6
weeks with concomitant DIP joint motion. Loss of PIP
joint flexion has been a concern, particularly for open
injuries and some authors have advocated for earlier
range of motion (ROM). Pratt and colleagues13 described
a postoperative protocol that included 3 weeks of
immobilization followed by 3 weeks of protected
motion with a dynamic extension splint. No patient in
her series had an extension deficit over 15°.
 Chapter 32:  Extensor Tendon Injuries—Primary Management
ZONE 4—PROXIMAL PHALANX
Zone 4 injuries are similar to zone 2 in many ways,
although in zone 4 the anatomy is more complex. A
majority of the injuries seen at this level are open and
partial lacerations are the norm. Examination of a
patient with an injury at this level includes evaluation
for an extensor lag at the PIP joint or weakness of active
extension. In the absence of an extensor lag with the
ability to extend against resistance nonsurgical treat­
ment is recommended. This includes PIP joint exten­
sion splinting and early protected motion. Many injuries
in this zone occur in the setting of an open fracture.
Treatment of an associated skeletal injury may influence
the choice of closed versus open treatment and the tech­
nique of rehabilitation. The “dorsal combined injuries”
involving an unstable open fracture and a tendon lac­
eration are a distinct pattern of injury. Rigid internal
fixation of the fracture is typically advocated with repair
of the extensor tendon. Larger defects of the extensor
mechanism can be bridged with tendon graft. Great
care is taken during either repair or graft reconstruction
to ensure proper length balance of the central band
and lateral band, as imbalance in the length would
induce loss of finger extension. Extensor adherence over
the proximal phalanx may occur, which can lead to
decreased digital flexion, with possible need for later
tenolysis and joint release.
Patients with an extensor lag and/or lack of extension
against resistance have an indication for exploration
and likely repair. Once again a variety of tendon repair
techniques are used. Frequently repair is followed by 4
to 5 weeks of immobilization, with subsequent therapy.
Recent biomechanical data have shown that repairs
using the Becker and interlocking horizontal mattress
techniques are stronger than some more traditional
techniques.14,15 This has led some authors to advocate
beginning range of motion at 3 weeks postrepair.16
ZONE 5—MCP JOINT
Injuries to the extensor mechanism in zone 5 occur over
the MCP joint, and are frequently open injuries. A high
prevalence of these open injuries occur due to human
teeth; it is critical to identify patients with these “fight
bites” and aggressively treat them with operative irriga­
tion and débridement of the MCP joint as well as repair
of the tendon, if indicated (Figure 32-5). Due to the
common positioning of the digits in flexion when the
injury occurs, and the positioning of the digits in exten­
sion during the examination of the wound in the clini­
cal setting, an injury that extends to the joint may be
missed, as the affected portion of the tendon is now
much more proximally located. A high index of sus­
picion is appropriate when evaluating open injuries
in this zone. Bite wounds here should be irrigated,
débrided, and left open.
351
Figure 32-5  Open zone 5 “fight bite” injury involving the
tendon and joint.
When tendon repair in this area is performed, proxi­
mal tendon retraction is rarely an issue, as the intact
sagittal bands and juncturae tendinea prevent signifi­
cant migration. Common suture techniques include the
modified Kessler, modified Bunnell, mattress, and
figure-of-eight. Care should be taken to avoid excessive
shortening of the tendon during repair, which can lead
to loss of flexion. Rehabilitation protocols are varied in
this region17,18 and include immobilization for 3 to 4
weeks with the wrist extended 45° and the MCP joints
in approximately 15° to 20° of flexion, followed by
mobilization.19-21 Alternate rehabilitation with a pro­
tected early motion protocol such as immediate con­
trolled active motion (ICAM) has been shown to be
effective, especially in long and ring fingers, which allow
for the best support of the digital “yoke.”22-26
Open sagittal band injuries should be repaired to
prevent subluxation of the extensor tendon away from
the side of injury. Displacement of the extensor tendon
from its central location may be associated with an
extensor lag or, in extreme cases, the inability to extend
across the MCP joint from a maximally flexed position.
Intrinsic contracture can result if left untreated. Closed
sagittal band injuries are frequently associated with
inflammatory systemic conditions, or related to blunt
trauma. Rupture of the sagittal fibers most often occurs
on the radial side of the middle finger, with ulnar dis­
placement of the extensor. Management of acute closed
sagittal band injuries includes immobilization in exten­
sion for 4 weeks, followed by a range of motion proto­
col.27,28 If closed treatment is unsuccessful, surgical
management includes repair of the torn sagittal band if
the tissues permit. A variant of this injury is the “boxer’s
knuckle,” which occurs via a direct blow to the extensor
mechanism over the MCP joint, leading to injury of
both the extensor mechanism and underlying joint
capsule.29 Reconstruction using a juncture or a slip of
352 Section 4:  Extensor Tendon Repair and Reconstruction
the extensor tendon routed around a lateral band or the
radial collateral ligament is used for patients requiring
reinforcement of the native tissues. Chronic radial sagit­
tal band injuries may require release of the ulnar sagittal
band and centralization of the extensor.
ZONE 6—DORSUM OF THE HAND
Zone 6 injuries over the dorsum of the hand are less
common, but are often associated with significant
trauma, including fractures and major soft tissue inju­
ries. The extensor in this zone is more oval or circular
in cross section and more amenable to core suture repair
with 3-0 or 4-0 nonabsorbable suture (similar to those
for flexor tendon injuries). Early dynamic splinting
or ICAM protocols are often appropriate for these
patients; however, they may also be treated with immo­
bilization for 4 weeks after surgical repair, followed by
a standard mobilization. Complex injuries may neces­
sitate extended rehabilitation due to other affected
tissue structures such as bone or skin. Patients with
complex injuries may benefit from acute tendon recon­
struction performed in combination with free tissue
transfer for soft tissue coverage.30 Extensor adherence
to surrounding structures may lead to either extensor
lag or poor flexion from resultant joint contractures.
Uninjured digits in the hand can be similarly affected
from lack of mobilization with joint contractures and
tendon adhesions. Evans and Burkhalter31 describe early
motion protocols for injuries at this level involving
dynamic extension splints. They report full extension in
over 90% of their patients and no tendon ruptures.
Newport and colleagues have analyzed several studies
that compare static immobilization to early controlled
movement for uncomplicated injuries in zones 5 to 8
and found that 54 to 95% good or excellent results
were obtained with immobilization versus at least
90% good or excellent results for the early controlled
motion.32 Five millimeters of tendon excursion is suffi­
cient to prevent adherence of the repaired extensor,
which is correlated with range of motion at the various
joints.33,34
ZONES 7, 8, AND 9—WRIST, DISTAL, AND
PROXIMAL FOREARM
Zone 7 and more proximal extensor injuries are less
common. Appropriate identification of the proximal
ends of the transected extensor tendons in these areas
can be difficult. Knowledge of local anatomy including
the compartments, location of the muscle bellies, and
caliber of the tendons aids with identification (Figure
32-6). The proximal ends may also be retracted due
to muscle contraction, which may require extending
the proximal dissection. The distal ends are rather easy
to identify, as a gentle tug on the tendon stump will
elicit the expected distal movement. The tendons are
repaired using a strong nonabsorbable core suture. If
Figure 32-6  Open zone 7 injury with multiple tendons and
nerve transections.
the tendon repair is located in the area of the extensor
retinaculum, a small section can be resected or a length­
ening of the retinaculum can be performed to prevent
bowstringing. The wrist is typically immobilized in 40°
extension, with the MCP joints held in neutral to slight
flexion for 3 to 4 weeks. Early motion of the IP joints
of the fingers is typically possible without undue stress
on the repairs.
The most common closed tendon injury at the wrist
is an extensor pollicis longus (EPL) rupture. Most fre­
quently occurring after closed treatment of a minimally
or nondisplaced distal radius fracture, the etiology is
thought to be secondary to ischemia in that region of
the tendon. The tendon ends are typically frayed, pre­
cluding end-to-end repair, thus reconstruction with
extensor indicis proprius (EIP) transfer or an interposi­
tion tendon graft are typically performed.35
Lacerations over the forearm may to injury of both
tendons and nerves. Nerve repairs should be performed
at the time of tendon repair. With multiple tendon inju­
ries, repair of all of the divided structures is recom­
mended (Figure 32-7). If the injury precludes direct
repair of all structures, repair to allow independent wrist
and thumb extension is the most important, and com­
bined extension of the digits is desired. Injuries at the
musculotendinous junction are challenging due to poor
strength of the repair in the muscle. Often a tendinous
portion can be found extending within the muscle belly
to a quite proximal extent and can be incorporated for
increased repair strength. Rehabilitation is similar to
zone 7 but may need to be modified based on the
mechanical strength of the repair in zone 8.
Zone 9 injuries are those in more proximal forearm
and result from sharp lacerations. Muscle, tendon, and/
or nerves, especially the posterior interosseous nerve
(PIN), are often simultaneously injured. Any nerve
 Chapter 32:  Extensor Tendon Injuries—Primary Management
Figure 32-7  Forearm laceration involving multiple tendon
injuries in zones 7 and 8.
injuries should be identified and repaired at the surgery.
The muscle bellies are repaired, frequently with a figure-
of-eight suture. Fascia can be used to augment the
muscle repair. Above elbow immobilization is applied
when the injured muscles originate from the humeral
epicondyles.
References
1. Newport ML, Blair WF, Steyers CM Jr: Long-term results of
extensor tendon repair, J Hand Surg (Am) 15:961–966, 1990.
2. Kalainov DM, Hoepfner PE, Hartigan BJ, et al: Nonsurgical
treatment of closed mallet finger fractures, J Hand Surg (Am)
30:580–586, 2005.
3. Garberman SF, Diao E, Peimer CA: Mallet finger: results of
early versus delayed closed treatment, J Hand Surg (Am)
19:850–852, 1994.
4. Kaplan EB: Anatomy, injuries, and treatment of the extensor
apparatus of the hand and digits, Clin Orthop Relat Res 13:24–
40, 1959.
5. Tocco S: Effectiveness of cast immobilization in closed mallet
finger injury: A prospective randomized comparison with
thermoplastic splinting, J Hand Ther 20:362–363, 2007.
6. Bendre AA, Hartigan BJ, Kalainov DM: Mallet finger, J Am
Acad Orthop Surg 13:336–344, 2005.
7. Okafor B, Mbubaeqbu C, Munshi I, et al: Mallet deformity
of the finger: five-year follow-up of conservative treatment,
J Bone Joint Surg (Am) 79:544–547, 1997.
8. Pike J, Mulpuri K, Metzger M, et al: Blinded, prospective,
randomized clinical trial comparing volar, dorsal, and custom
thermoplastic splinting in treatment of acute mallet finger,
J Hand Surg (Am) 35:580–588, 2010.
9. Hofmeister EP, Mazurek MT, Shin AY, et al: Extension block
pinning for large mallet fractures, J Hand Surg (Am) 28:453–
459, 2003.
10. Kardestuncer T, Bae DS, Waters PM: The results of tenoder­
modesis for severe chronic mallet finger deformity in chil­
dren, J Pediatr Orthop 28:81–85, 2008.
11. Rubin J, Bozentka DJ, Bora FW: Diagnosis of closed central
slip injuries. A cadaveric analysis of non-invasive tests, J Hand
Surg (Br) 21:614–616, 1996.
353
SUMMARY
Extensor tendon injuries are one of the common inju­
ries in the hand. Careful attention to the anatomical
details of the zone of injury and complicated mechani­
cal balance of the extensor system will determine
whether surgical or nonsurgical treatment is indicated.
As each component of extensor tendon over the fingers
tolerate little loss of tendon substances, in repairing the
extensor tendon, care should be taken to ensure minimal
shortening of the tendon substance to maintain intri­
cate mechanical balance of the extensor apparatus.
Though strength of repair is not as important as for
flexor tendons, a mechanically reliable repair method
should be considered. Extensor tendons injured at the
distal parts of the fingers, such as over the DIP or PIP
joint areas may develop joint deformities easily, leading
to chronic mallet finger or boutonniere deformities.
Correct splinting or surgical intervention at acute stage
is important to prevent development of these deformi­
ties. In many surgical cases, postoperative early motion
protocols help restore digital range of motion and
return patients to occupational and daily activities more
rapidly. Adhesions may develop, especially over the
fingers or at the extensor retinaculum, which may
require secondary tenolysis.
12. Cluett J, Milne AD, Yang D, et al: Repair of central slip avul­
sions using Mitek Micro Arc bone anchors, J Hand Surg (Br)
24:679–682, 1999.
13. Pratt AL, Burr N, Grobbelaar AO: A prospective review of
open central slip laceration repair and rehabilitation, J Hand
Surg (Br) 27:530–534, 2002.
14. Lee SK, Dubey A, Kim BH, et al: A biomechanical study of
extensor tendon repair methods: introduction to the running-
interlocking horizontal mattress extensor tendon repair tech­
nique, J Hand Surg (Am) 35:19–23, 2010.
15. Woo SH, Tsai TM, Kleinert HE, et al: A biomechanical com­
parison of four extensor tendon repair techniques in Zone IV,
Plast Reconstr Surg 115:1674–1681, 2005.
16. Zubovic A, Egan C, O’Sullivan M: Augmented (Massachusetts
General Hospital) Becker technique combined with static
splinting in extensor tendons repairs zones III to VI: func­
tional outcome at three months, Tech Hand Up Extrem Surg
12:7–11, 2008.
17. Chester DL, Beale S, Beveridge L, et al: A prospective, con­
trolled, randomized trial comparing early active extension
with passive extension using a dynamic splint in the rehabili­
tation of repaired extensor tendons, J Hand Surg (Br) 27:283–
288, 2002.
18. Crosby CA, Wehbe MA: Early protected motion after extensor
tendon repair, J Hand Surg (Am) 24:1061–1070, 1999.
19. Newport ML: Extensor tendon injuries in the hand, J Am Acad
Orthop Surg 5:59–66, 1997.
20. Newport ML: Zone I-V extensor tendon repair, Tech Hand Up
Extrem Surg 2:50–55, 1998.
21. Rayan GM, Murray D: Classification and treatment of
closed sagittal band injuries, J Hand Surg (Am) 19:590–594,
1994.
354 Section 4:  Extensor Tendon Repair and Reconstruction
22. Howell, JW, Merritt WH, Robinson SJ: Immediate controlled
active motion following zone 4-7 extensor tendon repair,
J Hand Ther 18:182–190, 2005.
23. Ip WY, Chow SP: Results of dynamic splintage following
extensor tendon repair, J Hand Surg (Br) 22:283–287, 1997.
24. Khandwala AR, Webb J, Harris SB, et al: A comparison of
dynamic extension splinting and controlled active mobiliza­
tion of complete divisions of extensor tendons in zones 5 and
6, J Hand Surg (Br) 25:140–146, 2000.
25. Matzon JL, Bozentka DJ: Extensor tendon injuries, J Hand
Surg (Am) 35:854–861, 2010.
26. Mowlavi A, Burns M, Brown RE: Dynamic versus static splint­
ing of simple zone v and zone vi extensor tendon repairs: A
prospective, randomized, controlled study, Plast Reconstr Surg
115:482–487, 2005.
27. Catalano LW 3rd, Gupta S, Ragland R 3rd, et al: Closed treat­
ment of nonrheumatoid extensor tendon dislocations at the
metacarpophalangeal joint, J Hand Surg (Am) 31:242–245,
2006.
28. Purcell T, Eadie PA, Murugan S, et al: Static splinting of exten­
sor tendon repairs, J Hand Surg (Br) 25:180–182, 2000.
29. Hame SL, Melone CP Jr: Boxer’s knuckle. Traumatic dis­
ruption of the extensor hood, Hand Clin 16:375–380,
2000.
30. Scheker LR, Langley SJ, Martin DL, et al: Primary extensor
tendon reconstruction in dorsal hand defects requiring free
flaps, J Hand Surg (Br) 18:568–575, 1993.
31. Evans RB, Burkhalter WE: A study of the dynamic anatomy
of extensor tendons and implications for treatment, J Hand
Surg (Am) 11:774–779, 1986.
32. Newport ML, Tucker RL: New perspectives on extensor tendon
repair and implications for rehabilitation, J Hand Ther
18:175–181, 2005.
33. Elliot D, McGrouther DA: The excursions of the long extensor
tendons of the hand, J Hand Surg (Br) 11:77–80, 1986.
34. Sharma JV, Liang NJ, Owen JR, et al: Analysis of relative
motion splint in the treatment of zone VI extensor tendon
injuries, J Hand Surg (Am) 31:1118–1122, 2006.
35. Hirasawa Y, Katsumi Y, Akiyoshi T, et al: Clinical and micro­
angiographic studies on rupture of the EPL tendon after distal
radial fractures, J Hand Surg (Br) 15:51–57, 1990.
 CHAPTER
33  
SAGITTAL BAND INJURIES—
PRIMARY AND SECONDARY
MANAGEMENT
Kristen E. Fleager, MD, Monina Copuaco, OTR, CHT, and
James Chang, MD
OUTLINE
Sagittal band injuries have many potential etiologies,
although rheumatic disease and trauma are the most
common. Open acute injuries with a suspicion of sag-
ittal band laceration should be expeditiously explored.
There is evidence to suggest that closed acute injuries
(less than 3 weeks) may do well with conservative
management consisting of immobilization followed
by protected motion. Patients who fail nonoperative
management or have chronic injuries (3 weeks or
longer) may be appropriate surgical candidates for
primary repair. If there is not sufficient tissue for
primary repair, a reconstructive approach using local
tendon tissue should be undertaken.
Subluxation or dislocation of the extensor tendon at the
metacarpophalangeal (MCP) joint is typically seen in
patients with rheumatoid arthritis but may also be seen
with trauma, congenital laxity of the sagittal band, infec-
tion, and iatrogenic injury. Spontaneous sagittal band
disruption has also been reported.1 A sagittal band
injury will often present with pain and swelling near the
MCP joint, with associated subluxation, or catching. The
radial sagittal band is typically damaged, with resultant
ulnar deviation of the involved finger. The long finger
is most frequently involved. Treatment options are mul-
tiple and include splinting, realignment with direct
repair, and various forms of tendon reconstruction.
ANATOMY AND BIOMECHANICS
The sagittal band is one component of the extensor reti-
nacular system, which forms a cylindrical tube with the
palmar plate (Figures 33-1 and 33-2). This tube sur-
rounds the metacarpal head and MCP joint.2 In the
central digits, the origin of the sagittal band is palmar
and blends with the palmar plate, flexor tendon sheath,
proximal annular pulley, and deep transverse metacar-
pal ligaments (DTML). The sagittal bands on the radial
side of the index finger and ulnar side of the small finger
differ, in that they do not blend with the DTML. The
insertion of the sagittal band is dorsal and tendinous,
and glides with the extensor system as the digits move.
The fibers superficial to the extensor digitorum com-
munis (EDC) tendon are thinner than the deep fibers,
especially in the central digits. The radial component of
the sagittal band is typically thinner and longer than the
ulnar component, explaining the predilection for radial-
sided injury.
The primary functions of the sagittal band are to help
extend the proximal phalanx and to stabilize the exten-
sor tendon in the midline over the dorsal aspect of the
MCP joint.3 The force displacing the tendon in the ulnar
direction is greatest in full extension, decreases from 0
to 60 degrees, and then increases again from 60° to 90°
of flexion.4 Significantly higher forces are required to
prevent additional displacement of an already ulnarly
displaced tendon, and it tends to displace further with
additional MCP flexion.
The long finger is most frequently involved5, likely
because the tendon to the long finger sits on top of the
transverse fibers with a relatively loose fibrous attach-
ment, and the long finger extensor hood attaches
more distally from the joint than that of the adjacent
tendons.6 In addition, the cross-sectional shape of the
extensor tendon of the long finger over the MP joint is
rounder and less anchored than that of the other exten-
sor tendons at that level.7 The injury is most often
located on the radial side, with subsequent displace-
ment of the extensor tendon in an ulnar direction.
Young and Rayan8 studied the anatomy and biome-
chanics of the sagittal band in 48 cadaveric digits and
concluded the following: (1) extensor tendon instability
following sagittal band disruption is most common in
the long finger and least common in the small finger;
(2) ulnar instability of the extensor tendon is due to
partial or complete radial sagittal band disruption, (3)
the degree of extensor tendon instability is determined
355
356 Section 4:  Extensor Tendon Repair and Reconstruction

Sagittal band Central slip

Transverse
retinacular
ligament

PIP Oblique MP
retinacular
DIP ligament

Dorsal volar
interosseus
Triangular Lateral Sagittal
ligament band band

DIP
PIP
Central slip Lumbrical
extension MP

Figure 33-1  Depiction of sagittal bands and surrounding structures.

Radial Ulnar

1
3
2
4
5

Figure 33-2  Cadaver dissection demonstrating sagittal

bands (arrows) and surrounding extensor retinacular system.

by the extent of sagittal band disruption, (4) proximal
rather than distal sagittal band compromise contributes
to extensor tendon instability, (5) great forces are
inflicted on the sagittal band while the MCP joint is in
full extension or less frequently in full flexion, which
may be the mechanism of its injury, and (6) wrist flexion
contributes to extensor tendon instability after sagittal
band disruption and may exacerbate the severity of its
injury.
Ishizuki reported on differences in anatomical intra-
operative findings, depending on if the injury was spon-
taneous or traumatic (Figure 33-3).1 Spontaneous
dislocations involve rupture of the superficial layer of
the sagittal band just radial to the extensor tendon,
while traumatic dislocations rupture both layers of the
B
Figure 33-3  A, The extensor apparatus at the level of
the MCP joint (transverse section): (1) extensor tendon;
(2) superficial layer of sagittal band; (3) deep layer of the
sagittal band; (4) loose connective tissue between the
sagittal band and dorsal capsule; (5) dorsal capsule. In the
spontaneous type of dislocation, the thin superficial layer of
the sagittal band is ruptured just radial to the extensor
tendon (arrow), and the extensor tendon is detached from
the radial and palmar connection with the deep layer of the
sagittal band. B, In the traumatic type of dislocation, both
layers of the sagittal band are ruptured usually at a site
several millimeters radial to the extensor tendon (arrow).
 Chapter 33:  Sagittal Band Injuries—Primary and Secondary Management
Figure 33-4  Severe ulnar drift of the fingers in a patient
with rheumatoid arthritis.
sagittal band several millimeters radial to the extensor
tendon.
CAUSES
The causes of sagittal band injuries are multiple, and
include degenerative disease, trauma, congenital, infec-
tion, and iatrogenic injury.9,10 Rheumatoid arthritis is
the most common cause of subluxation or dislocation
of the extensor tendon at the MP joint. It is most fre-
quently seen in advanced cases with ulnar deviation
(Figure 33-4) but may also be seen in cases without
severe deformity. Rheumatoid arthritis causes synovitis
of the MCP joint, which then leads to attenuation or
rupture of the sagittal bands. Traumatic injury may
involve a laceration of the hood, direct blow, or forced
flexion of the MCP joint. In a closed injury, the finger
is often forced into a flexed and ulnarly deviated posi-
tion against a tense extensor muscles, causing a tear in
the radial sagittal fibers. “Boxer’s knuckle,” a direct
impact over the MCP joint with a clenched fist, has also
been described as a mechanism of injury. Spontaneous
subluxation secondary to an underlying laxity of the
joint capsule may occur during simple activities of daily
living. The rare case of congenital extensor tendon sub-
luxation involves an ulnar drift of all the fingers, and is
sometimes part of the entity known as a “windblown
hand.”11
Infectious etiologies, such as from a human fight bite,
can cause destruction of the joint capsule, extensor
tendon and deep fascial spaces. Iatrogenic injury to
the sagittal band, such as during joint replacement or
MCP joint capsulotomy, may also occur. Such injury
may be avoided by completing the capsulotomy on the
ulnar aspect of the MCP joint, as opposed to the radial
side. Chronic myoclonic jerks in a patient with focal
epilepsy have also been reported to cause extensor
tendon dislocation.
357
I II III
Figure 33-5  Three types of sagittal band injury: type I,
mild injury with no instability; type II, moderate injury with
extensor tendon subluxation; and type III, severe injury with
tendon dislocation.
CLASSIFICATION
Rayan and Murray12 described three clinical types of
sagittal band injuries. Type I injury is a contusion
without tearing of the retinaculum, and demonstrates
no instability. Type II is a moderate injury with extensor
tendon subluxation, while type III is a severe injury with
tendon dislocation (Figure 33-5). Subluxation was
defined as “lateral displacement with painful snapping
of the extensor tendon with its border reaching beyond
the mid-line, but remaining in contact with the condyle
during full MP joint flexion.” Dislocation was defined
as “displacement of the tendon in the groove between
the two metacarpal heads.”
DIAGNOSIS
Diagnosis of a sagittal band injury is primarily based on
clinical findings and can be identified with a thorough
review of history and physical examination. Closed
injuries typically present with pain, swelling, and/or
ecchymosis of the involved MCP joint. Open injuries
will involve a laceration over the MCP joint, typically
on the radial side. The extensor tendon may dislocate
ulnarward into the intermetacarpal space, and the
patient may complain of catching, locking, or snapping.
It should be noted, however, that tendon displacement
is often be obscured by swelling. Partial ruptures of the
radial sagittal band will not present with subluxation of
the extensor tendon. Active extension may produce
ulnar angulation of the MCP joint and supination of the
finger. With time, the ulnar deviation deformity pre-
vents dorsal relocation of the extensor tendon, and the
patient may be unable to extend the joint (Box 33-1).
DIFFERENTIAL DIAGNOSIS
Metacarpal fractures and avulsion injuries may present
with swelling and pain about the MCP joint and should
be ruled out. Radiographs may include an anteroposte-
rior (AP), lateral, and Brewerton view (AP tangential
view of the metacarpal heads, used to visualize the bony
origin of the collateral ligaments) (Figure 33-6). Col-
lateral ligament injury will demonstrate instability with
358 Section 4:  Extensor Tendon Repair and Reconstruction
Box 33-1 Clinical Pearls: Diagnosis
Sagittal band injuries are typically on the radial side, leading
to ulnar displacement of the extensor tendon.
The long finger is most commonly involved.
Possible mechanisms of injury:
 Rheumatoid arthritis
 Finger forced into flexed and ulnarly deviated
position
 “Boxer’s knuckle”: direct impact over MCP joint with
clenched fist
 Spontaneous: during mild activity such as flicking or
snapping
 Infection (e.g., fight bite)
 Iatrogenic (e.g., during joint replacement, MCP
capsulotomy)
 Focal epilepsy
Congenital cases are rare but may present with an ulnar
drift of all of the fingers.
Presents with pain, swelling, and/or ecchymosis over   realignment with direct repair, and various forms of
MCP joint. Tendon displacement may be obscured by
swelling.
Patient complains of snapping, locking, or catching.
Partial ruptures of a sagittal band will not present with
tendon subluxation.
Do not confuse a sagittal band injury with:
 Metacarpal fracture or avulsion injury (rule out with
radiograph)
 Collateral ligament injury (will demonstrate instabil-
ity with lateral stress when MCP joint fully flexed)
 Trigger finger (snapping and tenderness will be
present on volar aspect of hand)
 Subluxation of the MCP joint
 Snapping of the junctura tendinum
60°
Figure 33-6  The Brewerton view is a tangential view of the
metacarpal heads that is useful in detecting fractures,
dislocation, or subluxation of the MCP joint.
lateral stress when the MCP joint is fully flexed. Pain
will be located deep in the groove between the metacar-
pal heads. Sagittal band injuries, in contrast, will dem-
onstrate instability with the MCP joint in extension and
be associated with more superficial tenderness. Radio-
graphs are essential, which may demonstrate bony
avulsion. Trigger finger will present with snapping or
locking, but will be present on the volar aspect of the
hand. Tenderness will be elicited directly over the A1
pulley. Snapping junctura tendinum simulating radial
sagittal band rupture has also been reported, and should
be considered.13
TREATMENT METHODS
Open injuries should be emergently explored, thor-
oughly irrigated, and repaired. Closed injuries have
multiple treatment options, which include splinting,
tendon reconstruction. Patients with an acute traumatic
dislocation may achieve satisfactory results with exten-
sion splinting of the MCP joint.14,15 Those who fail con-
servative treatment or who have a chronic dislocation
may benefit from surgical intervention. Koniuch and
colleagues demonstrated instability in lacerations
involving greater than two-thirds of the proximal sagit-
tal band, and recommended surgery for such injuries16
(Box 33-2).
Rayan and Murray12 described treatment options
based on their classification scheme and the chronicity
of the injury. Acute (within 3 weeks) sagittal band inju-
ries are initially treated with a buddy splint (for type I)
or palmar splint (for types II and III) for 3 weeks, fol-
lowed by protected range of motion 3 times daily for an
3 additional weeks. Buddy splinting is then continued
for 4 additional weeks while completing both active and
Box 33-2 Clinical Pearls: Treatment
Nonsurgical treatment: Closed acute injuries (<3 weeks)
may be treated initially with splinting.
Surgical indications: Chronic injuries (≥3 weeks), patients
who do not respond to nonoperative treatment, open
injuries with lacerations involving greater than two-
thirds length of the sagittal band.
Surgical methods
 If sufficient tissue is present, perform direct repair.
 Reconstructive options are reserved for patients with
scarring or deficient tissue.
 Sagittal band reconstructions utilizes local tissues
such as juncturae tendinae or a portion of the exten-
sor tendon.
 “Boxer’s knuckle” injuries are best treated with
primary direct repair of the sagittal band, without
capsular repair.
 Chapter 33:  Sagittal Band Injuries—Primary and Secondary Management 359

passive range of motion exercises. Chronic injuries
(longer than 3 weeks) are treated with buddy splinting
for 6 to 8 weeks. Patients with type II or III injuries, who
do not respond to nonoperative treatment, are then
candidates for surgical intervention. In their series of 28
nonrheumatoid patients, those treated within 3 weeks
of injury achieved satisfactory results with nonoperative
treatment.
Immobilization
MCP palmar splints should position the joint at a
neutral abduction-adduction position, and allow no
more than 20° of active MCP flexion (Figure 33-7). It
should allow motion at the IP joint, which prevents
stiffness. The splint may also be made in slight deviation
in the direction of the sagittal band injury (typically
radial), to decrease tension. Inoue and Tamura17 reported
on six patients seen within 2 weeks with traumatic
or spontaneous dislocations of the extensor tendons.
These patients were treated with a splint that stopped
MCP flexion at 10° to 20° but allowed active extension.
The IP joint was left free. All patients had full range
of motion and were free of symptoms. The authors
therefore concluded that all acute dislocations less than
2 weeks old should be initially treated with splinting.
A buddy splint immobilizes the injured digit to the
adjacent digit on the side of sagittal band injury (Figure
33-8). It works to minimize abduction forces, and
should fasten proximal to the PIP joint. Both MCP
palmar splints and buddy splints can be used for
nonoperative treatment, or as part of a postoperative
protocol.
Ragland and colleagues18 demonstrated success in
nonoperative treatment of closed sagittal band injuries
in nonrheumatoid patients with extensor tendon dislo-
cations. Patients were treated for 8 weeks with a sagittal
band bridge splint (Figure 33-9). This splint holds the
MCP joint in 25° to 35° of hyperextension, centralizing
the extensor tendon while the sagittal band heals. Active
motion of the DIP and PIP joints was encouraged.
Surgical Options
Surgical options are varied, depending on the complex-
ity of the injury. Simple, acute lacerations involving
greater than two-thirds of the sagittal band or with
associated subluxation may undergo realignment and

A B

C D
Figure 33-7  A–D, A flexion-block splint allows active extension but prevents flexion of the MCP joint past 20°. Motion of
the IP joint prevents stiffness.
360 Section 4:  Extensor Tendon Repair and Reconstruction

Figure 33-8  A buddy splint immobilizes the injured digit to

the adjacent digit on the side of the sagittal band injury. It
should fasten proximal to the PIP joint. B

primary repair with 4-0 braided suture (Figures 33-10

and 33-11). Congenital or spontaneous cases with suf-
ficient tissue may also undergo direct repair. Both Kettle-
camp and Ishiuki have reported good results with a
minimum follow-up of 1 year with direct repair.1,7 The
ulnar sagittal band may also be released to help central-
ize the EDC tendon.
Hame and Melone19 reported on eight professional
athletes with 11 “boxer’s knuckle” injuries who were
treated with centralization of the extensor tendon and
primary sagittal band repair. Seven joints had associated
capsular tears, and these were not repaired. The authors
thought that capsular repair would place excessive
tension on the repair and limit range of motion. Post-
operatively, the joint is immobilized at 60° of flexion C
for 6 weeks. Five months postoperatively, all athletes Figure 33-9  A–C, A sagittal band bridge splint provides
had returned to sports, were symptom free, and had full 25° to 35° more extension of the MCP joint compared to
range of motion. the adjacent digits. It helps maintain the EDC tendon in a
If unable to perform a direct repair of the radial sagit- reduced position.
tal band because of chronicity of injury, scarring, or
deficient tissue, several surgical options are available,
including those described by Wheeldon,20 McCoy,21 and
Carroll.22 A successful surgical repair must meet two Wheeldon20 reported using junctura tendinum to
requirements: (1) the tendon must be accurately aligned reconstruct the radial sagittal band of the long finger.
over the MCP joint to diminish the forces causing dis- The junctura tendinum is separated from its attachment
location to occur, and (2) the repair must be able to to the ring finger tendon and brought over to be sutured
withstand the ulnar forces incurred during flexion of the in the line of the torn aponeurosis, preventing further
joint. dislocation. However, use of the junctura tendinum may
 Chapter 33:  Sagittal Band Injuries—Primary and Secondary Management
Figure 33-10  Preoperative view of patient who sustained a
dorsal hand laceration with suspicion of ulnar sagittal band
injury.
A
B soradial aspect of the MCP joint, as well as rupture of
Figure 33-11  A, Exploration demonstrates a complete
laceration of the ulnar sagittal band and underlying capsule.
B, Direct repair of the ulnar sagittal band was possible
because of the early intervention.
361
not always be possible because of its irregular location,
inadequate length, or complete absence (Figure 33-12).
McCoy and Winsky21 described using a distal slip of
the extensor tendon to reconstruct the sagittal band. A
4-cm dorsal incision is made along the radial side of the
MCP joint, and skin flaps are reflected. Beginning 1 cm
proximal to the joint, the radial third of the extensor
tendon is stripped back to a point 3 mm proximal to the
level of the articular surface of the metacarpal head. A
suture is placed to prevent additional tearing. The strip
is then looped around the lumbrical tendon and sutured
to itself. Prior to placing the suture, tension is carefully
adjusted with the MCP joint at 95° of flexion. The repair
is tested under direct visualization with flexion and
extension of the MCP joint, and tightened as necessary.
Carroll and colleagues22 reported using a distally
based ulnar slip of the EDC to reconstruct the sagittal
band in patients who had previously failed conservative
management. The EDC tendon is first centralized by
releasing the ulnar sagittal band. The ulnar slip of the
EDC is then looped around the radial collateral liga-
ment and carefully tensioned to allow full flexion. The
EDC slip is then sutured to the EDC tendon.
The common themes of the above repairs are: (1)
wide exploration of the sagittal band complex, freeing
the tendon and sagittal band from the underlying
scarred capsule; (2) identification of stout material to
which to anchor the repair; (3) ideally, use of either the
juncturae tedinae or portion of the extensor tendon as
a pedicled tendon graft; (4) release of any tight portion
of the ulnar sagittal band that would cause excessive
ulnar pull; and (5) full range of motion from MCP joint
extension to flexion to test the adequacy of repair.
Postoperatively, the MCP joint is typically immobi-
lized for 4 to 6 weeks. MCP motion is then started with
a goal to regain full flexion. IP motion is started 2 weeks
after surgery. Koniuch16 has recommended the use of
dynamic splinting in the postoperative period. Excessive
stiffness of the MCP joint should be avoided at all costs.
INJURIES TO THE THUMB
Much like the other four digits, the radial component
of the thumb at the MCP joint is more critical to exten-
sor pollicis longus (EPL) stabilization than the ulnar
component.23 Subluxation or dislocation of the EPL
tendon is rare but has been reported. Rheumatoid
arthritis is one potential cause secondary to a bouton-
niere deformity of the thumb. A congenital case of bilat-
eral thumb contracture secondary to dislocation of
extensor tendons over the MCP joint of both thumbs
has also been reported.24 Traumatic damage to the dor-
the EPL tendon after a distal radius fracture may also
lead to EPL ulnar dislocation.25-27 Treatment of an injury
to the thumb sagittal band is similar to that of the
remaining digits.
362 Section 4:  Extensor Tendon Repair and Reconstruction

Ulnar Radial

Lumbrical
Tendon slip
(McCoy)

Ulnar Scarred radial

sagittal sagittal band
fibers
Ulnar released
subluxation

RCL

A Injury B Primary suture C Junctura tendinum D Tendon slip E Tendon slip

(Kettlekamp) (Wheeldon) (McCoy) (Carroll)
Figure 33-12  Methods of extensor hood reconstruction. A, Ulnar subluxation of the EDC tendon caused by a torn radial
sagittal band. B, Primary suture of the radial sagittal band centering the EDC tendon. C, The ulnar juncture tendinum is
released from the adjacent tendon and sutured to the palmar radial sagittal band remnant of the deep intermetacarpal
ligament. D, The distal tendon is splinted on the radial side and wrapped around the lumbrical muscle. E, An ulnar, distally
based slip of the EDC is looped around the radial collateral ligament (RCL).

References
1. Ishizuki M: Traumatic and spontaneous dislocation of exten-
sor tendon of the long finger, J Hand Surg (Am) 15:967–972,
1990.
2. Rayan GM, Murray D, Chung K, et al: The extensor retinacular
system at the metacarpophalangeal joint: Anatomical and
histological study, J Hand Surg (Br) 22:585–590, 1997.
3. Smith RJ: Balance and kinetics of the fingers under normal
and pathological conditions, Clin Orthop Relat Res 104:
92–111, 1974.
4. Hunter JM, Mackin EJ, Callahan AD: Rehabilitation of the Hand
and Upper Extremity, ed 5, St Louis/London/Philadelphia/
Sydney/Toronto, 2002, Mosby, pp 507–512.
5. Araki S, Ohtani T, Tanaka T: Acute dislocation of the extensor
digitorum communis tendon at the metacarpophalangeal
joint, J Bone Joint Surg (Am) 69:616–619, 1987.
6. Kettelkamp DB, Flatt AE, Moulds R: Traumatic dislocation of
the long finger extensor tendon: A clinical, anatomical, and
biomechanical study, J Bone Joint Surg (Am) 53:229–240,
1971.
7. Wheeldon FT: Recurrent dislocation of the extensor tendons
in the hand, J Bone Joint Surg (Br) 36:612–617, 1954.
8. Young CM, Rayan GM: The sagittal band: anatomic and bio-
mechanical study, J Hand Surg (Am) 25:1107–1113, 2000.
9. Andruss RJ, Herndon JH: Ulnar subluxation of the extensor
digitorum communis tendon: a case report and review of the
literature, Iowa Orthop J 13:208–213, 1993.
10. Ovesen OC, Jensen EK, Bertheussen KJ: Dislocation to exten-
sor tendons of the hand caused by focal myoclonic epilepsy,
J Hand Surg (Br) 12:131–132, 1987.
11. Posner MA, McMahon MS: Congenital radial subluxation of
the extensor tendons over the metacarpophalangeal joints: A
case report, J Hand Surg (Am) 19:659–662, 1994.
12. Rayan GM, Murray D: Classification and treatment of closed
sagittal band injuries, J Hand Surg (Am) 19:590–594, 1994.
13. Jeon I, Seok J, Choi J, et al: Snapping junctura tendinum to
the small finger simulating radial sagittal band rupture: A
report of two cases, J Bone Joint Surg (Am) 91:1219–1222, 2009.
14. Bunnell S: Surgery of the Hand, Philadelphia/London/Mon-
treal, 1948, JB Lippincott, pp 670–671.
15. Ritts GD, Wood MB, Engber WD: Nonoperative treatment of
traumatic dislocations of the extensor digitorum tendons in
patients without rheumatoid disorders, J Hand Surg (Am)
10:714–716, 1985.
16. Koniuch MP, Peimer CA, VanGorder T, et al: Closed crush
injury of the metacarpophalangeal joint, J Hand Surg (Am)
12:750–757, 1987.
17. Inoue G, Tamura Y: Dislocation of the extensor tendons over
the metacarpophalangeal joints, J Hand Surg (Am) 21:464–
469, 1996.
18. Catalano LW, Gupta S, Ragland R, et al: Closed treatment of
nonrheumatoid extensor tendon dislocations at the metacar-
pophalangeal joint, J Hand Surg (Am) 31:242–245, 2006.
 Chapter 33:  Sagittal Band Injuries—Primary and Secondary Management
19. Hame SL, Melone CP: Boxer’s knuckle in the professional
athlete, Am J Sports Med 28:879–882, 2000.
20. Wheeldon FT: Recurrent dislocations of extensor tendons in
the hand, J Bone Joint Surg (Br) 36:612–617, 1954.
21. McCoy FJ, Winsky AJ: Lumbrical loop operation for luxation
of the extensor tendons of the hand, Plast Reconstr Surg
44:142–146, 1969.
22. Carroll C, Moore JR, Weiland AJ: Postraumatic ulnar sub­
luxation fo the extensor tendons: A reconstructive technique,
J Hand Surg (Am) 12:227–231, 1987.
23. Jaibaji M, Rayan GM, Chung KW: Functional anatomy of the
thumb sagittal band, J Hand Surg (Am) 33:879–884, 2008.
363
24. Rudigier J, Karnosky V: Surgical correction of congenital bilat-
eral dislocations of the extensor tendons of the thumb, Hand-
chir Mikrochir Plast Chir 20:89–92, 1988.
25. Churchill M, Citron N: Isolated subluxation of the EPL
tendon. A cause of ‘boutonniere’ deformity of the thumb,
J Hand Surg (Br) 22:790–792, 1997.
26. Cardon LJ, Toh S, Tsubo K: Traumatic boutonniere deformity
of the thumb, J Hand Surg (Br) 25:505–508, 2000.
27. Gong HS, Chung MS, Oh JH, et al: Ulnar subluxation of a
ruptured EPL tendon at the metacarpophalangeal joint: Case
report, J Hand Surg (Am) 34:910–913, 2009.
 CHAPTER
34  
TENDON TRANSFERS FOR
EXTENSOR TENDON
RECONSTRUCTION
Lance M. Brunton, MD, A. Bobby Chhabra, MD, and
Mollie O Manley, MD, MS
OUTLINE
Upper extremity extensor tendon injuries are often
detrimental to overall hand function and may lead to
significant patient disability. Insufficiency of the wrist,
thumb, and/or digital extensor tendons may be caused
by direct or indirect mechanisms or may be second-
arily attributable to systemic disease or radial nerve
dysfunction. This chapter will provide an overview of
tendon transfer methods to address extensor tendon
insufficiency, alternatives to tendon transfers for
various clinical scenarios, and guidelines for postop-
erative rehabilitation after reconstructive techniques.
The extensor muscles of the wrist and hand are con-
tained within the dorsal aspect of the forearm and are
all innervated by the radial nerve. At the level of the
wrist, the extensor tendons are divided into six com­
partments by tough fibrous septae of the extensor
retinaculum, numbered from radial to ulnar. The first
compartment contains the abductor pollicis longus
(APL) and extensor pollicis brevis (EPB). Anatomic
variation within this compartment includes potential
multiple tendon slips of the APL and a distinctly sepa-
rate compartment for the EPB.1 The second compart-
ment includes the extensor carpi radialis longus (ECRL)
and the extensor carpi radialis brevis (ECRB). The ECRB
is oriented ulnar to the ECRL. The third compartment
houses the extensor pollicis longus (EPL). This tendon
takes a sharp turn radially after it courses distal to the
ulnar aspect of Lister’s tubercle. Within the fourth com-
partment are the extensor digitorum communis (EDC)
and the extensor indicis proprius (EIP). The terminal
branch of the posterior interosseous nerve (PIN) and
accompanying interosseous vessels lie at the floor of this
compartment. The EIP is oriented ulnar to the index
EDC. The extensor digiti minimi (EDM) is the sole
tendon within the fifth compartment at the level of the
364
distal radioulnar joint (DRUJ). The final and most ulnar
sixth compartment encloses the extensor carpi ulnaris
(ECU). This tendon courses through a fibro-osseous
tunnel on the dorsal surface of the distal ulna, creating
a groove that is often evident on plain radiographs of
the wrist.
Extensor tendons are divided into zones of the hand
and forearm, which help to guide treatment. The zones
are numbered from 1 to 9 with odd numbered-zones
largely corresponding to underlying joints. Zone 1 over-
lies the distal interphalangeal joint (DIP) of the four
digits, and zone 9 extends proximal to the musculoten-
dinous junction. The extensor zones of the thumb are
altered because there is one less joint. In the thumb
zone T1 is over the interphalangeal joint (IP) and T3
over the metacarpophalangeal (MCP) joint, whereas in
the other digits the MCP joint would correspond to
zone 5. The carpal level is T5 for the thumb and zone
7 for the other digits.2
Injury or dysfunction of an extensor musculotendi-
nous unit may result from direct laceration, acute closed
rupture, chronic attritional wear, vascular insufficiency,
systemic inflammatory disease, or radial nerve denerva-
tion. There are several clinical scenarios where extensor
tendon injuries cannot be adequately repaired in
primary fashion and may require tendon transfer recon-
struction. A classic example is rupture of the EPL tendon
in association with nonoperative treatment of a distal
radius fracture. When faced with such a scenario, patient
factors such as comorbidities, accompanying injuries,
occupation, and compliance must be taken into account.
Basic principles of tendon transfer surgery remain para-
mount for achieving optimal results. The work of Starr
among injured military personnel in the early twentieth
century established a framework for tendon transfer
surgery and is summarized in Table 34-1.
More recent work has demonstrated that sarcomere
length may be measured in vivo and a single sample
 Chapter 34:  Tendon Transfers for Extensor Tendon Reconstruction
Table 34-1  Principles of Tendon Transfer Surgery
Applicable to Extensor Tendon Reconstruction
Expendable The choice of tendon for transfer
donor should not fully compromise existing
normal function.
One tendon for Splitting a transferred tendon for
one function separate functions will function only
to the shortest excursion of the
recipient tendons.
Direction A straight line of pull maximizes
function of the transfer.
Similar excursion Donor and recipient excursion
should be comparable.
Similar strength Donor and recipient strength should
be comparable. One grade of
recipient strength will be lost, even
for the most successful transfers.
Joint mobility Tendon transfers will not function in
the setting of contracted joints. Near
full passive mobility of distal joints
must be established preoperatively.
Synergy Antagonistic muscles must provide a
stabilizing effect for the recipient.
Tenodesis Taking advantage of the tenodesis
effect of the hand enhances tendon
transfer function; wrist arthrodesis
should be avoided if possible.
Tissue Tendon transfers should be delayed
equilibrium until adjacent bone and soft tissue
injuries are healed and mature.
Power versus Weaker motors are used for position
positional motors and stronger motors for power.
represents the entire muscle.3 Consequently, transferred
musculotendinous units may be set at a sarcomere
length specific to the muscle being replaced. Friden4
astutely recognized that surgeons typically overtighten
transfers, thinking they will relax over time, when in
reality the sarcomeres are overstretched and only fire at
28% of the maximum force of the muscle. This may in
part account for transfers losing one grade of strength.
Overly tightened transfers become somewhat of a
passive tenodesis.5
Wrist kinematics plays a role in tendon transfer. The
“dart thrower’s” arc, described as combined wrist exten-
sion and radial deviation through combined wrist
flexion and ulnar deviation, is the functional motion for
most activity. It is argued that with some tendon trans-
fers, this motion is either not restored or compromised.
For example, if the flexor carpi ulnaris (FCU) is sacri-
ficed for transfer in a patient with radial nerve palsy, the
dart thrower’s arc may be restricted.
365
Traumatic extensor tendon injury may be direct or
indirect and further classified as acute or chronic. The
acute treatment of these injuries is covered earlier in this
textbook. Occasionally, the diagnosis is missed or the
injury is neglected, especially in the setting of poly-
trauma, altered mental capacity, or in patients with poor
understanding of a condition or limited access to
medical resources. The chronicity of the condition often
alters the type of treatment that can be rendered. Cases
that would ordinarily be treated by direct repair are
instead addressed by delayed reconstruction, and tendon
transfer surgery is an indispensible option in these clini-
cal scenarios.
The first description of extensor attritional rupture
was a case report of two patients by Vaughn-Jackson in
1948. Both patients had rupture of the ring and small
EDC in proximity to the distal end of the ulna; the
“syndrome” of progressive extensor ruptures from ulnar
to radial now bears the author’s name.6 Almost a decade
later, another case report demonstrated six patients with
attritional extensor ruptures associated with rheumatoid
arthritis (RA). The authors speculated that rupture
resulted from attritional changes caused by localized
rheumatoid synovitis.7 In patients with RA, the ECU
tendon subluxates volarly, the wrist deviates radially,
and the digital extensors course directly over a dorsally
prominent distal ulna.
Radial nerve dysfunction compromises the extension
capabilities of the wrist and hand. The radial nerve
essentially innervates the entire dorsal aspect of the
forearm musculature. The radial nerve proper innervates
the triceps, lateral portion of brachialis, anconeus, bra-
chioradialis, and ECRL. At the level of the elbow, the
radial nerve proper divides into its superficial sensory
branch and the PIN. The PIN innervates the remaining
extensor muscles in the forearm including the ECRB
(with some variability), supinator, APL, EPB, EIP, EDC,
EDM, and ECU. The radial nerve may be injured directly
from a penetrating injury or often indirectly in asso­
ciation with humeral shaft fractures. It may also be
injured iatrogenically during surgical approaches to the
arm. Depending on the level and extent of the nerve
injury, wrist extension, digit extension, and/or thumb
extension may be compromised. Lack of active wrist
extension will severely affect power grip of the hand.
Digit extension is mostly compromised at the level
of the MCP joints because IP joint extension receives
significant contributions from the median and ulnar-
innervated intrinsic musculature (lumbricals and inter-
ossei) of the hand. A variety of tendon transfers have
been described to improve function without creating
imbalance within the hand. In devising an appropriate
transfer, available muscles that can substitute for the lost
function are considered and the above principles of
tendon transfer surgery guide the ultimate choice and
technique.
366 Section 4:  Extensor Tendon Repair and Reconstruction

METHODS OF TREATMENT
Traumatic Injury of EPL
Regardless of the mechanism of injury, treatment of an
EPL rupture follows a general algorithm: primary repair
without transposition, primary repair with transposi-
tion, intercalary tendon autograft, tendon transfer, and
thumb IP fusion. Direct repair is clearly the most desir-
able and can be accomplished if tendon retraction is
minimal and the cut ends are healthy. This sometimes
requires a radially directed transposition of the EPL
tendon away from its normal course adjacent to the
ulnar aspect of Lister’s tubercle to achieve increased
length and a more direct line toward the thumb. When
the EPL tendon appears atrophied or degenerative, the
cut ends are debrided until healthy tendon is evident. If
direct repair is impossible even after transposition, an Figure 34-1  EIP-to-EPL transfer. The EPL rupture is
intercalary tendon autograft may be used. The obvious identified. The EIP is identified over the index MCP joint
disadvantages are that autografts are essentially avascu- (ulnar to the common extensor tendon), transected, and
pulled through the proximal incision.
lar and that two repair sites must heal during rehabilita-
tion. The most common available autograft for this
purpose is the palmaris longus (PL), present in approxi-
mately 80%–85% of people. Alternatives include the
long or ring flexor digitorum superficialis (FDS), plan-
taris, or a toe extensor tendon.
Prior to considering a thumb IP arthrodesis as a last
resort, a final option is tendon transfer. In this regard, the
EIP is classically chosen for transfer to the distal cut end
of the EPL. The EIP is a good option for transfer to
the EPL due to its similar line of pull and amplitude.
Prior to harvesting this donor, the patient must demon-
strate independent EIP function by extending only the
index finger while keeping the other digits flexed. Explo-
ration is carried out to identify the ruptured EPL near
the scapho-trapezo-trapezoidal (STT) joint, and once
tendon transfer is deemed appropriate, a transverse inci-
sion is made over the dorsum of the index MCP joint. The
EIP is identified as ulnar to the index EDC and tagged. Figure 34-2  EIP-to-EPL transfer. A tendon passer is used
Another incision is made proximal to the extensor reti- to pass the EIP through the EPL and a Pulvertaft weave is
naculum in the distal forearm, and the EIP is identified created after appropriate tensioning.
as the most distal muscle belly in the fourth compart-
ment. The EIP is confirmed as the tagged tendon in the
distal wound. The tendon is cut distally and brought follow up of 4.3 years.9 In a similar retrospective case
through the more proximal incision (Figure 34-1). The series, the tendon transfer group trended toward less
EIP is tunneled and coapted to the distal EPL stump by extension and decreased strength, so the authors con-
Pulvertaft weave or directly sutured to the extensor cluded that people requiring more dexterity and power,
mechanism at the thumb MCP level (Figures 34-2 and such as musicians or surgeons, should have a free tendon
34-3). The tension should be set in wrist extension so graft.10
that the tip of the thumb touches the tip of the index
finger. With passive wrist flexion, the thumb IP joint Systemic Disease
should fully extend. The thumb is then immobilized for Extensor tendon ruptures are common in the setting of
4 weeks with 0° IP flexion and 20° of wrist extension.8 inflammatory arthropathies such as RA. The reconstruc-
A recent study performed by Schaller and colleagues tive ladder of direct repair, adjacent tendon coaptation,
compared intercalary PL autograft to EIP tendon trans- and tendon transfer is followed. In the setting of RA,
fer for EPL reconstruction. They found no major differ- however, tendon failure by attenuation is rarely ame-
ence in thumb function or complications after a mean nable to direct repair. These patients typically present in
 Chapter 34:  Tendon Transfers for Extensor Tendon Reconstruction 367

Table 34-2  Common Tendon Transfers for Radial

Nerve Dysfunction
Procedure Wrist MCP Joint Thumb
Boyes PT to FDS (RF) to 1 FDS (MF)
2
(1960) ECRB EDC to EPL
1
2FDS (MF) to FCR to APL
EIP and EPB

Jones PT to FCU to EDC FCR to EPL,

(1921) ECRB/L III-IV, FCR to EPB, and APL
EDC II and EIP
Merle PT to 1
2 FCU to EDC PL to EPB
d’Aubigne ECRB/L and APL
(1946)
1
2 FCU to EPL
Riordan PT to FCU to EDC PL to EPL
(1983) ECRB
Starr (1922) PT to FCR to EDC PL to EPL
and Brand ECRB
(1985)
Tsuge and PT to FCR to EDC PL to EPL
Adachi ECRB
Tenodesis of
APL to BR

Figure 34-3  EIP-to-EPL transfer. Depiction of the finished

transfer.
delayed fashion after the tendon ends have retracted and
scarred to adjacent tissue. Once full small joint passive
motion is reestablished, the best option is often tendon
transfer. Briefly, the EIP may be transferred to a ruptured
EPL and a long/ring FDS transferred to a ruptured EDC.
If needed, silicone MCP arthroplasties may be per-
formed and rehabilitated prior to a tendon transfer.8
Radial Nerve Dysfunction
The most commonly described series of tendon trans-
fers to address a permanent high (or low) radial nerve
deficit were adopted in response to injuries suffered by
soldiers from the first two world wars. Others have
drawn on their early experience and described adapta-
tions to these procedures with specific goals in mind.
Several of these contributors and their corresponding
transfers of choice are summarized in Table 34-2.
Restoration of Wrist Extension
In high radial nerve deficits, innervation to the ECRL,
ECRB, and ECU is lost and active wrist extension is
absent.11 The pronator teres (PT) is the most reliable
available tendon to address this deficit and is typically
routed to the ECRB for a potentially more centralized
and balanced wrist extension arc. Abrams and col-
leagues confirmed the suitability of the PT by showing
that its muscle fiber length and cross-sectional area are
comparable to the ECRB.12 This transfer is sometimes
performed early after a recognized radial nerve palsy, to
maintain wrist extension, maximize the tenodesis effect,
and aid in early retraining, even if later nerve recovery
restores innervation to the wrist extensor muscles. At
the very least, it may help to prevent wrist flexion con-
tracture and aid in power grasp with improved wrist
positioning. An incision is made on the volar-radial
aspect of the mid-forearm over the insertion of the PT
tendon. The PT must be harvested with a long strip of
periosteum and freed proximally to ensure maximum
excursion. The tendon is then passed subcutaneously
around the border of the radius superficial to the BR
and ECRL. The PT is sutured to the ECRB just distal to
the musculotendinous junction. This connection may
be reinforced with a free ECRL tendon graft. The transfer
is tensioned with the wrist in approximately 45° of
extension.13
Occasionally, patients with a low radial nerve palsy
(PIN palsy) affecting only the ECU and/or ECRB may
demonstrate excessive radial deviation of the wrist
during active extension. To address this imbalance, the
ECRL may be transferred to the ECU or ECRB and effec-
tively increase relative ulnar deviation during wrist
extension and subsequently maximize power grasp.
Restoration of Thumb Extension
The classic tendon transfer to restore thumb extension
is PL to EPL. Comparable excursion is obtained and a
368 Section 4:  Extensor Tendon Repair and Reconstruction

combination of thumb abduction at the MCP joint and musculotendinous junction. The FCR is then tunneled
extension at the IP joint is achieved with the positioning subcutaneously toward the dorsal forearm. The FCR is
of this transfer. It must be first identified that the patient coapted to several of the thickest EDC tendons by Pul-
has a PL tendon, as it is absent in 15% to 20% of the vertaft weave, while the diminutive tendons are sutured
population. This is determined by having the patient to neighboring EDC tendons further distally. Equal ten-
oppose the thumb to the small fingertip while maxi- sioning is difficult, but should be done with the wrist
mally flexing the wrist, at which time it is readily evident and MCP joints in neutral and the FCR under maximal
or palpable. An incision is made on the dorsal aspect of pull (Figure 34-4).
the wrist and the EPL is identified and cut at the mus-
culotendinous junction. The EPL tendon is rerouted
from the third extensor compartment across the ana-
tomic snuff box to pass along the radial border of the
thumb metacarpal. The PL is then identified, freed prox-
imally, and cut at the level of the distal wrist flexion
crease. The tendons are coapted by Pulvertaft weave in
line with the thumb metacarpal. Tensioning of this
transfer should be done with the wrist in neutral and
maximum tension on both ends.13
For patients without a PL, the long or ring FDS is used
and may be brought either around the radius or through
the interosseous membrane (IOM) in the distal forearm.
A slip of the brachioradialis tendon may also be an
adequate motor to substitute for EPL function. A last
option is to include the EPL in the FCU to EDC transfer Extensor
described next. digitorum
Extensor
pollicis communis
Restoration of Digit Extension longus
While the aforementioned transfers for wrist and thumb
extension are consistent among Brand, Jones, and Boyes, Extensor carpi
they all differ in their transfer for restoring digit exten- radialis longus
sion. Brand chose the flexor carpi radialis (FCR) because
of its proximity to the wrist extensors and its adequate Extensor carpi
excursion to power all of the digital extensors simulta- radialis brevis
neously. Critics of the Jones transfer of the flexor carpi
ulnaris (FCU) cite the sacrifice of the most powerful
wrist flexor with ulnar deviation, especially in light of
the more physiological and functional “dart-thrower’s” Flexor carpi
radialis
arc of wrist motion. This transfer should be avoided in
Extensor
a manual laborer who requires wrist ulnar deviation for digitorum
power grasp activities such as hammering. The Boyes communis
transfer uses the ring FDS tendon directed through the
IOM for a straighter line of pull and sufficient excursion. Pronator
A disadvantage to this technique may be increased scar- teres
ring and adhesion formation through the IOM and
therefore some have advocated routing the superficialis
tendon around the radius, especially in adults. The long
finger FDS may compromise power grasp less than the
ring FDS, and its architecture resembles that of the
digital extensors to a closer degree.
The Brand transfer for restoring digit extension uti-
lizes the FCR tendon. An incision is made over the distal
volar forearm between the FCR and PL. The FCR is
identified, cut near its insertion and freed proximally to Brand transfer
allow proper excursion and direction. A second longi- Figure 34-4  Diagram of Brand transfer. (From Trumble TE,
tudinal incision is made in the central dorsal forearm. Rayan GM, Baratz M: Principles of Hand Surgery and Therapy,
The EDC tendons are identified and divided at their ed 2, Philadelphia, 2010, Saunders, page 304).
 Chapter 34:  Tendon Transfers for Extensor Tendon Reconstruction
The original Jones transfer for digit extension utilized
both the FCU and FCR. Today, some surgeons favor the
stronger FCU over the FCR. A volar-ulnar incision is
made in the distal forearm, and the FCU tendon is cut
just proximal to its insertion at the pisiform and freed
proximally. The distal muscle fibers are excised off the
FCU tendon, debulking it for later use. Another incision
may be made more proximally over the FCU muscle
belly for additional untethering of fascial attachments
to increase excursion, but care must be taken to avoid
the innervation of the muscle at its proximal 2 inches.
A third incision is made over the dorsal forearm, through
which the FCU is passed. The FCU is coapted to the EDC
tendons in a similar fashion to the Brand transfer. Some
surgeons avoid including the EDM during transfer for
fear of overextending the small digit, but it should be
included when a substantial extensor lag exists after the
other EDC tendons have been secured. The FCU tendon
should have a straight line of pull from the medial epi-
condyle to the EDC. The transfer should carefully incor-
porate each digital extensor to keep all four MCP joints
extending uniformly.
Last, the Boyes transfer for digit extension uniquely
passes the donor FDS musculotendinous units through
the IOM. A longitudinal incision is made in the radial
distal forearm to approach the volar aspect of the IOM.
A transverse incision is made in the distal palm in line
with the long and ring fingers. The FDS tendons are
identified, divided proximal to Camper’s chiasma, and
passed subcutaneously to the more proximal incision.
Two large windows are made in the IOM proximal to
the pronator quadratus muscle without violating the
anterior and posterior interosseous vessels. The muscle
bellies of the FDS are then passed through the IOM. An
incision is made on the dorsal forearm and the rerouted
donor tendons are delivered to the dorsal surface. The
long FDS is brought to the radial side of the wrist and
interwoven to the EIP and EPL. The ring FDS is taken
ulnarly and sutured to the EDC. This transfer is ten-
sioned with the wrist in 20° of extension and FDS under
maximal tension with an assistant keeping the patient’s
digits and thumb clenched into a fist.13
TREATMENT ALTERNATIVES
Tendon transfers for radial nerve dysfunction have been
used reliably for almost 90 years, but these procedures
are not without drawbacks. Tendon transfers are a
balance between restoring function and introducing
additional dysfunction. An alternative to sacrificing
“expendable” tendons that is gaining momentum is the
sacrifice of “expendable” nerves. Repair or nerve grafting
of proximal lesions has historically poor results because
of scar infiltration, large reinnervation distances, and
irreversible loss of target motor endplates after 18 to 24
months.14 Some argue that tendon transfers lead to
unnatural ergonomics.15 Nerve transfer has theoretical
369
Figure 34-5  Median to radial nerve transfer, shown in a
cadaveric forearm. The pledget has been placed under the
two nerve transfers. The distal transfer (left) is a median
nerve branch to the PL sutured to a radial branch to the
ECRB and the more proximal transfer (right) is a median
nerve branch to the FCR sutured to the PIN.
advantages over nerve autograft because of decreased
donor site morbidity, pure motor donors, and shorter
reinnervation distances. In addition, nerve transfers can
be accomplished in situations that tendon transfers are
less advantageous, such as in the presence of significant
joint stiffness.16 Distal motor nerve reconstruction is
more optimal because of dissection and coaptation
away from the zone of injury.17 Furthermore, the brain
is better equipped to adapt to nerve rather than tendon
transfers. For a high radial nerve palsy, branches of the
median nerve in the proximal forearm may be sacrificed
without appreciable compromise of other hand/wrist
function. Redundant branches to the FCR, FDS, and PL
muscles may be used for nerve transfer to the PIN and/
or independent nerve branches to the wrist extensors16
(Figure 34-5). However, one must balance these advan-
tages with the possible risk of injury to uninvolved
donor nerves such as the median and ulnar nerves.
REHABILITATION
The principles of tendon rehabilitation are as important
as the principles of transfer surgery. Traditionally, three
phases of rehabilitation are recognized, each of which
lasts for approximately 3 weeks. An initial period of
immobilization allows early healing and avoids inad-
vertent damage to repair sites during the acute inflam-
matory phase. This is followed by early passive range of
motion to allow further healing and protection of the
repair site while ensuring adequate tendon gliding, min-
imizing scar adhesions, and preventing joint contrac-
ture. During this phase, dynamic extension splints may
be fabricated to provide more reliable passive mobility
while protecting the repair and restricting the urge to
attempt active motion prematurely. Finally, active range
of motion is initiated and the central nervous system is
trained to fire the transferred musculotendinous unit to
370 Section 4:  Extensor Tendon Repair and Reconstruction
achieve a different function than it is accustomed to
performing. Extensor lags are common and may be
treated with static night-time extension splinting.
Gradual strengthening and return to vocational and
avocational activities is pursued as tailored to the indi-
vidual patient.
As tendon repair techniques have improved, rehabili-
tative protocols have adapted to shorten recovery time.
Some surgeons now recommend immediate active
range of motion in an effort to speed recovery and
decrease the necessity of secondary tenolysis surgery.
Early active extension protocols are started in the first
few days postoperatively. The postoperative splint is
removed and a custom thermoplastic splint replaces it.
The patient is then instructed to start active extension
out of the splint with increasing frequency as the days
and weeks progress. Another form of accelerated reha-
bilitation is a dynamic splinting protocol. A device is
attached to the splint with a rubber band traction mech-
anism that passively extends the affected joint. A recent
study comparing early active to dynamic splinting pro-
tocols after EPL reconstruction found no difference at 8
weeks between groups.18 The authors theorized, however,
that patients were not as aggressive in their early active
home exercises for fear of doing something wrong or
References
1. Jackson WT, Viegas SF, Coon TM, et al: Anatomical variations
in the first extensor compartment of the wrist. A clinical and
anatomical study, J Bone Joint Surg (Am) 68:923–926, 1986.
2. Matzon JL, Bozentka DJ: Extensor tendon injuries, J Hand
Surg (Am) 35:854–861, 2010.
3. Lieber RL, Ponten E, Burkholder TJ, et al: Sarcomere length
changes after flexor carpi ulnaris to extensor digitorum com-
munis tendon transfer, J Hand Surg (Am) 21:612–618, 1996.
4. Friden J, Lieber RL: Evidence for muscle attachment at rela-
tively long lengths in tendon transfer surgery, J Hand Surg
(Am) 23:105–110, 1998.
5. Peljovich A, Ratner JA, Marino J: Update of the physiology
and biomechanics of tendon transfer surgery, J Hand Surg
(Am) 35:1365–1369, 2010.
6. Vaughan-Jackson OJ: Rupture of extensor tendons by attrition
at the inferior radio-ulnar joint. Report of two cases, J Bone
Joint Surg (Br) 30:528–530, 1948.
7. Straub LR, Wilson EH: Spontaneous rupture of extensor
tendons in the hand associated with rheumatoid arthritis,
J Bone Joint Surg (Am) 38:1208–1317, 1956.
8. Feldon P, Terrono AL, Nalebuff EA, et al: Rheumatoid arthritis
and other connective tissue diseases. In Green DP, Hotchkiss
RN, Pederson WC, Wolfe SW, editors: Green’s Operative Hand
Surgery, ed 5, Philadelphia, 2005, Churchill Livingstone–
Elsevier, pp 2068–2074.
9. Schaller P, Baer W, Carl HD: Extensor indicis-transfer com-
pared with palmaris longus transplantation in reconstruction
of extensor pollicis longus tendon: A retrospective study,
Scand J Plast Reconstr Surg Hand Surg 41:33–35, 2007.
10. Pillukat T, Prommersberger KJ, van Schoonhoven J: Compari-
son of the results between reconstruction of the extensor
pollicis longus tendon using a free interposition tendon graft
and extensor indicis transposition, Handchir Mikrochir Plast
Chir 40:160–164, 2008.
overstressing the repair. Another group compared early
dynamic splinting to static splinting after ECRL to EPL
reconstruction; they found better range of motion,
shorter rehabilitation period, shorter time off work, and
better movement of the thumb.19 A systematic review of
rehabilitation protocols after extensor tendon repair
compared immobilization, early controlled mobiliza-
tion, and early active mobilization. While immobiliza-
tion has led to comparatively inferior results, the
difference between the other two protocols disappears
by 3 months postoperatively.20
SUMMARY
The work of early hand surgeons laid the foundation for
reconstructive alternatives for loss of extensor tendon
function to injury, disease, or nerve impairment. These
techniques are now employed by most well-trained and
technically proficient practicing hand specialists. Recent
contributions have focused on enhancing tendon repair
and accelerating rehabilitative efforts to optimize patient
outcome. We have summarized the classically described
tendon transfers to treat upper extremity extensor dys-
function and challenge the next generation to think of
new ways to address these difficult problems with inno-
vative techniques and rehabilitative protocols.
11. Omer GE Jr: Tendon transfers in radial nerve paralysis. In
Hunter JM, Schneider LH, Mackin EJ, editors: Tendon and
Nerve Surgery in the Hand, St Louis, 1997, Mosby Year–Books,
425–431.
12. Abrams GD, Ward SR, Friden J, et al: Pronator teres is an
appropriate donor muscle for restoration of wrist and thumb
extension, J Hand Surg (Am) 30:1068–1073, 2005.
13. Green DP: Radial nerve palsy. In Green DP, Hotchkiss RN,
Pederson WC, Wolfe SW, editors: Green’s Operative Hand
Surgery, ed 5, Philadelphia, 2005, Churchill Livingstone–
Elsevier, pp 1113–1129.
14. Nath RK, Mackinnon SE: Nerve transfers in the upper extrem-
ity, Hand Clin 16:131–139, 2000.
15. Lowe JB 3rd, Sen SK, Mackinnon SE: Current approach to
radial nerve paralysis, Plast Reconstr Surg 110:1099–1113,
2002.
16. Brown JM, Tung TH, Mackinnon SE: Median to radial nerve
transfer to restore wrist and finger extension: Technical
nuances, Neurosurgery 66(3 Suppl Oper.):75–83, 2010.
17. Tung TH, Mackinnon SE: Nerve transfers: indications, tech-
niques, and outcomes, J Hand Surg (Am) 35:332–341, 2010.
18. Giessler GA, Przybilski M, Germann G, et al: Early free active
versus dynamic extension splinting after extensor indicis
proprius tendon transfer to restore thumb extension: A pro-
spective randomized study, J Hand Surg (Am) 33:864–868,
2008.
19. Justan I, Bistoni G, Dvorak Z, et al: Evaluation of early
dynamic splinting versus static splinting for patients with
transposition of the extensor carpi radialis longus to the
extensor pollicis longus, In Vivo 23:853–857, 2009.
20. Talsma E, de Haart M, Beelen A, et al: The effect of mobiliza-
tionon repaired extensor tendon injuries of the hand: A
systematic review, Arch Phys Med Rehabil 89:2366–2372,
2008.
 CHAPTER
35  
SOFT TISSUE COVERAGE FOR
EXTENSOR TENDON
RECONSTRUCTION
Michel Saint-Cyr, MD, FRCS(C)
OUTLINE
A myriad of options exist for soft tissue reconstruction
and coverage of exposed extensor tendons. This can
range from simple skin grafting with or without turn-
over adipofascial flaps to free flaps in more complex
cases. Principles of proper patient and wound evalua-
tion, radical débridement, early coverage, and rehabili-
tation are paramount to maximize function. Transfer
of intrinsic flap (i.e., flap from the injured the hand)
should be considered first to cover local and small area
soft tissue defect. Local or regional flap such as radial
or ulnar forearm flap, dorsal interosseous artery flap,
or lateral arm flap may be considered to cover the
defect in the dorsum of the hand. Anterior thigh flap
or other vascularized distant flaps should be consid-
ered if the defects are extensive and located over the
dorsum of the hand or forearm. Thorough débride-
ment is required before embarking on complicated
reconstructive procedures, and postoperative motion
of the hand and wrist is important to prevent joint
stiffness and tendon adhesions. Despite increased
technical requirements and length of operation, free
flap reconstruction often results in fewer postoperative
complications due to better vascularization, which is
important when early postoperative mobilization or
adjuvant therapy is required.
Often, extensor tendon exposure, lacerations, or tendon
loss will require coverage with well-vascularized tissue
to promote proper tendon healing and early mobiliza-
tion. Adequate coverage also helps minimize any sub-
sequent scarring, in an environment that is already
prone to significant adhesions and contracture forma-
tion. Therefore, it behooves the reconstructive hand
surgeon to provide well-vascularized tissue with either
an intrinsic, locoregional, or distant free flap to provide
stable soft tissue coverage. The dorsal skin of the hand
has many qualities that allow flexion and extension of
the digits. The increased skin laxity, pliability, and thin-
ness also make the dorsum of the hand an excellent
donor site for local flaps applicable to extensor tendon
coverage. Flap selection will ultimately be dictated by
the size and location of the defect, donor site availabil-
ity, and recipient tissue characteristics.
Goals of this chapter will be to outline initial evalu-
ation and management principles in the presence of
exposed extensor tendons of the upper extremity follow-
ing injury. Principles of flap selection and use will
be discussed to provide stable coverage and expedite
rehabilitation and maximize function.
EVALUATION AND TREATMENT
As with any upper extremity–mutilating hand injury,
ruling out other severe systemic injuries is paramount.
Before embarking in a complex reconstruction, the
patient needs to be stabilized and all other life-
threatening injuries need to be addressed and resolved.
Patient-specific factors such as overall general health
condition, associated comorbidities, profession, socio-
economic status, age, and compliance to therapy need
to be considered when selecting the type of reconstruc-
tion. There are also wound-specific factors such as defect
size as well as mechanism of injury, such as crush, pene­
trating versus blunt trauma, amputation, etc. All wound
factors need to be considered as well as the zone of
injury and availability of local or distant tissue for flap
coverage.
WOUND DÉBRIDEMENT
Early radical débridement, of all nonviable tissue under
tourniquet, control is pivotal prior to any attempt at
locoregional or free flap soft tissue reconstruction. The
critical step involves débridement of all marginally and
questionably viable tissue to convert a contaminated
wound into a clean wound and thus minimize risks of
subsequent infection. This also allows a clear evaluation
of all injured and missing structures. Early aggressive
débridement should be performed over traditional
serial débridement whenever possible. Serial débride-
ment can delay final wound closure and make assess-
ment of tissue viability difficult, and trigger a cascade of
371
372 Section 4:  Extensor Tendon Repair and Reconstruction

additional tissue loss from desiccation due to prolonged

dressing changes. Early débridement and reconstruction
also help to achieve the ultimate goal of early mobiliza-
tion and return to function, which is critical in the upper
extremity.
The general assessment is done, ideally, in the operat-
ing room under tourniquet control. The upper extremity
is exsanguinated and a tourniquet is elevated and used
to provide a blood-free field, so as to better expose and
identify potentially devitalized tissue. All devitalized
tissue is then débrided and the wound is extirpated very
much like a tumor from the periphery towards the center
and within well-defined natural tissue planes. The
wound bed is resected entirely thus converting it from
a contaminated to a noncontaminated wound. Follow-
ing wound débridement, and once the extensor tendons
have been either grafted or repaired, healthy coverage
can be provided with either an intrinsic, locoregional,
or free flap, as needed. A major prerequisite is adequate
wound débridement to minimize any risk of infection,
wound breakdown, and flap loss. Any initial wound
Figure 35-1  Dorsal hand soft tissue defect following
that cannot be débrided thoroughly is best débrided first-stage radical débridement, under tourniquet control.
serially after 24 or 48 hours. A negative pressure dressing This wound was clean enough to be covered.
can be applied temporarily using a white sponge over
exposed extensor tendons so as to minimize any risk of
desiccation. Note that negative pressure therapy should helps minimize any risk of infection due to the presence
be used sparingly and only as a temporizing measure of residual necrotic tissue (Figure 35-1).
prior to definitive closure, which should be performed
TIMING OF RECONSTRUCTION
ideally within the first week. The upper extremity is
very sensitive to the timing of reconstruction, and any Reconstruction should be attempted as early as possible
prolonged immobilization will have a definite negative once adequate débridement is achieved. Advantages of
impact on final range of motion due to progressive early reconstruction include primary wound closure,
stiffness, joint contracture, and swelling. Early coverage coverage of vital structures, shorter hospitalization
allows patients to enter an aggressive rehabilitation course, avoidance of multiple procedures and multiple
program to maximize their range of motion. painful dressing changes, and early rehabilitation and
Once the wound has been properly débrided, the mobilization. An absolute indication for immediate
tourniquet is released and all nonbleeding and nonvi- primary reconstruction includes exposure of recon-
able tissue is reexcised. Wound edges are inspected for structed or native arteries and veins. Contraindications
bright red bleeding, and the wound is irrigated with a for immediate reconstruction include an unstable
bulb syringe only. Pulse lavage is not used and can lead patient that cannot tolerate a prolonged operative pro-
to extensor tendon friability and additional soft tissue cedure, and patients in whom amputation and pros­
trauma. Therefore, we only use triple antibiotic saline thesis would provide a better functional result than
with bulb irrigation. reconstruction.
Choice of extensor tendon coverage, working from If delayed reconstruction is selected or necessary,
distal to proximal, will be based on the level of injury then all joints must be actively or passively mobilized
as well as the availability of nontraumatized soft tissue to maintain motion. Prolonged use of negative pressure
in the proximity of the wound. Clearly, replacing like wound therapy dressings in the hand without passive
with like is the ideal condition. All defects that are and active mobilization is to be condemned as this can
replaced with local tissue of similar color, texture, pli- lead to severe stiffness and fibrosis.
ability, and sensation will provide a better outcome than
non loco-regional flaps. The resulting defect, following SOFT TISSUE COVERAGE AND
radical débridement, will also be much larger than the RECONSTRUCTION
initial wound size. Knowing that stable soft tissue cover-
age can be provided regardless of defect size should be Intrinsic Flaps
impetus for providing aggressive initial débridement. Clearly, if paratenon is available over the exposed exten-
This not only serves to expedite reconstruction but also sor tendon, a simple form of coverage can involve either
 Chapter 35:  Soft Tissue Coverage for Extensor Tendon Reconstruction
a split- or full-thickness skin graft, which is harvested
from the either the forearm, the hypothenar region or
groin. Note that skin grafts harvested further from the
defect will be less cosmetically matched compared to
more local skin graft options. Skin grafts harvested from
the hand or from the forearm would provide better skin
match compared to more distant skin grafts such as the
proximal forearm, or groin.
Turnover and Distally Based Adipofascial Flap
If the exposed extensor tendon is devoid of paratenon,
then a skin graft is not an option. A simple form of
reconstruction can include a turnover adipofascial flap,
which can be used to cover small-to-moderate sized
defects. These are then covered with a split-thickness
skin graft. Adipofascial flaps can be very useful for resur-
facing small exposed extensor tendon defects in the
digits as well as the dorsum of the hand. These can flaps
can be based off of small perforators from the dorsal
metacarpal arteries when covering defects in the hand
or dorsal digital branches when covering dorsal digital
defects. These can be wide based and are simply turned
over under elevated skin flaps and skin grafted to provide
well-vascularized coverage over the exposed extensor
tendons. Turnover adipofascial flaps need to be widely
based to maximize perforator incorporation into the
flap, as well as subcutaneous veins. When covering
digital defects, the flap is distally based and incorporates
a maximal amount of arterial perforators and subcuta-
neous veins for venous outflow. Closure of the skin flaps
that have been elevated should not be performed under
any tension, so as to minimize any risk of venous con-
gestion of the adipofascial turnover flap. These flaps are
simple to elevate, provide quick and easy coverage
options for small defects with exposed tendons, and
offer minimal morbidity to the donor site.
Reverse Cross-Finger Flap
Extensor tendon exposure in zones 1 through 4 can be
covered with reverse cross-finger flaps. The reverse cross-
finger flap, first described by Pakiam in 1978, is an
excellent local flap for soft tissue coverage of exposed
extensor tendons in the dorsal digit. Its vascular supply
is provided by the dorsal digital branches of the digital
arteries, as well as small subcutaneous veins and venae
comitantes from the dorsal digital branches. Subcutane-
ous veins from the cross-finger flap can also be used as
venous flow through veins for replants to bridge both
recipient and donor veins. The reverse cross-finger flap
is then covered with either a split- or full-thickness skin
graft for definitive coverage. The flap is elevated as
follows: The adjacent donor digit is used for a cross-
finger flap. The mid-axial skin incision is made proximal
to the defect, and the skin flap is elevated just above the
subcutaneous tissue in a direction that is opposite the
side of the defect. The adipofascial flap is then harvested
373
down through paratenon in the opposite direction of
the elevation of the overlying skin flap. This is taken
from mid-axial line to mid-axial line. Care is taken to
not damage any of the dorsal branches of the digital
artery when harvesting this flap. The flap is then turned
over to cover the adjacent digit dorsal defect and provide
good coverage for the exposed extensor tendon. The
cross-finger adipofascial flap is covered with a split-
thickness skin graft and the donor site is closed primar-
ily with its hinged skin flap. The hand is immobilized
for 2 to 3 weeks, preferably 3 weeks, and the division
and inset of the flap is performed after 2 to 3 weeks,
with revisions to the donor or recipient site as needed.
The patient is splinted in a position of function for 3
weeks to minimize any contractures. In compliant
patients, the patient can begin light active range of
motion after the surgery but needs to be very compliant
(Figure 35-2).
Metacarpal Artery Island Flaps
The dorsal aspect of the hand represents an invaluable
and expendable donor site for dorsal digital coverage of
exposed extensor tendons. A sound knowledge of the
vascular anatomy of the hand and digits’ dorsal skin has
led to many innovative flap designs for this area. This
knowledge is an important prerequisite for the safe
application of these flaps. The blood supply to the
dorsal skin of the hand and digits is provided by (1) the
dorsal metacarpal arteries, which vascularize the proxi-
mal portion of the hand and (2) the dorsal perforating
metacarpal arterial branches from the deep palmar arch,
which supply the distal hand and proximal phalanx.
These two major arterial systems form the basis for
direct and reverse dorsal metacarpal artery (DMA) flaps.
First Dorsal Metacarpal Artery Flap
The first dorsal metacarpal artery flap (FDMA flap, i.e.,
kite flap), described by Foucher and Braun,1 provides two
major applications in hand reconstruction: (1) dorsal
hand wound coverage and (2) thumb reconstruction.
In Foucher’s anatomical study of 30 injected cadav-
eric hands, the FDMA originated from the radial artery
in 28 of 30 specimens and from the dorsalis superficialis
antebrachialis artery in 2 of 30 cases. From there, it
courses distal to the extensor pollicis longus tendon,
and proximal to the radial artery’s entry between both
heads of the first dorsal interosseous (DIO) muscle. The
FDMA travels parallel to the dorsal surface of the second
metacarpal, and superficial to the first DIO muscle
fascia, with some fibers occasionally covering the vessel.
The FDMA then continues distally and anastomoses
at the level of the metacarpal neck with dorsal perfor­
ating branches from the palmar metacarpal arteries
of the deep palmar arch. These perforator branches
form the basis of the reverse flow FDMA island flap.
They anastomose with three different arterial systems:
374 Section 4:  Extensor Tendon Repair and Reconstruction

(1) distally with the dorsal branches of the proper

palmar digital arteries, (2) proximally with branches of
the DMA, and (3) laterally with adjacent DMA perforat-
ing branches (Figure 35-3).
Intact
skin
The FDMA flap is designed over the dorsum of the
island Defect index finger’s proximal phalanx along the mid-radial
and mid-ulnar lines of the finger (see Figure 35-3).
Distal and proximal limits include the proximal inter-
phalangeal (PIP) joint and metacarpophalangeal (MCP)
joint, respectively; however, an extended flap can also
be harvested by including skin from the dorsum of the
middle phalanx. Inclusion of the dorsal skin of the MCP
joint can make dissection of the pedicle safer because
Elevated thin the layer of subcutaneous tissue is very thin at this level.
full-thickness
A lazy S, or Bruner-type incision, is marked from the
A skin flap
head of the second metacarpal bone to the apex of the
first interosseous web space. This design allows for gen-
erous exposure and an en block dissection of the pedicle
without skeletonization and undue risks of vascular
damage.
Elevation of the FDMA flap begins distally by incising
the flap outline over the dorsal proximal phalanx in a
radial to ulnar direction, just above the paratenon layer.
The lazy S, or zigzag incision, is made and the lateral
skin flaps are raised subdermally to develop a subcuta-
neous pedicle. Sensory branches of the radial nerve and
one or more subcutaneous veins are identified proxi-
mally and included in the pedicle. The radial border of
Elevated the second metacarpal bone is then exposed and dissec-
full-thickness tion continues deeper to include the first dorsal inter­
subcutaneous osseous muscle fascia. This fascia is sharply incised
flap with intact and carefully dissected off the interosseous muscle in a
B skin island
radial direction, until the ulnar border of the first meta-
carpal bone is reached. The FDMA lies just superficial
Reversed flap covering to the first dorsal interosseous fascia, thus requiring
recipient defect and inclusion of the latter during flap elevation to prevent
reconstructing avulsed
eponychial defect
damage to the pedicle. For this same reason, some
authors even advocate raising a cuff of first dorsal inter-
osseous muscle in case the FDMA lies deeper. Pedicle
dissection continues in a proximal direction and all
small perforating branches penetrating the interosseous
fascia are coagulated to yield a maximal pedicle length,
Thin
which can vary from 6 to 8 cm. The pedicle is raised
full-thickness
skin graft with a generous cuff of subcutaneous fibrofatty tissue
Originally elevated without skeletonization. If required, tunneling is created
thin full-thickness
skin flap covering by undermining subcutaneous skin, and the flap is
donor defect transferred into the defect without tension, compres-
sion, or kinking. Nevertheless, when harvesting an
C FDMA flap, an overlying skin bridge over the pedicle
Figure 35-2  Step-by-step description of a reverse cross-
should also be harvested so as to avoid tunneling and
finger flap elevation. Either a thin split-thickness or full- possible pedicle compression. We perform this for all
thickness skin graft can be used to cover the wound. intrinsic pedicle flaps. The arc of rotation of the FDMA
flap allows it to reach the thumb tip, volar second MCP
joint, distal antebrachial region, and fifth MCP joint.
The donor site is covered with a full-thickness skin graft
(see Figure 35-3).
 Chapter 35:  Soft Tissue Coverage for Extensor Tendon Reconstruction 375

D
Figure 35-3  A, Dorsal tissue defect of left thumb with exposed phalanges and loss of extensor pollicis longus tendon.
B, Harvest of a 3.0 × 5.5-cm flap based on the dorsal metacarpal artery with a skin island kept over the pedicle to avoid
tunneling the flap and compression to the flap and vascular compromise. C, The FDMA flap was harvested over the first and
second interosseous muscle with incorporation of the fascia to not injure the pedicle. A wide base of subcutaneus tissue of
the flap was harvested to maximize arterial inflow and venous outflow. The skin paddle can be extended passing the PIP joint
for a longer flap, and this flap can also be made sensate by including a dorsal branch of the ulnar or radial digital nerve, or the
digital nerves of the thumb. D, Final inset of the FDMA flap with well-vascularized coverage over the thumb. Note that the
FDMA flap is not tunneled. The donor site is covered with a full-thickness skin graft.

The first dorsal interosseous muscle fascia must be
included in flap elevation to avoid inadvertent injury
to the FDMA. The pedicle should not be skeletonized
and should be raised with a generous cuff of fibrofatty
tissue.
Second Dorsal Metacarpal Artery Flap
The second dorsal metacarpal artery (SDMA) flap is a
reliable sensate flap with a wide arc of rotation.2-4 Like
the FDMA flap, it serves as a useful and reliable tool for
coverage of hand and thumb defects. This flap can be
combined with the FDMA island flap to harvest the
entire second web space for reconstruction of thumb
degloving injuries.
The SDMA generally runs along a line joining the
anatomical snuffbox and second web space. In 23 of
29 (79%) cadaveric hands studied by Early and Milner,
the SDMA originated from the dorsal carpal arch. In the
remaining six specimens, the SDMA originated from the
deep palmar arch, the FDMA, the anterior interosseous
artery, or the radial artery. The SDMA passes deep to the
extensor digitorum and extensor indicis muscles of the
index finger, and superficial to the second dorsal inter-
osseous muscle fascia. As the SDMA reaches the second
376 Section 4:  Extensor Tendon Repair and Reconstruction

web space, one or more large perforators can be found
between the second and third metacarpal heads in the
second intermetacarpal space. These perforators origi-
nate from the deep palmar arch and pass dorsally to
communicate with the SDMA to supply the dorsal skin.
The perforators arise at the level of the metacarpal necks
and give off distal branches, which anastomose with the
dorsal cutaneous branches of the PPD arteries. These
perforator vessels form the basis of the extended SDMA
flap and the reverse flow SDMA flap.
The SDMA runs in an oblique line between the ana-
tomical snuffbox and the center of the second web
space, between the heads of the second and third meta-
carpal bones. Depending on defect size and location,
the flap can be designed over the second intermetacar-
pal space, over the proximal phalanx of the middle
finger, or over the superficial web space. The proximal
intersection of the extensor tendons to the index and
middle fingers can be considered the pivot point of
the flap.
The flap is incised circumferentially and dissected off
the extensor tendon paratenon of the proximal phalanx.
Dissection is performed in a distal-to-proximal fashion.
When the second web space is reached, the communi-
cating perforator from the palmar metacarpal artery
must be identified and ligated. An S-shaped incision is
then made from the base of the flap and carried proxi-
mally over the SDMA toward the anatomical snuffbox
until the required pedicle length is obtained. Skin flaps
are elevated in a subdermal plane with appropriate
superficial veins and branches of the radial nerve. Dis-
section is deepened along the ulnar aspect of the
index extensor tendons. After radial retraction of these
tendons, the SDMA can be seen coursing over the second
dorsal interosseous muscle and fascia. The SDMA
pedicle is dissected from the second dorsal interosseous
muscle much like the FDMA (i.e., with a generous cuff
of fascia and muscle), until the flap safely reaches its
intended destination. The donor site is closed primarily
or with a full-thickness skin graft.
As in the dissection of the first dorsal metacarpal
artery flap, the second dorsal interosseous fascia should
be included during the elevation of an SDMA flap to
avoid inadvertent injury to the SDMA. In addition, the
pedicle should not be skeletonized and should be
raised with a generous cuff of fibrofatty tissue to mini-
mize risks of venous congestion, vasospasm, and vascu-
lar injury.
Perforator-Based DMA Flap
As described by Quaba and Davidson,5 the reverse flow
dorsal metacarpal flap can be harvested without incor-
porating the DMA. Dissection of the flap proceeds from
proximal to distal, and is carried above the dorsal inter-
osseous fascia without including the DMA. The flap may
be raised on the second, third, or fourth intermetacarpal
space and is designed as an ellipse, which can extend
from the MCP joint to the wrist crease (Figure 35-4).

A B
Figure 35-4  A, Soft tissue defect in the right long finger with exposed extensor tendon following repair. This defect is an
excellent indication for a perforator-based metacarpal artery flap. In this cased, an SDMA perforator-based flap “Quaba flap”
was used. The same flap can be raised from the third and fourth DMA perforators. B, The axis of the flap was designed parallel
to the third metacarpal and extends from the intermetacarpal head space, to the distal wrist crease, and not beyond this
point. A pinch test is used to estimate the maximal width of the flap. A larger flap can be harvested but the donor site will
require a skin graft.
 Chapter 35:  Soft Tissue Coverage for Extensor Tendon Reconstruction 377

The flap width and length can vary from 1 to 3.5 cm Thumb Dorsal Radial Artery Flap
and 2 to 9 cm, respectively. This flap is an excellent A thumb dorsal radial artery flap can be used for smaller
option for dorsal digital coverage. It will easily cover defects in the dorsum of the thumb. This is based on
defects involving exposed MCP joint, proximal phalanx, recurrent branches from the radial digital artery. Vascu-
and even the PIP joint (see Figure 35-4). This flap is larity is ensured by the communication between both
elevated suprafascially from proximal to distal with the the ulnar and radial digital arteries of the thumb via
overlying skin and subcutaneous tissue from the dorsum dorsal branches of the digital artery and communicating
of the hand. The axis of the flap is parallel to the meta- branches along the dorsum of the thumb. The flap is
carpals, and dissection is stopped just distal to the junc- elevated on the dorsal radial aspect of the thumb overly-
turae tendinum, where a major cutaneous perforator ing the MCP joint and is dissected from proximal to
can be found originating from the dorsal metacarpal distal, leaving a wide base of fibrofatty tissue along the
artery. The recurrent cutaneous perforator branch of the pedicle (Figure 35-5). Inset is performed under minimal
DMA, which communicates with the deep carpal arch tension, and the donor site is either closed primarily or
or metacarpal artery at the level of the metacarpal neck, closed with a skin graft. Any exposed pedicle that cannot
is found just distal to the intertendinous connections be covered with primary closure should be skin grafted
and represents the pivot point of the flap. The arc of to minimize any compression. This skin graft can be
rotation varies from 0° to 180° and can cover the excised at a later date, but often the swelling and soft
dorsum of the metacarpal bone, web space, and dorsal tissue contracture will minimize any need for revisions
proximal and middle phalanges, up to the distal inter- in the future.
phalangeal (DIP) joint. This modification converts the
standard axial type reverse flap into a reverse perforator Local Flaps
flap via this recurrent branch. The advantages of this Dorsal hand defects can be either covered with local,
modification include ease of elevation and thinner cov- regional, or distant flaps. Many dorsal hand defects with
erage for dorsal digital defects. exposed extensor tendons can be covered with either
Karacalar and Özcan6 have described a modified
version of the reverse flow dorsal metacarpal flap. Their
flap had an extended arc of rotation and covered the
distal phalanx in five patients. It is based on the
second and third intermetacarpal spaces as well as
connections between the dorsal branches of the digital
artery and the terminal branches of the DMA at the level
of the proximal phalanx. The largest flap size measured
7 × 3 cm. Flap survival rate was 100%. Dissection is
similar to dissection of the Quaba reverse flow dorsal
metacarpal flap but is carried more distally. The perfo-
rating recurrent branch of the dorsal metacarpal artery
is ligated and a pedicle is developed based on connec-
tions between the dorsal branches of the digital artery
and the terminal cutaneous branches of the DMA over
the proximal phalanx. Pedicle skeletonization should A
be avoided and a generous cuff of fibrofatty tissue
should be harvested with the flap. Angiographic studies
by Yang and Morris confirm the anatomical basis of this
flap modification.7 This modification allows coverage of
more distal defects at the level of the distal phalanx,
which could not be treated with a standard reverse flap
design.
Care must be taken to harvest the flap while respect-
ing integrity of the paratenon if a skin graft is antici-
pated. The flap inset is performed under minimal
tension. The flap should preferably not be tunneled to
minimize any risk of congestion and ischemia, and B
sutures are taken out 2 weeks later, and light active range Figure 35-5  A, Soft tissue defect in the right thumb with
of motion is begun after 1 to 2 weeks. This flap is an landmarks drawn for a dorsal radial thumb flap. B, Harvest
excellent option for all exposed extensor tendons within of the flap with a large cuff of subcutaneous tissue kept
the digit from the MCP joint to the DIP joint. surrounding the pedicle.
378 Section 4:  Extensor Tendon Repair and Reconstruction
a pedicle radial forearm flap, posterior interosseous
artery flap, or dorsal ulnar artery flap. These are three
very good options when the forearm has not been
compromised.
Radial Forearm Flap
The flap provides excellent thin and pliable skin
coverage for reconstruction of soft tissue defects of the
dorsal hand. It may be harvested with a vascularized
segment of radius for reconstruction of metacarpal
bone defects and with palmaris longus tendon for
extensor tendon defects. Additional composite recon-
struction is also possible by incorporating antebrachial
cutaneous nerve.
The flap is supplied by the multiple septocutaneous
perforating branches of the radial artery in the forearm,
and flap territory extends from lower third of the volar
aspect of the arm proximally to the flexion crease dis-
tally. Distal width is from the extensor pollicis longus
tendon radially to the extensor carpi ulnaris tendon
ulnarly and proximally from lateral to medial epicon-
dyles. The diameter of the artery is approximately
2.5 mm, and that of the concomitant veins 1.3 to
2.5 mm. The typical radial forearm flap creates rather
marked scar in exposed forearm and need sacrifice of
a main artery truck,8 which became less used than
before, because a myriad of other options are currently
available.
Alternatively, for small to medium-sized defects, a
perforator-based radial forearm flap can also be used
without sacrifice of the radial artery. At least one major
radial artery perforator can be found within 2 cm from
the radial styloid.
Posterior Interosseous Artery Flap
The posterior interosseous flap is also a very credible
option for dorsal coverage. The pedicle can be found
from the lateral epicondyle to run in between the ECU
and the EDQ. Dissection proceeds from proximal to
distal, and identification of the posterior interosseous
artery is found with perforators emanating from the
septum between both the previously mentioned
muscles. Pivot point is just proximal to the distal radio-
ulnar joint, and care must be taken to protect the pos-
terior interosseous nerve during dissection. This flap
will cover small to moderate-sized defects of the dorsum
of the hand and is a viable option when the radial
forearm flap is not available.
Becker Flap (Ulnar Artery Dorsal Perforator Flap)
The dorsal ulnar artery fasciocutaneous flap was first
described by Becker and Gilbert in 1988, which is vas-
cularized by the ascending branch of the dorsal ulnar
artery without sacrifice of the ulna artery.9 The Becker
flap is in essence a pedicle perforator flap based of
the ulnar artery and can provide excellent coverage
for exposed defects on the ulnar and dorsal aspect of
the hand.
The flap is raised as an island flap subfascially, and
dissection is started from the ulnar side of the wrist and
forearm from proximal to distal. The pedicle is exposed
by retracting the flexor carpi ulnaris tendon radially and
the major perforator pedicle can be seen emerging from
ulnar artery 2 to 5 cm proximal to the pisiform. The
dorsal ulnar artery is dissected down to the origin of the
ulnar artery to allow rotation of the flap 180° and to
prevent inadvertent pedicle kinking and twisting. For
smaller flaps, the donor site can be closed primarily; if
not, then a split-thickness skin graft is used for closure.
Free Flaps
Free flap reconstruction is now well established for pro-
viding a safe and reliable means of obtaining wound
closure and composite structural repair. With current
success rates of over 95%, and the availability of mul-
tiple donor sites, free flaps offer virtually unlimited
freedom in complex reconstruction of the dorsum of the
hand. Key requirements for soft tissue reconstruction
include provision of a stable bony framework, adequate
recipient vessels outside the zone of injury, adequate
blood supply of tissue adjacent to the recipient site, a
stable patient, and a surgeon experienced in microsur-
gery. Free tissue transfer for extensor tendon coverage is
indicated when local pedicle flaps cannot be harvested
outside the zone of injury or when soft tissue defects are
extensive.
Several key features favor the use of free flaps over
pedicled or local flaps, including avoiding additional
donor site burden or surgical trauma to an already com-
promised region, including avoiding sacrifice of a major
blood vessel, and providing ample well-vascularized
tissue to promote wound healing, minimize infection,
and enable coverage of larger wounds. A composite
reconstruction using vascularized bone, tendon, and
nerve is also generally easier to design. The structural
complexity and aesthetic demands of a recipient site
may also dictate that a graded approach using the recon-
structive ladder is not always appropriate. In these cir-
cumstances, free flap soft tissue reconstruction should
always be considered early in the treatment algorithm if
a better end result can be anticipated. Despite increased
technical requirements and length of operation, free
flap reconstruction often results in fewer postoperative
complications due to better vascularization, which is
important when early postoperative mobilization or
adjuvant therapy is required.
Free flap reconstruction is contraindicated in pati-
ents with significant comorbidities. Diabetes, cigarette
smoking, corticosteroids, and immunosuppressants
may lead to wound healing complications. Presurgical
angiography may be required following high-energy
injuries to the upper extremity where vascular injury is
 Chapter 35:  Soft Tissue Coverage for Extensor Tendon Reconstruction
suspected or in patients with extensive atherosclerotic
disease.
The availability of free flap donor sites is extensive
and selection should involve not just coverage but
should be tailored and individualized to meet the recip-
ient site requirements. Consideration should also be
given to the function and aesthetics of both the recipient
and donor sites. There are now a myriad of free flap
options for dorsal hand coverage, and ultimately the
choice of flap is determined by both patient donor site
characteristics and surgeon preference. The following
should be evaluated in the recipient site: dimensions,
the color and texture of the tissues surrounding the
defect, structures needing reconstruction, available
recipient vessels, level of contamination, and the need
to restore sensation. Following radical débridement the
wound is often much larger and deeper than antici-
pated, and the microvascular anastomosis must be
placed well out of the zone of injury. It is therefore
desirable to choose a flap with a large and reliable cuta-
neous territory and a long pedicle of large caliber,
enabling anastomosis out of fields of trauma, thus
reducing the risk of vessel spasm and thrombosis at the
anastomosis. Available flaps include lateral arm flap,
scapula/parascapular flap, anterolateral thigh flap, tho-
racodorsal artery perforator flap, etc.10,17
Fasciocutaneous flaps provide excellent coverage for
dorsal hand defects and provide an excellent gliding
surface for tendons and joints in the hand. The ability
to easily and quickly reelevate fasciocutaneous flaps is
a definitive advantage when staged reconstruction of
bone, nerve, or tendon is anticipated under the flap.
Lateral Arm Flap
The lateral arm flap is excellent for providing thin cover-
age for small to medium defects of the hand. It can be
harvested as a composite flap, incorporating a segment
of up to 10 cm in length of the humerus or a segment
of vascularized triceps tendon for extensor tendon
reconstruction (Figure 35-6).
The flap is located on the lateral aspect of the upper
arm, centered on a line drawn from the insertion of the
deltoid to the lateral epicondyle, and spans the distal
half of the lateral arm and the proximal third of the
dorsolateral forearm. The pedicle is the posterior radial
collateral artery and venae comitantes, which is 0.75 to
2.0 mm in diameter and varies from 6 to 8 cm in length
(see Figure 35-6).
The flap can be designed with a 6- to 8-cm width,
which allows primary closure of the wound. If the width
is larger, the donor site requires skin grafting. It can also
be harvested as a pure fascial flap with split-thickness
skin grafting, which provides excellent coverage of
exposed extensor tendons when ultra-thin flap coverage
is required (Figure 35-7). This flap also can be designed
as a sensate flap based on the antebrachial cutaneous
379
Brachialis m.
Ant. radial
Brachioradialis m.
collateral a.
Radial Radial n. Triceps m. Lower lateral Posterior radial
collateral a. cutaneous n. collatral a.
of the arm
Figure 35-6  Schematic demonstrating the major
landmarks and pedicle for the lateral arm flap.
nerves of the arm and forearm. During dissection the
posterior cutaneous nerve of the forearm is usually
sacrificed.
Scapula/Parascapular Flap
The scapula and parascapular flaps afford consistent
vascular anatomy, an easily accessible vascular pedicle,
good vessel diameter and length, and flap safety and
reliability. The flap is also useful for dorsal hand cover-
age hand reconstruction and can also be combined with
the latissimus dorsi or serratus muscle on the same
subscapular system for additional coverage.
Anterolateral Thigh (ALT) Flap
The ALT flap includes a large and reliable adipocutane-
ous territory, minimal donor site morbidity, capability
for sensory neurorrhaphy, long vascular pedicle, and the
potential for flap thinning in the primary or secondary
setting to improve flap contour.10 Multiple components
can be raised on different perforators from the lateral
femoral circumflex artery, including separate skin
paddles, the vastus lateralis muscle, and iliac crest,
enabling accurate reconstruction of complex three-
dimensional multicomponent defects.
The flap is based on the descending branch of the
lateral femoral circumflex artery, located between the
rectus femoris and vastus lateralis muscles, with a per-
forator almost always found at the midpoint of a line
between the anterior superior iliac spine and the supero-
lateral aspect of the patella. The perforator is musculo-
cutaneous in approximately 80% of cases. The pedicle
can be up to 15 cm in length with an average arterial
external diameter of 2 to 3 mm (Figure 35-8).
Flaps in excess of 40 cm in length have been safely
harvested based on only one perforator. Primary closure
can be achieved if the flap width does not exceed 8 to
380 Section 4:  Extensor Tendon Repair and Reconstruction

A B

C D
Figure 35-7  A, Contracture of the dorsum of the left hand in a 50-year-old male patient due to extensive burn. B, Defect
size following resection of burn scar, tenolysis, and MCP joint capsulotomies. C, Lateral arm flap skin paddle design based on
size and geometry of defect template. D, Flap inset following microanastomosis of posterior radial collateral artery end-to-side
to radial artery and vena comitans end-to-end to dorsal vein.

10 cm. The flap may be harvested in the suprafascial
or subfascial plane. There is a reduced incidence of
muscle herniation with suprafascial dissection, although
a 5-cm radius cuff of deep fascia should be preserved
around the perforator. A sensate flap can be achieved by
incorporating the lateral femoral cutaneous nerve (see
Figure 35-8 and Figure 35-9).
Other options for dorsal hand coverage also include
muscle flaps. Keep in mind that we prefer to use skin
flaps for dorsal hand coverage in the event that second-
ary reconstruction or revisions are required in the form
of tenolysis. If tenolysis is anticipated in the future, or
capsulotomy, it is much easier to reelevate a fasciocuta-
neous flap rather than a muscle flap, although muscle
flaps will atrophy very nicely and provide excellent
cosmesis and coverage. This is preferentially reserved
for patients that do not have any extensor tendon loss
or defects and have simply only exposed extensor
tendons.
Adipofascial flaps, such as the temporoparietal fascial
flap, are also a viable option for extensor tendon recon-
struction. We prefer to use an ALT adipofascial flap or
an ALT flap as opposed to a temporoparietal flap due to
ease of dissection, large flap size potential, and minimal
donor site morbidity.
SECONDARY PROCEDURES
Secondary procedures may be required following the
initial flap coverage, and these may involve, for example,
flap debulking, tenolysis, capsulotomy, tendon grafting
following Hunter rod removal, etc. One major advan-
tage of using a fasciocutaneous flap for extensor tendon
coverage is the ability to easily reelevate the flap at a
later stage for tenolysis or other procedures. This can
even be performed under local anesthesia using a “wide-
awake” approach to better judge the effects of surgery.
If the flap requires debulking we prefer to wait at least
3 months postoperatively before performing liposuc-
tion. Peripheral incisions and excess skin removal are
performed an additional 3 months later to ensure ade-
quate vascularity.
SUMMARY
Soft tissue coverage of extensor tendons in the hand
and digits that have either been primarily repaired or
grafted is of paramount importance to promote proper
 Chapter 35:  Soft Tissue Coverage for Extensor Tendon Reconstruction 381

E
Figure 35-8  A, Extensive degloving injury, following a motor vehicle accident, of the dorsal right hand, with bone, extensor
tendon, and soft tissue defects. Note complete loss of EDC tendons on the dorsum of the distal forearm and hand. B, A
fasciocutaneous ATL flap was selected for coverage instead of a muscle flap in anticipation for future secondary surgeries and
need to reelevate the flap. C, ALT flap harvest with extension of fascia lata showing well vascularized tissue. D, Long extensor
tendon grafts harvested from the leg for primary extensor tendon reconstruction. E, Flap coverage after tendon grafting to
reconstruct the EDC tendons.
382 Section 4:  Extensor Tendon Repair and Reconstruction
B
Figure 35-9  A, Hand motion and cosmetics 6 months postoperatively following coverage of a dorsal hand with an ATL flap,
which is in the case shown in Figure 35-8. B, Flap appearance after liposuction performed 3 months postoperatively.
gliding, minimize adhesion, and maximize function.
The reconstructive surgeon needs to have a wide arma-
mentarium of flap options for exposed extensor tendon
coverage. Any extensor tendon devoid of adequate soft
tissue will be at high risk for delayed wound healing,
tendon desiccation, contracture, stiffness, and potential
loss of hand function. The combination of adequate
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review of 72 cases and technical refinements, J Reconstr Micro-
surg 14:39–48, 1998.
17. Gosain AK, Matloub HS, Yousif NJ, et al: The composite
lateral arm free flap: vascular relationship to triceps tendon
and muscle, Ann Plast Surg 29:496–507, 1992.
 CHAPTER
36  
TREATMENT OF BOUTONNIÈRE
AND SWAN-NECK
DEFORMITIES
Fraser J. Leversedge, MD, and Felicity G.L. Fishman, MD
OUTLINE
The treatment of boutonnière and swan-neck deformi-
ties of the digits is guided by the etiology and staging
of the condition, primarily differentiated as being the
sequelae of trauma or as a part of the spectrum of
rheumatoid disease. A thorough evaluation should
include consideration for the current or potential
pathology of adjacent joints, the active and passive
motion of involved joints, subjective concerns for pain
or instability, and radiographic assessment. Careful
assessment of the deformity is critical to the decision
on an appropriate and individualized treatment strat-
egy. The primary goals of treatment of boutonnière
and swan-neck deformities are to alleviate pain and
to improve function. Treatment ranges from splinting
and therapy to operative intervention. The surgical
procedures include ligament repair or reconstruction
and tenodesis or arthrodesis. Long-standing and severe
deformities are difficult to correct and consequently
full function of the digits may not be achieved. Patient
selection is critical to achieving successful surgical
outcomes.
The intricate and coordinated functions of the hand and
digits rely extensively on the complex but balanced
interactions between the extrinsic and intrinsic muscu-
lature of the hand. Alterations in the relationships
between these extrinsic and intrinsic systems due to
trauma or secondary to the effects of systemic disease
may cause the development of functional deformities
such as a boutonnière or swan-neck deformity. Such
changes may be acute or chronic in nature. Treatment
for these conditions should be guided by a comprehen-
sive evaluation of the patient, a consideration for associ-
ated injuries or structural deficiencies, the timing of
injury, and the severity of the deformity. Importantly, a
functional assessment and recognition of the patient’s
activity requirements and expectations are critical for
creating a plan of care.
The boutonnière and swan-neck deformities of the
digits are differentiated as being the sequelae of trauma,
or as a part of the spectrum of rheumatoid disease.
POST-TRAUMATIC DEFORMITY
Post-Traumatic Boutonnière Deformity
Post-traumatic boutonnière (or “buttonhole”) deformi-
ties, characterized by hyperextension of the meta­
carpophalangeal (MCP) joint, flexion of the proximal
interphalangeal (PIP) joint, and hyperextension of the
distal interphalangeal (DIP) joint, are caused by disrup-
tion of the central slip. Attenuation of the triangular
ligament allows the lateral bands to migrate volar to the
PIP joint axis of rotation, transforming the lateral bands
into a flexion force at the PIP joint and extension force
at the DIP joint (Figure 36-1).
Traumatic injuries to the central slip can be divided
into two groups: (1) Closed injuries: Typically, avulsion
of the central slip from its insertion occurs due to a
hyperflexion injury or volar dislocation of the PIP joint.
An associated avulsion fracture from the dorsal base of
the middle phalanx may be present. (2) Open injuries:
Lacerations to the dorsal digit can disrupt the central
slip directly.
Often, patients present with complaints of “jamming”
or spraining the affected digit and the clinician should
be suspicious of a central slip injury particularly in the
presence of localized swelling, ecchymosis, and/or ten-
derness to the dorsal PIP joint and a loss of full active
PIP joint extension; a lack of motion should not be
disregarded as a consequence of swelling or pain. Early
diagnosis may be complicated by the delayed develop-
ment of the deformity, often 2 to 3 weeks following
initial injury.
Physical examination findings supportive of an acute
central slip injury include: (1) A 15° to 20° extension
lag at the PIP joint with the wrist and MCP joint held
in full flexion.1 (2) Absence or weakness of resisted
active extension of the PIP joint with the PIP joint
383
384 Section 4:  Extensor Tendon Repair and Reconstruction
CS
clb
Figure 36-1  Lateral view of the digit demonstrating the
volar subluxation of the lateral bands (clb) in a simulated
boutonniere deformity (central slip [CS]). (Reprinted with
permission: © 2004 Leversedge FJ, Goldfarb CA, Boyer MI.)
starting in 90° of flexion.2,3 (3) Elson test: The patient
attempts to extend actively the PIP joint of the involved
finger against resistance from a 90° starting position
over the edge of a table. The absence of extension force
at the PIP joint accompanied by fixed extension of the
DIP joint confirm disruption of the central slip as exten-
sion forces are being transferred to the DIP joint by the
lateral bands.4,5 (4) Boyes test: A positive test may be
found in progressive stages of boutonnière deformity
but is not reliable for the diagnosis of acute central slip
injuries.5 Loss of active flexion of the DIP joint with the
PIP joint held in passive extension due to tension across
the lateral bands following disruption of the central
slip. Active flexion of the DIP is possible with the PIP
joint flexed.
After a traumatic injury to the central slip, the bou-
tonnière deformity generally progresses through five
stages6:
1. Disruption of the central slip results in resting
flexion of the PIP joint and weak extension of the
middle phalanx via the lateral bands
2. Absent active PIP joint extension combined with
attenuation of the triangular ligament and con-
tracture of the transverse retinacular ligaments
results in the volar migration of the lateral bands
3. Extension forces are transmitted through the
lateral bands, causing hyperextension at the DIP
joint
4. Progressive contracture of the PIP joint volar plate
and the oblique retinacular ligament causes fixed
flexion contracture at the PIP joint
5. Progressive articular degeneration occurs after pro-
longed and untreated pathology
Post-Traumatic Swan-Neck Deformity
Post-traumatic swan-neck deformity is characterized by
the inability of the terminal slip to extend the DIP joint
combined with laxity of the PIP volar plate resulting in
hyperextension of the PIP joint and flexion of the DIP
joint. Attenuation of the transverse retinacular ligament
coupled with hyperextension of the PIP joint leads to
dorsal migration of the lateral bands in relation to the
PIP joint axis of rotation, thereby exerting an extension
force on the PIP joint and a flexion force on the DIP
joint.
Laxity or incompetence of the volar plate can be
caused by dorsal dislocation of the PIP joint. Recurrent
injury may lead to chronic dorsal instability of the PIP
joint. Conversely, terminal tendon avulsion from its
insertion at the base of the distal phalanx may cause an
imbalance in the extensor mechanism, resulting in
hyperextension of the PIP joint.
Patients may present with a history of acute injury
or recurrent dorsal PIP hyperextension injuries cul­
minating in progressive subluxation or dislocations,
often unrecognized. Patients presenting with a chronic
“mallet” deformity should arouse suspicion for PIP
hypermobility. On physical examination, the affected
digit will exhibit PIP joint hyperextension and DIP joint
flexion posturing, often with MCP joint flexion. For
patients with flexible PIP and DIP joint deformities,
active and passive motion of the PIP joint should be
assessed and a Bunnell’s intrinsic tightness test should
be performed.
Bunnell’s intrinsic tightness test: Increased resistance to
passive PIP joint flexion with the MCP joint in extension
compared with flexion indicates a relative shortening of
the intrinsic muscle–tendon units.
The post-traumatic swan-neck deformity may prog-
ress through four characteristic stages7:
1. Full passive PIP joint range of motion
2. Intrinsic tightness secondary to prolonged hyper-
extension of the PIP joint
3. Fixed hyperextension of the PIP joint regardless of
MCP position due to attenuation and contraction
of the transverse retinacular ligament and dorsal
subluxation of the lateral bands
4. Articular degeneration and fixed hyperextension
deformity of the PIP joint
RHEUMATOID DEFORMITY
Rheumatoid Boutonnière Deformity
of the Fingers
Rheumatoid boutonnière deformities occur due to pro-
gressive erosion of the central slip, transverse retinacular
ligaments, and the triangular ligament by the destructive
synovitis characteristic of rheumatoid arthritis. As the
restraints provided by triangular ligament are lost, the
lateral bands migrate in a volar direction, transforming
 Chapter 36:  Treatment of Boutonnière and Swan-Neck Deformities
them into a flexion force at the PIP joint. The continued
flexion deformity of the PIP joint results in contractures
of the oblique retinacular ligament, the volar plate, and
the collateral ligaments; progression from a flexible to
a fixed deformity of the PIP joint occurs with time. The
classic boutonnière deformity involves flexion of the
PIP joint and hyperextension of the DIP and MCP joints
and evolves through three stages.8 Stage I is considered
a mild, involving PIP joint synovitis and a passively cor-
rectable flexion deformity of the PIP joint. Stage II, or a
moderate deformity, involves a flexion contracture of
the PIP joint and concomitant MCP joint hyperexten-
sion. Stage III involves a fixed contracture of the PIP
joint and destruction of the articular surfaces.
Rheumatoid Swan-Neck Deformity
of the Fingers
Swan-neck deformities associated with rheumatoid
disease are characterized by hyperextension of the PIP
joint and concurrent MCP and DIP flexion deformities.
A swan-neck deformity may be caused by primary
pathology affecting the MCP, the PIP, or the DIP joint.7
 MCP joint pathology: The characteristic rheumatoid
digital deformity of flexion and ulnar drift leads
to imbalance of the extensor mechanism. The PIP
is hyperextended by the extension force exerted
across the PIP by the dorsal shift of the lateral
bands. The MCP joint component of a swan neck
deformity is flexion, which can be secondary to
chronic synovitis with degeneration of the sagittal
bands, intrinsic tightness, and/or articular destruc-
tion resulting in volar subluxation of the MCP
joint.
 PIP joint pathology: The volar plate of the PIP joint,
the collateral ligaments, and the insertion of the
flexor digitorum superficialis (FDS) tendon can
become attenuated in rheumatoid disease, result-
ing in PIP hyperextension. Also, progressive atten-
uation of the transverse retinacular ligaments
results in a loss of the normal restraints to the
dorsal migration of the lateral bands, leading to
PIP joint hyperextension.
 DIP joint pathology: Synovitis of the DIP joint may
cause attenuation and eventual rupture of the ter-
minal extensor tendon. Subsequently, the extensor
forces are concentrated at the PIP joint, resulting
in a hyperextension deformity of the PIP joint.
Nalebuff classified rheumatoid swan-neck deformities
into four distinct types7:
 Type I—Fully mobile and flexible PIP joint, regard-
less of MCP joint position
 Type II—Active and passive PIP joint motion is
limited with MCP joint held in extension due to
intrinsic tightness
385
 Type III—Decreased PIP joint motion in all posi-
tions of MCP joint flexion and extension
 Type IV—Fixed extension contracture of the PIP
joint with degeneration of PIP joint articular
cartilage
Rheumatoid Thumb Deformity
Thumb deformity associated with rheumatoid disease
may be classified based on changes specific to the car-
pometacarpal (CMC), MCP, and interphalangeal (IP)
joints, as outlined by a modified classification system of
six types initially proposed by Nalebuff.9,10
The most common rheumatoid thumb deformity is
the type I (boutonnière) deformity. This is characterized
by IP joint hyperextension and MCP joint flexion
without primary involvement of the CMC joint. Typi-
cally, the type I deformity begins with proliferative syno-
vitis within the MCP joint, which leads to attenuation
of the extensor pollicis brevis (EPB) tendon insertion
and expansion of the extensor hood. Concurrently, the
collateral ligaments become attenuated and the exten-
sor pollicis longus (EPL) is displaced ulnar and volar to
the MCP joint axis of rotation. Subsequently, the proxi-
mal phalanx becomes subluxed palmarly relative to the
metacarpal head and the altered pull of the intrinsics
and the EPL leads to IP joint hyperextension and MCP
joint flexion. Radial abduction of the thumb metacarpal
can occur in compensation for MCP joint flexion. Type
I deformities are further divided into stages: (1) stage I,
or mild: PIP joint synovitis and mild fully correctable
extensor lag; (2) stage II, or moderate: marked flexion
deformity of PIP joint, flexible or fixed; and (3) stage
III, or severe: PIP articular destruction.
The second most common rheumatoid thumb defor-
mity is the type III (swan-neck) deformity (Figure
36-2).9,11 CMC joint synovitis leads to erosion of the
articular surface and capsular attenuation, which con-
tributes to the dorsal and radial subluxation of the CMC
joint. An adduction contracture of the metacarpal devel-
ops due to the alteration in forces across the CMC joint
with daily activities such as pinch and grasp. Compensa-
tory MCP joint hyperextension and IP joint flexion,
characteristic of a type III swan-neck deformity, is poten-
tiated as functional compensation for the progressive
adduction contracture.12
METHODS OF TREATMENT
Post-Traumatic Boutonnière Deformity
Nonoperative Management
Generally, non-surgical management is indicated for
closed injuries within 8 to 12 weeks from the time of
injury. This treatment is appropriate when the anatomi-
cal length relationship between the central slip and the
lateral bands is restored after correction of the defor-
mity. Nonoperative treatment can also be attempted in
386 Section 4:  Extensor Tendon Repair and Reconstruction

A B
Figure 36-2  A, Palmar and lateral clinical photograph of a swan-neck deformity of the thumb; B, lateral radiograph of
the thumb demonstrating a swan-neck deformity involving CMC joint subluxation, metacarpal adduction contracture,
hyperextension of the MCP joint, and thumb IP joint flexion. (Reprinted with permission: © 2004 Leversedge FJ, Goldfarb CA,
Boyer MI.)

the cases with a volar dislocation or central slip avulsion

fracture if the PIP joint is stable and acceptable joint and
fracture reductions are achieved.
PIP joint extension splinting is applied when full
passive extension and congruent reduction of the PIP
joint is maintained. Supplemental transarticular Kirsch-
ner wire fixation can be considered. If a flexion contrac-
ture of the PIP joint is present, progressive static splinting
or serial casting, or dynamic extension splinting is uti-
lized in the attempt to restore a supple joint.
The splinting is maintained at all times for 6 to 8
weeks to completely immobilize the PIP joint. After this
period, following reevaluation to confirm stable reduc-
tion, the patient is transitioned to buddy straps during
the day and night-time extension splinting for an addi-
tional 4 to 6 weeks. Throughout the duration of the PIP Figure 36-3  A figure-of-eight ring splint (Silver Ring Splint;
joint splinting, the patient is instructed for active and Charlottesville, VA) used to prevent PIP joint hyperextension
passive DIP joint range of motion exercises. in a mild, flexible swan-neck deformity. (Reprinted with
permission: © 2004 Leversedge FJ, Goldfarb CA, Boyer MI.)
Operative Management
Surgical intervention should be considered for patients
who have failed 3 months of conservative treatment, considered. As PIP joint flexion and grip strength are
such as extension splinting, and for open injuries or compromised rarely with a boutonnière deformity, the
patients with fixed deformity and associated degenera- surgeon should avoid trading active digital flexion for
tive joint changes. Full passive extension of the PIP joint improved extension.
should be sought prior to surgical reconstruction.
Burton and Melchior emphasized that boutonnière Post-Traumatic Swan-Neck Deformity
reconstructions are generally more successful in patients Nonoperative Management
with flexible joints and that a first-stage joint contrac- Although nonoperative treatment is rarely effective in
ture release, followed by an exercise and splinting treating post-traumatic swan-neck deformities, a small
program, can sometimes obviate the need for further subset of patients with flexible deformities who are
procedures.13 If arthritic changes are present, a soft tissue capable of actively initiating PIP joint flexion may
reconstruction may not yield a satisfactory outcome benefit from a trial of figure-of-eight ring splinting to
and, therefore, PIP joint reconstruction with arthrodesis maintain the lateral bands in their anatomical position
or arthroplasty with extensor reconstruction should be and to prevent PIP joint hyperextension (Figure 36-3).
 Chapter 36:  Treatment of Boutonnière and Swan-Neck Deformities
Operative Management
Surgical reconstruction is indicated for those patients
with a flexible deformity who have failed nonoperative
management, for patients with flexible deformities
who cannot actively initiate PIP joint flexion, and for
patients with a fixed deformity. Mobilization and volar
transfer and tenodesis of the lateral bands to prevent
PIP joint hyperextension can be performed for patients
with flexible deformities. For those with fixed deformi-
ties, treatment is determined by the status of the PIP
joint articular surfaces. If the articular surfaces are
preserved, release of the PIP joint with concomitant
procedures to restore flexion may prove beneficial.
However, if the articular surfaces are degenerated, PIP
joint arthrodesis is considered.
Rheumatoid Deformity—General
Surgical correction of both rheumatoid boutonnière
and swan-neck deformities is guided by the stage of
deformity present. Goals include relief of pain and
improvement of overall function of the digit.14 Fortu-
nately, the advances in medical pharmaceutical treat-
ments for rheumatoid arthritis have reduced the rate of
disease progression. It remains important, however, to
perform a thorough global examination, including the
entire upper limbs and the cervical spine, as a localized
area of pathology might influence reconstructive options
elsewhere. Pending treatments of the spine and lower
extremities may influence the timing of upper extremity
intervention due to consideration of ambulatory aids of
devices. In the upper extremity, the pathology of the
elbow and/or wrist should be considered in the preop-
erative planning for hand and digital reconstruction.
Rheumatoid Boutonnière Deformity
Nonoperative Management
Nonoperative treatment includes pharmacologic therapy
as well as low-profile PIP joint extension splinting and/
or buddy strap use. Intra-articular corticosteroid injec-
tions and oral anti-inflammatory medications are uti-
lized to decrease joint synovitis.
Operative Management
For the stage I rheumatoid finger, surgical intervention
should be considered for patients who have failed to
improve with conservative treatment or have a substan-
tial functional deficit. PIP joint synovectomy can be
beneficial for persistent joint synovitis despite pharma-
cologic intervention. Additionally, if attenuation of the
soft tissue over the dorsal PIP joint is present, central
slip reconstruction and dorsal repositioning of the
lateral bands may be indicated. Sectioning of the termi-
nal extensor tendon over the dorsal middle phalanx may
ease limitations caused by DIP joint hyperextension.
In patients with stage II disease, if the cartilage of
the PIP joint is preserved, reconstruction of the central
387
Figure 36-4  Lateral radiograph of the finger following PIP
joint arthrodesis using a tension-band technique. Typically,
due to hardware prominance, the pins and wire are removed
at a time commensurate with osseous union and bony
maturation. (Reprinted with permission: © 2004 Leversedge
FJ, Goldfarb CA, Boyer MI.)
slip and terminal extensor tendon release may be indi-
cated.12,15 For severe deformities in stage III, destruction
of the PIP joint will limit reconstructive options.
Arthrodesis of the PIP joint is a reliable option for
relieving pain and for improving function by creating a
stable digit. Arthrodesis of the PIP joint may be consid-
ered, also, for patients with a fixed flexion contracture
of the PIP joint without articular destruction (Figure
36-4). Implant arthroplasty of the PIP joint with con-
comitant terminal extensor release is a less reliable
option based on a history of soft tissue instability.16-18
Rheumatoid Swan-Neck Deformity
Nonoperative Management
Digital splinting, such as a figure-of-eight ring splint,
can be applied to type I deformities with minimal PIP
joint synovitis, in attempting to prevent PIP joint hyper-
extension and to improve initiation of PIP joint flexion.
Operative Management
Surgical treatment is guided by the type of deformity
present. For type I deformities, it is important to deter-
mine the primary etiology of the flexible swan-neck
deformity. The deformity may be the result of DIP joint
synovitis as extension forces are transferred to the PIP
joint, or more commonly, the result of PIP synovitis and
weakness of the volar PIP joint restraining structures.
The MCP joint must be evaluated carefully, as flexion
contracture at the MCP joint or subluxation of the
extensor tendon at this level should be addressed prior
to, or at the same time of, surgical correction of the
swan-neck deformity. If passive range of motion of the
388 Section 4:  Extensor Tendon Repair and Reconstruction
PIP joint is near normal, DIP joint arthrodesis may be
considered. Postoperatively, the DIP joint is protected
in a mallet-finger splint and the PIP joint is left free to
promote mobilization. In patients with type I swan-
neck deformities who are unable to initiate PIP joint
flexion from a resting hyperextended position, soft
tissue reconstructive procedures that prevent PIP joint
hyperextension may be considered. These procedures
include volar skin dermodesis, oblique retinacular liga-
ment reconstruction, lateral band tenodesis,19 and PIP
joint flexor tenodesis.2,20
In type II swan-neck deformities, intrinsic tightness
results in the MCP joint being held in extension and PIP
joint motion is limited both actively and passively. As
with type I deformities, the presence of MCP joint
pathology and intrinsic tightness should be considered
prior to surgical intervention for correction of the swan-
neck deformity. If MCP joint arthroplasty or intrinsic
release is performed, flexor tenodesis of the PIP joint
may be necessary. Intrinsic release may be performed as
described by Nalebuff, in which the lateral band and
extensor hood are exposed via a dorsal approach, and a
1-cm segment of the lateral band and sagittal band
fibers is excised.7,14
Type III deformities generally require more extensive
soft tissue reconstructive procedures, as PIP joint con-
tractures and lateral band adhesions have developed.
There is decreased active and passive motion of the PIP
joint with fixed positioning of the lateral bands, dorsal
to the PIP joint axis of rotation. Reconstruction involves
lateral band release and volar translocation, dorsal
PIP joint capsulectomy, collateral ligament release, and
extensor tenolysis.16,19,21,22
Type IV deformities are characterized by degenerative
changes of the PIP joint articular surfaces in combina-
tion with a fixed hyperextension deformity of the PIP
joint. Typically, soft tissue procedures alone will not
achieve improved function or provide substantial pain
relief. Options for type IV deformities include implant
arthroplasty and arthrodesis.16,22
Rheumatoid Thumb Deformity
Nonoperative Management
The treatment includes pharmacologic therapy, includ-
ing intra-articular corticosteroid injections and oral
anti-inflammatory medications to decrease joint syno-
vitis. Functional splinting using custom-molded ther-
moplast materials or neoprene may be beneficial for
stabilization of the thumb for pinch and grasp activities
and for positioning of the thumb tip for dexterity-
related tasks.
Operative Management
Surgical correction of type I, or boutonnière, thumb
deformities is based on the subtype: mild, moderate, or
severe. In mild type I deformities, although soft tissue
reconstruction has a high incidence of deformity recur-
rence, it may be indicated as substantial functional
improvements can be achieved.10 EPL tendon rerouting
coupled with synovectomy of the MCP joint will lead
to an increased extensor moment at the MCP joint via
the dorsal MCP joint capsular attachment of the EPL.9
In moderate type I deformities, a fixed MCP joint
deformity is present. Appropriate planning includes
assessment of the CMC and IP joints. The relative condi-
tion of these adjacent joints may guide a decision to
proceed with arthroplasty or arthrodesis of the MCP
joint. If the CMC or IP joint pathology necessitates or
has resulted in fusion, it may be desirable to preserve
motion at the MCP joint with an implant arthroplasty,
avoiding arthrodesis at consecutive joints. Extensor
reconstruction, including EPL rerouting, can be per-
formed concomitantly with arthroplasty of the thumb
MCP joint to augment extensor and abductor forces.23
Following extensor reconstruction and MCP joint
arthroplasty, the thumb MCP joint is splinted in exten-
sion for 4 to 6 weeks, allowing for CMC and IP joint
exercises. If arthrodesis of the MCP joint is performed,
the joint is positioned for fusion in approximately 15°
of flexion and in slight pronation. Several surgical
options are available for arthrodesis of the thumb MCP
joint, including tension band wire fixation, crossing
Kirschner wires, headless compression screws, or plate
and screw fixation.24 Postoperatively, interphalangeal
joint motion is encouraged; however, the fusion site
is protected until radiographs demonstrate evidence
of union.
Severe type I deformities are characterized by fixed
deformities of both the MCP and interphalangeal joints.
Often, the condition of the interphalangeal joint will
warrant arthrodesis. Options for MCP joint arthrodesis
and arthroplasty are the same as for moderate type I
rheumatoid thumb deformities. The CMC joint should
be considered carefully in severe deformities as it is
affected commonly in this stage of the disease process.
Motion sparing procedures are preferred, and include
resection or hemiresection arthroplasty with ligament
reconstruction and soft tissue interposition arthro-
plasty.24 The use of a trapezial implant arthroplasty
should be considered carefully in the rheumatoid popu-
lation due to the higher risk for dislocation or implant
failure.24
Type III rheumatoid swan-neck deformities are
divided into subtypes: mild, moderate, and severe. Mild
type III deformities consist of isolated CMC joint patho­
logy. Therefore, surgical correction is directed toward
alleviation of CMC joint discomfort and dysfunction. If
conservative treatment fails to provide symptomatic
relief, CMC hemitrapeziectomy or trapeziectomy and
ligament reconstruction with soft tissue interposition
arthroplasty are considered. Moderate type III deformi-
ties are characterized by mild MCP joint involvement
 Chapter 36:  Treatment of Boutonnière and Swan-Neck Deformities
(flexible deformity) in addition to CMC joint patho­
logy. Progressive MCP joint hyperextension should be
addressed concurrently with surgical intervention for
CMC joint involvement. MCP joint volar plate capsu-
lodesis, sesamoidesis, or volar tenodesis can be coupled
with CMC hemitrapeziectomy or trapeziectomy and
ligament reconstruction with soft tissue interposition
arthroplasty. Transarticular pin stabilization of the MCP
joint in 20° to 30° of flexion for 3 to 4 weeks postop-
eratively protects the joint while permitting early motion
of the interphalangeal joint.
The severe type III deformity consists of CMC joint
dislocation, adduction contracture of the metacarpal,
and fixed MCP joint hyperextension. Each of these com-
ponents should be addressed in the surgical interven-
tion performed for severe type III rheumatoid thumb
deformities. Generally, arthrodesis of the MCP joint is
warranted to correct the rigid MCP joint hyperexten-
sion. Treatments options for the CMC joint are the same
as those for mild and moderate deformities, including
CMC resection arthroplasty and ligament reconstruc-
tion or tendon interposition arthroplasty. Often, adduc-
tion contracture of the thumb metacarpal is corrected
with metacarpal base resection during resection arthro-
plasty of the CMC joint; however, if the correction is
inadequate, fasciotomy of the first dorsal interosseous
and adductor muscles and, rarely, first web to space
reconstruction with z-plasties, may be performed.24
SURGICAL PROCEDURES
Boutonnière Reconstruction
Primary Central Slip Repair
A dorsal approach is used, preserving the extensor
paratenon. The central slip is isolated and redundant
fibrous tissue is excised after assessing central slip length
with the PIP joint held in extension. In certain cases, a
V-Y advancement is required if tissue is insufficient. If
an avulsion fracture is present, the fragment is carefully
elevated, preserving the central slip attachment. If the
fragment is smaller and fixation with Kirschner wires
or screws is inappropriate, then the fragment is excised
and the central slip is repaired directly to the dorsal
base of the middle phalanx using a suture anchor or
pullout suture method. If a larger fragment, amenable
to fixation, is present, then it is anatomically reduced
and stabilized with two small Kirschner wires or screws.
The lateral bands are restored to their anatomical
location. Incising the transverse retinacular ligaments
may be required to permit mobilization dorsal to the
axis of rotation of the PIP joint. The lateral bands are
stabilized in their anatomical position using non­
absorbable suture. Following repair, the PIP joint is
maintained in full extension for 6 weeks. Often, a trans­
articular Kirschner wire is used to temporarily stabilize
the joint.15,17,18,21,25-27
389
Central Slip Reconstruction Using Local Tissue
Several methods have been described for central slip
reconstruction using local tissues when insufficient
central slip is available for direct repair and a flexible
deformity is present:
1. Snow’s Technique.28 The proximal stump of the
central slip is isolated from surrounding tissues. A
distally based flap of extensor tendon, sufficient to
span the central slip deficit is elevated sharply and
is turned back on itself. The flap is repaired to the
lateral bands using nonabsorbable suture. Follow-
ing repair, passive PIP joint flexion of greater than
60° without excessive tension on the repair site
should be possible.
2. Aiche’s Technique.29 The radial and lateral bands/
conjoined lateral bands are isolated by longitudi-
nal division from the trifurcation of the extrinsic
extensor tendon to the triangular ligament. The
dorsal half of each lateral band / conjoined lateral
band are mobilized dorsally and are sutured
together using nonabsorbable suture. Relocation
of the remaining lateral band is recommended if
it remains volar to the PIP joint axis of rotation.
3. Littler and Eaton’s Technique.30 The radial and ulnar
lateral bands/conjoined lateral bands are isolated
and incised over the middle phalanx. The ORL
must be preserved; otherwise, DIP joint extension
will be compromised. The divided lateral bands
are mobilized dorsally and sutured into the inser-
tion of the central slip. This method is not indi-
cated in the presence of severe attenuation of the
central slip.
4. Matev’s Technique.31 The lateral bands/conjoined
lateral bands are isolated longitudinally. The ulnar
lateral band is divided at the level of the DIP joint
and the radial lateral band is incised at the mid-
point of the middle phalanx. The proximal stump
of the ulnar lateral band and the distal stump of
the radial lateral band are sutured over the dorsal
digit, thereby lengthening the lateral band. The
proximal stump of the radial lateral band is sutured
into the remaining central slip and the base of the
middle phalanx in order to assist with PIP joint
extension. The PIP joint is held in extension for
6 weeks postoperatively, with or without transar-
ticular Kirschner wire fixation (Figure 36-5).
Central Slip Reconstruction Using Tendon Graft
A dorsal exposure of the digit is used, elevating full-
thickness skin flaps and preserving the extensor
paratenon. The central slip remnant is isolated and ele-
vated from the surrounding tissues. An autologous
tendon graft, often the ipsilateral palmaris longus (PL)
tendon, is harvested and is passed through an osseous
tunnel created through the dorsal base of the middle
390 Section 4:  Extensor Tendon Repair and Reconstruction
Matev technique
Figure 36-5  Illustration of Matev’s technique for extensor
reconstruction.
phalanx. The two limbs of the tendon graft are weaved
into the lateral bands with the digit held in neutral. A
temporary, transarticular Kirschner wire may be placed
to stabilize the joint and to protect the reconstruction.
Extensor Tenotomy
It is indicated in the presence of a flexible deformity and
in patients for whom prior PIP joint surgery has been
unsuccessful.26 This procedure can be considered in con-
junction with PIP joint arthrodesis. The terminal tendon
is isolated and is elevated proximally over a distance of
1.5 cm from the underlying DIP joint and middle
phalanx.
The terminal tendon is incised transversely, distal to
the triangular ligament. The ORL must be preserved so
as to not compromise DIP joint extension. The incised
tendon ends are separated by passively extending the PIP
joint and passively flexing the DIP joint (Figure 36-6).
Swan-Neck Reconstruction
PIP Joint Flexor Tenodesis
A check-rein to PIP hyperextension can be created using
a slip of the FDS tendon.17,18,21,32-34 The flexor sheath is
exposed from the base of the digit to the A4 pulley via
a Bruner or mid-axial incision. The membranous portion
LS
clb
O TRL
TT
ORL
Figure 36-6  Location of extensor tenotomy (solid vertical
line “I”) distal to the triangular ligament and proximal to the
ORL insertion at the terminal tendon. Lateral view of the
digit demonstrating the coalescing fibers of the lateral slip
(LS) and oblique fibers of the extensor apparatus (O) which
combine to form the conjoined lateral band (clb). The two
conjoined lateral bands combine to form the terminal
tendon (TT), which inserts into the dorsal base of the distal
phalanx. The transverse retinacular ligament (TRL) prevents
dorsal subluxation of the lateral bands. The oblique
retinacular ligament (ORL) passively links the PIP and DIP
joints as it travels from volar to dorsal from the fibro-
osseous gutter (middle third of the proximal phalanx and A2
pulley) to the proximal aspect of the distal phalanx through
the extensor tendon. (Reprinted with permission: © 2004
Leversedge FJ, Goldfarb CA, Boyer MI.)
of the flexor sheath, from the distal margin of the A2
pulley to the proximal margin of the A4 pulley is ele-
vated, exposing the flexor tendons. One slip of the FDS
tendon is identified and divided at the level of the
decussation, preserving its insertion into the middle
phalanx. The free, proximal end of the divided FDS
slip is passed from deep to superficial (dorsal to volar)
through a transverse incision in the A2 pulley, approxi-
mately 3mm from the distal margin of the pulley. The
tendon slip is sutured back onto itself using nonabsorb-
able suture, tensioning the repair to hold the PIP joint
in approximately 20° of flexion (Figure 36-7).
After surgery, the repair is protected in a dorsal block-
ing splint with the PIP joint at approximately 30°
flexion for 6 to 8 weeks; protected flexion exercises are
started at 2 to 3 weeks.
Lateral Band Tenodesis
The extensor apparatus is exposed via a dorsal curvilin-
ear incision. Cleland’s ligaments are divided and the
flexor sheath is accessed. The dorsally subluxated lateral
band is dissected free from the central slip and the tri-
angular ligament; the lateral band is left intact proxi-
mally and distally. The lateral band is translocated volar
to the PIP joint axis of rotation and is stabilized by a
 Chapter 36:  Treatment of Boutonnière and Swan-Neck Deformities
A4
Flexor
digitorum
superficialis
(FDS)
tendon
A2
A B
Figure 36-7  Illustration of the volar digit demonstrating
(A) the incised FDS slip proximally at the FDS decussation in
relation to the A2 and A4 pulleys and (B) the passage of the
FDS slip through a transverse incision in the A2 pulley and
repair back onto itself, holding the PIP joint in 20° to 30°
flexion.
dorsally based flap of the flexor sheath at the level of
the PIP joint.
Alternatively, the lateral band may be incised at its
distal insertion into the terminal tendon and rerouted
from proximal to distal through a 0.5- to 1.0-m segment
of the flexor sheath. The tendon slip is repaired subse-
quently to its insertion at the terminal extensor tendon
(Figure 36-8).
The repair is protected postoperatively with a dorsal
blocking splint, which maintains the PIP joint in greater
than 30° flexion for 6 to 8 weeks. Early protected digital
flexion exercises are encouraged.
Oblique Retinacular Ligament Reconstruction
ORL reconstruction may be indicated in the presence of
a well-preserved DIP joint when a flexible swan-neck
deformity develops as the result of a chronic mallet
injury. The digit is exposed via an incision from the
MCP joint flexion crease along the radial midaxial line,
curving dorsally to end over the DIP joint. The radial
neurovascular bundle is protected and the A2 pulley
and the terminal tendon slip are identified. A suitable
graft (ideally the ipsilateral PL tendon, when present) is
harvested. The graft is sutured to the terminal tendon
slip using nonabsorbable suture and the free end of the
391
A
A4 Lateral
band
B
Figure 36-8  Illustration of the lateral digit demonstrating:
A, Incision of the lateral band at its insertion into the
terminal tendon; B, the lateral band is elevated, brought
proximally to be re-routed through a 1-cm portion of the A2
pulley before being repaired back to the terminal tendon
insertion over the dorsal DIP joint.
graft is passed volarly, deep to the radial neurovascular
bundle, and is sutured to the distal margin of the A2
pulley after appropriate tensioning. The A2 pulley may
be stabilized by passing the tendon graft from deep to
superficial through a small incision 2 to 3 mm proximal
to the distal and lateral margin of the pulley, before
folding it back upon itself and securing it with nonab-
sorbable suture. Prior to suture repair, the DIP joint is
held in full extension and the PIP joint in 25° of flexion
using temporary, transarticular Kirschner wires that are
left in place for approximately 6 weeks.
Type III Swan-Neck Reconstruction
Via a dorsal curvilinear incision, the extensor apparatus
is exposed. The following procedures are considered, as
indicated: (1) lateral band release from the central
tendon and from the triangular ligament; (2) dorsal PIP
joint capsulectomy; (3) release of the radial and ulnar
collateral ligaments symmetrically from dorsal to volar
as needed to permit passive flexion of the PIP joint to
90°; (4) lateral band stabilization volar to the PIP joint
axis of rotation is not required, typically, as they trans-
late passively with PIP joint flexion; and (5) the PIP
joint in 20° flexion is stabilized using a transarticular
Kirschner wire that is removed 2 to 3 weeks postopera-
tively. The reconstruction is protected in a forearm-
based splint, which may be removed to permit MCP and
DIP joint motion.
SUMMARY
The treatment of boutonnière and swan-neck deformi-
ties of the digits is guided by the etiology and staging
of the condition, primarily differentiated as being the
sequelae of trauma or as a part of the spectrum of rheu-
matoid disease. Treatment may range from splinting
392 Section 4:  Extensor Tendon Repair and Reconstruction
and therapy to operative intervention and, therefore, the
careful assessment of the patient and the deformity is
critical to the formulation of an appropriate and indi-
vidualized treatment strategy. A thorough and global
evaluation of the extremity should include consider-
ation for the current or potential pathology of adjacent
joints, the active and passive motion of involved joints,
subjective concerns for pain or instability, and pertinent
radiographic assessment. In patients with rheumatoid
disease, reconstruction for wrist and/or MCP joint
pathology may influence decision-making for PIP and
DIP joints, including surgical techniques and the
sequence of reconstruction.
A boutonnière deformity, post-traumatic or rheuma-
toid, develops from an injury to the central slip at the PIP
joint. The deformity may evolve in a progressive fashion
secondary to trauma and, therefore, may not be imme-
diately appreciated clinically following injury. Outcomes
are improved with early diagnosis, particularly utilizing
the Elson test. However, if the diagnosis is within 2 to 3
months of the time of injury, extension splinting (with
or without use of a temporary transarticular Kirschner
wire holding the PIP joint in extension) is an effective
treatment. Surgical intervention for boutonnière defor-
mities that have failed conservative treatment range from
central slip reconstruction with lateral band reposition-
ing to PIP joint arthroplasty and arthrodesis.
Swan-neck deformities are characterized by laxity of
the PIP volar plate and an inability of the terminal slip
to extend the DIP joint, leading to hyperextension of
the PIP joint and flexion of the DIP joint. In patients
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thumb deformity, J Hand Surg (Am) 15:999–1003, 1990.
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joints. Determination as to the specific type of defor-
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Nonoperative treatment rarely leads to a favorable
outcome in patients with an advanced swan-neck defor-
mity. However, the flexible swan neck deformity may be
treated successfully in a figure-of-eight splint. Surgical
options for rheumatoid and post-traumatic swan neck
deformities include volar positioning of the lateral band
with tenodesis, oblique retinacular ligament reconstruc-
tion, DIP arthrodesis, and PIP joint arthroplasty or
arthrodesis.
Boutonnière or swan-neck deformity of the thumb
can develop in the presence of rheumatoid disease. It is
imperative to assess both individually and collectively
the status of the CMC, MCP, and IP joints in formulat-
ing a treatment plan. Operative intervention varies,
with options ranging from soft tissue reconstruction
procedures to arthroplasty and arthrodesis. In the CMC
joint, implant interposition arthroplasty may have an
increased failure rate due to poor soft tissue restraints
and an increased risk of dislocation.
Ultimately, the primary goals of treatment of swan
neck and boutonnière deformities are to alleviate pain
and to improve function. Preoperative patient educa-
tion will help to avoid unrealistic expectations and or
the consequences of unanticipated outcomes. Patient
selection and thorough preoperative evaluation are criti-
cal to guiding appropriate intervention and to achieving
successful outcomes.
11. Ratliff AH: Deformities of the thumb in rheumatoid arthritis,
Hand 3:138–143, 1971.
12. Flatt AE: The Care of the Arthritis Hand, St Louis, 1995, Quality
Medical Publishing, pp 263-264.
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In Green DP, Hotchkiss RN, Pederson WC, editors: Green’s
Operative Hand Surgery, ed 4, New York, 1999, Churchill
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14. O’Brien ET: Surgical Principles and planning for the rheuma-
toid hand and wrist, Clin Plast Surg 23:407–420, 1996.
15. Urbaniak JR, Hayes MG: Chronic boutonniere deformity: an
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16. Boyer MI, Gelberman RH: Operative correction of swan-neck
and boutonniere deformities in the rheumatoid hand, J Am
Acad Orthop Surg 7:92–100, 1999.
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arthroplasty in the proximal interphalangeal joint of the
hand, J Hand Surg (Am) 10:796–805, 1985.
18. Takigawa S, Meletiou S, Sauerbier M, et al: Long-term assess-
ment of Swanson implant arthroplasty in the proximal inter-
phalangeal joint of the hand, J Hand Surg (Am) 29:785–795,
2004.
19. Gainor BJ, Hummel GL: Correction of rheumatoid swan-neck
deformity by lateral band mobilization, J Hand Surg (Am)
10:370–376, 1985.
 Chapter 36:  Treatment of Boutonnière and Swan-Neck Deformities
20. Curtis R: Sublimis tenodesis. In Edmonson AS, Crenshaw AH,
editors: Campbells’s Operative Orthopaedics, ed 6, St Loius,
1980, CV Mosby, p 319.
21. Kiefhaber TR, Strickland JW: Soft tissue reconstruction for
rheumatoid swan-neck and boutonniere deformities: long
term results, J Hand Surg (Am) 18:984–989, 1993.
22. Strickland JW, Boyer M: Swan neck deformity. In Strickland
JW, editor: The Hand. Master Techniques in Orthoapedic Surgery
Series, Philadelphia, 1998, Lippincott-Raven, pp 459–470.
23. Figgie MP, Inglis AE, Sobel M, et al: Metacarpal-phalangeal
joint arthroplasty of the rheumatoid thumb, J Hand Surg
(Am) 15:210–216, 1990.
24. Stein AB, Terrono AL: The rheumatoid thumb, Hand Clin
12:541–550, 1996.
25. Wilczynski M, Boyer MI, Leversedge FJ: Operative reconstruc-
tion of boutonnière and swan-neck deformities. In Wiesel S,
editor: Operative Techniques In Orthopaedic Surgery, Philadel-
phia, 2011, Wolters Kluwer/Lippincott Williams & Wilkins,
pp 2619–2633.
26. Meadows SE, Schneider LH, Sherwyn JH: Treatment of the
chronic boutonniere deformity by extensor tenotomy, Hand
Clin 11:441–447, 1995.
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27. Towfigh H, Gruber P: Surgical treatment of the boutonniere
deformity, Oper Orthop Traumatol 17:66–78, 2005.
28. Snow JW: Use of a retrograde tendon flap in repairing a
severed extensor in the PIP joint area, Plast Reconstr Surg
51:555–558, 1973.
29. Aiche A, Barsky AJ, Weiner DL: Prevention of boutonniere
deformity, Plast Reconstr Surg 46:164–167, 1970.
30. Littler JW, Eaton RG: Redistribution of forces in the correction
of boutonniere deformity, J Bone Joint Surg (Am) 49:1267–
1274, 1967.
31. Matev I: Transposition of the lateral slips of the aponeurosis
in treatment of long-standing “boutonniere deformity” of the
fingers, Br J Plast Surg 17:281–286, 1964.
32. Thompson JS, Littler JW, Upton J: The spiral oblique retinacu-
lar ligament (SORL), J Hand Surg (Am) 3:482–487, 1978.
33. Kleinman WB, Petersen DP: Oblique retinacular ligament
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Surg (Am) 9:399–404, 1984.
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1992.
 CHAPTER
37  
VASCULARIZED TENDON
GRAFT FOR EXTENSOR
TENDON RECONSTRUCTION
Roberto Adani, MD, Luigi Tarallo, MD,
Massimo Corain, MD, and Jean Claude Guimberteau, MD
OUTLINE
This chapter describes different vascularized compo­
site tissue graft procedures incorporating tendons to
reconstruct the tendons and overlying soft tissue
defects in the hand. The options are the dorsalis pedis
flap, the radial forearm flap, and the ulnar artery–
based island flap. The radial island fasciotendinous
flap is an excellent evolution of the radial forearm flap
for coverage of soft tissue defects of the hand; we rec­
ommend this composite fascial flap to reconstruct the
dorsum of the hand that requires simultaneous grafts
of two or three tendons.
Composite tissue loss of the hand involving tendon
defects represents a great clinical challenge. These injuries
require restoration of both skin coverage and tendon
function. These injuries are approached by different ways:
multistage reconstructions of soft tissue then tendon, or
single-stage vascularized composite tissue grafting.1
Multistage reconstructions include skin coverage
with distant flaps and tendon grafting in a later stage.2
Nonvascularized tendon grafts in conjunction with ped­
icled flaps or free tissue transfer are termed partially
vascularized tissue transfer.1 Skin,3-8 fascial,9-11 and muscle
flaps12,13 can be used for this purpose. A completely
vascularized single-stage reconstruction uses a compos­
ite flap in which different tissue components (skin,
tendon, and nerve) are included.
In 1979, Taylor and Towsend14 described for the first
time a composite free flap, with attached vascularized
segments of the extensor hallucis brevis to the great toe
and the extensor digitorum longus to the second toe.
Subsequently, several authors15-19 have described good
results for the treatment of compound injuries with the
dorsalis pedis composite flap; this flap provides four
vascularized tendons (extensor digitorum communis
[EDC]) of adequate length.
Reid and Moss20 modified the radial artery forearm
flap to include flexor tendons from forearm. The tendons
394
can be included are the palmaris longus (PL) and a strip
of the brachioradialis tendons along with fascia and
skin, and a slip of flexor carpi radialis (FCR) tendon.21,22
The ulnar island flap of the forearm allows for the inclu­
sion of the PL and a strip of the flexor carpi ulnaris
(FCU) tendons.23,24
OPERATIVE TECHNIQUES
Dorsalis Pedis Cutaneotendinous Free Flap
The surgical procedure uses two operative teams: one to
harvest the cutaneotendinous free flap and the other to
prepare the recipient site. A pattern outlining the soft
tissue defect on the dorsum of the hand is transferred
to the dorsum of the foot centered on the second meta­
tarsal bone using Doppler examination. It is helpful to
also outline the venous drainage. Flap elevation begins
distally between the first and the second toes, identify­
ing the first dorsal metatarsal artery that is tied and
sutured to the distal skin margin. The flap is elevated
from distal to proximal and laterally to medially below
the level of the first dorsal metatarsal artery. The flap is
dissected to include in continuity, the long toe extensors
to the second through fifth toes tendons, keeping the
areolar tissue around the tendons, vessels, and nerves
with the flap. The extensor digitorum tendons are fol­
lowed proximally and are divided, according to the
number of destroyed tendons in the hand. Care should
be taken to preserve the paratenon on the extensor hal­
lucis longus tendon, which is left on the foot. During
elevation, the long saphenous vein or median dorsal
vein is preserved, In addition, the superficial peroneal
nerve must be included in the flap. Finally, the extensor
retinaculum is divided and the dorsalis pedis artery can
be traced until a sufficient pedicle length is obtained.
Radial Artery Forearm Island Flap With
Vascularized Tendons
This is a modification of the radial artery forearm flap.
Preoperatively, an Allen test must be done to ensure the
 Chapter 37:  Vascularized Tendon Graft for Extensor Tendon Reconstruction
Figure 37-1  Skin incision for harvesting the ulnar artery-
based skin flap incorporating half of the FCU tendon.
presence of a complete vascular palmar arch. The pres­
ence of a PL tendon is also confirmed. The pattern of
the dorsal defect is outlined around the radial vessels,
and the flap is raised including skin and fascia. Two 7- to
8-cm-long strips of FCR tendon and brachioradialis
tendons might be included in the flap with the PL
tendon, if it is present. Care is taken to preserve the
areolar tissue around the tendons, which receive their
blood supply from the deep fascia. The radial artery and
its venae comitantes are ligated proximally, and the flap
is mobilized distally. Due to cosmetic reasons, this flap
is less favored by many surgeons in recent years.
Ulnar Artery–Based Island Flap With
Vascularized Tendons (Used by J.C.G.)
At the distal third of the wrist, just proximal to the flexor
retinaculum, the ulnar artery on its lateral side gives off
one or two branches of around 1 mm in diameter to the
distal part of the FCU tendon. Two types of arterial
branching can be observed, either directly from the
ulnar artery or from the dorsal branch of the ulnar
artery. These vascular branches are constant and easily
identified on the lateral side of the pedicle. It is possible
to carry out not only tendinous vascular transfers but
also a cutaneotendinous transfer, and even the triple
transfer of skin, tendon, and bone.
Preoperative evaluation includes the Allen test and
Doppler testing to ascertain that the radial artery pro­
vides adequate blood supply to the hand. Angiography
of the arm is also advisable. A bayonet-shaped incision
is first traced and then made on the medial side of the
forearm, the axis of the incision overlying the lateral
border of the flexor carpi ulnaris (Figure 37-1). The
ulnar pedicle is dissected and all its branches are care­
fully separated and divided.
First, the cutaneous branches between the ulnar
artery and the skin, emerging from the volar aspect of
the pedicle and which are the principal components
of the ulnar forearm flap, are then carefully isolated.
395
Figure 37-2  Ulnar artery island skin flap with the FCU
tendon connecting to the flap by fascia.
Then, the ulnar pedicle is separated from the ulnar nerve
on its dorsal aspect along its whole length from the
lower third of the forearm to Guyon’s canal. This ulnar
skin flap is raised together with the FCU tendon.
The FCU tendon is longitudinally split into two parts.
One is maintained in place with the muscle and the
other one (i.e., the medial part) is transected at its distal
insertion on the triquetrum. The proximal portion is
transected at the musculotendinous junction. All the
other branches of the ulnar artery are ligated, except
branches to the skin flap on the anterior side and to the
periosteum in the event of a bone transfer. The ulnar
pedicle is dissected distally and the combined tendon–
skin transfer is performed (Figure 37-2).
The FCU and ulnar skin transfer is generally used as
a retrograde flap by preserving the inflow from the distal
portion of the ulnar artery. One method is by transpos­
ing to the anterior and radial side for thumb and index
reconstruction. The other method is transposing to the
ulnar and posterior direction. Because the transfer is
oriented on the lateral side of the hand, caution has to
be taken concerning the sensory branches of the radial
nerve. Sutures for extensor tendon reconstruction are
various, from simple sutures to Pulvertaft weaves.
POSTOPERATIVE CARE
We perform split-thickness skin grafting on the defect
immediately following flap harvesting. When the dor­
salis pedis flap is used, the ankle, foot, and toes are
splinted to prevent movement under the graft. When the
radial forearm flap is used, the wrist and the fingers are
immobilized for 10 days with the wrist in 20° to 30° of
extension with the metacarpophalangeal (MCP) joints
in 50° of flexion and the interphalangeal (IP) joints in
extension.4
Initially, the hand is splinted with the wrist at 30° of
extension and MCP and IP joints in 0°. In our case
series, these injuries have been managed with variable
periods of immobilization after repair; nevertheless,
396 Section 4:  Extensor Tendon Repair and Reconstruction

rehabilitation of the extensor tendon has recently been

settled in favor of early mobilization.25
Mobilization is started after 1 week, allowing 0° to
30° movements at MCP joints with IP joints free to
move during exercise. The flexion movement of MP
joints is gradually increased, and after 5 weeks MCP and
IP joints are left free to move during the day with night
splinting. The splint is continued for 6 weeks. Patient
motivation is very important: without the patient’s
active participation, functional recovery could be very
limited.
OUTCOMES A
Between 1988 and 2008, the lead author (R.A.) and his
colleagues treated 21 patients with composite loss of
tendon and skin on the dorsum of the hand. The skin
defects ranged from 8 × 5 cm to 11 × 13 cm. The interval
from injury to flap transfer ranged from 2 to 40 days,
with an average of 14 days. The time between injury and
reconstruction was long because initial trauma in most
cases were treated elsewhere and referred to us later. The
number of transferred tendons in each patient was three
on average. We used cutaneotendinous dorsalis pedis
flap in 8 cases, and the radial tendinous island flap in
13 cases (a cutaneous flap in 10 cases and a fascioten­
B
dinous flap in 3 cases).
The aim of extensor tendon reconstruction is to
achieve free gliding of the tendons and normal finger
movement. The transferred tendons function well in
our patients. In one case the flexion of the fingers
and the extension of MCP joints were full, but there were
IP joint extension deficits of the middle, ring, and little
finger due to the original interosseous muscle avulsion.
Tendon adhesions markedly limiting hand motion
were seen only in one case; tenolysis was necessary. In
the donor site, toe extension was weak. However, toe
motion was not impaired because the short extensors of
the toes were intact. Partial skin graft loss at the donor
C
site occurred in the majority of the cases treated with
dorsalis pedis flap but did not require additional surgery
except that skin grafting was redone in one patient with
radial artery flap. Hypertrophic scarring occurred in all
patients at the donor site; however, this improved with
time, particularly in the foot.
Ulnar artery–based composite flap tendon transfer
was performed in 14 patients by J.C.G. and his col­
leagues. There were no cases of complete necrosis, but
there was one case of partial skin loss because the flap
was passed in a subcutaneous tunnel. The sacrifice of the
ulnar artery is the main disadvantage. In the long term,
the flap may remain somewhat swollen for 3 or 4 months.
D
It may be necessary to reshape the skin flap in the months
that follow. The tissue quality is excellent, being fine, fat Figure 37-3  A case of skin defect and EPL tendon defect
free, and virtually hairless (Figure 37-3). There are over the proximal part of the thumb. A and B, An island
minimal concerns at the donor site. The scar on the ulnar artery flap with the FCU tendon was transferred to
forearm is usually very limited and not hypertrophic. cover skin defect and reconstruct the EPL tendon. C and
D, Postoperatively, the cosmetic appearance is excellent
and thumb extension was restored.
 Chapter 37:  Vascularized Tendon Graft for Extensor Tendon Reconstruction 397

DISCUSSION
The dorsum of the hand is covered by a thin skin with
little subcutaneous tissue, underneath which lie the
extensor tendons; traumatic loss of skin is often associ­
ated with extensor tendon defects. These injuries are
conventionally treated with primary distant flap transfer
(axial and random pattern flaps, groin flap, etc.) and
secondary tendon grafts or transfers.2 The treatment
does not yield satisfactory results either aesthetically or
functionally because of the need for immobilization of
the hand in a nonfunctional position and bulky flap
coverage.14,15 Moreover, the risk of tendon adhesions
may require the staged tendon reconstruction preceded A
by silicone rubber tendon implants in the first stage.26
Multiple operations also require a prolonged period of
physiotherapy and functional recovery.
The partially vascularized tissue transfer allows the
hand to be placed in a functional position and ensure
early mobilization. Flaps of various forms can be
used: island or free skin flaps, island or free fascial
flaps, island or free muscle flaps. Fascial and muscle
flaps do not always allow immediate tendon repair.9-12
Tendon reconstruction is more difficult under muscle
or fascial than with cutaneous flaps.27 Muscle flaps are
too bulky, requiring subsequent thinning, and they
adhere to tendon grafts extensively.6,7 This have been
B
partially solved by using partial superior latissimus or
partial medial rectus flaps; in this way, the debulking
rate has decreased, which may allow one-stage tendon
reconstruction.13
Distally based radial3,4 and ulnar5 flaps sacrifice a
major vascular supply to a hand, and this may jeopar­
dize blood flow to an already compromised area.6
Scheker and colleagues6 used primary tendon grafts
covered by a free flap from either the lateral arm or groin.
Free tendon grafts were placed through a subcutaneous
tunnel under the flap. This technique may damage the
flap vessels, which has resulted in hematomas, causing
C
tendon adhesion.8 To minimize this problem, the groin
flap can be harvested along with a sheet of external
oblique aponeurosis preserving the vascular connec­
tions between it and the under surface of the groin flap.
This aponeurosis is used to create a gliding surface for
tendon grafts, reducing tendon adhesion.8
The vascularized flap incorporating extensor tendons
allows one-stage reconstruction of all lost structures.
The vascularized tendon grafts may heal faster with less
adhesion.14 Hand motion can be initiated earlier because
union of the tendon junction is achieved sooner than D
with conventional tendon grafts.21 The dorsalis pedis
Figure 37-4  A case of severe friction injury to the dorsum
cutaneotendinous flap has been used most commonly. of the hand caused by road accident. A, Loss of skin and
It can provide four vascularized tendons of adequate EDC tendons of index, middle and ring fingers and extensor
length completely surrounded by paratenon and loosely indicis proprius tendon. B, Transfer of dorsalis pedis artery
attached to skin as thin as that on the dorsum of the flap with extensor tendons. C and D, Aesthetic and
hand (Figure 37-4). functional results.
398 Section 4:  Extensor Tendon Repair and Reconstruction

A B C

D E F
Figure 37-5  A patient with severe friction injury on the dorsum of the hand. A, Loss of skin and extensor tendons to the
middle and ring fingers. B, Dorsalis pedis artery flap of 7 × 11 cm with two extensor digitorum longus tendons of the toe was
harvested and transferred to the hand. The extensor digitorum longus tendons were sutured to the extensor communis
tendons in the dorsum of the hand. C, Immediate postoperative view. D–F, Aesthetic and functional results.

In our cases, tenolysis was not necessary and a defat­
ting procedure was never used with the dorsalis pedis
flap. Recently, the dorsalis pedis flap has been less
used as a free skin flap transfer because of variations
in donor site anatomy, delayed wound healing, tedious
dissection, and scar formation on the dorsum of the
foot.21,27-29 However, the cosmetic appearance of the
donor site of the foot is rather acceptable in our patients
after dorsalis pedis flap transfer (Figure 37-5). These
patients believe the overall benefits of the procedure
outweighed the donor-site morbidity. There was only
minimal functional deficits. Delayed donor site healing
was common in this series of patients and late wound
breakdown was also common. However, this rarely
produced a significant long-term functional deficit.27
None of our patients had ulcerations, and all were able
to walk normally. Only two patients had contractures
of the skin at the grafted area overlying the extensor
hallucis longus tendon and the extensor digiti minimi
tendon with minimal deficits of toe plantar flexion
(Figure 37-6).
We believe that some technical pearls can help reduce
donor site problems associated with dorsalis pedis flap.
The size of the flap should be limited and surgeons
should avoid raising the flap too distally: the morbidity
of the donor site is related to both the site and the loca­
tion of the flap harvested. In the literature, increased
morbidity seems to accompany harvested flaps that
extend to within 2 cm of the metatarsophalangeal
(MTP) joint crease.28 In contrast, when the flap was
raised 2 cm or more proximal to the MTP joint crease,
there were no problems with the distal portion of the
donor site.
Some authors20, 21 preferred a radial forearm cutaneo­
tendinous flap. The flap transfer is quick and simple, but
only a limited number of tendons are available. The PL
tendon can be taken completely with strips of the FCR
tendon and the brachioradialis tendon as vascularized
grafts (Figure 37-7). The sacrifice of the radial artery
does not generally cause significant problems. In cases
of severe hand trauma, use of the reverse radial forearm
flap can be contraindicated.6 In our cases, there were few
donor site complications. To minimize donor site mor­
bidity, the radial border of the flap should not be
extended beyond the radial border of the forearm and
the FDS muscle must be imbricates over the FCR tendon
 Chapter 37:  Vascularized Tendon Graft for Extensor Tendon Reconstruction
A B C
D E
to prevent exposure of this tendon.4 The cosmetic
appearance of the flap donor site could be improved
covering it with artificial dermis (Integra, Integra Life­
sciences, Plainsboro, NJ, USA).30 However, in recent
years, more surgeons prefer not to use this site as a
donor because of obvious cosmetic reasons in the
forearm.
An evolution of the radial forearm cutaneotendinous
flap is the radial island fasciotendinous flap.31 This radial
fascial flap in combination with vascularized extensor
399
F
Figure 37-6  A patient with hot press injury. A, Loss of
dorsal skin and all extensor tendons to the four fingers.  
B, Defects of all extensor tendons in the dorsum of the
hand. C, Harvest of a free cutaneous tendinous dorsalis
pedis flap including four extensor digitorum longus
tendons: intraoperative view showing tendon
reconstruction. D, Immediate postoperative result.
E–G, Aesthetic and functional results of the hand.
tendons has not been popular. Reid and Moss20 used a
radial artery–based flap of fascia and tendon alone,
leaving the forearm skin unattached. The fascia flap
includes nerve and tendon units to facilitate true com­
posite tissue reconstructive efforts,10 which provide thin,
pliable tissue with no or minimal donor site morbidity.
We have used radial forearm cutaneotendinous flap in
three cases thus far (Figure 37-8). We obtained excellent
functional and aesthetic results in the hand with
minimal donor site morbidity. None of the patients had
400 Section 4:  Extensor Tendon Repair and Reconstruction
A B
D E
symptoms of cold intolerance due to the sacrifice of the
radial artery, or functional deficits due to the harvesting
of the tendons. The outcomes of the use of this flap are
encouraging.
SUMMARY
The dorsalis pedis flap, radial forearm cutaneotendi­
nous flap, and island ulnar artery flap may provide good
options for one-stage simultaneous reconstruction of
skin and tendon defects on the dorsum of the hand. In
our patients, we achieved good cosmetics and function
after these composite flap procedures.
When grafting of three or four tendons is required, the
dorsalis pedis flap can be used with careful management
of the donor site. The radial forearm cutaneotendinous
C
F
Figure 37-7  A, A case of hot press injury on the
dorsum of the hand with section of EDC tendon of
the middle finger and loss of EDC tendons of the
ring and little fingers and extensor digit minimi
proprius. B, Intraoperative débridement of the
dorsal wound. C, Reconstruction with radial
artery cutaneotendinous island flap; detail of
reconstruction of the extensor apparatus of the
little finger with PL tendon. D–F, Aesthetic and
functional results after surgery. G, Donor site
result in the forearm.
flap can also be applied in cases of one or two extensor
tendon reconstruction, as much as it is a simpler tech­
nique, with no microsurgical risks, and followed by
minor complications. The dorsalis pedis flap and radial
forearm flap are less often used now because of the donor
site morbidity.
Based on our preliminary results in a series of three
patients, we believe that radial island fasciotendinous
flap represent an excellent evolution for coverage of
soft tissue defects of the hand and we recommend the
use of this composite fascial flap in the reconstruction
of cutaneotendinous injuries of the dorsum of the
hand that require the use of two or three tendon grafts.
Harvesting a small dorsalis pedis flap or ulnar side
island flap for reconstruction of extensor tendon in the
 Chapter 37:  Vascularized Tendon Graft for Extensor Tendon Reconstruction 401

A B C

D F G
Figure 37-8  A patient with injury to the dorsum of the hand. A, Soft tissue defect located on the dorsum of the hand with
absence of extensor tendons from the index and middle finger. B, The forearm fascia flap was raised on a distal pedicle with a
strip of the brachioradialis and flexor carpi radialis tendons. C and D, The flap was transferred to the dorsum of the hand and
is covered with a full-thickness skin graft. E and F, Aesthetic and functional results. G, Appearance of the donor site in the
forearm.

dorsum of the digits remains a practical and attractive composite tissue grafting in one stage is expected to
option. confer the best opportunity to patients for functional
The replacement of combined loss of skin and recovery, allowing patients a relatively rapid return to a
tendons on the dorsum of the hand with vascularized normal life.

References
1. Dessai SS, Chuang DC, Levin SL: Microsurgical reconstruc­
tion of the extensor system, Hand Clin 11:471–482, 1995.
2. Winspur I: Distant flaps, Hand Clin 1:729–739, 1985.
3. Soutar DS, Tanner NS: The radial forearm flap in the manage­
ment of soft tissue injuries of the hand, Br J Plast Surg 37:18–
26, 1984.
4. Jones NF, Jarrahy R, Kaufman MR: Pedicled and free radial
forearm flaps for reconstruction of the elbow, wrist, and
hand, Plast Reconstr Surg 121:887–898, 2008.
5. Grobbelaar AO, Harrison DH: The distally based ulnar artery
island flap in hand reconstruction, J Hand Surg (Br) 22:204–
211, 1997.
6. Schecker LR, Langley SJ, Martin DL, et al: Primary extensor
tendon reconstruction in dorsal hand defects requiring free
flaps, J Hand Surg (Br) 18:568–575, 1993.
7. Sundine M, Scheker LR: A comparison of immediate staged
reconstruction of the dorsum of the hand, J Hand Surg (Br)
21:216–221, 1996.
8. Jeng SF, Wei FC, Noordhoff MS: The composite groin fascial
free flap, Ann Plast Surg 35:595–600, 1995.
9. Weinzweig N, Chen L, Chen ZW: The distally based radial
forearm fasciosubcutaneous flap with preservation of the
radial artery: An anatomic and clinical approach, Plast
Reconstr Surg 94:675–684, 1994.
402 Section 4:  Extensor Tendon Repair and Reconstruction
10. Carty MJ, Taghinia A, Upton J: Fascial flap reconstruction of
the hand: A single surgeon’s 30-year experience, Plast Reconstr
Surg 125:953–962, 2010.
11. Buehler MJ, Pacelli L,Wilson KM: Serratus fascia “sandwich”
free-tissue transfer for complex dorsal hand and wrist avul­
sion injuries, J Reconstr Microsurg 15:315–320, 1999.
12. Brody GA, Buncke HJ, Alpert BS, et al: Serratus anterior
muscle transplantation for treatment of soft tissue defects in
the hand, J Hand Surg (Am) 15:322–327, 1990.
13. Parrett BM, Bou-Merhi JS, Buntic RF, et al: Refining outcomes
in dorsal hand coverage: Consideration of aesthetic and donor
site morbidity, Plast Reconstr Surg 126:1630–1638, 2010.
14. Taylor GI, Townsend P: Composite free flap and tendon trans­
fer: An anatomical study and a clinical technique, Br J Plast
Surg 32:170–183, 1979.
15. Hentz VR, Pearl RM: Hand reconstruction following avulsion
of all dorsal soft tissues: A cutaneo-tendinous free tissue
transfer, Ann Chir Main 6:31–37, 1987.
16. Vila-Rovira R, Ferreira BJ, Guinot A: Transfer of vascularized
extensor tendons from the foot to the hand with a dorsalis
pedis flap, Plast Reconstr Surg 76:421–427, 1985.
17. Caroli A, Adani R, Castagnetti C, et al: Dorsalis pedis flap with
vascularized extensor tendons for dorsal hand reconstruction,
Plast Reconstr Surg 92:1326–1330, 1993.
18. Lee KS, Park SW, Kim HY: Tendocutaneous free flap transfer
from the dorsum of the foot, Microsurg 15:882–885, 1994.
19. Cho BC, Lee JH, Weinzweig N, et al: Use of free innervated
dorsalis pedis tendocutaneous flap in composite hand recon­
struction, Ann Plast Surg 40:268–276, 1998.
20. Reid CD, Moss LH: One-stage flap repair with vascularized
tendon grafts in a dorsal hand injury using the “Chinese”
forearm flap, Br J Plast Surg 36:473–479, 1983.
21. Yajima H, Inada Y, Shono M, et al: Radial forearm flap with
vascularized tendons for hand reconstruction, Plast Reconstr
Surg 98:328–333, 1996.
22. Adani R, Marcoccio I, Tarallo L: Flexor coverage of dorsum of
hand associated with extensor tendons injuries: A completely
vascularized single-stage reconstruction, Microsurg 23:32–39,
2003.
23. Glasson DW, Lovie MJ: The ulnar island flap in hand and
forearm reconstruction, Br J Plast Surg 41:349–353, 1988.
24. Guimberteau JC, Panconi B, Boileau R: Mesovascularized
island flexor tendon: new concepts and techniques for flexor
tendon salvage surgery, Plast Reconstr Surg 92:888–903, 1993.
25. Koul AR, Patil RK, Philip V: Complex extensor tendon inju­
ries: early active motion following single-stage reconstruc­
tion, J Hand Surg (Eur) 33:753–759, 2008.
26. Cautilli D, Schneider LH: Extensor tendon grafting on the
dorsum of the hand in massive tendon loss, Hand Clin
11:423–429, 1995.
27. Tomaino MM: Treatment of composite tissue loss following
hand and forearm trauma, Hand Clin 15:319–333, 1999.
28. Samson MC, Morris SF, Tweed AE: Dorsalis pedis flap donor
site: Acceptable or not? Plast Reconstr Surg 102:1549–1554,
1998.
29. Chen HC, Buchman MT, Wei FC: Free flaps for soft tissue
coverage in the hand and fingers, Hand Clin 15:541–554,
1999.
30. Murray RC, Gordin EA, Saigal K, et al: Reconstruction of the
radial forearm free flap donor site using integra artificial
dermis, Microsurg 31:104–108, 2011.
31. Adani R, Tarallo L, Marcoccio I: Island radial artery fascioten­
dinous flap for dorsal hand reconstruction, Ann Plast Surg
47:83–85, 2001.
 CHAPTER
38  
STATE OF THE ART FLEXOR
TENDON REHABILITATION
Karen M. Pettengill, MS, OTR/L, CHT, and
Gwendolyn Van Strien, LPT, MSc
OUTLINE
There are three approaches to management of the
repaired flexor tendon during the first few weeks:
immobilization, passive mobilization (passive flexion
and active or passive extension), and active flexion
initiated within the first several days. The “classic”
early passive mobilization programs have been modi-
fied, improving results. While the literature now sup-
ports the efficacy of early active mobilization over
early passive and early passive mobilization over
immobilization, there is little evidence behind indi-
vidual techniques. Rehabilitation programs must be
individually designed, based on such factors as char-
acteristics of injury and repair, concomitant injuries,
patient access to therapy, and patient ability to perform
a given program. This requires close surgeon–therapist
collaboration. There are a number of ways to safely
progress active flexion programs and to provide splint
protection. Splints (or orthoses) are dorsal and provide
some protection from excessive extension through
metacarpophalangeal joint and wrist position; the
traditional wrist and finger positions have been modi-
fied over the years. One published active flexion
plan involves a splint with a wrist hinge. Growing
evidence suggests greater incorporation of neuro­
muscular theory and purposeful activity into therapy,
preventing loss of cortical representation of involved
digits and facilitating recovery of fluid functional
motion. We need more specific measures of functional
outcomes for both surgery and therapy, to better rep-
resent the success of each individual’s rehabilitation.
Methods of rehabilitation after flexor tendon repairs are
evolving. Earlier chapters examined the anatomy,
healing, surgical repair and other aspects in great detail,
offering a biological, mechanical, and surgical basis for
establishment of current rehabilitation principles and
methods. It is well recognized that the first few weeks
following repair are crucial in flexor tendon rehabilita-
tion: Management during this phase will determine the
success of the repair. In discussing the various rehabilita-
tion programs available, we will focus almost entirely
on the first few weeks, with discussion of basic concepts
and techniques, and rationale for advancing the program
according to individual patient and surgical factors. We
will also examine emerging trends and issues in flexor
tendon rehabilitation, raising questions we hope to see
answered in the years to come.
In 1917, Harmer1 published his results of uncon-
trolled early active flexion and extension following
flexor tendon repair. Over the course of the past 100
years, we have come full circle in our approach: For a
long period, injured flexor tendons in the hand were
immobilized or resected, with later grafting. In the
1960s, passive mobilization programs were in vogue,
and today we have returned with greater sophistication
to active mobilization as the preferred approach. None-
theless, there is limited high-quality evidence support-
ing one form of early mobilization over another.2,3
IMMOBILIZATION
The more conservative approaches of immobilization
and/or resection and grafting were a response to the
complexity of the flexor tendons in zone 2, known as
“no man’s land.” Surgeons were understandably hesi-
tant to perform a repair at that level because of the
unacceptably high risk of rupture or development of
restrictive adhesions. In 1941, Mason and Allen4 found
that in immobilized repairs there was an initial drop in
repair strength, followed by a gradual increase. At 3
weeks, repair strength was equivalent to that on the first
postoperative day. Because of the observed dip in
strength, it was considered necessary to protect the
repair with complete immobilization for 3 weeks. Since
then research has supported the value of controlled
early mobilization of repairs. Even though immobiliza-
tion is no longer the preferred approach, there are many
cases in which this is the treatment of choice (e.g., in
young children).
When a repair must be immobilized, the cast or
splint is designed to keep the repaired flexor tendon on
405
406 Section 5:  Rehabilitation of Tendon Surgery
slack by positioning the wrist at neutral to 20° to 30°
of flexion, the metacarpophalangeal (MCP) joints in
40° to 70° of flexion, and the interphalangeal (IP)
joints at 0°. Following 3 weeks of immobilization, there
are two predictable problems. Since immobilized repairs
grow weaker before they return to their immediate post-
operative strength, we can expect a higher risk of rupture
with active motion in these patients. At the same time,
frustratingly, restrictive tendon adhesions will have
developed. Therapy in these cases focuses on increasing
tendon excursion while protecting the repair from
excessive stress. A 1991 article by Cifaldi Collins and
Schwarze5 describes a systematic approach to regaining
tendon function following initial immobilization of
repairs in zones 2 and 3. They provide timing guidelines
for initiating tendon gliding exercises, blocking and
other specifically targeted interventions to restore gliding
without overstressing the immobilized repair.
CONTROLLED EARLY MOBILIZATION
In earlier chapters, authors have covered the beneficial
effects of early motion on tendon healing and biome-
chanics, and the supporting research showing that early
mobilization of the repair provides at least a partial
solution to the problems of immobilization: better
adhesion control and increased repair strength.
EARLY PASSIVE MOBILIZATION
Before any significant research had been performed in
early mobilization of tendon repairs, forward-thinking
surgeons such as Kleinert6 and Duran7 had designed
postoperative management programs incorporating
controlled passive motion of the repair in the first 3 to
4 weeks. These programs involved protecting the tendon
repair by placing it on slack in a dorsal protective splint
in some degree of wrist and MCP joint flexion as
described above. For both programs, elastic traction
held the fingers in flexion. Therapy consisted of passive
flexion and either active or passive extension, to provide
passive tendon gliding of the flexor tendon with minimal
stress to the repair.
Kleinert’s technique, designed for zone 2 and which
he also advocated for zone 1, involved hourly active
extension against dynamic traction, followed by relax-
ation of the finger and passive flexion by means of the
elastic traction, premised on the theory that the flexors
would relax with resisted extension. However, later
research8,9 has shown that the desired relaxation of the
flexors does not occur consistently.
Over the years various authors have proposed modi-
fications of the Kleinert approach. To prevent or mini-
mize the risk of proximal interphalangeal (PIP) joint
flexion contractures, elastic resistance to extension
can be decreased by manually releasing rubber band
traction during active extension or by using a lighter
rubber band for exercises as in the Washington regimen
Figure 38-1  In this modification of the Kleinert program,
the patient manually releases rubber band traction during
extension to facilitate full PIP extension in an effort to avoid
development of a PIP flexion contracture.
(Figure 38-1).10 Some immobilize the interphalangeal
joints in extension at night, and others use the splint
design proposed by May and colleagues,11 with the
dorsal finger component ending at the PIP joint for
optimal PIP joint extension. At night a separate volar
piece is strapped on to the splint to keep the IP joints
in extension.11 In the same study, May and colleagues
examined the issue of using dynamic flexion for all four
fingers versus only the involved finger.11 They concluded
that incorporation of all four fingers contributed to
improved results by making passive flexion easier to
attain. Other authors10 have recommended incorporat-
ing only the involved finger in traction. Some practitio-
ners apply traction to only the involved finger(s) for
flexor digitorum profundus (FDP) repairs, in order to
facilitate inadvertent “cheating” with active motion of
the uninvolved providing limited active motion of the
involved finger(s).
To provide greater passive excursion of the FDP
through flexion of the distal interphalangeal (DIP)
joint, a palmar pulley can be added to redirect the
line of traction to the distal palmar crease (Figure
38-2).10,12,13 To mobilize the flexor pollicis longus (FPL),
the thumb MCP joint is immobilized and the IP joint
must be passively flexed, with active or passive exten-
sion (Figure 38-3).14
Duran’s approach7 involved less frequent mobiliza-
tion entirely through passive flexion and extension. His
exercises were designed to provide passive excursion of
the repair relative to surrounding tissues and differen-
tial glide between the FDP and flexor digitorum super­
ficialis (FDS) in zones 2 and 3. In 1980 Strickland and
Glogovac15 published a study showing improved results
in zone 2 repairs mobilized passively compared with
 Chapter 38:  State of the Art Flexor Tendon Rehabilitation
Figure 38-2  A palmar pulley at the distal palmar crease
redirects the line of traction to attain DIP flexion and thus
attain greater excursion of FDP tendon.
Figure 38-3  For FPL repairs, the MCP joint should be
immobilized in extension for IP joint passive flexion (whether
applied by elastic traction or manually).
immobilized repairs. For that study they used a modi-
fied version of the Duran approach, now known as
modified Duran. They eliminated the rubber band trac-
tion, splinting fingers in IP joint extension between
exercises, modified the wrist flexion angle in the splint,
and added composite passive flexion and active exten-
sion to the original exercises. Over the years the Strick-
land and Glogovac approach has been further modified
to include more frequent mobilization and other
variations.
A study by Cooney and colleagues16 found that incor-
porating synergistic wrist motion (SWM) would increase
passive flexor tendon excursion in zones 2, 3, and 5:
extending the wrist assists passive digit flexion via teno-
desis, while wrist flexion during digit extension uses
tenodesis to decrease stress on the repaired flexor(s) and
allows greater digit extension. Since then a number of
407
authors have looked at the stresses placed on the tendon
and the amount of excursion attained with SWM.9,17,18
Amadio and Tanaka19,20 have proposed a further modi-
fication on a passive SWM exercise. The wrist is in flexion
initially, with the fingers in extension, followed by
passive finger flexion, wrist extension and MCP joint
extension (holding the IP joints in flexion). The combi-
nation of wrist extension and MCP joint hyperextension
with the DIP and PIP joints fully flexed produces an
increase in flexor tendon tension. They hypothesize that
in vivo this small increase in tendon tension may
increase FDP excursion. An added benefit would be
control of any intrinsic muscle tightness developing in
response to blocking the MCP joints in flexion in the
splint.
EARLY ACTIVE MOBILIZATION
Although early passive mobilization produced improved
results,15 surgeons and therapists questioned whether
they could attain even better functional results with
techniques producing greater excursion of the repair
site. The model of passive excursion is logical and clearly
safe in theory, but in practice the repaired tendon and
adjacent tissues may be edematous, with added bulk
from sutures and related injuries. In those cases passive
flexion may simply fold the tendon or cause it to bunch
up due to the gliding resistance it encounters.
Once again, clinical development preceded support-
ing research: Surgeons and therapists began using con-
trolled active flexion to attempt to provide gentle
proximal tendon glide more effectively than was possi-
ble with passive flexion. As new suture techniques were
developed to provide improved strength and gliding
characteristics, therapists became more and more com-
fortable using active flexion for repair mobilization.
Hitchcock and colleagues21 showed that controlled
active mobilization actually increased the strength of
the repair in the first few postoperative days, in contrast
to the accepted dip in strength demonstrated in immo-
bilized repairs.
Savage22 studied the effect of wrist position on active
tension on the flexor tendon, or the force required to
flex the interphalangeal joints against the passive resis-
tance of the extensors. He found that the smallest
amount of force was required with the wrist in 45° of
extension, and the greatest amount of force was required
when the wrist was in 45° of flexion. Since then, other
authors23-28 have explored this problem in greater depth,
taking into account the total force exerted by the repaired
tendon, due to edema, joint stiffness, and the gliding
resistance at the tendon–pulley interface. In practice,
therapists must deal with the total work of flexion with
all of its components.
Savage’s work22 supported the concept of either posi-
tioning the wrist in extension during flexor mobiliza-
tion or incorporating synergistic wrist motion with
408 Section 5:  Rehabilitation of Tendon Surgery

Figure 38-4  The patient extends the wrist actively with

simultaneous passive digit flexion. (Modified from Cannon N:
Post flexor tendon repair motion protocol, Indiana Hand
Center Newsletter 1:13-18, 1993.)
finger flexion and extension. As a result, early mobiliza-
tion programs were adapted to bring the wrist into less
flexion, and in some cases, into extension. More recently
a study by Kursa and his colleagues9 provided additional
evidence, at least for FDS, for which greater forces were
recorded with finger flexion and extension when the
wrist was at 30° of flexion.
Active mobilization programs can be divided into
three basic approaches: active,29-32 assisted active,33 and
place-hold (active-hold).34-36 The first two programs are
self-explanatory. In place-hold programs the involved
fingers are placed in flexion and the patient holds the
position with a gentle muscle contraction. Assisted
active and place-hold flexion exercises are designed to
decrease the work of flexion by overcoming passive
resistance manually. All of these approaches assume
that the tendon will be protected through splint posi-
tion, and that work of flexion will be reduced through
edema control and passive exercises performed prior
to active flexion. Most published programs include a
dorsal protective splint with the MCP joints in some
degree of flexion, IP joints allowed to extend to 0° and
the wrist in slight flexion, neutral or slight extension to
decrease the work of flexion.29,32,33,35,36 One published
program, the Indianapolis program,34 adds an exercise
splint with a hinged wrist, allowing wrist extension to
30°, to incorporate SWM and thus both increase excur-
sion and decrease work of flexion (Figures 38-4 to
38-6). Although the authors do not state that the
program is for zone 2 repairs, the program is based on
the issues of excursion and work of flexion crucial to
rehabilitation of zone 2 injuries.
A recent study3 showed clearly superior results in
zone 2 flexor tendon repairs treated with active versus
passive mobilization. The authors used a hinged-wrist
splint program for active mobilization and a modified
Kleinert program for passive mobilization. The passive
mobilization program was conservative, starting active
flexion using place-hold with the wrist at neutral (within
the splint), and delaying true active flexion until 6
Figure 38-5  The patient maintains digit flexion with a
gentle active muscle contraction. (Modified from Cannon N:
Post flexor tendon repair motion protocol, Indiana Hand
Center Newsletter 1:13-18, 1993.)
Figure 38-6  The wrist is allowed to relax into flexion
with simultaneous digit extension (limited to 60° at the
metacarpophalangeal joints). (Modified from Cannon N: Post
flexor tendon repair motion protocol, Indiana Hand Center
Newsletter 1:13-18, 1993.)
weeks. Some of the interventions used by experienced
clinicians (functional activities, blocking exercises,
splinting to address joint and tendon tightness) were
introduced later than either of these authors would have
expected. An experienced clinician progresses the
program according to evaluation of tendon function:
e.g., slowing down the progression if tendon excursion
is returning rapidly and treating more aggressively in
the presence of severe adhesions. Although it may be
that the therapists overseeing the passive mobilization
program took some liberties with the stated timetable,
the article does not say so, leaving the impression that
all of the passively mobilized tendons were moved with
similar caution. If that is the case, then these patients
might have achieved better results if treated according
to current best practice in passive mobilization. This
diminishes the implications of the study, but not the
importance of its publication.
In choosing an appropriate early active mobilization
technique, there are several factors to consider: patient
 Chapter 38:  State of the Art Flexor Tendon Rehabilitation
selection, ways to control force of contraction (primarily
through wrist and digital position), timing of initiating
motion,24,25,28,37 and methods of reducing work of flexion
prior to exercise.
PATIENT SELECTION
Patient characteristics are difficult or impossible to
control, and should dictate the choice of program.
Therefore it is crucial to choose an approach that fits the
patient, rather than imposing unrealistic expectations
on a patient incapable of performing a complex
program. Recent research has found that a high percent-
age of patients are noncompliant with their home reha-
bilitation programs.38,39 In fact, in one study 67% of
patients with flexor tendon repairs removed the splint
against therapist instruction.39 The most common
reason given was hand washing: an all-too-familiar
story to an experienced hand therapist!
CONTROLLING FLEXION FORCE
There are a number of different ways to ensure that the
patient exerts the minimal flexion force needed to
achieve sufficient tendon excursion. Studies have shown
that placing the wrist in flexion increases the force
required to flex the fingers.9,22 Placing the wrist in neutral
or extension reduces the force required to flex the fingers.
Incorporating synergistic wrist extension with finger
flexion favors proximal gliding of the flexor tendons and
decreases the force required to flex the fingers. Forces
transmitted through the flexor tendons increase with
increasing active flexion of the fingers and wrist.9 To
determine the optimum splint position (or to choose
whether or not to use an SWM program), the therapist
must consider zone and type of injury. For example,
placing the wrist in slight extension benefits gliding of
the tendon repaired in zone 2 in the digits and reduces
the forces applied to the tendon during active finger
flexion. Nevertheless, some wrist flexion or a more
limited range of wrist synergistic motion should be
chosen to protect multiple nerve and tendon repairs in
zone 5, avoiding nerve compression by limiting degree
of wrist flexion, and limiting passive traction on nerve
and tendon repairs by limiting degree of synergistic
wrist extension. A lesser degree of MCP joint flexion in
the splint is appropriate in zone 2 and 3 injuries to
avoid development of intrinsic muscle tightness in con-
junction with adhesion formation.
Some authors recommend gradually increasing the
IP joint flexion demands over time. The Belfast proto-
col29,32 for zone 2 repairs sets increasing range of flexion
goals from week to week. Evans and Thompson35 used
a biomechanical model to calculate the force placed on
flexor tendon repairs at various points in the range of
flexion and concluded that a partial fist places consider-
ably less stress on the repair than does a full fist. On this
basis they proposed a program designed to elicit active
409
Figure 38-7  If the patient flexes to touch the second
finger with the first finger out of the way, the patient will
automatically tend to flex the PIP and MCP joints instead of
the DIP and PIP joints.
flexion (place-hold) with “minimal active muscle
tension” (MAMT) through partial digital flexion and
slight wrist extension.
Another convenient way to gradually increase the
amount of flexion over the first 4 weeks was proposed
by Sheila Harris (personal communication, 2010). The
patient is asked to place the four fingers of the uninjured
hand in the palm of the injured hand with the little
finger resting at the distal palmar crease and the fingers
perpendicular to the plane of the palm. In the first week
the patient flexes to touch the index finger. In the second
week the patient is asked to move away the index and
try to touch the middle finger (Figure 38-7). In the third
and fourth week the patient is asked to flex to touch the
ring and small finger respectively in the same way. A
useful modification was added by van Strien in order to
add more DIP joint flexion. By leaving the four fingers
of the uninjured hand in place and sliding the fingertip
across the dorsum of the fingers to reach the next finger
more DIP joint flexion is achieved (Figure 38-8). Not
only does this method gradually increase the force
exerted through the tendon, but with the modification
it also encourages the patient to flex both the PIP and
the DIP joints, thus theoretically achieving greater FDP
excursion and differential FDP/FDS glide.
Place-hold (active-hold) flexion may decrease the
force of muscle contraction, but only if the fingers are
partially flexed (as noted earlier), or if the wrist is syner-
gistally extended to assist passive proximal excursion. If
the fingertips are flexed to the DPC passively before con-
tracting the flexors to hold the position, there is a risk of
increasing the stress to the tendon if the passive flexion
produced only buckling or folding of the tendon (which
must now be unfolded, requiring a theoretically greater
amount of force than would be required for unassisted
410 Section 5:  Rehabilitation of Tendon Surgery
Figure 38-8  With the first finger kept in place, the patient
is encouraged to slide the fingertip down to the second
finger, thereby using DIP and PIP joint flexion rather than
just PIP and MCP joint flexion.
active flexion). We propose that assisted active flexion is
a safer way to decrease force of contraction.
Before active flexion exercises, work of flexion must
be minimized by decreasing the resistance to passive
flexion, not only through positioning to minimize resis-
tance from the extensors but also through reducing
resistance caused by edema and passively ranging the
finger joints to reduce stiffness. Cao and Tang24 found
that six cycles of digit motion in a chicken model sig-
nificantly decreased work of flexion.
INITIATING ACTIVE MOBILIZATION
Determining the best time to initiate active mobiliza-
tion is difficult, due to both conflicting evidence in the
literature24,25,27,28 and variability of patient healing char-
acteristics. It is widely accepted that active mobilization
is both safe and effective only if started within the first
postoperative week. In a recent study in a chicken
model, Tang and colleagues24 divided the early postop-
erative phase into three stages: days 0 to 3, increasing
resistance due to postoperative inflammatory edema;
days 4 to 7, further increase in resistance from edema;
and after days 7 to 9, hardening of the subcutaneous
tissue with development of adhesions. On the basis of
this and other studies,25,27,28,37 it is reasonable to assume
that in an otherwise appropriate patient, active flexion
may begin at 3 to 4 days, if edema and wound healing
appear well under control.
All of these studies further underline the importance
of controlling edema in order to decrease work of flexion
in the crucial early days. A patient with an unusually
edematous finger or other complications of healing
presents a dilemma: If motion is delayed for too long,
adhesions will have formed and subcutaneous tissue
will have hardened, but if motion begins early and
edema cannot be adequately controlled, there is a higher
risk of rupture.
FUNDAMENTAL CONCEPTS AND TECHNIQUES
OF EVALUATION AND TREATMENT
Choosing the most appropriate rehabilitation approach
requires an understanding of all the factors affecting
tendon healing and recovery of function. The mecha-
nism of injury will affect both surgical and therapy deci-
sions. A crush injury, for example, has a higher risk of
formation of restrictive adhesions, whereas a clean lac-
eration may be more easily repaired and may recover
function more easily. The effect of the level of injury is
discussed in Chapter 39.
The therapist must know what kind of repair was
performed. Despite all the recent evidence cited in pre-
vious chapters supporting the use of four-strand core
sutures and strong peripheral sutures for early active
flexion programs, many surgeons use a two-strand
Kessler and a simple running peripheral suture. In a
2006 survey of members of the Irish Hand Surgery
Society, Healy and colleagues40 found that a clear major-
ity preferred the latter to the former. In addition to the
type of repair, the therapist should be informed of any
intraoperative findings that may influence clinical deci-
sions, such as concomitant injuries, repairs performed
under tension, pulley resection, venting or repair, or
other repair characteristics that may affect gliding or
strength of the repair. Gliding resistance from surround-
ing tissues is not the only reason why active or passive
flexion may be difficult to attain. Postoperative edema
and joint stiffness in particular pose resistance to
motion, increasing the risk of rupture or repair deforma-
tion as well as decreasing repair mobility.
Amadio19 has proposed the concept of a safe zone,
which allows the therapist and surgeon to make deci-
sions about mobilizing tendons based on the various
factors increasing work of flexion (Figures 38-9 and
38-10). For example, if the repair is strong but bulky, it
will withstand the stress of active motion but will glide
poorly, and may even “catch” on surrounding tissues,
thereby exceeding its resistance to rupture. This would
lower the upper limit of the safe zone and could pre-
clude active motion. Likewise, if edema and joint stiff-
ness are not well controlled, the passive resistance to
flexion increases, and again may preclude safe active
mobilization. Recent work of Cao and colleagues and
Tang and colleagues has demonstrated increased tendon
repair strength and decreased gliding resistance with
partial excision of the A2 pulley,41,42 which suggests that
venting pulleys may further widen the “safe zone” as
described by Amadio.19
Such factors make it imperative that the therapist
gather all pertinent information through clear commu-
nication with the referring surgeon. Ideally, all hand
therapists should receive a copy of the operative report
 Chapter 38:  State of the Art Flexor Tendon Rehabilitation 411

Table 38-1  Assessment of Adhesions Based on

Strong grip
Clinical Findings (Modified Based on Groth)
Max strength in vitro
40 Adhesions* Clinical Findings†
Light grip Absent Tendons glide well; <5° discrepancy
Max strength in vivo between total active and passive
30
digital flexion.
Force (N)

Responsive ≥10% decrease in active motion lag

2 mm gap
20 is observed between one session and
Light active the next‡
Initial gap Unresponsive <10% decrease in active motion lag
10
Synergistic is observed between one session and
Safe zone
5
In vivo friction the next‡
Repair friction
Normal friction Passive motion *When adhesions are considered absent or responsive, the therapy
0.2 program does not need upgrading. When adhesions are
unresponsive, the therapist should consider upgrading the
Figure 38-9  Small safe zone for a four-strand repair with program.
40 N breaking strength. (Modified from Amadio PC: Friction †
Clinical findings were reworded from the Groth’s description for
of the gliding surface. Implications for tendon surgery and clarity based on the clinical judgment of the present authors.
rehabilitation, J Hand Ther 18:112-129, 2005.) ‡
Because frequency of therapy appointments varies according to
many factors, therapists should apply the definition of “responsive”
or “unresponsive” with due consideration to the number of days
between sessions.
Max strength
in vitro
40

Max strength response to intervention as absent, responsive, and unre-

at 1 week in vivo sponsive and suggested clinical observations that may
30
help assess adhesion severity. This classification is
Force (N)

further clarified and presented in Table 38-1. Groth’s

2 mm gap
20 Improve strength:
Faster healing
Stronger repairs
Initial gap
10
Reduce friction:
In vivo repair
5 Lubricants
In vitro repair Smoother repairs
Normal friction
0.2
Figure 38-10  Larger safe zone with increased suture repair
strength and faster healing, and reduced friction through the
use of lubricants and repairs with smooth gliding surfaces.
(Modified from Amadio PC: Friction of the gliding surface.
Implications for tendon surgery and rehabilitation, J Hand
Ther 18:112-129, 2005.)
as well as discussing with the surgeon any unusual
aspects of history, injury, and repair.
Observation and palpation are key skills for identify-
ing edema, joint stiffness, and wound complications
that could influence treatment planning. Edema and
range of motion should be measured objectively as dic-
tated by the characteristics of the injury and repair, and
the therapist must repeat measurement periodically to
assess the effectiveness of treatment and to determine
how best to advance or modify the program. Groth43
proposed a classification of adhesion severity and
system helps the therapist decide how to advance up the
proposed pyramid of force progression (graded passive
and active mobilization) safely and effectively (Figure
38-11).43 As published the pyramid does not address the
progression of synergistic wrist motion programs; at the
Annual Meeting of the American Society of Hand Thera-
pists in Boston in 2008, von der Heyde proposed a
modification of the pyramid that incorporates wrist
motion during the early weeks of therapy and proposes
progression to straight fist (DIP joints in extension as
MCP joints and PIP joints flex) and hook fist (MCP
joints in extension, IP joints flexed) before full fist to
decrease work of flexion in the early postoperative
period.
Coert and colleagues44 used positron emission tomog-
raphy (PET) imaging to determine cortical activity fol-
lowing 6 weeks of passive mobilization of a repaired
flexor tendon. In these patients changes in cortical func-
tion were evident, showing inefficient motor control
apparently due to deprivation of sensorimotor input.
Once active flexion was initiated, cortical function grad-
ually returned to normal, reflecting more efficient motor
control. The authors suggest that this inefficiency might
be avoided with active mobilization or use of other
techniques such as mirror therapy (with active flexion
of the contralateral hand) combined with passive mobi-
lization during the first 6 postoperative weeks.
412 Section 5:  Rehabilitation of Tendon Surgery

Resistive
isolated W
ris
joint motion tu
np
ro
Resistive hook and te
cte
straight fist d

Resistive composite fist

W
ris
Discontinuation of protective splint tp
ro
te
cte
d
Isolated joint motion

Hook and straight fist

Active composite fist

Place and hold

Passive protected extension

Pyramid of progressive force application

Figure 38-11  Progressive application of force to the repaired intrasynovial flexor tendon. (Modified from Groth G: Pyramid of
progressive force exercises to the injured flexor tendon, J Hand Ther 17:31-42, 2004.)

Many patients have a tendency to co-contract intrin-
sic or extrinsic extensor muscles in their first attempts at
active flexion. This can be very frustrating for the patient
and increases the difficulty of attaining flexor tendon
excursion. One way to overcome the problem is to
incorporate purposeful, goal-oriented activities, which
elicit more fluid and less effortful motion than do exer-
cises.45,46 For example, when asked to bend the tip of the
thumb following FPL repair, a patient may tend to
co-contract or use excessive force. When asked to encir-
cle a dowel with thumb and index finger, the same
patient, focusing on the task rather than the motion,
may easily and fluidly incorporate all involved muscles
in a functional tip pinch position including thumb IP
joint flexion. Once this position has been attained, the
patient can be asked to gently scratch the tip of the index
with the thumb fingernail, thus eliciting greater IP joint
flexion. Some patients benefit from performing the
same task first with the uninvolved hand or perhaps
simultaneously with both hands.
QUESTIONS AND ISSUES
There are many exercises, activities, splints, and adjunc-
tive modalities commonly used and anecdotally suc-
cessful. However, there is a dearth of evidence supporting
most of these techniques. For example, many therapists
routinely use ultrasound to aid recovery of tendon glide,
but this is supported only by extrapolation of theory
and basic science regarding the thermal and nonthermal
effects of ultrasound.
For that matter, there is insufficient evidence support-
ing use of any one tendon rehabilitation protocol over
others.2 With the exception of the Evans protocol for
zone 1 repairs, the published protocols either are
intended for zone 2 repairs or do not specify the zone.
The therapist must choose and adapt as needed the
program most appropriate to the patient. This may be
dependent on many variables, not the least of which is
cultural variation and differences in health care system
from one country to another. For example, some pub-
lished active mobilization protocols require closer mon-
itoring than others (some including postoperative
hospitalization), and may be feasible only within a
health care system that pays for frequent therapy or
postoperative hospitalization. Those protocols should
be adapted if used with a different patient population
or within a different health care system.
In comparing publications on surgical techniques
and rehabilitation programs, the reader must be alert to
the different systems that can be used to assess clinical
outcomes of flexor tendon repair. The most commonly
accepted and most logical is the modified Strickland
formula, in which the total active motion (TAM) of the
involved digit (excluding MCP joint motion, which may
be within normal limits even with severely adherent
repairs) is expressed as a percentage of normal. To
 Chapter 38:  State of the Art Flexor Tendon Rehabilitation
specifically evaluate FDP tendon function, DIP joint
flexion must be given greater weight, as suggested by
Moieman.47 None of the existing clinical outcomes
methods takes into account the position of the wrist
during measurement of finger flexion. Outcomes assess-
ments based on range of motion alone do not take into
account all of the factors (such as coordination, quad-
riga effect, individual digit differences, and patient per-
ception of function) that determine success. Existing
functional outcomes instruments such as the Disability
of the Arm, Shoulder, and Hand (DASH) questionnaire
are not specific enough to be of much value in evalua-
tion of flexor tendon repairs.
SUMMARY
Several distinct trends are apparent in current postop-
erative management of the repaired flexor tendon.
Dynamic traction into flexion (Kleinert technique) is
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 CHAPTER
39  
CUSTOMIZING FLEXOR
REHABILITATION BASED ON
ZONE OR TYPE OF INJURY
Fiona H. Peck, MCSP
OUTLINE
This chapter details the information that must be
assimilated before selecting an appropriate rehabilita-
tion regimen for flexor tendon repairs at all areas. The
postoperative management of these injuries depends
primarily on the extent of the injury, concomitant
damage to surrounding tissues, surgical methods, and
other factors. The type of tendon injury, timing and
strength of the repair, and the age and characteristics
of the patient all affect the details of the regimen.
Within each zone of injury, a number of anatomical
and biomechanical factors need to be considered in
the decision making process. In the absence of a defin-
itive evidence-based method of rehabilitation after
flexor tendon repairs, the surgeon and the therapist
together must customize the rehabilitation regimen
according to varying patient and surgical factors in
order to achieve favorable outcomes. The chapter also
describes the different types of regimen available,
detailing timing of motion, splintage, and the treat-
ment of associated complications.
In recent years a significant amount of research in the
field of flexor tendon treatment has contributed to
advances in both surgical and rehabilitation tech-
niques.1,2 There is an overwhelming amount of evidence
to show that carefully devised rehabilitation programs
are critical to achieving favorable outcomes following
primary flexor tendon repair in the digits, but very little
attention has been given to other zones of injury in the
hand and forearm. Whatever the level of injury, the
ultimate goal of both the surgeon and the therapist is
to minimize or modify peritendinous adhesions and
promote optimal tendon glide. At the same time the
tendon repair must be protected from excessive stress to
avoid gapping or rupture at the repair site.
Although early mobilization of primary flexor tendon
repairs is now accepted practice, there is no one defini-
tive rehabilitation regimen guaranteed to restore a full
range of active digital motion. Therapists dealing with
these injuries require not only specialized knowledge in
the field but also the ability to use advanced clinical
reasoning skills to select appropriate postoperative exer-
cise programmes.3 Early active motion in different forms,
used in conjunction with multistrand repair techniques,
has gained increasing popularity but application must
depend on consideration of a number of variables.1-3
The aim of this chapter is to examine the implications
of these variables on regimen selection and assist the
therapist with the provision of evidence-based practice
following primary flexor tendon repair at all levels.
CUSTOMIZING A REGIMEN
Specialized hand therapy clinics with easy access to
expert medical and nursing staff provide the best envi-
ronment for the treatment of these injuries. Therapists
with the responsibility for the selection of rehabilitation
programs must be well informed with regard to a variety
of different factors. There should be a good working
relationship and excellent communication between the
surgeon and the therapist. Access to accurate medical
records is also vital to the process and clear recording
of operative details will provide the therapist with the
relevant information.
EXTENT OF INJURY
Mechanism of Injury
The mechanism of injury can impact on the outcome of
tendon repairs. Clean cut injuries with the finger in
extension require less extensive surgical exposure and
the tendon can be easily retrieved and repaired with
minimal interference with the surrounding tissues or
loss of tendon length. In uncomplicated tendon injuries
and in the presence of a strong multistrand repair, the
therapist can be more confident in selecting an active
protocol. Ragged saw or crushing injuries involving
bone, joint, and neurovascular structures can be very
different and result in significant postrepair edema and
adhesion formation.
415
416 Section 5:  Rehabilitation of Tendon Surgery

Number and Type of Structures Damaged

Although single-digit injuries are common, the therapist
is often presented with more complex injuries. In the
presence of multidigit injuries, each digit may require
an individual exercise scheme according to the nature
of the injury. Controlled active motion regimens will be
unsuitable for severely injured digits and will therefore
restrict the use of this form of rehabilitation in adjacent
digits that are damaged to a lesser degree. After replanta-
tion surgery, there is a requirement to balance the needs
of both the flexor and extensor tendons. It is necessary
to adopt a regimen which safeguards the most vulner-
able structures.

Injuries to the Skin

The nature of the skin wounds affects the decision
making during rehabilitation. Untidy wounds, includ-
ing a crushing element, will impact the final outcome
and the therapist must prioritize the prevention of joint
and scar contracture. The therapist should differentiate
between incisions made during the surgery and those
that are part of the original injury. Carefully designed
surgical incisions made to access the tendon for explora-
tion and repair of the tendon and other structures will
minimize postoperative contracture. Random longitudi-
nal wounds which cross the metacarpophalangeal
(MCP) and the interphalangeal (IP) joints may cause
joint contracture.4 When the surgical incision is made
across these joints, active digital extension exercises and
prophylactic splinting should be incorporated into the
regimen to prevent loss of full joint extension.2-4
In more severe soft tissue injuries, the presence of
skin grafts or flaps necessary for wound closure delays
the start of postoperative mobilization until vascularity
is ensured. In digital-level injuries, care must be taken
not to impede joint motion or increase resistance to
tendon glide by the use of restrictive dressing. Dressings
should be shaped to reduce the resistance over the IP
joints and should cover the wound area only, avoiding
the use of circumferential adhesive tape (Figure 39-1).
Postoperative complications such as infection, heavily
exuding wounds or skin loss may require more substan-
tive dressings, which will result in delays in initiating
active motion. In cases where there is infection involv-
ing the tendon sheath, all motion should be delayed
until the infection is treated. Where the status of the
wound has the potential to impede active motion, for
example, in large open wounds with extensive edema,
mobilization must be confined to gentle passive exer-
cises to preserve tendon glide and minimize stress on
the repair until the restrictive swelling has reduced. In
the presence of heavily exuding wounds, dressings
should be removed on attendance for hand therapy, and
provided there is minimal edema, a controlled active
motion regimen may be initiated even in the presence
of skin loss.
Figure 39-1  Wound dressings must be kept to a minimum
and should not impede active motion following digital flexor
tendon repairs.
Injuries to Bone and Joint
Concomitant injuries to bone impact postoperative
management as the timing and type of exercises chosen
can be limited by the presence and characteristics of the
bony injury and the stability of fracture fixation. Primary
tendon repair is contraindicated in the presence of
complex unstable or intra-articular fractures.2 In the case
of stable, undisplaced fractures in the hand or digits, it
is possible to initiate an early motion regimen, provid-
ing supplementary splinting support for the fracture
while at rest and additional manual support when per-
forming exercises. Rigid fixation of fractures of the pha-
langes or metacarpals usually provides sufficient stability
to permit the early passive and active motion following
discussion with the surgeon regarding safety. Injuries to
more than one digit presenting with different patterns
of injury in each require individual exercise plans for
each digit. Care must be taken, however, initiating an
active motion protocol in complex injuries to the
middle, ring, and little fingers due to the quadriga effect
of the conjoined flexor digitorum profundus (FDP)
tendons. The most severely injured digit will dictate the
mobilization program and the therapist must devise
an exercise regimen that most effectively preserves the
tendon glide for each digit without placing excessive
stress on the repairs. This will be a combination of
 Chapter 39:  Customizing Flexor Rehabilitation Based on Zone or Type of Injury 417

passive only exercises for the more seriously injured

digits and careful active for those able to withstand
greater stress. In the presence of joint stiffness, restora-
tion of passive motion of the joint is imperative. Deep
lacerations to the digits may damage the palmar plate
or capsule of the IP joints, resulting in flexion contrac-
ture of the joints. Prophylactic extension splinting is
indicated to prevent the contracture from the early
stages of rehabilitation.

Injuries to Nerve
When nerves are repaired under tension, full range of
digital extension should be restricted in the early stages.
Major nerve injury at the wrist level is common, and
affects the details of the rehabilitation regimen. Con-
comitant median and ulnar nerve injuries at the wrist
or forearm levels, whether complete or partial, result in
some degree of intrinsic muscle paralysis and conse-
quent impairment of active digital motion. Under this
circumstance, special attention must be given to joint
positioning within the protective splint to optimize
tendon motion. Increased tendon excursion is facili-
tated if the MCP joints are positioned in 60° to 70° Figure 39-2  Following a strong multistrand repair of the
flexion with the wrist in neutral. Loss of sensation and flexor pollicis longus tendon active motion should be
cortical representation impacts the quality of motion isolated to the IP joint to preserve tendon glide.
during the early rehabilitation phase and delays func-
tional recovery.

Vascularity of Injured Structures Flexor Pollicis Longus (FPL) Injury

Injuries requiring revascularization (e.g., digital replan-
tation) require careful management. Early mobilization
regimens should not be initiated until the viability of
the digit is established. Whether damage to the vincula
affects adhesion formation remains uncertain.5
Triggering of the Repaired Tendon
Against the Pulley
Bulky tendon repairs may trigger and are prone to dis-
ruption when gliding through annular pulleys.5,6
TYPE OF TENDON INJURY
Complete or Partial Injuries
Complete divisions of tendon require protected mobili-
zation and a customized program of exercises with no
functional activity of the hand for at least 6 weeks. Less
severe forms of the partial tendon injury (cut through
less than 40% of the cross section) can be managed
conservatively without surgery. The patients should be
permitted to move their injured fingers without restric-
tions.7 Surgically repaired partial lacerations of the
tendon (cut through greater than 40% of the cross
section) are usually capable of withstanding the stresses
of an active motion protocol and are less likely to rupture.
The hand requires some form of dorsal splint protection
but this may be removed as early as 3 to 4 weeks.
The postoperative care of the repaired FPL tendon
requires special consideration. The FPL tendon appears
to have a greater tendency to rupture when active motion
regimens are applied following a two-strand core suture
with simple peripheral stitches.8,9 Recent studies support
the use of active motion programs following a multi-
strand core, even without an epitendinous suture.10,11 If
there is any doubt as to the ability of the repair to with-
stand active motion the therapist should use passive
motion techniques. When using a controlled active
motion regimen, care must be taken to ensure that
movement is isolated to the IP joint (Figure 39-2). A
neutral position at the wrist benefits both flexion and
extension at the IP joint. Positioning the wrist in exten-
sion can impede active extension at the IP joint and
place stress on the repair site.
OTHER FACTORS
Length of Time From Injury to Repair
The therapist should have knowledge of the impact that
delayed repair may have on expectations and outcomes.
Delaying the surgery for 7 to 10 days or more may result
in formation of adhesions and collapse of the sheath
and pulleys and the tendon becomes difficult to retrieve
because of muscle–tendon unit shortening. In these
cases, the repair may require increased postoperative
418 Section 5:  Rehabilitation of Tendon Surgery
protection in a flexed position with serial extension as
appropriate. In the author’s own experience long delays
in repairing flexor tendons in zone 2 have been shown
to impact significantly on outcome leading to less favor-
able results than those that are repaired within the first
48 hours.
The Type and Quality of the Repair
There has been a significant amount of research
devoted to improving the tensile strength of flexor
tendon repairs, permitting greater confidence in the
use of active mobilization regimens and resulting in
reduced rates of dehiscence.12-14 Although some have
demonstrated the successful application of active mobi-
lization regimen with two-strand repairs of varying tech-
niques, others have reported unacceptably high rates of
rupture.15-17
Before selecting an appropriate postoperative regimen
the therapist should be acquainted with the caliber and
type of both core and circumferential suture in each
particular case. Four- or six-strand core suture repairs
with 4-0 or 3-0 suture produce a repair strong enough
to accommodate early active motion of the repaired
digital flexor tendon. If the tensile strength of the repair
is judged not to withstand the forces generated during
active digital motion, alternative and safer methods of
maintaining tendon glide should be considered.18,19
Venting the constrictive part of a major pulley (such as
the A2) will decrease the resistance to the tendon.
Repairing the tendon just distal to the A2 pulley, without
venting the constrictive part of the pulley, may subject
the tendon to greater resistance during early active
tendon movement. Particular care should be taken
when instructing the patient to move the tendons that
are repaired just distal to the A2 pulley, as greater inci-
dence of rupture of the primary repair is experienced in
this area.
Patient Characteristics and Compliance
The ability to comply with a rehabilitation regimen,
which involves commitment to a strict exercise program
within a protective splint for several weeks, vary among
individuals. Age, medical and mental health, and socio-
economic factors influence the choice of postoperative
management. Repairs are at risk of rupture if the patient
removes the splint for function and of poor gliding
action if they do not perform the required exercises.
Enhancing compliance requires a confident, knowledge-
able, and enthusiastic therapist who develops a good
working relationship with the patient. Good communi-
cation, the provision of high quality information, and
the enlistment of family support are also necessary. A
regimen that is versatile and tailored to suit the lifestyle,
socioeconomic circumstances, and work commitments
of the patient also promotes cooperation. Negative
factors that are most likely to impact on compliance and
lead to poor outcomes are long travel distances to
therapy and long waiting times. Postoperative pain,
especially that which is neurogenic in origin, should be
effectively controlled as this will significantly affect
compliance and behavior.20,21 Despite the best efforts,
the therapist is often presented with patients who do
not or are unable to adhere strictly to the requirements
of the rehabilitation regimen for a variety of reasons. In
these situations a compromise must be reached to
prevent repair rupture while permitting the patient to
continue with certain aspects of their daily life.
Age
Both the very young and some elderly patients are not
able to comply with treatment. A complex active motion
regimen is not suitable for elderly patients with dimin-
ished cognitive function or physical impairment. In
these cases immobilization is the option of postopera-
tive care.
The choice of immediate aftercare following tendon
repairs in children depends solely on the maturity of the
child. The principles of postoperative management are
similar to those applied to adults but the ability to
comply with splinting and exercises must be carefully
considered. Older children and teenagers will be able to
follow a specific regimen, but younger children may
inadvertently use the hand in functional activity and a
splint guard is thus required to deter use of the injured
hand (Figure 39-3). Although younger children may
cooperate with a thermoplastic splint and a guard, they
will require assistance with mobilizing exercises and the
responsibility for this then falls to the carer. The selec-
tion of the type of exercises then depends on the capa-
bility of the carer and their ability to comply. Babies
and toddlers are at risk of dehiscence through falls and
Figure 39-3  The addition of a guard to the protective
splint permits unimpeded active flexion and extension and
deters functional use of the hand in a child following
reinsertion of the FDP tendon of the little finger.
 Chapter 39:  Customizing Flexor Rehabilitation Based on Zone or Type of Injury
Figure 39-4  An occlusive boxing glove–type dressing will
protect tendon repairs in very young children and babies.
functional activity and cannot follow mobilization regi-
mens. For this reason the hand should be immobilized
in a substantial, occlusive dressing for a period of 4
weeks. An effective way to protect the tendon repairs is
the application of an above elbow plaster of Paris or
resin cast. Nevertheless, both are prone to slippage and
may require removal under anesthesia in some children.
In our experience, a well-padded, occlusive, boxing
glove–type dressing using generous amounts of adhe-
sive tape to prevent removal is equally effective (Figure
39-4). This type of dressing can be easily reapplied in
an outpatient setting during the 4-week period of immo-
bilization, permitting inspection of the wound and
integrity of the repair along with passive exercises. The
paucity of literature on the subject leaves the therapist
with little guidance in this field. Much depends on the
ability of the child to cooperate with a regimen likely
to provide the most optimal outcome. Immobilization
for 4 weeks in the very young child has no detrimental
effects on the result.22
ZONE OF INJURY
Postoperative management should vary according to the
zone of injury. Therapists must possess an intimate
knowledge of the relevant anatomy and biomechanics
of each particular zone to customize the regimen accord-
ingly. Particular attention has been given in the litera-
ture to both surgery and rehabilitation in tendon repairs
419
Box 39-1 Zone 1 FDP Tendon Lacerations
Close to the Insertion (Zone 1A)*
 Requires reinsertion to the distal phalanx
 Risk of muscle-tendon unit shortening
 Risk of DIP joint flexion deformity
 Prioritize passive digital flexion
 Initiate careful active flexion from the DIP joint
 Kleinert regimen not appropriate
 In presence of delicate repair, Evans protocol affords
greater safety28
Distal to the A4 Pulley (Zone 1B)*
 Risk of snagging on the A4 pulley
 May include injury to the palmar plate
 Increased risk DIP joint fixed flexion deformity
 Emphasize active digital extension exercises
 Apply prophylactic digital extension splints
 Initiate careful active motion at the DIP joint to
ensure tendon glide through the pulley
Under the A4 Pulley (Zone 1C)*
 Difficult to repair
 Increased risk of tendon adherence
 Prioritize passive digital flexion
 Encourage careful active motion at the DIP joint to
ensure glide through the pulley
 Careful blocking of the PIP joint by the therapist will
facilitate this if necessary
 No blocking of the PIP joint by the patient to facili-
tate motion until after 6 weeks
*Subdivision of Moiemen and Elliot.
of zones 1 and 2, but there is very little to inform
evidence-based practice with regard of zones 3 to 5. The
therapist has to rely on a combination of the available
evidence for digital injuries, clinical reasoning skills,
and experience in dealing with zone 3 to 5 injuries.
Zone 1
The postoperative regimen is dictated by the type and
anatomical location of the surgical repair. Within zone
1, the FDP tendon lacerations are subdivided into three
areas (Box 39-1)23:
1. Under A4 pulley—there is an increased likelihood
of the formation of peritendinous adhesions if the
repaired tendon does not move smoothly through
the A4 pulley. Each 10° of the distal interphalan-
geal (DIP) joint motion produces 1 to 2 mm of
tendon glide up to a total of 7 mm in the unin-
jured finger.24 Following repair, edema and friction
to glide will reduce this excursion significantly and
therefore exercises should focus on achieving
active DIP joint motion where possible.25 Optimal
passive movement of the digit must be achieved
before careful active flexion is initiated at the DIP
joint (Figure 39-5).
420 Section 5:  Rehabilitation of Tendon Surgery
Active DIP joint flexion
Figure 39-5  Following repairs in zone 1 and zone 2 careful
active digital motion should be initiated from the DIP joint
to minimize stress on the repair site and promote differential
glide.
2. Distal to A4 pulley—Lacerations at the level of the
DIP joint may include concomitant damage to the
palmar plate resulting in increased potential for
flexion contracture. Particular attention should be
given to active extension exercises and prophylac-
tic extension splinting. At this level there is a risk
that the tendon may snag on the distal edge of the
A4 pulley, placing excessive stress on the repair site
and resulting in loss of DIP joint flexion. Close
attention to the intraoperative details are required
in defining rehabilitation parameters to minimize
the risk of rupture while maximizing tendon
motion.
3. At the FDP tendon insertion—Tendon divisions at
close proximity to the FDP tendon insertion
require reinsertion of the tendon to the distal
phalanx. The consequences of surgery at this level
are some degree of tendon shortening and
increased risk of DIP joint flexion deformity. Par-
ticular attention should be paid to motion of the
DIP joint with emphasis on maintaining passive
flexion. Active flexion of the DIP joint is applied
only following a strong repair which has no
reported impediment to gliding. The Kleinert-
type regimen, even with modification, is unsuit-
able because this regimen can not sufficiently
move the DIP joint.26 In the presence of a repair
which requires greater protection, the Evans pro-
tocol, using a dorsal block splint to restrict exten-
sion and limiting the arc of active motion to
between 45° and 75°, affords greater safety and
permits tendon glide of up to 3 mm in the early
phase.27
In closed avulsion injuries at the insertion of the FDP
tendon, selection of an appropriate rehabilitation
regimen is decided by the type of the injury,30 as detailed
in Box 39-2. In all types of avulsion injury controlled
active motion is usually desirable.
Box 39-2 Closed FDP Avulsion Injuries
Type 1—Tendon Retracted into Palm
 Muscle tendon unit may be shortened especially
after delay in treatment
 Loss of blood supply to the tendon
 Neutral position of wrist in protective splint
 Commence early action digital flexion initiated from
the DIP joint
 Prioritize active digital extension exercises
 Prioritize prevention of fixed flexion deformity at IP
joints
 Commence early passive finger extension stretching
without tension on the repair
 Remove protective splint and stretch IP joints into
extension with wrist and MCP joints in maximum
flexion
 Use digital extension splinting at night and between
exercise periods
Types II and III—Tendon Retracted to the PIP Joint
Level, With Small Bony Fragment (Type II) or
Remaining Distal to the A4 Pulley With Large Bony
Fragment (Type III)
 Less shortening of the muscle–tendon unit
 Delayed reinsertion has potential for favorable
outcome
 Tendon retains good blood supply
 Wrist position in protective splint 10° to 30°
extension
 Commence early action digital flexion initiated from
the DIP joint
 Prioritize active digital extension exercises
 Use prophylactic digital extension splinting at night
to prevent fixed flexion deformity
Rehabilitation Regimen for All 3 Types of Closed
FDP Tendon Avulsion Injuries
 Protective dorsal splint for 6 weeks
 Wrist position dependant on type of injuries
 MCP joints 30° flexion
 Restore optimal passive digital flexion
 Initiate early controlled active motion regimen
emphasizing DIP joint motion
 Hourly exercises; 10 repetitions of digital flexion
 Encourage active digital extension exercises
 Apply prophylactic digital extension splints
 Watch for complications arising from button reinser-
tion technique—Infection, edema catching/breaking
of exposed suture, and pain if this technique is used
 Excessive pain will impede compliance and motion
 Commence composite extension stretching at 6
weeks to treat muscle–tendon unit shortening
 Consider serial plaster of Paris casts at 6 weeks to
treat residual IP joint flexion deformities (see Figure
39-6)
 Return to light function at 6 weeks and contact
sports at 12 weeks
 Chapter 39:  Customizing Flexor Rehabilitation Based on Zone or Type of Injury
Figure 39-6  Serial plaster of Paris casts may be applied to
treat persistent fixed flexion deformities of the IP joints in
the later stages of rehabilitation.
In type I injuries, a careful passive stretching element
should be incorporated into the regimen taking care not
to place any stress on the repair. To facilitate this, the
hand should be removed from the protective splint and
all tension removed from the flexor tendon by position-
ing the wrist and MCP joints in maximum flexion while
carefully passively extending each IP joint individually.
Provision of a palmar splint should be considered for
use at night and between exercise periods and this may
be serially extended as rehabilitation progresses. At the
end of the protective phase residual flexion deformities
or shortening may be addressed by progressive stretch-
ing of the joints and composite stretching of the muscle
tendon unit with all joints in full extension. Despite
concerted effort flexion deformities may be a persistent
problem and serial plaster casting should be considered
as an early option (Figure 39-6).29
Type II and III injuries are less problematic as there
is little or no retraction and shortening of the muscle–
tendon unit. The surgical exposure required for reinser-
tion necessitates a lesser incision and the tendon
maintains good condition via an intact blood supply.
Delayed reinsertion often produces favorable outcomes;
however, there is still a tendency to develop flexion
deformity especially at the DIP joint and the therapist
must work within the rehabilitation regimen to prevent
or correct this. The technique of insertion should not
affect the choice of regimen but the therapist should be
aware of potential complications in the case of stitching
421
the tendon suture through the nail and tying over a
button. Infection, edema, catching, and breaking of the
exposed suture and pain impeding motion are some
common problems. The source of pain should be inves-
tigated as persistent discomfort will deter compliance
with exercise regimen. The therapist should also be
careful to instruct the patient that the suture should
remain in situ for 6 weeks as early inadvertent removal
may result in separation of the reinserted tendon espe-
cially in the presence of an early motion regimen.
Zone 2
Rupture of the repairs, cross adherence, triggering, or
snagging of the repair on the A2 pulley and finger joint
contracture are common complications in this area. The
essential aim of rehabilitation is to restore sufficient
tendon gliding but avoid rupture of the repair during
tendon motion. Another objective is the preservation of
differential glide of the FDS and FDP tendons if both
tendons are repaired. The exercise program should be
designed to promote differential tendon movement
(Box 39-3). Once passive flexion is regained, active
digital flexion exercises will promote optimal glide and
prevent cross adherence (Figure 39-7).
If the surgical repair is judged strong enough, an
active motion program can be applied. The therapist
should have a clear knowledge of the resistance the
repaired tendon may encounter during early active
finger motion. The presence of digital edema and posi-
tion of the MCP joint are important considerations. In
an edematous finger, where there is resistance to active
motion and tendon glide, placing the MCP joints in
excessive flexion within the dorsal splint will bias active
motion to the PIP joints and can impede the initiation
of flexion from the DIP joint. Confining motion to the
PIP joint only will encourage cross adherence, prevent-
ing differential glide. Therefore the patient should be
encouraged to attempt active DIP joint flexion at the
start of active finger flexion as in the early stages post
repair they may be unable to perform this action in the
inner range of motion30,31 Tang has demonstrated that
the strength of the repair decreases as the angle of
tension increases and patients should therefore be dis-
couraged from both performing composite flexion and
using maximal effort to flex the DIP joints at the end of
the range of flexion in the early postoperative stages.32
If optimal DIP joint range of motion is to be encour-
aged, active digital flexion should be initiated at this
joint. This can be facilitated in most patients by posi-
tioning the wrist joint in 10° to 30°extension and the
MCP joints in 30° of flexion.1,35
Flexion contractures of the IP joints are a common
complication and can occur even after simple clean
tendon injuries. Use of rubber band traction regimens
has been criticized for encouraging the development of
flexion contracture of the repaired fingers; thus, this
422 Section 5:  Rehabilitation of Tendon Surgery

Box 39-3 Author’s Rehabilitation Regimens for Flexor Tendon Injuries Zones 2 to 5

Rehabilitation Regimens: Common to All Zones 2 to 5

 Protective dorsal splint for 6 weeks: joint positions may be changed within this period
 Prioritize restoration of passive digital flexion in all patients
 Initiate early controlled active motion regimen in cooperative patients if surgical repairs are robust and tendon gliding
resistance is judged not particularly high
 Promote differential glide if multiple tendons are repaired
 Encourage active digital extension exercises—vital to prevent extension deficits of joints
 Apply digital extension splints if there is early loss of active extension or significant joint injury
 Incorporate early active wrist motion as appropriate
 At 6 weeks commence stretching of residual flexion deformity in conjunction with serial splinting/casting
 Commence light functional activity at 6 weeks
 Return to normal activities at 10 to 12 weeks

Special Considerations
Zone 2
 Set wrist position at 10° to 30° extension and MCP joint at 30° flexion
 Commence early active motion regimen at 4 to 5 days if appropriate
 Restore optimal passive digital flexion prior to active motion. Passive digital flexion stretches repeated until free motion
achieved especially in an edematous finger
 Encourage hourly exercises—10 repetitions of active digital flexion. No forced active flexion. Slowly increase range of
flexion over the first 3 weeks
 Prevent cross adherence of FDP to FDS by encouraging exercises, which promote differential glide (see Figure 39-7)
 Do not initiate place and hold maneuver until full active tendon glide is ensured
 Permit early active wrist motion in trust worthy patients
 Ruptures of the repairs are most frequent when the repair sites are distal or under the A2 pulley (zones 2B and 2C).*
Majority of ruptures are in the first 1 or 2 weeks post surgery. Therapist and patient must take care to avoid repair
rupture during motion
Zone 3
 Wrist position 10° to 30° extension
 MCP joints position 30° flexion in absence of nerve injury and intrinsic damage
 MCP joints position 60° to 70° flexion with intrinsic muscle injury or denervation
 Beware risk of fixed flexion deformity at MCP joints due to palmar scar

Zones 4 and 5
 With major nerve injury: wrist position neutral for 2 weeks
 Position MCP joints at 60° to 70° flexion to prevent claw finger deformity and maximize tendon excursion
 Delay wrist motion for 2 weeks
 At 6 weeks begin composite extension by stretching and serial splinting
 Beware risk of and prevent development of intrinsic muscle tightness. Avoid prolonged splinting; use prophylactic
passive stretching techniques. Incorporate early sensory re-education to preserve cortical representation
*Subdivision by Tang.

method of rehabilitation has become less popular and Zone 3

some surgeons advocate that they should be abandoned
altogether.33 Effective means of maintaining digital
extension should be incorporated from the early stages.
There are various reported methods from thermoplastic
palmar splints to strapping the digits into extension at
night and between exercise periods.34-36 Flexion contrac-
ture at the IP joints prolongs the rehabilitation, and
more importantly, these contractures tend to be persis-
tent, and are a major cause of poor outcomes in zone 2
tendon repair. They should be treated after 6 weeks by
stretching and palmar based extension splinting at night
(Figure 39-8).
There is little published information relating to zone 3
rehabilitation and therapists have been obliged to adapt
those rehabilitation regimens designed for zone 2 inju-
ries. Anatomical differences and injury characteristics,
however, necessitate modification to splinting and exer-
cise protocols. Lacerations in the mid-palm may include
damage or denervation of the lumbrical and interosse-
ous muscles with resultant loss of function and scarring.
Tendons are likely to adhere to surrounding structures
and the patient may experience difficulty in fully extend-
ing the IP joints and may even develop flexion deformi-
ties. Manual positioning of the MCP joints in greater
 Chapter 39:  Customizing Flexor Rehabilitation Based on Zone or Type of Injury 423

A B C D
Figure 39-7  To promote differential glide and prevent the development of fixed flexion deformity the components of an
active motion regimen should include four separate exercises. A, First, gentle active motion initiated at the DIP joint in a hook
type action. B, Second, active flexion at the PIP joints with the FDP tendons at rest. C, Third, once edema has subsided careful
composite flexion. D, In each exercise period, full active IP joint extension should be encouraged within the confines of the
splint.

Palmar extension splinting Palmar extension splinting
Zone 2 Zone 3
Tendon repair Tendon repair
Figure 39-8  Residual fixed flexion deformities and loss of
composite extension should be treated with palmar based
serial extension splinting 6 weeks following repairs.
flexion may be necessary during exercise periods to
facilitate IP joint extension and prevent the develop-
ment of joint contractures. Edema of the digits is rarely
a problem and free passive and active motion of both
the DIP and PIP joints should be encouraged. The wrist
should be positioned in 10° to 30° extension. If there
have been significant intrinsic muscle injuries, the MCP
joints should be positioned in 60° to 70° of flexion.
Care must be taken to ensure that an optimal range of
digital flexion can be achieved with the MCP joints in
this position to preserve tendon glide. Careful active
wrist motion with the digits in a relaxed semi flexed
position is permitted out of the splint in trustworthy
patients. Frequent monitoring of patients is required if
there has been intrinsic muscle damage or denervation.
This potent combination of flexor tendon and intrinsic
muscle injury can lead to claw deformity, which can
rapidly become fixed.
Flexion deformities of the MCP joints may also arise
as a result of palmar scar contracture but these are
usually easy to treat with serial extension splinting once
the dorsal protective splint has been removed (see
Figure 39-8).
Zone 4
Although tendon lacerations in this region are not
common, concomitant damage to the median nerve
and, less commonly, the ulnar nerve in Guyon’s canal
will result in intrinsic muscle paralysis and loss of sen­
sation. At this level, adhesions to the synovial sheath
and between the tendons in the restricted space under
the retinaculum very quickly become established. The
postoperative exercise regimen should promote the
maximum available tendon glide. An active motion
regimen is desirable, but the required amount of tendon
424 Section 5:  Rehabilitation of Tendon Surgery
motion can be hard to achieve for a number of reasons.
For example, wrist extension may increase tension on a
median nerve repair. A neutral position or slight flexion
of the wrist is generally the best compromise. After 2
weeks, the wrist can be gradually extended by altering
the splint to promote greater tendon glide.
Loss of intrinsic muscle action and muscle–tendon
unit shortening can result in a change in the resting
position of the digits. To facilitate tendon motion, the
MCP joints require positioning in a greater degree of
flexion than in digital injuries. Prior to application of
the protective splint active digital flexion should be
observed in varying positions of the MCP joints and the
position from which the greatest tendon excursion can
be achieved selected. In patients with severe clawing of
the digits, maintaining the MCP joint in 60° to 70°
flexion is recommended, to achieve active IP joint exten-
sion and a greater range of IP joint flexion. Active digital
flexion and differential glide exercises should be encour-
aged from the start of the rehabilitation. Active wrist
extension exercises in conjunction with active digital
flexion taking advantage of the tenodesis effect should
be initiated around 3 weeks, out of the splint in trust-
worthy patients.
Zone 5
Injuries at the level of the wrist and forearm may range
from an isolated tendon to a complex “spaghetti wrist”
involving neurovascular structures. In cases of injury to
isolated wrist tendons, the dorsal protective splint
should extend to the MCP joints only and the hand is
mobilized freely. The wrist should be positioned in
neutral or slight flexion depending on the tightness of
the repair and active wrist motion may commence at 3
weeks postoperatively. Patients can be permitted to
perform light activity but should be deterred from
strong gripping. When the injury involves multiple
tendon and nerve injuries, the splint position should
be dictated by (1) protection of the repaired structures,
(2) patient comfort, and (3) facilitation of active motion
regimens. In the presence of nerve injuries the wrist
should not be positioned in extension beyond neutral;
minimal wrist flexion is more appropriate in the early
postoperative period. The position of the wrist can be
gradually altered to achieve greater extension during the
first few weeks of the protective phase usually to a
maximum of 10° to 20°. Within the protective splint,
the MCP joints should be positioned to facilitate digital
flexion, inhibit the development of a claw deformity
and allow maximal IP joint extension. As in zones 3 and
4, 60° to 70° of MCP joint flexion is required depen-
dent on the degree of clawing and the presence of a
nerve injury. Digital edema is not usually present in the
early stages in injuries at this level and consequently
there is no restriction to passive IP joint motion. Passive
extension exercises with the MCP joints in maximal
flexion should be emphasized to prevent the develop-
ment of IP joint contracture, especially in the presence
of intrinsic muscle paralysis.
Active protocols are indicated as repairs are unlikely
to rupture. Exercises that focus on differential glide
should be incorporated to avoid adhesions between the
tendons, although this may not affect the outcomes.37
Another commonly seen consequence is adhesions
between the skin and the tendons. These do not usually
restrict tendon glide but can be of cosmetic concern to
the patient.
The protective splint should be removed at 6 weeks
after surgery. At this stage common complications are
loss of composite extension and fixed flexion deformi-
ties of the joints. Forearm based splints should be pro-
vided to achieve gradual restoration of extension. In the
presence of nerve injuries, anticlaw devices may be
required throughout the later stages of rehabilitation.
Sensory re-education techniques should also be
incorporated into the rehabilitation regimen from the
start of treatment. These are designed to assist in the
preservation of cortical representation of the hand by
modifying the functional reorganization, which will
inevitably occur within the somatosensory cortex.38
SELECTING A REGIMEN FOLLOWING
RE-REPAIR OF RUPTURES OF THE
SURGICALLY REPAIRED FLEXOR TENDON
At any stage during rehabilitation the patient may
report a loss of motion. This indicates rupture of the
surgically repaired tendon. The occurrence may vary
from an obvious sudden event during exercise or
unprotected use of the hand to a slower decrease in the
amount of movement as a gapping repair slowly gives
way altogether. The exact cause or time of rupture can
be unclear and may even be masked in cases of infec-
tion or significant edema. The rupture of the primarily
repaired flexor tendons in the hand can occur in a
period from several days to 6 weeks after surgery.15 The
repaired tendon is at most risk of rupture during the
first 2 weeks after repair with the second week being
the most dangerous. Diagnosis of a ruptured tendon is
made by examination of posture or manual tendon
testing, but recent advances in the technique of diag-
nostic ultrasound have made this process considerably
more efficient. If a re-repair is to be undertaken, it is
vital that the surgeon, therapist, and patient are involved
in any decision making. These decisions must be based
on the reason for the rupture, if known, and the likeli-
hood of a favorable outcome of the re-repair. In 1982
Leddy suggested that the best outcomes are likely if a
re-repair is undertaken soon after rupture and most
subsequent studies appear to support this although
careful consideration should be given to the little
finger.39-41 Some patients choose not to opt for further
surgery because of inability to commit to an extended
 Chapter 39:  Customizing Flexor Rehabilitation Based on Zone or Type of Injury
period of rehabilitation. The therapist should be aware
of the intraoperative findings of the re-repair before
embarking on rehabilitation, as the status of the
re-repair should differ from that of the original. An
understanding of the mechanics of the rupture is neces-
sary whether due to technical failure or excessive force
placed on the repair. Tendon ends may have softened
necessitating careful handling and making re-repair dif-
ficult to perform. The tendon may also be shortened
due to excision of the previous repair site requiring
careful postoperative positioning to ease the tension
across the repair site. Following a re-repair the therapist
should consider modifying the protocol and exercising
caution in the use of active motion until safety is
ensured. Generally, a lesser aggressive form of exercise
is prescribed for the repair of the ruptured primary
tendon repair.
Over the past 20 years, the materials and methods
used in the postoperative management of flexor tendon
injuries have changed considerably. Although plaster of
Paris was originally used for the entire 6-week period of
protection, it is now used only in the immediate post-
operative period. It has been superseded by thermoplas-
tic material, which provides greater comfort and
longevity. In the late 1970s, when mobilization of flexor
tendon repairs became popular, the passive flexion regi-
mens of Duran and Houser and Kleinert predomi-
nated.18,19 Although these passive regimens still have
their place, there has been a general transition to early
References
1. Elliot D: Primary flexor tendon repair-operative repair, pulley
management and rehabilitation: invited personal review,
J Hand Surg (Br) 27:507–513, 2002.
2. Tang JB: Indications, methods, postoperative motion and
outcome evaluation of primary flexor tendon repairs in Zone
2, J Hand Surg (Eur) 32:118–129, 2007.
3. Pettengill KM: The evolution of early mobilization of the
repaired flexor tendon, J Hand Ther 18:157–168, 2005.
4. Bruner JM: The zig-zag volar-digital incision for flexor-tendon
surgery, Plast Reconstr Surg 40:571–574, 1967.
5. Lindsay WK, Thomson HG: Digital flexor tendons: an experi-
mental study. Part I: The significance of each component of
the flexor mechanism in tendon healing, Br J Plast Surg
12:289–316, 1960.
6. Tang JB, Wang YH, Gu YT, et al: Effect of pulley integrity on
excursions and work of flexion in healing flexor tendons,
J Hand Surg (Am) 26:347–353, 2001.
7. Al-Qattan MM: Conservative management of zone II partial
flexor tendon lacerations greater than half the width of the
tendon, J Hand Surg (Am) 25:1118–1121, 2000.
8. Sirotakova M, Elliot D: Early active mobilization of primary
repairs of the flexor pollicis longus tendon, J Hand Surg (Br)
24:647–653, 1999.
9. Sirotakova M, Elliot D: Early active mobilization of primary
repairs of the flexor pollicis longus tendon with two Kessler
two strand core sutures and a strengthened circumferential
suture, J Hand Surg (Br) 29:531–535, 2004.
10. Giesen T, Sirotakova M, Copsey AJ, et al: Flexor pollicis
longus primary repair: further experience with the Tang
425
active motion or combined early passive-active motion
with resultant improvement in outcomes.1,2,8-11,17
SUMMARY
A skilled surgeon, experienced therapist, and compliant
patient are desirable requirements but not a guarantee
of an excellent result. Active motion regimens are best
in all zones of injury as they provide the optimal require-
ments for motion and tension following flexor tendon
repair. There are no standard protocols, however, and
therapists managing these injuries must assimilate a
considerable amount of information before selecting
the most appropriate treatment for each individual
patient. The pursuit of optimal tendon glide must not
take precedence over safety; however, there are a variety
of alternative options available with the potential to
achieve favorable outcomes.
Acknowledgments
I would like to thank Professor Gus McGrouther and
Mr. Stewart Watson, consultant hand surgeons at
Wythenshawe Hospital, Burns and Plastic Surgery Unit,
who read through my manuscript. The rehabilitation
regimens described in this chapter are the result of expe-
rience and close collaboration between the surgeons
and the therapists in South Manchester. I would also
like to thank my specialist hand therapy colleagues
Sarah Turner, Alison Roe, and Emma Kelly for their
contributions.
technique and controlled active mobilization, J Hand Surg
(Eur) 34:758–761, 2009.
11. Elliot D, Southgate CM: New concepts in managing the long
tendons of the thumb after primary repair, J Hand Ther
18:141–156, 2005.
12. Cao Y, Tang JB: Biomechanical evaluation of a four-strand
modification of the Tang method of tendon repair, J Hand
Surg (Br) 30:374–378, 2005.
13. Dona E, Gianoutsos MP, Walsh WR: Optimizing biomechani-
cal performance of the 4-strand cruciate flexor tendon repair,
J Hand Surg (Am) 29:571–580, 2004.
14. Birks M, Peck F, Lees V, et al: The influence of multistrand
repairs on the rupture rates of flexor tendon injuries in zone
II, BBSH Autumn Meeting 2008.
15. Elliot D, Moiemen NS, Flemming AF, et al: The rupture
rate of acute flexor tendon repairs mobilised by the con-
trolled active motion regimen, J Hand Surg (Br) 19:607–612,
1994.
16. Peck FH, Bücher CA, Watson JS, et al: A comparative study of
two methods of controlled mobilization of flexor tendon
repairs in zone 2, J Hand Surg (Br) 23:41–45, 1998.
17. Silfverskiöld KL, May EJ: Flexor tendon repair in zone II with
a new suture technique and an early mobilization program
combining passive and active flexion, J Hand Surg (Am)
19:53–60, 1994.
18. Duran RJ, Houser RG: Controlled passive motion following
flexor tendon repair in zones 2 and 3. In AAOS Symposium
on Tendon Surgery in the Hand, St Louis, 1975, Mosby,
pp 105–114.
426 Section 5:  Rehabilitation of Tendon Surgery
19. Lister GD, Kleinert HE, Kutz JE, et al: Primary flexor tendon
repair followed by immediate controlled mobilization,
J Hand Surg (Am) 2:441–451, 1977.
20. Dobbe JG, van Trommel NE, Ritt MJ: Patient compliance with
a rehabilitation program after flexor tendon repair in zone II
of the hand, J Hand Ther 15:16–21, 2002.
21. Sandford F, Barlow N, Lewis J: A study to examine patient
adherence to wearing 24-hour forearm thermoplastic splints
after tendon repairs, J Hand Ther 21:44–53, 2008.
22. Elhassan B, Moran SL, Bravo C, et al: Factors that influence
the outcome of zone I and zone II flexor tendon repairs in
children, J Hand Surg (Am) 31:1661–1666, 2006.
23. Moiemen NS, Elliot D: Primary flexor tendon repair in zone
1, J Hand Surg (Br) 25:78–84, 2000.
24. McGrouther DA, Ahmed MR: Flexor tendon excursions in “no
man’s land,” Hand 13:129–141, 1981.
25. Silverskiöld KL, May EJ, Törnvall AH: Flexor digitorum pro-
fundus tendon excursions during controlled motion after
flexor tendon repair in zone II: a prospective clinical study,
J Hand Surg (Am) 17:122–131, 1992.
26. Slattery PG, McGrouther DA: A modified Kleinert controlled
mobilization splint following flexor tendon repair, J Hand
Surg (Br) 9: 217–218, 1984.
27. Evans RB: Zone I flexor tendon rehabilitation with limited
extension and active flexion, J Hand Ther 18:128–140, 2005.
28. Leddy JP, Packer JW: Avulsion of the profundus tendon inser-
tion in athletes, J Hand Surg (Am) 2:66–69, 1977.
29. Colditz JC: Plaster of Paris: the forgotten hand splinting
material, J Hand Ther 15:144–157, 2002.
30. Cao Y, Tang JB: Investigation of resistance of digital subcuta-
neous edema to gliding of the flexor tendon: An in vitro study,
J Hand Surg (Am) 30:1248–1254, 2005.
31. Cao Y, Tang JB: Resistance to motion of flexor tendons and
digital edema: An in vivo study in a chicken model, J Hand
Surg (Am) 31:1645–1651, 2006.
32. Tang JB, Xu Y, Wang B: Repair strength of tendons of varying
gliding curvature: A study in a curvilinear model, J Hand Surg
(Am) 28:243–249, 2003.
33. Tang JB: Clinical outcomes associated with flexor tendon
repair, Hand Clin 21:199–210, 2005.
34. Savage R: The influence of wrist position on the minimum
force required for active movement of the interphalangeal
joints, J Hand Surg (Br) 13:262–268 1988.
35. May EJ, Silfverskiöld KL, Sollerman CJ: Controlled mobili­
zation after flexor tendon repair in zone II: a prospective
comparison of three methods, J Hand Surg (Am) 17:942–952,
1992.
36. Peck FH, Bucher CA, Watson SJ, et al: An audit of flexor
tendon injuries in zone II and its influence on management,
J Hand Ther 9:306–308, 1996.
37. Yii NW, Urban M, Elliot MD: A prospective study of flexor
tendon repair in zone 5, J Hand Surg (Br) 23:642–648, 1998.
38. Rosén B, Balkenius C, Lundborg G: Sensory re-education
today and tomorrow: A review of evolving concepts, Hand
Ther 8:48–56, 2003.
39. Allen BN, Frykman GK, Unsell RS, et al: Ruptured flexor
tendon tenorraphies in zone II: Repair and rehabilitation,
J Hand Surg (Am) 12:18–21, 1987.
40. Leddy JP: Flexor tendons–acute injuries. In Green DP,
editor: Operative Hand Surgery, New York, 1982, Churchill
Livingstone, pp 1347–1350.
41. Dowd MB, Figus A, Harris SB, et al: The results of immediate
re-repair of zone 1 and 2 primary flexor tendon repairs which
rupture, J Hand Surg (Br) 31:507–513, 2006.
 CHAPTER
40  
STATE OF THE ART OF
EXTENSOR TENDON
REHABILITATION
Ton A.R. Schreuders, PT, PhD, and
Gwendolyn Van Strien, lPT, MSc
OUTLINE
The extensor tendons have complex anatomical struc-
tures and mechanically they are dependent upon each
other. A large variety of protocols are available to
accommodate therapy for the varied extent and regions
of injuries. Generally, the protocols are classified into
three types: immobilization, early passive controlled
motion by means of dynamic splinting, and early
active motion. After digital extensor tendon laceration
and repair protective positioning of the finger is
important to release tension across the repair and to
prevent contracture of the joints of the finger. Main-
taining the joint(s) in an extended position will ease
tension on the tendon repair, and early motion can
prevent the joints from developing stiffness, a balance
that should be carefully planned. In zones 5 and 6,
most therapists and surgeons advocate early motion
(including dynamic splinting and active motion pro-
tocols). Though these early motion protocols produce
earlier recovery of hand motion, the late outcomes are
similar to immobilization protocols. Adhesion forma-
tion is less of a problem compared to the flexor tendon;
however, but in zone 7, where the extensor retinacu-
lum covers the extensor, occurrence of adhesions can
drastically hamper tendon gliding. After injuries in
this area, early movement of the tendon is critical to
ensure recovery of function. After tendon repair in
zone 8, early movement of the tendon may not be a
necessity. Early motion is usually implemented from
3 to 5 days postsurgery and therapy may need to con-
tinue for 2 to 3 months. In the initial days, edema
formation should be properly dealt with; information
about the severity of injuries, patient compliance, and
strength of surgical repairs should be taken into serious
consideration to decide rigor of the early motion.
The extensor tendons lie directly under the skin with
very thin subcutaneous tissue above. In most parts, the
tendons are thin and flat. The extensor tendons have
smaller excursion than the flexors and the forces gener-
ated by extensor muscles are weaker. The extensor mech-
anism (e.g., the structures of the extensor tendons on
the dorsum of the digits) consists of multiple tendon
slips intertwined and intimately covering the dorsum of
the phalanges.1
The extensor tendons do not have a synovial sheath
system, but at the wrist level (zone 7) (Figure 40-1),
the extensors are restricted by the extensor retinaculum
that forms six fibro-osseous compartments within
which 12 extensor tendons pass, which also help to
prevent bowstringing. Adhesion formation after exten-
sor tendon injuries is not uncommon, but because the
requirement of tendon excursion is low and adhesions
form under largely moveable skin, adhesions often do
not pose an important problem for function of the
extensor tendons. The extensor retinaculum at the wrist
functions as a pulley, keeping the wrist and finger exten-
sor tendons close to the axis of the carpus during
motion. At this location, dense adhesions may occur
between extensor retinaculum and the tendons, that
hinder tendon movement.
The architecture of the extensor tendon is complex,
especially at the proximal phalanx and middle phalanx
level (zones 3, 4, and 5). Here the extensor tendon gives
off the central slip and lateral bands and connecting
fibers, forming a broad expansion over the dorsum and
lateral aspects of the proximal phalanges with complex
intertwined tendon fibers.2 The fibers of this extensor
apparatus connect to the tendons of both the interosse-
ous and lumbrical muscles. The central slip is the direct
distal extension of the extensor digitorum communis
(EDC) tendon. Extensor tendons on the dorsal side of
the hand (zone 6) are separated tendons, but they have
connections through the juncturae tendinum.3 The
juncturae tendinum coordinate the opening of the hand
via the extension of thumb, digits and wrist, as well as
assist in force redistribution through the extensors.4
Because of the interconnections and multiple inser-
tions, the extensor tendons are less likely to retract when
427
428 Section 5:  Rehabilitation of Tendon Surgery
I sion or distally through joint flexion. Proximal move-
II
III
IV
V T-I
T-II
VI T-III
T-IV
VII T-V
VIII
Figure 40-1  Zones of extensor tendon injuries. (Copyright
of Judy Colditz.)
injured than are the flexor tendons. Loss of length in the
extensor tendon in the digits disturbs function of the
extensors, as structures in each segment are extremely
different. Shortening of a phalanx greatly impairs the
working capacity of the extensors.
GENERAL GUIDELINES FOR CARE AFTER
EXTENSOR REPAIRS
There have been fewer clinical investigations devoted to
surgery and rehabilitation of the extensor tendons than
the flexor tendons. Conceptually, many principles and
methods used in the postoperative care were derived or
modified after those for flexor tendons. Essentially, ade-
quate edema control and protection of the tendon
repair from excessive stress by eliminating inadvertent
hand use are important after surgery. Protective splint-
ing and instructions for home care should be given from
the first postoperative days.
As with care after flexor tendon repairs, therapy for
extensor tendons should start early after surgery, but care
should be taken not to create gapping or rupturing of
the suture site if early motion is initiated. The extensor
tendon can be moved proximally through joint exten-
ment of the tendon requires active contraction of the
extensor muscles (which are generally weaker compared
to the flexors). Active or passive flexion of the joints
produces distal glide of the extensor tendons. Similar to
the rehabilitation for the flexors, extensor tendon
therapy focuses on tendon gliding with a gradual
increase of load to the repaired tendon.
The development of protocols in flexor tendons was
spurred on by new suture techniques. Suture techniques
for extensors have not seen similar advances. Neverthe-
less, new extensor protocols have mostly followed the
same trends. Similarly, there are three types of protocols
for the extensors: (1) immobilization, (2) passive mobi-
lization with a dynamic extension splint, and (3) early
active mobilization.
The Initiation of Therapy: Timing
No studies have discussed specifically the optimal timing
to initiate motion of the extensor tendons. Following
flexor tendon repair, investigators have proposed initiat-
ing active flexion at postsurgical day 3 to 5, based on
experimental evidence.7 Though it is unsure whether we
can extrapolate the conclusions from the flexor tendon
research to the extensors, we generally adopt these con-
clusions, because of a paucity of investigation on exten-
sors in this regard.
Ideally, postoperative mobilization should be initi-
ated when the therapist has a wide margin of safety
between the tendon gapping strength and the load
required to initiate tendon gliding.5 Active tendon
gliding has to overcome resistance caused by (1) friction
between tendons and their surrounding structures;
(2) resistance resulting from joint stiffness, edema, and
adherence to surrounding tissues; and (3) resistance of
antagonist muscles.5 In zone 7, the tendon encounters
additional resistance from the restrictive extensor reti-
naculum, that covers the tendons tightly.
When the patient is immobilized for the first 3 or 5
days after surgery, extra care must be taken to ensure
correct positioning of the hand, which should be
checked at the first or second day with assessment of
pain, excessive swelling, or bleeding. An earlier dressing
change may be necessary.
Patient Referral Information
Detailed and specific information about the patient, the
injury, and operative procedures performed are helpful
in deciding protocols for individual patients. A copy
of the operative report is invaluable in this regard.
The therapist needs to know the mechanism of injury,
level and severity of the tendon injuries, and structures
repaired. It is also important to know the type of tendon
 Chapter 40:  State of the Art of Extensor Tendon Rehabilitation
repair and the strength of the repair. The surgeon should
inform the therapist if the tendon is frayed, if there is
the possibility of a postoperative infection, or if tissues
were seriously damaged. All these factors greatly influ-
ence the extent and amount of scar and the probability
of tendon adherence or repair rupture. Associated inju-
ries of bones, nerves, blood vessels, and skin should also
be taken into account in deciding protocols that best
suit the patient. Information on the use of skin grafts
and the location of repaired blood vessels is of great
importance since pressure over these areas should be
avoided by careful design of a splint. Finally, therapists
should obtain information regarding pertinent medical
conditions that may influence wound healing or the
normal progression of tendon healing.7
Record Keeping
Active and passive range of motion of the hand should
be regularly measured and recorded. Improvement of
range of motion is an indication for the effectiveness of
therapy and helps to decide if a protocol needs modifi-
cations. Function is assessed by measuring passive and
active range of motion of the joints. Extensor pollicis
longus (EPL) function, after a transfer of the extensor
indices to the EPL tendon, can be measured by the dis-
tance of thumb elevation from the surface of a table on
which the hand is placed flat.8 In addition, the Kapandji
thumb rule by giving a score (0-10 score; 0: to the meta-
carpophalangeal joint level of the index finger, and 10:
to the distal palmar crease of the little finger) to how far
the thumb can reach different parts of the fingers can
be used to score thumb opposition.9
The timing of initiating or modifying therapy and
frequency of exercises, such as active joint extension,
should be clearly recorded. The strength of finger and
wrist extension, pain, and potential signs and symptoms
of complex regional pain syndrome should also be
recorded.
REHABILITATION METHODS IN EACH ZONE:
FINGER EXTENSORS
Zones 1 and 2 (Mallet Finger)
Zones 1 and 2 extensor tendon injuries may involve
avulsion fracture from the base of the distal phalanx or
present as tendon disruption alone, leading to mallet
finger deformity. A full-time splint is usually applied
for 6 to 8 weeks with the DIP joint held in extension
for both types of mallet finger.10 After the initial 6 to 8
week splinting period, the splint should still be worn at
night and during strenuous activities for 2 to 6 weeks.
Several types of splint are available: foam-padded alu-
minum splints, molded plastic splints, and thermoplas-
tic splints. With splinting, most acute injuries achieve
a success rate of around 80%.11 Therapy after this
splinting period is not always continued.10,12 Patients
429
returning to their daily activities directly after splint
removal may risk a tendon re-rupture or develop a DIP
joint extension lag. The entire course of therapy can be
divided into the following phases:
First Phase (6 to 8 Weeks): Therapy During
Splinting Phase
After a mallet finger injury, a splint is applied to hold
the distal interphalangeal (DIP) joint in extension.13
It is preferable to apply a custom made splint to posi-
tion the DIP joint in submaximal extension, that is,
maximum extension that does not produce skin blanch-
ing. However, circulation is more often compromised
by too much pressure of the splint rather than too much
DIP joint hyperextension.
The splint should not include the proximal interpha-
langeal (PIP) joint and should allow full PIP joint
flexion. Nonelastic adhesive tape should securely fix the
splint to the volar skin of the middle part of the finger.
In the supple and hypermobile fingers, a mallet finger
injury encourages development of a swan neck defor-
mity. This can be prevented by adding a 30° extension
block for the PIP joint as part of the splint (Figure 40-2).
When the patient is less compliant or needs more
secure protection, a plaster of Paris or Quickcast cylindri-
cal cast is a good choice to immobilize the DIP joint.
Therapists often have difficulty keeping the DIP joint
extended while fabricating a plaster cast. This difficulty
may be overcome if an adhesive nonelastic tape is first
applied starting on the volar aspect of the distal end of
the finger and ending on the dorsum, crossing the DIP
joint crease and extending to the middle phalanx. This
tape holds the DIP joint in extension and the plaster of
Paris is easily applied over it. The tape also prevents the
plaster from slipping off as the plaster adheres to the tape.
With the splint/cast in place, the patient is instructed
to perform active PIP flexion exercises with the adjacent
fingers held in extension. With this exercise, the flexor
digitorum profundus (FDP) cannot be activated and the
flexor digitorum superficialis (FDS) will flex the PIP
joint only, eliminating flexion forces at the DIP joint.
Figure 40-2  A mallet finger splint often used by these
authors to immobilize the DIP joint and prevent PIP joint
hyperextension with a PIP joint extension block.
430 Section 5:  Rehabilitation of Tendon Surgery
The patient is instructed not to carry heavy objects
with the injured hand and to avoid playing contact
sports, etc. We prefer not to have the patient remove the
splint but have the therapist remove the splint carefully
every week. If the skin has signs of pressure or macera-
tion, the splint needs to be adjusted or an alternative
splint design considered.
Second Phase (6/8 to 10 Weeks): Initial Exercises
Without Splint
Only when there is no extension lag at the DIP joint can
the patient be allowed to start actively flexing the DIP
joint and gently increasing the flexion force. The active
exercises are done 3 to 5 times a day out of the splint.
The amount of DIP joint flexion can be controlled by
using a large diameter cylinder (Figure 40-3). With the
hand on top of the cylinder rolling it forward allows
some DIP joint flexion and rolling it backward provides
a passive assistance for DIP joint extension. The patient
then lifts the hand and holds this position for 5 seconds,
similar to place-hold active exercise. General instruc-
tions are to do the exercises slowly and stay within pain
limits. The splint is worn between exercises and at night.
Only when patients understand the exercises should
they do them independently at home.
Therapists should measure the active flexion and
extension of the DIP joint, and if there is adequate active
DIP extension, both the frequency of exercises and the
range of joint motion allowed can be increased gradually.
The range of flexion exercises can be increased by using
a smaller cylinder. Weaning off the splint gradually and
carefully increasing flexion range prevent a recurrence
of the mallet finger. Most patients require close monitor-
ing of splint wear and exercises during this phase.
Figure 40-3  In the first phase of exercises after a mallet
finger injury, the amount of DIP joint flexion is controlled by
using a large diameter cylinder. When the cylinder with the
hand on top is rolled forward it allows some DIP joint
flexion; rolling back the DIP joint is pushed into extension
similar to a place-hold exercise.
Third Phase (10 to 12 Weeks): Increase Loading
The range of active DIP joint flexion during exercises can
be increased and active extension of the DIP joint is
performed. Light daily activities can be started without
the splint and the time without splint can be gradually
increased. Night-time splinting continues. If at any time
a marked DIP joint extension lag occurs, joint flexion
exercises should be stopped and the splint reapplied for
4 extra weeks. The patient can return to all activities
once the splint can be discontinued during the day.
Nighttime splinting may be continued for another
month or two for some patients.
When therapy starts late or joint stiffness or other
complications develop during the course of therapy,
full DIP joint flexion may not be reached for 6 or 8
months. If a DIP flexion contracture has developed,
therapy should focus on correcting the flexion contrac-
ture first.
Zone 3: Central Slip Lesion
(Boutonnière Deformity)
Closed injuries are often missed in the acute stage
because the triangular ligament initially maintains
the dorsal positions of the lateral bands, helping to
maintain extension of the PIP joint. Only when the
triangular ligament yields and allows the lateral bands
to slip volarly will the lack of PIP joint extension
become apparent due to the developing boutonniere
deformity.14-16 Chronic bou­tonnière deformity leads to
flexion contracture of the PIP joint.
For a boutonnière deformity after closed injuries, the
underlying pathology is attenuation or partial disrup-
tion of the central slip and nonsurgical treatment is
attempted first. The goal is to immobilize the PIP joint
in extension to allow the attenuated tendons to heal. A
thermoplastic splint can be used to maintain the PIP
joint in full extension for 6 weeks on a full-time basis.
Others prefer the PIP joint to be pinned in extension for
the first 3 weeks, or even 5 to 6 weeks. The DIP joint
should be free and is allowed to move actively. The
immobilization by splinting should be extended beyond
6 weeks if extension lag continues to exist after initia-
tion of PIP joint flexion. After the splint is discontinued,
gradual active flexion of the PIP joint is initiated.
After surgical treatment of the persistent deformity or
surgical repair of an open, complete disruption of the
central slip, the goal of therapy is to protect the central
slip, prevent adhesions, prevent DIP joint stiffness and
extension lag, and maintain the length of the oblique
retinacular ligament (ORL).
Treatment protocols include immobilization, passive
early mobilization with a dynamic splint and immedi-
ate controlled active mobilization of the PIP joint.17-19
Maddy and Meyerdiercks advocate immobilizing
the PIP at 0° of extension with a static finger-based
splint for 3 to 31 2 weeks followed by another 3 weeks
 Chapter 40:  State of the Art of Extensor Tendon Rehabilitation
Figure 40-4  A Capener splint for correction of PIP joint
deformity.
of active flexion and assisted extension with a finger-
based dynamic extension splint.20
The dynamic extension splint in this study was a
custom-made spring coil finger-based splint, much like
a Capener splint (Figure 40-4). At 3 weeks, when the
dynamic splint was fabricated, a structured program
with three exercises was given to the patient: active DIP
flexion with the PIP blocked manually in extension,
active PIP flexion with the MP blocked in extension, and
composite active MP, PIP, and DIP flexion, with the
splint extending the PIP joint between repetitions of
each exercise.
Some authors start the early controlled mobilization
using a prefabricated spring coil dynamic PIP extension
splint (Capener) as early as 10 to 14 days postopera-
tively, following immobilization of the PIP joint in
extension with a static splint.21 Both groups initiated
active DIP flexion exercises with the PIP held in exten-
sion within the first week. However, with extensive
dorsal tissue damage or severed lateral bands the DIP,
exercises were postponed until 4 weeks post-operation.
Because the intent is to passively extend not against
the resistance of a flexion contracture but as an assist to
healing extensors, the spring coil does not need to be
very strong, and a lower force type can be chosen or
fabricated. The goal of the splint is to achieve maximum
extension at rest with the lowest possible force and at
the same time make active flexion easy to perform. The
position of full PIP extension (possibly 10° of hyper­
extension) in both the static and the dynamic splints is
critical for a successful outcome.23
The dynamic splinting can also be hand based,22,23 or
extending across the wrist. The wrist is usually placed in
30° extension, metacarpophalangeal (MCP) joints in
slight flexion, and interphalangeal (IP) joints fully
extended24,25 (Figure 40-5). The DIP joint is allowed to
actively flex to release the tension on the central slip
and to ensure some gliding of the intact lateral bands.
During the first week of active PIP joint flexion, the PIP
joint is allowed to flex up to 30° either by putting a stop
on the outrigger line, by adding a volar splint or by the
431
Figure 40-5  Dynamic extension splinting after surgical
repair of zone 3 extensor tendons. Here active flexion and
passive extension is achieved by the dynamic traction of the
extension splint.
patient grasping a large cylinder. PIP joint flexion is
increased by 15° each week.
From week 3, place-and-hold exercises for finger
extension can be incorporated by passively extending
the PIP joint and actively maintaining the joint at this
position. The exercises are done one to two hours with
10 repetitions each session.
At week 4, active PIP joint extension is started. The
patient continues to use a small finger extension splint,
such as a neoprene splint, during the day to support
extension. At week 5, achieving 90° of active PIP joint
flexion is the goal. Starting at week 6, light activities of
daily living are allowed. Resisted finger motion is started
at week 8. If the PIP joint has less than 60° of passive
flexion, corrective flexion splinting can be applied by
bandaging the fingers in flexion for periods of 10 to 15
minutes, several times a day. We emphasize that the
above program is progressed only when the patient
maintains full active PIP joint extension. If the patient
does not have full extension, the period of splinting in
extension should be prolonged, and more emphasis
should be given to extension than to flexion. Walsh and
colleagues22 compared the dynamic extension splint
with static splinting and the results suggested an earlier
return to work with less frequent therapy visits for the
dynamic extension splint group.
Early active digital extension is also used after surgical
repair of the extensor tendon in this zone. This method
advocated by Evans is known as Short Arc Motion.17 In
the active motion protocol, for the first 4 to 6 weeks, the
digit is immobilized in a finger based static splint in full
extension with the MCP joint excluded. Every hour the
patient is allowed to perform intermittent limited active
flexion and extension exercises using a template splint
(Figure 40-6). The patient actively flexes to the limits of
the template splint and actively extends to full extension.
The template splint supports only the PIP and DIP joints
432 Section 5:  Rehabilitation of Tendon Surgery
Full ext.
Template
splint
Limited
flexion
Figure 40-6  Limited active flexion and full extension
exercises of the PIP and DIP joints using a template splint.
and allows for 30° active PIP and DIP joint flexion in
the first 2 weeks, increasing 10° flexion each week.26
Exercises are performed 4 to 6 times a day. At 6 weeks,
both splints are discontinued, and exercises of full range
of active motion are started.
Evans and Thompson17,26 calculated that the amount
of force added on the repair was 3 N during early active
motion, which is well within the strength of most suture
techniques (about 20 N in the first week)6 and the 30°
flexion limit keeps the force within a safe zone.
Focusing on zones 2 and 3, the studies of Hung,27
Saldana,28 and Newport29 do not support the idea that
dynamic splinting has benefits over static splinting.
Therefore some regard static splinting to be as effective
and should be the standard care for simple extensor
tendon lacerations distal to the MCP joint, given its
simplicity and lower cost.
For chronic boutonniere deformity of PIP joint with
a flexion contracture of over 30°, serial casting is a
useful way to correct the deformity. The cast is applied
to the PIP joint and is changed approximately every 2
weeks; PIP joint extension is progressively increased by
5° to 10° after each change of the cast.
A frequent complication in treating closed bouton-
niere deformity is incomplete correction of the defor-
mity. However, an extension lag of about 20°, in the
presence of full PIP and DIP active flexion leads to little
functional disturbance of a finger, and therapy does not
necessarily need to continue if these degrees of digital
motion have been achieved.
Zone 4: Proximal Phalanx
In this zone, injuries to the tendon often cause no
functional loss because the wide extensor hood covers
more than half of the proximal phalanx. However, when
the tendon is repaired, due to the large contact area
to the underlying bone, it creates a substantial risk of
adherence. which restricts gliding of the extensor hood.
Therapists need to be aware of this extra risk and start
active gliding exercises as soon as possible. Protective
tendon gliding can be provided with a dynamic exten-
sion splint as in zone 3 injuries, or using gentle active
exercises similar to the short arc motion method advo-
cated by Evans.17
Zones 5 and 6: MCP Joint and Dorsum
of the Hand
In zone 5, the sagittal bands are responsible for main-
taining the extensor tendon central over the MCP joint.
Injuries may lead to subluxation of the extensor tendon.
The sagittal bands are tensed during MCP joint flexion.
Following sagittal band repair, MCP joint flexion should
be gentle. Flexing the IP joints while the MCP joint is
kept in extension reduces tension on the sagittal bands
and ensures some gliding of the tendon.
The zone 5 extensor tendon repair can adhere to the
MCP joint capsule. Immobilization of the joint in exten-
sion would lead to contracture of the collateral liga-
ments. To prevent these complications, use of a protocol
with early MCP joint flexion is beneficial.
In zone 6, the extensor tendon is more rounded than
distal extensor tendons and allows stronger surgical
repairs. Because of the juncturae tendinum connections
between the EDC tendons on the dorsum of the hand,
movements of adjacent finger(s) affect tension on the
repaired tendon. When the repair site is distal to the
interconnections, flexion of the adjacent digits may pull
through the interconnections on the proximal stump,
moving it distally, toward the distal stump, bringing the
tendon ends together. Therefore, splinting the adjacent
digits in slightly greater flexion or excluding the adjacent
digits from immobilization and allowing them to flex,
may reduce tension across the repair site. In contrast,
when the repair site is proximal to the interconnections,
flexion of the adjacent fingers may increase tension on
the repair site so the uninjured fingers should be held
in the same position in the splint. Zone 6 repairs benefit
from early motion protocols as postoperative edema on
the dorsum of the hand limits MCP joint flexion; early
motion facilitates reducing edema.
Lacerations of the extensor tendons in zones 5 and 6
are often treated with an early motion protocol using a
dynamic splint.27 Within 2 to 5 days postoperatively, a
dorsally based dynamic splint is applied holding the
wrist in 30° to 40° extension and dynamically extend-
ing the MCP joints to full extension via an outrigger
(loops around the proximal phalanx). At this time active
flexion of the MCP joints is allowed to 20° to 30° for
index and middle fingers, and 35° to 40° for the ring
and little fingers while the IP joints are actively extended.
The second exercise is to flex the IP joints while main-
taining extension of the MCP joints (active hook fist).
Exercises are done 5 times every 2 hours in the first 2
 Chapter 40:  State of the Art of Extensor Tendon Rehabilitation
Figure 40-7  Norwich exercise regimen. Combined active MCP and IP joint extension (lifting the extended digits off the
splint) and active MCP joint extension with IP flexion (making a hook fist within the splint).
weeks, and after that 10 times every hour. For patients
needing more support because they experience unrest
during sleep or exhibit a tendency toward development
of an extensor lag, a volar splint may be used to keep
the fingers in extension at night. At week 2, active flexion
of MCP joints is allowed to 45°, week 3 to about 60°
and week 4 to 90°. At week 4, place-and-hold exercises
for full finger extension are started and at week 6 the
splint is discontinued. Strengthening exercises are
started around week 7 and at 12 weeks the hand can be
used normally. Patients are progressed on this timetable
only if no extensor lag is observed.
For isolated EDC injuries in zones 5 and 6, the imme-
diate controlled active motion (ICAM) technique can
be used, as described by Howell and colleagues.30 This
method allows immediate active controlled motion by
using a yoke splint which places the injured finger in
MCP joint extension slightly greater than the adjacent
fingers, and a second splint is applied to hold the wrist
in 20° to 25° extension. The ICAM protocol has the
following three phases: (1) Days 0 to 21—Two splints
are worn full time and active composite finger flexion
exercises are started. (2) Days 22 to 35—The patient
continues to wear the yoke splint at all times but removes
the wrist splint only for wrist exercises. (3) Days 36 to
49—The wrist splint is discontinued but the patient
continues wearing the yoke splint while using the hand
but removes it for active finger motion exercises. In
Howell’s report 81% patients achieved excellent results
for both digital extension and flexion.30 Only five patients
developed a lag and there were no tendon ruptures.
The Norwich regimen31 designed for zone 5 and 6
extensor tendon rehabilitation is an active protocol
using a volar immobilization splint, which hold the
wrist in 45° extension, the MCP joints in 50° flexion,
and the IP joints in full extension. Two exercises are
performed for 4 weeks, 4 times a day, with 4 repetitions
each time (“the rule of four”). After loosening the digital
straps the following exercises are performed: combined
active MCP and IP joint extension (lifting the extended
digits off the splint) and active MCP joint extension
with IP flexion (making a hook fist within the splint)
433
Figure 40-8  The Norwich splint can be modified with a
V-shaped insert holding the MCP and IP joints at 0° when
extension lag persists.
(Figure 40-7). When extension lag persists, the splint
can be worn at night or part of the day, with a V-shaped
insert holding the MCP and IP joints at 0° (Figure
40-8). During weeks 4 to 6, the splint can be removed.
If an extension lag of the MCP joint is persistent and is
greater than 30°, splinting is resumed for 2 more weeks.
If no lag is present, active finger flexion exercises are
initiated at week 4 without wrist flexion.
A study by Bulstrode and colleagues32 compared the
outcomes of the Norwich regimen to immobilization of
all the joints of the hand and static extension splinting
of the wrist and MCP joints while leaving the IP joints
free. The total active range of digital motion in the
immobilization group was less at week 4. However, by
12 weeks, there was no statistically significant difference
between the three regimens, and all patients achieved
good or excellent results. The only significant finding
was reduced grip strength compared to the uninjured
hand at 12 weeks for the immobilization group.32 Other
investigators found better functional results for the
dynamic splint method over early active mobilization
at 4 weeks but failed to identify significant differences
in functional outcomes at 12 weeks.33 A study compar-
ing a dynamic outrigger splint with a static volar MCP
blocking splint also did not show statistically significant
differences in functional outcomes.34 There is no
434 Section 5:  Rehabilitation of Tendon Surgery
evidence of superior results in the long term for any of
the different treatment methods in these publications.
Still, all the authors recommended early mobilization
on the basis of lower cost and the simplicity of the early
active mobilization regimens with less time spent in
therapy and especially with simpler splint fabrication
and fewer adjustments. However, early mobilization has
achieved earlier return of grip strength, which may be a
reason to choose early mobilization over static treat-
ment.32,45 One group, however, states that with similar
outcomes the static regimen should be the treatment of
choice with poorly compliant patients, as it is both a
simple and an effective method.35
Ip and Chow36 and Kerr and Burczak37 used a dynamic
splinting regimen after extensor tendon repairs in zones
4 to 8, with good outcomes and no rupture of the repairs.
Newport and colleagues38 used static splinting for all
zones of injury and achieved similar good results. Static
splinting has been described by Blair and colleagues,39
Slater and colleagues,40 and much earlier by Stuart and
colleagues41 and Dargan.42 Soni and colelagues43 recom-
mended early active motion and consider it especially
beneficial in complex injuries distal to the MCP joint.
Zone 7: Extensor Retinaculum at the Wrist
In zone 7, the extensor tendons run through tight com-
partments formed by the extensor retinaculum and
distal radius. This restraining retinaculum increases the
risk for adhesions and limits gliding of the healing
tendon. For these reasons, early mobilization of the
tendon in this zone is preferred.
A practical treatment method is to splint the wrist in
30° to 40° of extension, and the MCP joints in 0° to
15° flexion for 3 to 4 weeks, allowing the PIP and DIP
joints full active range of motion. After 3 to 4 weeks the
MCP joints are left free but the wrist is still held in
extension in a splint. Wrist flexion is started and weaning
from the splint occurs while slowly increasing activities
over the next 2 weeks.44
Zone 8: Forearm
Injuries in the forearm involve tendons, the muscle–
tendon junction, or the muscle belly. Following surgery,
the wrist is immobilized in mild extension with a pro-
tective splint, but thumb and fingers are left out of the
splint. Although active digital motion can be allowed,
lifting of heavy objects should be avoided. Adhesions
occurring in this zone are unlikely to restrict tendon
motion.
REHABILITATION METHODS IN EACH ZONE:
THUMB EXTENSORS
The three thumb extensors, extensor pollicis longus
(EPL), extensor pollicis brevis (EPB) and abductor pol-
licis longus (APL), can be injured, mostly through open
wounds. Rehabilitation after repair is similar to that for
finger extensors. A static splint or a dynamic extension
splint is used for 4 to 6 weeks, followed by progressive
exercises of active thumb extension for a further 2 to 4
weeks. Between 70% and 90% of repairs of the EPL
tendons achieved excellent or good results, with these
protocols.46 Loss of thumb movement is often caused
by tendon adhesions to the bone and skin, with thicken-
ing of the dorsal joint capsules with scar formation.46
Zone T1
Although not seen as frequently as mallet finger, a
closed mallet thumb can be treated similarly to the
closed zone 1 digit injury with 6 to 8 weeks of immo-
bilization of the thumb with splinting. Afterward,
splinting is applied between exercises and at night for
an additional 2 to 4 weeks, and thumb extension is
allowed. However, a zone T1 laceration can also be
surgically repaired by virtue of the large size of the EPL
tendon as compared to the finger extensor.
After surgical repair, Elliot and Southgate46 place the
hand in a palmar plaster of Paris splint with the wrist in
30° of extension and both the MCP joint and the IP
joints in the neutral position. The tendon is mobilized
early after surgery in a dynamic extension splint, which
controls MCP joint flexion only, the loop being under
the proximal phalanx. The IP joint moves freely into
flexion and extension from the commencement of mobi-
lization. For the first 5 days, the hand rests in the splint.
From day 5, the MCP joint alone is actively flexed and
extended, with the sling under the distal phalanx and
the base of the thumb supported with the other hand.
In the second week, the patient actively flexes and extends
both MCP and IP joint together, aiming for the base of
the ring finger, 10 repetitions hourly. Between days 12
and 28, the patient performs active combined MCP and
IP joint flexion and opposition, aiming for the base of
the little finger. After 28 days, the same exercise are con-
tinued without the splint, active combined MCP and IP
joint flexion and opposition are continued and thumb
active abduction, adduction, and opposition exercise are
added. These exercises continue from week 8 onward.
Zone T2
Injuries to the extensor at the proximal phalanx of the
thumb can be immobilized in a hand-based splint,
holding the MCP and IP joint at 0° and the thumb radi-
ally extended. Gentle active exercises can be initiated at
3 weeks, progressing flexion of the thumb slowly while
splinting between exercise sessions.
Due to a high incidence of tendon-to-bone adher-
ence in this zone, early protective motion protocols
should be considered. Crosby and Wehbe18 use a
forearm-based splint, with the wrist in 20° to 30° of
extension, MCP joint at slight flexion of 10° to 20°,
with a rubber band holding the IP joint extended. Active
flexion of the IP joint is allowed, with the IP joint
 Chapter 40:  State of the Art of Extensor Tendon Rehabilitation 435

passively extended in the first 3 weeks. At weeks 4 to 5,

Rubber band
gentle active extension is initiated with the addition of
gentle active flexion of the IP joint. At week 8 and
beyond, graded resistive exercises are initiated. Elliot
and Southgate46 use the same regimen after zone T2 to
T4 EPL tendon repair as in zone T1.

Zones T3 to 5
Figure 40-9  Drawing showing the protective active thumb
The proximal zones of the thumb include the EPL,
motion with a forearm-based dynamic splint for the extensor
extensor pollicis brevis (EPB), and abductor pollicis tendons injured proximal to the MCP joint level of the
longus (APL). After repair of the APL tendon at zones thumb. The rubber band permits active MCP joint flexion
T3 and 4, the wrist is positioned at 30° extension, with and passive extension of the joint.
slight radial deviation and metacarpal extension. Exten-
sion is increased to 40° for zone T5 APL repair.
After EPL repair, immobilization by a static splint
worn full-time for 4 weeks, and starting active exercises
at 4 weeks is common practice. The splint can be dis-
carded at 6 weeks. However, if there is an extension lag
at 6 weeks, extension splinting is continued for another
2 weeks. If stiffness of the joints prevents full thumb
flexion and extension is normal or close to normal,
passive flexion exercises and flexion splinting should
start after 7 to 8 weeks.
Dynamic splinting protocols vary; for postoperative
management of a zone T4 to 5 laceration, Evans17 recom-
mended a dorsal forearm–based splint that positions
the wrist at 30 to 40° of extension, the carpometacarpal
joint at neutral, and the MCP joint at 0°. The IP joint is
held in neutral by a sling with dynamic traction. The
splint allows 60° of active IP joint flexion, which is pas-
sively brought back to extension via dynamic traction.
Evans now adds more motion when the patient is at
therapy. She does controlled passive motion to the MCP
joint of approximately 30° while the wrist is held in
maximum extension and the IP joint is held at 0°. To
ensure gliding, an “active hold” exercise is also done.
Crosby and Wehbe18 use a forearm-based splint and
rubber band traction to the proximal part of the thumb. Figure 40-10  A two-part forearm based thermoplastic
The MCP joint motion is not restricted. The rubber band splint with a removable plate allows flexion and extension of
traction produces MCP joint extension after active MCP the IP joint of the thumb following repair of the EPL tendon
in zones T 3 to 5. (Courtesy of Fiona Peck.)
joint flexion (Figure 40-9).
In the Manchester regimen (personal communica-
tion, with Fiona Peck, 2011), a 2 part forearm based of adhesions under retinaculum. At week 5 the splint is
thermoplastic splint is applied with wrist at 30° and removed. Active IP joint flexion and extension exercises
the MCP and IP joints at 0°. The thumb is positioned are continued and composite active MCP and IP joint
comfortably in abduction and extension. The remov- motion is encouraged to restore opposition. In the pres-
able plate allows active 0° to 60° IP joint flexion and ence of extensor lag, the splint continues to be worn at
extension exercises (Figures 40-10 and 40-11). In week night. Corrective passive flexion is initiated at 6 weeks
1, active IP joint flexion and extension exercises are if flexion is slow to progress. The patient returns to
initiated, progressing to 60° flexion during the first 3 normal activity by weeks 10 to 12.
weeks. No passive flexion is permitted and the splint is Hung and colleagues27 described a dynamic exten-
worn full time. At week 3, the splint is removed to sion splint for all EPL repairs that places the wrist at
perform careful wrist flexion and extension with thumb 40° extension and the thumb in mid-abduction/mid-
relaxed to encourage tenodesis action and promote extension. The IP joint is allowed to flex to 45° in the
tendon glide, especially in zone T5 where there is risk first week, and full flexion is allowed in the second
436 Section 5:  Rehabilitation of Tendon Surgery

week. In the third week, the MCP joint is allowed to flex
to 45°, increasing to full composite flexion by week 4.
The dynamic splint is discontinued in week 5 and is
replaced by a wrist cock-up for one additional week. For
T4 and proximal zone injuries, full active flexion of the
thumb is allowed within the dynamic splint, with the
wrist held in 20° of extension.
Browne and Ribik47 also allowed full flexion across
the palm in a dynamic outrigger splint. They began
Active IP joint flexion Active IP joint extension
Figure 40-11  Active flexion and extension of the IP joint of
the thumb within this splint following repair of the EPL
tendon. (Courtesy of Fiona Peck.)
motion 3 to 5 days after repair and continued exercise
in the splint for 5 weeks. Chinchalkar48 suggested active
wrist and thumb motion to start at 4 to 6 weeks for
injuries at the first extensor compartment.
CLINICAL EVIDENCE AND OUTCOMES
Currently few randomized comparative clinical studies
are available for extensor tendon injuries; rehabilita­
tion methods for individual patients are largely
decided according to personal preference and judg-
ment. Talsma and colleagues49 reviewed findings from
five studies (Table 40-1), about one of the three regi-
mens: (1) immobilization, (2) early controlled passive
mobilization (dynamic splinting), or (3) early active
mobilization. There is strong evidence that early con-
trolled mobilization regimens used after surgical repairs
in zones 5 and 6 lead to better recovery of both range
of motion and grip strength of the hand compared
with immobilization in the short term. Nevertheless,
no conclusive evidence can be uncovered regarding the
long-term (6 months) effectiveness of these regimens.
The methods used to assess the outcomes include Buck-
Gramcko, White, Miller11 and Dargan.42
Surgical repairs of open extensor tendon injuries fol-
lowed by appropriate postoperative care have generally
favorable outcomes.27-29,36 Ip and Chow36 reported 101
primary end-to-end extensor tendon repairs due to
clean-cuts or crush open injuries in zones 4 to 8 of all
fingers or zones 1 to 6 of thumbs in 84 patients treated
with dynamic splinting and passive mobilization.
Among 37 thumb extensor repairs, there were 67% (25
tendons) with excellent results, 30% (11 tendons) good,
and 3% (one tendon) fair by Buck-Gramcko criteria.

Table 40-1  Summary of Studies Comparing Outcomes of Extensor Rehabilitation Protocols49

Authors Interventions/Groups Zones Outcomes
45
Mowlawi et al Start 3 to 5 postoperative days 5, 6 ROM in group A was significantly
N = 34* A.  Dynamic extension splint 4 weeks better than group B at 4 to 8 weeks
B.  Immobilization for 3 weeks, active motion at   and grip strength was greater at 8
4 weeks weeks, but not at 6 months
Bulstrode et al32 A.  Immobilization in plaster, 4 weeks 5, 6 ROM in group B and C was better than
N = 42 B.  Extension splint: wrist in 30° and MCP joints A at 4 and 6 weeks not at 8 and 12
extended; IP joints free, 4 weeks weeks with a compared with B
C.  Extension splint: wrist in 45° and MCP in 50°
flexion, IP joints free, 4 weeks
Chester et al33 A.  Early active motion. with a static splint,   4 to 8 ROM was better with a compared with
N = 54 4 weeks B at 4 weeks, but not at 12 weeks
B.  Dynamic extension splint, 4 weeks No ruptures
Khandwala et al30 A.  Dynamic extension splint 4 weeks 4 to 8 ROM had no differences in two groups;
N = 100 B.  Early active with palmar blocking splint 4 weeks 1 rupture in group 1 and 2 in B
Russell et al35 A.  Immobilization 2 to 3 weeks and dynamic 5 to 8 ROM had no differences between A
N = 65 splint 4 weeks. and B.
B.  Immobilization, 4 weeks followed by static No ruptures
splint, 4 weeks
*N is the total number of patients.
 Chapter 40:  State of the Art of Extensor Tendon Rehabilitation
With Dargan criteria, 83% (50 tendons) of the finger
extensor tendons had excellent results; 9% (6 tendons)
were good; 6% (4 tendons) were fair; and 2% (one
tendon) had poor results. No tendon rupture was
recorded. Newport and colleagues38 reported that out of
91 fingers with surgical repair of open extensor tendon
injuries (zones 1 to 8, all treated with static splinting),
52% (47 tendons) achieved good or excellent results by
Miller criteria. For the thumb, 60% (6 out of 10 thumbs)
had good or excellent results. No rupture was reported.
Few studies have reported outcomes of surgical
repairs of extensor tendons after loss of tendon length
due to extensive tissue damage or complex extensor
tendon injuries in the fingers; persistent and marked
loss of active and passive motion of the fingers after
reconstructive procedures is a challenge for therapists.
Dynamic splinting or early active motion appears to
be beneficial to extensor tendon repair in some areas.
Comparing the dynamic extension splint regimens (early
controlled mobilization) with early active mobilization,
evidence indicated better total range of motion in the
early period (6 to 8 weeks) for the active motion proto-
col, but at three months postoperatively there were no
differences in motion between the two regimens.43
Because of the lack of clinical comparative studies
which provide high quality evidence to support the
use of any specific regimen, post operative treatment
regimens currently used in different units around the
globe vary enormously. We found ourselves hard put to
recommend any one particular way of rehabilitation,
but the therapy guidelines and essential approaches
and considerations described in this chapter should be
helpful in guiding therapists and surgeons in choosing
the post operative treatment best suited for their patient
and their setting. Not only is it important to choose
the most suitable regimen for each patient; it is also
important to make appropriate modifications or adjust-
ments to variable patient conditions to achieve the best
result possible. The ultimate goal of therapy is to achieve
a smoothly gliding tendon without risking rupture of
the repair, and to ensure early recovery of hand func-
tion. To provide further insight into the regimens cur-
rently used worldwide, we include regimens which were
kindly sent to us from several hand centers around the
globe. Their regimens for extensor tendon therapy are
given in the online contents of this chapter.
CONSIDERATIONS
Passive mobilization through dynamic splinting and
early active motion protocols allow for more rapid gain
of range of motion compared with static splinting.
References
1. Hanz KR, Saint-Cyr M, Semmler MJ, et al: Extensor tendon
injuries: acute management and secondary reconstruction,
Plast Reconstr Surg 121:109e–120e, 2008.
437
Nevertheless, we will need to make decisions about
which regimen to use in individual patients, considering
other issues, such as patient compliance, ages of patients,
and zones of injury, and the cost effectiveness of a pro-
tocol. Dynamic extensor splints are arguably the most
difficult to make and therefore time consuming. In addi-
tion, if such complicated splints result in less compliant
patients, we may need to look into more simple regi-
mens like immobilization or early active motion. In
comparing different regimens, it is necessary to integrate
variables such as patient compliance, cost, access to
physical therapy, risk of rupturing the repair, and
expected time off work. Rate and quality of wound
healing, and the site of adhesion formation may be
considered as well.
Therapists should aim for maximum functional
results by anticipating problems during the course of
treatment, by paying close attention to details concern-
ing splint and edema control, and by monitoring ROM,
especially extension lag, and by modifying treatment
regimens accordingly as we go along. Early referral and
good communication between therapist, surgeon and
patient throughout the entire treatment period is essen-
tial for achieving the best functional results.
Acknowledgments
Therapy protocols were kindly contributed from following
surgeons or therapists; protocols available in this book at
www.expertconsult.com are as follows:
1. Therapy Protocols After Extensor Tendon Repairs: St Andrew’s
Centre for Plastic Surgery, Broomfield Hospital, Chelmsford,
Essex, UK, from Dr. David Elliot
2. Therapy Protocols After Extensor Tendon Repairs of the Thumb:
St Andrew’s Centre for Plastic Surgery, Broomfield Hospital,
Chelmsford, Essex, UK, from Dr. David Elliot
3. Therapy Protocols After Extensor Tendon Repairs of Fingers, Mid
Essex Hospital Services, St Andrew’s Centre-Hand Therapy,
Essex, UK, from Dr. David Elliot
4. The Manchester Regimen for Postoperative Rehabiliation After
Finger Extensor Tendon Repairs, Manchester, UK, from Ms.
Fiona Peck
5. Protocols of Exercise After Repair of Extensor Tendon Injuries,
Queen Mary Hospital, The University of Hong Kong, Hong
Kong, China, from Dr. Wing Yuk Ip
6. Extensor Tendon Rehabilitation Program, Queen Mary Hospital,
The University of Hong Kong, Hong Kong, China, from Dr.
Wing Yuk Ip
7. Therapy Protocols After Extensor Tendon Repair, Springfield,
Mass, USA, from Ms. Karen Pettengill
8. Protocols of Sydney Hand Therapy & Rehabilitation Centre,
Sydney, Australia, from Ms. Rosemary Prosser
9. Therapy Protocols from Royal Free Hamstead NHS Trust,
London, UK, from Ms. Nikki Burr
2. Matzon JL, Bozentka DJ: Extensor tendon injuries, J Hand
Surg (Am) 35:854–861, 2010.
438 Section 5:  Rehabilitation of Tendon Surgery
3. Hirai Y, Yoshida K, Yamanaka K, et al: An anatomic study of
the extensor tendons of the human hand, J Hand Surg (Am)
26:1009–1015, 2001.
4. Pinar Y, Bilge O, Govsa F, et al: Anatomo-histological analysis
of the juncturae and their relations to the extensor tendons
to the dorsum of the hand, Surg Radiol Anat 31:77–83, 2009.
5. Amadio PC: Friction of the gliding surface. implications for
tendon surgery and rehabilitation, J Hand Ther 18:112–119,
2005.
6. Newport ML: Extensor tendon injuries in the hand, J Am Acad
Orthop Surg 5:59–66, 1997.
7. Rosenthal EA, Stoddard CW: Questions hand therapists ask
about treatment of tendon injuries, J Hand Ther 18:313–318,
2005.
8. Lemmen MH, Schreuders TAR, Stam HJ, et al: Evaluation of
restoration of extensor pollicis function by transfer of the
extensor indicis, J Hand Surg (Br) 24:46–49, 1999.
9. Kapandji AI: Clinical evaluation of the thumb’s opposition,
J Hand Ther 5:102–106, 1992.
10. Handoll HH, Vaghela MV: Interventions for treating mallet
finger injuries, Cochrane Database Syst Rev CD004574, 2004.
11. Baratz ME, Schmidt CC, Hughes TB: Extensor Tendon Inju-
ries. In Wolfe SW, Hotchkiss RN, Pederson WC, et al, editors:
Green’s Operative Hand Surgery, ed 5, Philadelphia, 2005,
Elsevier Churchill Livingstone, pp 187–217.
12. Kalainov DM, Hoepfner PE, Hartigan BJ, et al: Nonsurgical
treatment of closed mallet finger fractures, J Hand Surg (Am)
30:580–586, 2005.
13. Pratt AL: Is eight weeks’ immobilisation of the distal inter-
phalangeal joint adequate treatment for acute closed mallet
finger injuries of the hand? A critical review of the literature,
Br J Hand Ther 9:4–10, 2004.
14. Schreuders TAR, Soeters JNM, Hovius SER, et al: A modifica-
tion of Elson’s test for the diagnosis of an acute extensor
central slip injury, Br J Hand Ther 11:111–113, 2006.
15. Elson RA: Rupture of the central slip of the extensor hood of
the finger. A test for early diagnosis, J Bone Joint Surg (Br)
68:229–231, 1986.
16. Smith PJ, Ross DA: The central slip tenodesis test for early
diagnosis of potential boutonniere deformities, J Hand Surg
(Br) 19:88–90, 1994.
17. Evans RB: Immediate active short arc motion following exten-
sor tendon repair, Hand Clin 11:483–512, 1995.
18. Crosby CA, Wehbe MA: Early protected motion after extensor
tendon repair, J Hand Surg (Am) 24:1061–1070, 1999.
19. Boscheinen-Morin J, Davey V, Conolly WB: The Hand Funda-
mentals of Therapy, Oxford, 1997, Butterworth-Heinemann.
20. Maddy LS, Meyerdierks EM: Dynamic extension assist splint-
ing of acute central slip lacerations, J Hand Ther 10:206–212,
1997.
21. O’Dwyer FG, Quinton DN: Early mobilisation of acute
middle slip injuries, J Hand Surg (Br) 15:404–406, 1990.
22. Walsh MT, Rinehimer W, Muntzer E, et al: Early controlled
motion with dynamic splinting versus static splinting for
zones III and IV extensor tendon lacerations: A preliminary
report, J Hand Ther 7:232–236, 1994.
23. Thomes LJ, Thomes BJ: Early mobilization method for surgi-
cally repaired zone III extensor tendons, J Hand Ther 8:195–
198, 1995.
24. Schreuders TAR, Soeters JNM, Augustijn WA, et al: Dynamic
extension splint: Rotterdam design, J Hand Ther 10:240–241,
1997.
25. Schreuders TAR, Soeters JNM, Augustijn WA, et al: Develop-
ment of extensor lag in treating boutonniere deformity [letter;
comment], J Hand Ther 9:415, 1996.
26. Evans RB, Thompson DE: The application of force to the
healing tendon, J Hand Ther 6:266–284, 1993.
27. Hung LK, Chan A, Chang J, et al: Early controlled active
mobilization with dynamic splintage for treatment of exten-
sor tendon injuries, J Hand Surg (Am) 15:251–257, 1990.
28. Saldana MJ, Choban S, Westerbeck P, et al: Results of acute
zone III extensor tendon injuries treated with dynamic exten-
sion splinting, J Hand Surg (Am) 16:1145–1150, 1991.
29. Newport ML: Zone I-V extensor tendon repair, Tech Hand Up
Extrem Surg 2:50–55, 1998.
30. Howell JW, Merritt WH, Robinson SJ: Immediate controlled
active motion following zone 4–7 extensor tendon repair,
J Hand Ther 18:182–190, 2005.
31. Sylaidis P, Youatt M, Logan A: Early active mobilization for
extensor tendon injuries. The Norwich regimen, J Hand Surg
(Br) 22:594–596, 1997.
32. Bulstrode NW, Burr N, Pratt AL, et al: Extensor tendon reha-
bilitation a prospective trial comparing three rehabilitation
regimes, J Hand Surg (Br) 30:175–179, 2005.
33. Chester DL, Beale S, Beveridge L, et al: A prospective, con-
trolled, randomized trial comparing early active extension
with passive extension using a dynamic splint in the rehabili-
tation of repaired extensor tendons, J Hand Surg (Br) 27:283–
288, 2002.
34. Khandwala AR, Webb J, Harris SB, et al: A comparison of
dynamic extension splinting and controlled active mobiliza-
tion of complete divisions of extensor tendons in zones 5 and
6, J Hand Surg (Br) 25:140–146, 2000.
35. Russell RC, Jones M, Grobbelaar A: Extensor tendon repair:
mobilise or splint? Chir Main 22:19–23, 2003.
36. Ip WY, Chow SP: Results of dynamic splintage following
extensor tendon repair, J Hand Surg (Br) 22:283–287, 1997.
37. Kerr CD, Burczak JR: Dynamic traction after extensor tendon
repair in zones 6, 7, and 8: A retrospective study, J Hand Surg
(Br) 14:21–22, 1989.
38. Newport ML, Blair WF, Steyers CM Jr: Long-term results
of extensor tendon repair, J Hand Surg (Am) 15:961–966,
1990.
39. Blair WF, Steyers CM: Extensor tendon injuries, Orthop Clin
North Am 23:141–148, 1992.
40. Slater RR Jr, Bynum DK: Simplified functional splinting
after extensor tenorrhaphy, J Hand Surg (Am) 22:445–451,
1997.
41. Stuart D, Zambia L: Duration of splinting after repair of
extensor tendons in the hand, J Bone Joint Surg (Br) 47:72–79,
1965.
42. Dargan EL: Management of extensor tendon injuries of the
hand, Surg Gynecol Obstet 128:1269–1273, 1969.
43. Soni P, Stern CA, Foreman KB, et al: Advances in extensor
tendon diagnosis and therapy, Plast Reconstr Surg 123:727–
728, 2009.
44. Josty IC, MacQuillan AH, Murison MS: Functional outcomes
following surgical repair of wrist extensor tendons, Br J Plast
Surg 56:120–124, 2003.
45. Mowlavi A, Burns M, Brown RE: Dynamic versus static splint-
ing of simple zone V and zone VI extensor tendon repairs: A
prospective, randomized, controlled study, Plast Reconstr Surg
115:482–487, 2005.
46. Elliot D, Southgate CM: New concepts in managing the long
tendons of the thumb after primary repair, J Hand Ther
18:141–156, 2005.
47. Browne EZ Jr, Ribik CA: Early dynamic splinting for extensor
tendon injuries, J Hand Surg (Am) 14:72–76, 1989.
48. Chinchalkar SJ: Dynamic splinting for the repair of the first
extensor compartment tendons, J Hand Ther 21:292–296,
2008.
49. Talsma E, de Haart M, Beelen A, et al: The effect of mobiliza-
tion on repaired extensor tendon injuries of the hand: A sys-
tematic review, Arch Phys Med Rehabil 89:2366–2372, 2008.
Appendix 1 
Therapy Protocols After Extensor Tendon
Repairs: St Andrew’s Centre for Plastic
Surgery, Broomfield Hospital, Chelmsford,
Essex, UK
EXTENSOR TENDON REPAIRS
OF THE FINGERS
(i) Zones 5–8
(ii) Zone 9 with good strong repair of the intramuscular
tendon.
1. Theatre
POP Palmar (volar) splint applied after tendon
repair(s)—
Wrist −30°
MCPs +40°
PIP 0°
DIP 0°
2. 0–5 days (Week 1)
Rest in POP splint for 5 days. (Week 1)
Elevate hand above elbow at all times.
Shoulder and elbow exercises 5×5 per day (5 exer-
cises 5 times per day).
3. 6–13 Days (Weeks 1 and 2)
Day 6—Fabricate thermoplastic splint with same
joint angle of the MCP (+40°) but with splint only
extending distally to just proximal to the PIP joints.
X10 hourly—extend to MCP 0°+PIP 0° +DIP 0°,
passively extend fingers to MCP 0°+PIP 0° +DIP 0°
if there is extension lag,
then actively flex MCPs back to +40°,
then actively fully flex the PIP and DIP joints to full
flexion of both over the end of the splint.
Continue to elevate hand above elbow at all times.
Continue shoulder and elbow exercises 5×5 per day
(5 exercises 5 times per day).
X5 hourly—full thumb active flexion and extension.
X5 hourly—full forearm active supination and
pronation.
Adjust pain control as necessary to allow this regime.
Hygiene and splint check at 7 days and 14 days.
4. 14–28 Days (Weeks 3 and 4)
Day 14—Remold splint so MCP +70°.
X10 hourly—extend to MCP 0°+PIP 0° +DIP 0°,
(passively extend fingers to MCP 0°+PIP 0° +DIP 0°
if there is lag, and,
if lag persisting, fabricate splint for night wear at MCP
0°+PIP 0° +DIP 0°),
then actively flex MCPs back to +70°,
then actively fully flex the PIP and DIP joints to full
flexion of both over the end of the splint.
Continue to elevate hand above elbow at all times.
Continue shoulder and elbow exercises 5×5 per day
(5 exercises 5 times per day).
Continue X5 hourly—full thumb active flexion and
extension.
Continue X5 hourly—full forearm active supination
and pronation.
Hygiene and splint check at 21 and 28 days.
Ultrasound if necessary from week 3.
5. 28+ Days (4–8 weeks)
X10 hourly—full active flexion and extension of all
joints of fingers without splint.
X10 hourly—active wrist flexion and extension
exercises with the fingers relaxed (fingers in the
position of the fingers in the wrist tenodesis maneu-
ver—wrist flexion with fingers loosely extended and
wrist flexion with fingers loosely flexed).
Also start active radial and ulnar wrist movements.
Passive extension of wrist and fingers to neutral.
Gradually increase active combined wrist and finger
extension as comfortable.
Add active combined wrist and digit flexion exercises
at 6 weeks post-op if needed.
MCPs +70° splint worn at night and in busy places
to 8 weeks.
Continue shoulder and elbow exercises 5×5 per day
(5 exercises 5 times per day).
438.e1
438.e2 Section 5:  Rehabilitation of Tendon Surgery

Continue X5 hourly – full thumb active flexion and
extension + add active thumb abduction/adduc-
tion/opposition.
Continue X5 hourly – full forearm active supination
and pronation
From 4 weeks – light hand use but not lifting any-
thing more than 150 gm (6oz) = a full yogurt pot
6. 8 weeks onwards
Continue all exercises as above.
Passive finger flexion if required.
Dynamic flexion splinting if required.
From 8 weeks – return to light work and driving.
From 12 weeks – return to heavy work and contact
sports.
If there is extensor tendon tethering – forced passive
flexion exercises + massage dorsal skin of digit and
dorsum of hand with finger held in flexion +
ultrasound.

In Theatre Days 0–5 Week 1 Days 6–13 Weeks 1–2 Days 14 -28 Weeks 3–4 Day 28+ Weeks 4–8
POP Rest in POP splint Thermoplastic   Thermoplastic   Thermoplastic + 70°
Palmar Splint Splint to PIP level Splint to PIP level Splint to PIP level as
Made day 6 adjusted day 14 weeks 3/4
Wrist  −30° Wrist  −30° Wrist  −30° Wrist  −30° Splint only worn
MCPs  +40° MCPs  +40° MCPs  +40° MCPs  +70° at night and in busy
PIP 0°  DIP 0° PIP 0°  DIP 0° PIP 0°  DIP 0° PIP 0°  DIP 0° places
Fingers— Fingers— X10 hourly X10 hourly X10 hourly—full active
No movement No movement Full active extn. Full active extn. flexion and extension of
x 3 joints then x 3 joints then all joints of fingers
MCP flexn. + 40° MCP flexn. + 70° without splint
PIP/DIP flexn. full PIP/DIP flexn. full
Passively extend joints Passively extend joints to X10 hourly—full active
to neutral if necessary neutral if necessary wrist flexn. and
extension exercises with
the fingers relaxed
If lag persists, fit night From 4 weeks light hand
splint with all joints use—less than 150 gm
straight (full yogurt pot)
Elevate hand Elevate hand above Elevate hand above From 8 weeks—light
above elbow elbow elbow work/driving
Shoulder exercises Shoulder exercises 5x5 Shoulder exercises 5x5 From 12 weeks—heavy
5x5 times per day times per day times per day work/contact sports.
Elbow exercises Elbow exercises 5x5 Elbow exercises 5x5
5x5 times per day times per day times per day
X5 hourly—full thumb X5 hourly—full thumb
active flexion/extension active flexion/extension
X5 hourly—full forearm X5 hourly—full forearm
active supin./pronation active supin./pronation
Adjust pain control as Adjust pain control as
necessary necessary
Hygiene and splint Hygiene and splint
checks—7 & 14 days checks—21 & 28 days
Ultrasound if necessary
from week 3
Appendix 2 
Therapy Protocols After Extensor Tendon
Repair of the Thumb: St Andrew’s Centre
for Plastic Surgery, Broomfield Hospital,
Chelmsford, Essex, UK
Zones 1–4
1. Theatre
POP Palmar (volar) splint applied after tendon
repair(s)—
Wrist −30°
MCP 0°
IP 0°
2. 0–5 days (Week 1)
Rest in POP palmar (volar) splint for 5 days. (Week 1)
Elevate hand above elbow at all times.
Shoulder and elbow exercises 5×5 per day (5 exer-
cises 5 times per day).
3. 5–7 Days (Week 1)
Day 6—Fabricate thermoplastic dorsal dynamic
extension splint with same joint angle of the wrist
and thumb MCP and with the splint lifting off the
thumb at the mid-proximal phalangeal level so
that a sling can be attached around the distal pha-
langeal palmar (volar) surface.
When resting, the sling remains around the distal
phalanx.
X5 hourly, slide sling back under the proximal
phalanx and actively flex and extend the IP joint
alone.
X5 hourly, actively flex and extend the MCP joint
alone, with the sling under the distal phalanx and
the base of the thumb supported with the other
hand. Aim thumb tip for the base of the middle
finger during this maneuver.
Elevate hand above elbow at all times.
Shoulder and elbow exercises 5×5 per day (5 exer-
cises 5 times per day).
Full active pronation and supination of the forearm
5×5 per day.
Full active flexion and extension of all fingers 5×5 per
day.
Adjust pain control as necessary to allow this regime.
4. 7–14 Days (Week 2)
When resting, the sling remains around the distal
phalanx.
X5 hourly, slide sling back under the proximal
phalanx and actively flex and extend both MCP
and IP joints together, aiming for the base of the
ring finger ×10 hourly (may need to support the
base of the thumb).
Elevate hand above elbow at all times.
Shoulder and elbow exercises 5×5 per day (5 exer-
cises 5 times per day).
Full active pronation and supination of the forearm
5×5 per day.
Full active flexion and extension of all fingers 5×5 per
day.
Adjust pain control as necessary to allow this regime.
Hygiene and splint check at 7 days and 14 days.
5. 14–28 Days (2–4 Weeks)
Active combined MCP and IP flexion/opposition,
aiming for the base of the little finger ×10 hourly
(may need to support the base of the thumb).
Ultrasound from week 3 if needed.
Elevate hand above elbow at all times.
Shoulder and elbow exercises 5×5 per day (5 exer-
cises 5 times per day).
Full active pronation and supination of the forearm
5×5 per day.
Full active flexion and extension of all fingers 5x5 per
day.
Adjust pain control as necessary to allow this regime.
Hygiene and splint check at 21 days and 28 days.
6. 28+ Days (4–8 Weeks)
Continue X10 hourly—active combined MCP and IP
flexion/opposition, aiming for the base of the little
finger x10 hourly (may need to support the base of
the thumb)
+ add active thumb abduction/adduction/
opposition.
438.e3
438.e4 Section 5:  Rehabilitation of Tendon Surgery

X10 hourly—active wrist flexion and extension exer-
cises with the fingers relaxed (fingers in the posi-
tion of the fingers in the wrist tenodesis
manoeuvre—wrist flexion with fingers loosely
extended and wrist flexion with fingers loosely
flexed).
Also start active radial and ulnar wrist movements.
Passive extension of wrist and fingers to neutral.
Gradually increase active combined wrist and finger
extension as comfortable.
Add active combined wrist and digit flexion exercises
at 6 weeks post-op if needed.
Thumb splint worn at night and in busy places to 8
weeks.
Shoulder and elbow exercises 5×5 per day (5 exer-
cises 5 times per day).
Full active flexion and extension of fingers 5×5 per day.
Full forearm active supination and pronation 5×5 per
day.
From 4 weeks – light hand use but not lifting any-
thing more than 150 gm (6oz) = a full yogurt pot.
7. 8 weeks onwards
Continue all exercises as above.
Passive finger flexion if required.
Dynamic flexion splinting if required.
From 8 weeks – return to light work and driving.
From 12 weeks – return to heavy work and contact
sports.
If there is extensor tendon tethering – forced passive
flexion exercises + massage dorsal skin of digit and
dorsum of hand with finger held in flexion +
ultrasound.

Days 0–5 Days 5–7 Days 7–14 Days 15–28

In Theatre Week 1 Weeks 1–2 Weeks 1–2 Weeks 3–4 Day 28+ Weeks 4–8
POP Rest in POP Thermoplastic Thermoplastic Thermoplastic Splint only worn at night/in
Palmar Splint Splint Splint fitted on Splint worn at Splint worn at busy places
day 6* all times all times
Wrist  −30° Wrist  −30° Wrist  −30° Wrist  −30° Wrist  −30° Wrist  −30°
MCP  0° MCP  0° MCP  0° MCP  0° MCP  0° MCP  0°
IP  0° IP  0° IP  0° IP  0° IP  0° IP  0°
X5 per hr X5 per hr X10 per hr X10 per hr
Thumb Thumb Thumb Thumb Exercises****
Exercises** Exercises*** Exercises****
Ultrasound from + add active abd/add/opp.
week 3 as nec.
Elevate hand Elevate hand Elevate hand Elevate hand Elevate hand above elbow
above elbow above elbow above elbow above elbow
Adjust pain
control as nec.
Finger Finger Finger Finger Finger Finger
Exercises Shoulder Shoulder Shoulder Shoulder Shoulder
immediately Elbow Elbow Elbow Elbow Elbow
Forearm Forearm Forearm Forearm Forearm
exercises Exercises Exercises Exercises Exercises
5x5 times daily 5x5 times daily 5x5 times daily 5x5 times daily 5x5 times daily
X10 hourly—full active wrist
movements with fingers relaxed
Hygiene/Splint Hygiene/Splint Increased Activity*****
Checks–7&14d Checks-21&28d
*The Thermoplastic Dorsal Dynamic Extension Splint is made with the same joint angles of the wrist and thumb MCP and with the splint
lifting off the thumb at the mid-proximal phalangeal level so that a sling can be attached around the distal phalangeal palmar (volar)
surface. When resting, the sling remains around the distal phalanx.
**Five times hourly, the sling is slid proximally, under the proximal phalanx, and the IP joint alone actively flexed and extended. Five times
hourly, the MCP joint alone is actively flexed and extended, with the sling under the distal phalanx and the base of the thumb supported
with the other hand. The thumb tip is aimed for the base of the middle finger during this maneuver.
***Five times hourly, the sling is slid proximally, under the proximal phalanx, and both the MCP and the IP joint are actively flexed and
extended, with the thumb tip aimed for the base of the ring finger.
****Ten times hourly, the sling is slid proximally, under the proximal phalanx, and both the MCP and the IP joint are actively flexed and
extended, with the thumb tip aimed for the base of the little finger. After 28 days, the same exercises are continued without the splint.
*****From 4 weeks light hand use—less than 150 gm (full yogurt pot).
From 8 weeks—light work/driving.
From 12 weeks—heavy work/contact sports.
Appendix 3 
Therapy Protocols After Extensor Tendon
Repairs of Fingers: Mid Essex Hospital
Services, St Andrew’s Centre-Hand
Therapy, Essex, UK

ST ANDREW’S CENTRE – HAND THERAPY

EXTENSOR TENDON REPAIRS – FINGERS

Stone Splint – Weeks One to Four

This splint is to reduce the risk of the tendon(s) rupturing.

Weeks 1-4. A plastic splint will be made approximately 5 – 7 days after surgery. It is worn
continuously (24 hours) until 4 weeks after your surgery during which time you must
exercise your hand as instructed by your therapist. Do not use your hand, even unaffected
finger(s) and thumb.

Weeks 4-8. The splint is then worn for a further 4 weeks at night and when you are in
crowded places (e.g., shopping, using public transport). Do not drive until 8 weeks following
surgery. Your tendons are not strong enough and your insurance is invalid because of
your hand injury.

At 4 weeks after surgery you can begin to use your hand for very light activities only, not
lifting anything heavier than 6oz (150 grams) (e.g., yogurt pot).

At 8 weeks after surgery you can return to light work and driving.
From week 12 onwards you can return to heavy work after advice from your the surgeon
and the therapist.

EXERCISES FOR THE FIRST WEEK

You are required, as part of your treatment, to exercise as directed by your therapist
within the splint.

By gently exercising your hand, as instructed, these tendons will heal and are less likely to
become stuck or tightly caught in the scar.

1. Elbow and shoulder exercises – see separate sheet.

2. Straighten your thumb fully then bend it across your palm.

Repeat slowly 10 x each hour.

438.e5
438.e6 Section 5:  Rehabilitation of Tendon Surgery

3. Bend your fingers at all joints over the edge of the splint.
DO NOT push with other hand.

Then fully straighten your fingers.

The therapist may ask you to assist by straightening your fingers with your other hand.
Repeat slowly 10 x each hour.

• DO NOT bend or grip strongly with your fingers/thumb.

• DO NOT try to pick anything up with your injured hand.
• DO NOT let your hand hang down.
• DO NOT remove any of the splint or bandages. If you take the splint off against our
advice and it is lost or left at home, it will not be replaced!

You should ring us if:

• You feel pain, swelling, or discomfort
• The splint feels loose or is not fitting well
• You have any worries

Make sure you bring the splint with you to every appointment.

If any problems do occur please telephone the Hand Therapy Department at

01245 516009 between 8:30 a.m. and 2:00 p.m. Monday to Friday, ask for _____________.
It is very important that your hand and splint are checked by your therapist regularly.
It is your responsibility to attend your appointment.
Please telephone to cancel or change appointments.
 Chapter 40:  State of the Art of Extensor Tendon Rehabilitation 438.e7

ST ANDREW’S CENTRE – HAND THERAPY

EXTENSOR TENDON REPAIRS – FINGERS

Stone Splint - Weeks Four to Eight

You must continue to use your splint for protection (i.e., at night, outside the house, and at
times when your hand may get accidentally knocked) (e.g. by dogs, cats, and young
children).

Light activities can be started, you can lift 6 oz/150grams (e.g., a small yogurt pot), but
avoid straining (e.g., tying shoe laces, pulling on tight clothing/belts, tight taps, tops of
bottles, door handles).

EXERCISES

1. Continue all your hand exercises hourly, out of the splint (as advised by your
therapist).

2. Gently bend your wrist forwards with your fingers relaxed and straight. Hold for 5
seconds.

Gently bend your wrist backwards, keeping your fingers relaxed and slightly bent.
DO NOT push. Hold for 5 seconds.

Repeat slowly 10x each hour.

Make sure you bring the splint with you to every appointment.

If any problems do occur please telephone the Hand Therapy Department at

01245 516009 between 8:30 a.m. and 2:00 p.m. Monday to Friday, ask for _____________.
It is very important that your hand and splint are checked by your therapist regularly.
It is your responsibility to attend your appointment.
Please telephone to cancel or change appointments.
 Appendix 4 
The Manchester Regimen for
Postoperative Rehabilitation After Finger
Extensor Tendon Repairs, Manchester, UK

Timing Regimen
Zone 1 tendon avulsion, tear, avulsion-fracture, zone 1–2 surgical repair
Week 1 • Apply thermoplastic splint to immobilize DIP joint in full extension or slight hyperextension to be worn
full time.
• No active or passive DIP joint motion.
• Monitor regularly and ensure skin hygiene and compliance.
Week 6 • Following surgical repairs and avulsion fractures wean from splint at 6 weeks slowly over 2 weeks and
commence active DIP joint flexion and extension exercises.
Week 8 • After tendon avulsion and substance tears wean from splint at 8 weeks slowly over 2 weeks and
commence active DIP joint flexion and extension exercises if good active extension.
Week 12 • Continue to wear splint at night until 12 weeks.
• Commence passive flexion stretch at 12 weeks if flexion slow to recover.
Zone 3 and distal zone 4 surgical repair
Week 1 • Apply thermoplastic cylinder or gutter splint to immobilize DIP and PIP joint in full extension.
Week 2 • If lateral bands are uninjured shorten splint to allow active and passive DIP joint flexion and extension
exercises.
• No PIP joint flexion until 3 weeks.
Week 3 • Continue with splint but remove to commence 0°–30° active PIP joint flexion and extension exercises.
10 repetitions hourly progressing to 20 repetitions when comfortable.
• Continue DIP joint exercises in splint.
Week 4 • Progress to 0°–40° active PIP joint flexion if there is no loss of active extension. 20 repetitions every 2
hours replacing cylinder splint between exercise periods.
• Continue DIP joint exercises.
Week 5 • Progress to 0°–50° active PIP joint flexion. Continue with splint.
Week 6 • Remove splint and commence light functional activity and free active PIP and DIP joint flexion and
extension exercises.
• Continue with cylinder splint at night in presence of extensor lag.
• Commence passive flexion stretching.
Week 12 • Return to normal activity.
Zone 4 (proximal), 5, and 6 surgical repair
Week 1 • Apply 2 part thermoplastic forearm based splint. Wrist in 45° extension, MCP joints 0°, IP joints in full
extension. Include only affected digits but in Zone 6 include adjacent digit if tendon linked by juncturae.
Removable digital plate allows IP joint flexion and extension exercises (Figures 40-10 and 40-11).
• Commence active IP joint flexion and extension exercises. 10 repetitions hourly. Digital plate to be
replaced between exercises periods.

438.e8
 Chapter 40:  State of the Art of Extensor Tendon Rehabilitation 438.e9

Timing Regimen
Week 3–6 • Remove splint every 2 hours and commence active wrist flexion and extension exercises with digits
relaxed. Commence active MCP joint flexion and extension with wrist in flexion and IP joints extended.
Continue active IP joint flexion and extension exercises with MCP joints at 0°. 10 repetitions each
exercise. No composite flexion until 6 weeks.
Week 6 • Remove splint and commence composite flexion and extension exercises. Commence composite passive
flexion stretching. Allow light functional activity.
• Continue to wear splint at night in cases of extension loss.
• Return to normal activity once composite flexion regained.
Zone 7
Week 1 • Apply 2 part thermoplastic forearm based splint. Wrist in 21° extension, MCP joints 0°, IP joints in full
extension. Removable digital plate allows IP joint flexion and extension exercises.
• During weeks 1 and 2 IP joint flexion and extension exercises performed. 10 repetitions hourly.
Week 3–6 • Remove splint every 2 hours and commence gentle wrist motion with digits relaxed. No forced wrist
flexion.
• Commence active MCP joint flexion and extension with wrist at 0°.
• Continue IP joint active flexion and extension with MCP joints at 0°. 10 repetitions each exercise. No
composite flexion until 6 weeks.
Week 6 • Remove splint and commence composite flexion and extension exercises.
• Commence composite passive flexion stretching.
• Commence light functional activity.
• Continue to splint at night in presence of extensor lag.
Week 12 • Return to normal activity.
Zone 8
Week 1 • In combination tendon and muscle belly injuries or muscle bellies only apply high forearm based
thermoplastic splint. Wrist 45° extension. MCP joints 0°. IP joints in full extension. Immobilize for  
3 weeks.
Week 3 • For muscle bellies only remove splint and commence slow return to composite flexion.
• In cases of concomitant wrist tendon injury at 3 weeks reduce splint to allow unimpeded active MCP
and IP joint flexion and extension exercises. Remove splint 2 hourly for careful active wrist flexion and
extension exercises. 10 repetitions hourly.
Week 6 • Remove splint and commence composite active flexion and extension exercises.
• Commence composite passive flexion stretching.
Week 12 • Return to normal activity.

The Manchester Regimen for the Postoperative Rehabilitation Following Surgical Repair of Extensor Pollicis
Longus: Manchester, UK
Timing Regimen
Zone T—1 surgical repair, avulsion fracture, and substance tear if treated conservatively
Week 1 • Apply thermoplastic splint to immobilize the IP joint only in full extension. To be worn full time for  
6 weeks for avulsion fracture and post surgical repair and 8 weeks for substance tear.
• No active IP joint flexion or extension.
• Monitor regularly and ensure skin hygiene and compliance.
Week 6 • Following surgical repairs or avulsion fracture with large fragment wean from splint slowly over 2
weeks and commence 0°–30° active IP joint flexion and extension exercises. Gradually increase
range of active IP joint flexion if there is no loss of active extension.
• No passive flexion stretch.
• In avulsion or substance tear continue with splint.
438.e10 Section 5:  Rehabilitation of Tendon Surgery

Timing Regimen
Week 8 • Following avulsion or substance tear wean from splint slowly over 2 weeks and commence active IP
joint flexion and extension exercises. Gradually increase range of IP joint flexion if there is no loss of
active extension.
• No passive flexion stretch.
• All types to continue with splint at night in presence of extensor lag.
Week 12 • All types commence passive flexion stretch if required.
• All types return to normal activity.
Zone T—2 post surgical repair
Week 1 • Apply thermoplastic splint forearm splint with MP and IP joint in 0°. Thumb comfortably abducted
and extended.
Week 3 • Modify splint adding removable plate to commence 0°–30° active IP joint flexion and extension
exercises. 10 repetitions hourly.
Week 3–5 • Splint to be worn full time.
• Progress active IP joint flexion exercises increasing slowly 0°–60°.
Week 5 • Remove splint and commence light function. Increase active flexion and extension exercises.
• Continue with splint at night in presence of extensor lag.
Week 6 • Commence passive flexion stretch if required.
Weeks 10–12 • Return to normal activity.
Zones T—3–5 post surgical repair
Week 1 • Apply 2 part forearm based thermoplastic splint with wrist at 30°, MCP and IP joint at 0°. Thumb
comfortably abducted and extended. Removable plate to allow 0°–60° IP joint flexion and extension
exercises (Figs. 40-4, 40-5, and 40-6).
• Commence IP joint active flexion and extension exercises progressing to 60° flexion during the first  
3 weeks.
• No passive flexion stretch.
• Splint to be worn full time and immobilize at night.
Week 3 • Remove splint to perform careful wrist flexion and extension with thumb relaxed to encourage
tenodesis action and promote tendon glide especially in Zone T5 where there is risk of adhesions
under retinaculum.
Week 5 • Remove splint continue with active IP joint flexion and extension exercises.
• Commence composite active MCP and IP joint motion to restore opposition.
• Continue to wear splint at night in presence of extensor lag.
Week 6 • Commence passive flexion stretch if slow to regain flexion.
Weeks 10–12 • Return to normal activity.
Appendix 5 
Protocols of Exercise After Repair
of Extensor Tendon Injuries,
Queen Mary Hospital, The University
of Hong Kong, Hong Kong, China

Day Rehabilitation Program

Day 0 Extensor tendon injury rehabilitation program
Operation
Day 2 Dressing changed
Extension dynamic splint (Fig. 2) applied in occupational therapy department
Position: wrist 30° extension. MPJ and PIPJ full extension
Exercise program by physiotherapists
a. passive extension of MPJ and IPJ
b. active flexion of MPJ to 30°. IPJ to full flexion 1 against resistance of dynamic bands (with broad finger
straps at middle phalanx) 10 times hourly
c. no active extension
Discharged from hospital to hand class for alternate day treatment
Day 7 Splint adjusted to allow MPJ active flexion to 45° against traction system
Day 14 Splint adjusted to allow MPJ active flexion 1 to 60° against traction system
Sutures removed
Day 21 Splint adjusted to allow full active flexion of MPJ
Day 28 Should be able to regain full grip within splint
Day 35 Off splint
Exercise program
a. free active flexion and extension of fingers
b. gentle passive flexion of fingers
c. strong passive extension of fingers
d. wrist mobilization
Week 7 Active flexion and extension of finger against resistance
Passive flexion and extension of fingers
Gradual simultaneous active finger and wrist flexion
Week 8 Strengthening exercise

438.e11
 Appendix 6 
Extensor Tendon Rehabilitation Program, Queen
Mary Hospital, The University of Hong Kong,
Hong Kong, China

Zone IV → VIII
Thumb Zone I → V

Date *D1 1/52 *D8 2/52 *D15 3/52 *D22 4/52 *D29 5/52 *D36 6/52 *D43 7/52 *D50 8/52
Splintage Wrist 30° ext. Wrist 30° Wrist 30° Wrist 30° Wrist 30° ext. Off splint for wrist mobilization
MCP 15°–30° ext. ext. ext. *Off outrigger
+ outrigger MCP MCP MCP 0°
(dynamic band 15°–45° 15°–60° - full
at MP level, IP + outrigger + outrigger + outrigger
fully ext)
Active Extension No active fingers extension is allowed Free active fingers Free active Gentle Strong resistive
Movement extension within fingers resistive extension
cock up splint extension extension→
Flexion Active fingers flexion within splint & outrigger 10 times Free active fingers Free active Resistive Strong resistive
hourly flexion within fingers fingers flexion
cock up splint flexion flexion→
Passive Extension Passive extension of MCP & IPJs within the splint Strong passive extension of fingers
Movement
Flexion No passion flexion of fingers is allowed Gentle Strong Allow simultaneous
passive passive passive flexion of
flexion of flexion of fingers & wrist
fingers fingers
Remarks D14 Off Pressure Glove for scar as Work rehab in Occ
Stitches indicated Therapy as indicated
Appendix 7 
Therapy Protocols After Extensor Tendon
Repair, Springfield, Mass, USA
Zone of
Injury Immobilization
1–2 • 6–8 weeks full-time DIP
extension cylinder cast or
splint if not pinned.
• Gradually wean out of splint
(first for exercise only, then for
increasing time) and initiate
active flexion and extension.
3–4 • 3 weeks in IP extension if
referred too late for early
mobilization.
• Wean out of splint as above
and initiate AROM.
• Focus on full extension and
initiate passive flexion
cautiously after 7 weeks.
5–6 • 3 weeks in wrist and IP
extension, 15–20° MP flexion.
May leave IPs free for Zone 6.
• Wean out of splint as above
and initiate AROM. Focus on
attaining full extension while
increasing MP and composite
flexion.
7 • 3 weeks wrist extension and
15–20° MP flexion.
• Wean out of splint and initiate
active ROM. Focus on
differential glide between
extensors.
Passive Mobilization
— —
• Prefer not to use – if patient
can perform, can probably
also do well with Short Arc
Motion (SAM) (Evans, 1992).
• See Active Mobilization.
• 3 weeks in dynamic
extension splint with wrist at
40–45° and active flexion
without block to flexion
(similar to Evans and
Burkhalter, 1986).
• Wean out of splint and
initiate AROM.
• Prefer Immediate Controlled
Active Mobilization (ICAM)
(see Active Mobilization)
when a border digit not
involved.
• None for wrist extensors.
• Dynamic extension as for
Zones 5–6.
Active Mobilization
• 4 weeks Short Arc Motion (SAM)
with resting splint full extension,
exercise template splint allowing
30° PIP flexion (Evans, 1992).
• Modify exercise splint to increase
allowed PIP flexion weekly, and
discontinue at 4 weeks.
• Except for border digits, Immediate
Controlled Active Mobilization
(ICAM) (Howell et al, 2005).
• 1st 3 weeks: Yoke splint holding
MP(s) of involved finger(s) in
15–20° greater extension relative
to adjacent uninjured fingers.
Worn with separate 20–25° wrist
extension splint. Full motion as
allowed by splints.
• From 3–5 weeks wean out of wrist
splint and initiate wrist ROM
slowly.
• 5–7 weeks, yoke splint only.
Discontinue by 7 weeks.
• None for wrist extensors. For
digits, have considered but not
tried Evans (2002) combination of
dynamic extension with protected
short arc active extension in
therapy only.
438.e13
438.e14 Section 5:  Rehabilitation of Tendon Surgery

Zone of
Injury Immobilization Passive Mobilization Active Mobilization
T-1 • As for Zones 1–2 (IP extension • 3–5 weeks dynamic thumb —
fulltime 6–8 weeks). Wean out extension with MP extension
of splint slowly and initiate block, outrigger cuff at DIP
AROM. joint (Elliot, 2005).
• Blocked MP and IP flexion
first week.
• Thumb opposition to middle
finger tip second week.
• Full opposition third week.
Wean out of splint thereafter
as indicated.
T-2 to • 3 weeks in wrist extension, • Dynamic thumb extension —
5 thumb in extension and with MP extension block
abduction as determined by (Elliot, 2005). Protocol above
structures repaired.

References
Elliot D, Southgate CM: New concepts in managing the long
tendons of the thumb after primary repair. J Hand Ther 18:
141–156, 2005.
Evans R, Thompson D: An analysis of factors that support early
active short arc motion of the repaired central slip. J Hand Ther
5:187–201, 1992.
Evans RB: Clinical management of extensor tendon injuries. Reha-
bilitation of the Hand and Upper Extremity. E. J. Mackin, A. D.
Callahan, T. M. Skirven, L. H. Schneider and A. L. Osterman.
St. Louis, C.V. Mosby. 1: 542–582, 2002.
Evans RB, Burkhalter WE: A study of the dynamic anatomy of
extensor tendons and implications for treatment. J Hand Surg
(Am) 11:774–779, 1986.
Howell JW, Merritt WH, Robinson SJ: Immediate controlled active
motion following zone 4–7 extensor tendon repair. J Hand
Ther 18:182–190, 2005.
Appendix 8 
Protocols of Sydney Hand Therapy &
Rehabilitation Centre, Sydney, Australia

Exercises Out Time in

Zone Protocol Type Splint Exercises in Splint of Splint Therapy
3–4 SAM Splint position: Full extension, Immediately start Generally this is Total time in
template splints or other exercises following started at 6 therapy is
devices to limit flexion SAM protocol as weeks, but may be about 3
initially to 30 degrees. described by Evans. sooner at 4 weeks months, if
Some cases (e.g., crush Avoid stress on repair if the joint is stiff, difficulties
injuries) may switch to for 6 weeks. always monitoring maybe 4
Capener at 2 or 4 weeks. However if the to ensure months.
Splint stays on for: 6 weeks, joint is stiff and extension to 0 is
splinting may be longer   thick and glide maintained.
if there is a lag and the poor more vigorous Graded resisted
splint may be changed to exercises may be exercises are
Capener or neoprene in the commenced at 4 commenced  
day and static digit at night weeks. week 6.
Comments We use a “custom made” Capener that has very low tension (less than 300 g) that can be adjusted and
measured in order to facilitate the therapy program for Zone 3 PIP joint level injuries. Sometimes this works
better than taking splints on and off, but not always. An OFF the shelf Capener is ENTIRELY NOT appropriate
as they are all too strong (600 g plus). It is good to have some different options for different or difficult
situations.
Zone 5–6 Merrit or Merrit: Exercises as As described in the Total time in
Norwich Wrist extension splint in 45 described in original articles, therapy
(Depending on deg original articles graded resisted 3–4
referring plus hand piece with involved exercise is months
surgeon) digit 15 deg more commenced at 6
extension than adjacent weeks
digits
Norwich:
POSI type splint with wrist 45
deg ext
MP 45 deg flexion and IPs in
full ext
The splint stays on for 6
weeks and then 2 wks at
night and for travel
Comments The protocols used are generally reported but are sometimes changed depending on the healing of the
tissues, the patients scar and the mobility of the joint(s), and also what the surgeon found at the time of the
repair eg was it tight or was the tendon really mashed up. Also other factors like patient compliance, other
injuries to other structures in the hand can influence the protocol.
Zone 7 Immobilization Wrist in 40 degrees extension Active exercises start More vigorous active Total time in
Splinting is for 6 weeks then at 3 weeks exercises started therapy 3
weaned over 2–4 weeks at 6 weeks months

438.e15
 Appendix 9 
Therapy Protocols from Royal Free
Hampstead NHS Trust, London, UK

Exercises Out Total Time

Zone Protocol Type Splint and Positions Exercises in Splint of Splint in Therapy
3–4 Immobilization for Cylinder splint for PIP Active MCP/DIP 6–8 weeks unless
the first 3 joint which is joint flexion/ complications
weeks then extended, DIP free extension from
controlled unless lateral bands day 1
mobilization repaired PIP joint motion
MCP joint free commenced at
2–3 weeks full time 2–3 weeks as
until edema long as central
controlled and some slip can extend
extension central back to neutral
slip control visible 4–6 weeks increase
From 3–6 weeks   range of PIP joint
splint full time in flexion as long as
extension coming extension good
out for gentle PIP Passive flexion and
joint exercises. Splint commence some
stopped 6 weeks gripping after 6
unless complications weeks
Comments We delay PIP active mobilization protocol slightly especially if the PIP joint is swollen or the wound infected.
Zone 5-6 Active–Norwich Position: First appointment 4 wks post op: 8–10 weeks on
Wrist joint 20 start passive ext exercises out average
extension from splint of splint and
MP 30 flexion unless Active ext from start moving
extension lag noted: splint wrist joint
MCP in extension Active ext fingers Increase flexion
IP neutral from splint and if fingers
Splint full time 4 weeks extension good towards
with exercises within then gentle palm as long
splint flexion of fingers as extension
Splint for protection towards splint good
4-8 weeks as NB patient must be Light activities
required depending able to maintain with hand
on age/occupation/ extension MCP allowed
hand dominance, etc. joints before
Splint week 4–8 flexion is allowed
reducing gradually
Stop splinting at 8 wks

438.e16
 CHAPTER
41  
CURRENT STATUS AND FUTURE
A Current Status and Future of
Flexor Tendon Surgery
Peter C. Amadio, MD
CURRENT STATUS OF FLEXOR
TENDON SURGERY
Tendon surgery has certainly advanced over the past
century. Our repairs are stronger and more reproduc-
ible; most surgeons who deal with these injuries have
had some sort of training in the management of tendon
injuries, and within the past 60 years hand surgery has
developed as a specialty, while within the past 30 years
hand therapy has joined it as a recognized field of spe-
cialization. There are hand surgeons in nearly every
country on the planet; in the larger and more developed
countries, there are literally thousands of trained hand
surgeons and therapists.
One might think that, with all this progress, tendon
injuries would be a solved problem. But, despite our
best efforts, this is not the case. The average result after
surgery restores perhaps 80% of normal finger motion
when both tendons are cut in zone 2, and that assumes
a sharp laceration and a cooperative patient. Ragged
cuts, multiple injuries, and patients who are not able or
willing to cooperate with an early mobilization rehabili-
tation program still frequently end up with adhesions,
ruptures, infections, contractures, and other forms of
unsatisfactory results.
Why is this? Primarily because while our under­
standing of tendon healing, biomechanics, and physiol-
ogy has grown dramatically, our ability to improve
upon Mother Nature remains where it was in Sterling
Bunnell’s day—or, for that matter, Galen’s. We may
sometimes be able to avoid slowing down the healing
process, by better techniques, but we have not yet found
a method to speed things up. And we must face reality—
tendon injuries are most common in those who can
least afford time away from work for rehabilitation and
protection—mostly adolescents and young adults,
mostly male, and mostly in occupations where heavy
use of both hands is an expectation. And, while our
patients are often satisfied with less than normal motion,
for many of them, joint contractures and loss of motion
are unsightly at best, and functionally awkward for
many. In short, while the current state of tendon surgery
is better than it has ever been, it is not nearly as good
as those with injured tendons want it to be.
THE FUTURE OF FLEXOR TENDON SURGERY
What does the future hold for tendon surgery? A good
place to start is current research. These focus on two
general areas—accelerating the pace of tendon healing
and reducing adhesion formation. Along the way,
researchers in both areas must address a common
pitfall—too much load, too soon, will result in tendon
rupture, and a need for the patient to start all over again.
Speeding up tendon healing has already run down
one blind alley: once a tendon is moving, there is no
evidence that more load on a repair speeds healing or
reduces adhesions—all it can do is break the repair.
Thus, the only reason to create ever stronger repairs is
to permit a bit more of a margin of safety for early
mobilization, while at the same time not creating so
much bulk as to impede healing or gliding. In my
opinion, there is little more we can practically do in this
regard—current repairs are “good enough.”
What is needed to shorten tendon healing time? Two
things—cells, and matrix, and these are interrelated,
because making matrix requires cells—specifically,
fibroblasts initially, and then tenocytes. Tendons are not
very cellular, and the cells that are there are often trapped
in a dense collagen matrix. Adding cells from outside
the tendon should help, and there are several studies
now underway in animal models that should be trans-
latable to humans soon, delivering differentiated cells
or stem cells, either via a cell-seeded patch of some sort
between the cut tendon ends, or by literally attaching
the cells to the tendon suture. Add in the right mix of
cytokines, or perhaps even platelet-rich plasma, and we
should be able to develop a cocktail that can cut down
total healing time, and even better, accelerate the early
441
442 Section 6:  Current Status and Future
healing phase, so that repair strength grows faster in the
first few weeks, when the repair is in greatest jeopardy.
Reducing adhesions has always been possible, but at
a price—aggressive mobilization may result in tendon
rupture, and adhesion barriers are usually also healing
barriers. New research into more permeable barrier,
and ones that biodegrade over the critical first week
or two, when most adhesions begin to form, may do
the trick.
Finally, what to do when no tendon is available,
due to extensive injury, tumor resection, or some other
B Current Status and Future
Robert Savage, MB, FRCS, FRCS Ed Orth, MS
A reasonable starting point for considering the future
for tendon surgery would be to consolidate what we
know of best practice today, and to ensure that this
knowledge is as widely known as possible. Other chap-
ters in this book cover this in detail and as previously
reported in surgical history practitioners will choose
which bits of advice are most believable and applicable.
There now appears to be very strong evidence that mul-
tistrand tendon repairs give a more reliable outcome to
acute tendon division. Hopefully, the use of two-strand
core sutures is diminishing for it appears important that
at least a four-strand core suture should be used. This
should be combined with, at least, a simple peripheral
suture but a crossed or interlocked peripheral suture
adds further strength and gap resistance. A six-strand
core suture further improves repair strength, but it is
debatable whether addition of a crossed or interlocked
peripheral suture is beneficial. All these elements give a
repair that is, in the main, sufficiently robust to with-
stand the controlled active motion program and to
reduce the chance of rupture in the healing phase.
In laboratory testing, traditionally single static tests
have been used to describe the quality of a tendon
repair, but they do not mimic real life where a repair is
subject to repeated loads. Single static load tests are rela-
tively straightforward to perform in a laboratory and
clearly give a reasonable evaluation of a repair’s quali-
ties, but it is possible that tendon repairs have been
cause? Here, tissue engineering may help. While build-
ing a tendon from scratch is daunting, it may be pos-
sible to manipulate allograft tissue, seeding it with host
cells, and specialized surfaces in the middle for gliding,
and at the ends for attachment to tendon, muscle, or
bone. Such work is already proceeding.
In short, I think that the future for tendon surgery is
bright. With a decade, or two at the most, we should
have solved the remaining vexing problems of healing
and function and have begun to apply those solutions
clinically. The best is yet to come.
overrated (or underrated) and that cyclic load tests
would give more reliable information. Further con-
trolled studies comparing static and cyclic load testing
are indicated, and perhaps we should adopt cyclic load
tests for all laboratory studies.
Recent studies have shown that different mammalian
tendons have different physical characteristics. The com-
monly used and readily available pig flexor tendon
appears to be less like human flexor tendon than, for
example, sheep flexor tendon. The wide use of pig flexor
tendon could have produced some inaccurate informa-
tion and it may be better to use sheep tendon in
preference.
Many other technical problems in medicine and
surgery have been resolved by a gadget using the special
properties of a physical material and clever engineering.
The tendon repair would seem ripe for such a develop-
ment but currently we only have some relatively crude
barbed suture techniques and screw devices. Further
development of these ideas on a more refined scale
might yield something practical and strong.
Developments in post surgical rehabilitation may be
found, which combined with improved repair quality,
could lead to less restrictive and shorter splintage regi-
mens. As a parallel there are other aspects of trauma
surgery in which multipoint fixation; for example, distal
radius fractures, has enabled mobilization of the wrist
before the fracture has healed. We have not reached a

point where repair strength is sufficient to discard the
splint immediately after surgery, although possibly this
could come about, but presumably another means of
restricting finger activity would be required. A theoreti-
cal idea for reducing power to one finger could be devel-
oped: the injured finger would be held slightly more
flexed than the neighboring fingers reducing the tension
C Future of Tendon Surgery
of the Hand
Jin Bo Tang, MD
The repair of injured tendons is a fascinating field that
has attracted the particular attention of hand surgeons
over the past century. In the early 1970s, Verdan wrote
a classic review: “Half a century of flexor-tendon surgery.
Current status and changing philosophies” (J Bone
Joint Surg [Am] 52:472–491, 1972). In 1987, Hunter,
Schneider, and Mackin edited the book Tendon Surgery
in the Hand to summarize the progress.
The authors of the current book and our predecessors
have witnessed major paradigm shifts in both funda-
mental concepts and the practice of tendon repair. The
content of this book reflects the growing body of knowl-
edge and advances over the past 25 years. After almost a
century of efforts by basic scientists and surgeons, our
accumulated knowledge of basic scientific knowledge
offers both useful and meticulous guidance for clinical
practice, making it much more feasible to restore the
function of the hand. Principles of primary repair and
secondary reconstruction have been established; surgical
and postoperative care methods have been developed.
Armed with current guidelines for surgical repair and
postoperative care, well-trained hand surgeons can
expect to restore near-normal function of the hand and
digits after repair of injuries chiefly involving the tendons.
It appears that major scientific and technical obstacles
on the path to nearly optimal primary tendon repair
have been eliminated, except in a few specific instances.
Nevertheless, tendon injuries with delayed presenta-
tion, injuries in a complex wound setting, and injuries
Chapter 41C:  Future of Tendon Surgery of the Hand 443
within the flexor tendons of the injured finger yet allow-
ing it to move.
Other ideas will emerge!
Biological research may identify methods of acceler-
ating tendon healing and reducing adhesion. Current
tried techniques include grafts and locally applied
agents.
involving serious damages to multiple structures (such
as fractures or soft tissue defects), though not related to
the quality of tendon repair only, frequently result in
distinct loss of function. In many such cases, extensive
adhesions form; arduous staged reconstruction is neces-
sary. There is still no guarantee of functional recovery to
the level desired by both patients and surgeons. Fortu-
nately, the number of such cases declined drastically
after the inception of primary tendon repair in the
digital sheath area. Though relevant to surgery of the
tendon per se only partly, tendon transfers do not
restore full, or sometimes, major hand function after
nerve palsies.
It is difficult to precisely or inclusively predict future
developments in a field. Scientific and technical innova-
tions are by their nature unpredictable. Nevertheless, we
can summarize those areas where work is under way and
those that await answers and continuing efforts.
We will probably see the following changes in the
near future:
1. More widespread use of stronger surgical repairs.
We already see a trend towards use of stronger
surgical repairs. However, the speed of change
varies with the resources of the hospital and with
geographic region. I expect that strong surgical
repairs will become the method of choice for the
vast majority, if not all, of surgeons, particularly in
digital areas and for flexor tendons.
444 Section 6:  Current Status and Future
2. Early combined passive-active motion. It is clear
to me that combined passive-active motion is an
ideal way to rehabilitate repaired fingers. However,
regimens incorporating this principle can vary
enormously. I believe that rubber band traction
should be abandoned in digital flexor tendon
rehabilitation and that passive-only motion
reserved for patients who fail to comply with
active motion regimens. Generally, in each exer-
cise session, passive motion should precede active
motion to lessen resistance to tendon gliding.
3. Simplification of motion protocols. We currently
see a variety of protocols in different units, and
some are quite complex. The variation in proto-
cols that produce comparable clinical outcomes
indicates that some protocol details are of second-
ary importance. We should be cognizant that
current protocols are largely experience-based and
in fact constitute “expert opinions.” My opinion is
that workload of patients and therapists may be
reduced, without lowering rate of success. For
example, hourly exercise of repaired tendons
may not be necessary; four or five sessions of exer-
cise in a day would probably suffice. The number
of repetitions is increased in each session. This
would relieve the patients from hourly exercise
of the repaired fingers. In addition, it appears
unnecessary to actively move the finger through a
full range of motion, particularly in the initial 1
to 2 weeks. It is vital to keep in mind that the most
extreme portion of active finger flexion carries the
greatest risk of disrupting the repair. Partial active
finger flexion not only reduces the chance of over-
loading the tendon, but also diminishes pain and
discomfort. Nevertheless, passive finger motion
does need to be executed over the entire range.
4. Loosely controlled postoperative motion. In
patients whose tendon has been repaired with a
strong method, and after proper measures (such
as pulley release) have been taken to diminish
tendon gliding resistance, the finger can be
expected to actively move under less stringent pro-
tection or a substantially simplified protocol, pro-
vided such motion is not against resistance.
Employment of such hand motion perhaps will be
a major advance in the future.
The following changes may not occur in the near future,
but are likely in the years or decades to follow:
1. Biological approaches to increase intrinsic
tendon healing. Recent years have seen growing
realization of the impact of molecular biotechnol-
ogy on medicine. Molecular therapy catches public
imagination of future medicine, and offers thera-
peutic promise to regulating tendon healing. In
the future, efforts to accelerate tissue healing and
repair will find the tendon a perfect test ground
for transferring some basic scientific concepts to
the clinic, because tendons are composed mainly
of uniform collagen building blocks with aston-
ishingly little vascularization. Compared with
tissues rich in vasculature, enhancement of tissue
repair in tendons may be more attainable. We
expect that injection or implantation of bioactive
agents will fortify weak tendon healing capacity.
Currently, approaches with such potentials include
gene therapy, controlled release systems, or coated
surgical sutures; certainly novel methods would
emerge and will bring us even closer to this goal.
2. Reducing adhesion formation. Reducing adhe-
sions has been a constant theme in tendon surgery
and imputes for investigations. Limiting adhe-
sions is important not only for primarily repaired
tendon, but also after secondary tendon grafting
or tenolysis. Broadly, avoiding adhesion or scar is
desirable after all surgical interventions, but it is
particularly necessary for tendons, which glide
within a restrictive sheath. Surface modifications
of tendons, which have been the goal of Peter
Amadio and his colleagues for a decade, are impor-
tant to reduce not only gliding resistance but
adhesions as well. Such efforts likely offer great
potential for decreasing adhesions arising from
the tendon surface. Another fertile research area is
molecular methods to regulate tendon healing
and inhibit key mediators of scar formation.
However, we must be prepared to understand the
complex nature and interactions of molecular
events, and recognize the complexity of interven-
tions at the molecular level. Such approaches may
not prove easy and straightforward, particularly
when aimed at simultaneously maintaining
healing strength.
3. Engineered tendons for reconstruction of tendon
defects. This is certainly a worthwhile future direc-
tion. The work of researchers in James Chang’s lab
leads me to expect that decellularized allogenic
tendons will serve as a good scaffold clinically,
providing structural supports for cell seeding in
vitro before implantation or cellular ingrowths
from surrounding tissues in vivo. These tendons
bypass the major obstacle in generating scaffolds
that mimic the flexibility and loading capacity of
intrasynovial tendons. In contrast, it is hard to
speculate whether or how soon a “tendon” made
of biomaterials incorporated with cells in vitro or
in vivo will be used to replace a tendon graft; there
is a long road ahead of us. There is the open ques-
tion of whether we can ever produce materials
with the superb mechanical properties of natural
intrasynovial tendons. If we ever do reach that

goal, I expect it to happen in the quite distant
future.
4. Novel materials and methods to promote tendon
healing or a manufactured tendon substitute.
Basic scientific developments always offer novel
tools to battle against frustrating problems. Lately
emergent options constantly replace old ones,
though only very few among these may offer actual
solutions. Each innovation creates energy and
enthusiasm for tackling the problem. I expect that
novel materials and methods will be used to
produce tendon substitutes (or enhancing the
healing process). Nevertheless, tendons have many
unique requirements as a viable biologic tissue—
bearing both compressive and pulling forces
during motion, being firm enough to sustain com-
pression and flexible enough to accommodate
angular motion, while surrounded by a restrictive
sheath in some parts. The tendon should not be
bulky, but smooth and free of restraining adhe-
sion. Any manufactured tendon substitute must
possess these biological and mechanical qualities.
The following issues are unlikely to be overcome in
foreseeable future, and will thus continue to affect out-
comes: (1) less-qualified surgeons still repair a propor-
tion of cases; (2) particular injuries, such as those in the
little finger, will continue to be a problem; (3) severe
injuries involving multiple structures, whose outcomes
do not chiefly depend on treatment of tendon injuries,
limit the extent of recovery, and (4) socioeconomic con-
ditions limit the availability and affordability of surgery
and postoperative rehabilitation.
Chapter 41C:  Future of Tendon Surgery of the Hand 445
Finally, future development of our field includes the
education of qualified hand surgeons. This remains a
great concern and is also a pressing task. Scientific
advances have cleared the major obstacles encountered
50 years ago in repairing injured tendons. Nevertheless,
close-to-ideal outcomes are expectable only when sur-
geons have been well-trained in tendon repair and abide
by up-to-date surgical and postsurgical care guidelines.
Unfortunately, tendon injuries may have disastrous
clinical results if treated by unqualified surgeons.
In most regions of the world, it is not the current state
of scientific and technical knowledge that limits return of
clinically acceptable function after tendon injury; rather, it
is the lack of both trained surgeons and adequate rehabilita-
tion systems that prevents functional restoration of the injured
hand (Injury 37:1036–1042, 2006).
Therefore, in countries where hand surgery is not
fully recognized as an established surgical subspecialty,
surgeons should be encouraged to become specialists in
the hand. It should be realized that, development of
techniques and expansion of knowledge on treating
hand disorders make a general orthopedic or plastic
surgeon less likely to treat a tendon injury in the hand
proficiently. Poor mastery of surgical techniques and
lack of sufficiently precise knowledge of anatomy jeop-
ardize treatment outcomes. Ideal repair of lacerated
tendons is based on understanding of hand anatomy
and biomechanics, possession of fine surgical skills, and
knowledge of hand rehabilitation or cooperation with
hand therapists. Improving education and training is
one of the most momentous tasks among all that we
will have in the future.
 CHAPTER
42  
CHEMICAL MODIFICATION OF
TENDON GLIDING SURFACE
Yu-Long Sun, PhD, and Peter C. Amadio, MD
TENDON LUBRICANTS
The flexor digitorum profundus (FDP) tendon glides
within tendon sheath, which consists of annular liga-
ments or pulleys, during the movement of fingers. This
tendon-pulley system has a low coefficient of friction
(0.04), which is similar to that of articular cartilage
(0.014).1
Lubrication mechanism of articular cartilage has been
widely investigated.2,3 Hyaluronic acid (HA), lubricin,
and phospholipids are thought to be involved in the
lubrication of the cartilage–cartilage interface, acting
alone or in combination. HA is a polyanionic polysac-
charide, present in the intercellular matrix of most ver-
tebrate connective tissues, especially in synovial fluid.
The unique properties of HA result in a molecular
network that, in highly hydrated conditions, is extremely
viscoelastic and pseudoplastic, favorable rheological
properties for a potential lubricant. Lubricin, also known
as superficial zone protein and proteoglycan 4, is a gly-
coprotein which has been identified in synovial fluid4,5
and the superficial zone of articular cartilage.6 It has
been noted to lubricate articular cartilage with the same
lubricating properties as normal synovial fluid. Lubricin
is widely considered to be the principal lubricant in
joints.3,7 Furthermore, phospholipids, the major compo-
nent of all biological membranes, are known to contrib-
ute to joint lubrication and to lubricate other gliding
surfaces as well.8,9
HA and lubricin have been identified on the surface
of the FDP tendon.10-12 While phospholipids have not
been sought in tendon, it is reasonable to assume that
some are present, as phospholipids are found in all
living tissues. To assess the effect of HA, lubricin, and
phospholipids on tendon lubrication, the enzymatic
and chemical treatments were applied to remove them
from the surface of canine FDP tendons.13
Hyaluronidase can effectively digest HA. The effect of
the hyaluronidase digestion on the friction between
FDP tendon and its associated pulley was measured. The
friction between the FDP tendon and its pulley increases
after the FDP tendon is treated with hyaluronidase
(Figure 42-1).10,13 Therefore, HA has been assumed to
play a role in lubricating the surface of the FDP tendon.
This chapter does not appear in the print edition.
Phospholipase C selectively removes certain types of
phospholipids, such as phosphatidylcholine, without
destroying the extracellular matrix network.14 The
increase in friction after treatment with phospholipase
C suggests that phospholipids are present on the surface
of the FDP tendon, and that phospholipids help to
lubricate FDP tendon (see Figure 42-1). This conclusion
was further confirmed by the increase in friction after
treatment with lipid solvent. The increased effect of
lipid solvent compared to phospholipase C suggests
that phospholipids other than phosphatidylcholine
may also affect tendon lubrication.
Trypsin can digest lubricin as well as other extracel-
lular matrix proteins except collagen, the principal
protein in tendon. Trypsin digestion resulted in a sig-
nificant increase of friction of the FDP tendon (see
Figure 42-1). Although the increase of friction could
contribute to phospholipids, which could be carried by
lubricin and/or other extracellular matrix proteins, it
was found that the friction of the FDP tendons could
be further increased with trypsin after the elimination
of phospholipids with lipid solvent (see Figure 42-1).
Hence, the effect on friction could be due to a removal
of protein components, especially lubricin, a glycopro-
tein both known to have lubricating ability, although it
cannot exclude an effect from other proteins on the
tendon surface.
Many factors appear to contribute to the lubrication
mechanism of the FDP tendon. The research findings
are strongly suggestive of the presence of, and a role for,
proteins, HA, and phospholipids in tendon lubrication.
Phospholipids, HA and lubricin, may serve as boundary
lubricants in FDP tendon lubrication.
CHEMICAL SURFACE MODIFICATION
OF TENDON IN VITRO
Tendons attach muscle to bone and transfer the power
of the muscle to bone over a distance. The structure of
tendon is directly related its physical and physiological
function. The surface of tendons well adapts to their
mechanical environments.15 Tendons are characterized
based on their anatomic location as either intrasynovial
or extrasynovial.16-18 The intrasynovial tendons, such as
the FDP tendon, have parietal and visceral synovial
e1
e2 Chapter 42:  Chemical Modification of Tendon Gliding Surface
0.15
0.12
Friction (N)
* * * *
0.09
0.06
0.03
0 Figure 42-2  The chemical structure of hyaluronic acid.
Control HAase PLC LipSol Trypsin LipSol-
Try
Treatment
Figure 42-1  The friction of FDP tendons treated with
control solution (Control), hyaluronidase (HAase),
phospholipase C (PLC), lipid solvent (LipSol), trypsin, and the
combination of lipid solvent and trypsin (LipSol-Try).
sheaths that form a closed compartment that contains
synovial fluid for lubrication and nutrition. In extrasy-
novial tendons, such as the peroneus longus (PL)
tendon, there is a peritendinous sheet of loose fibrillar
tissue, the paratenon, which functions as an elastic
sleeve, permitting limited movement of the tendon
against the surrounding tissue. The extrasynovial auto-
graft, intrasynovial allograft, and the repaired flexor
tendon are the accepted procedures in flexor tendon
surgery. The chemical surface modification of these
tendons is described later.
Extrasynovial Autograft
Tendon graft plays an important role in reconstruction
to restore finger function in the cases of severe flexor
tendon damage, adhesion formation, and primary
tenorrhaphy rupture. As the potential sources of intra-
synovial tendons available for use as tendon autografts
are limited, the most donor tendons, such as palmaris
longus tendon, plantaris tendon, and long extensor
tendon, come from extrasynovial tendon sources in
clinical settings. Extrasynovial tendons have rougher
surfaces than intrasynovial tendons.19,20 The coating of
paratenon on the surface of extrasynovial tendon is
extremely susceptible to damage as the tendon repeti-
tively glides against the pulley. Extrasynovial tendons
create higher friction against a pulley compared to intra-
synovial tendons, particularly after multiple repetitive
motion.20-22 Animal models have shown that extrasyno-
vial tendon grafts are associated with more adhesions
to the surrounding tissue than intrasynovial tendon
grafts.19,23,24 Therefore, outcomes of extrasynovial grafts
may be improved by keeping paratenon intact as well
as low friction of the grafts.
HA is a linear, unbranched polysaccharide with a
high molecular weight. It is composed of a repeating
OH OH
O
O O
O HO
O
HO
OH NH
O n
HA Paratenon
HOOC HOOC
COOH CONH
COOH COOH
NH2
COOH
NH2 EDC CONH
CONH
NH2 COOH
Tendon
Figure 42-3  Chemical surface modification of
extrasynovial tendon with cd-HA. EDC is 1-ethyl-3- 
(3-dimethylaminopropyl)carbodiimide.
disaccharide that consists of N-acetyl-D-glucosamine
and D-glucuronic acid linked by a β1–4 glycosidic bond
(Figure 42-2).25 The disaccharides are linked by β1–3
bonds to form the HA chain. Each disaccharide has one
carboxyl group, which can be activated by carbodi-
imides at physiological condition to form an amine-
reactive O-acylisourea intermediate that quickly reacts
with an amino group to form an amide bond and
release an isourea. As amino group universally exists in
the protein components, such as collagen, the major
extracellular matrix in tendon, with the activation of
carbodiimides, HA could cross-link paratenon and
tendon and keep paratenon resist abrasion. Further-
more, HA is a lubricant of tendon. The chemical reac-
tion can tightly bind HA on the surface of tendon and
play a role in lubrication (Figure 42-3).
We performed a study to evaluate HA and carbodi-
imide derivatized HA (cd-HA) on the gliding of canine
PL tendon, an extrasynovial tendon.26 We found that
the gliding resistance of normal PL increased with the
increase of cycle of repetitive motion (Figure 42-4).
The administration of exogenous HA (1%) resulted in
the nonchange of gliding resistance in the first cycle of
motion after the administration. However, the gliding
resistance of PL treated with HA increased significantly
over five cycles of repetitive motion than normal PL did.
The quick discharge of the lubricating ability of exoge-
nous HA indicates the weak attachment of HA on the

1.2
Saline
1
HA
Gliding resistance (N)
0.8 cd-HA
0.6
0.4
0.2
0
Normal 1 5 10 20
Cycles
Figure 42-4  Gliding resistance of PL tendon treated with
saline, exogenous HA, or cd-HA over 100 cycles of repetitive
motion against pulley.
surface of the tendon. cd-HA, which is composed of
1% HA with 1% 1-ethyl-3-(3-dimethylaminopropyl)
carbodiimide hydrochloride (EDC) and 1% N-
hydroxysuccinimide (NHS), significantly decreased the
gliding resistance of the PL tendon compared with that
of normal PL tendon or the PL tendon treated with HA
only, at each corresponding cycle of repetitive motion.
This finding indicates the chemical modification
improves the attachment of HA and/or paratenon on
the surface of the PL tendon.
Although cd-HA improves the gliding of the PL
tendon, the gliding resistance decreased significantly
only in the first cycle of motion after the administration
and increased over 20 cycles of repetitive motion.
Gelatin, which serves as a carrier of HA and a cross-
linker and a cross-linker, was introduced to further
improve the gliding of the PL tendon. It was found that
all PL tendons treated with saline, 10% gelatin, or cd-HA
(1% HA, 0.25% EDC, and 0.25% NHS) showed similar
trends up to 500 cycles of repetitive motion22,27 (Figure
42-5). Over the first 200 cycles, the gliding resistance
increased linearly and then reached a plateau. There was
no significant difference in gliding resistance between
the saline-, gelatin-, and cd-HA–treated PL tendons for
any given number cycles of motion. For the PL tendon
treated with cd-gelatin (10% gelatin, 0.25% EDC, and
0.25% NHS) and cd-HA–gelatin (1% HA, 10% gelatin,
0.25% EDC, and 0.25% NHS), the gliding resistance
increased at a much more gradual rate over the 500
cycles. Beginning at 100 cycles of simulated flexion/
extension, the gliding resistance of tendons treated with
cd-HA–gelatin was significantly lower than that of the
saline-treated tendons. Starting at 200 cycles, the gliding
resistance of tendons treated with cd-gelatin was also
significantly lower than that of the saline-, gelatin-, and
cd-HA–treated PL tendons. Starting at 300 cycles, there
was also a significant difference in the gliding resistance
Chapter 42:  Chemical Modification of Tendon Gliding Surface e3
1.4
1.2
Gliding resistance (N)
1
0.8
0.6
0.4
0.2
50 100 0
0 100 200 300 400 500
Cycles
FDP cd-HA
Saline cd-gelatin
Gelatin cd-HA-gelatin
Figure 42-5  Gliding resistance of FDP tendons and PL
tendons treated with saline, gelatin, cd-HA, cd-gelatin, or
cd-HA–gelatin at different cycles of simulated motion.
between the PL tendon treated with cd-gelatin and the
PL tendon treated with cd-HA–gelatin (p < 0.05), with
the latter group having a lower gliding resistance at
comparable cycles of simulated flexion/extension. At
the 500th cycle, the increase in gliding resistance of
the cd-HA–gelatin treated PL tendons was roughly 4
times that of the FDP tendon, compared to a 20-fold
difference for the saline treated PL tendon. The gliding
of the PL tendon treated with cd-HA–gelatin almost
approached that of the FDP tendon. The chemical mod-
ification of the surface of the PL tendon with cd-HA–
gelatin also significantly improved its resistance to
abrasion. After 500 flexion/extension cycles, the sur­face
of untreated PL tendons was roughened, and the col-
lagen fibers covering the PL tendon surface were twisted
into large strands. In contrast, the surface of the PL
tendon treated with cd-HA–gelatin was still smooth
after 500 cycles of repetitive motion, and the normal
collagen fibers on the PL tendon surface remained
intact, similar to the FDP tendon.
The formula of cd-HA–gelatin and the curing time
were further optimized to improve the surface gliding
of extrasynovial tendon grafts.28,29 cd-HA–gelatin with
1% HA, 10% gelatin, 1% EDC, and 1% NHS showed
the best improvement of gliding of extrasynovial tendon
grafts. Meanwhile, it was found the curing time could
be as short as 5 minutes for this formula of
cd-HA–gelatin.
In addition to HA, lubricin also is believed a lubri-
cant of tendon. Can lubricin improve the gliding of
extrasynovial tendon grafts by itself or a chemical
approach? A study compared the lubricating ability of
e4 Chapter 42:  Chemical Modification of Tendon Gliding Surface
1.2
1.0
Gliding resistance (N)
0.8
0.6
0.4
0.2
0.0
0 200 400 600
Cycles
Saline
Lubricin
cd-gelatin
Figure 42-6  Gliding resistance of PL tendons treated with
saline, lubricin, cd-gelatin, cd-HA–gelatin, or cd-gelatin/
lubricin at different cycles of tendon motion.
canine PL tendons that were treated with saline, bovine
lubricin (260 µg/mL), cd-gelatin (10% gelatin, 1% EDC,
and 1% NHS), cd-HA–gelatin (1% HA, 10% gelatin, 1%
EDC, and 1% NHS), or cd-gelatin plus lubricin (260 µg/
mL lubricin was applied after cd-gelatin treatment).30
There was no significant difference in the gliding resis-
tance between the tendons treated with saline solution
and those treated with lubricin alone or between the
tendons treated with cd-HA–gelatin and those treated
with cd-gelatin plus lubricin (Figure 42-6). However,
the gliding resistance of the tendons treated with
cd-gelatin plus lubricin was significantly lower than that
of the tendons treated with saline solution, lubricin
alone, or cd-gelatin alone. The results indicate that
lubricin does have an important effect on tendon lubri-
cation. Like HA, lubricin may preferentially adhere to
tendon surface pretreated with cd-gelatin and when so
fixed in place.
The gliding of the canine PL tendon can be improved
with the chemical treatment of cd-gelatin, cd-HA–
gelatin, and cd-gelatin plus lubricin. The feasibility of
these approaches was tested with human ipsilateral
palmaris longus tendon, an extrasynovial tendon often
used for tendon grafting clinically. Human palmaris
longus tendons were treated with either saline, cd-HA–
gelatin, cd-gelatin plus lubricin, or cd-HA–gelatin plus
lubricin. After treatment, tendon gliding resistance
was measured during up to 1000 cycles of simulated
flexion and extension motion.31 The gliding resistance
of the PL tendons in the cd-HA–gelatin, cd-gelatin plus
lubricin, and cd-HA–gelatin plus lubricin groups was
0.9
0.8
0.7
0.6
0.5
0.4
0.3
0.2
0.1
800 1000
0.0
0 200 400 600 800 1000
cd-HA-gelatin Cycles
cd-gelatin
+ lubricin Saline cd- cd-HA-
cd-HA- gelatin + gelatin +
gelatin lubricin lubricin
Figure 42-7  Gliding resistance of PL tendons treated with
saline, cd-HA–gelatin, cd-gelatin/lubricin, or cd-HA–gelatin/
lubricin at different cycles of tendon motion.
significantly lower than that of the saline-treated control
after 1000 cycles (Figure 42-7). The gliding resistance
in these treatment groups decreased within the first 50
cycles and then increased at a much more gradual rate
over the 1000 cycles, with the cd-HA–gelatin plus lubri-
cin group being most stable. The results indicate that
the chemical modification can be applied in a variety of
extrasynovial tendons.
HA, lubricin, and phospholipids exist in native syno-
vial fluid and also are found to play the role of tendon
lubrication. Instead of using purified HA and lubricin,
native synovial fluid may serve as a lubricating material
to improve the gliding of extrasynovial tendon. Canine
PL tendons were treated with either saline, 1% EDC/1%
NHS, cd-gelatin, synovial fluid, synovial fluid plus 1%
EDC/1% NHS, or cd-gelatin–synovial fluid. The gliding
resistance was measured for 1000 cycles of simulated
flexion/extension motion. Same as HA and lubricin
only, synovial fluid alone did not improve the gliding
of the tendon (Figure 42-8). The gliding resistance of
the tendons treated with synovial fluid plus 1% EDC/1%
NHS, cd-gelatin, or cd-gelatin–synovial fluid was signifi-
cantly lower than the control group after 1000 cycles of
tendon motion. The gliding resistance of the tendon
treated with cd-gelatin–synovial fluid was significantly
lower than that of the tendon either treated with syno-
vial fluid plus 1% EDC/1% NHS or cd-gelatin. No sig-
nificant difference was found in the gliding resistance
between first cycle and 1000 cycles for the gliding resis-
tance of the tendon treated with cd-gelatin–synovial
 Chapter 42:  Chemical Modification of Tendon Gliding Surface e5

1.00

Gliding resistance (N) 0.80

0.60

0.40

0.20

0.00
0 100 200 300 400 500 600 700 800 900 1000
Gliding times

cd-SF-gelatin EDCNHS
cd-gelatin cd-SF
Control SF

Figure 42-8  Gliding resistance of PL tendons treated with saline, cd-HA–gelatin, cd-gelatin/lubricin, or cd-HA–gelatin/
lubricin at different cycles of tendon motion.

fluid. The results indicate that synovial fluid can be 0.6

applied by chemical approach to improve the gliding of *
extrasynovial tendon. 0.5 *
* †‡
Intrasynovial Allograft 0.4
Friction (N)

Intrasynovial tendon autografts may have better out- ** ‡

comes than extrasynovial autografts do. The autologous 0.3
†
intrasynovial tendons are rarely available for tendon *
grafts. However, intrasynovial tendon allografts are 0.2
more available and can be potentially used as flexor
0.1
tendon graft. In order to reduce immunogenicity and to
facilitate storage, allografts may be subjected to repeti-
0
tive freeze/thaw cycles and lyophilization.32 We found
First cycle 1000 cycles
that frictional force of the flexor digitorum profundus
Cycle
tendon, which was lyophilized and rehydrated in a
saline solution, was significantly increased in compari- Before Lyophilized After cd-HA
son with that of the normal FDP tendon (Figure 42-9).
*, **; p <0.05
With the surface modification of FDP tendon allograft †, ‡; p <0.05
with cd-HA–gelatin (1% HA, 10% gelatin, 1% EDC,
“and 1% NHS), the frictional force of the lyophilized Figure 42-9  The gliding resistance for the groups of
FDP tendon was significantly decreased in comparison normal tendons, untreated lyophilized tendons, and
with the untreated lyophilized tendon even after 1000 lyophilized tendons treated with cd-HA–gelatin.
cycles of repetitive motion in vitro (see Figure 42-9).
The results indicate that tendon surface modification
e6 Chapter 42:  Chemical Modification of Tendon Gliding Surface
with cd-HA–gelatin can improve the gliding ability of
lyophilized flexor tendons and therefore may improve
the utility of lyophilized tendon allografts as a tendon
graft substitute.
Flexor Tendon Primary Repair
With the development of surgical techniques and post-
operative controlled mobilization, the primary repair
after injury has been the mainstream in flexor tendon
surgery. Stronger repairs have been advocated to permit
early active mobilization and to reduce adhesion forma-
tion,33 but tendon adhesions and tendon repair rupture
remain a problem even with stronger repairs.34 The role
of friction as a source of adhesions has been investi-
gated. The data suggest that many strong repairs also
have higher friction35-37 and that this higher friction is
associated with poorer results in an animal model.38
The repair constantly increases the gliding resistance
of the flexor tendon.39 A number of suture techniques
were investigated to repair FDP tendon.35-37 The modi-
fied Kessler and modified Pennington techniques are
satisfied with relatively high breaking strength and low
gliding resistance. However, gliding resistance of the
FDP tendon repaired with these two techniques is sig-
nificantly higher than the intact FDP tendon.
The effects of chemical surface modification on
gliding and repair integrity were investigated during
simulated repetitive motion of a repaired tendon in
vitro.40 The gliding resistance between the FDP and the
proximal pulley was measured before laceration. After
the repair with modified Kessler technique, the tendons
were treated with saline, 1% HA, or cd-HA–gelatin (1%
HA, 10% gelatin, 0.25% EDC, and 0.25% NHS). Then
the gliding resistance of the tendons was measured up
to 500 cycles of repetitive motion. The results showed,
from the first cycle to the 10th cycle, no significant dif-
ferences in gliding resistance between the three testing
groups. From the 50th cycle onward, the friction was
significantly lower in the cd-HA–gelatin group than
in the control group. Neither breaking strength, nor
tendon stiffness, nor resistance or gap formation of the
repairs, was significantly different with the treatment of
cd-HA–gelatin.
The effects of lubricin chemical modification on the
gliding of repaired FDP tendons were also investigated
in vitro.41 Canine FDP tendons were completely lacer-
ated, repaired with a modified Pennington technique,
and treated with one of the following solutions: saline,
cd-HA–gelatin (1% HA, 10% gelatin, 1% EDC, and 1%
NHS), cd-gelatin plus lubricin (260 µg/mL), or cd-HA–
gelatin plus lubricin. After treatment, the gliding resis-
tance was measured up to 1000 cycles of simulated
flexion/extension motion. The gliding resistance of the
repaired FDP tendons in the cd-HA–gelatin, cd-gelatin
plus lubricin, and cd-HA–gelatin plus lubricin groups
decreased within the first 50 cycles and then increased
0.40
Increase in average gliding resistance (N)
0.30
0.20
0.10
0.00
–0.10
–0.20
–0.30
0 200 400 600 800 1000
Gliding cycles
Saline cd-HA-gelatin
cd-gelatin cd-HA-gelatin
+ Lubricin + lubricin
Figure 42-10  Increase in average gliding resistance of
repaired FDP tendon in the four treatment groups at
different cycles of tendon motion.
at much more gradual rate over the 1000 cycles (Figure
42-10). In these groups, the mean and peak gliding
resistance after 1000 cycles was still lower than the
initial gliding resistance before treatment, while the
gliding resistance in the saline control tendons increased
significantly over the 1000 cycles of testing. The repaired
tendons treated with cd-HA–gelatin plus lubricin had
the lowest gliding resistance comparing the tendons in
other three groups at same cycle of repetitive motion.
The surfaces of the repaired tendons appeared smooth
after 1000 cycles of tendon motion for the tendons
treated with cd-HA–gelatin, cd-gelatin plus lubricin,
and cd-HA–gelatin plus lubricin, while that of the saline
control appeared roughened. These results suggest that
tendon surface modification can improve tendon gliding
ability, with a trend suggesting that lubricin fixed on the
repaired tendon may provide additional improvement
over that provided by HA and gelatin alone.
EVALUATION OF CHEMICAL MODIFICATION
IN ANIMAL MODELS
The chemical surface modification succeeded in improv-
ing the gliding ability of extrasynovial tendon, intrasy-
novial tendon allograft, and the repaired flexor tendon
in vitro. It was also applied to improve digit function in
the canine models in vivo.42-45
 Chapter 42:  Chemical Modification of Tendon Gliding Surface e7

Table 42-1  Adhesion Scores in Extrasynovial Tendon Autografts

1W 3W 6W
Adhesion Score Saline Modified Saline Modified Saline Modified
0 1 7 0 1 0 0
1 2 1 0 5 0 5
2 5 0 2 2 0 2
3 0 0 6 0 8 1

cd-HA–Gelatin: Extrasynovial GLIDING RESISTANCE OF TENDON GRAFT

Tendon Autograft
0.6
The canine PL tendons were harvested and transplanted
Normal
to replace the FDP tendons in the second and fifth digits 0.5
cd-HA
of one forepaw.42,43 Prior to grafting, one of the PL
Saline
tendons was coated with cd-HA–gelatin (1% HA, 10% 0.4

Resistance (N)
gelatin, 0.25% EDC, and 0.25% NHS), while the other
was immersed in saline solution only. Adhesion and 0.3
digital normalized work of flexion were evaluated
0.2
after surgery at 1, 3, and 6 weeks. The adhesion score
of cd-HA–gelatin treated tendons was significantly
0.1
less than the saline treated tendons at all time points
(p < 0.05) (Table 42-1). All saline-treated graft digits at 0
6 weeks had severe adhesions at both the pulley and A 1-week 3-week 6-week
tendon bed, including the entire zone 2 area. The adhe-
sion score at 1 week in both groups was significantly less NORMALIZED WORK OF FLEXION (nWOF)
than at 3 and 6 weeks in their respective groups (treated
7
or control), with no significant difference between the
3- and 6-week results. In consistence with adhesion Normal
6
cd-HA
score, the normalized work of flexion of the tendons
nWOF (N-mm/degree)

5 Saline
treated with cd-HA was significantly lower than that of
the saline-solution-treated controls at each time point 4
(Figure 42-11). In addition, the gliding resistance of the
cd-HA group was significantly lower than that of the 3
saline-solution group at 3 and 6 weeks. The chemical 2
surface modification of an extrasynovial tendon auto-
graft with cd-HA–gelatin decreases adhesion formation 1
and improves the digital function in flexor tendon auto- 0
graft model in vivo. B 1-week 3-week 6-week

cd-HA–Gelatin: Intrasynovial
Tendon Allograft
A primary repair failure model was first created by lac-
erating and repairing the FDP tendons in zone 2 from
the second and fifth digits of dogs.44 The dogs were
allowed free active motion postoperatively. Six weeks
later, the tendons were reconstructed with use of FDP
allografts. In each dog, one allograft was treated with
cd-HA–gelatin (1% HA, 10% gelatin, 1% EDC, and 1%
NHS) and the other was treated with saline solution, as
a control. The dogs were restricted from free active
motion, but daily therapy was performed beginning on
postoperative day 5 and continued until 6 weeks after
the operation. The gliding resistance and mean work
Figure 42-11  The gliding resistance (A) and normalized
work (B) of flexion in the normal, cd-HA–gelatin–treated,
and saline-solution–treated groups at 1, 3, and 6 weeks. A
difference in symbols denotes a significant difference
between values (p < 0.05), with the triangle being
significantly less than the circle.
of flexion of the allografts treated with cd-HA–gelatin
were significantly less than those in the saline-solution
control group (Figure 42-12). This study indicates the
chemical modification with cd-HA–gelatin can improve
the digital function in flexor tendon allograft model
in vivo.
e8 Chapter 42:  Chemical Modification of Tendon Gliding Surface

cd-HA–Gelatin/Lubricin: Tendon Repair ((260 µg/mL). Passive synergistic motion therapy was

In this study, dogs were randomly assigned to either a started on the fifth postoperative day and continued
chemical treatment group or an untreated control until the dogs were killed on day 10, day 21, or day 42.
group.45 The second and fifth FDP tendons from each The prevalence of severe adhesions was decreased in the
dog were lacerated fully at the zone 2 area and then tendon treated with cd-HA–gelatin plus lubricin (Table
repaired. Following repair, the tendons in the chemical 42-2). The normalized work of flexion of the repaired
treatment group were treated with cd-HA–gelatin (1% tendons treated with cd-HA–gelatin plus lubricin was
HA, 10% gelatin, 1% EDC, and 1% NHS) plus lubricin significantly lower than that of the nontreated repaired
tendons at all time points (Figure 42-13). The results
indicate treatment with cd-HA–gelatin plus lubricin
appears to be an effective means of decreasing postop-
erative adhesions after flexor tendon repair.
GLIDING RESISTANCE
SUMMARY
*
0.5 Flexor tendon injuries are a frequent clinical problem.
n = 10
*
Restoration of tendon function after flexor tendon lac-
0.4
eration especially in zones 1 and 2 has been difficult.
The introduction of chemical surface modification and
Force (N)

0.3 n=8
the development of carbodiimide-derivatized gelatin
0.2
n = 18
0.1

0 * * * *
A Normal CHG Saline 5
nWOF (N-mm/degree)

* *
4 *
NORMALIZED WORK OF FLEXION
* * *
* 3
* *
1.6 n = 10 *
2 *
nWOF (N-mm/degree)

1.4
1.2 1 *
*
1
0
0.8
n=8 D-10 D-21 D-42
0.6
0.4 Normal FDP
n = 18 CHL
0.2
Repair-control
0
B Normal CHG Saline
Figure 42-13  The work of flexion normalized by the
Figure 42-12  The gliding resistance (A) and normalized proximal interphalangeal and distal interphalangeal angle
work (B) of flexion in the normal, cd-HA–gelatin–treated, (nWOF) of repaired FDP tendons with or without cd-HA-
and saline-solution-treated groups at 10, 21, and 42 days. gelatin plus lubricin (CHL) treatment and of the normal,
CHG, cd-HA-gelatin. contralateral digit at days 10, 21, and 42.

Table 42-2  Adhesion Scores in the Repaired FDP Tendon

10 Day 21 Day 42 Day
Adhesion Score Saline Modified Saline Modified Saline Modified
0 10 11 9 12 5 9
1 3 5 3 0 4 3
2 4 0 2 2 4 3
3 1 0 3 1 7 2
 Chapter 42:  Chemical Modification of Tendon Gliding Surface
incorporation of HA and lubricin successfully improved
the gliding ability of the extrasynovial tendon, intrasy-
novial tendon allograft, and the repaired flexor tendon
in vitro. The methods of chemical surface modification
also reduced adhesion formation and improved the
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 CHAPTER
43  
TENDON GLIDING: THE ROLE
AND MECHANICAL BEHAVIOR
OF CONNECTIVE TISSUES
Jean Claude Guimberteau, MD
OUTLINE
The work and experiments of the author and his col-
leagues, including surgeons, histophysiologists, and
biomechanical engineers, have convinced them that
current understanding about tendon physiology is to
be moved ahead. After carrying out in vivo dissections
and video-recording of the tissues existing between
the skin and tendons in carpal tunnel and forearm
areas, the author and his colleagues questioned some
basic mechanics of the tendon sliding. This chapter
presents a new approach of morphological studies,
and the author attempts to explain the existence of the
multimicrovacuolar collagenous dynamic absorbing
system. This system enables easy and extensive sliding
of the tendons without interference from surrounding
tissues, facilitating tissue interdependence. The multi-
microvacuolar collagenous dynamic absorbing system,
which initially seems chaotic and complex, is based
on the vacuolar concept, which is found in many parts
of the human body, and is structurally composed of
multiple interconnected fibrous tissues organized to
facilitate functional adaptation of the tendon during
movement.
For many years, the scientific explanations concerning
the natural mechanism of flexor tendon mobility in the
fingers were limited to the notion of a virtual space or
the existence of loose connective tissue organized in
layers, but the biomechanical foundations for these
theories were vague.1-3
The biomechanical characteristics and histological
findings of the structures around the tendons are some-
times confusing, and the roles and the definitions of the
paratenon, mesotendon, peritendon, and sheaths and
have largely varied among authors and their described
surgical procedures4-9 (Figure 43-1).
When surgical dissection is performed in vivo, visual
magnification demonstrates the presence of a varied
arrangement of tissue connections; a histological con-
tinuum with no clear separation between the skin, the
This chapter does not appear in the print edition.
hypodermis, the vessels, the aponeurosis, and the
muscles. Present everywhere are structures that allow
sliding to take place.
We present a view of physiology of tendon sliding in
human tissues, based on microanatomical observations
that we made with the aid of video recording and analy-
sis. We present new hypotheses concerning the organi-
zation of these subcutaneous tissues.
MATERIALS AND METHODS
In Vitro Study of the Paratenon
This study was carried out on 30 human upper limb
biopsies of flexor digitorum superficialis (FDS) and pro-
fundus (FDP) with their surrounding sheaths, and 26
animal samples including the flexor carpi radialis from
cattle where the organization is very similar to that of
the human flexor profundus (Figure 43-2).
The preparation was treated with potassium bichro-
mate, placed in formalin, and finally in caustic soda,
allowing for a softer and more complete hydrolysis
(Prof. J. P. Delage, INSERM Laboratories, Bordeaux,
France). It was then frozen and freeze-dried under stan-
dard conditions for dehydration. Afterward, it was dis-
sected under a binocular loupe at ×3.5 magnification.
Samples were taken, given a gold-metallic finish, and
then observed under the electron microscope. The
INSERM Laboratories (Prof. Herbage, Lyon, France)
helped us to analyze the chemical components of this
connective tissue.
In Vivo Study of Digital Zones 3, 4, and 5 by
Microanatomical Video Endoscopic
Observation
The tendon gliding system was observed and recorded
on video in 65 cases of tendon revascularization in
Kleinert’s zones 3, 4, and 5 after releasing the
tourniquet.
All of the patients gave their consent before surgery.
Of the 65 cases, 57 procedures were forearm island
reverse flaps. The remaining eight procedures were
e11
e12 Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues
A which was not interrupted despite the excursion and
B
Figure 43-1  When the tendon moves, the movement is
barely discernible. There is an absorbing system surrounding
the tendon. The capillary network around the tendon
changes as the tendon moves. Vascular network observed
during flexion (A), and during extension (B).
axillary flaps. Static and dynamic observations were
carried out using an endoscope with an attached camera
Tri CCD-HD-Image 1 22220055 Karl Storz endoscopy
fiber optic camera and Xenon Nova 201315 light source
at ×25 magnification.
Continuous sequences were captured on video during
flexion of the digital flexors to allow for subsequent
analysis.
RESULTS
In Vivo Observations
Macroscopic Observations
When the flexor tendon moves, its movement is barely
discernible in the palm. There is no dynamic repercus-
sion of the movement on the skin surface. However, the
flexor tendon excursion is at least 2 cm, without any
hindrance and without displacing any of the neighbor-
ing tissues in the palmar area or along the common
carpal sheath.
This suggests the existence of some sort of shock-
absorbing system.
It is also clear from observing the behavior of the
vessels of the common carpal sheath after revasculariza-
tion and during flexion and extension, that there is
apparent disorder and irregularity of shape of the micro-
vascular network. There are surprisingly complex forms
of vascular distribution, a finesse to the microvascular
network, which is much more complex than a simplistic
mechanistic distribution.10-14
When we observed the area around the tendon, we
noted an apparently circular longitudinal and periph-
eral vascularization, which seemed to represent a real
continuity between the sheath and the tendon, and
distension occurring during sliding and subsequent
return to the original position.
At first sight, this is not incompatible with classical
anatomical descriptions.
Ten-Fold Microscopic Examination
However, during flexion and extension of the tendon,
tenfold microscopic examination of zones 3, 4, and 5
enabled us to observe vascular patterns in different
planes of excursion and with different speeds of vessel
progression due to modifications in the capillary
network and depending on variations in tendon
movements (Figure 43-3). Small vessels are subjected
to deformation during movement but do not follow
any logical or rational sequence. Some vessels pro-
gress quickly, while others move more slowly, and
some overtake other vessels. The diameter of the vessel
seems to be of no importance in this process. There
is dynamic progression with no apparent order or
proportionality.
Very little research has been done to study this
mechanical phenomenon, since the issue was consid-
ered by many to have been solved by the concept of a
virtual space (i.e., the tendon slides in the carpal sheath
like a bullet in a gun barrel without touching the sides,
or rather, it slides in membranous or visceral layers or
by stratification of different coaxial layers).
In vivo observation has rendered this concept unac-
ceptable partly because it is surgically impossible to
define a clear field of dissection between the paratenon
and the tendon (Figure 43-4).
At 10-fold microscopic examination (Figure 43-5),
video observation at rest showed an inaccessible micro-
anatomical arrangement, a tissue-continuity, and a gel-
like tissue surrounding the tendon. We saw a glossy
structure stretching across the tendon. Within this
tissue, collagen fibers can be seen framing the vessels
in a random fashion. We were confronted with the
notion of global dynamics and continuous matter
between the tendon and the surrounding tissue, radi-
cally opposing the classical descriptions of sliding struc-
tures based on the notion of tissue stratification and
a virtual space between the tissue layers. Instead, we
 Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues e13

A B

C D
Figure 43-2  MVCAS shown under electron microscope. A, The flexor carpi radialis of cattle was harvested for observation.
B, Preparation frozen-dried samples. C, Appearance of the sliding structure, MVCAS, under the electron microscope (×5).
D, Findings under a higher power magnification. Tissues surrounding the tendon are made of microvacuoles (×25).
e14 Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues

found total histological continuity. It therefore became

necessary to investigate this tissue further in order to
gain better knowledge of its properties and its different
roles.

At 25-Fold Magnification
At 25-fold magnification, this glossy system consists of
loose connective tissue situated between the tendon and
its neighboring tissue, and is composed of intertwining
multidirectional filaments creating partitions that form
a new type of vacuole: three-dimensional, structured
microvacuolar volumes (Figure 43-6). Apart from some
adipocytes and fibroblasts, there are few cells in this
A multifibrillar network.
We called it the MultimicroVacuolar Collagenous
dynamic Absorbing System (MVCAS), to emphasize its
functional and architectural impact.15-17
4 This tissue network is a continuous structure com-
3 posed of billions of microvacuolar components that
1 must be considered as a three-dimensional network.
2
The basic component of this sliding framework is the
microvacuole.
The microvacuoles measure from a few microns to a
few hundred microns and are organized in a dispersed
branching fractal pattern. They have a pseudo-geometric
shape forming a basic polyhedron.
A microvacuole can be considered as a microvolume
(Figure 43-7); however, the organization differs accord-
ing to dynamic role—The greater the distance that the
B structure must travel, the smaller and denser are the
vacuoles; when stimulated, the structures can move
freely without anything else moving around them; and
under physical constraints, the structure is resistant,
adapting, and yet able to maintain shape. Its apparent
major role is to ensure the dynamics of movement and
absorb the shocks that this creates. The structure also
4
has a memory, so it returns to its initial position, pre-
1 3
2 serving its form and volume. Slight traction on this
microvacuolar system reveals mini air explosions that
prove the existence of a tissular pressure, which is dif-
ferent from atmospheric pressure.
As well as providing efficient movement, shape, form,
and filling space, this microvacuolar tissue plays two
other essential roles18 (Figures 43-8 and 43-9).
As an essential structural element, fibrils serve as a sup-
C
porting frame for the network of the blood supply,
Figure 43-3  A, Cold light variable magnification which accounts for the huge variety of blood supply
endoscope and 3 CCD camera. B, Intriguing vascular shapes. This frame constitutes the continuum of tissues
patterns that change in the capillary network depending   between the mobile tendon and the neighboring tissues,
on the direction of tendon movements during flexion and ensuring the collagenous, vascular, lymphatic, and
extension. C, Vessels are not all going at the same speed nervous continuity between the tendon, epitenon, and
and are in different planes. paratenon. Tissue continuum is total.
As a biomechanical and dynamic system, it has a
mixed role of combined transmission and absorption
of the stress. Thanks to this dynamical behavior, the
microvacuolar system permits the transmission and
 A B

C D
Figure 43-4  A, Traction on the paratendon during surgery. B, Searching for a space over the tendon surface. C, Network
between the tendon and the surrounding tissues: the MVCAS. D, The movable, elastic sliding tissues, MVCAS.

A B

C D
Figure 43-5  A, Peritendinous sliding system. B, Tissue continuity between tendon and microvacuolar distribution. C, 3D
MicroVacuola. D, Apparent fibrillar distribution in the dispersed branching pattern.
 A

Collagen I

Collagen VI
Collagen I

Collagen I
Co
lla
ge

B
nI

Polysaccharides, hyaluronan
Network of gly licans
colicans
Network of glycolicans of glyco
N etwork

C
Figure 43-7  A, Diagrams showing the microvacuoles
inside the MVCAS. B, Real microvacuole with a hexagonal
shape at the beginning of dissection. C, Microvacuole
hyperpressure after atmospheric pression exposure filled
D with GAG and the collagen type I, III, and IV framework.
Figure 43-6  A, Fibrils composed of collagen and elastin
delimit the microvacuoles. B, Magnification MVCAS under
the electron microscope. C, A microvacuola with a hexagonal
shape. D, Diagram of the basic building brick of the MVCAS:
the microvacuola filled with GAG and the frame contains
collagen types I, III, and IV.
 Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues
Figure 43-8  Collagen frameworks along with fibrils provide
support and nutrition.
absorption of the constraint across the tissue while at
the same time the surrounding tissues are not affected.
During progressive traction (2 N/cm2) (Figure 43-10),
the fibers rearrange themselves in response to the local
stress. As the stress increases, the fibers become more
aligned in the direction of the stress. All of the compo-
nent parts then turn so as to be oriented as much as
possible in the direction of the applied force. However,
this set of movements is difficult to analyze, so certain
fibers have to be selected for analysis on an arbitrary
basis. We therefore stained some fibers yellow and
observed their behavior.
Other internal factors need also be taken into account:
The fibrillar struts behave in a very peculiar manner.
First, in response to stretching a fibril becomes longer
by resembling a wormlike chain or a spring, which
means that it is capable of molecular rearrangement and
e17
Figure 43-9  Chaotic dynamic system showing a tendency
of pseudo-geometric arrangement.
can recover its initial form by returning to its initial
position (Figure 43-11). This mechanism seems to be
involved in minor forms of tension.
Second, the fibers undergoing mechanical stimula-
tion can divide in space into several other fibrils, which
enables an immediate dispersion and distribution of
the forces across the tissue space (Figure 43-12).
Third, the fibers are able to glide past each other
around a mobile focal point along the entire length of
both fibers (Figure 43-13). Because classic linear models
based on straight lines cannot account for these move-
ments, we are required to use fractal and nonlinear
mathematics to explain them.
These three dynamic abilities always coexist, which
allows the structure to move in three-dimensional space
and to respond optimally no matter what direction in
which it is stretched (Figure 43-14).
e18 Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues

A B C

D E F
Figure 43-10  A 200-fold magnification of fibrillary movements during traction. Time span between photographs A and F is
2 seconds. Diameter of fibrils = 10 µm. Two-dimensional analysis of what actually occurs in three dimensions. The fibrils
become oriented in the direction of traction but in a less-organized manner than the rules of linearity would have it.

Figure 43-11  Distention-retraction of a fiber.

 Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues e19

Figure 43-12  Division of a fiber into several fibrils that diffuse the stress three-dimensionally.

Figure 43-13  Fiber moves freely along axis of another fiber.

e20 Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues
Figure 43-14  Variation of fibrillar movements in the three dimensions of space opens a lot of dynamical opportunities. The
chaotic, pseudo-geometric distribution of the structures in vivo and the different ways in which the fibrils behave require a
specific vision of the system.
We have frequently observed glycosaminoglycan
(GAG) gel movements inside the fibers, the sliding
of drops along the fibrils, together with dilaceration,
absorption, and reconstitution. It is impossible to ignore
the role of GAG in response to traction (Figures 43-15
and 43-16).
In Vitro Observations
The sides of the intertwined microvacuoles are com-
posed of collagen fibers (75%, mostly type I, some type
III, IV, and VI collagens) and 20% elastin. Type I collagen
makes up 23% of the microvacuolar unit. Their diameter
ranges from a few to several dozen microns and they
vary in length, thus giving an overall disorganized
chaotic aspect. These microvacuoles contain a highly
hydrated proteoglycan gel (70%), which can change
shape during movement but whose volume remains
constant. Their lipid content (4%) is high. A major issue
in this system is the presence of water, which is omni-
present as soon as the skin is penetrated (Prof. Herbage,
INSERM Laboratories, Lyon, France). For this reason, no
biomechanical explanation for the sliding of subcutane-
ous structures can disregard the dynamics of the fluids
present (e.g., osmotic pressure and superficial tension).
DISCUSSION
This sliding tissue with its basic polyhedric shaped units
is to be found in every nook and cranny of our organ-
ism. The tissue, which used to be referred to as connec-
tive or areolar tissue, is totally continuous throughout
the fibers and their prolongations. Even the intermedi-
ary structures such as the deep premuscular fascia are
incorporated into this network and are connected with
it on their superior and inferior aspects, thereby increas-
ing the shock-absorbing properties of the tissue and
allowing the structures to move interdependently.
Whether it is in the abdominal, thoracic, dorsal, or ante-
brachial regions or in the scalp, this tissue network is
omnipresent (Figure 43-17).
Indeed, there is no space within the body where it is
not found. This fibrillar tissue network surrounds even
structures subject to relatively little movement—such as
nerves and the periosteum—although in these cases,
there are differences in the network itself and in the size
of the vacuoles. Indeed, it would seem that the MVCAS
occurs everywhere in the body.
The notion of tissue continuity provided by the mul-
timicrovacuolar collagenic absorbing system, MVCAS.
All of our observations support this tissue continuity
and the microvacuolar and fibrillar architecture. In tra-
ditional observations of this tissue, the concept of
sliding was thought to be due to several coaxial con-
joined layers with progressively decreasing diameters
framing the vascular structures, or to a virtual space
between visceral and membranous layers.
The layer closest to the tendon would move the
fastest, while the one farther away would move more
slowly. This concept of annular layers sliding between
each other based on the theoretical concept of virtual
space and a hierarchical tissular distribution seems
to be incorrect (see Figure 43-5). For this reason, we
have developed the concept of a tissue continuum. This
concept supposes that there is an association between
the way tissues are organized and how they behave.
 Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues
Figure 43-15  Three-dimensional sketch showing potential
for interfibrillar movement involving the three dynamic
capacities of the system.
It is important to highlight that, due to the dispersed
pattern of the fibrils and the cohesive nature of the
extracellular matrix, the sliding system forms a continu-
ous deformable framework performing three major
mechanical roles:
 Responding to any kind of mechanical stimulus in
a highly adaptable and energy-saving manner,
ensuring the complete movement of the tendon
 Preserving peripheral tissue stability, structures,
and shapes; providing information during action
and springing back to its original shape
 Ensuring the interdependence and autonomy of
the various functional units
e21
This sliding system and its multifibrillar organization
participating simultaneously in movement, restitution,
and the transfer of energy seem to be composed of ele-
ments developed from within this tissue rather than a
superposition of different tissues. We get the impression
of elements united to compose one sole tissue with
genuine continuity between the tendon, the sliding
tissue, and all surrounding tissues. The notion of layers
is replaced by a greater or lesser densification of the
MVCAS with a more or less specific cellularization. In
vivo observation has rendered the notion of tissue layers
unacceptable. This means that we need a new way of
thinking—a way of posing the problem in terms of
global dynamics and continuous matter and a theory
involving the concept of a tissue continuum. This is in
total contradiction with the traditional view of sliding
structures, tissue stratification, and virtual space between
tissue layers.
The microvacuole as the basic structural unit enables
the MCVAS to perform its function of filling space and
preserving form.19-23 This multimicrovacuolar collagenic
absorbing system is made of microvolumes and micro-
fibrils and is focused around the microvacuole, which
we can consider to be the basic framework unit. This
enables us to explain the very notion of form and the
fact that this form adapts to its environment but does
not change. We need to move to three dimensions to
really understand this.
It would seem that the existing polyhedron shape of
the microvacuole is the optimal shape for occupying
space with the most minimal arrangement. It is essential
to grasp that to fill space, living structures tend to adapt
geometrically simple forms such as polygons, spirals, or
cylinders.
By accumulation and superposition, these multimi-
crovacuolar polyhedric patterns under internal tension
will build an elaborate form. The concept of the micro-
vacuole explains the ability of the tissues to resist com-
pression and expansion while maintaining a stable
volume.
Efficient Dynamic Behavior
MVCAS is highly dynamic, and its components have
efficient dynamic behavior. Although the arrangement
of the structures is chaotic, with a dispersed pattern of
distribution, this flexible, polyhedric architecture is able
to assume many shapes, thereby providing stability and
efficient sliding.
We are now confronted with the dilemma of chaotic
architecture and optimal efficiency. Because of the exis-
tence of this sliding system, called the paratenon or
areolar or subsynovial connective tissue (SSCT)5 by
other investigators, the tendon displays optimal sliding
and can move smoothly and quickly without any hin-
drance and without disturbing anything around it,
e22 Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues

Figure 43-16  The multimicrovacuolar system during peritendinous sliding.

A B

C D
Figure 43-17  The sliding system in different sites. A, Forearm subcutaneous area. B, Thoracic wall. C, Thigh region.
D, Abdominal wall.
 Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues
thus allowing the tendon to move freely without trans-
ferring the movement to the surrounding structures.
This accounts for the absence of any dynamic repercus-
sions of the movement on the skin surface.
The essential function of the network is to ensure its
own efficient movement. Every structure component in
this network must permit movement while at the same
time ensuring shock absorption, which is indispensable
to avoid rupture of the mechanical elements within
the network. The question of how the microvacuolar
network behaves as a shock absorber, including the fact
that the closest vacuole to the moving structure under-
goes maximal deformation while those farthest away
hardly change shape, remains to be explained. These
two apparently conflicting roles must also be accompa-
nied by the spring-back memory function. It appears to
be a very elastic system that accommodates tendon
movement but does not disrupt the stretched collagen
fibers within the normal range of motion of tendon
motion.
These highly flexible, stressed or loaded fibrils take
various shapes during tendon sliding and movement
of extremities. The changes of interlacing, intertwining
fibrillar structures are created by the repetition of move-
ments, including distention, retraction, and compres-
sion during extremity movement. The system seems to
function optimally dynamically. The fibril movement
is highly organized and nicely coordinated, without
abnormal force distribution within the system, and the
motion of the tendon and other tissues is smooth and
efficient.
Due to the natural arrangement of the fibrils in their
seemingly chaotic or dispersed pattern and due to the
hydrophilic nature of the GAG in the extracellular
matrix, the microvacuole (which is a microvolume) is
able to adapt, change form, and return to its original
form. The MVCAS therefore displays chaotic patterns
and multiadaptive efficiency.
A Global System
This internal multifibrillar and microvacuolar architec-
ture is too repetitive not to be taken into account. Seen
in these terms, the whole structure of the body may
be considered as an immense collagen network. Going
from the macroscopic to the limits of the microscopic,
this network can be seen to stretch continuously from
e23
the peritendinous surface to the finest multimicro­
vacuolar organization, the ultimate boundary of the
mesosphere, before entering the realm of molecular
dynamics. The entire dynamic and structural continuum
may thus be explained and represented (Figure 43-18).
It may even be that this fundamental system obeys
dynamic and biomechanical principles that are subject
to influences other than gravity.
Anatomical Features
In order to transmit forces, this complex sliding system
must be resistant and able to adapt to environmental
and mechanical requirements. It must be able to con-
serve its mobility while maintaining its architecture and
adapting to the mechanical demands imposed on it. As
the function of different regions differ, its structures
therefore vary by anatomical sites according to changing
functional needs.
This type of microvacuolar sliding that we described
within a multimicrovacuolar framework has been seen
in zones 3, 4, and 5 of the flexor tendons. In the digital
fibrous sheath area, an efficient change in the subcuta­
neous tissue is observed. The digital sheath and the
sheath in the carpal tunnel area share some mechanical
characteristics, but each has its own specific morphologic
features and function.
CONCLUSION
The notion of virtual space between the sheath in the
carpal tunnel area and the flexor tendons or the absence
of any connecting tissue and especially vascular tissue
must be reconsidered. The vision described here has
resulted from anatomical observations performed on
fresh or formalin-treated cadavers. A different view of
the sliding system is therefore required. Based upon our
in vivo studies, a new sliding system can now be pro-
posed. The basic framework of this sliding tissue system
is the nonlinear, interconnecting, multimicrovacuolar
network, which seems chaotic and complex and yet
simultaneously shows graceful simplicity with one final
objective: to promote and facilitate sliding adaptation
and mobility. Future research in biology and chemistry
must examine the behavior of these basic structures,
which have long been neglected due to their apparently
self-evident nature.
e24 Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues

A B

C D

E
Figure 43-18  Progressive 50-fold enlargement of peritendinous area from the macroscopic to the pre-molecular conveys an
idea of the total tissue continuity of the sliding system with tendon. (Magnification: A, ×0; B, ×2, C, ×5, D, ×20, E, ×50.)
 Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues
References
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fluid and tendon sheath for flexor tendon nutrition. An exper-
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3. Littler JW: Free tendon grafts in secondary flexor tendon
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4. Verdan CE: Half a century of flexor-tendon surgery. Current
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5. Strickland JW, Glogovac SV: Digital function following flexor
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6. Strickland JW: Results of flexor tendon surgery in zone II,
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7. Hunter JM: Tendon salvage and the active tendon implant: A
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8. Paneva-Holevith E: Résultats du traitement des lésions mul-
tiples des tendons fléchisseurs des doigts par greffe effectuée
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9. Boyes JH: Flexor-tendon grafts in the fingers and thumb: An
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11. Lundborg G, Myrhage R, Rydevik B: The vascularization of
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2:417–427, 1977.
12. Schatzker J, Brånemark PI: Intravital observations on the
microvascular anatomy and microcirculation of the tendon,
Acta Orthop Scand Suppl 126:1–23, 1969.
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13. Smith JW, Ellinger CG: La vascularisation des tendons. In
Tubiana IR, editor: Traité de la Chirurgie de la Main, Paris,
1986, Masson, pp 375–380.
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the fingers, Chir Narzadow Ruchu Ortop Pol 39:265–270,
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15. Guimberteau JC: Journey to the tendon and satellite sheath
areas. In vivo anatomical observations of flexor tendon vascu-
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Brussels; 1999.
16. Guimberteau JC: New Ideas in Hand Surgery; Island Vascular-
ized Flexor Tendon Transfers, the Sliding System, France, 2001,
Aquitaine Domaine Forestier, pp 210.
17. Guimberteau JC, Panconi B, Boileau R: Mesovascularized
island flexor tendon: new concepts and techniques for flexor
tendon salvage surgery, Plast Reconstr Surg 92:888–903, 1993.
18. Zhao C, Amadio PC, Zobitz ME, et al: Gliding characteristics
of tendon repair in canine flexor digitorum profundus
tendons, J Orthop Res 19:580–586, 2001.
19. Guimberteau JC, Bakhach J: Subcutaneous tissue function:
the multimicrovacuolar absorbing sliding system in hand and
plastic surgery. In Siemonov MZ, editor: Tissue Surgery. New
York, 2006, Springer, pp 41–54.
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23. Thompson D: On Growth and Form, Cambridge, 1992, Cam-
bridge University Press.
 CHAPTER
44  
MOLECULAR BIOLOGY OF
TENDON HEALING
Chuan Hao Chen, PhD, Ya Fang Wu, MD, and
Jin Bo Tang, MD
The weak healing capacity of the injured tendons, intra-
synovial tendon in particular, is a critical issue underly-
ing difficulties in achieving optimal outcomes after
tendon surgery. After surgical repair, tendons ought to
be able to move to prevent adhesions; the weak healing
predisposes tendons to rupture during the early tendon
movement. In the early half of the 20th century, the
mechanisms of healing of primary end-to-end repair of
the intrasynovial tendon were not of great concern,
because secondary tendon grafting was advocated to
treat tendon injuries in the digits. In the 1950s and
1960s, the healing potential of primarily repaired
tendons in the sheath area became an essential question
facing hand surgeons. In the recent decades, the healing
of flexor tendons has been the subject of investigations
of a great number of investigators.
In the 1970s and 1980s, a number of elegant experi-
mental investigations demonstrated that cells in the
intrasynovial tendon segment can proliferate and par-
ticipate in the healing process, establishing the concept
of “intrinsic tendon healing.”1-7 Since 1990s, investiga-
tions into tendon healing biology have been directed
toward elucidation of molecular events underlying the
healing process and development of molecular thera-
peutic methods to enhance the healing or to decrease
adhesion formations. These investigations came from
several major laboratories around the world, under
investigators such as Abrahamsson,8-10 Chang,11-14 Gel-
berman, Boyer, and Thomopoulos,15-20 McGrouther,21-24
Mass,25,26 Tang,27-34 and Wolfe.35
Currently, laboratory research is focused on uncover-
ing gene expression patterns of the healing tendon and
exploring cellular and genetic therapeutic approaches to
strengthen weak intrinsic healing capacity. Work is also
aimed at improving the healing strength of the surgi-
cally repaired tendon.
TWO MECHANISMS OF INTRASYNOVIAL
TENDON HEALING
It is now generally believed that intrasynovial flexor
tendons heal through two mechanisms—intrinsic and
e26
extrinsic. Both intrinsic and extrinsic tendon healing
mechanisms come into play in a clinical setting. Intrinsic
healing takes place through proliferation of tenocytes
and production of extracellular matrix by intrinsic cells.
Extrinsic healing is the healing process brought about by
growth of tissues or cell seeding from outside the lacer-
ated tendon. Clinically, the participation of intrinsic
and extrinsic healing after tendon repair depends on the
condition of the tendon and surrounding tissues. Extrin-
sic cells participate minimally in the healing of clean-cut
wounds but can dominate healing when the intrinsic
healing is jeopardized by severe trauma to the tendon.
For a typically lacerated tendon, the healing process
generally consists of three stages: inflammation, colla-
gen production (or proliferation and repair), and col-
lagen remodeling.
The first stage is manifested with infiltration of
inflammatory cells, such as neutrophils. Monocytes and
macrophages are recruited to the injury site within the
first 24 hours, and phagocytosis of necrotic materials
occurs. After the release of vasoactive and chemotactic
factors, angiogenesis and proliferation of tenocytes are
initiated. Tenocytes then move into the site and start to
synthesize collagen III. The inflammation stage usually
lasts for a few days, followed by the collagen production
stage.
In the collagen production stage, which lasts for 5 to
6 weeks, the tenocytes produce large amounts of colla-
gen and proteoglycans at the repair site. In the early part
of this stage, tenocytes proliferate dramatically, but in
later weeks, inflammation subsides and cell prolifera-
tion is less obvious. Collagen I, which increases healing
strength, is produced abundantly in the later period.
At about 6 weeks after injury, the remodeling stage
begins. The first part of this stage is consolidation, which
lasts from about 6 to 10 weeks after the injury. During
this time, synthesis of collagens and glycosaminogly-
cans (GAGs) decreases, as does cellularity. The tissue
becomes more fibrous as a result of increased produc-
tion of collagen I, and the fibrils become aligned in the
direction of mechanical stress. The final maturation
This chapter does not appear in the print edition.

stage occurs after 10 weeks, and there is an increase in
cross-linking of the collagen fibrils, which makes the
tissue stiffer.
MOLECULAR BIOLOGY OF TENDON HEALING
Roles of Individual Growth Factors
A variety of molecules are involved in tendon healing.36
The roles of six growth factors have been studied associ-
ated with tendon healing in vivo or tenocyte prolifera-
tion in vitro:
1. Transforming growth factor (TGF). This molecule
is secreted by all of cell types participating in the
healing process and plays a role in wound healing
and scar formation. TGF-β has three isoforms: TGF-
β1, TGF-β2, and TGF-β3; they play different roles
in scar formation. While TGF-β1 and -β2 are known
to induce fibrotic changes and scar formation,
TGF-β3 may inhibit scar formation.37 Three iso-
forms are 60% to 80% homologous and are dimers
of 12.5-kDa polypeptides cleaved from larger pre-
cursors after being secreted from the cells into the
ECM. TGF-β is a master mediator in the pathogen-
esis of fibrosis and scar formation. Regarding
specific roles of TGF-β in flexor tendon healing,
Chang and colleagues found increased levels of
TGF-β1 mRNA in the sheath and the tendon itself
after tendon trauma. TGF-β receptors 1, 2, and 3
were upregulated as well. In in vitro studies, TGF-
β1 induced collagen I production by tenocytes.11
Chang and colleagues applied TGF-β1 neutralizing
antibodies to injured digital flexor tendons, and
this therapy increased the range of digital motion
of the toes operated upon in a rabbit model.13
2. Insulin-like growth factor (IGF). It is a single-
chain polypeptide hormone. The primary biologi-
cal action of IGF-1 is mitogenic activity for a broad
range of cells. Extracts from the epitenon and
internal compartment of avian flexor tendons
were found to contain IGF-1; these extracts could
stimulate DNA synthesis by tenocytes.8 In in vitro
culture of tenocytes, IGF-1 was found to increase
cell proliferation as well as stimulate synthesis of
DNA, collagen, and proteoglycan.9 Both IGF-1 and
IGF-2 were shown to promote proliferation of
tenocytes in vitro tenocyte culture.8-10
3. Platelet-derived growth factor (PDGF). PDGF
consists of a group of dimers, each of two chains
(A and B). Various grouping of these chains form
three isoforms (AA, BB, and AB). PDGF acts as a
chemoattractant and mitogen for fibroblasts,
endothelial cells, and smooth muscle cells. The
cell surface contains two kinds of receptors (α and
β) for PDGF binding. In fibroblasts, the β receptor
is predominant. Only the isoform BB of PDGF
Chapter 44:  Molecular Biology of Tendon Healing e27
binds to the β receptor. Investigations have focused
on the roles of PDGF-BB in tendon healing. Exog-
enous PDGF-BB stimulates collagen, proteogly-
can, and DNA synthesis of the tenocytes.18
Expression of PDGF-BB is increased after tendon
injuries in canine and chicken models.34,37
4. Vascular endothelial growth factor (VEGF).
VEGF has five isoforms (i.e., 121, 145, 165, 189,
and 206) distinguished by their number of amino
acids. Biological effects of these isoforms are
similar. VEGF121 and VEGF165 are the predomi-
nant isoforms secreted by most cells. VEGFs bind
to one of three VEGF receptors (VEGFR 1, 2, and
3) on the cell surface to exert their biologic effects.
The primary role of VEGF is to induce angiogen-
esis, including that in pathological conditions. In
a canine model, VEGF mRNA expression was
increased in healing flexor tendons.17,38,39 VEGF
expression may differ between the cells in endo-
tenon and epitenon at the repair site: 67% of the
cells in the endotenon at the repair site express
VEGF, but 10% of epitenon cells express VEGF.
Direct injection of VEGF increased the healing
strength of Achilles tendon in a rat model.
However, the effectiveness of direct use of VEGF in
synovial tendons has not been tested. We found
that AAV2-VEGF treatment significantly increased
the healing strength of the chicken flexor tendons
at postoperative weeks 3, 4, and 6.
5. Basic fibroblast growth factor (bFGF). bFGF
commonly presents as an 18-kDa, single-chain
polypeptide of 146 amino acids; other forms of
greater molecular weights (22, 22.5, and 24 kDa)
also exist. bFGF has a wide range of biological
effects, including induction of cell proliferation
and migration as well as stimulation of fibroblasts
to produce collagens and collagenase. There have
been several specific investigations of the roles of
bFGF in flexor tendon healing. Duffy and col-
leagues detected presence of bFGF in normal intra-
synovial flexor tendons.16 Chang and colleagues
found that bFGF levels were increased in flexor
tendons and sheath during healing from day 1 to
week 8.12 Tang and colleagues observed that exog-
enous bFGF acts on cultured chicken tenocytes to
accelerate cell proliferation and to promote col-
lagen I gene expression.27,28
Both direct delivery of bFGF and transfer of
bFGF cDNA via appropriate vectors to the healing
tendons have been tested to enhance tendon
healing.31,40-43 Direct delivery of bFGF was achieved
with direct injection of the bFGF,40 use of bFGF-
coated suture,41 or bFGF delivery through con-
trolled release system.42,43 Direct injection of bFGF
did not improve the healing strength of the tendon,
nor did bFGF delivered through controlled release
e28 Chapter 44:  Molecular Biology of Tendon Healing
system.40,43 After delivery of bFGF to the tendon,
biological reactions and increases in cellular pro-
liferation in the healing tendons were observed,
but mechanically, the healing strength was not
increased.43 Tendon repair with bFGF-coated surgi-
cal suture increased the tendon strength at week 3
after surgery, but not at week 6, in a rabbit model.41
AAV2-bFGF–treated tendons had a significantly
greater breaking strength than the nontreatment
control at weeks 2, 3, and 4 in a chicken model.31
6. Bone morphogenetic proteins (BMPs). BMPs are
a group of growth factors originally discovered by
their ability to induce the formation of bone and
cartilage. BMPs are considered to constitute a
group of pivotal morphogenetic signals, orches-
trating tissue architecture throughout the body.
There are BMPs 1 through 15 in this superfamily.
BMP14 is called growth differentiation factor-5
(GDF-5) as well; this factor was particularly studied
regarding its role in tendon healing and repair.
Hogan and colleagues44 found that growth differ-
entiation factor-5 (GDF-5, or BMP14) regulates
ECM gene expression in murine tendon fibro-
blasts. They isolated mice Achilles tendon fibro-
blasts and treated them with rGDF-5 (0 to 100 ng/
mL) for 0 to 12 days in cell culture. The temporal
effect of rGDF-5 on ECM gene expression was
analyzed for type 1 collagen and aggrecan expres-
sion. They found that expression of extracellular
matrix (ECM) genes procollagen IX, aggrecan,
matrix metalloproteinase 9, and fibromodulin
were upregulated. Proinflammatory reaction genes
were downregulated. rGDF-5 led to an increase
in total DNA, glycosaminoglycan (GAG), and
hydroxyproline (OHP). rGDF-5 treatment showed
improved collagen organization over controls.
No studies have directly investigated expression profile
of BMPs during intrasynovial tendon healing process.
However, studies were performed to determine relation
of BMPs with the healing in rat Achilles tendon. Elias-
son and colleagues45 investigated how mechanical
loading influences the gene expression of the BMP sig-
naling system in intact and healing tendons and how
the BMP signaling system changes during healing. They
studied four BMPs (OP-1/BMP-7, GDF-5/CDMP-1/BMP-
14, GDF-6/CDMP-2/BMP-13, and GDF-7/CDMP-3/
BMP-12), two receptors (BMPR1b and BMPR2), and the
antagonists follistatin and noggin. The Achilles tendon
was transected in rats. Ten tendons were analyzed before
transsection and in the early healing period after surgery.
All genes except noggin were expressed at all time points.
Loading strongly decreased the expression of follistatin.
They concluded that BMPs are involved in tendon
healing, and change after tendon loading. Bolt and col-
leagues46 showed that adenoviral vector–mediated
BMP-14 gene therapy increases tendon tensile strength
in a rat model of Achilles tendon injury 2 and 3 weeks
after surgery.
Chhabra and colleagues47 found that GDF-5 defi-
ciency delays Achilles tendon healing in GDF-5 −/−
mice. After injury, these mice took longer to reach peak
cell density and GAG and collagen content in the repair
site compared with normal control littermates. Aspen-
berg and Forslund48 found that implanting GDF-5 and
GDF-6–containing collagen sponge enhanced tendon
healing strength at 2 weeks after surgery in a rat Achilles
tendon model. Other studies also identified that exog-
enous GDFs stimulated healing of the Achilles tendon,
but this response was influenced by loading; without
loading, cartilage and bone formation was initiated.
Roles of Growth Factors and Cytokines
In Vivo
Chen and colleagues investigated the differences in
expression levels of six growth factors in lacerated and
surgically repaired flexor tendon in chicken toes.32 Con-
nective tissue growth factor (CTGF) and TGF-β had high
levels of gene expression in the early healing period
(Figure 44-1). Levels of expression of VEGF and IGF-1
genes were high or moderately high. Expression of the
TGF-β gene was upregulated after injury, whereas the
bFGF gene was downregulated at all time points
observed (Figures 44-1 and 44-2) and expressed at the
lowest levels among six growth factor genes 2 to 3 weeks
after surgery. The PDGF-B gene was minimally expressed
in injured tendon. Findings in immunohistochemical
staining corresponded to TGF-β, bFGF, and IGF-1 gene
expression (see Figure 44-2).
Schulze-Tanzil and colleagues49 reviewed the reports
of cytokines and growth factors on tendon healing and
summarized interrelations known between the interleu-
kin (IL)-1β, transforming growth factor (TNF)-α, IL-6,
and VEGF in tendon to assess their role in tendon
damage and healing. Multiple interrelations between
cytokines and ECM synthesis, catabolic mediators such
as matrix-degrading enzymes, inflammatory and angio-
genic factors (cyclo-oxygenase [COX]-2, prostaglandin
[PG]E2, VEGF, nitric oxide [NO]), and cytoskeleton
assembly are evident. Proinflammatory cytokines affect
ECM homeostasis, accelerate remodeling, amplify bio-
mechanical adaptiveness, and promote tenocyte apop-
tosis. This multifaceted interplay might both contribute
to and interfere with healing, which has relevance for
the development of novel therapeutic strategies.
Extracellular Matrix
Cao and colleagues in our laboratory studied expression
of ECM components from postsurgical day 3 to week
12 in a chicken model. Tendons exhibited drastic upreg-
ulation in the expression of collagens I, III, XII, and XIV
as early as 3 days after injury. After day 3, expression of

0.4
**
0.35
Levels of gene expression (target/GAPDH) 0.3
*
0.25
0.2
*
0.15
0.1
0.05
0
0 3
Time-points of the early healing period (days)
Figure 44-1  Changes in level of expression of six growth factor genes in the early healing period of a chicken FDP tendon
with real-time PCR analysis. Growth factor expression peaked at day 3, and CTGF and TGF-β expressed in the highest level.
(Modified from Chen CH, Cao Y, Wu YF, et al: Tendon healing in vivo: gene expression and production of multiple growth
factors in early tendon healing period, J Hand Surg [Am] 33:1834–1842, 2008.)
collagen I declined somewhat but remained at moder-
ately high levels after week 3. The collagen III gene was
upregulated progressively from day 3, with a drastic
increase from week 2 to 5. The fibronectin gene was
upregulated from week 2 to 8. Expression of aggrecan
and fibromodulin genes did not change after tendon
injury.
Matrix metalloproteinases (MMPs) act to modulate
metabolism of tendon healing. They play an important
role in the degradation and remodeling of the ECM.
They break down structural proteins of the ECM. Certain
MMPs, such as MMP-1, -2, -8, -13, and -14, have colla-
genase activity, capable of degrading collagen fibrils. The
activities of the MMPs are inhibited by endogenous
tissue inhibitors of metalloproteinases (TIMPs), a family
of four protease inhibitors (TIMP 1–4). Using the same
chicken model, Cao and colleagues investigated levels of
gene expression of MMPs and TIMPs from the early to
late healing periods in digital flexor tendons. MMP1 of
the tendon was upregulated and remained high in the
first 6 weeks after injury and dropped thereafter. TIMP2
and TIMP3 were downregulated after tendon injury in
the first 6 weeks after injury but were upregulated later.
Berglund and colleagues50 studied molecular events
during flexor tendon healing in a rabbit model of flexor
tendon injury. The mRNA expression for the growth
factors, MMPs, and TIMPs were measured in tendon and
tendon sheath tissue at several time points (3, 6, 21, and
42 days) representing different phases of the healing
process. They found that MMP-13 remained increased
Chapter 44:  Molecular Biology of Tendon Healing e29
VEGF PDGF
TGF-beta bFGF
CTGF IGF-1
*
*
*
** ** **
9 14 21
during the study period, whereas MMP-3 returned to
normal levels within the first week after injury. TIMP-3
was downregulated in the tendon sheaths. Cathepsin K
was upregulated in tendons and sheaths after injury.
Nerve growth factor (NGF) was present in both tendons
and sheaths, but unaltered. IGF-1 exhibited a late
increase in the tendons, while VEGF was downregulated
at the later time points. They demonstrated the presence
of NGF in flexor tendons and concluded that MMP-13
expression appears to play a more protracted role in
flexor tendon healing than MMP-3. The relatively low
levels of endogenous IGF-1 and VEGF mRNA following
injury support their potential beneficial role as exoge-
nous modulators to optimize tendon healing and
strength without increasing adhesion formation.
Intracellular Signal Pathways
Only the NFκB pathway was investigated in in vitro
tenocytes treated with exogenous bFGF and in in vivo
flexor tendon healing.38,51 Each of the key factors in the
NFκB pathway was found to be activated after exoge-
nous application of bFGF to the tenocytes’ culture
medium. In the healing flexor tendon in a chicken
model, NFκB gene was found to be upregulated.51
TENOCYTE APOPTOSIS DURING
TENDON HEALING
Apoptotic events in the healing digital flexor tendon
have been investigated recently.34,52 Nevertheless, teno-
cyte apoptosis can be an important event in the healing
e30 Chapter 44:  Molecular Biology of Tendon Healing

TGF-beta IGF-1 bFGF

Day 0

21

Figure 44-2  Immunohistochemical staining of three growth factors in the healing tendons. Great amount of TGF-β is
present in the tendon. Both bFGF and IGF-1 are present in a much lower amount compared with TGF-β. (Modified from
Chen CH, Cao Y, Wu YF, et al: Tendon healing in vivo: gene expression and production of multiple growth factors in early
tendon healing period, J Hand Surg [Am] 33:1834–1842, 2008.)

digital flexor tendon and can affect healing strength.
Investigations of Wu and colleagues have been aimed at
elucidating the relationship between cellular apoptosis
and proliferation in early tendon healing.34 At postop-
erative days 3, 7, 14, 21, and 28, Wu and colleagues
quantitatively analyzed the presence of apoptotic cells
in tendons using an in situ TUNEL assay (Figure 44-3),
and performed immunofluorescence staining with anti-
bodies to proliferating cell nuclear antigen (PCNA) to
assess proliferation (Figure 44-4), and Bcl-2 to assess
antiapoptotic effects. Apoptosis of tenocytes peaked at
day 3 (see Figure 44-3), which is followed about 10 days
later by the peak proliferation period. At days 14 to 28,
the number of apoptotic cells decreased significantly
compared with days 3 and 7, yet numbers remained
greater than those at day 0. At days 7 to 14, the number
of PCNA-positive cells peaked (see Figure 44-4). At days
7 and 14, the cells positively stained with Bcl-2 peaked.
These findings indicate that tenocyte apoptosis is accel-
erated within several days post-injury, followed by

A B
Figure 44-3  Tenocyte apoptosis is most obvious at day 3 after tendon laceration. The pictures show the cells with dark
brown nucleus stained with TUNEL are apoptotic cells (A ×200, B ×400). Nearly 50% of the tenocytes in the endotenon are
apoptotic at day 3.
Figure 44-4  Tenocyte proliferation peak at postsurgical
day 14. The picture shows positive PCNA-stained tenocytes,
which peak in number at day 14 (×200). Positive PCNA
staining indicates proliferation of the cells.
increases in cellular proliferation and activation of
molecular events to inhibit apoptosis in 2 to 4 weeks.
After 4 weeks, tenocyte proliferation persisted, but at a
rather lower level. Tenocyte apoptosis also declined
drastically (Figures 44-5 and 44-6). In the late healing
period, tenocyte apoptosis persisted, likely in response
to tendon remodeling, while tenocyte proliferation was
minimal or undetectable.52
Lui and colleagues53 found increases in tenocyte
apoptosis at the end of patellar tendon healing. They
investigated the role of apoptosis in cell turnover in a
rat central 1/3 patellar tendon donor site injury model.
The observations were made at days 4, 7, 14, and 28 and
months 2 and 6 after surgery. The total fibroblast-like
cell density in the center of the wound increased from
day 4 and thereafter steadily returned to normal. In situ
Chapter 44:  Molecular Biology of Tendon Healing e31
40 Bcl 2-positive cells
Positively-stained cells/field
PCNA-positive cells
35
30
25
20
15
10
5
0
0 3 7 14 21 28
Days
Figure 44-5  Changes of PCNA- and Bcl-2–positively
stained cells (Bcl-2 is an antiapoptotic protein) in the early
tendon healing period in a chicken model. Numbers plotted
in the graph show positively stained cells in the field under
high magnification (×400) over five time-points. (Data from
Wu YF, Chen CH, Cao Y, et al: Molecular events of cellular
apoptosis and proliferation in the early tendon healing
period, J Hand Surg [Am] 35:2–10, 2010.)
TUNEL assay showed few positive staining cells in the
wound at days 4 and 7. The percentages of TUNEL-
positive fibroblast-like cells showing morphological
characteristics of apoptosis increased sharply and
reached the maximum on day 28 (median, 31.4%). No
fibroblast-like cell was stained at month 6 and the
healed tissue was similar to that in a normal uninjured
tendon. A similar trend was observed with active
caspase-3 immunohistochemistry. They concluded that
an increase in apoptosis at the end of tendon healing
coincided with a decrease in cellularity.
The findings of Skutek and colleagues54 corroborate
that mechanical stretching directly activates intracellular
e32 Chapter 44:  Molecular Biology of Tendon Healing
Bcl 2-positive cells
50
PCNA-positive cells
Positively-stained cells (%)
40
30
20
10
0 enhancing flexor tendon healing. Delivery of cells
0 3 7 14
Days
Figure 44-6  Changes of percentage of PCNA- and
Bcl-2–positively stained cells in the field under high
magnification (×400) in a total population of the cells.
(Data from Wu YF, Chen CH, Cao Y, et al: Molecular events   the healing strength at the cost of increasing adhesion
of cellular apoptosis and proliferation in the early tendon
healing period, J Hand Surg [Am] 35:2–10, 2010.)
signaling pathways, which in turn induce apoptosis.
They investigated the response profile of human tendon
fibroblasts in terms of apoptosis in response to cyclic
stretching. They also found that cyclic mechanical
stretching activated stress-activated protein kinase
(SAPK)/Jun N-terminal kinase (JNK).
FUTURE FOR TENDON HEALING BIOLOGY
INVESTIGATION AND APPLICATION
The molecular mechanisms underlying tendon healing
are still poorly understood currently. Our understanding
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 CHAPTER
45  
MOLECULAR METHODS TO
PREVENT ADHESION
FORMATION
Armin Kraus, MD, and James Chang, MD
OUTLINE
Tendon adhesions are a significant problem, especially
after repair in zone 2. Tendon healing undergoes three
different phases—inflammation, proliferation, and
maturation—which can all be altered to reduce adhe-
sions. Intrinsic healing without contact to surrounding
tissue and therefore low adhesive potential can be
distinguished from extrinsic healing, where cell inva-
sion and vascularization take place from the surround-
ing with concomitant adhesions. Motion has shown
to decrease adhesions by mechanical disruption of
adhesions and by molecular alteration of tendon cells.
Artificial tendon grafts can be seeded with cells to form
an epitenon layer that could enhance gliding. Adding
or blocking various cytokines can reduce adhesion for-
mation, but cytokine interaction has shown to be
complex. Gene transfer or RNA interference are further
methods under investigation. Mesenchymal stem cells
have anti-inflammatory effects and may have the
potential to differentiate into a tenocyte-like pheno-
type, so that they could contribute to adhesion free
tendon healing. Despite promising results in the field
of molecular research, many of these insights remain
to be translated into clinical application.
CLINICAL SIGNIFICANCE
In the repair of flexor tendons, hand surgeons attempt
to achieve two main goals: stability of the repair and
gliding of the tendon. The problem of adhesion forma-
tion has been a challenge since the beginning of the
20th century. Initially this lead to the concept of a “no
man’s land” in the area of zone 2, a zone were primary
tendon repair was not indicated. As the tendon is gliding
through a tight fibro-osseus canal in this area, the likeli-
hood of adhesion formation was considered so high
that no direct tendon repair was recommended. As a
secondary procedure, tendon continuity was restored by
grafting. With the advent of more sophisticated suture
materials and surgical techniques and particularly with
more aggressive methods of early mobilization, an
e34
immediate tendon repair in zone 2 was considered to
be generally possible by a skillful surgeon. Nevertheless,
the results have since remained often less than
satisfactory.
From clinical experience, it can be seen that three
factors (“quality of repair,” “motion” in the sense of
early exercise, and “inflammation”)1 have an impact on
the degree of adhesion formation. While the quality of
a tendon repair is still up to the surgeon, strategies from
the toolbox of molecular medicine are under investiga-
tion to modulate tendon healing on the molecular or
cellular levels, to decrease those inflammatory effects
that are responsible for adhesion formation, and to find
new ways to prevent loss of tendon gliding.
PATHOPHYSIOLOGY
In its healing process, the tendon undergoes three
distinct phases: inflammation, proliferation, and
maturation/remodeling. The inflammatory phase is
characterized by the migration of T-lymphocytes and
phagocytotic cells into synovial sheath and epitenon.
Platelets adherent at the injury site release a variety of
cytokines such as platelet-derived growth factor (PDGF),
transforming growth factor (TGF)-β, or insulin-like
growth factor (IGF) that activate the migrating cells.2
These migrating cells are responsible for phagocytosis
of cell debris and for deposition of a preliminary extra-
cellular matrix.
In the proliferation phase, collagen synthesis and vas-
cularization are enhanced.3 The remodeling phase is
characterized by rearrangement and organization of col-
lagen fibers.4 At this state, adhesions become more
apparent.
In contrast to many other tissues, there are two dif-
ferent mechanisms involved in tendon healing: the
extrinsic and the intrinsic pathway. In extrinsic healing,
extracellular matrix producing cells are invading the lac-
erated tendon from its periphery. This pathway described
by Potenza and colleagues5 was for some time consid-
ered to be the prevailing and maybe only mechanism
of healing in a lacerated tendon.
This chapter does not appear in the print edition.
 Chapter 45:  Molecular Methods to Prevent Adhesion Formation
Lundborg and others, however, have shown that
tendon healing is also possible independent from the
adjacent tissue. When a sutured tendon was kept inside
the knee joint space of a rabbit without contact to a
tendon sheath or other connective tissue surfaces, the
tendon healed without forming adhesions. This intrin-
sic healing process allows a restitution of tendon conti-
nuity by cells out of the epitenon and endotenon
without forming adhesions to its surrounding.6
McGrouther and colleagues showed in vitro that the
extrinsic pathway naturally is the more active one and
starts to be active at an earlier time-point.7 This means
that tendon healing naturally tends toward forming
adhesions and that a therapeutic approach should aim
at enhancing the intrinsic pathway and suppressing the
extrinsic.
TREATMENT
Quantification of Tendon Adhesions
Measurement of the degree of adhesion formation is
mainly semiquantitative. In addition to macroscopic
observation, investigators use either biomechanical
testing or image analysis of histologic sections to quan-
tify the degree of adhesions. Biomechanical testing is
also dependent on factors such as joint stiffness. Histol-
ogy is dependent on section location and direction and
cannot quantify the rigidity of adhesions. Therefore, the
ideal measurement for the quantitative analysis of adhe-
sion formation remains elusive.
Conventional Pharmacological Treatment
Before the era of molecular medicine, various pharma-
cological agents have been investigated. Local and sys-
temic steroids, nonsteroidal anti-inflammatory drugs,
hyaluronic acid, 5-fluorouracil, and others have been
used. However, none of these substances have been suit-
able for routine clinical use. Lubricin, a mucinous gly-
coprotein responsible for the boundary lubrication of
articular cartilage, has been used to prevent adhesion
formation in a canine model of tendon repair.8 The
application of this substance led to a decreased adhe-
sion formation, although it is at the expense of repair
strength. Clinical value of this agent therefore is yet to
be elucidated.
Biomaterials to Prevent Adhesion Formation
As described earlier, the majority of adhesion formation
is considered to be caused by extrinsic rather than by
intrinsic healing. Therefore, attempts with blocking
materials and membranes have been made to prevent
adhesion formation caused by the exterior. Before the
area of molecular treatment, attempts have been made
to use materials such as silicone or gelatin sponge. Using
hydroxyapatite or alumina sheaths for covering a tendon
suture site in the chicken model,9 Siddiqi and colleagues
e35
showed a reduction of adhesions at the plantar site, but
mild to moderate adhesions both at the ends of the
sheaths and at the plantar contact site to the bone. Ishi-
yama and colleagues reported a phospholipid polymer
hydrogel to effectively prevent adhesion formation in a
rat and in a chicken model.10 They explained this by a
microstructure with a pore size less than 8 to 10 µm that
is capable of preventing extrinsic inflammatory cells
from getting into contact with the tendon surface but
allowing the passage of cytokines and growth factors
required for healing. Tenenhaus and colleagues11
claimed a similar mechanism to be active in adhesion
prevention when they wrapped tendon repair sites with
a collagen-GAG membrane (Integra) in a chicken model.
This material has been used particularly in burn surgery
and is known to possess good biocompatibility.
Motion
From clinical experience, it is known that early active
motion treatment helps to prevent adhesion formation
after tendon repair. Various explanations for this obser-
vation can be conceived. First, it might be due to
mechanical reasons that newly forming adhesions are
interrupted by motion. Recent research, however, has
also shown an effect of motion on a molecular level.
Strain and shear forces can be exerted onto cultured cells
by using a cell bioreactor, which is simulating the condi-
tions of motion.12 By exercising mechanical shear stress
on tenocytes in vitro (Figure 45-1), Fong and colleagues
showed an “antifibrotic” gene expression pattern—that
is, an upregulation of matrix-metalloproteinases and
a downregulation of collagen I and III as well as of
TGF-β.13 Not only cells in culture but also cell-seeded
grafts made from acellularized cadaver tendons can be
treated by mechanical force before implantation. Ange-
lidis and colleagues used a cell bioreactor to exert a
cyclic load of 1.25N on cell-seeded tendon scaffolds
Rotating cone Tissue culture plate
0.5°
Tenocytes
Figure 45-1  Tenocytes may be exposed to shear forces
induced by a cone viscometer to simulate tendon motion in
vitro. An “antifibrotic” gene expression pattern can thereby
be obtained.
e36 Chapter 45:  Molecular Methods to Prevent Adhesion Formation

for 5 days. Subsequent biomechanical testing showed
higher tensile strength of the bioreactor-treated tendons
compared to untreated controls. Moreover, the seeded
cells (adipoderived stem cells and skin fibroblasts)
showed an orientation parallel to the direction of force
on the scaffold. Further studies will have to show
whether this orientation also helps to prevent adhesion
with the surroundings.
The concept of mimicking the molecular events
induced by motion stress seems appealing, as this could
increase repair strength, decrease the formation of adhe-
sions, and minimize the risk of dehiscence caused by
motion therapy.
Prevention of Adhesions in Tendon Grafting
The formation of adhesions is an even greater problem
in tendon grafting than it is in tendon repair. Com-
monly used grafts such as the palmaris longus tendon
lack an extrasynovial sheath and are therefore highly
susceptible to adhesion formation. Furthermore, the
function of artificial grafting materials has been poor.
On the other hand, the use of allografts or xenografts is
limited due to immunological reasons, as these anti-
genic stimuli generally lead to excessive fibrosis, a fact
that is most detrimental in the gliding region of zone
2.14 Acellularization of cadaver tendons could be a way
to obtain a nonimmunogenic scaffold for tendon repair
with the right mechanical properties. Zhang and col-
leagues acellularized rabbit tendons by treating them
with trypsine/EDTA + Triton-X solution.15 These acel-
lularized scaffolds could be repopulated with epitenon
and endotenon cells. Reseeding the acellularized
tendons with tenocytes has been shown to improve
their biomechanical properties, mainly ultimate tensile
strength and elastic modulus.16 It may be speculated
that the newly formed epitenon layer (Figure 45-2) can
also inhibit adhesion formation, which has to be proved
in further preclinical studies.

A B

C D
Figure 45-2  Acellularized tendon scaffolds seeded with various cell types after 6 weeks in vivo. A, Epitenon tenocytes.
B, Sheath fibroblasts. C, Bone marrow–derived MSCs. D, Adipocyte-derived stem cells. Note preservation of collagen
framework, single epitenon-like layer on surface (individual cells indicated by black arrows), and distribution of endotenon-like
cells in center of grafts (individual cells indicated by white arrows).
 Chapter 45:  Molecular Methods to Prevent Adhesion Formation
FLEXOR TENDON WOUND HEALING CASCADE
INFLAMMATORY PROLIFERATIVE REMODELING
Neutrophil and Angiogenesis Collagen
macrophage reorganization
chemotaxis VEGF
bFGF
PDGF PDGF
TGF-β
Cell proliferation
IGF-1
bFGF
PDGF
Collagen synthesis and
extracellular matrix deposition
TGF-β
bFGF
PDGF
Figure 45-3  Although the interaction of cytokines is highly
complex, each cytokine is supposed to make a major
contribution to one or several certain aspects of tendon
healing in the three distinct phases.
Cytokines
As a variety of cytokines are active in the process of
tendon healing (Figure 45-3), blocking the “proadhe-
sion” and substituting the “antiadhesion” ones could be
a powerful strategy in preventing tendon adhesions.
However, there are several obstacles to overcome before
this approach will come to fruition. The number of pos-
sible cytokines involved is large, and there may be
several cytokines that are still unidentified. Second, the
above classification into “proadhesion” and “antiadhe-
sion” is overly simplified. A cytokine may perform con-
tradictory effects depending on the time and location of
its activity. The exact regulation of cytokine secretion
and activation is regulated by various paracrine feed-
back loops that will be very difficult to simulate. Never-
theless, promising results already have been obtained
when certain cytokines were either substituted or
blocked.
Platelet-Derived Growth Factor and
Fibroblast Growth Factor
By exogenous application of the cytokines PDGF-BB
and bFGF, Gelberman and colleagues have shown an
increased expression of lubricin and hyaluronic acid,
which promote gliding.17 By local administration of
PDGF to a tendon repair site in a canine model, the
same group showed an increase in cell proliferation and
matrix maturation without an increase of adhesion
formation.18
e37
RANGE OF MOTION
40
Range of motion (degrees)
*
35
30
25
20
15
10
5
0
*p <0.05 1
Control Low-dose M6P
Low-dose Decorin High-dose M6P
High-dose Decorin
Figure 45-4  Range of motion of rabbit forepaws treated
with the TGF-β antagonists decorin and mannose-6-
phosphate (M6P). Significant improvement (*) was achieved
by local administration of low-dose M6P (1 mg/100 µL).
Insulin-Like Growth Factor
IGF is a cytokine also of interest in the process of tendon
healing. It has been shown to posses anti-inflammatory
properties19 and to increase the production of collagen
and proteoglycan as well as DNA synthesis in flexor
tendon specimens in vitro.20 However, the ultimate
proof of whether IGF is effective in preventing intrasy-
novial tendon adhesions is yet to be determined.
Transforming Growth Factor-β
TGF-β is a cytokine that is related to various processes
in wound healing. Because TGF-β was upregulated espe-
cially in the inflammatory cells of the tendon sheath,21
this cytokine has become a target in the effort to prevent
adhesion formation.
By using mannose-6-phosphate as an inhibitor of
TGF-β production in an in vivo model of tendon repair
in rabbits, Bates and colleagues could achieve a signifi-
cantly improved range of motion in the operated digits
(Figure 45-4).22 Similarly, mannose-6-phosphate has
been shown to be effective in blocking TGF-β–induced
production of collagen I in tenocytes in vitro.23 Because
mannose-6-phsophate is nontoxic, nonimmunogenic,
and easy to produce, it will be an interesting agent for
future clinical applications.
In the intracellular pathway triggered by TGF-β, the
Smad proteins play a vital role. Katzel and colleagues
showed decreased scarring after FPL repair in Smad3-
deficient mice.24 By using a blocking agent of the Smad
pathway, likewise, Au and colleagues found diminished
connective tissue deposition and a decreased number of
myofibroblasts in rat skin wound healing.25
Smad 2 and 3 are phosporylated by TGF-β receptors
while Smad 1, 5, and 8 are phosphorylated by bone
e38 Chapter 45:  Molecular Methods to Prevent Adhesion Formation
morphogenetic protein (BMP) receptors and mediate
BMP signals.26 The group of BMPs is characterized by
high complexity of their signaling functions. BMP-12 is
known to play a role in the differentiation of stem cells
into tenogenic cells.27 It further has been shown to
increase proliferation of tenocytes and the production
of procollagen I and III and to decrease the production
of decorin.28 A role in the formation of adhesions there-
fore is likely for BMP-12, but the exact mechanisms are
yet to be elucidated.
Vascular Endothelial Growth Factor
There is evidence from in vivo studies that tendon
healing is possible without vascularization, but just by
mere diffusion.29 If neovascularization should contrib-
ute to adhesion-free tendon healing, it would have to
occur from intratendinous vessels. Gelberman and col-
leagues have shown that this type of neovascularization
takes place in a canine model of tendon repair.30 New
blood vessels were formed in tendon regions during the
healing process that were previously avascular. However,
vascular endothelial growth factor (VEGF), a cytokine
playing a role in angiogenesis, has not been found to
improve tendon vascularity and adhesion prevention
yet. In an in vitro model, VEGF gene transfer led to an
increase in TGF-β production, which was related to
increased adhesion formation.31 The authors concluded
that VEGF was not a critical factor to substitute in order
to promote tendon strength or to decrease adhesion
formation.
Epidermal Growth Factor
Epidermal growth factor (EGF) is another cytokine that
plays a role in tendon healing. It has been shown to be
present not in tenocytes but in migrating inflammatory
cells during the healing process.32 Another study showed
EGF to have a stimulatory effect on tenoblast migration
in culture.33 Further studies must elucidate whether EGF
would increase or decrease adhesion formation in zone
2 tendon repair.
Gene Silencing
In addition to blocking the effect of a cytokine by an
antagonist protein or natural inhibitor, blocking the
gene expression of an adhesion-causing protein such as
TGF-β is another strategy. The use of micro-RNA
(miRNA) or small interfering RNA (siRNA) is a method
to silence gene expression.34 miRNA typically consists of
single-stranded RNA at a length of 19 to 25 nucleotides
that binds to a corresponding sequence of messenger
RNA and inhibits the translation of the respective
protein. siRNA binds to complementary RNA and leads
to degradation of this complex by endonuclease cleav-
age. Chen and colleagues showed an effective decrease
in TGF-β production using miRNA directed against
TGF-β RNA both in vitro and in vivo.35 As in other fields
of medical research where gene silencing offers promise,
such as in HIV therapy, cancer treatment, or the therapy
of neurological disorders, protective treatment against
tendon adhesion by gene silencing may be possible.
Because the site of tendon repair is easy to access, selec-
tive local administration could rule out systemic adverse
events. By coupling silencing RNA with target-selective
carriers such as ligand-coated nanoparticles, an even
more specific way of delivering the agent to its domain
could be provided. Adverse effects of silencing RNAs
such as unspecific downregulation of genes and compe-
tition with endogenous silencing RNAs36 are still to be
overcome. Unlike in chronic diseases that would require
lifelong administration of RNA interference, short-term
treatment during the period of tendon healing should
be more easily tolerated.
Stem Cells
With the knowledge that scarless healing is possible
in the fetal stage,37 one might conceive that stem cell
mechanisms are a key to adhesion free tendon healing.
From embryonic stem cells, pluripotent cells that
can renew indefinitely in vitro can be derived. These
cells are capable of differentiation into tissues of all
three germ lines. The use of donor embryonic stem
cells raises various ethical concerns in humans and
involves the drawback of immune rejection by the
recipient.
Recent research has shown that somatic cells can also
be altered to become pluripotent. These cells are called
“induced pluripotent stem cells” (iPS). Takahashi and
colleagues transfected adult human fibroblasts with the
developmental genes Oct3/4, Sox2, Klf4, and c-Myc and
could thereby successfully transform these cells into a
phenotype that was similar to embryonic stem cells in
morphology, proliferation, surface antigen profile, gene
expression, epigenetic status of pluripotent cell-specific
genes, and telomerase activity.38 Theoretically, this
method could produce a self-renewing cell for every
individual with a capacity to transform into every
favored tissue type without the problem of immune
rejection. Thus, tendon healing free of scars and there-
fore free of adhesions may be conceived in the future as
this technology is further developed.
Despite these groundbreaking achievements, various
obstacles are still to be overcome before clinical use of
this technology is possible. When retroviral transfection
is used, this will yield high efficiency but contains the
risk of tumorigenesis as the viral genome is incorpo-
rated into the genome of the host cell. This problem
could be overcome by modern vectors completely
devoid of prokaryotic elements such as plasmids or
linear dumbbell-shaped expression cassettes, as their
integration rate into the host genome is far below the
spontaneous mutation rate.39 Furthermore, iPS seem to
be highly susceptible for tumor induction themselves.
 Chapter 45:  Molecular Methods to Prevent Adhesion Formation
In Takahashi and colleagues’ experiments, subcutane-
ous implantation of iPS into mice lead to teratoma
formation in 25% of the cases.
Conversely, multipotent adult stem cells do not raise
the same ethical concerns as do embryonal stem cells,
immunogenic reactions can be avoided by taking the
cells from the recipient individual, and their teratoge-
nous potential seems to be far lower than that of embry-
onal stem cells.40 Mesenchymal stem cells (MSCs) were
initially derived from the bone marrow, but that method
of harvest is a major procedure. Adipocyte-derived stem
cells are an interesting alternative as they are abundant
in adipose tissue and are easier to harvest by
liposuction.
MSCs have been successfully used in various disor-
ders such as myocardial infarction, meniscus repair, or
treatment of spinal cord injury. Concerning their use in
tendon healing, MSCs exert two main functions that can
be important for adhesion free healing.
First, stem cells are known to possess immunosup-
pressive capabilities.41 Their ability of homing at a site
of inflammation by chemotaxis toward inflammatory
cytokines makes them particularly suitable for suppres-
sion of local inflammatory processes. Initially, MSCs
are activated by immune cells that are secreting pro­
inflammatory cytokines such as interferon (IFN)-γ,
tumor necrosis factor (TNF)α, interleukin (IL)-1α, or
IL-1β.42 Subsequently, MSCs produce soluble mediators
such as nitric oxide, prostaglandin E2, indoleamine
2,3-dioxygenase, IL-6, and human leukocyte antigen
(HLA)-G. These mediators have an influence on a variety
of immune cells. Particularly, regulatory T cells are
induced and dendritic cells are directed toward an anti-
inflammatory phenotype.
Second, MSCs are known to be able to differentiate
into various cell lines—bone, cartilage, muscle, bone
marrow stroma cells, adipose tissue, and connective
tissue. A differentiation of MSCs toward mature teno-
cytes could therefore be conceived. Characterization of
the mature tenocyte phenotype is difficult, as a defini-
tive marker is missing. Various markers have been pro-
posed by different groups, such as collagen I, collagen
III, tenascin C, tenomodulin, scleraxis, decorin, aggre-
can, elastin, thrombospondin 4, thrombospondin 5
(also called cartilage oligomeric matrix protein, COMP),
and others.43 Scleraxis, a basic helix-loop-helix tran-
scription factor, is regarded to be highly specific for
tenocytes by some authors44,45 and is thought to regulate
the expression of tenomodulin, a transmembrane gly-
coprotein with an antiangiogenetic C-terminal domain.
However, scleraxis also has been detected in other cell
types such as osteocytes and chondrocytes.43 Tenascin is
an extracellular matrix protein that is highly expessed in
musculoskeletal tissues mainly during regenerative and
healing processes.46 It is upregulated by mechanical
strain but is also not exclusively tendon specific.
e39
Despite these difficulties, recent studies on nonhu-
man cells give promising evidence that a tenogenic dif-
ferentiation of mesenchymal stem cells toward tenocytes
may be achieved. In vitro studies in animal models have
shown the expression of the tenogenic genes decorin and
tenomodulin, Collagen Ia1, six1, six2, scleraxis, eya1, and
EphA4 after exogenous exposure to BMP-12.47 After
BMP-12 gene transfer, an upregulation of collagen type
I and scleraxis in rhesus monkey MSCs could be shown.27
There is also some evidence that interaction with teno-
cytes could induce mesenchymal stem cells toward a
tenogenic line. Luo and colleagues co-cultured rat bone
marrow MSCs and tenocytes in an indirect co-culture
system that allowed passage of soluble factors.48 They
noted an increased expression of the tendon-related
genes collagen I, collagen III, tenascin C, and scleraxis
compared to the control group. This gives evidence that
no direct cell contact is needed for tenogenic differentia-
tion of MSCs. The soluble factors that play the key role
in this process remain to be identified.
Further evidence is required to prove whether these
differentiated cells will be able to overtake the relevant
functions of tenocytes at a site of tendon repair and
contribute to scarless and adhesion-free healing.
Gene Therapy
Gene therapy is a strategy that may deliver the cytokine
genes to the tendon repair site. For the insertion of genes
into a recipient cell, nonviral and viral vectors are avail-
able. Nonviral gene transfer includes chemical methods
such as lipofection and physical methods such as elec-
troporation, microbubble-enhanced ultrasound, ballis-
tic delivery (“particle gun”), magnetofection, and laser
poration.
Nonviral methods are nonpathogenic but have lower
efficiency than viral methods. Furthermore, chemical
nonviral vectors may be toxic, and physical manipula-
tion may be harmful to the cells. On the other hand,
viral vectors are more efficient but have the potential
risk of immunogenicity and of causing genetic muta-
tions in the host cell. Various attempts of gene transfer
to tendons have been made. Nakamura and colleagues
successfully transferred the PDGF gene into rat tendons
in a liposome-mediated manner.49 Despite a transfec-
tion rate of only 2%, there was enhanced angiogenesis
and collagen I synthesis over a period of 4 weeks. As this
was not a model of intrasynovial tendon repair, further
studies will have to show whether PDGF is a suitable
cytokine to prevent adhesion formation in such a
setting. In another model of extrasynovial tendon
healing (gap formation in the medial collateral liga-
ment of the rabbit, no suture), the same group admin-
istered antisense-oligonucleotide against decorin
mRNA.50 They noted a higher abundance of larger col-
lagen fibrils, higher tensile strength, and better biome-
chanical properties compared to the control group.
e40 Chapter 45:  Molecular Methods to Prevent Adhesion Formation
CONCLUSIONS
The repair of flexor tendons that is free of adhesions in
zone 2 of the hand is a very complex problem. Various
efforts have been made in the past with pharmacologi-
cal agents, mainly to reduce inflammation, and with
physical barriers to reduce adhesion formation. More
recent attempts have used various cytokines with prom-
ising results. The blockade of TGF-β seems to effectively
reduce adhesion formation in the experimental setting.
For more specific cytokine delivery, genetic modification
strategies at a tendon repair site are possible, but obsta-
cles such as vector toxicity, low transfection efficiency,
unstable transfection, and the possibility of mutagene-
sis remain to be overcome.
To solve the problem of adhesion formation after
tendon grafting, seeding of a graft with recipient cells
could prevent adhesion formation by providing a gliding
layer and by reducing immune response with subsequent
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 CHAPTER
46  
TENDON REPAIRS IN
REPLANTATION SURGERY
Ren Guo Xie, MD, Jun Tan, MD, and Jin Bo Tang, MD
Tendon injuries are an integral part of complex tissue
injuries involved in the digital and forearm amputation.
Recovery of active movement of the hand and wrist after
replantation of digits or forearm depends on ample
tendon gliding. Tendon injuries in the amputation can
present as tidy cut or avulsion injuries of the tendons,
caused by knife or machine cuts, or by crush avulsion
injuries, respectively. Loss of a segment of bones or a
part of soft tissues in the trauma area is very common.
After patients are brought into the hospital, the
patients should be thoroughly evaluated regarding the
conditions of entire body and degrees of tissue loss or
contusion locally. The wound should be carefully
assessed about severity of contamination and potential
of infection.
SURGERIES AND TENDON REPAIRS
Digital Replantation
Surgery
Digital amputation after clean-cut injuries does not
have loss of tendon substance (Figure 46-1), but the
level of tendon cut may not be the same as those in the
tendons, particularly the flexor tendon. The proximal
tendon ends retracted to the proximal phalanx or the
palm. During crush and avulsion injuries, both flexor
and extensor tendons can be avulsed from more proxi-
mal parts of the tendon (Figures 46-2 and 46-3). Addi-
tional incisions are needed to find the proximal ends
and do end-to-end repair. In the thumb, both flexor
pollicis longus (FPL) and extensor pollicis longus (EPL)
tendons are usually cut without loss of tendon sub-
stance (Figure 46-4), and tendon avulsion from the
thumb is also sometimes seen. Surgical priority should
be given first to the bony fixation and re-establishment
of vascular circulation. Ideally, tendons are repaired in
all the cases. During replantation surgery, though slightly
shortening of phalanges are necessary, tendons do not
usually require shortening. Trimming the rugged tendon
ends is required, which usually only produces about
0.5 cm shortening of the tendon substance.
Both 2-strand Kessler and cruciate repair methods are
now used popularly for flexor tendon repair (Figure
e42
46-5). In our unit, we use a cruciate or an U-shaped
four-strand repairs (Figures 46-5 and 46-6). We do not
repair the FDS tendon. The FDS tendons are excised,
because it is not possible to obtain good gliding and
prevent adhesions after injuries to multiple tissues
including bones involved in digital amputation. During
surgery, we attempt to preserve the annular pulleys and
synovial sheath as much as possible. Frequently, we
incise or left open the sheath around the area of digital
amputation. It is not possible to perform complicated
pulley reconstruction during the replantation surgery, as
this is not possible and lengthen the surgery. It is a
practical way to leave completely disrupted annular
pulleys open without surgical repair or reconstruction.
It is not infrequent that we see that the A2 pulley is
almost entirely damaged by the trauma, or is signifi-
cantly shortened during surgery. In the case of thumb
amputation, the FPL tendon must be repaired.
As for extensor tendon repair, shortening of the digits
has great impact on function of extensors. We usually
manage to repair the extensor tendon with running con-
tinuous or locked running stitches or figure-of-eight
suture. When phalanges are shortened, extensor tendons
can be sutured with some overlapping of the cut
portions.
Postoperative Care
To avoid disturbance to vascular circulation and ensure
stable fixation of phalanges, replanted digits do not
undergo early mobilization. For the first 3 or 4 weeks,
the reattached digits are immobilized. After 3 or 4
weeks, the patients can be instructed to perform light
passive motion of the digits. Active motion of the fingers
can be started from 4 or 5 weeks (or even later) after
surgery. Therapies should be given to lessen digital
edema and improve digital circulation when the digit
motion starts.
Outcomes
Recovery of active range of finger motion after digital
replantation is generally poor. Many replanted digits
have only limited active flexion. The specific reports that
discussed digital motion range after digital replantation
This chapter does not appear in the print edition.

A
B is usually not possible and making a full fist is rarely
Figure 46-1  A clean-cut total amputation through the
middle phalanx of the index finger, presenting an ideal
indication for repair of the flexor and extensor tendons. In
this kind of tidy digital amputation, the phalanx was not
shortened, and flexor and extensor tendons were repaired   motion and function are actually due largely to the loss
in the same way as usually do for clean-cuts of flexor or
extensor tendons.
Figure 46-2  A crush-avulsion amputation of the index
finger.
Chapter 46:  Tendon Repairs in Replantation Surgery e43
Figure 46-3  Both the flexor and extensor tendons were
pulled out after disruption at the palm and wrist levels. The
tendons were repaired through additional incision in the
palm and wrist.
are rare. In our experience, we observed total range of
active motion of the distal and proximal interphalan-
geal (DIP and PIP, respectively) joints of about 60° to
80° degrees of digital flexion. These degrees of motion
in IP joints provide the hand with rather practical func-
tion for making a light grip or picking up. Powerful grip
achievable. Joint stiffness occurs to a great percentage of
the replanted digits. In our unit, we note varied degrees
of finger joint stiffness (i.e., limitations in passive digital
motion) in almost all the cases. Limitations of digital
of passive digital motion range, rather than impaired
tendon function.
A few reports indicated effectiveness of tenolysis after
digital replantation. In 1989, Jupiter and colleagues
reported 37 replanted digital units and four thumb
replantations with a flexor tendon tenolysis at an average
of 10 months after replantation.1 The results were
assessed by measuring total active range of motion
(TAM), potential active motion, and by the Strickland
criteria. The TAM increased from a mean pretenolysis of
72° to 130°. The potential active motion increased from
a mean of 43% to 70% after tenolysis. Both of these
improvements were statistically significant. By Strick-
land criteria, 13 digits were rated excellent, 11 good, 6
fair, and 11 poor. The thumbs had two fair results and
two poor results. Poor results were also seen in crush or
avulsion amputations, hands with more than two digits
amputated, and those requiring a PIP joint capsulotomy.
Complications included tendon rupture and infection.
The results support flexor tendon tenolysis after replan-
tation of fingers but not replanted thumbs.
Ross and colleagues (2003) specifically reported
the tendon function after digital replantation.2 They
e44 Chapter 46:  Tendon Repairs in Replantation Surgery
C FDP tendon during replantation.
Figure 46-4  A, Thumb amputation distal to the IP joint.
B and C, Both FPL and EPL tendons were repaired directly
and the replanted thumb has good cosmetic appearance   injury. TAM values were not affected by age, type of
and function after surgery.
retrospectively reviewed 48 patients (103 digital rays)
who underwent replantation. Average TAM (sum of the
DIP, PIP, and MCP joints) for all digits was 129°. Zone
1 and zone 5 injuries had better TAM than injuries in
zones 2, 3, and 4, which had TAM values not signifi-
cantly different from one another. Avulsion injuries
fared significantly worse than other mechanisms of
B
Figure 46-5  Two methods often used in flexor tendon
repair during replantation surgery. A, Two-strand modified
Kessler repair. B, Four-strand cruciate repair.
C
Figure 46-6  A four-stand repair method, i.e., the U-shaped
repair, the senior author developed using a looped suture.
A–C, Method of repair is shown. This is used to repair the
bone fixation, number of arteries repaired, or number
of digits injured. Digits with both the FDP and FDS
tendons repaired had significantly better TAM values
relative to one-tendon fingers. Similarly, fingers treated
with an “early” mobilization regimen also exhibited
better movement.
Secondary Tenolysis
Tenolysis is indicated for the patients who have suffi-
ciently ample passive motion of the digits but whose
degrees of active digital flexion are markedly smaller.

Therefore, only a very limited number of patients are
ideally indicative of secondary tenolysis because loss of
passive digital motion is common. Tenolysis is usually
carried out about 6 months or one year after surgery.
Postoperative 3 months are too early for this surgery.
Most patients seen in our department who needs
secondary tenolysis are operated one year after replanta-
tion surgery. When passive motion is restricted, a con-
siderable number of patients may not want to accept a
secondary operation to improve passive joint motion
followed by tenolysis. Under this circumstance, we do
not strongly urge the patients to have the surgery,
because the improvement after tenolysis is not as great
in these patients. Adhesions in extensor tendons are
common, but they are not as problematic as for flexor
tendons. Should these cases undergo the tenolysis,
simple release of the extensor tendon adhesions usually
is required. Care should be given especially to the pres-
ervation of integration of reattached vessels, and the
dissection should not extend too far away. Early passive
and active motion of the digit should be initiated after
tenolysis if the tendons are not found frayed.
Yu and colleagues (2003) reported that 79 digits of
55 patients received 102 secondary procedures follow-
ing replantation.3 They divided the procedures into two
groups, occurring before or after 2 months following
replantation. The procedures in the early group were
mainly for soft tissue coverage (92%), and those in that
late group were mainly for tendon (67%) to improve
function. Factors associated with higher incidence of
early secondary procedures included multiple-finger
injury, avulsion or degloving injury, and level of injury
proximal to zone 3 in finger replantation. However,
younger patients and those with proximal level replan-
tation in fingers had more late secondary procedures.
Flexor tenolysis procedure significantly improved the
digital function after replantation.
Eggli and colleagues (2005) reported 23 patients
with restricted motion after 32 combined digital injuries
or amputations in zone 2 treated with tenolysis.4 With
an average follow-up of 5 years, significant functional
improvement was achieved in 28 of 32 digits (88%).
TAM improved on average 51° after dorsal tenolysis, 55°
after palmar tenolysis, and 63° after combined dorso-
palmar tenolysis. Using Buck-Gramcko’s criteria, 15
digits were rated excellent, 8 good, 4 fair, and 5 poor.
Complications consisted of 16% flexor tendon ruptures
after palmar or combined tenolyses. In contrast, dorsal
tenolysis proved to be a safe procedure. Prerequisites for
success are compliant patients who are willing to
undergo therapy for at least 3 months postoperatively.
Palm Replantation
Surgery
Amputation through palm is rarely caused by clean cuts.
Most often, machine cutting or crush-cutting injuries
Chapter 46:  Tendon Repairs in Replantation Surgery e45
lead to amputation through palm. At this level, the
amputation involves multiple flexor and extensor
tendons, and intrinsic muscles. Chances of infection
increase in palm amputation. Thorough irrigation and
débridement are important. Similarly, surgical priority
should be given to stable fixation of the metacarpal
bones and reestablishment of vascular circulation.
Both core and peripheral repairs are used for flexor
tendons, but for extensor tendons, a running or cross-
stitch suture of sufficient suture purchase or a core
suture (mostly two-strand repair) should be used.
Peripheral sutures can be loosely added for flexor
tendons. This is less important in the palm area than in
the digital area, because this area accommodate more
space for the bulky repair site. Strength of the flexor
tendon remains important; we recommend four-strand
repair made with 4-0 or 3-0 sutures rather than two-
strand repair in the flexor tendons of the palm. Using a
looped suture or a system with one needling leading
two suture strands greatly simplify the surgery and
reduce operation time. In our unit, we also use a cruciate
four-strand repair. The FDS tendons are excised and
not repaired; some surgeons attempt to repair one or
two FDS tendons in the palm, which is also a feasible
option. Palm amputation may not involve a FPL tendon
cut. If the FPL tendon is lacerated, the FPL must be
repaired.
Postoperative Care
After surgery, the hand is placed in protective cast with
the wrist in slight extension and the MCP joint slightly
flexed and IP joints extended. Some surgeons place the
wrist in slight flexion. For the first 3 weeks, the hand is
immobilized. Passive digital flexion can be prescribed,
but generally motion range should be limited and
should be initiated after 10 days or 2 weeks when edema
subsides. Light active motion over a very limited range
can be ordered as well, just producing mild finger
motion. Starting passive motion of the digits prevents
digital stiffness. Motion also helps reduce persistent
edema of the hand and digits. After 3 weeks, the patients
can be instructed to perform passive motion of the
digits, together with active motion of the fingers. Hand
edema can be serious in the first days after surgery, and
when persistent, therapies should be given to lessen
digital edema and improve digital circulation when the
digit motion starts.
Outcomes
After palm replantation, the hand can be expected to
recover to rather realistic hand functions. Ample active
digital flexion can expected if no serious adhesions
occur. The overall digital function is better after surgery
of palm than digital replantation. Stiffness in the digital
joints does not usually develop if the passive motion
therapies are properly initiated. Nevertheless, when
e46 Chapter 46:  Tendon Repairs in Replantation Surgery
postsurgical therapy guidelines are not established or
timely ordered, the hand with successfully replanted
palm may end up with very limited function. Due to the
damage to intrinsic muscles, function of the digital MCP
joint can be affected, and grip and pinch strengths
reduce substantially. Therapies should continue to post-
surgical 6 months or over one year.
Tenolysis
Tenolysis in the palm can be much more safely done
than in the replanted digits. The passive motion of the
digits and wrist are usually ample. Consequently, a
higher percentage of the patients with palm replanta-
tion are indicative of secondary tenolysis. The palm pro-
vides greater space to release the tendon from adhesions
with less danger to damage the reestablished vascular
supplies, although surgeons should still take great care
not to hamper the vessels. Tenolysis is carried out about
6 months after surgery and should be under the condi-
tion that solid union of the metacarpus is achieved.
After tenolysis, the patients are instructed to perform
early active motion to prevent reoccurrence of the adhe-
sion, and the motion therapies should continue for 2
or 3 months.
Foream Replantation
Surgery
Amputation through forearm, especially distal forearm,
is caused by work-related injuries or crushing during
accidents. At this level, the amputation involves multi-
ple flexor and extensor tendons, major arteries, and
nerve trunks. Bony fixation should be accomplished first
during the surgery, followed by vascular anastomosis to
establish circulation. The radius and ulna are usually
shortened for 2 to 3 cm.
There is no need to particularly shorten the tendon,
but the rugged tendon parts are excised to obtain healthy
tendon substance for surgical repair. A core suture
(mostly two-strand repair or a four-strand repair) should
be used for both extensor and flexor tendons. Peripheral
sutures can be loosely added. Whether the repair site is
bulky or not is not a great concern, because this area
accommodates more space for tendon to glide. The
surgeons should pay particular attention not to mis-
match the tendon ends. Strength of the flexor tendon
remains important; we recommend four-strand repair
such as cruciate repair or U-shaped repair (see Figure
46-5 and Figure 46-6), made with 4-0 or 3-0 sutures.
Our colleagues (Zun Shan Ke, MD) used the U-shaped
4-strand repair made with looped nylon suture, supple-
mented with locking running peripheral suture in cases
of forearm replantation, followed by early tendon mobi-
lization. They impressively obtained good function.
Repair of the FDS tendon is not a necessity. To reduce
operation time, the FDS tendon may not be repaired or
may be connected with simpler suture. The lacerated
FPL must be repaired and major wrist flexors (flexor
carpi radialis and ulnaris, FCR and FCU) should be
repaired. Almost all the extensor tendons are worth
repairing, except for the extensor indicis proprius (EIP)
and extensor digiti minimi (EDM). Preferably the EPL
tendon should be repaired with a stronger surgical
method.
Postoperative Care
After surgery, the hand is placed in a well-padded pro-
tective cast with the hand in the functioning position or
neutral position, with the thumb web widely opened.
For the first 3 weeks, the hand is immobilized. After 1
week, after serious hand edema subsides, passive digital
flexion can start, but generally only a mild range of
passive motion should be prescribed. Light active
motion over a very limited range can be ordered as well.
Motion helps reduce persistent edema of the hand.
Early dynamic splinting and digital motion can be initi-
ated in selected patients who can follow the instruction
of the therapist in a setting with well-established reha-
bilitation guideline. After 3 weeks, the cast fixation
should be continued, with the hand in functional posi-
tion. Passive and active finger motion programs can be
upgraded gradually. Similarly, hand edema is serious in
the first week after surgery and, if persistent, therapies
should be given to lessen digital edema and improve
digital circulation when the digit motion starts. After 6
to 8 weeks, when the radiograph confirms that bony
healing is solid, the amplitude of motion and repetition
of the motion can be increased. For the patient with
forearm replantation, much progress can be expected
even months after surgery, and continuation of thera-
pies to 6 months or one year is worthwhile.
Outcomes
Outcomes of the forearm replantation vary greatly,
depending on the degree of injuries, structures repaired,
and, in particular, the recovery of nerve function. Passive
motion of the hand may not be impaired, but hand
function may be greatly reduced due to usually partial
or poor recovery of nerve function. Grip and pinch
strengths reduce substantially.
Scheker and colleagues (1995) reported that the
results of replantation at the wrist and distal forearm are
better than at the metacarpal level.5 Their study evalu-
ated a new postoperative protocol for replantation at
the metacarpal, wrist, and distal forearm levels. Three
days after replantation, the patient was placed in a
dynamic crane outrigger splint with MCP joint control,
compensating for intrinsic muscle function loss. From
4 to 12 weeks, an anticlaw splint alternated with the
outrigger splint. After 12 weeks, a dynamic wrist exten-
sion orthosis was added to the anticlaw splint. Eleven
patients (4 replantations at the transmetacarpal level,
3 at the wrist area, and 4 in the distal forearm) had

this protocol. For distal forearm replantations, TAM of
fingers averaged 216°, grip strength 42 lb, and pinch
strength 7.2 lb with 75% good or excellent results. For
wrist replantations, TAM of fingers averaged 243°, grip
strength 37 lb, and pinch strength 10.6 lb with 100%
good or excellent results. For transmetacarpal replanta-
tions, TAM of fingers averaged 189°, grip strength 37 lb,
and pinch strength 5.6 lb, with 75% good and excellent
results.
Tenolysis
Tenolysis can improve function of most patients after
replantation in the forearm. Surgery can be performed
from 6 months to several years after surgery. Function
of both extensor and flexor tendons can be improved
after surgical release. Similarly, tenolysis should not be
performed within 6 months after surgery, and before
solid union of the radius and ulna is achieved. After
tenolysis, the patients are instructed to perform early
active motion immediately after surgery, and the motion
therapies should continue for months.
References
1. Jupiter JB, Pess GM, Bour CJ: Results of flexor tendon tenoly-
sis after replantation in the hand, J Hand Surg (Am) 14:35–
44, 1989.
2. Ross DC, Manktelow RT, Wells MT, et al: Tendon function
after replantation: prognostic factors and strategies to enhance
total active motion, Ann Plast Surg 51:141–146, 2003.
3. Yu JC, Shieh SJ, Lee JW, et al: Secondary procedures following
digital replantation and revascularisation, Br J Plast Surg
56:125–128, 2003.
4. Eggli S, Dietsche A, Eggli S, et al: Tenolysis after combined
digital injuries in zone II, Ann Plast Surg 55:266–271,
2005.
5. Scheker LR, Chesher SP, Netscher DT, et al: Functional
results of dynamic splinting after transmetacarpal, wrist, and
distal forearm replantation, J Hand Surg (Br) 20:584–590,
1995.
Chapter 46:  Tendon Repairs in Replantation Surgery e47
FUNCTIONAL EVALUATION
In the early days of digital replantation, flexor tendons
were not repaired, and secondary tendon reconstructed
was preferred.6,7 The treatment guidelines for the tendon
repairs in replantation have been changed. Currently,
under favorable conditions, repairs of both extensors
and flexor tendons are an integral and important part
of replantation surgery.8,9
Functional evaluations of patients after digital replan-
tation include (1) range of motion, passive and active;
(2) recovery of sensation; (3) muscle power; (4) grip
strength; (5) pain; (6) cold tolerance; (7) ability to
resume previous or new occupation; (8) ability to inte-
grate the replanted parts into daily life and functional
use; (9) patient satisfaction with the replanted part; and
(10) cosmetic appearance.10 While all the above criteria
are important to the normal life, Buncke and colleagues11
stated that among all factors influencing outcomes,
“experience has shown that the two most critical issues
are sensibility and tendon gliding.”
6. Komatsu S, Tamai S: Successful replantation of a completely
cut-off thumb, Plast Reconstr Surg 42:374–377, 1968.
7. Tamai S: Digit replantation: analysis of 163 replantations in
an 11 year period, Clin Plast Surg 5:195–209, 1978.
8. Meyer VE, Chen ZW, Beasley RW: Basic technical consider-
ations in reattachment surgery, Orthop Clin North Am 12:871–
895, 1981.
9. Morrison WA, O’Brien BM, Macleod AM: Digital replantation
and revascularization: A long term review of one hundred
cases, Hand 10:125–134, 1978.
10. Steichen JB: Management of flexor tendon injury associated
with digital replantation or revascularization. In Hunter JM,
Schneider LH, Mackin EJ, editors: Tendon Surgery in the Hand,
St Louis, 1987, CV Mosby, pp 156–169.
11. Buncke HJ, Alpert BS, Johnson-Giebink R: Digital replanta-
tion, Surg Clin North Am 61:383–394, 1981.
 Appendix
SYMPOSIUM DISCUSSION 1
Symposium of Flexor Tendon Injury, The 10th
Congress of International Federation of Societies
for Surgery of the Hand (IFSSH)
March 12, 2007
The Sydney Convention Center, Sydney, Australia
(Figure 1)
The discussion followed the symposium presentations
by panelists.
Panelists: Robert Savage, Jin Bo Tang, Michale Riccio,
and Peter Amadio
Moderators: Peter Amadio and Stephen Coleman
Peter Amadio:  Let’s start the discussion of this session.
It seems all of us are moving towards venting a certain
part of the important pulleys and using strong repairs.
What do you think about importance of individual
annular pulley?
Robert Savage:  If other pulleys are intact, the A2 pulley
may not be as important as thought in terms of  suture. To my knowledge, the grasping and locking
preventing bowstringing and maintaining normal
mechanics of the tendon gliding. I think partial inci-
sion or partial removal of the A2 pulley has no
adverse influence; I leave such partial defects of the
pulley unrepaired. The lack of importance of other
individual pulleys in the presence of a mainly intact
pulley system has been proven biomechanically in
the past more than 10 years.
Peter Amadio:  How about the A4 pulley?
Robert Savage:  It may not be important as well if others
are intact. I would not repair it if it is the only annular
pulley injured.
Peter Amadio:  What method do you use for tendon
repairs?
Jin Bo Tang:  My colleagues and I use the latest modi-
fication of 6-strand repair with looped suture for the
profundus tendon. For FDS tendon, it cannot afford
more than 4-strand core suture, so a four-strand
repair using one group of looped suture is used to
make a U-shaped repair.
Peter Amadio:  What kind of suture material?
Jin Bo Tang:  4-0 nylon.
Peter Amadio:  Dr. Riccio, what sutures are you
using?
Michale Riccio:  Pretty similar, I use 4-0 or 3-0 sutures
to make core stitches, but in children, I use a 5-0
suture instead. It is not necessary to do early motion
of the digit in children.
446
Peter Amadio:  How about treatment of the partially
lacerated FDP tendon and the FDS tendon? I repair
a partial cut of the FDP when the cut is over 60% to
70% of the cross-section. If the cut is less than 50%
to 60%, trimming the tendon wound is an option.
This reduces the chance of triggering, but does not
reduce the tendon strength. I repair the FDS tendon
if possible, but prefer to remove a slip of the FDS
tendon when the gliding of the FDP appears tight
with the sheath or pulleys.
Michale Riccio:  I agree that we may not need to repair
the FDS tendon in all occasions. In some cases, it is
very difficult to repair this tendon; we have to leave
it unrepaired. Otherwise, the both tendons would be
bulky, but whether not repairing the FDS reduces the
flexion power of the finger is a concern, which
remains uncertain.
Audience:  This is a question for Dr. Tang. First I appreci-
ate the incredibly excellent work done in flexor tendon
from Dr. Tang. One thing I did not understand in the
work you’re doing: how far to place the grasping
suture should be placed 3 or 4 mm away from the cut
edge of the tendon. As to the traditional technique,
too much of the distance will bring about more tissues
within the suture, which will affect tendon gliding.
Jin Bo Tang:  Our original speculation is if a suture is
placed with sufficient grasping or locking area, these
repairs would produce equal strength. However,
during the test, the repair with shorter suture pur-
chase had much lower repair strength. This may
relate to the stiffness of the tendon and grasping
power of the suture. With smaller suture purchase,
the stiffness may be much less and easy to deform
and gap. Also the length of core suture purchase will
affect the share of the loads among the core suture
and peripheral sutures. If the core suture is very short,
the load can be largely loaded into peripheral sutures,
which is disrupted more easily, then the load will be
on the core suture entirely; core suture will be dis-
rupted. This is my explanation. We also found that if
the core suture purchase is beyond 7 mm, such effects
do not exist; almost equal repair strength was found
from 7 mm to 12 mm.
Audience:  We have just heard about venting, removal,
or not repairing a part of important pulleys, such as
the A2. I think this is a dangerous idea. Removal of
the pulley may cause bowstringing and this is oppo-
site to traditional suggestions of not violating these
important structures, such as A2 and A4 pulleys.

Figure 1  Symposium of flexor tendon injury in The 10th
Congress of the IFSSH, Sydney, March 12, 2007. On the
podium (from left to right): Stephen Coleman, Peter Amadio,
Robert Savage, Jin Bo Tang, and Michale Riccio. (Courtesy of
Bin Wang.)
Jin Bo Tang:  We perform simple venting of the A2
pulley when other annular pulleys are not injured.
With the other parts of the sheath intact, partial
venting of the A2 pulley is acceptable. Clinically, if
we see a wound limited to the area of the A2 pulley,
or not extending to another annular pulley, we leave
a part of injured A2 pulley unrepaired, or more often,
we incise or remove a part of the A2 pulley to allow
repair or smooth tendon gliding. If the wound is
extensive, with other pulleys, such as A1, PA, injured,
we should take great care to preserve the A2 pulley.
In those cases of tendon injury with A1 and PA lac-
erations, the tendon is usually cut proximal to the
A2. It does not interfere with tendon motion, thus
not needing venting.
Peter Amadio:  What is the length you vent the pulley?
Jin Bo Tang:  I incise the A2 pulley to 2/3 of the length
of this pulley.
Peter Amadio:  How about Dr. Riccio?
Michale Riccio:  About the same.
Jin Bo Tang:  The important message is that we really
need to know the detail of anatomy of the A2 pulley.
In the adult middle finger, this pulley is quite long,
about 2 cm. This pulley even has different density in
its middle, distal, or proximal parts. The diameters of
these parts are also different. I think either distal,
proximal, or their combination with the middle part,
can be incised or excised to free the tendon motion,
without any clinical problems. I have done it over
years, and still continue to do it. I do not suggest the
incision of the entire A2 pulley.
Peter Amadio:  We are at the right time to end this
session now. Great discussion of the panelists and
from the audience! Thank you.
Appendix: Symposium Discussion 2 447
SYMPOSIUM DISCUSSION 2
Symposium of Flexor Tendon and Carpal
Disorders, The Pre-Congress of The 11th
Congress of International Federation of Societies
for Surgery of the Hand (IFSSH)
October 28, 2010
Affiliated Hospital of Nantong University,
Jiangsu, China (Figure 2)
Panelists: Daniel Mass, Michael Sandow, Robert Savage,
Steve K. Lee, and Jin Bo Tang
Moderator: Jin Bo Tang
Michael Sandow:  Bad repair leads to bad outcomes.
Good repair does not guarantee good outcomes, but
it helps. I used modified Kessler repair (two-strand)
using 4-0 nylon or similar, Kleinert traction, and
flexed wrist splint. We failed to obtain satisfactory
results in some cases. We then changed to a four-
strand single cross grasp repair (“Adelaide repair”)
using 3-0 braided polyester (Ethibond or similar)
with immediate active mobilization, extension block
splint with the wrist extended. I reviewed the results
between 1996 and 2002, 89% follow-up, 71% good
or excellent results, 4.5% rupture rate. Modified
Kessler is a simple repair of poor biomechanics. Its
core suture has inherent grapping potential; its grasps
are easily deformable. The transverse passes in the
tendon may not be a good design.
Michael Sandow:  I have some concern for definitions
of “grasp” and “loop.” I looked up the dictionary:
“Grasp” denotes function, to hold onto something,
but “loop” denotes form, shape. “Locking grasp” and
“looping grasp” appear more appropriate.
Jin Bo Tang:  I probably would not change these terms,
because most hand surgeons are familiar with them,
but we need to give them clearer definitions.
Michael Sandow:  In Green’s textbook about the grasp-
ing, the suture is looped around the tendon sub-
stance, and is pulled to the opposite direction. The
grasping loop slips over the tendon substance in the
illustration. The difference between “grasp” and “lock”
is that if the suture changes its form by tension to the
tendon, it has a poor hold on the tendon and the
strength of repair is decreased. If the suture does not
change its form, it is a lock, and the strength does
not decrease as the hold gets stronger under load.
Jin Bo Tang:  No suture techniques in clinical use actu-
ally have grasping suture pulled at two opposite
directions. The techniques in use have grasp being
pulled in one direction parallel to the longitudinal axis
of the tendon, and in the other side another pull vertical
to the long axis of the tendon. This is the way the grasp-
ing loops act in the Kessler and other grasping repairs.
The drawings in that textbook need to be modified.
448 Appendix: Symposium Discussion 2
Figure 2  Panelists touring the Biomechanics Laboratory
of the Hand Surgery Research Center in the Hospital of
Nantong University immediately before the Symposium.
From the left to the right: Robert Savage, Steve K. Lee,
Daniel Mass, Michael Sandow, Ya Fang Wu, and You Lang
Zhou.
Michael Sandow:  I agree. We put modified Kessler
repair in porcine flexor tendon and observed the
deformation of the tendon after preloading. The
transverse passes of the Kessler repair shortened and
tendon was narrowed remarkably. With two single
cross placed into the tendon, without a transverse
arm across the tendon end, we see little narrowing of
the tendon.
Steve K. Lee:  What do you use for peripheral stitches?
Michael Sandow:  I use a simple peripheral suture. If it
is a big tendon or is not too irregular, I use Silfver-
skiöld method. But, for most tendons, we think
simple epitendinous suture is adequate. Unless you
expect the peripheral stitches to bring about a lot of
strength, simple suture is better.
Daniel Mass:  The complex peripheral stitches may be
caught by pulleys.
Michael Sandow:  Absolutely. In Kessler suture, when
we loaded the tendon, the epitendinous suture failed
first, followed by Kessler suture; when four-strand
single-cross suture is used, the epitendious suture
failed in the same time as the core suture, without
gapping first.
Robert Savage:  Some of the studies showed that Ade-
laide core with Silfverskiöld decrease the rate of
rupture of the repair. Do you feel you will train your
residents to do that repair?
Michael Sandow:  I am very happy you call it “Adelaide”
repair, not the modified …, modified Savage repair.
Robert Savage:  You have done a good job.
Michael Sandow:  We did Adelaide with a simple epi-
tendinous repair and had few ruptures. We had rup-
tures with two repairs of 4-0 nylon that registrars
used to repair these tendons; the hand was out of the
splint after surgery. With 3-0 Ethibond suture, we had
no rupture at all in our recent series. I think adding
Silfverskiöld will unnecessarily complicate the repair
of the four-strand core repair. It is much more com-
plicated when we do it.
Jin Bo Tang:  I have never used Silfverskiöld suture, as
we can easily increase the strength of core suture.
Complex peripheral suture brings about a lot of
suture over the tendon surface and this repair is also
difficult to perform. Is that very difficult to perform
such cross-stitch on the dorsal surface of the tendon?
Michael Sandow:  Our discussion here is quite gentle;
actually we had quite hot discussion in Adelaide with
Dr. Silfverskiöld. He works in Adelaide and he pub-
lished the method when he was in Sweden, and then
came back to work in Australia.
Jin Bo Tang:  How about the tension of your core
suture?
Michael Sandow:  The tension is sufficient to maintain
the cooptation of tendon ends. I do not mind having
some gap between the ends, so no bunching or catch-
ing by the sheath.
Jin Bo Tang:  Would other panelists maintain some
tension across the repair site of the tendon, or leave
gaps between the ends?
Michael Sandow:  I mean I will add some tension at the
time of repair when temporary fixation is in place,
but after removal of the fixation, it is best to see that
the tendon is smooth and not bunching, but it is fine
if there are small gaps between the ends. I do not
intentionally leave gaps between the ends when
suturing the tendons.
Steve K. Lee:  I have been using interlocking horizontal
mattress locking sutures. It is similar to Silfverskiöld,
but with interlocks. That is based on the work we
have done in the lab. Michael Hausman called it a
“Chinese finger trap.”
Daniel Mass:  What I usually do is to put epitendinous
stitches to the back of the tendon first. You lock the
stitch each time and make the tendon ends kissing.
Then you put core suture and end with putting the
epitendinous suture in the front of the tendon.
Daniel Mass:  Most people are actually still using the
Kessler. This is what they learned and what they have
used.
Michael Sandow:  I think the Kessler is such a rubbish
method for repairing the tendon; it has very poor
biomechanics, gapping very easily.
Jin Bo Tang:  Many people and papers talk about adding
Pennington locks into the Kessler. Either a grasping
and locking Kessler is not strong. We had a study
several months ago and asked two surgeons to make
two groups of Kessler repairs, with and without 
Pennington lock. We couldn’t find any difference in
the strength, except 2 to 3 N differences in the gap
force.
 Appendix: Symposium Discussion 2 449

Michael Sandow:  You are right. A study showed what- interlocking horizontal mattress suture provides
ever you put grasping, Pennington locking Kessler or good strength. In doing this repair, each bite has to
just a simple loop around the tendon end, the suture be slightly away from the cut edge to not converge.
would deform the tendon and form a loop around Daniel Mass:  I use running locks in epitendionus
the tendon, which actually does not act much suture, instead of interlocking suture. We tested it,
differently. without a core suture; it is adequately strong. Prob-
Jin Bo Tang:  Is the Kleinert method of motion still ably it is not as strong, but the superficialis is flat, and
common in the United States? people don’t get the rotation right and actually
Daniel Mass:  I think it is declining. More therapists use narrow the Camper’s chiasm. Just doing one slip is
the Duran method and the place-and-hold exercise. easier and adequate.
Jin Bo Tang:  Do you actively move after secondary Steve K. Lee:  For the superficialis tendon, I would repair
tendon graft? both slips, but quickly reduce it to one slip if there is
Daniel Mass:  I do active finger motion after tendon any issue with tendon gliding. The Mayo group wrote
graft, with no-resistance, in a wrist extension splint about the benefits of repairing just one slip. It seems
or cast putting the wrist in 20° of extension and the many people are moving in that direction.
MCP joint in 60° of flexion and the IP straight. For Jin Bo Tang:  Great talks and discussion. Thank you!
kids, I put a cast, and in adults, I put a splint. I left 
a big hole in the cast, so the finger can move in 
kids. In the unreliable patients, you can do the same
thing.
Robert Savage:  Controlled “active” motion began in a
report in 1989 about the Belfast regimen. Variable
results were reported later, including those from
Manchester and Essex, with some ruptures. In a lab
study of pulleys, I noticed, and other noticed too,
that if you do not move the finger through the full
range, you are not putting the maximal load to the
tendon. The other ways of performing active motion
more easily include putting the wrist in extension: to
explain, the wrist flexed position causes the finger
extensors to become tight, and so finger flexion will
become difficult. In wrist extension, the finger exten-
sors are slack and flexion of the fingers requires much
less force. Also if the MCP joints are held in a neutral
or slightly flexed position, you will find it easy to flex
the DIP joint. Figure 3  “Work done only a few years, not decades, ahead
Steve K. Lee:  Most people who do primary repair may of others actually would not make a great difference to the
still have up to 10% rupture after early active motion; overall progress in a field.”
that’s 1 out of 10. Those results are not that great.  —Prof. Seiichi Ishii (back row, second from the left)
Dr. Richard Gelberman came to speak to the New commented humbly on May 26, 2010, in Tokyo, when
talking about his early work and contribution on intrinsic
York Society for Surgery of the Hand, saying “tenoly-
healing capacity of the flexor tendon in early 1970s. The
sis was necessary in 20% of (his) patients. There 
photograph was taken on that day (second from the right,
is still a lot of research to be done.” We looked at  back row, Prof. Poong-Teak Kim, and second from the right,
the strength of different repair and materials. Fiber- front row, Prof. Masamichi Usui). Prof. Ishii was honored as
wire has the greatest strength and the least knot “Pioneer of the Hand Surgery” in the Congress of the IFSSH in
volume (bulk). We recommend 6 knots with Fiber- October 2010 for his early work on the tendon and other
wire for repairs. Among epitendinous sutures, the contributions.
 A Postscript About Progression of Thought
on Primary Tendon Repair
Jin Bo Tang, MD
I have set out to describe how my thinking pertaining
to flexor tendon surgery has progressed over more than
20 years.
My first work on the tendon started in 1988 with a
study of sheath closure using chicken models. Direct
closure of the sheath was found to be no better than
partial excision, and direct sheath closure at the delayed
primary stage was actually harmful to tendon gliding.
This conclusion differed from a mainstream tenet at that
time that sheath closure was beneficial to preventing
adhesions and maintaining nutrition. My ensuing work
fostered an idea that ample space inside the sheath cavity
(not closure or reconstructive surgery of the sheath per
se) is vitally important to healthy tendon healing and
gliding. A key piece of evidence that led me to this con-
sideration was that, given an equal extent of adhesions,
tendons whose sheaths were enlarged with interposing
grafts exhibited better gliding than those within tightly
closed sheaths. Increasing the volume inside the sheath
is thus considered imperative to both healing and
gliding of the tendon. I should give great credit to Pro-
fessor Seiichi Ishii, who earnestly mentored and sup-
ported my investigations in 1988 and 1989. Particular
credit is due to this great man for creating the adhesion
grading criteria used in the investigation. Prof. Ishii is
an early pioneer in the area of “intrinsic healing” of the
tendon. He initiated in vitro culture work to demon-
strate the capability of tenocytes to proliferate and to
repair wounds as early as 1971, and published 3 years
later. In 2010, when I talked to him about this early
work, he calmly commented that work done only a few
years, not decades, ahead of others actually would not
make a great difference to the overall progress in a field.
He is an exemplary pioneer in science, humble in accept-
ing credit, yet dedicated and nurturing toward young
investigators.
My second work was on subdivision of zone 2 in late
1989. At that time, I began independently treating hand
cases and regularly repaired zone 2 tendon injuries. In
practice, I found that recording the site of injuries and
outcomes of treatment in subdivisions of zone 2
appeared not only necessary, but important in discuss-
ing treatment of these tendons. Literature in the 1970s
and 1980s had been unclear regarding the exact site in
450
reporting methods and outcomes. I sketched out zoning
methods by observing hand specimens in the Depart-
ment of Anatomy. Later, in the early 1990s, my case
series indicated differences in results of tendon repairs
between zone 2C and other subzones. The repairs in the
area covered by the A2 pulley were found to produce
the worst outcomes.
It was my awareness of worse outcomes in zone 2C
that directed me to conducting studies focusing on the
A2 pulley and its corresponding tendon segment in
1993–94. Clinically I compared the outcomes of repair
to non-repair of the superficialis tendon in this particu-
lar area, and found worse outcomes when the superfi-
cialis was repaired. These clinical results prompted me
to return to the anatomic laboratory to specifically study
the morphology and mechanics of tendons and pulleys.
There, I began to realize that purposeful incision of a
part of the A2 pulley can be a feasible clinical option to
improve treatment results.
This idea of active release of the A2 pulley encoun-
tered great opposition when presented to a symposium
later. Though this study was published in The Journal of
Hand Surgery (British) in 1995, even with clinical data
the idea of purposeful pulley-venting was printed only
as an abstract in Chinese. There was considerable resis-
tance to this “dangerous” initiative against deeply rooted
traditional recommendations.
In late 1998, I read a report by Dr. David Elliot and
his colleagues of reporting results of tendon repairs in
subzones of zone 2 and venting of the A2 and A4
pulleys, which inspired me to send a letter to start com-
munication with Dr. Elliot and to plan a 5-day visit to
him in June of 1999. In Dr. Elliot’s house in the middle
of a wheat field by Chelmsford, Dr. Elliot and I spent 
no less than 3 entire days “randomly” discussing any
topics we could think of relating to tendon repair, taking
notes on ideas that came up during conversations. Dr.
Elliot showed me a manuscript in which he proposed
to subdivide zone 1. We agreed that a precise and clear
determination of the site of tendon laceration is funda-
mental to any discussion of treatment. Dr. Elliot’s take
was as follows: most people who do not feel a need 
to subdivide the zones probably have not had enough
cases to allow for observing differences in treatment
 A Postscript About Progression of Thought on Primary Tendon Repair
results. We discussed the methods of repairs and the
need of stronger surgical repair; in the later years, I
learned that Dr. Elliot and his colleagues started routine
use of the six-strand core repair using the looped suture
that I have favored. We agreed that a part of the pulleys
can be incised and that sheath closure is not important—
still at that time I did not recognize the importance of
pulley-venting to the extent that I would later—the
venting may be vital to achieve predictable treatment
outcomes. We were surprised by our similar approaches
in A2 pulley treatment without prior awareness of one
another. Dr. Elliot actually started to perform pulley-
venting in early 1995.
I established a research center for the hand in 1995
and had a group of investigators working on tendon
projects since then. Before that, I was mostly alone on
my journey. Drs. Ren Guo Xie, Bin Wang, and Yu-tong
Gu were the earliest to join in mechanical testing of
tendon repair strength and in vivo studies, followed by
Drs. Zhi Ming Cui, Jun Tan, Yan Xu, and Zun Shan Ke.
Over the past years, Drs. Yi Cao, Bei Zhu, Chuan Hao
Chen, and Ya Fang Wu performed a series of excellent
mechanical and molecular studies. On the clinical side,
Drs. Ren Guo Xie, Bin Wang, and Jun Tan have been
active in applying novel surgical and rehabilitation
methods for years. All have been extremely dedicated;
to them I should give great credit. The research center
has entered into full function since 1997. Over the past
15 years, we have investigated individual factors that
may affect tendon repair strength with in vitro mechani-
cal testing; modified test models under curvilinear
loading conditions; tested novel surgical repair methods;
examined the effects of pulley integrity or venting on
tendon gliding and adhesions with in vivo models; and
explored molecular methods which may be used in
enhancing tendon healing or limiting adhesions. In
these investigations, the study had been set up with
detailed discussion within the group. In order to allow
myself to remain involved in some vital steps and
monitor or participate the project directly, I rather strictly
limit the number of people participating in investigation
at the same time. In investigations that have led to major
conclusions, I repeated and verified key experimental
steps together with colleagues. Often independent inves-
tigators have worked on projects at different times, with
a portion of study contents overlapping, to verify each
other’s conclusions in a blinded way. To avoid bias, I do
not usually explain expected results to fellow investiga-
tors. I consider our conclusions reliable only when they
are obtained without a clear purpose of proving a pre-
conceived conclusion and are repeatedly proven by dif-
ferent investigators among us. Not infrequently, a study
is published years later, after it has undergone blinded
self-verification, sometimes carried out by researchers
451
who lack background knowledge about the project but
have strong technical skills, so they do not know what
we are trying to prove. We intend not only to publish
our findings, but also to publish with greater confidence,
with results that withstand the test of time.
Our hand surgery service for disorders of hand and
upper extremity became a department in 2002, and has
continuously expanded to its current size of 12 staff
surgeons and 110 hospital beds. Over the past 10 years,
my colleagues and I have steadily modified our surgical
techniques and rehabilitation protocols. Most of the
novel methods or technical modifications that my col-
leagues and I have applied to the clinic were derived
directly from our laboratory results. We also adopted a
few clinical treatment rules directly from laboratory
studies, e.g., optimal core suture purchase and ideal
grasping/locking sizes in a surgical repair, etc. Motion
protocols have been amended with new components,
such as passive motion prior to active motion in each
exercise session and initiation of finger motion 3 to 5
days after surgery. These modifications stemmed from
studies of factors affecting strength of tendon repair,
postoperative edema, resistance to tendon movement,
etc. We have been able to prove the safety of judicious
surgical venting of the pulleys through clinical follow-up
and established simplified multistrand repairs as the
standard method for zone 2 tendon repairs. Though we
still face challenges of composite tissue loss/damage
with tendon injuries—including tendon injuries involv-
ing bones or after multiple reconstructions—It is the my
opinion and that of my colleagues that it is possible to
achieve close-to-normal recovery of function in clean-
cut tendon injuries in the finger. The outcomes of repairs
of tendon injuries in the fingers are no longer unpredict-
able, which is a major advance.
My colleagues and I share the belief that attention to
the intricate details of surgical repair is vital to the
success of any given method. Equally important is the
clear and precise mastery of the surgical anatomy of the
tendon and its pulleys. Junior surgeons may frequently
not attend to details of surgical repair techniques such
as ensuring sufficiently large tendon substance within a
suture’s grasps or locks and adding some tension across
the repair, and may possess no clear mental picture of
anatomy during surgery. Without attention to such
details, the repair may be disrupted or gap easily, and
the sheath or pulleys could be treated erroneously. Sur-
geons who adopt an established method may report the
end-results that vary enormously depending on the sur-
gical details. Thus attention to surgical details should be
adequately emphasized. Technical details and mastery
of anatomy need to be passed from experienced sur-
geons to junior staff members in classrooms and at the
operation table.