MasterCases in Hand and Wrist Surgery 0865779813, 3131277416, 3913984054, 9780865779815

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MASTERCASES Hand and Wrist Surgery

Thieme

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MASTERCASES Hand and Wrist Surgery Kevin D. Plancher, M.D. Associate Clinical Professor Department of Orthopaedics Albert Einstein College of Medicine New York, New York and Chief of Congenital Hand Service Blyethdale Children’s Hospital Valhalla, New York and Plancher Orthopaedics and Sports Medicine New York, New York and Greenwich, Connecticut Assistant to the Editor Timothy Luke, M.D. Fellow Plancher Orthopaedics and Sports Medicine New York, New York

Thieme New York • Stuttgart

Thieme Medical Publishers, Inc. 333 Seventh Ave. New York, NY 10001 Editorial Assistant: Judith Tomat Associate Editor: Owen Zurhellen Director, Production and Manufacturing: Anne Vinnicombe Production Editor: Becky Dille Marketing Director: Phyllis Gold Sales Manager: Ross Lumpkin Chief Financial Officer: Peter van Woerden President: Brian D. Scanlan Compositor: Compset, Inc. Printer: Everbest Printing Co. Library of Congress Cataloging-in-Publication Data is available from the publisher. Copyright © 2004 by Thieme Medical Publishers, Inc. This book, including all parts thereof, is legally protected by copyright. Any use, exploitation or commercialization outside the narrow limits set by copyright legislation, without the publisher’s consent, is illegal and liable to prosecution. This applies in particular to Photostat reproduction, copying, mimeographing or duplication of any kind, translating, preparation of microfilms, and electronic data processing and storage. Important note: Medical knowledge is ever-changing. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy may be required. The authors and editors of the material herein have consulted sources believed to be reliable in their efforts to provide information that is complete and in accord with the standards accepted at the time of publication. However, in the view of the possibility of human error by the authors, editors, or publisher, of the work herein, or changes in medical knowledge, neither the authors, editors, or publisher, nor any other party who has been involved in the preparation of this work, warrants that the information contained herein is in every respect accurate or complete, and they are not responsible for any errors or omissions or for the results obtained from use of such information. Readers are encouraged to confirm the information contained herein with other sources. For example, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this publication is accurate and that changes have not been made in the recommended dose or in the contraindications for administration. This recommendation is of particular importance in connection with new or infrequently used drugs. Some of the product names, patents, and registered designs referred to in this book are in fact registered trademarks or proprietary names even though specific reference to this fact is not always made in the text. Therefore, the appearance of a name without designation as proprietary is not to be construed as a representation by the publisher that it is in the public domain. Printed in China 5 4 3 2 1 TMP ISBN 0-86577-981-3 GTV ISBN 3 13 127741 6

TABLE OF CONTENTS Foreword . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . List of Contributors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

x xi xii xiii

SECTION I: ENVIRONMENTAL INJURIES TO THE DERMIS 1. Thermal, Chemical, and Electrical Burns, Ziv M. Peled and Jonathan S. Schreiber . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2. Injuries to the Dermis: Cold Injuries, Sokaratis Varitimidi, Robert J. Goitz, and Dean G. Sotereanos . . . . . . . . . . . . . . . . . . . 3. High-Pressure Injection Injuries, Kevin D. Plancher . . . . . . . . . .

3 9 14

SECTION II: INFECTIONS 4. 5. 6. 7. 8.

Felons, Sam Moghtaderi and Kevin D. Plancher . . . . . . . . . . . . . Paronychia, Sam Moghtaderi and Kevin D. Plancher . . . . . . . . . . Pyogenic Arthritis, Kevin D. Plancher . . . . . . . . . . . . . . . . . . . . . Web-Space Infections, Kevin D. Plancher . . . . . . . . . . . . . . . . . . Supporative Flexor Tenosynovitis, John C. P. Floyd and Waldo E. Floyd III . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9. Herpetic Whitlow, Kevin D. Plancher . . . . . . . . . . . . . . . . . . . . . 10. Bites to the Hand, Kevin D. Plancher . . . . . . . . . . . . . . . . . . . . . 11. Mycobacterial Tenosynovitis, John C. P. Floyd and Waldo E. Floyd III . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

21 25 30 36 42 47 50 55

SECTION III: COMPRESSION NEUROPATHY A. Median Nerve 12. Carpal Tunnel Syndrome, Kevin D. Plancher . . . . . . . . . . . . . . . 13. Pronator Syndrome, Kevin D. Plancher . . . . . . . . . . . . . . . . . . . . 14. Anterior Interossus Nerve Syndrome, Michael F. Bothwell and Kevin D. Plancher . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

63 70 75

B. Ulnar Nerve 15. Cubital Tunnel Syndrome, Eric Freeman, Dennis Rodin, and Kevin D. Plancher . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16. Ulnar Tunnel Syndrome, Robert M. Szabo . . . . . . . . . . . . . . . . .

80 87

C. Radial Nerve 17. Posterior Interosseus Syndrome, William B. Geissler . . . . . . . . . .

96 v

TA B L E O F C O N T E N T S

D. Cervical Nerve 18. Cervical Root Compression, Bradley M. Thomas, John M. Olsewski, and Jerry G. Kaplan . . . . . . . . . . . . . . . . . . . . 102 19. Complex Regional Pain Syndrome Type I (Reflex Sympathetic Dystrophy), Carole W. Agin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 108

SECTION IV: NERVE INJURIES/PALSIES 20. Acute Nerve Laceration, Kevin D. Plancher . . . . . . . . . . . . . . . . 117 A. Nerve Palsies 21. Low Median Nerve Palsy, Kevin D. Plancher . . . . . . . . . . . . . . . 122 22. Ulnar Nerve–Tendon Transfer, Mark S. Cohen . . . . . . . . . . . . . . 129 23. High Radial Nerve Palsy, Kevin D. Plancher . . . . . . . . . . . . . . . . 134

SECTION V: VASCULAR DISORDERS 24. Arterial Aneurysms, Kevin D. Plancher . . . . . . . . . . . . . . . . . . . . 145 25. Cannulation Injuries, Leon S. Benson . . . . . . . . . . . . . . . . . . . . . 152 26. Extravasation Injuries, Leon S. Benson . . . . . . . . . . . . . . . . . . . . 158

SECTION VI: CONTRACTURES 27. Dupuytren’s Contracture, Jack Abboudi and David S. Zelouf . . . . . 167 28. Stiff Joints, Shelly M. Sailer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 174

SECTION VII: TENDON INJURIES 29. 30. 31. 32.

A. Tenosynovitis Flexor Stenosing Tenosynovitis: Trigger Finger and Thumb, Kevin D. Plancher . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . De Quervain’s Disease, Kevin D. Plancher . . . . . . . . . . . . . . . . . Flexor Carpi Radialis Tunnel Syndrome, Kevin D. Plancher . . . . Flexar Carpi Ulnaris Calcific Tendinitis, Richard W. Barth . . . . .

B. Tendon Repair 33. Acute Laceration of Flexor Tendons, Mark S. Rekant . . . . . . . . . 34. Delayed Treatment of Flexor Tendons: Staged Tendon Reconstruction, Lawrence H. Schneider . . . . . . . . . . . . . . . . . . . 35. Chronic Lacerations of Extensor Tendons, Angela A. Wang and Michelle Gerwin Carlson . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36. Avulsions of the Flexor Digitorum Profundus, Donald M. Lewis and Randall W. Culp . . . . . . . . . . . . . . . . . . . . vi

183 188 193 198 202 209 215 219

TA B L E O F C O N T E N T S

SECTION VIII: FRACTURES AND DISLOCATIONS OF THE HAND 37. 38. 39. 40.

41. 42. 43.

44.

A. Phalanx Fractures Distal Phalangeal Fractures, Kevin D. Plancher . . . . . . . . . . . . . . Mallet Fractures, Kevin D. Plancher . . . . . . . . . . . . . . . . . . . . . . Proximal Phalangeal Shaft Fractures, Kevin D. Plancher . . . . . . . Proximal Phalangal Condylar Fractures, Carrie R. Swigart . . . . . B. Metacarpal Fractures Metacarpal Neck Fractures, Kostas J. Constantine and Thomas R. Kiefhaber . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Metacarpal Shaft Fractures, Robert J. Goitz, Sokratis Varitimidis, and Dean G. Sotereanos . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Metacarpophalangeal Joint Injuries: Fractures (Intraarticular) at the Base of the Proximal Phalanx, An Arthroscopic Technique, Joseph F. Slade III and John D. Mahoney . . . . . . . . . . . . . . . . . . . Metacarpal Head Fractures, Paul R. Greenlaw and Mark R. Belsky . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

C. Dislocations: Phalanx and Metacarpals 45. Volar Dislocations of the Proximal Interphalangeal Joint, Lisa L. Lattanza and Steven Z. Glickel . . . . . . . . . . . . . . . . . . . . . 46. Lateral Dislocations of the Proximal Interphalangeal Joint, Christopher H. Martin and Steven Z. Glickel . . . . . . . . . . . . . . . . 47. Dorsal Dislocations of the Proximal Interphalangeal Joint, Rosa L. Dell’Oca and Amy Ladd . . . . . . . . . . . . . . . . . . . . . . . . . . 48. Distal Interphalngeal Joint Dislocations, John D. Wyrick . . . . . . 49. Dorsal Metacarpophalangeal Dislocations (Irreducible), Benjamin Chang and Mark Katz . . . . . . . . . . . . . . . . . . . . . . . . . 50. Volar Metacarpophalangeal Dislocations (Irreducible), Benjamin Chang and Mark Katz . . . . . . . . . . . . . . . . . . . . . . . . .

51. 52.

53. 54. 55.

D. Thumb and Carpometacarpal Joints Ulnar Collatreal Ligament Injuries: “Skier’s Thumb”, Kevin D. Plancher . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Carpometacarpal Joint Injuries: Bennett’s Fractures (Arthroscopic and Percutaneous Screw Technique), Joseph F. Slade III and John D. Mahoney . . . . . . . . . . . . . . . . . . . Carpometacarpal Joint Injuries: Bennett’s Fractures (Wire Technique), Michael Jablon . . . . . . . . . . . . . . . . . . . . . . . . Complex Fractures at the Base of the Thumb: Rolando Patterns, John A. Girotto, Shrika Sharma, Thomas J. Graham . . . . . Carpometacarpal Joint Dislocation, Andrew L. Haas and Kevin D. Plancher . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

227 232 238 246

252 258

265 271

277 282 287 296 300 305

310

319 325 331 337 vii

TA B L E O F C O N T E N T S

SECTION IX: FRACTURES AND DISLOCATIONS OF THE WRIST A. Wrist Fractures and Dislocations 56. Scaphoid Fractures: “Classic” Volar Approach, Kevin D. Plancher . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 345 57. Percutaneous Treatment of Proximal Pole Scaphoid Fractures, Joseph F. Slade III and John D. Mahoney . . . . . . . . . . . . . . . . . . . 351 58. Scaphoid Nonunion, James W. Vahey and Kevin D. Plancher . . . . . 359 B. Fractures of the Distal Radius 59. Radial Styloid Fractures, James H. Calandruccio . . . . . . . . . . . . . 369 60. Extraarticular Distal Radius Fractures, Kydee K. Sheetz and Matthew D. Putnam . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 375 61. Intraarticular Distal Radius Fractures: Volar Approach, Dorsal Approach, and Arthroscopic Reduction, Kevin D. Plancher . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 380

SECTION X: WRIST INSTABILITY AND ARTHROSCOPY 62. Acute Perilunate and Lunate Dislocations, Kevin D. Plancher . . . . 63. Scaphulonate Instability, Steven F. Viegas and Manuel F. DaSilva . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 64. Lunotriquetral Instability, Loryn P. Weinstein and Allen T. Bishop . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65. Dorsal Capsulodesis for Midcarpal Instability, William K. Feinstein and David M. Lichtmann . . . . . . . . . . . . . . 66. Tears of the Triangular Fibrocartilage Complex, Phillip E. Blazar and Scott D. Mair . . . . . . . . . . . . . . . . . . . . . . .

391 398 405 411 417

SECTION XI: ARTHRITIS OF THE HAND AND WRIST A. Osteoarthritis 67. Osteoarthrits: Proximal Interphalangeal Joint (Silastic Implants), Thomas Bienz and A. Lee Osterman . . . . . . . . . . . . . . . . . . . . . . . 68. Osteoarthritis: Carpometacarpal Joint (Ligament Reconstruction with Tendon Interposition), Vincent Ruggiero and Andrew K. Palmer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69. Scapholunate Advanced Collapse, Andrew H Borom and David B. Siegel . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70. Triscaphe Degenerative Arthritis, Andrew E. Caputo and H. Kirk Watson . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

425

433 440 445

B. Rheumatoid Arthritis 71. Rheumatoid Arthritis: Distal Interphalangeal Joint Arthrodesis, R. John Naranja, Jr. and Kevin D. Plancher . . . . . . . 450 viii

TA B L E O F C O N T E N T S

72. Rheumatoid Arthitis: Proximal Interphalangeal Joint Arthrodesis, R. John Naranja, Jr. and Kevin D. Plancher . . . . . . . 456 73. Rheumatoid Arthritis: Metacarpophlangeal Joint Reconstruction Arthroplasty, R. John Naranja, Jr. and Kevin D. Plancher . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 462

SECTION XII: CONGENITAL ANOMALIES OF THE HAND A. Failure of Formation 74. Short Below-Elbow Amputation, Robert T. Ciocco and Scott H. Kozin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75. Transverse Deficiency of the Digits, Scott H. Kozin . . . . . . . . . . 76. Radical Deficiency (Radical Clubhand), Alexander D. Mih . . . . 77. Ulnar Deficiency (Ulnar Clubhand), Scott H. Kozin . . . . . . . . .

471 478 484 488

B. Undergrowth 78. Brachydactyly, Scott H. Kozin . . . . . . . . . . . . . . . . . . . . . . . . . . . 494 79. Hypoplastic Digits and Hands, Scott H. Kozin . . . . . . . . . . . . . . 499 80. Reconstruction of a Type II Hypoplastic Thumb, Allan E. Peljovich and Peter M. Waters . . . . . . . . . . . . . . . . . . . . . 505 C. Failure of Differentiation 81. Congenital Radioulnar Synostosis, Allan E. Peljovich and Peter M. Waters . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 514 D. Duplication of Parts 82. Polydactyly and Bifid Thumb, Kevin D. Plancher . . . . . . . . . . . . 521 E. Overgrowth 83. Macrodactyly, Ann E. Van Heest and James House . . . . . . . . . . . . 526

SECTION XIII: TUMORS OF THE HAND AND WRIST 84. Ganglions, Kevin D. Plancher and Michael Bothwell . . . . . . . . . . 85. Lipoma, Kevin D. Plancher and Michael Bothwell . . . . . . . . . . . . 86. Giant Cell Tumor of the Tendon Sheath (Benign), Kevin D. Plancher . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87. BenignVascular and Malignant Vascular Tumors, Earl W. Brien and Stuart H. Kuschner . . . . . . . . . . . . . . . . . . . . . 88. Enchondroma, Kevin D. Plancher and Michael Bothwell . . . . . . . 89. Osteochondroma, Kevin D. Plancher and Michael Bothwell . . . . 90. Osteoid Osteoma, Kevin D. Plancher and Michael Bothwell . . . .

535 541 544 548 553 556 559

INDEX . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 562

ix

FOREWORD Textbook surgical education usually follows a predictable format involving fairly in-depth descriptions of various pathologic conditions including etiology, pathophysiology, symptomatology, diagnostic procedures, conservative management, and surgical treatment. Although there is variation in the emphasis different books place on each of these areas, the reader is obliged to absorb a plethora of information and add it to his or her knowledge base by rote retention. Trying to assimilate large amounts of clinically relevant information from these texts is confusing and difficult for all of us who are not blessed with photographic memories. In the MasterCases text Hand and Wrist Surgery, Kevin Plancher and his superb authors are to congratulated for breaking the mold and providing an amazingly comprehensive series of concise discussions of 90 different clinical conditions affecting the hand and wrist. Each begins with a short history and clinical presentation of a clinical case that will be used to guide the diagnostic and treatment sequence that will be used to illustrate the management of a specific condition. The authors then proceed with the physical examination, diagnostic studies, differential diagnoses, diagnosis, nonsurgical management, and surgical treatment with clear, thorough and well illustrated descriptions of the technique that they favor. Alternative treatment methods are included as are post-operative management and possible complications. Helpful “pearls” and “pitfalls” are included in the margin of each case. All case discussions are concise and relevant without superfluous and confusing verbage. The educational impact of this unique approach is considerable. With the clinical case in mind, the reader can easily follow the ensuing sequence of diagnostic and treatment considerations as if it were a patient under their own care. Unquestionably, the overall appreciation of that particular condition and the cerebral retention of important clinical information will be greater using this “user friendly” format. Dr. Plancher’s simplified format makes the learning pleasurable and enhances one’s ability to study many different conditions at one setting without confusing material between different conditions as is so easily done in more conventional surgical books. Kevin Plancher and his excellent complement of authors are to be congratulated for providing a superb text that will serve as examination preparation equally well. James W. Strickland M.D.

x

PREFACE Hand and wrist surgery is not a young discipline. The ability to find a specific procedure, well described with helpful hints, to make your trip to the operating room successful can be daunting. The various types of treatments described for the same procedure in textbooks can be overwhelming to a reader. The specific goal of this book is to allow a practicing surgeon, fellow, or resident physician and medical student to understand the most basic and advanced concepts to perform surgical procedures for some of the most common wrist and hand procedures. Each chapter contains a different, well-illustrated surgical procedure written in a concise manner. The format of each chapter is the same throughout the book. This book, written by many well-known experts who perform these exact procedures, provides the essential points to allow the surgeon to perform surgery successfully on the hand and wrist. The color photos and drawings guide you through the operation visually. While this textbook never substitutes for informed journal reading, I believe it will stand alone on the shelf when the need arises to find an injury that a physician must handle and have a coherent simple approach to a patient in need of treatment whether it is elective, urgent, or even emergent. This book may also be used for preparing for board-type examinations as a methodical way to review various injuries of the wrist and hand. While this text was not made to be as comprehensive as possible, I hope that in the future we will increase the number of surgical cases to challenge all of us as we strive for perfection when treating our patients. I look forward to your comments and thoughts. Kevin D. Plancher, M.D.

xi

ACKNOWLEDGMENTS To all the contributing authors: I apologize for the delay in getting this textbook to our bookshelves. I am deeply grateful for all your efforts and expertise. Many of you sacrificed weekends, vacations, and time away from family to complete the task at hand. I am very grateful to Ms. Becky Dille, a professional whose endless hours made this book a reality. Ms. Judith Tomat, who tirelessly reviewed and compiled each chapter to perfection with enthusiasm and energy. Deliah Cohen, Gary Schnitz, and Ron Boisvert for their artistic skill and illustrations, their artwork allows us to read the words with ease, through their gift to help our eyes. To the President of Thieme, Brian Scanlan, whose belief in this project, with willingness to stretch the limits of all rules to complete a book, I say thank you! To Karen Briggs, who behind the scenes, along with Tim Luke, M.D., completed Herculean writing, organizing, and editing, and made this book a reality. To my staff in New York and Connecticut for putting up with too many meetings and distractions, I cannot thank you enough for your patience and dedication. Thanks to my mentors, Drs. Richard Gelberman, James W. Strickland, James Steichen, Bill Kleinman, Hill Hastings, Rick Idler, and Tom Fischer who held my hand yet still allowed me to grow, each in their own way. Mostly I need to thank my patients for teaching me so much in more than a decade that I am honored to edit such a book.

xii

LIST OF CONTRIBUTORS Jack Abboudi, M.D. Clinical Instructor Department of Orthopaedic Surgery Jefferson Medical College Philadelphia, Pennsylvania

Allen T. Bishop, M.D. Professor of Orthopedic Surgery Department of Orthopaedic Surgery Mayo Clinic College of Medicine Rochester, Minnesota

Carole W. Agin, M.D., M.P.A.

Philip E. Blazar, M.D. Assistant Professor of Orthopaedic Surgery Harvard Medical School and Orthopaedic Surgeon Department of Orthopaedic Surgery/Hand and Upper Extremities Bringham Women’s Hospital Boston, Massachusetts

Andrew E. Caputo, M.D. Co-Director of Hand Surgery Service Hartford Hospital and Connecticut Children’s Medical Center and Associate Clinical Professor Department of Orthopaedic Surgery University of Connecticut Health Center Farmington, Connecticut And Attending Surgeon Connecticut Combined Hand Surgery Fellowship Hartford, Connecticut

Michael F. Bothwell, PA-C Plancher Orthopaedics & Sports Medicine PLLC 1160 Park Avenue New York, New York

Benjamin Chang, M.D. Department of Surgery University of Pennsylvania Children’s Hospital of Philadelphia Philadelphia, Pennsylvania

Earl W. Brien, M.D. Director of Muscloskeletal Tumor Cedar Sinai Medical Center and Assistant Professor King Drew University Orthopaedic Hospital Los Angeles, California

Roberta T. Ciocco, OTR/L Director of Occupational Therapy Shriners Hospitals For Children Philadelphia, Pennsylvania

Richard W. Barth, M.D. Assistant Clinical Instructor Department of Orthopaedic Surgery George Washington University and Georgetown University Washington D.C. Leon S. Benson, M.D. Associate Professor of Clinical Orthopaedic Surgery Illinois Bone & Joint Institute, LTD Department of Orthopaedic Surgery Northwestern University Medical School Glenview, Illinois Mark R Belsky, M.D. Associate Clinical Professor of Orthopaedic Surgery Tufts University School of Medicine, Boston, Massachusetts and Chief of Orthopaedic Surgery Newton-Wellesley Hospital, Newton, Massachusetts Andrew H. Borom, M.D. Tallahassee Orthopaedic Clinic Tallahassee, Florida Thomas Bienz, M.D. Gem City Bone and Joint Laramie, Wyoming

James H. Calandruccio, M.D. Assistant Professor Department of Orthopaedics University of Tennessee–Campbell Clinic Memphis, Tennessee

Mark S. Cohen, M.D. Associate Professor Director, Hand and Elbow Section Director, Orthopaedic Education Department of Orthopaedic Surgery Rush University Medical Center Chicago, Illinois Kostas J. Constantine, M.D. Fredricksberg Ambulatory Surgery Center Board Member Fredricksberg Orthopaedics Associates Mary Washington Hospital Fredricksberg, Virginia

xiii

LIST OF CONTRIBUTORS

Randall W. Culp, M.D., F.A.C.S. Assoicate Professor of Orthopaedic, Hand and Microsurgery Thomas Jefferson University The Philadelphia Hand Center Philadelphia, Pennsylvania Manuel F. DaSilva, M.D. Department of Orthopaedic Surgery and Rehabilitation University of Texas Medical Branch Galveston, Texas Rosa L. Dell’Oca M.S., M.D William K. Feinstein, M.D. Metropolitan Orthopedics St. Louis, Missouri John C. P. Floyd, M.D. Orthopaedic Resident Department of Orthopaedic Surgery State University of Newy York at Stony Brook Stony Brook, New York Waldo E. Floyd III, M.D. Clinical Professor of Surgery (Hand) Macon Orthopaedic and Hand Center Mercer University School of Medicine Macon, Georgia Eric Freeman, M.D. South Island Orthopaedics Cedarhurst, New York William B. Geissler, M.D. Professor, Division of Hand and Upper Extremity Surgery and Head of Section of Arthroscopic Surgery and Sports Medicine Department of Orthopaedic Surgery and Rehabilitation University of Mississippi Medical Center Jackson, Mississippi xiv

Michelle Gerwin Carlson, M.D. Attending Surgeon, Hospital for Special Surgery Assistant Professor of Orthopaedic Surgery Cornell University Medical College New York, New York John A. Girotto, M.D. Director, Cleft and Craniofacial Anomalies Center and Assistant Professor Pediatrics and Plastic and Reconstructive Surgery Golisano Children’s Hospital Strong Memorial Hospital Rochester, New York Steven Z. Glickel, M.D. Director, Hand Surgery Service St. Luke’s Roosevelt Hospital Center and Assistant Clinical Professor of Orthopaedic Surgery Columbia University St. Luke’s Roosevelt Hospital Center New York, New York Robert J. Goitz, M.D. Chief of Hand and Upper Extremeity Surgery University of Pittsburgh Medical Center Pittsburgh, Pennsylvania Thomas J. Graham, M.D. Chief Curtis National Hand Center Union Memorial Hospital Baltimore, Maryland Paul R Greenlaw, M.D. Tufts Orthopaedics Residency New England Medical Center/ Floating Hospital for Children Boston, Massachusetts

Andrew L. Haas, M.D. Associate Director of Sports Medicine South Florida Institute of Sports Medicine Fort Lauderdale, Florida James House, M.D. Professor Emeritus University of Minnesota Hospital Department of Orthopaedic Surgery Minneapolis, Minnesota Michael Jablon, M.D. Department of Orthopaedic Medicine Saint Francis Hospital Chicago, Illinois Jerry G. Kaplan, M.D. Director EMG Laboratory Associate Professor of Neurology Albert Einstein College of Medicine Bronx, New York Mark Katz, M.D. Division of Hand Surgery Department of Orthopaedic Surgery University of Pennsylvania Philadelphia, Pennsylvania Thomas R. Kiefhaber, M.D. Hand Surgery Specialists Cincinnati, Ohio Scott H. Kozin, M.D. Associate Professor Department of Orthopaedic Surgery Temple University and Hand Surgeon Shriners Hospital for Children Philadelphia, Pennsylvania Stuart H. Kuschner, M.D. Lane and Kuschner Medical Group Beverly Hills, California

LIST OF CONTRIBUTORS

Amy Ladd M.D. Professor, Hand and Upper Extremity Surgery Stanford University Stanford, California

Sam Moghtaderi, M.D. Montefiore Medical Center Albert Einstein College of Medicine Bronx, New York R. John Naranja Jr., M.D.

Lisa L. Lattanza, M.D. Assistant Clinical Professor Department of Orthopaedic Surgery University of California San Francisco, California Donald M. Lewis, M.D. Muir Orthopaedics Specialists Walnut Creek, California David M. Lichtman, M.D. Clinical Professor Department of Orthopaedic Surgery University of Texas Southwestern Dallas, Texas and Chairman and Residency Program Director John Peter Smith Hospital Fort Worth, Texas John D. Mahoney, M.D. Department of Orthopaedic Surgery George Washington University Washington, D.C. Scott Mair, M.D. Assistant Professor Division of Orthopaedic Surgery University of Kentucky Lexington, Kentucky Christopher H. Martin Assistant Professor University of Utah Hospital Salt Lake Orthopaedic Clinic Salt Lake City, Utah Alexander D. Mih, M.D. The Indiana Hand Center Associate Professor Department of Orthopaedic Surgery Indiana University School of Medicine Indianapolis, Indiana

John M. Olsewski, M.D. Associate Professor of Clinical Orthopaedic Surgery Albert Einstein College of Medicine Bronx, New York and Director of Orthopaedic service Soundshore Medical Center of Westchester New Rochelle, New York A. Lee Osterman, M.D. Chairman, Division of Hand Surgery and Professor of Orthopaedic Hand and Microvascular Surgery and President The Philadelphia Hand Center Thomas Jefferson University Hospital Philadelphia, Pennsylvania Andrew K. Palmer, M.D. Professor of Orthopaedics, Division Chief of Hand Surgery State University of New YorkUpstate Medical University Syracuse, New York Ziv M. Peled, M.D. Hartford, Connecticut Allan E. Peljovich, M.D., M.P.H. Clinical Instructor of Orthopaedics Department of Orthopaedic Surgery Atlanta Medical Center The Hand and Upper Extremity Center of Georgia Atlanta, Georgia

Kevin D. Plancher, M.D. Associate Clinical Professor Department of Orthopaedics Albert Einstein College of Medicine New York, New York and Chief of Congenital Hand Service Blyethdale Children’s Hospital Valhalla, New York and Plancher Orthopaedics and Sports Medicine New York, New York and Greenwich, Connecticut Matthew D. Putman, M.D. Associate Professor, Director of Hand Surgery Fellowship University of Minnesota Department of Orthopaedic Surgery Minneapolis, Minnesota Mark S. Rekant, M.D. Assistant Professor of Orthopaedic Surgery Department of Orthopaedic Surgery Thomas Jefferson University Philadelphia, Pennsylvania Dennis Rodin, M.D. Waterbury Orthopaedic Associates Waterbury, Connecticut Vincent Ruggiero, M.D. State University of New York-Health Science Center at Syracuse Syracuse, New York Shelly M. Sailer, O.T.R./L., C.H.T. Clinical Specialist in Upper Extremity Rehabilitation Department of rehabilitation Medicine Harborview Medical Center University of Washington Seattle, Washington

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LIST OF CONTRIBUTORS

Lawrence H. Schneider M.D. Clinical Professor Department of Orthopaedic Surgery, Division of Hand Surgery Jefferson Medical College of the Thomas Jefferson University Philadelphia, Pennsylvania Jonathan S. Schreiber, M.D. Assistant Clinical Professor Chief, Division of Plastic Surgery John Dempsey Hospital Farmington, Connecticut

Robert M. Szabo, M.D., M.P.H. Professor of Orthopaedics and Plastic Surgery Deartment of Orthopaedics University of California Medical Center Sacramento, California Bradley M. Thomas, M.D. Chief of Sports Medicine Department of Orthopaedic Surgery Harvor/University of California at Los Angeles Medical Center South Bay Orthopaedic Specialists Torrance, California

David B. Siegel, M.D. Southwest Shoulder Elbow and Hand Center Tucson, Arizona Joseph F. Slade, III, M.D. Yale University School of Medicine New Haven Connecticut Dean G. Sotereanos, M.D. Professor and Vice Chairman Department of Orthopaedic Surgery Allegheny Orthopaedic Associates Pittsburgh, Pennsylvania Carrie R. Swigart, M.D. Assistant Clinical Professor Department of Orthopaedics and Rehabilitation Yale University School of Medicine New Haven, Connecticut

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Peter M. Waters, M.D. Department of Orthopaedic Surgery Boston Children’s Medical Center Boston, Massachusetts

James W. Vahey, M.D. Orthopaedic Hand and Microvascular Surgeon Hand Associates of the Nevada Dessert Las Vegas, Nevada

H. Kirk Watson, M.D. Clinical Professor Department of Orthopaedics University of Connecticut Medical School Farmington, Connecticut And Assistant Clinical Professor Department of Surgery (Plastic) Yale School of Medicine New Haven, Connecticut

Ann E. Van Heest, M.D. Associate Professor Department of Orthopaedic Surgery University of Minnesota Minneapolis, Minnesota

Loryn P. Weinstein, M.D. Resident Department of Orthopaedic Surgery Mayo Clinic College of Medicine Rochester, Minnesota

Sokratis Varitimidis, M.D. Research Assistant Department of Orthopaedic Surgery University of Pittsburgh Medical Center Pittsburgh, Pennsylvania

John D. Wyrick, M.D. Director of the Upper Extremity Division of Orthopaedic Surgery and Associate Director of Orthopaedic Trauma and Assistant Professor University of Cincinnati College of Medicine Cincinnati, Ohio

Shrika Sharma, M.D. Kydee K. Sheetz, M.D. University of Minnesota Department of Orthopaedic Surgery Minneapolis, Minnesota

Angela A. Wang, M.D. Fellow in Hand and Microvascular Surgery Hospital for Special Surgery New York, New York

Steven F. Viegas, M.D. Professor and Chief, Division of Hand Surgery Department of Orthopaedic Surgery and Professor Department of Anatomy and Neurosciences University of Texas Medical Branch Galveston, Texas

David S, Zelouf, M.D. Clinical Instructor Department of Orthopaedic Surgery Jefferson Medical College Hand Surgeon, Philadelphia Hand Center Philadelphia, Pennsylvania

DEDICATION To my wife Jill S. Plancher, Esq. A source of inspiration for those lucky to know her And Brian, Jamie, and Megan An apology for all the missed evenings, weekends, and vacations

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Section I

Environmental Injuries to the Dermis

Thermal, Chemical, and Electrical Burns Ziv M. Peled and Jonathan S. Schreiber

Injuries to the Dermis: Cold Injuries Sokaratis Varitimidi, Robert J. Goitz, and Dean G. Sotereanos

High-Pressure Injection Injuries Kevin D. Plancher

THERMAL, CHEMICAL, AND ELECTRICAL BURNS

1 Thermal, Chemical, and Electrical Burns Ziv M. Peled and Jonathan S. Schreiber

History and Clinical Presentation A 77-year-old man undergoing chemotherapy for lung cancer was seen in consultation by the plastic surgery service after suffering a burn injury to the dorsum of his right hand. A previous intravenous (IV) site had infiltrated in the man’s right hand and this was removed. A different site was begun in another location for administration of mitomycin C. The chemotherapeutic agent extravasated at the site of the first IV line in the right hand, resulting in a chemical burn. PEARLS • There are multiple ways to treat burns of the hand, depending on the degree of the burn and associated injuries. Several principles should always be kept in mind and are critical to a successful outcome. These are early debridement and edema/infection control, early wound coverage, and early mobilization. Adherence to these simple principles will likely prevent or minimize common postburn complications such as flexion contractures and boutonniere deformities. • When completing the dissection of a distally based flap, the surgeon should examine the flap for evidence of venous congestion. If venous congestion is noted, a venous anastomosis should be performed to achieve adequate flap drainage. This technique, although infrequently necessary, can improve flap viability.

PITFALLS • Evaluation of a burn wound is challenging because the thickness of burn is often difficult to determine initially.

Physical Examination On initial examination the involved skin and subcutaneous tissue were cellulitic with a small area of necrosis. Initial debridement was performed in the office and revealed that the wound extended to the level of the deep subcutaneous tissue. The extensor tendons were noted to be covered by soft tissue and paratenon. Normal saline dressings were used to promote granulation tissue for possible future split-thickness skin grafting. Despite meticulous wound care, the overlying soft tissue became necrotic and required further debridement with resultant broad exposure of the extensor communis tendons. Minimal granulation tissue formation was noted. The patient was subsequently admitted to the local university hospital for workup and definitive treatment.

Differential Diagnosis Thermal burns Chemical burns Electrical burns

Diagnosis Chemical Burn The patient had a chemical burn caused by extravasation of mitomycin C. Tissue necrosis and sloughing is known to occur with extravasation of several types of chemotherapeutic agents and is well described with the use of mitomycin C. This tissue reaction has been known to occur at sites distant from the injection site.

Alternative Methods of Management The primary goal in the treatment of all hand injuries is to restore optimal function. There are multiple ways to treat burns of the hand, depending on the thickness 3

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and extent of the burn and associated injuries. Several principles should always be kept in mind. Early debridement, edema/infection control, early wound coverage, and early mobilization are critical to a successful outcome. Adherence to these simple principles will likely prevent or minimize the most difficult postburn complications such as flexion contractures and boutonniere deformities. Superficial burns usually heal spontaneously within 10 days. In this representative case, the full-thickness wound would take a very long time to heal by secondary intention. This is not ideal because the scar tissue that forms would result in restricted function and mobility. On the other hand, the early motion that is required to prevent joint stiffness and reduce edema formation may inhibit healing. Deeper wounds that would take more than 2 weeks to heal on their own, therefore, should be treated by excision and coverage with a graft or flap. Placement of full-thickness or split-thickness skin grafts have been used successfully in treating both superficial and partial-thickness burns of the hand. Furthermore, the success of these techniques has been augmented by the use of Unna’s boot dressings, fibrin glue, and even semipermeable membrane dressings, all of which have been reported to help improve graft take. In this case there was exposure of deeper structures (i.e., tendons) classifying this injury as a full-thickness burn. Tendons rarely accept skin grafts and therefore require flap coverage after excision and debridement. Flap coverage is an excellent option in injuries of the hand because of the ability to cover the wound while providing a smooth surface for joint and tendon motion and the potential for early mobilization with physical therapy. A variety of flaps have been described for coverage of hand wounds after burn injury (Table 1–1). Each technique has its unique advantages and disadvantages. Local flaps such as the homodigital flap have been successfully used to treat defects of the hand. The benefits of this technique include a one-stage procedure and the use of skin with similar thickness, appearance, and elasticity. The limitation of this flap is the limited area of skin for coverage and the ability to cover only very distal hand injuries. A more traditional technique is the use of a two-stage groin flap. This flap has the advantage of ample suitable skin for coverage, but the resultant immobilization of the involved hand makes this option less appealing in most patients. Recently, neurocutaneous ulnar nerve/artery flaps have been described. Aside from similar skin characteristics, these flaps have the reported advantage of preserved cutaneous sensation in the flap. Unfortunately, these flaps require a more involved dissection and there is limited experience with them. Another option is the distally based radial or ulnar forearm flap. These flaps can cover large defects, provide skin with characteristics similar to the recipient site, do not require staged procedures or immobilization, and do not require extensive dissection or, in many cases, vascular anastomoses. Another option is a free flap. Radial forearm free flaps from the opposite arm and temporoparietal free flaps with split-thickness skin graft (STSG) have both been described. The need for a vascular anastomosis and the risk of flap Table 1–1 Treatment Options for Fourth-Degree Hand Burns

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Type

Example

Local flap Distant flap Distally based fasciocutaneous flaps Neurocutaneous flaps

Homodigital flap, advancement flap Groin flap Radial or ulnar forearm flap Ulnar artery/nerve flap

THERMAL, CHEMICAL, AND ELECTRICAL BURNS

Figure 1–1. Right hand angiogram showing radial artery blood supply.

loss are the major disadvantages. The decision or method of reconstruction can be thought of as a “reconstructive ladder.” Each wound needs to be evaluated carefully and the decision for coverage is determined by many factors. The extent and site of the wound as well as associated injuries help to determine the method of coverage.

Surgical Management The patient was brought to the operating room where the edges of the wound were excised, leading to a defect measuring 5 cm by 7 cm. Intraoperative Doppler examination of the radial and ulnar vessels confirmed previous angiogram findings. Prior to operative intervention and after establishing adequate renal function, the patient underwent an angiogram of the right upper extremity. This study revealed that the radial artery was the dominant blood supply to the right hand. In addition, the palmar and dorsal arches were widely patent (Fig. 1–1). The arm was then exsanguinated and a tourniquet raised to 250 mm Hg. Dissection of the ulnar artery was initiated next to the flexor carpi ulnaris muscle near the wrist. The ulnar artery was then clamped, and the tourniquet released. Good blood flow into the hand was noted. An island of skin the same size as the defect was marked over the ulnar artery in the proximal forearm. The remaining length of the ulnar artery was then freed from the surrounding soft tissue, taking care to preserve the perforators to the skin island. The artery was transected in the proximal forearm, and adequate retrograde flow was observed in the stump of the ulnar artery, with excellent capillary refill in the skin. The ulnar-based fasciocutaneous flap was tunneled through the intact dorsal subcutaneous tissue of the wrist to cover the dorsal hand wound (Fig. 1–2). The flap was then secured into position in two layers. The donor site was partially closed by undermining the soft tissues medially and laterally to allow for tension-free approxUlnar artery

Ulnar nerve

FDS FCU

Figure 1–2. Ulnar artery flap for dorsal defect. 5

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Figure 1–3. Flap site at day 7 postoperative.

imation of the wound edges. Two areas proximally and distally were unable to be closed primarily and required a split-thickness skin graft (0.015-inch thick). Xeroform gauze was placed over the graft donor site and the STSG on the forearm. Doppler interrogation of the flap revealed good pulsatile blood flow. A volar splint was then placed to stabilize the hand and wrist. A site on the flap was marked for future arterial Doppler monitoring. The patient was placed on perioperative antibiotics and enteric-coated aspirin. He was discharged from the hospital 48 hours later after an uneventful postoperative course. The splint was kept in place for 7 days. Both flap and donor site healed well without complication (Figs. 1–3 and 1–4). Physical therapy was begun with both active and passive range of motion exercises 1 week postoperatively. The patient reported minimal functional impairment, but he did exhibit a 10-degree extensor lag of his fingers. He was able to make a fist and had normal wrist function.

Complications The complications associated with burns to the hand could be related to the extent of injury, the vehicle of injury, or the actual methods used to repair that injury. Skin and soft tissue contractures are common problems than can result from several factors including inadequate skin coverage, insufficient postoperative rehabilitation, or altered wound healing (e.g., hypertrophic scar formation). Boutonniere deformities can result from soft tissue contractures over the dorsal aspect of the digits. If addressed early enough, splinting may be sufficient to correct the problem, but often

Figure 1–4. Donor site at day 7 postoperative. 6

THERMAL, CHEMICAL, AND ELECTRICAL BURNS

arthrodesis is necessary. Web-space syndactyly is another related soft tissue complication that usually requires excision and grafting to correct. Nerve injury is often seen in cases of electrical burns. The ensuing fibrotic reaction may require neurolysis or even nerve grafting. Electrical burns represent a unique challenge for several reasons. For one, the extent of injury is often far greater than apparent on initial examination. Also, deeper structures are very frequently involved with accompanying subfascial edema. This should lower the threshold for fasciotomy, should evidence of compartment syndrome arise. Chemical burns are managed in the same manner as thermal burns. The key difference lies in what to do with the offending agent. In the vast majority of cases, copious water lavage is the most expeditious and least expensive way to remove harmful chemicals. Neutralization should be approached carefully, as it can sometimes lead to a second chemical reaction, which can further injure the tissues of the hand. Although no complications were noted in this particular case, distally based flaps are not without their disadvantages or potential complications. There can be a large donor site defect that may require a second procedure to repair and that can lead to a poor cosmetic result. In our case, complete closure of the donor site necessitated the use of an STSG. Postoperative venous congestion may require a second operation for a venous anastomosis to provide adequate flap drainage. Any distally based flap requires sacrificing one of the major vascular supplies to the hand that can lead to arterial insufficiency infused in the inappropriate patient (e.g., a patient with vasculitis or poor peripheral circulation). Finally, because a major vessel supplying the hand must be sacrificed, the remainder of the vascular supply must be well studied to ensure adequate postoperative blood flow. Hence, an unequivocal Allen’s test must be present or an angiogram may be required with the recognition that it is an invasive procedure and has its own accompanying set of potential complications.

Suggested Readings Barillo DJ, Harvey KD, Hobbs CL, Mozingo DW, Cioffi WG, Pruitt BA. Prospective outcome analysis of a protocol for the surgical and rehabilitative management of burns to the hands. Plast Reconstr Surg 1997;100:1442–1451. Belliappa PP, McCabe SJ. The burned hand. Hand Clin 1993;9:313–324. Bentivenga PE, Deane LM. Chemical burns of the upper extremity. Hand Clin 1990;6:253–259. Bertelli JA, Paglieli A. The neurocutaneous flap based on the dorsal branches of the ulnar artery and nerve: a new flap for extensive reconstruction of the hand. Plast Reconstr Surg 1998;101:1537–1543. Boeckx W, Vandevoort M, Blondeel PH, Van Raemdonck D, Vandekerckhove E. Fibrin glue in the treatment of dorsal hand burns. Burns 1992;18:395–400. Boswick IA. Management of the burned hand. Hand Clin 1990;6:297–303. Grobbelaar AO, Harrison DH. The distally based ulnar artery island flap in hand reconstruction. J Hand Surg [Br] 1997;22B:204–211. Hallock GG. Distal-based flaps for reconstruction of hand burns. J Burn Care Rehabil 1997;18:332–337. 7

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Hallock GG. Homodigital flaps-especially for treatment of the burned hand. J Burn Care Rehabil 1995;16:503–507. Harrison DH, Parkhouse N. Experience with upper extremity burns—the Mount Vernon experience. Hand Clin 1990;6:191–209. Jostkleigrewe F, Brandt KA, Flechsig G, Bruck JC, von Donnersmarck GH, Muhlbauer W. Treatment of partial thickness burns of the hand with the preshaped, semipermeable Procel burn cover: results of a multi centre study in the burn centres of Berlin, Duisburg and Munich. Burns 1995;21:297–300. Nuchtern JG, Engrav LH, Nakamura DY, Dutcher KA, Heimbach DM, Vedder NB. Treatment of fourth-degree hand burns. J Burn Care Rehabil 1995;16:36–42. Press B. Thermal electrical and chemical injuries. In: Aston SJ, Beasley RW, Thome CHM, eds. Plastic Surgery. Philadelphia: Lippincott-Raven; 1997:161–190. Puddicombe BE, Nardone MA. Rehabilitation of the burned hand. Hand Clin 1990;6:281–291. Salisbury RE, Dingeldein GP. The burned hand and upper extremity. In: Greene DP, ed. Operative Hand Surgery. New York: Churchill Livingstone; 1988. Sanford S, Gore D. Unna’s boot dressings facilitate outpatient skin grafting of hands. J Burn Care Rehabil 1996;17:323–326. Torres-Gray D, Johnson J, Mlakar J. Rehabilitation of the burned hand: questionnaire results. J Burn Care Rehabil 1996;17:161–168.

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INJURIES TO THE DERMIS: COLD INJURIES

2 Injuries to the Dermis: Cold Injuries Sokratis Varitimidis, Robert J. Goitz, and Dean G. Sotereanos

History and Clinical Presentation A 48-year-old, right hand dominant man was admitted to the emergency room 24 hours after a fall from a 20-foot height while hiking. The hikers who found the patient reported he had been exposed to temperatures below 0°C with only a light blanket.

Physical Examination

PEARLS • Rapid rewarming of the hand in a whirlpool at 40° to 44°C for 15 to 30 minutes • Protection of the skin with aloe vera or silver sulfadiazine is encouraged. Consider blister aspiration • Administration of a nonsteroidal antiinflammatory drug (NSAID) if not contraindicated by other medical problems. • Observe for ischemia and demarcation for up to 2 months before amputation is performed. • Triple-phase bone scan may help guide early salvage with debridement and flap coverage if young age or bilateral involvement.

PITFALLS • Slow rewarming may cause more tissue damage. • Early debridement of blisters should be avoided. • Amputation of the frostbitten part before a clear line of demarcation appears is strongly contraindicated, unless aggressive early salvage is considered.

On examination, the patient denied pain, but his left hand was discolored and mottled, and he had diminished sensation. He was unable to flex or extend the fingers of his left hand. His core body temperature was 34°C, and his vital signs were normal. His body was immediately rewarmed with warm oral and intravenous fluids. Tetanus prophylaxis was given and the affected hand was placed in circulating warm water (42°C) for 30 minutes. Within 24 hours, blisters were noted on his digits (Fig. 2–1) and he had significant pain. The hand continued to exhibit diminished sensation, and the digits appeared ischemic. The entire skin of the hand was covered with aloe vera ointment and dressed with a sterile soft dressing. An axillary block was performed to provide a sympathetic block to aid in pain control.

Diagnostic Studies Three days after admission, a bone scan was performed. It showed no activity in the fingers or distal palm. An arteriogram of the left upper extremity revealed no flow distal to the wrist (Fig. 2–2).

Figure 2–1. Blisters developed on the left hand 24 hours following rewarming. 9

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Figure 2–2. Arteriogram without flow distal to the palm.

Differential Diagnosis Acute frostbite Raynard’s disease Raynard’s syndrome Vascular disease Neurogenic disease

Acute Frostbite The diagnosis of acute frostbite injury can be made immediately by the patient’s history and examination. Acute thrombosis may be considered but is less likely when considering the history of extended cold exposure.

Diagnosis Frostbite of the Hand Frostbite may be defined as damage to tissue as a result of sustained exposure to low environmental temperatures. Ice crystals form in the extracellular space, resulting in an osmotic gradient, cellular dehydration, and electrolyte imbalance. In addition, direct injury to endothelial cells may result in thrombus formation. The combina10

INJURIES TO THE DERMIS: COLD INJURIES

tion of cellular dehydration, vasoconstriction, and thrombus formation may result in severe peripheral vascular collapse and ischemia. Rewarming may also result in further damage to tissues. As the crystals melt, the osmotic gradient reverses and the cells swell. If incomplete rewarming occurs, a cycle of alternating freezing and warming may cause even greater damage to tissues. In addition, metabolites of arachidonic acid have been shown to increase after frostbite injury and may also contribute to vasoconstriction. There are multiple factors influencing the severity of injury and the eventual outcome. The most important factors are the degree of cold penetrating the tissues and the duration of exposure. Additional factors that promote heat loss are immobility, hyperventilation, inadequate protective clothing, contact with moisture or bare metal, and the wind-chill effect. Host factors include alcohol, age, mental illness, compromised peripheral vasculature, and infection. Angiography has been used clinically to help determine the extent of vascular constriction and tissue ischemia from cold injuries. During the healing phase angiography can provide information on new collateral circulation to the affected region. Triple phase bone scanning has been found to correlate directly with the final extent of tissue damage and may be useful as early as 48 hours after the injury. Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) have also been used to assess vascular occlusion and degree of tissue ischemia with reasonable success.

Nonsurgical Treatment The management of frostbite is started immediately upon presentation. After stabilizing the patient’s general condition, emphasis is placed on regulating body temperature through air circulation, body warmers, and warm liquids administered both orally and parenterally. The affected area is rapidly rewarmed in circulating warm water (40° to 44°C) for 15- to 30-minute intervals. This process may be quite painful and usually requires administration of parenteral analgesics. Regional anesthesia may also be considered if severe pain is encountered. Multiple studies have confirmed the benefits of rapid rewarming versus slow rewarming (Table 2–1). Surface blisters appear within the first 24 to 48 hours after rewarming, and evidence suggests that blisters contain metabolites of arachidonic acid, which may potentiate Table 2–1 Management of Algorithm of Acute Cold Injury to the Hand 1. Stabilize the patient 2. Systemic rewarming with warm environment and warm fluid resuscitation 3. Rewarming of the extremity with circulating warm water (40° to 44°C) for 15- to 30-minute intervals 4. Tetanus prophylaxis 5. Analgesics and/or sedatives 6. Elevation of the affected extremity 7. Application of aloe vera on intact blisters and silver sulfadiazine cream on ruptured blisters; consideration of blister aspiration 8. Nonsteroidal antiinflammatory drug (NSAID) 9. Early immobilization followed by early range of motion exercises after 48 to 72 hours 10. Consideration of axillary block to provide sympathectomy and pain control 11. Antibiotics only if infection is present 11

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progressive dermal ischemia. Topical application of aloe vera to intact blisters is recommended because aloe is a topical thromboxane inhibitor and may combat its vasoconstricting effects. Aspiration of blisters is another way to lessen their ischemic effect. Ruptured blisters are treated with 1% sulfadiazine cream. Systemic antibiotics are used if infection is apparent. Tetanus prophylaxis is administered according to usual guidelines. Ibuprofen is also administered to inhibit the effects of arachidonic acid metabolites and has been shown to decrease the amount of tissue ischemia and subsequent necrosis. Functional splinting with custom-made orthoses may be helpful in patients who exhibit progressive contractures.

Surgical Treatment Absolute indications for early surgical intervention are for infection or escharotomy if viability is compromised secondary to the eschar. Midlateral incisions of a digit allow for decompression and may heal by secondary intention. Traditionally, surgical intervention for digital frostbite has paralleled treatment for ischemic digits. That is, allowing for clear demarcation of nonviable tissue prior to amputation maximizes retention of viable tissue and minimizes possible need for revision amputation or possible infection if necrotic tissue is retained. In the case presented, the patient was observed for 6 weeks, at which time it was determined that all five digits and half of the palm were necrotic and mummified; amputation of the hand at the level of demarcation was performed (Fig. 2–3). All

Figure 2–3. Amputation just proximal to the level of mummification. 12

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necrotic tissues (skin, tendons, and bone) were removed and the wound was closed primarily with healthy skin. More recently, attempts have been made to salvage ischemic digits secondary to frostbite injury. Greenwald et al have described an algorithm based on the triple-phase bone scan performed within the first 7 days postinjury. They recommended debridement of ischemic tissues that require high metabolic activity for the survival of tissue such as skin and subcutaneous tissue within the first 7 to 10 days, followed by early flap coverage of the remaining metabolically less active tissues such as bone, tendons, and nerves. They reported on two cases with reasonable results.

Suggested Readings Barker JR, Haws MJ, Brown RE, et al. Magnetic resonance imaging of severe frostbite injuries. Ann Plast Surg 1997;38:275–279. Baxter H, Entin MA. Experimental and clinical studies of reduced temperatures in injury and repair in man. Plast Reconstr Surg 1950;5:193. Gralino BJ, Porter JM, Rosch J. Angiographs in the diagnosis of frostbite. Radiology 1976;119:301–105. Greenwald D, Cooper B, Gottlieb L. An algorithm for early aggressive treatment of frostbite with limb salvage directed by triple-phase scanning. Plast Reconstr Surg 1998;102:1069–1074. Heggers JP, Robson MC, Manavalen K, et al. Experimental and clinical observations on frostbite. Ann Emerg Med 1987;16:1056–1062. Hosen JH, Fidler MD. Frostbite of the hand. In: Green DP, ed. Operative Hand Surgery. 3rd ed. New York: Churchill Livingstone; 1993:2061–2066. McCauley RL, Heggers JP, Robson MC. Frostbite: methods to minimize tissue loss. Postgrad Med 1990;88:67–68. Mehta RC, Wilson MA. Frostbite injury: prediction of tissue viability with triplephase bone scanning. Radiology 1989;170:511–514. Mills WJ Jr. Frostbite: a method of management including rapid thawing. Northwest Med 1966;65:119–125. Ozyazgan I, Tercan M, Melli M, et al. Eicosanoids and inflammatory cells in frostbitten tissue: prostacyclin, thromboxane, polymorphonuclear leukocytes, and mast cells. Plast Reconstr Surg 1998;101:1881–1885. Punja K, Grahm M, Cartotto R. Continuous infusion of epidural morphine in frostbite. J Burn Care Rehabil 1998;19:142–145. Robson MC, Heggers JP. Evaluation of hand frostbite blister fluid as a clue to pathogenesis. J Hand Surg 1981;6:43–46. Shumacker HB Jr, Lempke RE. Recent advances in frostbite. Surgery 1951;30: 873–904. Weatherley-White RCA, Knize DM, Geisterfer DJ, Paton BC. Experimental studies in cold injury: circulatory hemodynamics. Surgery 1969;66:208–214. 13

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3 High-Pressure Injection Injuries Kevin D. Plancher

History and Clinical Presentation A 28-year-old, right hand dominant man presented with an injury to the left hand. The patient was operating a high-pressure paint gun and tried to clear the nozzle with his free hand during operation of the equipment. The patient wiped the jet opening of the high-pressure gun with his left index finger when the gun discharged into his palm, producing a pressure of 5000 psi.

Physical Examination PEARLS • The time between the injection and treatment may determine the severity and treatment of the injury (less than 24 hours essential). • Tissues that survive the initial injection injury but still contain grease, paint, or oil heal slowly and may develop multiple oleogranulomas of varying sizes. • In time, the oleomas drain through sinuses or open directly through the skin • Wide open incision and debridement; do not try for cosmesis because of high risk for loss of digit or hand

PITFALLS • The appearance of the wound does not determine the severity of the injury. • Amputation is more likely if debridement is delayed more than 10 hours, especially with low viscosity substances. • Without diagnosis and treatment, a compartment syndrome with subsequent necrosis usually destroys tissue viability. • Do not use small openings for debridement. 14

The paint stream struck the palm with such pressure that the liquid penetrated the skin and spread widely throughout the underlying fascial planes and tendon sheaths. To assess the severity of the injury, the type of injected material and the time of the injection were determined. Circulation surrounding the injury was assessed by observing the general skin color and temperature and capillary refill. To confirm dual circulation to hands and fingers, the Allen’s test was performed (Fig. 3–1). Anterior forearm compartment was evaluated by passive wrist and finger extension. Distention of the tissue and the resulting inflammatory reaction caused

Figure 3–1. (A–D) Demonstration of digital Allen’s test to confirm circulation of fingers.

HIGH-PRESSURE INJECTION INJURIES

marked ischemia of the tissue. Treatment was not delayed to avoid tissue necrosis, fever, and leukocytosis.

Diagnostic Studies Standard preoperative laboratories are performed. Radiographs can be used to determine any associated fractures. Preoperative roentgenograms can assist in determining the surgical strategy by identifying subcutaneous air, debris, or unanticipated fractures.

Differential Diagnosis Bites Puncture wounds

Diagnosis High-Pressure Injection Injury to the Palm The index finger is the most frequently injured digit, followed by the palm and long finger (Fig. 3–2). If the patient delays treatment, the digit may appear erythematous or cold, edema and intense pain may develop, and loss of digit is ensured. Injuries to the digits are often associated with more morbidity than those to the hand because of potential for development of compartmental syndrome. The severity of the injury is first diagnosed by the type of fluid. Injection injuries with grease guns result in ischemia and chemical irritation, but inflammation is less severe than with paint injuries. The highest risk of early tissue necrosis and gangrene are seen with injuries involving paint, paint solvent, and paint thinner. Other fluids such as grease, oil, and other mechanical fluids may cause no reaction during the first 48 hours following the injection. However, fibro-

Figure 3–2. Paint gun injury to the palm in another patient. Note the swelling and edema. 15

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Figure 3–3. Debridement may include opening of fingers along nonpinch, nonprotective border surfaces.

sis, oligogranuloma formation, and draining sinuses may occur. The amount of fluid injected determines the degree of vascular compression. Large volumes of fluids are associated with increased vascular compression. If the fluid was at high pressure, the result is an extension of the fluid penetration, and this may result in a larger area of spread of the injected material. Timely diagnosis and treatment are the most important factors, as the risk of amputation increases as the time from injury to treatment increases.

Nonsurgical Management Initial nonsurgical treatment of injection injuries may include prophylactic, broadspectrum antibiotics. The patient should also have a tetanus update and be provided with analgesics. The injury must be splinted and elevated. The patient should then be referred immediately as an emergency to a hand specialist for surgical intervention. As symptoms increase, surgical consultation should not be delayed, as this may lead to tissue necrosis. Depending on the severity of compression, injections of clean air or water can be managed conservatively, with caution.

Surgical Management Most high-pressure injection injuries require emergency surgical debridement because of extreme tissue toxicity. Prompt surgical debridement optimizes tissue salvage. Debridement may include opening of fingers along nonpinch, nonprotective border surfaces (Fig. 3–3). The distended tissues are opened through large incisions. A longitudinal incision (Fig. 3–4B) can be made over the injection site to ensure a

Figure 3–4. The distended tissues are opened through large incisions. (A) Transverse incision. (B) Longitudinal incision. (C) Combined longitudinal and transverse incisions. (D) Third lumbrical canal. 16

HIGH-PRESSURE INJECTION INJURIES

Figure 3–5. Incisions to drain infection of the thenar spaces. (A) Dorsal longitudinal incision. (B) Dorsal transverse incision. (C) Volar thenar crease incision. (D) Volar transverse incision.

wide opening. Alternative approaches are utilized when necessary (Fig. 3–4A,C,D). A dorsal thumb web-space incision can be used to debride the thenar space (Fig. 3–5C,D), and an alternative volar approach can be utilized (Fig. 3–5A,B). The midpalmar space is opened with a midpalmar incision, which may be extended proximally to include the carpal tunnel. With paint injuries, all paint must be immediately removed form the wound, tissue, and digital arteries. In most cases, wounds are left open for serial debridement. Early amputation may be considered with severe paint injection injuries. Antibiotics are given postoperatively, and the hand is immobilized and elevated. Amputation rates for injection injuries range from 15% to 50%.

Postoperative Care Most patients return to the operating room and undergo open packing. Patients may use whirlpool therapy. Supportive wound care should be provided by a certified occupational hand therapist.

Complications The most common complication is amputation due to tissue necrosis. Infection is also a common complication, as is compartment syndrome (Fig. 3–6). Complications may vary depending on the type of liquid injected and the time from injury to treatment.

Figure 3–6. Incisions for decompression of compartment syndromes in the hand, dorsal incisions. 17

E N V I R O N M E N TA L I N J U R I E S T O T H E D E R M I S

Suggested Readings Christodoulou L, Melikyan EY, Woodbridge S, Burke FD. Functional outcome of high-pressure injection injuries of the hand. J Trauma 2001;50:717–720. Couzens G, Burke FD. Veterinary high pressure injection injuries with inoculations for larger animals. J Hand Surg [Br] 1995;20B:497–499. Curka PA, Chisholm CD. High-pressure water injection injury to the hand. Am J Emerg Med 1989;7:165–167. Fialkov JA, Freiberg A. High pressure injection injuries. J Emerg Med 1991;9:367–371. Flotre M. High-pressure injection injuries of the hand. Am Fam Physician 1992;45: 2230–2234. Lewis HG, Clarke P, Kneafsey B, et al. A 10-year review of high-pressure injection injuries to the hand. J Hand Surg [Br] 1998;23B:479–481. Mrvos R, Dean BS, Krenzelok EP. High pressure injection injuries: a serious occupation hazard. J Toxicol Clin Toxicol 1987;25:297–304. Pinto MR, Turkula-Pinto LD. High-pressure injection injuries of the hand: a review of 25 patients managed by open wound technique. J Hand Surg [Am] 1993;18A: 125–130. Schnall SB, Mirzayan R. High-pressure injection injuries to the hand. Hand Clin 1999;15:245–248,viii. Schoo MJ, Scott FA, Boswick JA Jr. High-pressure injection injuries of the hand. J Trauma 1980;20:229–238. Sirio CA, Smith JS Jr, Graham WP 3d. High-pressure injection injuries of the hand: a review. Am Surg 1989;55:714–718. Vasilevski D, Noorbergen M, Depierreux M, Lafontaine M. High-pressure injection injuries to the hand. Am J Emerg Med 2000;18:820–824.

18

Section II

Infections

Felons Sam Moghtaderi and Kevin D. Plancher

Paronychia Sam Moghtaderi and Kevin D. Plancher

Pyogenic Arthritis Kevin D. Plancher

Web-Space Infections Kevin D. Plancher

Supporative Flexor Tenosynovitis John C. P. Floyd and Waldo E. Floyd III

Herpetic Whitlow Kevin D. Plancher

Bites to the Hand Kevin D. Plancher

Mycobacterial Tenosynovitis John C. P. Floyd and Waldo E. Floyd III

FELONS

4 Felons Sam Moghtaderi and Kevin D. Plancher

History and Clinical Presentation A 15-year-old, left-hand dominant boy with insulin-dependent diabetes mellitus who monitors his blood glucose via multiple daily finger sticks presented to his physician complaining of extreme throbbing pain of his right middle fingertip for the past 24 hours.

Physical Examination Examination of the affected finger demonstrated the volar aspect of the tip to be swollen, hard, and erythematous. The distal phalanx was extremely tender and somewhat fluctuant, but there was no pain in the distal interphalangeal joint or the more proximal regions of the finger. The dorsum of the phalanx, including the nail and periungual areas, appeared normal.

Diagnostic Studies PEARLS • Often history of skin-penetrating injury • “Throbbing pain” keeps patient from sleeping • Conservative therapy effective for cellulitis—before the onset of pain • Gram-negative coverage is essential in empiric antibiotic treatment of diabetics and immunocompromised patients • Immobilization for first 48 hours, then active ROM exercises at dressing changes

PITFALLS • Best routine incision is controversial • In subcutaneous dissection, must avoid approaching the flexor tendon sheath • Multitude of complications for neglected felon

Anteroposterior and lateral plain film radiographs of the finger were obtained and demonstrated no abnormal findings.

Differential Diagnosis Cellulitis Flexor tenosynovitis Herpetic whitlow Metastatic tumor

Diagnosis Felon of the Right Middle Finger A felon is a bacterial infection of the distal pulp space of the fingers or thumb. As first described by Kanavel, the anatomy of the distal phalanx is unique, with the volar pulp space a confined sac, and fine fibrous septa connecting the subcutaneous layer to the bone (Fig. 4–1). An abscess in this region can lead to tensioning of the fibrous strands, increased pressure within the pulp space, and essentially a compartment syndrome with neurovascular compromise. In this way, a felon is distinguished from a simple superficial cellulitis, which may precede it. The patient with a felon presents with a swollen, hard, fluctuant, and erythematous fingertip, typically complaining of a throbbing pain so severe that it has kept him from sleeping. There is usually a history of some penetrating trauma to the fingertip, which served as the inoculating event (splinter, broken glass, etc.), although it may have 21

INFECTIONS

Figure 4–1. Schematic anatomic drawing of digital pulp sac.

been rather inconsequential and forgotten by the patient. It is also possible that the organisms entered in retrograde fashion via the eccrine or sebaceous glands in the finger pad. Although diabetics and immunocompromised patients are generally at higher risk for hand infections, those who require routine blood monitoring via finger sticks have an additional risk for inoculating so-called finger stick felons. Skin flora comprises the organisms commonly seen in felons, and most often it is Staphylococcus aureus or other gram-positive organisms. A suppurative flexor tenosynovitis can be clinically distinguished as it typically involves most of the digit, and certainly more proximal areas than just the distal phalanx. Flexor tenosynovitis has a characteristic pain elicited by passive motion of the interphalangeal joints. Although quite rare, there have been several reported cases of metastases of various tumors to the distal fingers, which at first presentation were misdiagnosed as felons. A felon does not display any radiographic changes, though radiographs are nonetheless recommended to rule out bony pathology such as tumor or osteomyelitis (the latter being a possible late sequela of an untreated felon). It is important to distinguish herpes infections of the fingertip from bacterial felons. Herpetic whitlow is a self-limited viral infection caused by the herpes simplex virus. It is transmitted by skin-to-skin contact, and is often seen in medical and dental personnel, as well as in children. The course of the presentation of a herpes lesion is much longer than that of a felon, which is typically quite acute. Herpetic whitlow may present with swelling and erythema, but typically displays fluid-filled vesicles as well. The diagnosis is usually made clinically, although it is possible to confirm it by use of a Tzanck prep or viral culture. It is important to distinguish herpetic whitlow from bacterial infections, as a surgical incision for the former can lead to complications involving the entire digit or systemic spread, and is contraindicated.

Nonsurgical Management Infection of the pad of the finger can be managed nonoperatively if the superficial cellulitis, as is typically the case during the first 48 hours, has not spread. In such instances, elevation, warm soaks, and a course of oral antibiotics (typically dicloxacillin or a first-generation cephalosporin to cover gram-positives and skin flora) suffice. In the case of a diabetic or immunocompromised patient, however, additional gram-negative coverage is essential. 22

FELONS

Surgical incision is indicated as soon as the patient’s pain and physical exam indicate increased pressures in the pulp space, despite the absence of fluctuant abscess.

Surgical Management A felon requires surgical drainage both to clear the infection and to relieve the intracompartmental pressure and prevent neurovascular compromise. All of the procedures outlined here are typically done using local anesthesia and under tourniquet control. There is little disagreement over when surgical management is indicated. There is, however, controversy over the most appropriate surgical approach for routine incision and drainage of felons. The goal, similar in all techniques, is to adequately drain the abscess while minimizing damage to neurovascular structures and scar formation in critical areas. Most surgeons use a unilateral longitudinal approach, where an incision is made on the unopposing lateral side of the digit (ulnar for the fingers and radial for the thumb), beginning just dorsal to and 5 mm distal to the distal interphalangeal (DIP) joint flexion crease and continuing lateral to the nail edge to a point just distal to the unattached portion of the nail (Fig. 4–2). The incision is deepened by blunt dissection with a hemostat or similar instrument, until the abscess is adequately opened for draining. Extreme care must be taken so as not to dissect in a proximal direction, to reduce the likelihood of piercing the flexor tendon sheath and causing an iatrogenic tenosynovitis. An alternative approach, suggested by Kilgore for routine drainage of all felons, is the longitudinal volar incision. He contends that scar formation is minimal, and that there is actually more likelihood of neurovascular damage when the lateral approach is used. Most authors, however, prefer the lateral approach, citing concerns about scar formation over the most important tactile region of the fingertip. Volar incisions are typically used only when the abscess is smaller and localizable to the volar pad, or when a sinus tract already exists. The longitudinal volar incision is made in the midline extending from the tip of the pad to within several millimeters of the DIP joint flexion crease proximally. It is important not to cross the flexion crease, as a subsequent scar will then lead to a flexion contracture. Alternatively, the volar incision can be made transversely over the point where the abscess is best localized. In either case, once the skin incision is made, blunt subcutaneous dissection is performed as above, taking care not to dissect too far proximally to endanger the tendon sheath.

Figure 4–2. Incisions of the distal phalanx. (A) Volar longitudinal incision. (B) Volar oblique incision. (C) Axial incision. (D) Axial incision extending to the tip. 23

INFECTIONS

When the abscess is entered, intraoperative cultures should be obtained for definitive identification and susceptibility testing of the involved organisms. After adequate drainage is achieved, the wound is irrigated and packed with sterile gauze or nonadherent dressing. The digit is splinted and elevated for the first 48 hours. Subsequently daily warm soaks are applied and active range-of-motion exercises are performed at dressing changes. A 10- to 14-day course of empiric antibiotic treatment is typically begun postoperatively. However, the regimen should be changed to a more focused coverage once culture results are obtained.

Complications A delay in proper treatment of a felon can have severe complications. These include formation of a sinus tract in addition to spread of the infection in either direction, leading to osteomyelitis, flexor tenosynovitis, septic arthritis of the DIP joint, as well as paronychia on the dorsum of the finger. Proper recognition of a felon is essential, as the complications of an untreated felon can be severe enough to lead to amputation of the digit.

Suggested Readings Abrams RA, Botte MJ. Hand Infections: treatment recommendations for specific types. J Am Acad Orthop Surg 1996;4:219–230. Jebson PJL. Infections of the fingertip. Hand Clin 1998;14:547–555. Jebson PJL, Watson PA. The natural history of the neglected felon. Iowa Orthop J 1996;16:164–166. Kanavel AB. Infections of the Hand. 7th ed. New York: Lea & Febiger; 1939. Kilgore ES Jr. Treatment of felons. Am J Surg 1975;130:194–198. Louis DS, Jebson PJL. Mimickers of hand infections. Hand Clin 1998;14:519–530. Mann RJ. Infections of the Hand. New York: Lea & Febiger, 1988. Neviaser RJ. Infections. In: Green DP, ed. Operative Hand Surgery. 3rd ed. New York: Churchill Livingstone; 1993. Polayers IM, Arons MS. The treatment of herpetic whitlow: a new surgical concept Plast Reconstr Surg 1980;65:811–817. Rose BA, Wood FM. Metastatic bronchogenic carcinoma masquerading as a felon. J Hand Surg 1983;8:325–328.

24

PA R O N Y C H I A

5 Paronychia Sam Moghtaderi and Kevin D. Plancher

History and Clinical Presentation A 34-year-old, right hand dominant woman presented to her physician complaining of a red, tender area surrounding the nail of the third finger of her right hand. She had received a manicure 3 days prior to the onset of symptoms.

Physical Examination The periungual areas of the affected digit appeared erythematous and swollen, and were tender to palpation over the radial paronychial fold and the eponychium (Fig. 5–1). There was also elevation of the proximal nail bed with pus extruding from below.

Diagnostic Studies The diagnosis of paronychia is generally clinical, and does not require any diagnostic studies. PITFALLS • Must differentiate from herpetic infections, for which incision and drainage (I&D) is typically contraindicated • In making incisions, care must be taken to avoid damage to nail matrix • Nonsurgical treatments typically not effective for chronic paronychia

PEARLS • Paronychia is the most commonly seen infection of the hand • Warm soaks and antibiotics effective if there is no drainage or fluctuance • Eponychial marsupialization for chronic paronychia; also remove nail if signs of involvement

Differential Diagnosis Herpetic whitlow Acute paronychia Chronic paronychia

Diagnosis This patient’s presentation is typical of acute paronychia, an infection of the soft tissue folds surrounding the fingernail. The clinical presentation initially consists of localized tenderness of the paronychial region, with subsequent erythema,

Figure 5–1. Schematic anatomic drawing of nail complex and its components.

25

INFECTIONS

Figure 5–2. Acute paronychia, with characteristic erythema and swelling.

swelling, and fluctuance (Fig. 5–2). Frank drainage and elevation of the nail plate are also seen. Acute paronychia are often seen in nail biters, as well as after manicures or ingrown nails. The etiology of such infection is a break in the soft tissue seal on the dorsal periphery of the nail, allowing entry, colonization, and abscess formation by the offending organism. The infection begins in the lateral (paronychial) nail fold, and may spread to include the proximal nail fold (eponychium). In severe cases, the lesion may reach the contralateral paronychia, and is termed a runaround or horseshoe infection. Since a paronychia is essentially an infected abscess, definitive treatment typically requires surgical drainage. Typically, Staphylococcus aureus is the involved organism. Chronic paronychia are persistent, indurated infections of the eponychium, and present somewhat differently from acute paronychia. It is typically seen in people whose hands are chronically exposed to water with detergents and alkali, such as cleaning workers, bartenders, and kitchen staff. The etiology is thought to include an initial bacterial infection, typically followed by superinfection and colonization of the eponychium with a fungus such as Candida albicans. There is subsequent episodic inflammation and drainage, as well as a fibrosis and thickening of the eponychium secondary to the chronic low-grade inflammatory response. The patient presents with less severe erythema and fluctuance than acute paronychia, and typically does not report as much localized tenderness. A typical sign of chronic paronychia is the appearance of longitudinal grooves on the dorsal surface of the nail plate, secondary to the long-term damage to the germinal tissues in the eponychium. Both acute and chronic paronychia have been noted with an increased incidence in diabetics, immunocompromised patients, and those receiving anti-retroviral therapy. The most important entity to distinguish from paronychia in the differential diagnosis is herpetic whitlow, a self-limited viral infection of the fingertips caused by 26

PA R O N Y C H I A

the herpes simplex virus. It is transmitted by skin-to-skin contact, and is often seen in medical and dental personnel, as well as in children. As with paronychia, herpetic whitlow may also present with swelling and erythema, though typically patients have disproportionately greater pain than in the case of bacterial infections. Vesicles are also seen, containing fluid that may be clear or turbid, but is never purulent. The diagnosis is usually made clinically, though it is possible to confirm it by use of a Tzanck prep or viral culture. It is important to distinguish herpetic whitlow from bacterial infections, as a surgical incision for the former can lead to complications involving the entire digit or systemic spread, and is contraindicated.

Nonsurgical Management Nonsurgical treatment of an acute paronychia should be attempted only in the earliest stage, where the infection has not progressed to more than a mild localized erythema and swelling. In such cases, a regimen consisting of an oral antibiotic with Staphylococcus coverage (e.g., dicloxacillin 250 to 500 mg po q6h), along with warm saline soaks and rest, may be adequate. Typically, however, by the time the patient presents to a physician, there is already abscess formation and fluctuance requiring drainage. Conservative treatment of chronic paronychia by use of topical or systemic antibiotic and antifungal agents has almost universally been unsuccessful. It is thought that the process of fibrosis and chronic injury in the eponychium leads to a diminished vascular supply and decreased delivery of such drugs. As previously stated, herpetic whitlow should generally be treated conservatively and typically runs a self-limited course of ~21 days. A notable exception is when bacterial superinfection is seen along with an abscess. In such cases the abscess may be carefully drained, with systemic acyclovir administered to reduce the likelihood of complications.

Surgical Management The goal of surgical intervention for a paronychia is to allow a thorough drainage of the purulent collection. At the same time, however, it is imperative that invasion of the nail bed be kept to a minimum to avoid future growth deformities. All of the procedures described may typically be performed under a digital block anesthesia. In cases where there is only involvement of one of the lateral nail folds, a true skin incision is not necessary. A No. 11 or No. 15 blade is used to completely lift the paronychium from the nail plate, opening the abscess in the nail fold and allowing drainage. Care must be taken to direct the sharp edge of the scalpel toward the paronychial fold and away from the nail bed, to avoid an injury to the nail matrix that may result in scarring or growth deformities. If there is any involvement of the nail bed, it is best also to remove the affected side of the nail plate, using a Freer elevator to gently separate the lateral third of the nail from the nail bed, and then using a small pair of scissors to make a longitudinal cut and remove the nail plate. When there is involvement of the eponychium and proximal nail in addition to the lateral fold, a single incision is made beginning at the midpoint of the paronychial fold and proceeding proximally through the eponychium to reach 27

INFECTIONS

Figure 5–3. Single-incision technique for irrigation and debridement of acute paronychia.

the base of the nail. The soft tissues are elevated, and the proximal third of the nail is bluntly separated and excised with scissors (Fig. 5–3). In severe cases where a runaround or horseshoe infection involves both sides of the finger, a similar incision is made on the opposite side as well, and the entire eponychium is elevated. Chronic paronychia are treated somewhat differently. Keyser and Eaton describe a technique of eponychial marsupialization that has been highly effective at clearing the persistent infection. A crescent of tissue ~1 mm proximal to the eponychial fold and 5 mm in width at its largest point is removed along with its subcutaneous tissue, taking care to not penetrate so deep as to encroach on the germinal nail matrix (Fig. 5–4). Bendar and Lane subsequently reported success by removing only the superficial soft tissue, and excising the nail plate in cases where it was involved. We agree that the latter approach provides adequate treatment while minimizing unnecessary trauma to the nail bed. In all of the above cases, the wound is thoroughly irrigated and packed with plain gauze or a nonadherent dressing. An oral antibiotic regimen is begun, and the dressing is kept on for 48 to 72 hours, at which point warm saline soaks are regularly performed until the irritation subsides.

Figure 5–4. Eponychial marsupialization for treatment of chronic paronychia.

28

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Suggested Readings Abrams RA, Botte MJ. Hand infections: treatment recommendations for specific types. J Am Acad Orthop Surg 1996;4:219–230. Bendar MS, Lane LB. Eponychial marsupialization and nail removal for surgical treatment of chronic paronychia. J Hand Surg 1991;16A:314–317. Hurst LC, Gluck R. Herpetic whitlow with bacterial abscess. J Hand Surg 1991; 16A:311–314. Jebson PJL. Infections of the fingertip. Hand Clin 1998;14:547–555. Keyser JJ, Eaton EG. Surgical cure of chronic paronychia by eponychial marsupialization. Plast Reconstr Surg 1976;58:66–70. Louis DS, Jebson PJL. Mimickers of hand infections. Hand Clin 1998;14:519–530. Neviaser RJ. Infections. In: Green DP, ed. Operative Hand Surgery. 3rd ed. New York: Churchill Livingstone; 1993:1033–1036. Polayers IM, Arons MS. The treatment of herpetic whitlow—a new surgical concept. Plast Reconstr Surg 1980;65:811–817. Russo F, Collantes C, Guerrero J. Severe paronychia due to zidovudine-induced neutropenia in a neonate. J Am Acad Dermatol 1999;40:322–324. Tosti A, Piraccini BM, D’Antuono A, Marzaduri S, Bettoli V. Paronychia associated with antiretroviral therapy. Br J Dermatol 1999;140:1165–1168.

29

INFECTIONS

6 Pyogenic Arthritis Kevin D. Plancher

History and Clinical Presentation A 35-year-old, right hand dominant woman presented with a swollen right index finger. She reported previously having a large piece of wood that entered her finger near the metacarpophalangeal (MP) joint, but stated that she had removed the wood. A puncture wound was present over the joint and she has had progressive tenderness of the finger and increased pain with activity. Her wound has now dramatically changed after spending the weekend working in the garden.

Physical Examination Examination reveals a warm finger with a joint effusion and surrounding soft tissue edema at the proximal interphalangeal (PF) joint of the index finger. Active and passive joint range of motion is painful. The painful joint with no evidence of cellulitis was aspirated through skin that was sterilized. The fluid obtained was turbid.

Differential Diagnosis PEARLS • Diagnosis can be confirmed on aspiration. • Early intervention avoids cartilage damage in a joint. • Always send aspiration to the lab for cell count.

PITFALLS • Assume that joint swelling will resolve with elevation and conservative treatment (antibiotics) • Avoid a small incision under local anesthesia rather than wide debridement and irrigation in an operating room under regional anesthesia. • Never assume the type of infection until the labs and culture and sensitivities dictate the correct antibiotic treatment.

30

Gout Psoriatic arthritis flare Systemic lupus erythematosus

Diagnostic Studies Synovial fluid analysis includes Gram stain, cultures, and sensitivity testing. In septic arthritis, the joint fluid contains a white blood cell count over 50,000/mm3. The polymorphonuclear count should be over 75% and the synovial fluid glucose is 40 mg or lower. Radiographs are taken to rule out an occult fracture and to assess the joint space for loose or foreign bodies. When treatment is been delayed, radiographs can be useful to determine the extent of articular cartilage destruction and bone loss.

Diagnosis Pyogenic Arthritis Index Finger Based on the clinical exam and the laboratory values of the synovial fluid, Gram stains, and cultures, the diagnosis of pyogenic arthritis was ruled in as the diagnosis. The most common organism isolated from septic hand joints is Staphylococcus aureus. Contamination of the joint can occur by several mechanisms including

PYOGENIC ARTHRITIS

hematogenous or contiguous spread and postoperative infectious. Direct implantation of organisms can also occur from a hand injury during a brawl, or penetration from a nail, knife, etc. High suspicion for joint infection is important when the MP joints are involved. This is the case because these joints are the major target sites for lacerations secondary to coming in contact with human teeth during fistfights.

Nonsurgical Treatment Because septic arthritis can cause articular cartilage destruction and osteomyelitis, aggressive surgical treatment is recommended. Nonsurgical treatment is not recommended for any open joint laceration that is suspected to have occurred from a bite or contact with a contaminated object.

Surgical Treatment Once the diagnosis has been made (Fig. 6–1), the patient should be started on appropriate antibiotic (Table 6–1) and proceed with aggressive treatment of incision and drainage of the joint. This aggressive treatment is important to minimize the cartilage destruction and osteomyelitis.

Figure 6–1. Swollen proximal interphalangeal (PIP) joint with pyogenic arthritis preoperative in another patient.

31

INFECTIONS

Table 6–1 Antibiotic Choice Specific to Organism Treatment Organism

Preferred Drug

Dosage

Staphylococcus aureus

Cefazolin Vancomycin (MCRS) Penicillin G Ceftriaxone Ticarcillin Ticarcillin Ampicillin-sulbactam (Unasyn) Ampicillin-sulbactam (Unasyn) Ceftriaxone Ethambutol Biaxin

1 g IV q8h 500 mg IV q6h 2– 4 million units IV q4h 1 g IV q12h 3 g IV q6h 3 g IV q6h 3 g IV q6h

Streptococcus spp. Haemophilus influenzae Pseudomonas aeruginosa Serratia spp. Pasteurella multocida Eikenella corrodens Neisseria gonorrhoeae Mycobacterium marinum

3 g IV q6h 1 g IV q12h 2500 mg po q day ⫻ 6 months 500 mg po bid ⫻ 6 months

The procedure to drain the proximal interphalangeal (PIP) joint is to make a midaxial incision on either side of the joint that will allow adequate drainage (Fig. 6–2). Care should be taken to avoid injury to the neurovascular bundles. In the fingers, section the transverse retinacular ligament. The extensor lateral band is retracted dorsally, and the neurovascular bundle is retracted toward the palm. Once the collateral ligament is identified, a longitudinal incision is made parallel and palmar to the ligament, separating the accessory collateral ligament. A portion of the collateral ligament is removed and the joint is drained. The specimens are sent to the lab for aerobic and anaerobic cultures. The joint space must be copiously irrigated, and the fibrinous and synovial debris is debrided. The wound can be packed to allow for continuous bedside irrigation, or, if joint debridement has been adequate, the wound can be loosely closed. A bulky dressing is applied with a splint. If the joint or bone has been destroyed, removal may be required. Antibioticimpregnated spheres can be useful in reconstruction of the joint with arthrodesis or bone grafting once the infection has been eliminated. In severe cases, amputation may be required.

Figure 6–2. Procedure to drain the PIP joint is to make a midaxial incision on either side of the joint that will allow adequate drainage.

32

PYOGENIC ARTHRITIS

Figure 6–3. Alternative surgical approach to the PIP joint for exposure and joint debridement. Dorsal midline approach.

Alternative Treatment An alternative surgical approach is the dorsal midline approach (Fig. 6–3).

Postoperative Management It is important to keep the hand elevated for 24 hours following initial irrigation and allow the hand to rest so that the soft tissues do not swell. The bandage must be changed and checked for adequate drainage of the wound, or, rather, ensure that no fluid is collecting in the joint. As the wound calms down and dries up, the patient starts range-of-motion exercises. Wound checks should be continued. The appropriate antibiotics should be prescribed, and the patient must complete the full course of the treatment.

Complications Narrowing of the MP and PIP joints after apyogenic infection is treated (Fig. 6–4). 33

INFECTIONS

Figure 6–4. Radiograph demonstrating the narrowing of the metacarpophalangeal (MP) joint of the ring finger. This is three years after a previously septic joint. Anteroposterior (AP) view.

Suggested Readings Boustred AM, Singer M, Hudson DA, Bolitho GE. Septic arthritis of the metacarpophalangeal and interphalangeal joints of the hand. Ann Plast Surg 1999;42: 623–628. de Vries H, van der Werken C. Septic arthritis of the hand. Injury 1993;24: 32–34. Harris PA, Nanchahal J. Closed continuous irrigation in the treatment of hand infections. J Hand Surg 1999;24B: 328–333. Harth M, Ralph ED, Faraawi R. Septic arthritis due to Mycobacterium marinum. J Rheumatol 1994;21:957–960. Hausman MR, Lisser SP. Hand infections. Orthop Clin North Am 1992;23:171– 185. Marinella MA. Group G streptococcal septic arthritis of an interphalangeal joint. Clin Exp Rheumatol 1996;14:577–578. Murray PM. Septic arthritis of the hand and wrist. Hand Clin 1998;14:579–587. 34

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Nemoto K, Yanagida M, Nemoto T. Closed continuous irrigation as a treatment for infection in the hand. J Hand Surg 1993;18B:783–789. Rothe M, Rudy T, Stankovic P. Treatment of bites to the hand and wrist-is the primary antibiotic prophylaxis necessary. Handshir Mikrochir Plast Chir 2002;34: 22–29. Tonta K, Kimble FW. Human bites of the hand: the Tasmanian experience. Aust N Z J Surg 2001;71:467–471.

35

INFECTIONS

7 Web-Space Infections Kevin D. Plancher

History and Clinical Presentation A 32-year-old right hand dominant woman complains of increased pain in her right hand with swelling and redness, and is worried because her fingers are spreading apart. She said she stabbed herself with a pencil last week and does not remember a lot of pain or bleeding at the time of the injury. She does remember seeing a puncture wound on her hand that turned into a small blister and then a callus. She did not seek any medical help at that time and is now concerned because of the pain and appearance of her hand. She does not have diabetes and is not allergic to any medications.

Physical Examination The patient is comfortable moving her hand but has pain when removing her hand from her jacket sleeve. She has obvious swelling of her second web space and distal to her distal palmar crease. The swelling is more pronounced on the palmar aspect but is still seen dorsally in the second web space. She has some abduction of her index finger at rest and is able to flex and extend her fingers actively but reports generalized pain in her palm. She has fluctuance and tenderness of the web space and cellulitis of the distal hand and forearm (Fig. 7–1). Her hand and all digits have no signs of vascular compromise.

A

B

Figure 7–1. (A) Hand with edema over second dorsal web space held in position of minimal pain. (B) Hand with extensive swelling happens often after neglect from what was thought to be a simple injury. 36

W E B - S PA C E I N F E C T I O N S

PEARLS • Two incisions used to clear infections • Recurrence can be avoided with early diagnosis when cellulitis is present. Rule out flexor tenosynovitis • Collar button abscess should always be suspected if there is tissue reaction out of all proportion to the size of the superficial component of the abscess.

PITFALLS • Lack of recognition of collar button access • Inadequate drainage and dissection • Avoid local anesthetic block to ensure deep debridement. • Flaps to open wounds should not be shallow to avoid flap necrosis.

Figure 7–2. Classic pain on extension of a digit with fusiform swelling and tenderness in patients with flexor tenosynovitis.

Kanavel’s sign was used to distinguish a deep infectious tenosynovitis from a superficial cellulitis although pain with finger extension was present in this patient (Fig. 7–2).

Diagnostic Studies Posteroanterior and lateral radiographs of the hand do not identify any foreign objects and no bone or soft tissue abnormalities.

Differential Diagnosis Pyoderma gangrenosum Gout Volar web-space infection

Diagnosis Second interdigital web-space infection resulting in a collar-button abscess. A web-space abscess may develop from an infected callus on the volar side of the distal palm. The abscess may spread to the dorsal aspect of the space, resulting in a “collar button” abscess (Fig. 7–3).

Figure 7–3. Collar button abscess. Note infection extends from volar to dorsal area. This can result from a simple injury such as a stabbing from an indelible pen. 37

INFECTIONS

Table 7–1 Antibiotic Treatments Infectious Organism

Antibiotic of Choice

Pasteurella Eikenella Escherichia coli Enterobacter Pseudomonas Serratia

Ampicillin, penicillin Ampicillin, penicillin First- or second-generation cephalosporin Aminoglycoside, cephalosporin Aminoglycoside, cephalosporin Aminoglycoside, cephalosporin

Nonsurgical Treatment For superficial cellulitis, IV antibiotics are used. If infectious tenosynovitis is diagnosed within 24 to 48 hours of onset of symptoms, it may be treated with antibiotics, splinting, and hand elevation. Operative treatment is usually required. Antibiotic treatments are described in Table 7–1. The digits can keep a flexed posture because of involvement of the tendon sheath from time to time.

Surgical Treatment Treatment for a collar button abscess involves prompt surgical drainage. When an hourglass abscess is present, it requires both volar and dorsal incisions. We also make sure that no incision is placed transversely across the web space because of subsequent scar contraction and resulting full-finger abduction. Several different incisions have been advocated for the palmar incision. Incision is begun just proximal to the ulnar end of the proximal flexion crease of the radial digit of the two involved fingers (Fig. 7–4A), and continued proximally and ulnarward, stopping just distal to the midpalmar crease overlying the metacarpal of the ulnar digit involved. After the skin is divided, the subcutaneous tissue is spread with a clamp until any purulent material is encountered. The abscess is enlarged longitudinally. The surgeon applies compression from the dorsum web space while the wound is retracted. Increased drainage can be seen in the depth of the wound if there is a deep collar button abscess. A second incision is made on the dorsum of the infected hand. This incision begins at the level of the metacarpophalangeal (MP) joints (Fig. 7–4B). It lies between the metacarpals and is extended distally in a straight line to end at the base of the involved web for a distance of 1 to 1.5 cm. The deep tissues are divided in a plane toward the palmar abscess. When the dorsal collection is entered, the opening is enlarged in the direction of the wound. After the infection has been evacuated and the wound irrigated, drains, made of gauze wicks, are placed into both wounds. The hand is dressed in a compressive dressing with a plaster splint; this is removed in 48 to 72 hours and soaks are started with a supervised hand therapy program. Active motion is encouraged.

Alternative Technique The palmar surface approach is made with a zigzag incision starting just proximal to the web and stopping just distal to the midpalmar crease (Fig. 7–4C). The flaps are 38

W E B - S PA C E I N F E C T I O N S

B

A

C

Figure 7–4. (A) Incision is begun just proximal to the ulnar end of the proximal flexion crease of the radial digit of the two involved fingers. (B) Second incision is made on the dorsum of the infected hand. This incision begins at the level of the metacarpophalangeal (MP) joints. This photo depicts a normal hand with incision marked. (C) Palmar surface approach is made with a zigzag incision starting just proximal to the web and stopping just distal to the midpalmar crease.

39

INFECTIONS

Figure 7–5. Hand in compressive dressing with manual irrigation system in place.

reflected and the deep tissues dissected in the web while the digital arteries and nerves are retraced to either side. To provide ample exposure of the volar and dorsal compartments of the dumbbell-shaped abscess, the superficial transverse metacarpal ligament and other fibers of the palmar fascia are divided. A 1.5 cm dorsal longitudinal incision is made between the bases of the proximal phalanges. Generous communication between the two incisions is established. A drain, 16-gauge polyethylene catheter, is inserted into the palmar wound and sutured to the skin to prevent accidental removal. The volar wound is sutured around the catheter. A small Penrose drain is placed into the dorsal wound. Manual irrigation with saline is done to be certain that the irrigating solution exits dorsally. The hand is dressed in a compressive dressing and supported with a plaster splint (Fig. 7–5). Continuous irrigation with sterile saline at the rate of 100 mL/hr is maintained for 48 hours. The outflow spills and collects onto the dressing. The hand is then inspected, and if it is found to be free of infection, the catheter and drain are removed. Exercises are started in a dry dressing.

Complications Scar contraction resulting in loss of full-finger abduction. Missed diagnosis with cellulitis leading to necrosis of small fingers of the hand (Fig. 7–6).

A

B

Figure 7–6. (A) Original web-space infection untreated and now with cellulitis extending through the midpalmar space. Seen in a patient with atypical mycobacterium. (B) Artwork showing midpalmar space. 40

W E B - S PA C E I N F E C T I O N S

Suggested Readings Hausman MR, Lisser SP. Hand infections. Orthop Clin North Am 1992;23:171– 185. Jebson PJ. Deep subfascial space infections. Hand Clin 1998;14:557–566. Kanavel AB. Infections of the hand. In: A Guide to the Surgical Treatment of Acute and Chronic Supperative Processes in the Fingers, Hand, and Forearm. Philadelphia: Lea and Febiger; 1943:17–410. Neviaser RJ. Acute infections. In: Green DP, Hotchkiss RN, Pederson WC, eds. Green’s Operative Hand Surgery. 4th ed. Philadelphia: Churchill Livingstone; 1999: 1033–1047. Rothe M, Rudy T, Stankovic P. Treatment of bites to the hand and wrist-is the primary antibiotic prophylaxis necessary. Handshir Mikrochir Plast Chir 2002;34: 22–29. Siegel DB, Gelberman RH. Infections of the hand. Orthop Clin North Am 1988; 19:779–789. Tonta K, Kimble FW. Human bites of the hand: the Tasmanian experience. Aust N Z J Surg 2001;71:467–471.

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8 Supporative Flexor Tenosynovitis John C. P. Floyd and Waldo E. Floyd III

History and Clinical Presentation A 52-year-old insulin-dependent diabetic man presented to his primary care physician 4 days after sustaining a palmar stab wound while sharpening a knife. Due to swelling and erythema about the wound overlying the palmar aspect of the fourth metacarpophalangeal joint, the patient was admitted to the hospital and placed on parenteral cefazolin. Significant medical history included insulindependent diabetes mellitus, peripheral vascular disease, and coronary artery disease. Bilateral above the knee amputations, multiple coronary artery bypass grafts complicated by wound healing problems, and drug allergies to vancomycin, sulfa, doxycycline, clindamycin, and ceftazidime characterized his medical history. The patient had undergone a limited incision and drainage procedure by an orthopedic surgeon in the palmar wound just proximal to the A-1 pulley. The flexor tendons were reported to have been intact. Purulent fluid had been expressed from a rent in the flexor tendon sheath. The sheath was further incised and irrigated through a pediatric feeding tube. Purulent material was obtained for cultures and sensitivities. Despite oral amoxicillin management, purulent drainage and erythema persisted, prompting hand surgery referral.

Physical Examination On presentation to the hand surgeon, the palmar wound was draining serous fluid and there was no flexor tendon function (Fig. 8–1). Flexor tendons were visible within the wound, with a significant amount of surrounding nonviable tissue. Further surgical intervention was deemed appropriate. PEARLS • Early diagnosis followed by early antibiotic and surgical intervention • Adequate drainage of infection • Appropriate antibiotic management based on cultures

PITFALLS • Necrotic tissue removal necessary • Complications result from inadequate drainage of infection

42

Diagnostic Studies Anteroposterior and lateral radiographs of the left hand were positive for arterial calcification and soft tissue swelling.

Differential Diagnosis Posttraumatic nonspecific inflammation Cellulitis Pyogenic, fungal, or mycobacterial infection Flexor tendon sheath infection with rupture of the flexor tendons Septic arthritis Osteomyelitis Foreign body

S U P P O R AT I V E F L E X O R T E N O S Y N OV I T I S

A

Figure 8–1. (A) Ongoing palmar drainage and lack of wound healing following limited palmar drainage of suppurative ring finger flexor tenosynovitis. (B) Due to rupture of necrotic flexor tendons, the digit rested in full extension, rather than the characteristic semiflexed posture of flexor tenosynovitis.

B

Diagnosis The diagnosis was flexor tendon rupture secondary to suppurative flexor tenosynovitis. Kanavel outlined the four classic, cardinal signs of digital flexor tenosynovitis: (1) fusiform digital swelling, (2) semiflexed digital posture, (3) significant pain associated with passive extension of the digit, and (4) exquisite tenderness along the 43

INFECTIONS

Interphalangeal joints rest in flexion Diffusely swollen finger

Increased pain with passive digital extension

Pain to palpation over flexor tendon sheath

Kanavel's Four Signs of Flexor Tendon Sheath Infection

Figure 8–2. Kanavel’s cardinal signs of suppurative digital flexor tenosynovitis are (1) fusiform digital swelling, (2) semiflexed digital posture, (3) pain with passive digital extension, and (4) pain along the flexor tendon sheath. Pain with passive digital extension is the earliest and most sensitive sign.

entire flexor tendon sheath (Fig. 8–2). All four signs are present in an advanced case and a combination of one or more signs is found in less severe cases. However, in this case, the semiflexed posture was not present as the flexor tendons had ruptured secondary to the advanced process. High-dose parenteral antibiotic management should be instituted at the time of diagnosis and continued postoperatively. Cultures and sensitivities guide the choice of antibiotic management. An infectious disease specialist best manages complex antibiotic therapy. The risk of infections in high-risk individuals should play an important part in the diagnosis. Diabetes and peripheral vascular disease are associated with hand infections refractory to medical intervention. To prevent the serious sequelae of suppurative flexor tenosynovitis, the treating physician must maintain a high index of suspicion for this diagnosis. Adequate drainage of the flexor tendon sheath and removal of necrotic tissue were necessary.

Surgical Management The transverse, open, draining, palmar wound was extended proximally ulnarward and distally radially, and full-thickness flaps were elevated. The flexor tendons were confirmed to be ruptured, and the edges of the tendons were quite friable. There was no frank pus present. With pressure over the palmar aspect of the digit, serous fluid could be expressed from the tendon sheath. The necrotic flexor tendons had become a protected focus of infection, necessitating their excision. With ring finger flexion, the distal tendons could be delivered into the palmar wound. An ulnar midaxial incision was begun distally at the level of the digital whorl and carried back to the ulnar midaxial line at the distal interphalangeal joint level and back to the ulnar midaxial line at the proximal interphalangeal joint level. Subcutaneous tissue was divided and a full-thickness volar flap was elevated containing the neurovascular bundles. The flexor tendon sheath was opened proximally distal to the A-4 pulley. The profundus was divided distal to the A-4 pulley and was completely excised. The flexor superficialis was divided at its insertion and was completely excised. Aerobic and anaerobic cultures were obtained. The digital and palmar incisions were loosely approximated, leaving the transverse wound open. The wounds were dressed and a volar splint was applied, immobilizing the wrist in slight dorsiflexion.

Postoperative Management The patient’s postoperative care consisted of daily dressing changes and whirlpool therapy. Due to the patient’s multiple drug allergies, no parenteral antibiotics were 44

S U P P O R AT I V E F L E X O R T E N O S Y N OV I T I S

administered. Cultures were positive for Staphylococcus aureus susceptible to vancomycin, gentamicin, rifampin, Bactrim, and tetracycline. Infectious disease consultation was obtained. Two weeks postoperative, wounds were healing well with no evidence of active infection. As the protected focus of nonviable flexor tendon tissue had been removed, the decision was made in this complex case not to proceed with a vancomycin desensitization program. The surgical approach, independent of further antibiotic administration, resulted in healing and resolution of the infectious process. Once the infection began to abate, a lighter dressing to enable early motion replaced the splint. Following wound healing, resolution of infection, recovery of passive motion, and the development of tissue equilibrium, delayed flexor tendon reconstruction may be considered in such cases.

Alternative Methods of Management Selected early cases of flexor tenosynovitis may be managed with parenteral intravenous antibiotics, splinting of the hand in the functional position, and elevation. In early cases, Kanavel’s signs are limited to pain with passive digital extension. More advanced cases are characterized by the additional findings of a semiflexed digital posture and pain along the entire flexor digital sheath. Significant improvement must occur within 24 hours with complete resolution of presenting signs by 48 hours. Patients initially presenting with all four of Kanavel’s signs demand more urgent surgical intervention. Closed tendon sheath irrigation is an excellent surgical management technique, which should be instituted early in severe cases and in those less severe cases that do not quickly respond to intensive antibiotic management. This technique requires a zigzag incision in the palm proximal to the A-1 pulley of the involved digit. At the proximal margin of the A-1 pulley, the flexor tendon sheath is excised, and cultures are obtained. A second incision is made in the midaxial line over the distal portion of the middle digital segment sheath distal to the A-4 pulley. A long 16- or 18-gauge flexible catheter is directed from the A-1 pulley into the flexor sheath for a distance of up to 1.5 to 2 cm. A small rubber drain is directed from the distal wound to beneath the A-4 pulley proximally. Following proximal wound closure around the catheter, the system is tested for patency by flushing the catheter with sterile saline and observing the effluent from the distal wound/drain. The hand is then immobilized with a splint secured by a soft dressing with the catheter and drain exposed. Postoperatively the sheath is continuously or intermittently flushed with saline. After 24 hours, if the signs of infection have resolved, then the catheter and drain are removed and mobilization begun.

Complications The most important method for prevention of further complications is adequate drainage. If inadequate drainage occurs, adhesions, tendon rupture, and osteomyelitis can result. The use of antibiotic treatment in combination with inadequate drainage can result in the development of resistant organisms. 45

INFECTIONS

Suggested Readings Burkhalter WE. Deep space infections. Hand Clin 1989;5:553–559. Floyd WE III, Troum S, Frankle MA. Acute and chronic sepsis. In: Peimer CA, ed. Surgery of the Hand and Upper Extremity. 1st ed. New York: McGraw-Hill; 1996:1741. Glass KD. Factors related to the resolution of treated hand Infections. J Hand Surg 1982;7A:388–394. Kanavel AB. Infections of the Hand: A Guide to the Surgical Treatment of Acute and Chronic Suppurative Processes in the Fingers, Hand, and Forearm. Philadelphia: Lea & Febiger; 1912. Kanavel AB. Infections of the Hand. 7th ed. Philadelphia: Lea & Febiger; 1943. Mann RJ, Peacock JM. Hand infections in patients with diabetes mellitus. J Trauma 1977;17:376–380. McGrath MH. Infections of the hand. In: May JW, Littler JW, eds. Plastic Surgery. Philadelphia: Saunders; 1990:5529–5556. Neviaser RJ. Closed tendon sheath irrigation for pyogenic flexor tenosynovitis. J Hand Surg 1978;3A:462–466. Neviaser RJ. Tenosynovitis. Hand Clin 1989;5:525–531. Neviaser RJ. Infections. In: Green DP, ed. Green’s Operative Hand Surgery. 3rd ed. New York: Churchill Livingstone; 1993:1021–1038. Stern PJ, Staneck JL, McDonough JJ, et al. Established hand infections: a controlled prospective study. J Hand Surg 1983;8A:553–559.

46

HERPETIC WHITLOW

9 Herpetic Whitlow Kevin D. Plancher

History and Clinical Presentation A 23-year-old nursing student, working in the intensive care unit for the first time, treated a patient without gloves. The patient reported symptoms of pain and burning or tingling of the infected digit. Erythema and edema followed with the development of vesicles on an erythematous base over the next 7 to 10 days. These vesicles are filled with clear or cloudy fluid.

Physical Examination On examination, the patient’s finger is tender and edematous. Unlike a felon, the pulp space is not swollen. Examination revealed grouped vesicular lesions, which progressed to ulcers at 2 weeks (Fig. 9–1), and extension of the infection into subungual space and lymphangitic streaking was found. In the following 7 to 10 days the vesicles dried and began to heal (Fig. 9–2, different patient).

Diagnostic Studies Diagnosis of herpetic whitlow is usually based on clinical presentation. The diagnosis can be confirmed with a Tzanck smear, which reveals characteristic multinucleated giant cells. Other smears, stains, and serologic tests can be used for diagnosis of primary infections. Herpes antibody titers can also be used to confirm the diagnosis.

Figure 9–1. Grouped vesicular lesions of the index finger.

Figure 9–2. In the following 7 to 10 days the vesicles dry and begin to heal.

47

INFECTIONS

PEARLS • Distinguishing between a felon and herpetic whitlow is important, because incision and drainage is contraindicated for herpetic whitlow. • Splint and elevate • Level of suspicion is high in dental personnel

Differential Diagnosis Cellulitis Felon Paronychia Pyogenic infections

Diagnosis Herpetic Whitlow of the Index Finger

PITFALLS • Surgical treatment can lead to bacterial superinfection, viremia, and encephalitis. • Do not undertake irrigation and debridement unless bacterial infection warrants treatment.

Diagnosis of herpetic whitlow is usually based on presentation of the affected digit with the characteristic lesions and the patient’s history. In health care workers (dentists, dental hygienists, nurses, physicians), infection is usually due to exposure to infected oropharyngeal secretions of patients (herpes simplex virus type 1). This can easily be prevented by use of gloves and by scrupulous observation of universal fluid precautions. In the general adult population, herpetic whitlow is most often due to autoinoculation from genital herpes; therefore, it is most frequently secondary to infection with herpes simplex virus type 2 (HSV-2). Infection involving the finger usually is due to autoinoculation from primary oropharyngeal lesions as a result of finger-sucking or thumb-sucking behavior in patients with herpes labialis or herpetic gingivostomatitis. Care should be taken as viral shedding may occur for another 12 days and the lesions may be infective. The paronychial region should be examined for abscesses indicating a concomitant pyogenic infection. The oral cavity should be examined for preexisting herpetic lesions. Herpetic whitlow may be accompanied by axillary and epitrochlear adenopathy with lymphangitis of the forearm.

Nonsurgical Management The infection resolves spontaneously in 2 to 3 weeks and treatment is directed toward the patient’s symptoms relief. In primary infections, topical acyclovir 5% has been demonstrated to shorten the duration of symptoms and viral shedding. Oral acyclovir may prevent recurrence. Use antibiotic treatment only in cases complicated by pyogenic infections or bacterial superinfections.

Surgical Technique In most cases, surgical treatment is not recommended and if undertaken, it can lead to bacterial superinfection, viremia, and encephalitis. In rare instances, with an abscess and concomitant pyogenic infections, surgical incision and drainage may be warranted.

Suggested Readings Gill MJ, Arlette J, Buchan K. Herpes simplex virus infection of the hand. A profile of 79 cases. Am J Med 1988;84:89–93. Haedicke GJ, Grossman JA, Fisher AE. Herpetic whitlow of the digits. J Hand Surg 1989;14B:443–446. 48

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Hurst LC, Gluck R, Sampson SP, Dowd A. Herpetic whitlow with bacterial abscess. J Hand Surg 1991;16A:311–314. Klotz RW. Herpetic whitlow: an occupational hazard. AANA J 1990;58:8–13. McNicholl B. Recurrent herpetic whitlow. Arch Emerg Med 1990;7:124–125. Smith E, Hallman JR, Pardasani A, McMichael A. Multiple herpetic whitlow lesions in a patient with chronic lymphocytic leukemia. Am J Hematol 2002;69:285–288. Walker LG, Simmons BP, Lovallo JL. Pediatric herpetic hand infection. J Hand Surg 1990;15A:176–180. Weisman E, Troncale JA. Herpetic whitlow: a case report. J Fam Pract 1991;33: 516,520.

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10 Bites to the Hand Kevin D. Plancher

History and Clinical Presentation A 17-year-old college student presented to the emergency room with an open wound to the dorsum and a piece of human tooth in the wound. The patient reported he had been in a bar brawl last evening. Closed fist injuries are encountered almost exclusively in young males, usually occurring during adolescence through the fourth decade of life. Although toddlers are notorious for biting each other, these injuries tend to be superficial and low risk.

Tendon Capsule

PEARLS • Open lavage with adequate debridement to avoid complications. • Early intervention to avoid collar button abscess • Appropriate immediate antibiotic coverage • Must evaluate the wound in the same position as the injury occurred to appreciate the depth

A

PITFALLS • Undertreatment with closure of wound seen after 8 hours from injury • Underestimation of full depth of penetration to wound and joint B

50

Figure 10–1. (A) Tooth from bite severing skin and entering metacarpophalangeal (MP) joint of the hand. (B) Although the wound looks small and innocuous, when the digit is in extension the penetration is much deeper. Adequate debridement and opening of the wound are essential.

BITES TO THE HAND

Physical Examination If the bite results in a puncture wound that is swollen, red, and painful, the wound is likely to be infected. Patients with infection may have an elevated temperature, swollen glands, or a history of fever. Any loss of motion or sensation in the fingers suggests that a tendon or nerve has been severed. If a flexor tendon has been severed, the patient will be unable to extend or flex some portion of the finger. When a nerve has been lacerated, there is a loss of sensation over the tip of the finger. Closed fist injuries often result in injury to the extensor tendon and its sheath. When a closed fist injury occurs to someone with a clenched fist, the bacterial load is often carried back into the hand as the tendon slides back to its relaxed state (Fig. 10–1). This means that the problem of contamination cannot be easily resolved using normal methods of irrigating and cleaning a wound. Patients who present with dog or cat bites have a wounded area that is painful, red, and swollen. Abscess formation may develop.

Diagnostic Studies Wound cultures are used to diagnose the infecting organisms. Aerobic and anaerobic cultures should be included. For human bites, the most common infecting organisms include Staphylococcus aureus, streptococci, and Eikenella corrodens. For cat bites, cultures should be examined for Pasteurella multocida. For dog bites, Straphlococcus aureus, Streptococcus viridans, Bacteroides spp., and P. multocida may be cultured. All patients with lacerations over the metacarpophalangeal joint should be x-rayed for retained teeth fragments, regardless of patient-reported history. Radiographs are used to exclude fractures or foreign bodies (e.g., teeth). Radiographs can be used to determine if osteomyelitis is present, which has been frequently reported in cat bites.

Differential Diagnosis Puncture wound Insect bite Other animal bite Marine animal bite

Diagnosis Human Bite to the Hand There are two major mechanisms of human bites to the hand. An example of penetrating trauma is a closed fist injury, in which one person strikes another in the mouth, causing a fight bite to the hand. If the hand is clenched in a fist, laceration of the skin over the knuckle may damage a tendon sheath or tendon, as well as surrounding tissue or underlying bones of the joint. Wounds over the fingers or other surfaces of the hand are the result of a direct and deliberate (“chomping”) human 51

INFECTIONS

Figure 10–2. Unusual presentation of a human bite of the ulna aspect of the hand affecting the 5th volar MP.

bite (Fig. 10–2). The most common site of injury is the third and fourth digits at the metacarpophalangeal joint. Osteochondral fractures are common. Bite wounds to the hand may cause cellulitis and abscess. Human bite wounds are particularly virulent because of the gram-positive and anaerobic bacteria present in the mouth.

Nonsurgical Management Patients who present less than 1 day following injury may not have signs of sepsis, and wound exploration and swabbing for aerobic and anaerobic cultures to determine antibiotic treatment may be sufficient. Treatment includes antibiotics and close observations. If their injury is treated within 8 hours, then the wound may be closed, whereas any wound after that time should be left open. Close observation in all cases must be performed. Antibiotics recommended may include penicillin G, ampicillin, carbenicillin, or tetracycline for E. corrodens, and a cephalosporin for Staphylococcus organisms. For dog bites, most suspected organisms are sensitive to penicillin. Tetanus prophylaxis should also be included with the use of antibiotics in dog bite injuries. The organism in cat bites, P. multocida, is usually sensitive to penicillin.

Surgical Management In patients where treatment is delayed, signs of sepsis may be present. For these bite wounds, open joint drainage and irrigation may be necessary. A wide-open incision should be used for the irrigation and debridement. Several liters should be used in the irrigation. This is followed by close observation in the hospital and IV antibiotics. Frequently the tooth will penetrate the metacarpophalangeal joint where the cartilage is particularly sensitive to infection. Every puncture wound near the proximal 52

BITES TO THE HAND

B

A

Figure 10–3. (A) Hand showing the wound from a bar altercation. (B) Open debridement. Note how little obvious damage is seen in extension.

knuckle must be treated aggressively with exploration, irrigation, antibiotics, and drainage (Fig. 10–3). Human saliva contains more than 109 bacteria per milliliter, and the risk of infection is great. Human bite wounds to the hand thus should rarely, if ever be closed. Animal bite wounds can be closed loosely after debriding the wound edges and thoroughly irrigating in select cases where time is crucial. Oral antibiotics are administered; however, in advanced cases, IV antibiotics should be used.

Postoperative Care Bite wounds are wrapped in a bulky dressing. Motion exercises can be started at 24 hours after drainage. Follow-up visits should be mandatory at 48 and 72 hours following treatment. The patient should cleanse the wound daily (Fig. 10–4).

Figure 10–4. Six months follow-up and old scar is seen from wound left open after a human bite. 53

INFECTIONS

Complications Complications from bite injuries include osteomyelitis, which is frequently reported in cat bites, fractures, joint stiffness, and arthritis. Less common complications include digital amputation, systemic sepsis, and death.

Suggested Readings Aslam A, Dickinson JC. Dog bite bones too—a tale of fractures in adult hands. Injury 1999;30:374–376. Dire DJ. Cat bite wounds: risk factors for infection. Ann Emerg Med 1991;20: 973–979. Dire DJ, Hogan DE, Riggs MW. A prospective evaluation of risk factors for infections from dog-bite wounds. Acad Emerg Med 1994;1:258–266. Grant I, Belcher HJ. Injuries to the hand from dog bites. J Hand Surg 2000;25B: 26–28. Griego RD, Rosen T, Orengo IF, Wolf JE. Dog, cat, and human bites: a review. J Am Acad Dermatol 1995;33:1019–1029. Hausman MR, Lisser SP. Hand infections. Orthop Clin North Am 1992;23:171– 185. Kelly IP, Cunney RJ, Smyth EG, Colville J. The management of human bite injuries of the hand. Injury 1996;27:481–484. Lewis KT, Stiles M. Management of cat and dog bites. Am Fam Physician 1995; 52:479–490. Mennen U, Howells CJ. Human fight-bite injuries of the hand. A study of 100 cases within 18 months. J Hand Surg 1991;16B:431–435. Moran GJ, Talan DA. Hand infections. Emerg Med Clin North Am 1993;11:601– 619. Perron AD, Miller MD, Brady WJ. Orthopedic pitfalls in the ED: fight bite. Am J Emerg Med 2002;20:114–117. Tsai E, Failla JM. Hand infections in the trauma patient. Hand Clin 1999;15: 373–386. Wiggins ME, Akelman E, Weiss AP. The management of dog bites and dog bite infections to the hand. Orthopedics 1994;17:617–623.

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MYCOBACTERIAL TENOSYNOVITIS

11 Mycobacterial Tenosynovitis John C. P. Floyd and Waldo E. Floyd III

History and Clinical Presentation A 66-year-old man employed as a machinist was referred for further evaluation of limited range of motion and swelling in his left hand and distal forearm, which had been progressive over the past 8 months. The patient had been impaled over the volar aspect of the volar forearm by a saltwater catfish fin 18 months previously. The patient’s surgical and medical history was otherwise negative.

Physical Examination The patient had limited range of motion in the thumb and small finger and a 4 ⫻ 5 cm cystic mass over the volar aspect of the wrist and distal forearm (Fig. 11–1). Over the volar aspect of the thumb, there was marked swelling about the flexor tendon sheath. To a lesser degree, the small finger was also swollen over the flexor sheath and rested in slight flexion at the interphalangeal joints. There was limitation of composite digital flexion, but all flexor tendons were intact. Neurovascular examination of the hand was normal. No evidence of axillary or epitrochlear node involvement was present.

Diagnostic Studies Anteroposterior and lateral radiographs of the left hand were positive for soft tissue swelling. No evidence of osseous involvement was present. A magnetic resonance imaging scan demonstrated a 4 ⫻ 5 ⫻ 3 cm mass volar to the pronator quadratus

A

B

Figure 11–1. (A) Progressive hand and wrist swelling. (B) Eighteen months following a penetrating volar wrist injury by a saltwater catfish. (With permission from Floyd WE III, Foulkes GD. Tuberculous, mycotic, and granulomatous disease. In: Peimer CA, ed. Surgery of the Hand and Upper Extremity, 1st ed. New York: McGraw-Hill; 1996.)

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INFECTIONS

PEARLS • High index of suspicion • Obtain a thorough history of possible exposure • Surgical debridement is key to affecting a cure • Obtain infectious disease consultation

Figure 11–2. Magnetic resonance imaging scan demonstrating a solid soft tissue mass volar to the pronator quadratus. (With permission from Floyd WE III, Foulkes GD. Tuberculous, mycotic, and granulomatous disease. In: Peimer CA, ed. Surgery of the Hand and Upper Extremity, 1st ed. New York: McGraw-Hill; 1996.)

PITFALLS • For species-specific diagnosis, culture is necessary. • Treatment should be modified to the specific species.

without evidence of bone involvement (Fig. 11–2). The mass was homogeneous and had a signal intensity consistent with soft tissue.

Differential Diagnosis Neoplasm Fungal infection Mycobacterial infection Bacterial infection

Diagnosis Microbacterial Infection The diagnosis was a horseshoe abscess of noncaseating granulomatous disease secondary to mycobacteria other than tuberculosis (MOTT). Cultures were positive for Mycobacterium avium-intracellulare complex. A major cause of granulomatous infections is mycobacteria. Two of the earliest identified mycobacteria were Mycobacterium tuberculosis and Mycobacterium leprae. Tuberculosis remains the most common pathologic organism of this genus. Hansen’s disease or M. leprae has long been recognized as a separate species, but leprosy is far less common in most parts of the United States than some of the more newly recognized species. “Atypical mycobacteria” has traditionally meant a mycobacterium that is neither tuberculosis nor leprosy. An increased understanding of all nontuberculosis infections has led to the introduction of the term mycobacteria other than tuberculosis (MOTT). Timpe and Runyon first showed MOTT to be pathogenic in humans in 1954. The Runyon classification system has been used to delineate species on the basis of pigment production or growth rate in culture. Runyon groups I, III, and IV have been identified as pathogenic in humans. Mycobacteria may be identified immediately with acid-fast stain, but most often, as in this case, MOTT is not seen. Current microbiologic methods may take 8 to 10 56

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weeks to identify the slow-growing MOTT. In vitro sensitivities may not be available for at least another week. MOTT infections have become more frequently recognized, especially in immunocompromised patients. Contemporary culture and diagnostic techniques have led to the recognition of several new species of nonpulmonary infections within the immunocompetent population. Fifteen percent of all mycobacterial infections and an even larger percentage of extrapulmonary mycobacterial infections are of the “atypical” variety. They are most commonly encountered in tropical and subtropical areas. At our institution, we saw 28 extrapulmonary MOTT infections over the last 4 years compared with nine M. tuberculosis extrapulmonary infections over the same period. Because the hand is the major manipulator of the environment, the hand is more likely to be inoculated with saprophytic bacteria. Infection occurs by either cutaneous or deep (noncutaneous) pathways. Cutaneous infections are far more common. Abrasions on the extremities involving an aquatic environment (swimming pools, aquaria, fishing) are the prototypical cases. These infections can spread proximally with multiple abscesses resembling sporotrichosis. Deep infections in the adult patient present as a spectrum of disease progressing from tenosynovitis to septic arthritis. All species of MOTT can be acquired from prior trauma except Mycobacterium kansasii, which usually shows no clear mode of inoculation. Mycobacterium marinum is the most common cause of MOTT infections of the upper extremity followed in frequency by M. kansasii. Symptoms appear slowly and are only occasionally characterized by typical inflammatory criteria. A thorough remote and recent history is essential in raising suspicion of a MOTT infection, because MOTT infections are indolent and may present long after inoculation.

Surgical Management A zigzag incision was made over the volar aspect of the wrist. The median nerve was identified and carefully protected. A large mass was present about the flexor tendons. The mass was opened and contained multiple rice bodies (Fig. 11–3). A frozen section biopsy demonstrated the presence of granulomatous disease. Figure 11–3. Significant rice body formation was encountered upon excision of the flexor compartment. Histopathology demonstrated noncaseating granulomatous inflammation, and cultures identified Mycobacterium avium-intracellulare complex. (With permission from Floyd WE III, Foulkes GD. Tuberculous, mycotic, and granulomatous disease. In: Peimer CA, ed. Surgery of the Hand and Upper Extremity, 1st ed. New York: McGraw-Hill; 1996.) 57

INFECTIONS

Figure 11–4. The thumb and little finger flexor sheaths, respectively, represent the distal extent of the radial and ulnar bursae. The potential spaces may communicate at the distal forearm level through Parona’s space volar to the pronator quadratus muscle. Inoculation at any site within this space may produce a horseshoe abscess involving the thumb and little finger flexor tendons sheaths as well as a deep compartment infection of the level of the distal forearm.

This evidence of granulomatous tenosynovitis indicated the need for flexor tenosynovectomy. Complete tenosynovectomy was performed with removal of diseased tissue from about all flexor tendons. Thumb and little finger distal flexor tenosynovectomies were performed. Findings demonstrated a horseshoe abscess pattern of involvement of the radial and ulnar bursae through Parona’s space (Fig. 11–4). The “eight pack” recently emphasized by Patel provides a simple pattern that should be followed when collecting a specimen for further diagnosis. The “eight pack” consist of smears (Gram stain, acid-fast stain, and fungal KOH stain) and cultures (aerobic, anaerobic, acid fast at 37°C, acid fast at 30°C, and fungal).

Postoperative Management An infectious disease specialist consultation was obtained. The patient was placed on a planned 30-day course of rifampin and ethambutol. He developed a rash thought to be secondary to the ethambutol, and this medication was discontinued after 2 weeks. His wounds continued to improve without further evidence of infection, and hand function improved with a formal rehabilitation program. 58

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Alternative Methods of Management Multidrug therapy is acceptable for initial treatment of less severe cases of granulomatous disease. The efficacy of antibiotic management in MOTT infections has not been clearly established. Most MOTT infections are sensitive, at least in vitro, to antimycobacterials, but this may not translate into an in vivo response. We believe thorough surgical debridement should be the primary therapy for all known deep granulomatous infections. M. tuberculosis often responds to chemotherapy alone, but once a diagnosis of a MOTT infection is confirmed, treatment should be modified to the specific species. In the case of most MOTT infections, surgical debridement is the primary means of effecting a cure, but adjunctive treatment with antibiotics is considered appropriate. These drugs have multiple side effects and are best managed by an infectious disease specialist familiar with their use.

Complications Failure to make the correct diagnosis and inadequate surgical debridement are significant problems in MOTT infections. The immunocompetence of the patient should be established, and infectious disease consultation should be obtained.

Suggested Readings Dawson DJ, Blacklock ZM, Ashdown LR, Bottger EC. Mycobacterium asiaticum as the probable causative agent in a case of olecranon bursitis. J Clin Microbiol 1995;33:1042–1043. Floyd WE III, Foulkes GD. Tuberculous, mycotic, and granulomatous disease. In: Peimer CA, ed. Surgery of the Hand and Upper Extremity. 1st ed. New York: McGrawHill; 1996:1766. Foulkes GD, Floyd JCP, Stephens JL. Flexor tenosynovitis due to Mycobacterium asiaticum. J Hand Surg [Am] 1998;23A:756. Gunther SF, Elliott RC, Brand RL, Adams JP. Experience with atypical mycobacterial infection in the deep structures of the hand. J Hand Surg [Am] 1977;2:90–96. Gunther SF, Levy CS. Mycobacterial infections. Hand Clin 1989;5:591–598. Hurst LC, Amadio PC, Badalamente MA, et al. Mycobacterium marinum infections of the hand. J Hand Surg [Am] 1987;12A:428–435. Kelly PJ, Karlson AG, Weed LA, Lipscomb PR. Infections of synovial tissues by Mycobacteria other than tuberculosis. J Bone Joint Surg Am 1967;49A:1521–1530. Leung PC. Tuberculosis of the hand. Hand 1978;10:285–291. Patel MR. Chronic infections. In: Green DP, ed. Green’s Operative Hand Surgery, 4th ed. Philadelphia: Churchill Livingstone; 1999:1048–1050. Runyon EH. Anonymous mycobacteria in pulmonary disease. Med Clin North Am 1959;43:273–290. Timpe A, Runyon EH. The relationship of “atypical” acid-fast bacteria to human disease. A preliminary report. J Lab Clin Med 1954;44:202–209. 59

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Visuthikkosol V, Aung PS, Navykarn T, Nitiyanant P. Tuberculosis infections of the hand and wrist. J Med Assoc Thai 1992;75:45. Wolinsky E. Mycobacteria. In: Davis BD, Dulbecco R, Eisen HH, Ginsberg HS, eds. Microbiology. 3rd ed. Philadelphia: Harper & Row; 1980:724–742. Wyngaarden JB, Smith LH, Bennett JC. Cecil Textbook of Medicine. 19th ed. Philadelphia: WB Saunders; 1992.

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Section III

Compression Neuropathy

A. Median Nerve Carpal Tunnel Syndrome Kevin D. Plancher

Pronator Syndrome Kevin D. Plancher

Anterior Interossus Nerve Syndrome Michael F. Bothwell and Kevin D. Plancher

B. Ulnar Nerve Cubital Tunnel Syndrome Eric Freeman, Dennis Rodin, and Kevin D. Plancher

Ulnar Tunnel Syndrome Robert M. Szabo

C. Radial Nerve Posterior Interosseus Syndrome William B. Geissler

D. Cervical Nerve Cervical Root Compression Bradley M. Thomas, John M. Olsewski, and Jerry G. Kaplan

Complex Regional Pain Syndrome Type 1 (Reflex Sympathetic Dystrophy) Carole W. Agin

C A R PA L T U N N E L S Y N D R O M E

12 Carpal Tunnel Syndrome Kevin D. Plancher

History and Clinical Presentation A 46-year-old right hand dominant woman presents with symptoms of numbness 5 cm proximal to the right wrist crease as well as loss of sensation in her palm over the thumb area. She noticed her hands go to sleep while driving her car. Her symptoms have been present for 4 to 6 weeks, and have been progressively getting worse. The patient denies cramping in her hand and has no palmar hypersensitivity. She needs to shake her hands out at night and experiences numbness or tingling to the fingertips. The patient spends ~6 hours a day working on a computer.

Physical Examination

PEARLS • Avoid the limited open technique in patients with distorted anatomy, fracture of the distal radius, or fracture dislocation of carpus. • Avoid this technique in patients with marked thenar wasting, or complete or near loss of sensory perception. • Always extend the excision proximally to allow adequate visualization if limited technique does not provide direct visualization.

PITFALLS • Do not use this technique in recurrent carpal tunnel syndrome for a repeat procedure when an open procedure was done previously. • Never exert force in passing instruments across the ligament without good visualization to avoid cutting the median nerve.

A positive Tinel’s sign is present directly over the palmar cutaneous branch of the median nerve, which the patient says simulates her numbness and tingling to the thenar eminence. In addition to this, she has an area of numbness of 3 ⫻ 2 cm directly over the area of innervation at the palmar cutaneous branch of the median nerve in her palm. Her Phalen’s test is positive and her Tinel’s test to the wrist is negative. Her median nerve compression test is positive and her Weber static two-point discrimination is greater than 1 cm to all her median innervated digits. The patient’s grip strength is 110 on the left and 110 on the right on the Jamar dynometer. Pinch is 18 pounds on the left and 18 pounds on the right. All measurements are an average of three trials.

Diagnostic Studies Radiographs are negative for bony or soft tissue abnormalities. Electromyograms (EMGs) show nerve conduction velocities significantly slowing at the median nerve distribution more on the sensory fibers, even to the index with proximal conduction and ulnar conduction normal.

Differential Diagnosis Carpal tunnel syndrome Neuroma Arthritis Thyroid disease Diabetes mellitus Tenosynovitis Gout 63

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Diagnosis Moderate Carpal Tunnel Syndrome with Compression of the Palmar Cutaneous Branch of the Median Nerve Carpal tunnel syndrome is one of the most common conditions of the hand. Swelling of the median nerve or compression of the median nerve by surrounding structures causes sensory and motor disturbances (Fig. 12–1). Chronic repetitive stress on the carpal tunnel and the median nerve within it is the most common cause of idiopathic carpal tunnel syndrome. Occupations that require stress on the wrist, such as typing and carpentry, often lead to a high incidence of carpal tunnel syndrome. Sporting activities that involve repetitive or continuous flexion and extension of the wrist, such as cycling, throwing sports, racquet sports, archery, and gymnastics, also predispose individuals to carpal tunnel syndrome. Carpal tunnel syndrome can be diagnosed by obtaining a careful patient history. Common complaints include nocturnal paresthesia, a heavy feeling, or hands going to sleep. Pain may radiate up the arm to the shoulder and neck. Patients also complain of weakness that hinders their ability to grasp objects. Numbness when gripping objects may prevent the patient from being able to lift objects. Nonoperative treatments include activity modification, splinting (Fig. 12–2), magnetic support wraps, and injections (Fig. 12–3). In younger patients with early stages of carpal tunnel syndrome, these modalities may relieve symptoms. Following failed conservative treatment, patients may require surgical intervention to regain lost function. Open carpal tunnel release has been shown to relieve symptoms of median nerve compression for many years (Fig. 12–4). Endoscopic carpal tunnel re-

Figure 12–1. Dumbbell appearance of median nerve after chronic constriction. 64

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Figure 12–2. Custom carpal tunnel splint with wrist in neutral alignment.

Figure 12–3. Injection with a high rate of success when done as demonstrated. (Illustration courtesy of The Indiana Hand Center and Gary Schnitz.)

Figure 12–4. Classic open carpal tunnel incision. 65

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lease was shown to reduce tissue trauma and speed postoperative recovery. However, the endoscopic technique requires extensive equipment and has a steep learning curve. In our patients, we perform a limited open incision carpal tunnel release. This technique combines the advantages of the open procedure with the advantage of reduced tissue trauma and postoperative morbidity of endoscopic release.

Surgical Treatment The patient is brought into the operating room and a localized injection of anesthesia is injected at the wrist and into the carpal canal (Fig. 12–5). A 2- to 2.5-cm incision (Fig. 12–6) is made parallel to the radial side of the ring finger and one-third distal to and two-thirds proximal to a proximal line extending slightly off of the distal border of the thenar muscle. A Miltex retractor is positioned in the wrist. The superficial palmar fascia is incised in line with its fibers and the retractor is placed deeper into the wound (Fig. 12–7). A Ragnell retractor is placed in the distal aspect of the incision. The soft tissue is spread to identify the fat, which pouches up at the distal aspect of the transverse carpal ligament. Distal and proximal tissues are retracted until at least one third of the distal transverse carpal ligament can be visualized. The ligament is then incised for a distance of 1 cm. The distal end of the ligament is cut until the fat overlying the superficial palmar arch is exposed. The contents of the carpal tunnel, including the median nerve, can now be identified and protected throughout the remainder of the operation (Fig. 12–8). A smooth blunt pilot instrument is then placed proximally between the underside of the transverse carpal ligament and the carpal tunnel contents (Fig. 12–9). The instrument is withdrawn and a palmar stripper is then placed under the ligament and into the wound under direct visualization. This sharp instrument is designed to prepare a channel through the thick connecting tissues directly palmar to the ligament. The stripper is inserted into the groove that was formed by the distal division of the ligament and pushed proximally until resistance is felt. The design of the instrument prevents it from penetrating the ligament. The stripper is removed and a double pilot instrument is introduced. This instrument, with long, dull lower and upper skids, allows for full visualization of the passageway beneath the ligament. It provides an area for the cutting “tome” to enter and allows for safe passage above and below the transverse carpal ligament. The pilot is removed and the “tome” guide is

Figure 12–5. Local anesthesia administered to the proximal palm. 66

Figure 12–6. Under tourniquet, the palmar incision is made and deepened through the palmar fascia.

A

Figure 12–7. The self-retaining Holzheimer retractor is placed in the wound.

B

Figure 12–8. (A) The surgeon, although not seeing this anatomy, must understand all the relationships within the wrist. (B) Anatomic relationships. (Illustration courtesy of The Indiana Hand Center and Gary Schnitz.)

Figure 12–9. The blunt pilot is placed in the depths of the wound between the underneath surface of the transverse carpal ligament and the contents of the carpal canal. 67

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Figure 12–10. The carpal tunnel tome-cutting blade.

inserted between the undersurface of the transverse carpal ligament and the carpal tunnel contents. To allow for complete division of the transverse carpal ligament, the “tome” guide is placed proximally. The patient’s wrist is fully hyperextended and positioned in a neutral alignment. The cutting “tome” is inserted into the prepared ligament and passed proximally (Fig. 12–10). The cutting “tome” should not be reintroduced after the primary ligament transection. The cutting “tome” is removed and the contents of the carpal tunnel can be inspected (Fig. 12–11). The skin is closed and a soft dressing is applied to the palm and wrist (Fig. 12–12). Digital range-of-motion and tendon gliding exercises are taught to the patient in the operating room. The patient returns in 2 weeks for suture removal.

A

C

68

B

Figure 12–11. (A) Median nerve exposed and radial and ulna leaf bisected. (B) Division of the transverse carpal ligament by proximal passage of the carpal tunnel “tome.” (C) The carpal tunnel release using the carpal tunnel “tome.” (Illustrations courtesy of The Indiana Hand Center and Gary Schnitz.)

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Figure 12–12. A soft tissue, bulky dressing placed after successful division of the transverse carpal ligament.

Complications Complications that may occur include stiffness, nerve injury, vascular injury, infections, and incomplete release. Although complications are rare, inaccurate diagnosis may predispose the patient to complications. Patients with recurrent carpal tunnel syndrome or with distorted anatomy due to fractures or dislocations should never undergo limited open incision carpal tunnel release. Open carpal tunnel release should also be performed in patients who have neurologic deficits in the thenar muscle area and near complete loss of sensory perception.

Suggested Readings Agee JM, McCarroll HR Jr, Tortosa RD, Berry DA, Szabo RM, Peimer CA. Endoscopic release of the carpal tunnel: a randomized prospective multicenter study. J Hand Surg 1992;17A:987–995. Braun RM, Rechnic M, Fowler E. Complications related to carpal tunnel release. Hand Clin 2002;18:347–357. Brown RA, Gelberman RH, Seiler JG III, et al. Carpal tunnel release: a prospective, randomized assessment of open and endoscopic methods. J Bone Joint Surg 1993; 75A:1265–1275. Lee WP, Plancher KD, Strickland JW. Carpal tunnel release with a small palmar incision. Hand Clin 1996;12:271–284. Plancher KD, Idler RS, Lourie GM, Strickland JW. Recalcitrant carpal tunnel. The hypothenar fat pad flap. Hand Clin 1996;12:337–349. Plancher KD, Parekh SR. Limited open incision carpal tunnel release. Tech Hand Upper Extrem Surg 1998;2:64–71. Vasen AP, Kuntx KM, Simmons BP, Katz JN. Open versus endoscopic carpal tunnel release: A decision analysis. J Hand Surg 1999;24A:1109–1117.

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13 Pronator Syndrome Kevin D. Plancher

History and Clinical Presentation A 35-year-old woman presents to our office with symptoms of forearm discomfort consisting of fatigue-like pain and numbness in her hand. She works long hours on a computer and reports that this repetitive activity is what reproduces the symptoms in her right arm; however, she denies any symptoms at night. The condition has been gradually getting worse.

Physical Examination The patient presents with symptoms of general forearm pain in addition to paresthesias and hypersthesia in the thumb, index finger, long finger, and radial half of the ring finger. There is pain on flexion of the long finger at the proximal interphalangeal (PIP) joint. Sensory symptoms are also present over the thenar eminence in the distribution of the palmar cutaneous nerve. Patient experiences pain on palpation of the median nerve in the proximal forearm. In addition, the pronator teres muscle can be tender, firm, or enlarged. Tinel’s sign is present on the nerve site just distal to the elbow and paresthesias increase with mild compression of the proximal muscle mass of the pronator teres. Phalen’s test is negative.

Diagnostic Studies

PEARLS • EMG slowing in the forearm, not in the carpal tunnel • Tinel’s sign in the proximal forearm • Pain on long finger flexor digitorum superficialis (FDS) flexion • Negative Phalen’s test • No nocturnal symptoms • Numbness of the palmar cutaneous branch of the median nerve • Pain on resistance to pronation

PITFALLS • Numbness of the radial 31⁄2 digits • Full knowledge of the anatomy to avoid a complication on exploration is essential. 70

Electrodiagnostic tests are suggestive, but not always diagnostic. Although slowing will often show in the forearm, it does not always show in the carpal canal. The threshold testing with Semmes-Weinstein monofilaments may reveal decreased sensibility over the distribution of the median nerve. Needle electromyography (EMG) may be useful if fibrillations, positive sharp waves, and reduced interference patterns are noted in the pronator quadratus and flexor pollicis longus (FPL). It is important to note that the EMG does not differentiate median nerve lesions at the pronator teres from those more proximal.

Differential Diagnosis Carpal tunnel syndrome Compartment syndrome Pronator syndrome

Diagnosis Pronator Syndrome of the Right Arm Pronator syndrome is defined by functional problems of the median nerve due to some mechanical abnormality at the level of the forearm. This disturbance in

P R O N ATO R S Y N D R O M E

function is often related to the path of the nerve through the middle of the pronator teres muscle. A concise and clear physical exam is the best indicator for diagnosis of pronator syndrome, which is similar to carpal tunnel, but less common. Both syndromes involve the median nerve and therefore have similar symptoms; the syndromes are usually differentiated based on the physical exam. Keys to the physical exam are to note the areas of tenderness and the presence of a positive Tinel’s sign. It is possible that both conditions coexist with medial nerve entrapment at the proximal forearm and the wrist. Correlating the physical exam with the EMG study aids in correctly diagnosing the patient’s symptoms. No motor symptoms or weakness is present with a pronator syndrome.

Surgical Management The initial incision usually begins 5 cm proximal to the elbow flexion crease unless either a supracondyloid process or accessory bicipital aponeurosis has been identified. If this is the case, the incision should begin no less than 10 cm proximal to the crease (Fig. 13–1). The incision curves distally just medial to the biceps tendon, zigzags across the antecubital crease, and curves back medially for 5 cm in the proximal forearm. Next, the medial antebrachial cutaneous nerve is identified and isolated as it continues along the basilic vein. The median nerve is then identified and isolated in a similar manner. If a supracondyloid process or accessory bicipital aponeurosis had been identified preoperatively, the median nerve is identified and isolated in the most proximal portion of the incision and then traced distally. The supracondyloid process or accessory bicipital aponeurosis is then dealt with if present. It is important to explore the median nerve completely, as other, more proximal, sites of compression may exist at the same time. The median nerve is then dissected distally. The bicipital aponeurosis is incised and the nerve followed to the proximal end of the superficial or humeral head of the pronator teres. Retraction of the head is needed to identify any variation in the nerve’s path in relation to the two pronator heads. Any tendinous or fibrous bands within the pronator are identified and incised (Fig. 13–2). In those cases where the median artery penetrates the median nerve, interfascicular dissection may be used to enlarge the passage. Great care should be taken to avoid ligation of the artery. It is the dominant blood supplier to the median nerve

Figure 13–1. Incision for exploration of median nerve in the proximal forearm. 71

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Median nerve

B

Deep head A pronator teres Fibrous arch

C

Median nerve

Superficial head pronator teres Median nerve

Anterior interosseous nerve

Flexor digitorum muscle arch D

Figure 13–2. (A) The median nerve passes between the superficial and deep heads of the pronator teres muscle. (B) Anatomy of the median nerve in the forearm of a patient with pronator syndrome. (C) The median nerve passing superficial to the deep head and through the superficial head and being compressed by a fibrous arch of this anatomic variant muscle. (D) The median nerve accompanies the anterior interosseous nerve (AIN) underneath a tight arch of the flexor digitorum superficialis (FDS) muscle. 72

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30% of the time and also significantly serves the index and long fingers in some cases. Next, the superficialis arcade is explored. The arch should be incised, especially if thickened, as it may be a source of compression. The surgeon should carefully dissect distal to the arch, paying attention to the possible presence of anatomic variations such as accessory muscles. All sites of nerve compression should be released as the nerve is isolated. At this time the tourniquet should be deflated. Hemostasis should be verified, and a bipolar cautery can be used as needed. The pronator teres is reattached if detachment was necessary. When reattaching the pronator teres, careful attention should be paid so as not to shorten and therefore tighten the attachment. This by itself could cause a new compressive lesion. Epineurotomy, internal neurolysis, and subcutaneous transposition of the median nerve are not necessary and may even prove harmful. The subcutaneous layer is closed with 4–0 absorbable sutures and the skin edges with 5–0 simple sutures. The extremity is then placed in a bulky, plaster-reinforced, sterile, above elbow dressing. It should be positioned such that it maintains 90 degrees of flexion at the elbow, 45 degrees of pronation in the forearm, and slight flexion in the wrist to keep the nerve in a position of minimal tension.

Postoperative Care Ten days postoperatively, the sutures are removed and replaced with Steri-strips. Immobilization in a long arm cast in the same position is continued for 2 additional weeks, after which all immobilization is discontinued. At this time, gentle range of motion exercises are started. The patient should be instructed to avoid resistive activities for 6 to 8 weeks after surgery. Although there are some individual variations, most patients with pronator syndrome surgery are back to full function within 3 months.

Alternative Methods of Management In general, the pronator syndrome can often be treated using protection (Fig. 13–3), rest, ice, compression, elevation, medications, and modalities. Protection entails modifying activity and equipment to allow proper healing and prevention of further injury. It is important to explain to the patient that rest does not mean cessation of

Figure 13–3. Long arm splint used in position of comfort. 73

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activity, but modifying activities that may further aggravate the injury. Ice is used to alleviate pain and help control swelling. Compression is used to prevent swelling, but it should be used with caution because if compression is not placed correctly, it could aggravate the nerve entrapments. Elevation is used to prevent venous stasis around the injury, which can lead to increased inflammation and pain. Medications used include nonsteroidal antiinflammatory drugs (NSAIDs) and corticosteroids, although very rarely. Modalities include ultrasound, electrical stimulation, and friction massage.

Complications There are few surgical complications reported. The medial antebrachial cutaneous nerve is at risk during exposure. The entire course of the nerve must be explored in the cubital region to inspect all possible sites of compression. Scars may become hypertropic or unsightly.

Suggested Readings Dawson DM. Entrapment neuropathies of the upper extremities. N Engl J Med 1993;329:2013–2018. Mysiew WJ, Colachie SC III. The pronator syndrome: an evaluation of dynamic maneuvers for improving electrodiagnoistic sensitivity. Am J Phys Med Rehabil 1991;70:274–277. Nuber GW, Assenmacher J, Bowen MK. Neurovascular problems in the forearm, wrist, and hand. Clin Sports Med 1998;17:585–610. Olehnik WK. Manske PR, Szerzinski J. Median nerve compression in the proximal forearm. J Hand Surg 1994;19A:121–126. Plancher KD, Peterson RK, Steichen JB. Compressive neuropathies and tendinopathies in the athletic elbow and wrist. Clin Sports Med 1996;15:331–371. Rehak DC. Pronator syndrome. Clin Sports Med 2001;20:531–540. Weinstein SM, Herring SA. Nerve problems and compartment syndromes in the hand, wrist, and forearm. Clin Sports Med 1992;11:161–188.

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ANTERIOR INTEROSSEOUS NERVE SYNDROME

14 Anterior Interosseous Nerve Syndrome Michael F. Bothwell and Kevin D. Plancher

History and Clinical Presentation A 28-year-old weight lifter presents with weakness in his ability to pinch over the last 6 months after having an interscalene block for shoulder surgery. He also reports an ache in his forearm but no other pain or numbness. The patient is an avid weight lifter but reports no specific trauma or previous history of problems in the same area.

Physical Examination When a patient is asked to pinch, active flexion of the distal interphalangeal (DIP) index is impossible (Fig. 14–1). There is an inability to flex the interphalangeal joint of the thumb and the distal phalangeal joint of the index finger secondary to weakness of the flexor pollicis longus (FPL) and the index flexor digitorum profundus (FDP), with weakness of the pronator quadratus. A positive Tinel’s test over the proximal forearm is also seen with pain radiating distally. The patient reports intermittent pain in the proximal portion of the volar forearm, with no atrophy or sensory changes. PEARLS • Accurate attempt at pinch by patient is crucial to diagnosis— “OK” sign tip to tip. • Weight lifters often have hypertrophy of the forearm muscles leading to this diagnosis. • Complete hemostasis is essential during surgery with tourniquet, but limit time to ensure speedy recovery.

PITFALLS • Inaccurate diagnosis can lead to unnecessary surgery. • Understanding anatomy in the forearm is crucial to successful recovery. • Position of the patient’s neck in shoulder surgery should be monitored by the anesthesiologist and surgeon.

Differential Diagnosis • • • • •

Isolated rupture of the flexor pollicis longus (FPL) Rupture of the index flexor digitorum profundus (FDP) Laceration of the nerve Tumor of the forearm Anterior interosseus nerve palsy

Figure 14–1. Typical pinch sign with flattening of index pulp and classic palsy of the anterior interosseous nerve with “ok” sign on left hand.

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Diagnostic Studies Electromyogram (EMG) will confirm the diagnosis of anterior interosseous nerve syndrome (AINS) in most cases if the test is focusing on the individual muscles, FPL/FDP index, and pronator quadratus. Nerve conduction tests are often normal. X-rays should also be taken to ensure there is no underlying cause or fracture.

Diagnosis Anterior Interosseous Nerve Palsy Kiloh and Nevin first described AINS in 1952. It is seen sporadically in athletes resulting from a violent muscle contracture from aggressive forearm exercises. Trauma and structural anomalies can also cause AINS. Isolated AINS also may be seen in acute brachial neuritis caused by sports or postanesthesia from an interscalene block. Anatomically, it is caused by the compression of the anterior interosseous branch of the median nerve by fibrous bands from the deep head of the pronator teres or flexor digitorum superficialis (FDS), anomalous vessels or muscles, flexor carpi radialis brevis, or palmaris profundus. Its origin is usually 5 cm below the level of the medial epicondyle. It travels through the forearm distally with the median nerve. It gives off a motor branch to the FPL. The anterior interosseous nerve exclusively innervates the FDP to the index finger, whereas the FDP to the middle finger is innervated by the anterior interosseous nerve 50% of the time, escaping paralysis. This syndrome has been reported in various types of athletes such as baseball pitchers, tennis players, gymnasts, weight lifters, and football players.

Nonsurgical Management Treatment of anterior interosseous nerve palsy should be based on the specific etiology. Conservative treatment consisting of ice, rest, and nonsteroidal antiinflammatory drugs (NSAIDs) should continue for 8 to 12 weeks before surgery becomes an option. Some authors have recommended continued nonsurgical treatment for longer periods of time up to 6 months. A postanesthetic acute brachial neuritis of the anterior interosseous nerve (AIN) should be given at least 4 months of conservative treatment before surgery becomes an option. There have been documented cases of return up to 18 months after onset. It has been noted that the return in such cases is often unpredictable, and there has not been total recovery.

Surgical Management Surgical decompression offers a more rapid recovery in most cases. If there is no clinical or EMG improvement in the 8- lumen, 12-week period after injury, surgical exploration should be undertaken. Surgical exploration consists of identifying the median nerve from the proximal forearm and following the AIN distally, identifying all its branches on the way (Fig. 14–2). The incision should start ~5 cm above the medial epicondyle. It extends distally over the medial flexor muscle mass (Fig. 14–3A). The median nerve is identified proximal medial to the brachial artery. It is followed distally to the superficial head of the pronator teres. The pronator teres is mobilized and separated from the flexor 76

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Figure 14–2. Incision to allow adequate exposure of median nerve.

carpi radialis, allowing exposure of the nerve. The nerve is exposed where it emerges from beneath the fibers of the flexor digitorum sublimis. The nerve is traced proximally by retracting the flexor carpi radialis laterally and pronator proximally and by separating the fibers of the flexor digitorum sublimis (Fig. 14–3B). The nerve is then exposed over its course. The AIN emerges from the posteromedial side of the nerve after passing through the two heads of the pronator teres and supplies the FPL, the

A

B

Figure 14–3. (A) Line drawing showing course of the anterior interosseous nerve (AIN). (B) Photograph of the AIN illustrating arch of the flexor digitorum superficialis prior to release. 77

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Figure 14–4. Anterior interosseous nerve with decompression in progress.

Figure 14–5. Complete release of the median nerve (AIN branch).

radial half of the flexor profundus, and the pronator quadratus (Fig. 14–4). In most cases, the median and anterior interosseous nerves pass through the superficial and deep heads of the pronator teres (Fig. 14–5). Postoperatively, a bulky dressing and long armed splint are applied, keeping the elbow in 90 degrees of flexion and the forearm in 45 degrees of pronation. These should remain on for 10 to 14 days. They are then changed and sutures are removed. Immobilization should continue with a custom splint for an additional 4 weeks, after which light range-of-motion exercises are started under the supervision of a hand therapist. Weight lifting may not resume until 6 months postoperative recovery.

Suggested Readings Butters KP, Singer KM. Nerve lesions of the arm and elbow. In: Deter JC, Drez DJ, eds. Orthopaedic Sports Medicine: Principles and Practice. Philadelphia: WB Saunders; 1994:802–870. Campion D. Electrodiagnostic testing in hand surgery. J Hand Surg 1996;21A: 947–956. Eversmann WW Jr. Entrapment and compression neuropathies. In: Green DP, ed. Operative Hand Surgery, 3rd ed. New York: Churchill Livingstone; 1993:1341–1385. Goodman CE. Unusual nerve injuries in recreational athletes. Am J Sports Med 1983;11:244–277. Long RR. Nerve anatomy and diagnostic principles. In: Pappas AM, ed. Upper Extremity Injuries in the Athlete. New York: Churchill Livingstone, 1995:53–54. Lubahn JD, Cermak MB. Uncommon nerve compression syndromes of the upper extremity. J Am Acad Orthop Surg 1998;6:378–386. Posner MA. Compressive neuropathies of the median and radial nerves at the elbow. Clin Sports Med 1990;9:343–363. Rennels GD, Ochoa J. Neuralgic amyotrophy manifesting as anterior interosseous nerve palsy. Muscle Nerve 1980;3:160–164. 78

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Schantz K, Riegels-Nielsen P. The anterior interosseous nerve syndrome. J Hand Surg 1992;17B:510–512. Spinner M. The anterior interosseous nerve syndrome with special attention to its variations. J Bone Joint Surg 1970;52A:87–94. Szabo RM, Gilberman RH. The pathophysiology of nerve entrapment syndromes. J Hand Surg 1987;12A:880–884. Weinstein SM, Herring SA. Nerve problems and compartment syndromes in the hand, wrist, and forearm. Clin Sports Med 1992;11:161–188. Whitaker JH, Richardson GA. Compressive neuropathies. In: Strickland JW, Rettig AC, eds. Hand Injuries in Athletes. Philadelphia: WB Saunders; 1992: 209–228.

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15 Cubital Tunnel Syndrome Eric Freeman, Dennis Rodin, and Kevin D. Plancher

History and Clinical Presentation A 46-year-old right hand dominant man presented with numbness and tingling down the ulnar aspect of his left forearm and hand. Increased activities exacerbated his complaints. The patient reported that his symptoms were worse upon awakening in the morning. He had no impairment in his activities of daily living.

Physical Examination

PEARLS • The “no touch” technique when handling the ulnar nerve minimizes the risk of iatrogenic injury to the nerve itself as well as to its branches and blood supply. • Avoid small incisions for adequate decompression.

PITFALLS • Failure to release potential sites of compression proximally (i.e., the medial intermuscular septum and arcade of Struthers) may result in recurrence of symptoms despite adequate decompression of the cubital tunnel. • Avoid injury to the MABC nerve to allow for normal sensation on posterior and inside 1⁄2 of elbow.

80

There was no apparent forearm or hypothenar wasting of the left upper extremity. Range of motion of the elbow was measured as 0 to 125 degrees bilaterally. Areas were then examined for tenderness or ulnar nerve subluxation. There was tenderness with deep palpation over the cubital tunnel. Tinel’s test was negative at the cubital tunnel, carpal tunnel, and Guyon’s canal. The patient was examined for abduction of the small finger with extension (Wartenberg’s sign), which was negative. Earle’s test was negative (Fig. 15–1). Grip strength measured 60 pounds on the left and 65 pounds on the right. Intrinsic motor strength was 5/5 bilaterally, and there was no evidence of claw hand. On sensory examination, the patient had paresthesias in the fifth digit and ulnar aspect of the fourth digit. Two-point discrimination was greater than 10 mm in the fifth digit and ulnar aspect of the fourth digit, and less than 6 mm in the first, second, and third digits.

Diagnostic Studies Anteroposterior and lateral radiographs of the left elbow showed no abnormalities. In patients with a history of trauma, a cubital tunnel projection radiograph can be performed to exclude osteophytes. Magnetic resonance imaging (MRI) can be helpful in the diagnosis, especially in patients who have undergone previous surgeries. If the diagnosis of cubital tunnel syndrome is not certain, electromyography (EMG) may be helpful in determining the diagnosis and appropriate care.

Figure 15–1. Ability to cross the index and long fingers tests the ulna nerve (small muscles of the hand).

C U B I TA L T U N N E L S Y N D R O M E

Differential Diagnoses Cervical spine arthrosis Cervical spine disk disease Syringomyelia Thoracic outlet syndrome Pancoast tumor Ulnar nerve entrapment in Guyon’s canal Cubital tunnel syndrome

Diagnosis Cubital Tunnel Syndrome The patient was diagnosed with ulnar nerve compression at the level of the cubital tunnel. Cubital tunnel syndrome is now being diagnosed with increasing frequency. Our understanding of the dynamic nature of the pathophysiology has allowed us to improve its management. After an appropriate history and physical examination are performed, the diagnosis of ulnar nerve compression can be made. Following the diagnosis, it is crucial to determine the level of the lesion. In addition to a thorough physical examination, electrodiagnostic studies can be of great assistance in obtaining the definitive diagnosis. For this patient, electrodiagnostic studies were performed following 6 weeks of conservative treatment with no resolution of symptoms. EMG and nerve conduction studies revealed compression of the ulnar nerve at the level of the cubital tunnel in a sensory distribution. The elbow flexion test is the most diagnostic test for cubital tunnel syndrome. The test involves the patient’s flexing the elbow past 90 degrees, supinating the forearm, and extending the wrist. Results are positive if discomfort is reproduced or paresthesia occurs within 60 seconds. The addition of shoulder abduction may enhance the diagnostic capacity of this test.

Nonsurgical Management Conservative treatment of cubital tunnel syndrome is often successful with complete resolution of symptoms. Symptoms can be reduced by avoiding the activities that contribute to the nerve compression. This may include avoiding elbow flexion and resting on the elbow. In this case, the patient was placed in a long arm splint with the elbow flexed at 45 degrees. The splint was worn at night for 6 weeks. Activity modification was also attempted without relief of symptoms. Oral antiinflammatories may also be helpful in alleviating symptoms. When nonoperative modalities have failed over a period of 4 to 6 months, there are various surgical options.

Surgical Management The patient was placed in the supine position on the operating table and the left upper extremity was prepped and draped in the usual sterile fashion. Intravenous antibiotics were given prophylactically. A sterile, well-padded tourniquet was then applied and inflated to 250 mm Hg following exsanguination. The intraoperative 81

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Triceps Biceps Brachialis

Flexor digitorum profundus

Arcade of Struthers Intermuscular septum Medial epicondyle

Osborne’s ligament

Flexor carpi ulnaris

Figure 15–2. Course of the ulnar nerve seen proximal to dorsal with the flexor carpi ulnaris (FCU) lifted.

incision is marked out carefully to avoid injury to the median antebrachial cutaneous branch (Figs. 15–2 and 15–3). An incision was made on the medial surface of the elbow beginning 10 cm proximal to the epicondyle and extending distally ~15 cm (Fig. 15–4). The subcutaneous tissue was sharply dissected until the two heads of the flexor carpi ulnaris were identified (Fig. 15–5). At this point, the arcuate ligament of Osborne may be visualized and divided, revealing the ulnar nerve in the cubital tunnel. To fully expose the ulnar nerve, the insertion of the flexor carpi ulnaris was dissected from the epicondyle. The articular and muscular branches (flexor carpi ulnaris, flexor digitorum profundus) are identified and carefully dissected. Vessel loops were placed around the ulnar nerve, which was removed from its bed and reflected anteriorly. The nerve is freed from the surrounding soft tissue in a “notouch” technique (Fig. 15–6A). The medial intermuscular septum is released proximally to the arcade of Struthers (Fig. 15–6B). A trough was then made 3 cm for the medial epicondyle in the flexor pronator mass. The ulnar nerve was placed within

A

B

Figure 15–3. (A) Points of compression needed to be released for successful decompression. (B) Surface anatomy including an excision to avoid injury to the MABC.

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A

B

Figure 15–4. (A) Patient with MABC exposed. (B) Ulnar nerve dissection with MABC nerve unharmed during the dissection.

Figure 15–5. The ulna nerve dividing the two heads of the FCU tendon.

A

B

Figure 15–6. (A) Intraoperative photo demonstrating the branch of the medial antebrachial cutaneous nerve. (B) The medial intermuscular septum is released proximally to the arcade of Struthers.

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A

B

C

Figure 15–7. (A) The intramuscular transposition of the ulnar nerve after trough, and complete medial intermuscular septum pronator release (proximal is to the right in this photo). (B) Intraoperative photo demonstrating the intermuscular transposition. (C) Intraoperative photo demonstrating the muscle fascia loosely re-approximated.

the trough (Fig. 15–7), and the overlying muscle fascia was loosely reapproximated (Fig. 15–7C). The elbow was taken through a range of motion, and no compression of the ulnar nerve was noted. The wound was copiously irrigated with warm normal saline. The tourniquet was deflated and meticulous hemostasis was obtained. The skin was closed and a sterile dressing was applied. The arm was splinted in a position of 45 degrees of elbow extension, full pronation, and 15 degrees of wrist flexion. The splint was used intermittently for a period of 6 weeks. At 2 weeks postoperatively, the patient began range-of-motion exercises, and at 6 weeks the patient was without complaints and symptoms. The patient was able to throw a softball 4 months following surgery. 84

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Table 15–1 Alternative Methods of Management Surgical Procedure

Advantages

Disadvantages

In situ decompression

High recurrence rate Increased incidence of ulnar nerve subluxation

Medial epicondylectomy

Minimal dissection and nerve disturbance Decreased length of post-operative immobilization Preservation of ulnar nerve blood supply

Subcutaneous transposition

Technically easy

Submuscular transposition

Increased protection of nerve

Elbow instability Flexor pronator weakness Medial antebrachial cutaneous neuroma Vulnerable to trauma More technically demanding

Alternative Methods of Management Alternative methods of management are in situ decompression, medial epicondylectomy, and anterior transposition of the ulnar nerve. Each method has advantages and disadvantages and none has been clearly shown to be superior to the others (Table 15–1). In situ decompression, described by Osborne in 1957, divides the flexor carpi ulnaris aponeurosis (ligament of Osborne), which decompresses the roof of the cubital tunnel. Medial epicondylectomy removes the floor of the cubital tunnel. This procedure consists of osteotomizing the epicondyle and reattaching the flexor pronator mass to the surrounding soft tissues. Various techniques of anterior transposition of the ulnar nerve have been described. In this procedure, the nerve is completely removed from the tunnel, thereby eliminating potential sites of compression. Subcutaneous transposition involves the creation of a sling in the subcutaneous tissues (Fig. 15–8). The ulnar nerve is removed from its bed and is protected within the sling. A second method of transposition consists of placing the nerve in an intramuscular trough of the flexor pronator mass. It is important that the fibrous septa of the musculature be removed to prevent adhesion formation. In a submuscular transposition, the ulnar nerve is positioned beneath the flexor pronator mass.

Figure 15–8. Successful subcutaneous transposition of the ulnar nerve.

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Complications Complications from surgical intervention of cubital tunnel syndrome vary according to the specific procedure performed. They generally include persistent symptomatology, elbow instability, medial antebrachial cutaneous neuroma, painful scar, and reflex sympathetic dystrophy. Recurrence of preoperative symptoms may be due to scarring or adhesion formation. This can occur both in in situ decompression and transposition of the ulnar nerve. In addition, failure to release all potential sites of compression will result in persistent symptoms. This most frequently occurs proximally at the arcade of Struthers and medial intermuscular septum.

Suggested Readings Amadio PC, Beckenbaugh RD. Entrapment of the ulnar nerve by the deep flexor pronator aponeurosis. J Hand Surg 1986;11A:83–87. Apefelberg DB, Larson SJ. Dynamic anatomy of the ulnar nerve at the elbow. J Plast Reconstr Surg 1973;51:76–79. Campbell WW, Pridgeon RM, Riaz G, et al. Variations in the anatomy of the ulnar nerve at the cubital tunnel: pitfalls in the diagnosis of ulnar neuropathy at the elbow. Muscle Nerve 1991;14:733–738. Dellon AL. Review of treatment results for ulnar nerve entrapment at the elbow. J Hand Surg 1989;14A:688–700. Dimond M, Lister G. Cubital tunnel syndrome treated by long-arm splintage. J Hand Surg 1985;10:432. Earle SA, Valstou C. Crossed-fingers and other tests of ulnar nerve motor function. J Hand Surg 1980;5:560–565. Eisen A, Dannon J. The mild cubital tunnel syndrome. Neurology 1974;24:608–613. Kincaid J, Phillips LH II, Daube JR. The evaluation of suspected ulnar neuropathy at the elbow. Arch Neurol 1986;43:44–47. Novak CB, Lee GW, Mackinnon SE, Lay L. Provocative testing for cubital tunnel syndrome. J Hand Surg 1994;19A:817–820. O’Driscoll S, Horii E, Carmichael SW, et al. The anatomy of the cubital tunnel and its relationship to ulnar neuropathy. Abstracts of American Society of Surgery of the Hand 45th annual meeting, 1990, edition 5503:3–11. Osborne GV. The surgical treatment of tardy ular neuritis. J Bone Joint Surg [Am] 1957;39B:782. Posner MA. Compressive ulna neuropathy at the elbow. JAAOS 1998;6:282–298. Spinner M, Kaplan EB. The relationship of the ulnar nerve to the medial intermuscular septum in the arm and its clinical significance. Hand 1976;8A:239–242. Sunderlund S. Nerve and Nerve Injuries. Baltimore: Williams & Wilkins; 1968:816–828. Wadsworth TG, Williams JR. Cubital tunnel external compression syndrome. Br Med J 1973;1:662,666. 86

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16 Ulnar Tunnel Syndrome Robert M. Szabo

History and Clinical Presentation A 59-year-old right hand dominant physician fell off a curb on the outstretched hand 14 months prior to this evaluation. At that time, he was treated for a fracture at the base of his right fifth metacarpal and a fracture of his left radial neck. He noticed paresthesias along the ulnar side of his right fifth finger and right-sided hand weakness. The patient is a non–insulin-dependent diabetic who suffered a subarachnoid hemorrhage complicated by uncontrolled seizures, for which he had a hippocampectomy and still takes carbamazepine (Tegretol). PEARLS • Routine release of the ulnar tunnel in patients with carpal tunnel syndrome and mild ulnar symptoms is not indicated; carpal tunnel release alone increases the volume of the ulnar tunnel and changes its shape from triangular to ovoid. • Anatomy in this area is quite variable, so always start dissection proximal to the wrist crease and proceed distally and anticipate anomalies. • Clawing of the small and ring fingers is seen much earlier with compression of the ulnar nerve at the wrist than at the elbow because of the intact flexor digitorum profundus innervation.

PITFALLS • Patients with coexisting polyneuropathy may benefit from ulnar tunnel release but should be warned that not all of their symptoms may resolve. • Do not cross the wrist crease with a perpendicular incision or a hypertrophic scar may form.

Physical Examination Point tenderness was noted over the hook of the hamate. There were no other areas of tenderness, signs of previous trauma, or any swelling, masses, or bruits. Sensibility testing with Semmes-Weinstein monofilaments revealed 3.61 in the little finger and ulnar half of the ring finger and 2.44 in the remainder of the hand. Two-point discrimination was 7 mm in the little finger and ulnar half of the ring finger and 6 mm in the remaining fingers. Light-touch perception was normal on the dorsal-ulnar aspect of the hand and wrist. Nerve percussion and Phalen’s tests were negative. Manual motor testing was 5/5 throughout except for 0/5 of the third palmar interosseous muscle and the first dorsal interosseous muscle, which was 2/5 with moderate atrophy present. Mild clawing of the ring and small fingers was present, as was a positive Froment-Jeanne sign. Wrist range of motion was symmetric except for flexion, which was 45 degrees on the right compared with 80 degrees on the left. Key pinch on the right was 0 lb compared with 7 lb on the left. Tip pinch was 2 lb on the right and 7 lb on the left. Grip strength at the second setting was 60 lb on the right and 65 lb on the left. The Adson’s, hyperabduction, military brace positioning, and 3-minute elevation, as well as the Allen’ test, were normal.

Diagnostic Studies Anteroposterior, lateral, and oblique radiographs and a carpal tunnel view of the right hand revealed no acute fractures, subluxations, or dislocations. A chest radiograph was normal. Computed tomography of the wrist revealed small bone fragments adjacent to the base of the fifth metacarpal predominantly along its palmar-radial aspect. The hook of the hamate appeared intact. In the presence of a normal Allen’s test, Doppler studies were not performed. Nerve conduction study results are shown in Table 16–1. 87

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Table 16–1 Nerve Conduction Studies Nerve Right Ulnar Motor Motor Motor Sensory Sensory

Segment

Latency (ms)

Amplitude (µV )

Distance (cm)

Conduction Velocity (m/s)

Wrist → below elbow Below elbow → above elbow Wrist → first dorsal interosseous Palm → wrist Wrist → fifth dorsal interosseous

3.1/7.3 7.3/10.1

11.7K/12.5K 13K

22.5 18

54 64

3.6

0.6K*

14.5

2.6 No response*

5.0K*

10

*Indicates abnormal value.

Electromyographic Study Results There was no evidence of abnormal spontaneous activity in the right flexor digitorum profundus, abductor digiti minimi, or the abductor pollicis brevis. In the right first dorsal interosseous muscle there was increased insertional activity with 2+ (present at multiple sites) fibrillations and 2+ positive sharp waves; recruitment frequency was 30 to 40 Hz (normal: 5 to 15 Hz); the interference pattern was decreased and discrete, indicating marked loss of motor units; amplitude was decreased with the first recruitment = 1000 µV and the duration of the voluntary motor unit potentials was increased.

Differential Diagnosis Brachial plexus injury Upper plexus Lower plexus Cervical root compression Ulna nerve tunnel compression Elbow Wrist Corvical disk disease The ulnar nerve, containing fibers from the ventral rami of C8 and T1, is the terminal branch of the medial cord of the brachial plexus. Pathologic compression of the ulnar nerve occurs most commonly either at the elbow (cubital tunnel syndrome) or at the wrist where the ulnar nerve passes through the confines of the canal of Guyon (ulnar tunnel syndrome). With either of these conditions the patient may present with numbness along the little finger and ulnar half of the ring finger, often accompanied by weakness of grip, particularly in activities in which torque is applied to a tool, and rarely by wasting of the intrinsic musculature in the hand. The site of the compression may be determined by a careful physical examination; pain at the medial aspect of the elbow, a positive percussion test at the cubital tunnel, or exacerbation of symptoms by full flexion of the elbow suggests cubital tunnel syndrome. Sensory involvement on the ulnar dorsal aspect of the hand also suggests cubital tunnel syndrome, as the dorsal cutaneous branch of the ulnar nerve originates proximal to the canal of Guyon. Weakness of the deep flexors to the ring and 88

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little fingers as well as weakness of the flexor carpi ulnaris signal proximal ulnar nerve entrapment. Grip and pinch strength measurements may demonstrate weakness in more advanced lesions. Examination of the patient with symptoms of ulnar nerve compression should begin at the neck to rule out cervical disk disease or arthritis. Provocative maneuvers including Adson’s, hyperabduction, military brace positioning, and 3-minute elevation should be used to screen for thoracic outlet syndrome. Range of motion of the elbow should be observed and the ulnar nerve palpated during flexion-extension to determine subluxation. Percussion over the ulnar nerve can be performed to evoke a positive Tinel’s sign; however, nearly 24% of asymptomatic people have this finding. The elbow flexion test in cubital tunnel syndrome is analogous to the wrist flexion test (Phalen’s test) in diagnosing carpal tunnel syndrome. It is performed by maximally flexing the patient’s elbow with forearm supination and wrist extension. Symptoms of paresthesias in the ulnar nerve distribution within 1 minute constitute a positive test. False positives, however, occur in 24% of the normal population. Sensory examination of the hand including the dorsum should be performed using Semmes-Weinstein monofilaments. Sensibility testing is an important part of the workup of a patient with an ulnar nerve compression lesion. Much of the misunderstanding over which test is better at detecting an abnormality has been cleared up with our understanding the fundamental nature of what each test is measuring. Four sensory tests are available which test different fiber populations and receptor systems. Touch fibers, group A␤, can be divided into slowly and quickly adapting fiber systems. A quickly adapting fiber signals an on-off event, and a slowly adapting fiber continues its pulse response throughout the duration of the stimulus. Static twopoint discrimination and Semmes-Weinstein monofilament tests evaluate the slowly adapting fibers, whereas vibration and moving two-point discrimination tests evaluate the quickly adapting fibers. Each fiber system is associated with a specific sensory receptor. Each clinical test of sensibility is related to a receptor group and is classified as either a threshold test or a test of innervation density. A threshold test measures a single nerve fiber innervating a receptor or group of receptors. An innervation density test measures multiple overlapping peripheral receptive fields and the density of innervation in the region being tested. Static and moving two-point discrimination are innervation density tests, which require overlapping of different sensory units and complex cortical integration. These are reliable tests in assessing functional nerve regeneration after nerve repair where brain input is radically altered but are not sensitive to the gradual decrease in nerve function seen in nerve compression. Cortical organization is intact in compression neuropathy, as the integrity of the sensory relay system remains uninterrupted. Two-point discrimination may remain intact even if only a few fibers are conducting normally to their correct cortical end points. Semmes-Weinstein monofilament and vibration tests are threshold tests and are more likely to detect a gradual, progressive change in nerve function as a greater proportion of large nerve fibers are lost whereas smaller fibers maintain their normal central connections. Clinically, threshold tests are clearly more sensitive in evaluating compressive neuropathies. At present, Semmes-Weinstein monofilament testing is simpler, less expensive, and equally as reliable and sensitive as vibration testing. The value of nerve conduction studies is that often they provide the only objective evidence of the neuropathic condition. Electrodiagnostic testing remains the diagnostic gold standard, yet it entails several pitfalls. It is highly operator dependent, and so should be done with the same equipment and operator each time. Nerve conduction velocities and latencies can be compared with published popula89

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tion norms, to the contralateral nerve, to other nerves in the same extremity, or to previous tests in the same patient. Systemic conditions (including age-dependent alterations in nerve conduction) may confound the comparisons. Decreased dorsal ulnar sensation can help localize a lesion to be proximal to the wrist. Motor examination should carefully grade the flexor carpi ulnaris, flexor digitorum profundus, little and ring fingers, and the intrinsic muscles of the hand. One must keep in mind that median nerve fibers may supply some of the intrinsic hand muscles in 7.5% of limbs via a Martin-Gruber anastomosis. Electrodiagnosis is helpful in establishing the diagnosis of cubital tunnel syndrome, localizing the level of the lesion, and differentiating other or concomitant neuropathic lesions. The classic finding is focal slowing of conduction in the ulnar nerve segment that crosses the elbow. The lower limit of normal motor conduction velocity across the elbow is 49 m/second, with the elbow flexed to 135 degrees, and the across-elbow segment normally has a conduction velocity within 11 m/second of the forearm segment. Short segment stimulation studies can increase the sensitivity of the exam and be highly specific in identifying the precise point of conduction block; however, they are prone to error in velocity calculations. A latency change greater than 0.4 millisecond (ms) over a 1-cm segment of nerve is considered abnormal. Electromyography demonstrates whether or not axonal degeneration has occurred. The first dorsal interosseous muscle is affected most commonly. The abductor pollicis brevis should be examined to exclude a C8/T1 nerve root or inferior brachial plexus lesion. Thoracic outlet syndrome most commonly involves the medial components of the brachial plexus and may be mistaken for ulnar nerve compression. Plain radiographs in two orthogonal planes should be obtained to rule out posttraumatic deformity, neoplasm, cervical ribs, or other possible bony causes of the nerve condition. A carpal tunnel view can sometimes show a hook of the hamate fracture, but often computed tomography is needed to visualize this injury. Magnetic resonance imaging (MRI) has a specific role in the workup of this condition. For instance, MRI can be extremely helpful in assessing the extent of a soft tissue mass like a ganglion causing ulnar tunnel syndrome. An apical tumor of the lung can also compress or invade the inferior brachial plexus, causing ulnar nerve symptoms. A chest x-ray to rule out a Pancoast tumor should be obtained whenever the patient gives a history of smoking, ulnar nerve symptoms, and shoulder pain.

Diagnosis In 1861 Guyon, a French urologist, described a “loge” or a space in the hypothenar region of the wrist where the ulnar nerve bifurcates, and he prophesied compression of the ulnar nerve could be found here. Written in French, his word loge was subsequently translated to mean “canal,” and thus originated the name for the anatomic region we now call Guyon’s canal. Entrapment at this level may present with pure motor, sensory, or mixed symptoms depending on the precise location of compression. Space-occupying bony or soft tissue lesions may be causative; ganglia and other soft tissue masses are responsible for 32% to 48% of cases of ulnar tunnel syndrome. Another 16% of cases are due to muscle anomalies. Ganglia arising from the triquetrohamate joint are responsible for over 85% of the nontraumatic causes of ulnar tunnel syndrome. Other causes of ulnar tunnel syndrome include thrombosis or pseudoaneurysms of the ulnar artery, edema secondary to burns, and inflammatory arthritis. The distal ulnar tunnel, which is 4 to 4.5 cm in length beginning at the proximal edge of the palmar carpal ligament and ending at the fibrous arch of the hypothenar 90

ULNAR TUNNEL SYNDROME

Figure 16–1. Schematic drawing of the distal ulnar tunnel showing the location of the three zones. Zone 1 (coarse stippling), zone 2 (lines), zone 3 (fine stippling). P, pisiform; H, hamulus; A, ulnar artery; N, ulnar nerve. (With permission from Gross MS, Gelberman RH. The anatomy of the distal ulnar tunnel. Clin Orthop 1985;196:238–247.)

muscles, is divided into three zones to allow more accurate localization of ulnar nerve compressive lesions (Fig. 16–1). Zone 1 is the area proximal to the bifurcation of the nerve. Beginning at the edge of the palmar carpal ligament, it is ~3 cm in length, bounded dorsally by the flexor digitorum profundus and transverse carpal ligament, palmarly and laterally by the palmar carpal ligament, and medially by the pisiform and flexor carpi ulnaris. Compression in zone 1 causes combined motor and sensory deficits and is most likely due to ganglions or fractures of the hook of the hamate but has been reported to occur from an anomalous muscle. Even though the hook of the hamate is in zone 2, compression of the ulnar nerve by fracture just proximal to its bifurcation can produce mixed motor and sensory symptoms. Compression in this zone has also been reported to occur from an anomalous arching pattern of the ulnar nerve piercing the flexor carpi ulnaris tendon. Zones 2 and 3 travel alongside each other from the bifurcation of the ulnar nerve to just beyond the fibrous arch of the hypothenar muscles. Although bifurcation is the most common pattern, the ulnar nerve may trifurcate at this point into two common digital sensory branches and a motor branch. Zone 2 is bounded palmarly by the palmaris brevis muscle, fibrous arch, and hypothenar muscles; dorsally by the pisohamate and pisometacarpal ligaments, triquetrohamate joint, and opponens digiti minimi muscle; laterally by the transverse carpal ligament, flexor digiti minimi muscle, and the hook of the hamate; and medially by the superficial branch of the ulnar nerve and the abductor digiti minimi muscle. Zone 2 surrounds the deep motor branch, and compression in this region produces motor deficits without sensory disturbances. Again, ganglions and fractures of the hook of the hamate are the most likely causes, but an anomalous intrinsic muscle can also be responsible for symptoms. 91

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The motor branch leaves the tunnel, passing underneath the fibrous arch of the hypothenar muscles, entering the interval between the abductor digiti minimi and flexor digiti minimi muscles, piercing the opponens digiti minimi, and then curving radially and dorsally around the hook of the hamate. Zone 3 is bounded palmarly by the palmaris brevis muscle and ulnar artery; dorsally by the hypothenar fascia; laterally by the motor branch of the ulnar nerve; and medially by the abductor digiti minimi muscle. Zone 3 surrounds the superficial branch of the ulnar nerve, and compression in this zone produces pure sensory deficits. Synovial inflammation has been reported to cause compression in zone 3. More frequently, however, compression in zone 3 is due to a vascular lesion resulting from thrombosis or aneurysm of the ulnar artery, but an anomalous abductor digiti minimi, which has an incidence of 1.5%, can also be responsible. Just distal to the ulnar nerve bifurcation, the superficial branch gives off two small motor branches to the palmaris brevis muscle and then becomes purely sensory coursing deep and ulnar to the artery. The clinical characteristics of nerve compression in the ulnar tunnel can largely be correlated with the distinct regional anatomy in this area of the wrist. Symptoms include pain in the wrist with numbness, tingling, or burning, with radiation into the ring and little fingers. Pain is usually a less significant aspect of the presentation than in carpal tunnel syndrome. Sustained hyperextension or hyperflexion of the wrist accentuates symptoms. Intrinsic weakness, which occurs, progresses to atrophy in the hand if compression is not relieved. The diagnosis of an ulnar tunnel syndrome consists of first demonstrating the presence of an ulnar nerve lesion at the wrist and then determining the underlying cause. Although the cause may be purely mechanical, it may be potentiated by a coexisting systemic disorder like diabetes or a more proximal lesion of the same nerve (double crush phenomenon). It is important not to develop “tunnel” vision early in the diagnostic process, but rather to consider the possibility of additional places where the nerve may be compressed.

Nonsurgical Management In the absence of an identifiable lesion, alterations of repetitive activities, splint immobilization of the wrist in neutral, and nonsteroidal antiinflammatory drugs (NSAIDs) may alleviate symptoms.

Surgical Management Operative intervention is recommended for those patients refractory to conservative care or with documented anatomic lesions. Regardless of the suspected site of compression, the ulnar nerve should be visualized and released in its entirety within Guyon’s canal. Acute ulnar neuropathy following a wrist fracture is unusual but warrants special concern. This injury is seen in young patients with high-energy distal radius fractures with marked dorsal displacement of the distal fragment. Based on clinical and anatomic studies, Vance and Gelberman recommended that any patient with immediate complete ulnar neuropathy following a wrist fracture should undergo immediate fracture reduction, with particular attention to eliminating dorsal displacement of the radial and/or ulnar fracture(s). If ulnar nerve function does not improve in 24 to 36 hours, Guyon’s canal should be explored and the ulnar 92

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nerve decompressed. Any patient with progressive ulnar neuropathy after treatment for a wrist fracture should have immediate exploration and decompression of the ulnar nerve. Regardless of the expected pathology, the ulnar nerve should be explored proximally from the distal forearm into the palm throughout all three zones. Some surgeons routinely release the carpal canal when decompressing Guyon’s canal and perform this operation via an extended carpal tunnel incision. Regional or general anesthesia is used as is a tourniquet. A consideration in planning the skin incision is the anatomy of the palmar cutaneous branch of the ulnar nerve. According to Engber, the classic position for this nerve is ulnar to the ring finger ray. Although only found to be present in 5 of 21 cadaver dissections, injury to it may lead to painful neuromas. Although it is widely believed that there exists an internervous plane in the palm in the axis of the ring finger between the palmar cutaneous branches of the median and ulnar nerves, more careful dissections have demonstrated that this area in the palm is variably innervated by the nerve of Henle (the nervi vasorum of the ulnar artery) and multiple ulnar cutaneous branches. Dissection in the palm should avoid these small cutaneous nerves whose injury may lead to persistent incisional tenderness. The pisiform and hook of the hamate, which is 1 cm distal and radial to the pisiform, are used as anatomic landmarks. The incision begins 3 cm proximal to the wrist along the radial border of the flexor carpi ulnaris tendon, crosses the wrist crease at an angle of 60 degrees, with the apex radial, continues distally bisecting the interval between the pisiform and the hamate directed toward the web space between the little and ring fingers, and then is angled across the palm proximal and parallel to the proximal transverse palmar crease (Fig. 16–2). In the proximal incision, the flexor carpi ulnaris is reflected ulnarly and the ulnar nerve is identified dorsal and medial to the ulnar artery and tagged with a small rubber drain. Blunt dissection of the subcutaneous fat safeguards the palmar cutaneous branch of the ulnar nerve. The forearm and palmar fascia are divided in line with the skin incision. The ulnar nerve is traced distally into Guyon’s canal between the

Figure 16–2. Incision for exploring Guyon’s canal. 93

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Superficial branch of ulnar nerve

Hamate Deep branch of ulnar nerve

Pisohamate ligament Volar carpal ligament

Pisiform

FCU Ulnar artery

Figure 16–3. The ulnar nerve courses through Guyon’s canal between the volar carpal ligament and the transverse carpal ligament. P, pisiform; H, hamate. (With permission from: Szabo RM. Entrapment and compression neuropathies. In: Green DP, ed. Operative Hand Surgery. 4th ed. New York: Churchill Livingstone; 1999:1431.)

volar carpal ligament and the transverse carpal ligament (Fig. 16–3). The palmaris brevis muscle is elevated ulnarly and the volar carpal and pisohamate ligaments are incised. The fibrous origin of the hypothenar muscles often forms a thick arch just distal to the pisohamate ligament inserting on the hamate that should be incised. The motor branch is traced underneath the fibrous arch between the abductor digiti minimi and flexor digiti minimi and through the opponens digiti minimi. The floor of Guyon’s canal is explored looking for masses, fibrous bands, anomalous muscles, fractures particularly of the hook of the hamate, and any other unusual pathology. The ulnar artery is examined, the tourniquet is deflated, the ulnar artery is reexamined, and hemostasis is obtained. The skin is approximated and a bulky plaster reinforced hand dressing applied with the wrist in slight dorsiflexion. Sutures are removed in 10 days and splinting is continued in 20-degree wrist dorsiflexion for an additional 2 weeks. Tenderness may persist in the palm, particularly if the hook of the hamate was excised. A gel-padded sleeve to protect the palm along with scar massage and desensitization therapy is often appreciated. Sensibility and motor function will return depending on the severity and length of time of compression.

Suggested Readings Campbell WW, Pridgeon RM, Sahni KS. Short segment incremental studies in the evaluation of ulnar neuropathy at the elbow. Muscle Nerve 1992;15:1050–1054. Denman EE. The anatomy of the space of Guyon. Hand 1978;10:69–76. Engber WD, Gmeiner JG. Palmar cutaneous branch of the ulnar nerve. J Hand Surg 1980;5A:26–29. Fahrer M, Millroy PJ. Ulnar nerve compression neuropathy due to an anomalous abductor digiti minimi—clinical and anatomic study. J Hand Surg 1981;6A:266–268. 94

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Failla JM. The hypothenar adductor muscle: an anomalous intrinsic muscle compressing the ulnar nerve. J Hand Surg 1996;21A:366–368. Gelberman RG. Ulnar tunnel syndrome. In: Gelberman RH, ed. Operative Nerve Repair and Reconstruction. Philadelphia: Lippincott; 1991:1131–1143. Gross MS, Gelberman RH. The anatomy of the distal ulnar tunnel. Clin Orthop 1985;196:238–247. Guyon F. Note sur une disposition anatomique propre à la face antérieure de la région du poignet et non encore décrite par le docteur. Bull Soc Anat Paris 1861;6:184–186. Hilburn JW. General principles and use of electrodiagnostic studies in carpal and cubital tunnel syndromes. Hand Clin 1996;12:205–221. Kang HJ, Yoo JH, Kang ES. Ulnar nerve compression syndrome due to an anomalous arch of the ulnar nerve piercing the flexor carpi ulnaris: a case report. J Hand Surg 1996;21A:277–278. Kleinert HE, Hayes JE. The ulnar tunnel syndrome. Plast Reconstr Surg 1971;47: 21–24. Lindsey JT, Watumull D. Anatomic study of the ulnar nerve and related vascular anatomy at Guyon’s canal: a practical classification system. J Hand Surg 1996;21A: 626–633. Rayan GM, Jensen C, Duke J. Elbow flexion test in the normal population. J Hand Surg 1992;17A:86–89. Shea JD, McClain EJ. Ulnar-nerve compression syndromes at and below the wrist. J Bone Joint Surg 1969;51A:1095–1103. Szabo RM, Gelberman RH. Peripheral nerve compression. Etiology, critical pressure threshold, and clinical assessment. Orthopedics 1984;7:1461–1466. Szabo RM, Gelberman RH. The pathophysiology of nerve entrapment syndromes. J Hand Surg 1987;12A:880–884. Szabo RM, Gelberman RH, Dellon AL, Yaru NC, Dimick MP. Vibratory sensory testing in acute peripheral nerve compression. J Hand Surg 1984;9A:l04–109. Taleisnik J, Szabo RM. Compression neuropathies of the upper extremity. In: Chapman MW, Madison M, eds. Operative Orthopaedics. Philadelphia: Lippincott; 1993:1419–1435. Thomson A. Third annual report on the Committee of Collective Investigation of the Anatomical Society of Great Britain and Ireland for the year 1891–1892. J Anat Physiol 1893;27:183. Vance RM, Gelberman RH. Acute ulnar neuropathy with fractures at the wrist. J Bone Joint Surg 1978;60A:962–965.

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17 Posterior Interosseous Syndrome William B. Geissler

History and Clinical Presentation A 52-year-old right hand dominant carpenter and avid golfer presented with complaints of pain well localized to the right extensor muscle mass just distal to the elbow joint that had persisted for 6 months. He describes the pain as aching in character with burning that radiates along the anatomic course of the forearm extensor muscles. He has noticed a slowly enlarging mass over the dorsal proximal forearm and complains of weakness in grip strength and diminished endurance. He has no complaints of sensory loss to the hand or forearm. He denies any history of trauma.

Physical Examination

PEARLS • Brachioradialis splitting approach provides excellent easy exposure to the radial tunnel for decompression. • Easier to identify nerve proximally and trace out distally • Consider posterior approach for mass compressing distal aspect of radial tunnel.

PITFALLS • Beware of cervical radiculopathy presenting as posterior interosseous syndrome. No sensory symptoms in posterior interosseous syndrome. • Beware tendon rupture in rheumatoid patients presenting as posterior interosseous nerve syndrome. Treatment is entirely different. • Revisions usually secondary to incomplete release of nerve through supinator. Compression of posterior interosseous nerve has been reported at distal edge of supinator. 96

The right forearm measured 2 cm larger than the left in circumference and measured 5 cm distal to the lateral epicondyle. A palpable mass was noted over the dorsal proximal forearm, and the patient was tender to palpation over the radial nerve as it passed through the mobile muscle mass at and just distal to the radial head. Slight tenderness to palpation was noted over the same area to the left forearm but not as severe. Palpation directly over the lateral epicondyle caused mild discomfort, less severe than over the course of the nerve. Full passive flexion of the wrist and fingers with the elbow in extension reproduced the pain. Resisted supination with the extended arm similarly reproduced the pain symptoms. Radial deviation was observed with wrist extension. The patient was able to fully extend the interphalangeal joints, but he could not fully extend the metacarpophalangeal joints beyond 45 degrees.

Diagnostic Studies Anteroposterior, lateral, and oblique radiographs of the right elbow did not show any bony abnormalities. An abnormal soft tissue shadow was noted on the lateral radiograph dorsally. Magnetic resonance imaging of the proximal forearm revealed

Figure 17–1. Magnetic resonance image demonstrating a large lipoma overlying the proximal radius. Note the distended supinator muscle.

POSTERIOR INTEROSSEOUS SYNDROME

a mass consistent with a lipoma involving the supinator muscle (Fig. 17–1). Electromyographic and nerve conduction studies of the bilateral upper extremities demonstrated denervation of the extensor digitorum communis and extensor carpi ulnaris. The abductor pollicis longus and extensors pollicis longus and brevis were spared.

Differential Diagnosis Radial tunnel syndrome Cervical radiculopathy Lead poisoning Systemic connective tissue disease Hysterical wrist drop Posterior interosseous syndrome

Diagnosis Posterior Interosseous Syndrome Radial tunnel syndrome involves compression of the posterior interosseous nerve branch of the radial nerve. Radial tunnel syndrome is defined when there is an absence of muscular involvement and the diagnosis of posterior interosseous syndrome is defined when there is muscular weakness and atrophy in the efferent distribution. The posterior interosseous nerve is not a purely motor nerve. It carries gamma-afferent fibers from the muscles it innervates. This can be demonstrated by the discomfort experienced by squeezing any muscle belly. The posterior interosseous nerve also supplies sensory afferent fibers to the radiocarpal, intercarpal, and carpometacarpal joints. Patients describe an aching, burning discomfort in the mobile extensor wad musculature, which may radiate distally down the forearm. The radial nerve rises from the posterior cord of the brachial plexus. About 4 cm proximal or distal to the radiocapitellar joint, the radial nerve divides into two large terminal branches: the radial sensory and posterior interosseous nerves. Anatomic compressive factors in posterior interosseous syndrome include the fibrous bands from the anterior capsule, origin of the extensor carpi radialis brevis, radial recurrent leash of vessels, and the arcade of Frohse. These structures compress the nerve in elbow extension, passive forearm pronation with wrist flexion, and resisted supination. Active forearm supination has been reported to produce five times greater pressure than passive forearm pronation. Unlike radial tunnel syndrome, many causes of posterior interosseous nerve syndrome other than purely anatomic have been described. Trauma primarily resulting in radial head fracture or dislocation may result in palsy of the posterior interosseous nerve. Any space-occupying lesions may compress or injure the nerve in the radial tunnel. Ganglions, lipomas, and fibromas have all been reported to compress the posterior interosseous nerve with resulting muscle weakness. Magnetic resonance imaging may be helpful if a mass is suspected. The posterior interosseous nerve may become compressed in patients with rheumatoid arthritis secondary to inflammation or subluxation of the radial head. This can be differentiated by the tenodesis effect by flexion and extension of the wrist. Pain is frequently the primary initial complaint followed by muscle weakness or paralysis, which may develop over a period of several weeks. Occasionally, weakness 97

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may occur dramatically overnight following unaccustomed exercise. The sequence of muscular involvement follows no set pattern. Patients with motor involvement may notice weakness and radial deviation with wrist extension. This is because the radial nerve proximal to the radial tunnel innervates the extensor carpi radialis longus and brevis. Patients maintain the ability to extend the interphalangeal joints of the fingers, but may be unable to extend the metacarpophalangeal joints beyond 45 degrees. Partial paralysis may result in the loss of extension of the small and ring fingers alone, producing the false appearance of an ulnar claw hand. However, the metacarpophalangeal joints would not be hyperextended and the ulnar nerve intrinsic musculature would be intact. Thumb extension may or may not be involved. There is no sensory loss.

Differential Diagnosis Other conditions that must be differentiated from posterior interosseous nerve syndrome include cervical radiculopathy, inflammatory arthritis, lead poisoning, and hysterical wrist drop. Radial tunnel syndrome is defined when there is lack of motor involvement. Examination of the elbow should always include an evaluation of the cervical spine. A Spurling’s maneuver is helpful to evaluate for cervical radiculopathy along with a thorough neurologic examination. Cervical radiographs should be performed if there is any question of cervical involvement. Patients with cervical pathology also usually present with sensory symptoms. Patients with rheumatoid arthritis may present with sudden loss of metacarpophalangeal extension secondary to acute extensor tendon rupture or posterior interosseous nerve palsy. Patients with posterior interosseous nerve palsy may be differentiated from ruptured extensor tendons by examining the tenodesis effect of wrist flexion-extension. The metacarpophalangeal joints extend with wrist flexion if the extensor tendons are intact, suggesting that the lack of extension is secondary to posterior interosseous nerve palsy. Electromyographic studies also are helpful in this situation. Lead poisoning may produce a high radial nerve palsy without sensory loss. Patients would then present with involvement of the brachioradialis and radial wrist extensors. Lead poisoning is further confirmed by classical gingival discoloration and by blood and urine studies. Hysterical wrist drop presents with inability to extend both the interphalangeal and metacarpophalangeal joints (Table 17–1). Table 17–1 Diagnosis and Differentiating Findings Diagnosis

Differentiating Findings

Radial tunnel syndrome Cervical radiculopathy

No motor involvement Spurling’s maneuver Distal sensory complaints Altered reflexes Abnormal cervical radiograph Positive rheumatoid factor Wrist tenodesis effect High radial nerve palsy Weak radial wrist extensors Positive blood/urine studies Inability to extend interphalangeal joints with metacarpophalangeal joints in flexion

Rheumatoid arthritis Lead poisoning Hysterical wrist drop

98

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Nonsurgical Management Nonsurgical management of posterior interosseous syndrome includes rest, splinting, and activity modifications. Oral antiinflammatory agents may be helpful, primarily for pain relief. Corticosteroid injections generally have minimal benefit because the neuropathology is compression, not active synovitis. Job or avocation changes may be of some benefit. Appropriate splintage should be provided if muscle paralysis is present. It is extremely important to emphasize full passive range-of-motion exercises to the involved joints in cases of muscle paralysis to prevent contracture. Patients with acute motor weakness without evidence of a mass may demonstrate spontaneous recovery.

Surgical Management Indications for surgical management include clinical or electrophysiologic denervation without change or improvement over 60 to 90 days. Patients with a confirmed mass compressing the radial tunnel should be considered primarily for surgical management. A symptomatic radial tunnel that progresses to extensor motor paralysis is an indication for operative decompression. The radial tunnel may be decompressed through one of three approaches— brachioradialis-splitting, anterior, and dorsal—which have all been described to release the radial tunnel. The brachioradialis-splitting approach provides excellent exposure to the entire radial tunnel and is easy to perform. The dorsal approach may be utilized particularly when a mass is present involving primarily the supinator muscle.

Brachioradialis-Splitting Approach A 6-cm curved or straight incision is made over the mobile wad starting at the level of the cubital fossa and extending distally. Dissection is bluntly taken down to the fascia to protect the cutaneous nerves. The brachioradialis is then bluntly split, aiming toward the radial head. Blunt dissection and retraction with a blunt retractor reveal the radial nerve within a fibrofatty layer. Dissection proximally demonstrates the radial nerve as it divides into the posterior interosseous and the sensory nerve branches. The fibrous bands are released over the radial nerve. Bipolar electrocautery is necessary to release the leash of recurrent radial vessels. The posterior interosseous nerve is then traced as it passes under the proximal edge of the extensor carpi radialis brevis. Occasionally, the nerve gives off motor branches to the muscle at this location, and these need to be protected. The proximal edge of the supinator (Arcade of Frohse) is then identified. Care must be taken to identify the proximal edge of both the extensor carpi radialis brevis and the supinator. It is easy to release only the extensor carpi radialis brevis, thinking this was the supinator. The supinator should be released throughout its entire length in posterior interosseous syndrome. Meticulous hemostasis is mandatory before closure.

Posterior Approach The posterior approach is useful when a mass is present in the supinator causing muscle paralysis, as more distal decompression of the nerve is easier from this 99

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Figure 17–2. Exposure of the radial tunnel by the dorsal approach. The surgical dissector points to the posterior interosseous nerve as it is tented over the lipoma involving the supinator muscle.

Figure 17–3. Photograph of the lipoma following excision.

approach. A 6-cm incision is made over the dorsal proximal forearm parallel with an imaginary line extending from the lateral epicondyle to Lister’s tubercle. The interval between the extensor carpi radialis brevis and extensor digitorum communis is developed. This interval is easier to develop distally than proximally. The posterior interosseous nerve is identified as it exits distally through the supinator and is traced proximally (Figs. 17–2 and 17–3).

Anterior Approach The anterior approach leaves a large unsightly scar. Although identification of the radial nerve is easy proximally through this approach, it becomes more difficult to fully release the posterior interosseous nerve distally. Care must be taken not to injure the lateral antebrachial cutaneous nerve. This approach is rarely used for radial tunnel decompression. Postoperatively, the wrist and elbow are supported in a sugar-tong–type splint for 1 week. The patient is then placed in a wrist support splint and range-ofmotion exercises are initiated. Resistive exercises are started at 6 weeks and are progressed.

Suggested Readings Derkash RS, Niebauer JJ. Entrapment of the posterior interosseous nerve by a fibrous band in the dorsal edge of the supranator muscle and erosion of a groove in the proximal radius. J Hand Surg 1981;6A:524–526. Eaton CJ, Lister GD. Radial nerve compression. Hand Clin 1992;8:345–357. Fardin P, Negrin P, Sparta S, et al. Posterior interosseous nerve neuropathy—clinical and electromyographical aspects. Electromyogr Clin Neurophysiol 1992;32:229–234. Lister GD, Belsole RB, Kleinert HE. The radial tunnel syndrome. J Hand Surg 1979;4:52–59. 100

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Marshall SC, Murray WR. Deep radial nerve palsy associated with rheumatoid arthritis. Clin Orthop 1974;103:157–162. Ogino T, Minami A, Kato H. Diagnosis of radial nerve palsy caused by ganglion with use of different imaging techniques. J Hand Surg 1991;16A:230–235. Spinner M. The arcade of Frohse and its relationship to posterior interosseous nerve paralysis. J Bone Joint Surg 1968;50B:809–812.

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18 Cervical Root Compression Bradley M. Thomas, John M. Olsewski, and Jerry G. Kaplan

History and Clinical Presentation A 49-year-old right hand dominant electrician presented with complaints of progressive weakness in his right arm. He also described having pain in his neck extending down the front of his arm to his hand. He was having difficulty lifting objects with his right hand and performing repetitive-type motions, with weakness of his right shoulder and biceps. He reported occasional numbness in his thumb and index finger while at work. He did not recall any trauma to his neck or arm. He denied bowel or bladder dysfunction, and was not experiencing disturbances in his gait. On further questioning he denied any history of smoking, diabetes, or hypertension. He also denied night pain. PEARLS • Spurling’s maneuver reproduces a patient’s arm pain and paresthesias by turning the patient’s head toward the symptomatic side and extending the neck. This position decreases the size of the neuroforamina. • Use an EMG to differentiate first-degree shoulder problems from a C5 root problem. • Biceps weakness may be the first sign of rotator cuff disease, although a herniated C6 root can give similar findings.

PITFALLS • Patients with sensory changes in the thumb and index finger may have carpal tunnel syndrome and not a C6 radiculopathy. • Check for a local Tinel’s and Phalen’s sign. • An incomplete cervical spine exam in a patient with upper extremity problems often leads to an incorrect diagnosis. • A full cervical spine x-ray series should be used to see on oblique films encroachment on the foramina by osteophytes. 102

Physical Examination Examination revealed a patient in no acute distress, with a full range of motion of the cervical spine. Reproduction of his right arm pain was elicited with extension of the neck and rotation of his head to the right (Spurling’s maneuver). He appeared to have mild deltoid wasting on his right with prominence of his acromion. Motor testing was symmetric with 5/5 strength in bilateral deltoids, biceps, triceps, wrist flexors, wrist extensors, finger flexors, finger extensors, and hand intrinsics. His deep tendon reflexes were 2+ and symmetric, with the exception of the biceps reflex, which was depressed on the right side compared with the left. He had a negative Hoffman’s sign and his gait was within normal limits. Tinel’s and Phalen’s testing of the median nerve at the wrist were not provocative.

Diagnostic Studies Radiographs taken included an anteroposterior, lateral, obliques, and flexion/extension laterals of the cervical spine. There is evidence of multilevel degenerative changes, with principal changes at the C5-C6 level. These changes include loss of C5–6 disk height on the lateral and narrowing of the C6 neural foramen with encroachment on the foramina by osteophyte on the oblique views (Fig. 18–1). Magnetic resonance imaging (MRI) of the cervical spine showed evidence of multilevel mild cord impingement with disk herniation at C3–4, C4–5, C5–6, and C6–7, along with focal increased signal intensity within the cord at the C5–6 level on the T2-weighted images consistent with cord edema (Fig. 18–2). There is also bilateral foraminal narrowing on the axial images at the C5–6 level (not shown). A needle electromyogram (EMG) was performed, which showed membrane instability of the C6 innervated muscles on the right side. C5, C7, and C8 muscles were normal. The nerve conduction studies did not exhibit peripheral nerve slowing as evidence for peripheral nerve compression.

A

B

Figure 18–1. (A) Lateral radiograph of the cervical spine showing multilevel degenerative changes with narrowing at the C5–6 disk space. (B) Oblique radiograph showing narrowing and osteophyte (4) formation within the C5–6 neuroforamen.

Figure 18–2. T2-weighted sagittal magnetic resonance imaging (MRI) of the cervical spine shows disk herniations at C3 lumen 4, C4–5, C5–6, and C6–7, along with focal increased signal intensity within the cord at the C5–6 level on the images consistent with cord edema. 103

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Differential Diagnosis Carpal tunnel syndrome Rotator cuff tear C5 radiculopathy C6 radiculopathy Brachial neuritis Thoracic outlet syndrome

Diagnosis C6 Radiculopathy Cervical radiculopathy represents impingement of an exiting cervical nerve root generally caused by herniated disk material or from degenerative cervical spondylosis, or commonly a combination of the two. In cases where the etiology is a herniated disk, the symptoms are more acute in onset and may be exacerbated by coughing or other Valsalva-type maneuvers. Cervical spondylosis as a cause for radiculopathy has an insidious onset, with degenerative changes occurring at the disk and the zygapophyseal and neurocentral joints (Fig. 18–3). Other causes of cervical root irritation or compression include intraspinal tumors, infection, inflammatory arthritic changes, and chemical irritation from neurohumeral factors. The presentation of cervical radiculopathy begins with varying degrees of pain, paresthesias, and motor weakness in the neck and upper extremity. Significant neck pain is often associated with the radicular pain and sensory changes, which generally follow a dermatomal distribution. Breast pain and angina-like symptoms should also be considered as potential radicular complaints. Weakness and reflex changes are also root specific, but significant overlap exists in the muscular innervation of the upper extremity and may occasionally be confusing. Table 18–1 outlines the clinical symptoms and findings seen with individual root involvement, and other potential causes for similar findings.

Intervertebral foramina (neuroforamen)

Cervical nerve root Articular process (facet joint)

Vertebral body 104

Cord

Disk

Uncinate process (joint of Luschka)

Figure 18–3. Axial anatomy of the cervical spine at the level of the disk and exiting nerve root at the intervertebral foramina. Note the disk herniation on the left side impinging the nerve root.

CERVICAL ROOT COMPRESSION

Table 18–1 Clinical Symptoms and Physical Findings Seen in Individuals with Cervical Root Involvement and Other Potential Causes for Similar Findings Root

Level

C3

C2–3

C4

C3–4

C5

C4–5

C6

C5–6

C7

C6–7

C8

C7–T1

Pain or Sensory changes

Motor

Reflex

Diagnosis with Similar Findings

Back of the neck Mastoid region Ear Back of the neck Along the trapezius Anterior neck Side of the neck to top of the shoulder Over the deltoid Lateral side of the arm and forearm Thumb and index fingers Back of the forearm to the middle finger

X

X

“Tension headache”

X

X

Myofascial pain

Deltoid Rotator cuff

X

Primary shoulder problem

Biceps Wrist extensors

Biceps Brachioradialis

Carpal tunnel syndrome (CTS) Upper trunk BPN

Triceps Wrist flexors Finger extensors

Triceps

Ulnar side of the forearm to the ring and small fingers

Finger flexors Intrinsics

X

CTS Pronator syndrome Radial tunnel synd. Posterior cord BPN Ulnar nerve entrapment at Guyon’s canal or the cubital tunnel AIN palsy Lower trunk BPN

AIN, anterior interosseous nerve; BPN, brachial plexus neuropathy.

The physical exam should be focused on identifying a dermatomal distribution of radicular complaints and sensory changes. Specific muscle group weakness and reflex changes as compared with the opposite side should also be recorded. Special tests like the previously mentioned Spurling’s sign and the Valsalva maneuver can reproduce a patient’s radicular complaints by decreasing the size of the neuroforamina. Davidson’s shoulder abduction relief sign functions to relieve a patient’s radicular complaints with abduction of the shoulder and presumably decreased tension on the cervical root. In this patient’s presentation a typical C6 radiculopathy is present with neck pain radiating down the biceps region of the arm to the lateral aspect of the forearm into the thumb and index fingers. Although he did not exhibit weakness on testing, he did report difficulty maintaining biceps strength with repetitive motion, and he had a depressed biceps reflex. Spurling’s maneuver was provocative for reproducing his radicular pain. The radiographs and MRI are significant for loss of C5–6 disk space, C6 neural foramen narrowing, encroachment on the foramina by osteophyte, and focal cord edema at the C5–6 level. The EMG confirmed denervation at the C6 level.

Differential Diagnosis Other conditions that may mimic C6 radiculopathy include other level radiculopathies, carpal tunnel syndrome, rotator cuff tendinopathies, brachial neuritis, and thoracic outlet syndrome. 105

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Clinical neurophysiologic testing is very important for differentiating radiculopathy from peripheral neuropathies. Needle EMG has traditionally been the most useful electrophysiologic tool for diagnosing cervical radiculopathy. If compression produces axonal interruption in some fibers, the EMG reveals changes in muscles from decreases in motor unit action potentials to fibrillation potentials of muscles. In radiculopathy the nerve compression is proximal to the dorsal primary ramus, which should produce changes in the paraspinal muscles, differentiating this lesion from a brachial plexus injury or more distal nerve compression. The sensory changes involving the thumb and index finger seen in C6 radiculopathy are also present in carpal tunnel syndrome. The differences can be seen in the dorsal and volar distribution of sensory changes in the hand and the proximal findings associated with radiculopathy. Coexisting distal nerve entrapment and cervical radiculopathy can occur, known as the double crush phenomenon. EMG is useful for differentiation of proximal versus distal nerve entrapment, with nerve conduction velocities identifying peripheral neuropathy. Pain that originates in the neck and extends to the shoulder and arm is very typical for radiculopathy, but patients with rotator cuff disease often have associated neck pain due to shoulder weakness and trapezium muscle spasm. In addition, biceps weakness may be a subjective complaint with rotator cuff disease due to an associated biceps tendinopathy causing pain and restricted motion. Specific testing of the rotator musculature and an MRI of the shoulder are helpful in diagnosing a rotator cuff tear. Proximal arm pain and weakness may be present in brachial neuritis. In this condition of unknown etiology a patient might awaken with shoulder pain and arm weakness without an inciting event. The symptoms are usually self-limited and treated symptomatically. Again, electrodiagnostic testing along with a thorough history and physical examination should differentiate this entity from radiculopathy. Thoracic outlet syndrome may involve nerves of the brachial plexus and may present with weakness and numbness of the hand. Physical findings of asymmetric pulses, vascular bruits, and a positive Adson’s test are tips to suspect thoracic outlet syndrome.

Nonsurgical Management The majority of patients with first-time symptoms of radiculopathy may be managed nonoperatively. Initial management should include immobilization in a soft collar with the neck slightly flexed, antiinflammatory medications, and physical therapy. Narcotic medications may be used in conjunction with nonsteroidal antiinflammatory drugs (NSAIDs) in the acute period in cases of severe pain. Physical therapy consists of heat and ultrasound modalities to make the patient more comfortable, cervical traction, and stretching exercises when tolerated. Epidural or selective nerve root corticosteroid injections are also an option, but require accurate needle placement around an irritated nerve root. Improvement in symptoms should be seen within 2 weeks; if symptoms worsen or marked neurologic deficits are present, more aggressive management should be considered.

Surgical Management Cases of cervical radiculopathy that require surgical intervention are those with unrelenting pain despite conservative management, progressive neurologic deficit, 106

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upper extremity weakness, and nerve root compression that is proven diagnostically and correlates clinically. Surgical choices include anterior cervical diskectomy and fusion as described by Robinson, or posterior diskectomy involving a hemilaminectomy or foraminotomy. The anterior approach is considered the best option for the acute disk herniation to decompress the nerve root from impinging disk fragments in the intervertebral foramen, and for cases where the nerve root is compressed by osteophytes from the joints of Luschka (Fig. 18–3). This anterolateral approach in the neck takes advantage of the fascial plane between the carotid sheath laterally and the trachea and esophagus medially, which affords visualization of the entire surgical spine. The posterior approach is useful for cases of chronic compression due to degenerative changes at the facet joints, and for cases where several levels need to be addressed. Both approaches produce excellent results for relieving radiculopathy, but the anterior approach is more consistent for relieving axial neck pain. Postoperatively, the patients are immobilized in a hard collar in cases of fusion and a soft collar if a simple diskectomy is performed.

Suggested Readings An HS. Cervical root entrapment. Hand Clin 1996;12:719–730. Bohlman HH, Emery SE, Goodfellow DB, et al. Robinson anterior cervical discectomy and arthrodesis for cervical radiculopathy. J Bone Joint Surg 1993;75A: 1298–1307. Dumitru D. Electrodiagnostic Medicine. Philadelphia: Hanley & Belfus; 1995. Levine MJ, Albert TJ, Smith MD. Cervical radiculopathy: diagnosis and nonoperative management. J Am Acad Orthop Surg 1996;4:305–316. Lomen-Hoerth C, Aminoff MJ. Clinical neurophysiologic studies: which test is useful and when? Neurol Clin 1999;17:65–74. Morgan G, Wilbourn AJ. Cervical radiculopathy and coexisting distal entrapment neuropathies: double-crush syndromes? Neurology 1998;50:78–83. Persson LC, Moritz U, Brandt L, Carlsson CA. Cervical radiculopathy: pain, muscle weakness and sensory loss in patients with cervical radiculopathy treated with surgery, physiotherapy, or cervical collar. A prospective, controlled study. Eur Spine J 1997;6:256–266. Saal JS, Saal JA, Yurth EF. Nonoperative management of herniated cervical intervertebral disc with radiculopathy. Spine 1996;21:1877–1883. Stewart JD. Focal Peripheral Neuropathies. 2nd ed. New York: Raven Press; 1993.

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19 Complex Regional Pain Syndrome Type 1 (Reflex Sympathetic Dystrophy) Carole W. Agin

History and Clinical Presentation

PEARLS • When presented with a questionable case of CRPS early after symptom development, a three-phase bone scan may be helpful. • CRPS (RSD) is often a diagnosis of exclusion.

PITFALLS • Radiologic studies performed late in the disease process may show changes secondary to disuse atrophy, which may be caused by other medical conditions. • If the sympathetically maintained pain is the result of a persistent but treatable condition, the condition needs to be treated. Treating only the signs/symptoms of CRPS without addressing the underlying condition may prove futile. • If the patient has a diagnosed psychiatric illness (i.e., posttraumatic stress disorder, depression), this must be treated or it can adversely affect any potential improvements obtained from other treatment modalities. 108

A 50-year-old woman was undergoing magnetic resonance imaging (MRI) with contrast. Intravenous access was started in her right antecubital fossa. As the infusion of gadolinium was started, the patient reported a burning pain in her arm from the antecubital fossa to her fingers. Her forearm and hand swelled. As the swelling increased, she reported numbness and cyanosis. Over the next few days the swelling resolved. Slowly sensation returned to her arm; however, the patient reported a constant burning pain. The patient also noted changes in the color of her hand and pain with movement of her wrist, elbow and shoulder.

Diagnostic Studies There are no radiologic findings that are pathognomonic for complex regional pain syndrome (CRPS) type 1, reflex sympathetic dystrophy (RSD). Radiologic findings are often nonspecific, and many findings are a result of prolonged disuse, which is attributable to the pain associated with the syndrome. However, imaging studies can support a diagnosis of CRPS (RSD). Fine detail radiography may help to suggest the presence of CRPS. Early radiologic changes seen with sympathetic hyperdysfunction include patchy demineralization of the epiphyses and short bones of the hands and feet. Periarticular osteoporosis in long bones and diffuse osteoporosis in small bones may be seen on plain radiographs. Subperiosteal resorption, striation, and tunneling of the cortex may occur. Comparison with the unaffected limb is always required. Unfortunately, these findings may be seen whenever there is disuse of a limb. As CRPS advances, patchy osteopenia may be seen. Triple-phase scintigraphy has also been used to help diagnosis CRPS (RSD). Three-phase bone scanning measures the uptake of a radionucleotide tracer at three different times: arterial phase, measured seconds after the injection of tracer; soft tissue phase, measured after several minutes have passed; and mineral phase, measured hours after the tracer is given. The triple-phase bone scan pattern most consistently seen in a patient with CRPS (RSD) is that of increased flow to the involved extremity and delayed static images that show diffusely increased uptake activity throughout the involved extremity, usually in a periarticular distribution. MRI studies may show skin thickening and tissue edema. Nuclear bone density measurements have been used to follow the progression of the syndrome.

Differential Diagnosis Peripheral neuropathy disease Inflammatory disease

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Infectious disease Vascular disease Connective tissue disorder Reflex sympathetic dystrophy CRPS (RSD) is often a diagnosis of exclusion. Other causes of similar pain complaints include peripheral neuropathies, which may also present with neuropathic pain. Traumatic injuries to nerves may present with dysesthesia and hyperpathia, but without the sympathetic component. Inflammatory and infectious causes for pain needed to be ruled out when autonomic dysfunction is the primary presenting symptom. Examples of this would include tenosynovitis and bursitis. Vasculitis and vascular disorders can also manifest with similar findings. In many instances vascular diseases present with bilateral symptoms. Raynaud’s disease produces vasospasm that will lead to findings of pallor, cold skin, and potentially cyanosis. Connective tissue disorders also have to be ruled out. Myofascial pain may also present with a nondermatologic distribution of pain. These patients may report burning pain as a symptom and have tender trigger points in the affected muscles. Malingering and psychiatric disorders must also be ruled out as a cause of the patient’s unremitting pain, which presents out of proportion to the inciting event.

Diagnosis Complex Regional Pain Syndrome, Type 1 (Reflex Sympathetic Dystrophy) The Committee on Taxonomy of the International Association for the Study of Pain (IASP) recently renamed reflex sympathetic dystrophy as complex regional pain syndrome type 1. This new taxonomy was promulgated in an attempt to establish uniform diagnostic criteria. This will aid in the development of treatment protocols for the syndrome. Previously many symptom constellations were included within the category of RSD, making treatment pathways and outcome studies difficult. A study done to evaluate the validity of the IASP’s CRPS diagnostic criteria to distinguish between CRPS and other neuropathies showed that the new classification did assist in improved accuracy of diagnosis. To meet criteria for CRPS type 1 a patient must present with regional pain outside of the distribution of a single peripheral nerve and out of proportion to the inciting event. CRPS has been reported to develop after compression/crush injuries, lacerations, fractures, sprains, burns, or surgery. Allodynia and hyperalgesia are typically present. Abnormalities in skin blood flow (causing changes in skin temperature and color), abnormal sudomotor activity, and edema are also present. Dystonia and weakness, although not necessary for the diagnosis, may also be present. Trophic changes and personality changes may develop as the disease progresses. CRPS type 2 has all of the same signs and symptoms; however, it follows injury of a major peripheral nerve.

Methods of Management As the pathophysiology of CRPS type 1 (RSD) is not well understood, multiple treatment protocols have been described. The consensus is that these patients do best with a multidisciplinary treatment plan (Table 19–1). This includes regional blockade (Fig. 19–1), physical therapy, pharmacologic therapy, and psychological 109

Table 19–1 Treatment Modalities Pharmacologic

Interventional Technique

Physical Modalities

Psychological Interventions

Antidepressants, TCAs, SSRIs

Sympathetic blockade Stellate ganglion Lumbar sympathetic IV regional

Physical/occupational therapy

Psychiatric evaluation

Membrane stabilizers Anticonvulsants Local anesthesia Antiarrhythmic

Spinal cord stimulator

Contrast baths

Cognitive behavior skills

NSAIDs

TENS

Relaxation training

Topical medications EMLA Capsaicin

Heat/cold

Imagery

Opiates

Massages

Hypnosis

Clonidine Calcitonin NSAID, nonsteroidal antiinflammatory drug; TCA, tricyclic antidepressant; TENS, transcutaneous electrical nerve stimulation; SSRI, selective serotonin reuptake inhibitor.

Figure 19–1. Anatomy of the neck and placement of the needle for a stellate ganglion block. 110

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intervention. The earlier the syndrome is diagnosed and treatment is started, the better the chances for complete recovery.

Pharmacologic Therapy Kingery reviewed the literature with respect to controlled clinical trials for CRPS. He found great disagreement as to the effectiveness of many of the medications currently being used in the treatment of CRPS. He concluded that further doubleblind controlled studies are needed. Tricyclic antidepressants (TCAs) have been well studied in neuropathic pain. TCAs (amitriptyline, nortriptyline, desipramine) inhibit monoaminergic transmitters by blocking reuptake of serotonin and norepinephrine. The dose used for treatment of neuropathic pain is typically much less than antidepressant doses. The selective serotonin reuptake inhibitors (paroxetine, sertraline), although used anecdotally in chronic CRPS, have not been formally studied for this purpose. The mechanism of action of nonsteroidal antiinflammatory drugs (NSAIDs) is the inhibition of cyclooxygenase. This leads to a reduction in the production of pain mediators and a reduction in inflammation. NSAIDs may be helpful in the early stages of CRPS type 1; however, the potential for gastrointestinal complications and renal failure must be considered if continued use is to be recommended. Membrane stabilizing medications are also used. This category includes anticonvulsants, local anesthetics, and antiarrhythmic agents. Gabapentin, a selective voltage-gated Ca2+ channel blocker, has shown some efficacy in managing pain in CRPS. Gabapentin has reduced side effects and an improved efficacy-to-toxicity ratio when compared with phenytoin and carbamazepine. Lidocaine, mexiletine, and tocainide effect sodium channels. Lidocaine has been used intravenously in the management of neuropathic pain. Intravenous lidocaine therapy is often followed by oral treatment with mexiletine. Topical medications have been tried for the hyperpathia and allodynia associated with CRPS. Topical application of local anesthetics, lidocaine, and prilocaine (eutectic mixture of local anesthetics, EMLA) has been tried recently in the treatment of neuropathic pain in patients with CRPS type 1 (RSD). Topical capsaicin causes a reversible depletion in substance P and calcitonin gene-related peptide from the C-fiber nerve terminals. There are anecdotal reports of its use for localized hyperalgesia; therefore, it can be tried for patients with CRPS with local areas of pain. Patients need to be informed that initially its application may cause increased pain. This is secondary to the release of substance P that occurs. The use of opioids in the treatment of neuropathic pain, and specifically in CRPS, has not been studied. Opioids are useful in nociceptive pain, and their effect is related to interaction at the level of the spinal cord with the opioid receptors. Although their use may be considered controversial in chronic, nonmalignant pain, a patient with unremitting pain should be tried on opioid therapy. This should occur early on in the treatment. It is important to control the patient’s pain utilizing all available means so that active physical therapy can be pursued and disuse atrophy avoided. As is true whenever using opioids, constipation should be expected and treated prophylactically. There have been anecdotal reports of the use of other medications for CRPS. Medications that inhibit ␥-aminobutyric acid (GABA), such as baclofen, have been reported to be useful in neuropathic pain. Controlled studies of their use in CRPS have not yet been done. Clonidine has been shown to be useful when topically applied 111

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to areas of hyperalgesia. It acts by blocking release of catecholamines presynaptically. Clonidine has also been administered epidurally and intrathecally in patients with CRPS. These patients are at a much greater risk for hemodynamic complications when the drug is used transdermally. Subcutaneous calcitonin has been shown to be effective in treatment of spontaneous pain. Its use in CRPS has not yet been documented. In the early stages of CRPS a patient may benefit from a trial of corticosteroids. This is particularly true for patients who present with edema or other signs of inflammation.

Regional Blockade Regional blockade, specifically sympathetic nerve blocks, are useful in both establishing the diagnosis as well as in the treatment of CRPS (RSD). Patients with CRPS report relief of pain with sympathetic blocks, which is very useful in giving patients the analgesia that they require to participate in a physical therapy regimen. If a patient responds positively to a trial of sympathetic block, these blocks should be repeated as long as the patient continues to be afforded increasing duration of pain relief and symptom improvement with subsequent blocks. In addition to assessing the level of pain relief reported by the patient, patients should be assessed for signs of a sympathetic block. Blocks of the sympathetic nervous system interrupt nociceptor visceral and somatic afferents and vasomotor, sudomotor, and visceromotor fibers. One would therefore look for signs of increased blood flow to the limb(s) involved. As cutaneous blood flow affects skin temperature and this is controlled by the sympathetic nervous system, an increase in skin temperature should occur. This can be measured using surface temperature monitors or plethysmography. The limb should be examined for visual signs of increased vasculature. Blocking of sudomotor functions can be measured using Ninhydrin, cobalt blue, or starch-iodide. A quantitative sudomotor axon reflex test (QSART) can also be used. For CRPS affecting the upper limb a stellate ganglion block is usually performed. Many patients develop Horner’s syndrome (enophthalmos, miosis, anhidrosis, and ptosis) after a stellate (cervicothoracic) ganglion block. Block of the thoracic sympathetic chain is technically difficult, requiring radiologic guidance, and is not commonly done. For CRPS affecting the lower extremities, sympathetic blockade is done either by performing a lumbar sympathetic block or by an epidural injection. If required, continuous blocks can be done.

Intravenous Regional Blocks (Bier Blocks) Intravenous regional blocks allow for prolonged exposure of the affected limb to the ganglionic blocking agent. In the United States this technique is typically performed with bretylium. Bretylium accumulates in adrenergic nerves and blocks norepinephrine release. These blocks have also been performed with guanethidine and reserpine.

Spinal Cord Stimulation Spinal cord stimulation is hypothesized to affect pain based on the gate control theory whereby stimulation of large myelinated fibers blocks pain transmissions through smaller pain fibers (Fig. 19–2). 112

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Figure 19–2. Patient with spinal stimulation of large myelinated fibers that in theory blocks pain transmissions through smaller pain fibers.

Patients who either do not respond to regional blocks, medications, or physical therapy, or are unable to pursue those treatment options secondary to unacceptable side effects, may be candidates for spinal cord stimulation. All patients must meet strict selection criteria and have a successful trial with a temporary lead. A trial is deemed successful if the patient reports a decrease in pain, a reduction in medication requirements, and an improvement in function.

Physical Therapy Physical therapy should be done concurrently with medications and sympathetic blocks in the treatment of severe CRPS. It can be the main treatment modality for children with CRPS. Multiple physical therapy modalities have been used to treat CRPS. These include range-of-motion exercises, muscle strengthening and conditioning, massage, paraffin wax, contrast baths, ultrasound, and transcutaneous electrical nerve stimulation (TENS).

Psychiatric/Psychological Intervention Secondary to the potential chronic pain and disability associated with CRPS, patients should be sent for psychological evaluation early on in their treatment. Patients often benefit from cognitive-behavioral skills training. Some patients may require ongoing psychiatric intervention. 113

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Complications Early diagnosis of CRPS is essential for pain relief and restoration of function. The incidence of poor outcomes is significantly higher in patients who present with a duration of CRPS greater than 12 months, in the second and third stages of disease, and in cases with coexisting nerve injuries or compression as a consequence of initial trauma. Studies have shown a correlation between CRPS and psychosocial disorders. This may complicate treatment.

Suggested Readings Aprile AE. Complex regional pain syndrome. AANA J 1997;65:557–560. Galer BS, Bruehl S, Harden RN. IASP diagnostic criteria for complex regional pain syndrome: a preliminary empirical validation study. International Association for the Study of Pain. Clin J Pain 1998;14:48–54. Geertzen JH, Dijkstra PU, Groothoff JW, ten Duis HJ, Eisma WH. Reflex sympathetic dystrophy of the upper extremity–a 5.5-year follow-up. Part II. Social life events, general health and changes in occupation. Acta Orthop Scand Suppl 1998; 279:19–23. Kingery WS. A critical review of controlled clinical trials for peripheral neuropathic pain and complex regional pain syndromes. Pain 1997;73:123–139. Raj PP. Reflex sympathetic dystrophy. In: Raj PP, ed. Pain Medicine. St. Louis: Mosby-Year Book; 1996:466–481. Sandroni P, Low PA, Ferrer T, Opfer-Gehrking TL, Willner CL, Wilson PR. Complex regional pain syndrome I (CRPS I): prospective study and laboratory evaluation. Clin J Pain 1998;14:282–289. Schiepers C, Bormans I, De Roo M. Three-phase bone scan and dynamic vascular scintigraphy in algoneurodystrophy of the upper extremity. Acta Orthop Belg 1998; 64:322–327. Stanton-Hicks M, Baron R, Boas R, et al. Complex regional pain syndromes: guidelines for therapy. Clin J Pain 1998;14:155–166. Stanton-Hicks M, Janig W, Hassenbusch S, Haddox JD, Boas R, Wilson P. Reflex sympathetic dystrophy: changing concepts and taxonomy. Pain 1995;63:127–133. Walker SM, Cousins MJ. Complex regional pain syndromes: including “reflex sympathetic dystrophy” and “causalgia.” Anaesth Intensive Care 1997;25:113–125. Wasner G, Backonja M, Baron R. Traumatic neuralgias. Complex regional pain syndromes (reflex sympathetic dystrophy and causalgia): clinical characteristics, pathophysiologic mechanisms and therapy. Neurol Clin 1998;16:851–868. Wong GY, Wilson PR. Classification of complex regional pain syndromes. New concepts. Hand Clin 1997;13:319–325. Zyluk A. The reasons for poor response to treatment of posttraumatic reflex sympathetic dystrophy. Acta Orthoped Belg 1998;64:309–313.

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Section IV

Nerve Injuries/ Palsies

Acute Nerve Laceration Kevin D. Plancher

A. Nerve Palsies Low Median Nerve Palsy Kevin D. Plancher

Ulnar Nerve-Tendon Transfer Mark S. Cohen

High Radial Nerve Palsy Kevin D. Plancher

AC U T E N E R V E L AC E R AT I O N

20 Acute Nerve Laceration Kevin D. Plancher

History and Clinical Presentation A 20-year-old right hand dominant male laborer caught his left hand in a circular saw with the “guard” off. He has a laceration to his left index finger and can’t feel the tip of his finger, and has an open bleeding wound.

Physical Examination On physical examination, the patient has an acute open laceration involving the radial side of the right index finger. A careful motor examination was performed. The functioning level of specific muscles is determined to assist with identifying peripheral nerve injuries. A two-point sensory discrimination test (Fig. 20–1), as determined by the Weber two-point discrimination test, using a dull pointed eye caliper applied in the longitudinal axis of the digit without blanching the skin, and a twopoint discrimination (2-PD) (both moving and static), Semmes-Weinstein monofilaments, and vibrometer tests were used to assess the status of the nerves. Denervated skin responds differently to stimuli; when the injured hand is placed in water, innervated skin wrinkles and denervated skin does not. This test can be helpful in determining the affected peripheral nerves in the hand in unconscious patients.

PEARLS • Microscopic repair is always more accurate. • Occupational therapy postoperatively will successfully complete a desensitization program. • The area of injury must be defined for successful functional nerve repair.

PITFALLS • Clean ends of nerve must be sewn together to avoid a neuroma in continuity. • Missed diagnosis with a devascularized finger may lead to amputation • Range of motion must be controlled with splinting.

Diagnostic Studies Radiographs were performed to rule out associated fractures.

Differential Diagnosis Vascular injury Muscle laceration Neurologic disorder Nerve laceration

Figure 20–1. Weber static two-point sensory discrimination test.

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Diagnosis Acute Laceration, Radial Nerve, of the Index Finger Neurapraxia is the mildest form of nerve injury. This usually involves demyelination without axon disruption and degeneration. This type of injury has a relatively short recovery time, and full function is expected without intervention. Axonotmesis occurs when axons, myelin, and associated internal nerve structures are disrupted. These injuries often result from situations in which traction overcomes the inelastic internal structures but leaves the elastic epineurium intact. When axons are disrupted and the endoneurium and the rest of the nerve are intact, degeneration and regeneration occur. This is the first stage of injury that shows an advancing Tinel’s sign. Because the endoneurium is intact, regeneration should be full with complete sensory and motor function regained. Another type of injury occurs when the axons and the endoneurium are damaged and the perineurium and epineurium are intact. This leaves the blood–nerve barrier intact but provides a disorganized bed through which the axons can travel. Nerve regeneration may be slowed due to infiltration of scar tissue or a smaller number of axons capable of survival and regeneration. An advancing Tinel’s sign, though somewhat slowed, should be present. The worst form of closed nerve damage is when all structures are damaged except the epineurial covering. This disables the intact axons and no conduction down the nerve is possible. Surgical intervention is required to restore function. A Tinel sign is present at the level of injury and does not move distally because the regenerating nerve is kept from advancing by large amounts of scar tissue or debris. Neurotmesis is the most severe type of injury. This class of injury is easy to diagnose because it usually involves an open wound with nerve deficits. Surgical repair is a requirement for any return in function to occur. Results following the surgical repair of digital nerves are inconsistent. Among the factors that could impact on outcomes are the amount of direct trauma to the nerve, the length of nerve that has been traumatized, and the age of the patient. Increased tension on the repair has also been shown to effect the final results. Nerve repair never results in the return of full sensibility. However, reasonable protective sensibility to light touch and pin pricks can be obtained. Two-point discrimination can approach normal in as many as one patient in three (33%).

Surgical Management After usual draping and prepping of the patient, the skin is marked. The patient is supine and a regional anesthetic is administered. If multiple structures need to be repaired, then general anesthesia is used and the arm is exsanguinated using a tourniquet on the forearm or arm. Incision use for this procedure is a midaxial incision because it offers the best extensile exposure to the palm and finger. Some surgeons use a Bruner zigzag to expose the nerve, but we feel excessive scarring results with this type of incision. Gross exploration is accomplished under loupe magnification using tenotomy or other scissors. After initial exploration, using a microscope for high-power magnification, identify the nerve and trim any necrotic or bruised tissue until normal fascicles are 118

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A

B

C

Figure 20–2. (A) Intraoperative exposed injured radial digital nerve to the index finger. (B) Epineurial repair of a nerve. (C) Fascicular repair of nerve.

found (Fig. 20–2A). Then transect the nerves perpendicular to the main axis and carefully examine them to ensure that they are healthy and uninjured fascicles are found (Figs. 20–2B,C). Several sequential transections may be indicated before finding appropriate endings for repair. Use a systematic approach consisting of a simple suture first being placed on either side of the nerve anteriorly. and this is followed by another in the midline posteriorly. The intervening epineurium is then sutured (Fig. 20–3). Many surgeons suggest the use of 9-0 or 10-0 nylon or Prolene sutures. If the nerve is under too much tension, the sutures will not hold. If there is any question about increased tension on the digital nerve repair, grafting should be considered because holding a digit in flexion to oppose nerve endings often leads to contracture. Closure of the wound is accomplished with simple sutures. A bulky bandage is wound circumferentially around the digit to help diminish swelling. A dorsal and palmar splint may be applied.

A

D B

C

Figure 20–3. Epineurial repair of a nerve. (A) Suture outside-in from one end. (B) Suture from inside-out on the matching other end. (C) Nerve laceration systematically approximated with complete repair and epineurial vessels correctly aligned. (D) Intraoperative photo showing nerve repaired. 119

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Figure 20–4. Dorsal block splint for protection of repair in a multiple nerve lacerated hand with digital flexion begun and an early range-ofmotion program.

Postoperative Management Splinting is done for a period of 3 weeks (Fig. 20–4), but one sequela can be stiffness in the interphalangeal joints. Absent undue tension on the repair and full extension, range-of-motion exercises can be started at the time of suture removal or earlier depending on the quality of the repair. Hand therapy following nerve repair is individualized, and many patients require no specific therapy. If stiffness does develop, supervised hand therapy and dynamic therapy are useful interventions. Regeneration of the nerve is followed by measuring the paresthesia radiating distally from the level of nerve repair when the nerve is percussed (Tinel’s sign). As regeneration continues, the focus of the paresthesia migrates distally. As migration and healing continue, sensibility is noted proximal to Tinel’s sign.

Complications Nerve surgery has complications similar to those found in other kinds of surgeries. Among the more common of these are infection, hematoma, seroma, and injury to surrounding structures, including vascular structures. Of unique concern during nerve surgery is the possibility of downgrading function by further injuring the nerve, particularly in mixed nerve injuries.

Suggested Readings Allan CH. Functional results of primary nerve repair. Hand Clin 2000;16:67–72. Birch R, Raji AR. Repair of median and ulnar nerves. Primary suture is best. J Bone Joint Surg 1991;73B:154–157. Cabaud HE, Rodkey WG, Nemeth TJ. Progressive ultrastructural changes after peripheral nerve transection and repair. J Hand Surg 1982;7A:353–365. Chow JA, Van Beek AL, Meyer DL, Johnson MC. Surgical significance of the motor fascicular group of the ulnar nerve in the forearm. J Hand Surg 1985;10A:867–872. de Medinaceli L, Prayon M, Merle M. Percentage of nerve injuries in which primary repair can be achieved by end-to-end approximation: review of 2,181 nerve lesions. Microsurgery 1993;14:244–246. 120

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Diao E, Vannuyen T. Techniques for primary nerve repair. Hand Clin 2000;16:53–66. Fu SY, Gordon T. Contributing factors to poor functional recovery after delayed nerve repair: prolonged denervation. J Neurosci 1995;15:3886–3895. Hobbs RA, Magnussen PA, Tonkin MA. Palmar cutaneous branch of the median nerve. J Hand Surg 1990;15A:38–43. Jabaley ME. Techniques in nerve repair. In: Hunter JM, Schneider LH, eds. Tendon and Nerve Surgery in the Hand: A Third Decade. St. Louis: Mosby; 1994:89–94. Jarvik JG, Kliot M, Maravilla KR. MR nerve imaging of the wrist and hand. Hand Clin 2000;16:13–24. Lundborg G, Dahlin LB, Danielsen N, et al. Nerve regeneration across an extended gap: a neurobiological view of nerve repair and the possible involvement of neuronotrophic factors. J Hand Surg 1982;7A:580–587. Millesi H. Techniques for nerve grafting. Hand Clin 2000;16:73–91. Smith KL. Anatomy of the peripheral nerve. In: Hunter JM, Schneider LH, eds. Tendon and Nerve Surgery in the Hand: A Third Decade. St. Louis: Mosby; 1994: 11–18. Vanderhooft E. Functional outcomes of nerve grafts for the upper and lower extremities. Hand Clin 2000;16:93–104. Wilgis EF, Brushart TM. Nerve repair and grafting. In: Green DP, ed. Operative Hand Surgery. Vol. 2. New York: Churchill Livingstone; 1993:1315–1340.

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21 Low Median Nerve Palsy Kevin D. Plancher

History and Clinical Presentation A 17-year-old girl presents following operative repair of a tendon with ulnar and median nerve injuries to the distal forearm. Her surgery was ~1 year ago. She is now unable to achieve thumb abduction or metacarpal flexion, and she has noticed severe clawing of her digits. She has been in occupational therapy for 1 year. She would like to be able to grip wide-mouthed objects, as she was once able to do.

Physical Examination PEARLS • The EIP muscle belly must be freed from surrounding soft tissue completely so that when the tendon is transferred dorsally, the muscle fibers are not angulated. • The use of the EIP in lieu of the FDS spares the tendon for use in an intrinsic transfer if necessary. • No pulley is required for the Burkhalter transfer.

PITFALLS • The EIP may not be sectioned distal to the sagittal band. Loss of independence of index MP joint extension may then occur with a small extension lag at the MP joint. • If there is an injury to the ulna distal forearm, scar may cause adhesions as it is in the path of the transfer. • This EIP transfer just reaches the site of insertion with little or no leftover tendon. Beware, and be prepared if the transfer is short.

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The patient cannot oppose her thumb to the little finger. Her skin is supple and there is no contracture in her first digital web space.

Diagnostic Studies Plain radiographs were read as normal. Nerve conduction and electromyogram (EMG) were performed and revealed a combined low median and ulnar nerve palsy.

Diagnosis The thumb is key in providing strength for prehensile pinch and grasp. Opposition is a complex motion involving abduction, flexion, and rotation of the carpometacarpal (CMC) joint and flexion and rotations of the metacarpophalangeal (MP) joint. Median nerve palsy deprives the thumb of its ability to oppose. Restoration of opposition requires the presence of transferable functioning tendons and a thumb that has adequate mobility without contractures. At the level of the wrist, the median nerve lies between the flexor carpi radialis (FCR) and the palmaris longus tendons. The nerve lies volar to the flexor pollicis longus and the flexor digitorum profundus. The nerve then enters the carpal tunnel beneath the transverse carpal ligament. In the carpal canal the nerve may begin to branch to supply the median-innervated hand intrinsic muscles.

Surgical Management (Burkhalter EIP Transfer) This transfer of the extensor indicis proprius (EIP) to the abductor pollicis brevis (APB) was descried by Burkhalter in 1974 and is perfect for patients with an isolated thenar paralysis due to low or high median nerve injury. The transfer achieves excellent thumb abduction, pronation, and MP flexion.

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Figure 21–1. Relationship of extensor indicis proprius (EIP) on the ulnar side of the extensor digitorum communis (EDC), seen over the index metacarpal (right hand dorsal approach).

With the patient under either general or regional anesthetic, a tourniquet is applied to exsanguinate the operative extremity. The planned incisions are outlined and a longitudinal incision is made over the index MP joint. The EIP tendon is then identified ulnar to the extensor communis tendon (Fig. 21–1). An incision is then made on the ulnar side of the EIP, through the sagittal band, and extended distally. A similar incision is made on the radial side, separating it from the extensor digitorum communis, and then connecting it to the distal incision on the ulnar side (Fig. 21–2). The sagittal band is repaired at this point in the operation to avoid an extensor lag. Once the distal attachment of the EIP is released, a linear incision is made over the dorsal, ulnar aspect of the distal forearm and the deep fascia is divided longitudinally. The EIP tendon and muscle are identified and delivered to the proximal wound. If delivery is hampered by adhesions or connection of the EIP tendon in the dorsum of the hand, another incision may be required to free the tendon and muscle belly fully. Once the EIP and muscle belly are freed, a small longitudinal incision is made just distal to the pisiform, and a subcutaneous tunnel is created across the forearm from the dorso-ulnar distal forearm incision to this second incision distal to the pisiform (Fig. 21–3A). Care should be taken to ensure that the tunnel is large enough to accept the muscle belly of the EIP or it may prevent full excursion of the donor tendon. The tendon can be passed through the tunnel using a tendon passer or hemostat. 123

Figure 21–2. Distal EIP is sutured to the EDC tendon and transferred subcutaneously to the midforearm.

Figure 21–4. The EIP is sewn into place, weaved into the APB tendon.

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Figure 21–3. (A) Clinical photo of the EIP tendon being pulled subcutaneously from dorsal to volar to be distal to the pisiform. (B) The EIP is transferred from the distal ulna volar forearm to the insertion of the abductor pollicis brevis (APB) subcutaneously.

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A second subcutaneous tunnel is made across the palm to the thumb MP joint. The line of pull is estimated by placing the donor tendon to the proposed insertion site on the distal thumb metacarpal (Fig. 21–3B). Regardless of the method of attachment used, the transferred tendon needs to be securely fixed in place. This can be accomplished using a bone tunnel or weaving the EIP through the abductor pollicis brevis (Fig. 21–4). The thumb is placed in full opposition to the small finger. The EIP transfer is tensioned and secured. The tourniquet is then released, hemostasis is obtained, and the wounds are closed (Fig. 21–5). When the procedure is completed, a bulky hand

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Figure 21–5. (A,B) Artwork of volar and dorsal incisions of the hand and forearm closed once the tension of the transfer is secured and tested with the tenodesis effect. (C) Clinical photo of EIP transfer complete with all skin wounds closed.

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dressing is applied to maintain the positional thumb opposition, and the index finger is splinted in extension to avoid an extensor lag at the MP joint.

Alternative Techniques Brand’s technique involves splitting the EIP tendon into two slips. One slip is woven through the APB, passed distal to the MP joint, and then attached to the extensor pollicis longus tendon (Fig. 21–6). The second slip passes subcutaneously across the extensor mechanism dorsally and is attached to the adductor pollicis on the ulnar side of the MP joint. This technique is useful in those patients with complete loss of thenar musculature function and an unstable MP joint. The Royle-Thompson method also splits the EIP tendon into two slips. One is passed through a drill hole in the metacarpal neck from radial to ulnar with the metacarpal pulled to the highest degree of opposition as possible. The other half is passed dorsally over the extensor hood at the MP joint and through a small tunnel in the fascia and periosteum at the base of the proximal phalanx. The two slips are tied together. The proximal insertion into the head of the metacarpal serves to assist in the rotation of the thumb while the distal insertion achieves slight rotation of the MP joint without causing flexion.

Figure 21–6. With a severe median and ulnar paralysis, the EIP tendon is split and the Royle-Thompson SP modification is used.

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Figure 21–7. An alternative transfer such as a Riordan or Sterling Bunnell seen in this clinical photo with the flexor digitorum superficialis (FDS) ring as the donor tendon.

Use of the flexor digitorum superficialis (FDS) ring as an alternative technique was popularized by Sterling Bunnell (Fig. 21–7).

Postoperative Management The bulky hand dressing with splints is maintained until the sutures are removed at 10 to 14 days after surgery. Hand therapy is initiated to maintain motion in the fingers. An Orthoplast splint is custom fit to maintain wrist flexion and full thumb opposition for a total of 4 weeks. Range of motion, tendon gliding, and retraining exercises are begun at 4 weeks.

Complications Complications with poor results after the opposition tendon transfers often are due to an adduction contracture of the first metacarpal. This problem may be avoided by release of the contracture prior to the tendon transfer, whether it is by a surgical or conservative fashion. Flexion or extension contractures of the MP joint of the thumb often reflect the position of the transfer relative to the MP joint axis. The transfer should be sutured more dorsally if there is a flexion contracture and reattached more volarly if there is an extension contracture. Other common complications with any transfer are placing the donor tendons under inadequate tension, or placing a repair in a poorly vascularized soft tissue bed. These complications, along with a web contracture, or inappropriate splinting can often be avoided if precision handling of all tendons is done along with understanding the important general principles of tendon transfers.

Suggested Readings Anderson GA, Lee V, Sundaraej GD. Opponensplasty by Extensor Indicis and Flexor Digitorum Superficialis Tendon Transfer. Brand PW. Biomechanics of tendon transfers. Orthop Clin North Am 1974;5:205. Burkhalter WE. Tendon transfer in median nerve palsy. Orthop Clin North Am 1974; 5:271–281. 127

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Conney WP. Tendon transfer for median nerve palsy. Hand Clin 1998;4:155–165. Hollister A. Giurintano, DJ. Thumb movements, motions and moments. J Hand Ther 1995;8(2):106–114. Thompson CF. Fusion of the metacarpals of the thumb and index finger to maintain functional positions of the thumb. J Bone Joint Surg [Am] 1942;24:907. Thomson TC. A modified operation for opponens paralysis. J Bone Joint Surg [Am] 1942;24:632.

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22 Ulnar Nerve-Tendon Transfer Mark S. Cohen

History and Clinical Presentation A 57-year-old man presents for evaluation of his dominant hand. He complains of a deformity involving his small and ring fingers with loss of function, especially fine motor skills. He relates his problem to a laceration he suffered at the wrist level several years prior. He also reports numbness in his small and ring fingers. He denies any radicular symptoms or problems with his contralateral hand. PEARLS • Ulnar nerve dysfunction leads to a claw deformity with asynchronous motion, weakened grip, and loss of lateral finger mobility and sensation. • Various tendon transfers can restore clawing and asynchronous digital flexion. To improve weakness of grasp, the transfer must utilize a wrist muscletendon unit. Using a digital motor simply redistributes balance within the hand. • Transfer selection is based on patient age, requirements, tendon availability, and compliance.

PITFALLS • Claw deformity can result from a variety of conditions including lesions of the ulnar nerve, lower cervical roots, inferior brachial plexus, and more generalized neurologic conditions (e.g., motor neuron disease). • The diagnosis requires a careful history, physical examination, and often electrodiagnostic studies. • Contraindications to tendon transfers include an uncooperative patient, a lack of expendable donor tendons, and stiff digits without full passive mobility.

Physical Examination Obvious atrophy is visible in the hand involving the intrinsic musculature. The small and ring fingers are positioned in a claw deformity, although passive interphalangeal joint extension is present and the joints are supple. The patient has difficulty abducting and adducting his digits. His flexor digitorum profundus function to the small and ring fingers is intact (he can actively flex his small and ring distal interphalangeal joints). Sensory examination reveals diminished two-point discrimination in the small and ulnar half of the ring fingers.

Diagnostic Studies Roentgenograms were obtained of the hand including the wrist. They were within normal limits. Electrical studies were obtained and revealed a complete ulnar nerve lesion at the wrist level with denervation present in all ulnar nerve innervated intrinsic muscles tested (interossei and hypothenar muscles). No reinnervation potentials were present. The thenar muscles were electrically normal and there was no evidence of a peripheral neuropathy or radiculopathy.

Differential Diagnosis Brachial plexus injury Upper plexus Lower plexus Cervical root compression Peripheral nerve dysfunction Charcot-Marie-Tooth disease Ulna nerve tunnel compression Cubital tunnel (source) Pancoast tumor Tendon lacerations Laceration of the ulna nerve at the wrist The differential diagnosis of a claw deformity of the hand with loss of sensation in the ulnar nerve distribution is somewhat limited. One assumes a lesion of the ulnar 129

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nerve or possibly the lower cervical nerve roots (C8–T1) or inferior brachial plexus. Cervical nerve root compression typically results in neck pain with radicular symptoms down the arm. Weakness and atrophy would be expected in the thenar and hypothenar musculature, which are both innervated by the lower cervical and first thoracic nerve roots. A lesion of the lower brachial plexus (e.g., a Pancoast tumor of the lung apex) would result in similar findings. The ulnar nerve is most commonly compressed at the elbow (cubital tunnel syndrome) or at the wrist (ulnar tunnel syndrome). Intact function of the two ulnar flexor digitorum profundus tendons would point to a more distal lesion in the lower forearm or wrist. Lastly, one must rule out other causes of peripheral nerve dysfunction such as a generalized peripheral neuropathy or hereditary motor-sensory neuropathy (CharcotMarie-Tooth disease). Intrinsic atrophy with or without sensory loss may be seen in syringomyelia or motor neuron disease (amyotrophic lateral sclerosis, ALS). These typically result in symmetric disease. The history, physical findings, and corroborative electrical studies aid in localizing the nerve lesion and ruling out a more generalized disease process.

Diagnosis The diagnosis is a low complete ulnar nerve palsy. The ulnar nerve innervates the four dorsal interossei, the three volar interossei, the two ulnar lumbricals, the hypothenar muscles and typically the deep head of the flexor pollicis brevis. It supplies sensation to the small finger and ulnar half of the ring finger. A claw deformity develops due to imbalance between absent intrinsic (interossei and lumbricals) and intact extrinsic muscle function. The claw deformity is more pronounced in the ring and small fingers due to the intact index and middle finger lumbricals, which are innervated by the median nerve. Clawing is more significant in a low ulnar nerve palsy than a lesion at the elbow due to the intact flexor digitorum profundus tendons to the ring and small fingers. These tend to accentuate the flexion posture of the interphalangeal joints. Loss of ulnar nerve function can be quite disabling. The intrinsic muscles are responsible for simultaneous flexion of the metacarpophalangeal (MP) joints and extension of the interphalangeal (IP) joints (the intrinsic-plus position). Although full finger flexion and extension is present, with intrinsic loss the fingers tend to roll up during flexion due to asynchronous motion of the MP and IP joints (MP flexion does not begin until IP flexion has been completed). IP joint extension requires contraction of the extrinsic extensor tendons (extensor digitorum communis). This leads to MP joint hyperextension and contributes to the claw posture. The ability to place the hand around objects such as a glass or doorknob is lost. These activities requires the intrinsic-plus posture. All fine motor skills that require simultaneous MP flexion and IP extension, such as writing or threading a needle, are similarly impaired. Lastly, pinch and grip strength are markedly diminished due to loss of the interossei and hypothenar muscles.

Nonsurgical Management Conservative treatment of ulnar nerve dysfunction relies on the use of external splints to block clawing of the digits. A lumbrical bar splint is commonly utilized for this purpose (Fig. 22–1). It is a static splint, usually made of Orthoplast by a hand 130

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Figure 22–1. A lumbrical bar splint blocks metacarpophalangeal (MP) hyperextension in individuals with a claw deformity secondary to ulnar nerve dysfunction. This allows the long extensor tendons to extend the IP joints and corrects the claw deformity. It does not improve asynchronous digital flexion.

therapist, that fits over the dorsum of the metacarpal head and proximal phalanges. It does not improve grip strength or integrated MP and IP motion. It does, however, block MP hyperextension of the ring and small fingers, thereby correcting the claw deformity. This enables the extrinsic extensor tendons to fully extend the IP joints. It also prevents fixed proximal IP joint contractures from occurring.

Surgical Management If a compressive neuropathy or isolated nerve disruption is identified, decompression or nerve repair is indicated. Unfortunately, with complete ulnar nerve transection, full recovery seldom occurs following repair. This is due to the mixed motor and sensory function of the ulnar nerve as well as the complex motor innervation of the many intrinsic muscles of the hand. Recovery is especially guarded in older individuals, in high lesions, and in nerve loss requiring grafts for reconstruction. Furthermore, motor end plates cannot be functionally reinnervated years after paralysis. In this setting, tendon transfers are the only option available to restore ulnar nerve function. There are many surgical procedures described to treat patients with intrinsic muscle paralysis. Tendon transfers are described to correct the claw deformity and integrated MP and IP joint motion, improve grip and pinch strength, and restore lateral deviation of the fingers (Fig. 22–2A). All require a motivated patient and full passive mobility of the digits. The choice of transfer depends on the age and needs of the patient, the availability of donor tendons, and the level of the palsy. In this patient, a simple transfer was decided on that would correct the claw deformity and restore synchronous finger flexion. This was thought to be most appropriate for his functional demands. Loss of grip strength was not one of his complaints, and thus a transfer involving a wrist tendon was not chosen. The only way 131

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Figure 22–2. (A) Preoperative claw posture of the hand. Note the minimal clawing of the index and middle fingers due to the intact radial two lumbrical muscles innervated by the median nerve. (B) Stiles-Bunnell transfer utilizing the flexor digitorum superficialis (FDS) tendon of the middle finger to correct the ring and small finger clawing and asynchronous flexion. The tendon has been longitudinally split. (C,D) Following transfer, the ulnar digits are rebalanced and digital motion is now synchronous without a claw posture.

to improve grip strength is to use a wrist motor-tendon unit, which adds power to the hand. This, however, requires the use of free tendon grafts to augment tendon length, and thus is a more complicated operative procedure. A Stiles-Bunnell transfer was chosen, which utilizes a flexor digitorum superficialis (FDS) tendon to restore MP flexion and IP extension and redistribute balance within the hand (Fig. 22–2B). The FDS has excellent amplitude and force with little functional morbidity as a donor. As this patient had a low ulnar nerve palsy with only ring and small finger clawing, a single FDS tendon from the middle finger was transferred. Through a palmar incision, the FDS was harvested and split longitudinally. These were then passed through the lumbrical canals (palmar to the MP joints) and sutured into the lateral bands of the extensor mechanism of the ring and small fingers. When the wrist was passively flexed and extended intraoperatively, the ulnar digits no longer assumed a claw posture. Postoperatively, the patient was placed in a short arm dorsal blocking splint with the wrist in 20 to 30 degrees of flexion and the MP joints in ~60 degrees of flexion for 3 weeks. Active flexion and extension of the fingers was allowed within the limits of the splint. A hand-based lumbrical bar splint was then worn for an additional 2 weeks. At 5 weeks postoperative, the patient had regained synchronous digital flexion and extension without clawing (Fig. 22–2C,D). Functional use was encouraged. 132

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Suggested Readings Brand PW. Tendon transfers for correction of paralysis of intrinsic muscles of the hand. In: Hunter JW, Schneider LH, Mackin EJ, eds. Tendon Surgery of the Hand. St. Louis: Mosby; 1987:439–499. Burkhalter WE. Ulnar nerve palsy. In: Gelberman RH, ed. Operative Nerve Repair and Reconstruction. Philadelphia: JB Lippincott; 1991:729–746. Hastings H, Davidson S. Tendon transfers for ulnar nerve palsy: evaluation of results and practical treatment considerations Hand Clin 1988;4:167–178. Omer GE. Ulnar nerve palsy. In: Green DP, Hotchkiss RH, Pederson WC, eds. Green’s Operative Hand Surgery. 4th ed. Philadelphia: Churchill Livingstone; 1999: 1527–1541. Smith RJ. Tendon transfers to restore intrinsic muscle function to the fingers. In: Smith RJ, ed. Tendon Transfers of the Hand and Forearm. Boston: Little, Brown; 1987:103–133.

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23 High Radial Nerve Palsy Kevin D. Plancher

History and Clinical Presentation A 31-year-old right hand dominant construction worker fell from a scaffold and sustained a middle to distal third humerus fracture. He came to the emergency room 1 year ago with pain and an inability to perform wrist extension and finger and thumb extension. At that time the emergency room physician placed the patient in a sling and told him to follow up with an orthopedic surgeon. One year, 4 months later, after unsuccessful restoration of his hand and wrist function, the patient comes in, concerned because he is unable to perform any radial nerve function with the hand and wrist.

Physical Examination The patient has shoulder range of motion of 0 to 165 degrees of forward flexion. External rotation is to 45 degrees. Elbow range of motion is from 0 to 125 degrees. Active wrist flexion is to 50 degrees. Although passively wrist extension is full with a supple joint, active wrist range of motion is not present. Digital range of motion was tested, and the patient was able to flex all digits and the thumb interphalangeal (IP) joint. He could not extend his fingers beyond an M2 grade (Fig. 23–1). There was numbness noted over the dorsal aspect of the thumb and hand. The ulnar and median innervated muscles were tested and found to be intact. All tendons, including radial innervated, were found to be present and working (tenodesis effect).

Diagnostic Studies Posterior anterior, lateral, and oblique radiographs were taken of the wrist and forearm and showed no bony abnormalities. Anterior, posterior, and lateral views of the humerus were taken and showed a well-healed middle to distal one-third shaft humerus fracture with an intramedullary rod in place with acceptable alignment. An electromyogram (EMG) was originally obtained 4 months after the injury and revealed absent brachioradialis action potentials. The patient had a new EMG showing no change in response to

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Figure 23–1. (A,B) Clinical photos of a drop wrist with inability to extend metacarpophalangeal (MP) joints due to a radial nerve palsy. 134

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PEARLS • The Jones/Tsuge/Boyd modified transfer for high radial nerve palsy preserves power grip because it does not use the flexor digitorum superficialis and leaves the flexor carpi ulnaris intact. • This transfer (Jones/Tsuge/ Boyd) provides independent EPL function. • In a patient who needs a strong grip but does not need individual finger extension, the use of flexor carpi radialis is often selected for digital extension.

PITFALLS • The Jones/Tsuge/Boyd modified transfer for high radial nerve palsy requires the presence of a palmaris longus and two fully functional wrist flexors. • The Jones/Tsuge/Boyd transfer does not provide independent finger extension. • The Jones/Tsuge/Boyd modified transfer may cause mild ulnar deviation of the wrist.

the brachioradialis, as well as no response to the extensor digitorum communis, extensor pollicis longus, as well as to the extensor carpi radialis brevis (ECRB).

Differential Diagnosis Tendon laceration extensor pollicis longus (EPL) Tendon laceration ECRB, extensor carpi radialis longus (ECRL) Radial nerve palsy Mixed nerve palsy

Diagnosis High Radial Nerve Palsy The physical examination and diagnostic studies necessitated a discussion about a high radial nerve palsy without any good prognosis for recovery. Radial nerve injuries that occur in the proximal one third of the forearm result in a low radial nerve palsy (Fig. 23–2). Low radial nerve palsies are characterized by loss of thumb extension, abduction, and finger extension, and by lack of grasp. The level of injury can also be diagnosed by the “hanging of the wrist.” If the wrist is straight, the level is above the elbow. If the wrist is extended but radial deviated (ECRL intact), the level of injury is below the elbow. The radial nerve originates on the posterior cord of the brachial plexus, just above the axilla. The nerve passes posteriorly and laterally in close approximation to the

Figure 23–2. Anatomy of radial nerve as it crosses the elbow to branch into the posterior interosseus nerve (PIN). 135

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Figure 23–3. Anatomy of the volar and dorsal forearm essential for understanding successful transfer of the tendons in a radial nerve palsy.

humerus throughout its course. The nerve is protected by the long and lateral heads of the triceps. Fractures, such as a displaced spiral oblique fracture, can severely damage the nerve in this area. The sensory branch of the radial nerve becomes subcutaneous underneath the brachioradialis in the distal forearm. The radial nerve provides motor branches to the triceps, brachioradialis, and supinator, and the wrist, finger, and thumb extensors (Fig. 23–3). The radial nerve provides sensory innervation to the posterior and inferolateral arm, posterior forearm, and dorsal radial wrist and hand. The treatment of fractures with associated radial nerve palsy is controversial. An EMG that revealed a nonfunctioning brachioradialis at 4 months from the date of injury may require, as was done, a nerve exploration. Nerve exploration may reveal a stretched and contused radial nerve that may be lacerated as well, presumably by the fracture (bone spicules). Now with no recovery, the hand and wrist function will be restored with tendon transfers.

Nonsurgical Treatment Observation is indicated in some nerve palsies associated with fractures. Since return of normal function can be anticipated at 3 to 6 months, surgical management should be undertaken at this time. 136

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Surgical Management Preoperative planning is essential for all operative cases, but especially for those involving tendon transfers. The principles for tendon surgery must be adhered to prior to any successful tendon transfer. Principles such as one donor for wrist extension, one donor for finger extension, and one donor for thumb extension must be strictly adhered. Passive range of motion of the wrist and fingers must always be maintained, as described in our conservative treatment, prior to any elective tendon transfer with preoperative wrist extension splinting all completed prior to the day of surgery. There are many options for high radial nerve palsy. This transfer is a modified Jones/Tsuge/Boyd: 1. Pronator teres to ECRB 2. Flexor carpi radialis to the finger extensors [extensor digitorum communis (EDC)] 3. Palmaris longus to extensor pollicis longus 4. Tenodesis of abductor pollicis longus These donor muscles are preferred as they preserve power grip by leaving the flexor carpi ulnaris intact and do not use the flexor digitorum superficialis. On the other hand, this transfer requires two excellent wrist flexors and the palmaris longus. If these tendons are not present, this transfer cannot be used and an alternative must be selected. A skin incision is made at the junction of the upper and middle thirds of the radial side of the forearm and extends distally to approximately 3.0 cm proximal to the radial styloid. The incision moves dorsally to the fourth dorsal compartment. A short transverse incision is made just proximal to the volar wrist flexion crease over the flexor carpi radialis and the palmaris longus insertion to identify these structures. The pronator teres is identified at the insertion of the midshaft of the radius on the dorsal aspect of the forearm and is detached from the 3.0-cm strip of periosteum. The muscle is then freed proximally to the midline of the forearm. It is essential that slow and meticulous dissection occurs, as the 3.0-cm strip of the periosteum is quite necessary to maintain length when attempting to suture this strip into the ECRB (Fig. 23–4). With the palmaris longus and the flexor carpi radialis transected at the wrist and freed proximally to the midforearm, both tendons are moved dorsally through a

Figure 23–4. Clinical photo of pronator teres prepared for transfer to the extensor carpi radialis brevis (ECRB). (Photo courtesy of S. Kozin) 137

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Figure 23–5. (A) The flexor carpi radialis (FCR) tunneled subcutaneously into the dorsal aspect of the forearm to meet the common finger extensors. (B) The palmaris longus tunneled to meet the extensor pollicis longus (EPL) on the dorsum to allow for thumb extension.

subcutaneous dissection opened up with a hemostat (Fig. 23–5). The ECRB is cut at the midforearm, and the wrist is held at 50 to 60 degrees of extension. The pronator teres is then sutured to the ECRB without tension (Fig. 23–6). The wrist should move into ~30 degrees of wrist dorsiflexion when placed against gravity at rest and flexion with the tenodesis effect. The remaining part of the procedure, that is finger extension and thumb extension, is now completed. If prior to beginning finger extension and thumb extension the wrist has a slight position of ulnar deviation due to the loss of the flexor carpi radialis, suturing must occur on the distal end of the ECRL with some tension to the distal aspect of the ECRB to compensate. The extensor digitorum communis as well as the extensor minimi quinti are cut at the midforearm level. It is important to not include the extensor indicis proprius in this transfer. The flexor carpi radialis is split and sutured to each tendon separately. The tendon length is checked by using the tenodesis effect with palmar flexion of the wrist, and observation of full finger extension. With the wrist in full dorsiflexion, each finger should be able to flex fully to a position of function. The third compartment of the wrist is open, and the extensor pollicis longus is freed up. The tendon is cut ~5.0 to 7.0 cm proximal to the radial styloid and sutured to the palmaris longus with the thumb metacarpophalangeal joint in 20 degrees of flexion and the wrist in 30 degrees of extension. The distal end of the abductor pollicis longus (APL) is looped around the brachial radialis just proximal to the radial styloid. The APL is then sutured to 138

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Figure 23–6. Suturing the pronator teres to the ECRB.

itself and the brachial radialis with the first metacarpal held in extension, and the wrist in 30 degrees of full extension. This tenodesis effect is completed to make certain no restricted wrist motion is seen (Fig. 23–7). If full ulnar deviation of the wrist is restricted by the tenodesis effect, the APL is loosened to the appropriate tension. The tourniquet that was used at the beginning of the procedure is let down. Hemostasis is obtained and the wounds are closed. The arm is placed in a volar splint that holds the wrist at ~45 to 50 degrees of dorsiflexion. The finger should be positioned with 30 degrees of palmar flexion at the metacarpophalangeal (MP),

Figure 23–7. The distal abductor pollicis longus (APL) sutured to itself for a tenodesis effect (see text). 139

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Figure 23–8. The completed tendon transfer for a patient with high radial nerve palsy.

proximal interphalangeal (PIP), and distal interphalangeal (DIP), and the thumb is placed in abduction with 30 degrees of flexion at the MP and interphalangeal (IP) joints (Fig. 23–8).

Postoperative Management After approximately 4 weeks all splints are removed, and a volar custom splint made by a hand therapist is applied with extension slings for the MP joint of the fingers. Active range-of-motion exercises of the fingers are begun at 3 to 4 weeks, and the wrist at 6 weeks. Splinting as protection is done for 8 to 12 weeks postoperatively often yields excellent results.

Alternative Procedures Patients who develop severe wrist contractures should consider undergoing a wrist arthrodesis rather than a tendon transfer. Patients with multiple nerve injuries and insufficient tendon donors to allow for a transfer should also consider a wrist arthrodesis. Patients who are totally disabled and who do not want surgical intervention can use splints custom-made by a certified occupational hand therapist. 140

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Complications Complications in correction of high radial nerve palsy are several and include overcorrection, undercorrection, and soft tissue bed problems. Overcorrection is one of the most common complications in this transfer. Overcorrection of a wrist drop may be due to excessive shortening, that is, too much tension in the transfer. This complication can easily be resolved with testing the hand in the operating room with the tenodesis effect. When overcorrection is present due to adherent tendon transfers, passive palmar flexion of the wrist will be limited. The transfer should be reexplored and the tendons lengthened if not recognized intraoperatively. It is important to note that if the pronator teres was used as a tendon donor, it may prove very difficult to lengthen this transfer at a second return visit to the operating room. Undercorrection of the wrist drop is usually due to a transfer that has been sutured too long. To test the transfer length, with the patient in a postoperative wrist drop, the patient’s forearm is supinated so the ulnar side of the wrist is parallel to the examination table. If active wrist dorsiflexion does not improve, the transfer requires shortening. Shortening the tendon by 1.0 cm can increase dorsiflexion by 15 to 20 degrees. To achieve more dorsiflexion with the pronator teres, the ECRB is sutured more distally. If the wrist can dorsiflex with gravity eliminated, the patient’s problem is probably one of muscle imbalance, and not in a technical error such as suturing too long. Contracture of a soft tissue bed with resultant failure of a tendon transfer can be avoided. Adhering to the general principles of tendon transfers often leads to good results. Restoring function to the wrist, with extension as well as digital extension, in most cases can be achieved with a successful tendon transfers. The severity of the deformity and functional goals need to be discussed preoperatively with the patient prior to undertaking any type of tendon transfer in these complex patients.

Suggested Readings Boyles JH. Tendon transfers for radial palsy. Bull Hosp Joint Dis 1960;21:97. Brand PW. The Hand and Upper Limb. In: Lamb, DW, ed. The Paralyzed Hand vol 2, New York: Churchill Livingstone; 1987:190–213. Goldener JL, Kelly JM. Radial nerve injuries. South Med J 1958;51:873–883. Riordan DC. Tendon transfers in hand surgery. J Hand Surg [Am] 1983;8:748–753. Scuderi C. Tendon transplants for irreparable radial nerve paralysis. Surg Gynecol Obstet 1949;88:643–651. Strickland JW, Kleinman WB. Tendon transfers for radial nerve paralysis. Master Tech Orthop Surg 1998;20:303.

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Section V

Vascular Disorders

Arterial Aneurysms Kevin D. Plancher

Cannulation Injuries Leon S. Benson

Extravasation Injuries Leon S. Benson

ARTERIAL ANEURYSMS

24 Arterial Aneurysms Kevin D. Plancher

History and Clinical Presentation A 38-year-old left hand dominant woman is seeking treatment for a tender mass in the palm of her hand. The patient had fallen with a glass bottle in her hand 2 weeks earlier and had sustained a puncture wound to the ulnar aspect of her right palm. At that time active arterial bleeding persisted despite direct pressure on the wound with a compressive dressing. She was originally treated in the emergency department with irrigation and exploration with cauterization of a “superficial” vessel and wound closure.

Physical Examination Removal of her sutures of the skin resulted in pulsatile bleeding from the wound. The bleeding continued despite direct manual compression on the wound (Fig. 24–1). Manual compression of the ulnar and radial arteries individually at the wrist crease did not stop the bleeding. Bleeding only ceased with manual compression of both arteries. The Allen’s test was performed and found the ulnar artery not patent. The color of the hand when performing the Allen’s test, to the ulnar side of the wrist, showed lack of perfusion to the radial side of the wrist (Fig. 24–2).

PEARLS • Use of a tourniquet and appropriate anesthesia for adequate visualization and microscopic dissection of the artery • Meticulous microscopic dissection with tension-free anastomosis • Postoperative supervised therapy and appropriate incision care

PITFALLS • Vein graft selection too small • Inadequate graft length or anastomosis sewn under tension • Failure to maintain proper graft orientation

Diagnostic Studies Radiographs of the patient’s hand were obtained. Doppler flow assessment, pulse volume recordings, and angiography were also obtained. Angiography provided definitive information regarding the location and extent of arterial injury (Fig. 24–3).

Figure 24–1. Manual compression of the wrist with a saturated dressing in the patient with persistent bleeding.

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Figure 24–2. The Allen test. (A) Compression of both the ulnar and radial arteries. (B) Demonstrating no blood flow to the hand. (C) Release of only the radial artery in this example gives a negative test for the radial artery. (D) Release of only the ulnar artery in this example gives a positive Allen test for the ulnar artery.

A

B

Figure 24–3. (A) Arteriography of the forearm and digital subtraction angiography of the palm. (B) Close-up view of the palm. 146

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Differential Diagnosis Ganglions Nerve tumors Other soft tissue masses Raynaud’s disease Pseudoanerysm of the palm

Diagnosis Pseudoaneurysm of the Palm Aneurysms are classified into two groups: traumatic and nontraumatic. Traumatic aneurysms can be subgrouped into true and false aneurysms. True aneurysms occur after blunt trauma to the upper extremity. These arise from occupational hazards, thoracic outlet syndrome, or a malignancy. Damage occurs to the arterial wall media to cause vessel dilation. False aneurysms occur from a penetrating arterial injury or from a complete rupture of the vessel wall when continuity is maintained by the surrounding soft tissue. Hemorrhage from the vessel forms a contiguous hematoma that forms a fibrous shell adjacent to the vessel. Stab wounds, gunshots, and displaced fractures, or recurrent bleeding from hemophilia are all causes of a false aneurysm. Other causes of a false aneurysm include arterial punctures from blood gas analysis, cannulation of a vein or axillary arterial injury during a brachial plexus injection, as well as unrecognized arterial bleeders during operations. Diseases associated with peripheral aneurysms include Kawasaki’s syndrome, Buerger’s disease, and hemophilia.

Nonsurgical Management While the patient is waiting for results of clinical tests, several nonsurgical options are available. The patient may be prescribed a vasodilator for partial obstructions to a blood vessel. Nitropaste placed on the finger or affected site has also been used, as has sublingual nifedipine. Surgery is indicated if symptoms persist and survival of the finger or hand is in question.

Surgical Management Treatment of upper extremity aneurysms consists of exploration, resection, and vascular reconstruction depending on the location and type of aneurysm. The most common true and false aneurysms reported to date are the ulnar artery aneurysms. The redundant artery allows for an end-to-end repair. Digital artery aneurysms are rare. In the absence of ischemic signs, when an arterial thrombosis is present in a digit, ligation rather than reconstruction is the treatment of choice (Figs. 24–4 and 24–5). The patient was administered general anesthesia and the arm was exsanguinated, and a tourniquet inflated to 250 mm Hg. The wound was explored under loupe magnification and a 2 by 3 cm pseudoaneurysm was located, emanating from the superficial palmar arch between the common digital arteries to the ring and little 147

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Figure 24–4. Arterial anastomosis of the wrist.

Figure 24–5. Arterial anastomosis of the digits of the hand.

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A

C

B

Figure 24–6. (A) Note aneurysm in the depth of the wound. (B) Close inspection of the aneurysm out of the depth of the wound. (C) Aneurysm to be resected with arch brought back together.

fingers (Fig. 24–6A). The mass occupied the entire space between the two arteries and a 1-cm segment of the superficial arch appeared thin-walled and fibrotic at the origin of the pseudoaneurysm (Fig. 24–6B). Proximal and distal control of the vessel was obtained with a vascular loop around the superficial arch at the base of the common digital arteries. Resection of the pseudoaneurysm was done, and then the free ends of the arch were brought together easily (Fig. 24–6C). A primary anastomosis in this position was formed by an intersection with the superficial palmar arch and the third and fourth common digital arteries. If there is concern that the tension produced by such an anastomosis could lead to occlusion, then a timed Allen test should be performed. This test can be performed by closing the cut ends of the superficial palmar arch with microvascular clamps. Vessel loops provided occlusion of the arch on both sides proximal to the common digital arteries. Normal color and turgor was noted with brisk capillary refill in the ring and little fingers within 3 seconds after release of either the ulnar or the radial side of the superficial palmar arch. If the arteriogram shows digital flow and the Allen test has demonstrated sufficient flow at rest, you will not need to perform a vein graft, and the superficial palmar arch can be ligated (Fig. 24–7). A timed Allen test was again performed, with occlusion of the radial and ulnar arteries at the wrist crease. Brisk capillary refill was again noted within 3 seconds after sequential release of the occlusion of the arch. A patient-oriented approach is always necessary, and patient selection is important because the patient must be willing to play an active, cooperative role in the perioperative period. Postoperatively, extensive rehabilitation is seldom necessary after vein grafting in ulnar artery thrombosis, and the hand is placed in a bulky compressive dressing 149

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A

B

C

Figure 24–7. End-to-side and end-to-end anastomoses as a technique used to regain blood flow when necessary.

with dorsal splints. This dressing allows the fingers freedom to move and active range of motion. Supervised occupational hand therapy is added if the patient has difficulty with range of motion. A soft dressing is left in place for 2 weeks, at which time the sutures are removed. The foot is dressed with a compressive dressing, which is removed at 5 days. A support stocking is recommended for 6 to 8 weeks, and if the main portion of the saphenous vein has been harvested, the patient is advised that there will be some swelling of the foot, which will diminish over time. At the time of discharge, the patient is instructed on appropriate anticoagulation therapy, and at 2 weeks, if the wounds are healing, the patient is allowed increased use of the hand, but is not allowed to return to unrestricted activities for 6 to 8 weeks. Specific strengthening exercises are given only if the patient has pain or stiffness.

Alternative Methods of Management Concerns with vein graft harvesting include selecting a vein graft that is too small along with iatrogenic damage of the graft during dissection. The length of the graft is crucial, as is meticulous dissection to avoid saphenous or other sensory nerve damage. Hemostasis at the branches is important as well as sustaining that hemostasis 150

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Figure 24–8. The graft and surgical technique in arteries that do not match completely secondary to size.

post-graft harvesting. This procedure requires extensile exposure, attention to detail, and careful hemostasis. Postoperative wound appearance may be enhanced by appropriate drainage, careful hemostasis, and subcuticular closure of vein donor sites. Using Steri-strips for 6 to 12 weeks and having the patient use a sunscreen may minimize scar spread and disfigurement. Adequate exposure helps minimize technical errors during anastomoses, and the microscopic portion of the procedure should be “easy.” Failure to maintain the graft in the proper orientation when placing it is problematic, because twisting the graft more than 60 degrees will compromise patency rates (Fig. 24–8). The role of intussusception anastomoses or mechanical couplers has yet to be delineated in arterial reconstruction with vein grafts. When appraising the anastomosis, it is vital to have uncompromised flow, and if it is compromised, it must be redone.

Complications With patent vein grafts, ulcerations should heal and symptoms should improve, but complete elimination of pain, cold intolerance, and neural dysfunction is uncommon. Improvement, not cure, is the expectation, and the patient should understand that before proceeding with the operation.

Suggested Readings Adham MN, Seradge H. Treatment of thrombosed thumb artery aneurysm: a report of four cases. J Hand Surg 1997;22A:750–752. Axe MJ, McClain EJ. Complete involvement of the ulnar nerve secondary to an ulnar artery aneurysm. A case report. Am J Sports Med 1986;14:178–180. Duchateau J, Moermans JP. False aneurysm of the radial artery. J Hand Surg 1985; 10A:140–141. Gelberman RH, Blasingame JP. The timed Allen test. J Trauma 1981;21:477–479. Gelberman RH, Blasingame JP, Fronek A, Dimick MP. Forearm arterial injuries. J Hand Surg 1979;4:401–408. Ho PK, Weiland AJ, McClinton MA, Wilgis EF. Aneurysms of the upper extremity. J Hand Surg 1987;12A:39–46. Murphy RX Jr, Korngold JM, Jaffe JW, Scarlato M. Bilateral radial artery pseudoaneurysms associated with bilateral ulnar artery atresia: a case report. J Hand Surg 2000;25A:565–570.

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25 Cannulation Injuries Leon S. Benson

History and Clinical Presentation The hand surgery service was called to evaluate the thumb and index finger of a 75-year-old woman. The patient had been admitted to the hospital 1 week previously for heart failure. Twenty-four hours after admission she became increasingly hypotensive and was transferred to the intensive care unit. A Swan-Ganz catheter was placed, the patient was intubated, and a left wrist arterial line was inserted. On hospital admission day 7, the patient was still in the intensive care unit and intubated but she was slowly improving. However, it was then noted that her thumb and index finger, which had looked “dusky” on the previous day, were now turning black and rigid (Figs. 25–1 and 25–2) even though the radial artery catheter had been removed on the previous day.

Physical Examination Examination of the left hand demonstrated dry gangrene of the thumb that was sharply demarcated distal to the midportion of the proximal phalanx. The left index finger also demonstrated dry gangrene, although a more gradual zone of transition was present, with grossly necrotic tissue being present circumferentially distal to the distal interphalangeal joint. No other soft tissue compromise was noted about the hand. A normal ulnar pulse was easily palpable at the wrist, whereas a radial pulse was undetectable, either by palpation or Doppler examination. A small puncture wound and 3-cm ecchymotic area were present where the radial pulse normally would have been palpable. Nursing staff noted that this was the site of arterial line placement when the patient was first admitted to the intensive care unit. The line, which was an 18-gauge angiocatheter, had been removed 2 days earlier when it seemed to be dysfunctional.

Figure 25–1. Clinical presentation of the volar surface with a black and rigid appearance with sharp demarcation demonstrating dry gangrene. 152

Figure 25–2. Clinical presentation of the dorsal surface with a black and rigid appearance with sharp demarcation demonstrating dry gangrene.

C A N N U L AT I O N I N J U R I E S

PEARLS • Up to 20% of patients have an incomplete ulnar arterial arch in which the thumb and index fingers are completely dependent on the radial artery for blood flow. • The timed Allen’s test is the simplest and cheapest way to accurately screen for patients with incomplete arterial arch anatomy. • Twenty-gauge Teflon catheters are associated with less thrombosis production in the radial artery than larger (18-gauge) heparin-coated polyethylene catheters. • Constant irrigation of the catheter greatly reduces thrombus formation. • Allen’s test is inconclusive if blushing of the hand is delayed for 10 to 15 seconds. • The overall incidence of radial artery thrombosis after cannulation has been estimated to ~10 to 25%. • If prolonged arterial monitoring is required, the temporal artery is a good choice. It is totally expendable and can easily be used for 5 to 7 days without clotting. Access can be achieved with a small incision under local anesthesia. • Pretreating the patient with a single, 600-mg dose of aspirin has been shown to diminish the frequency of radial artery thrombosis from cannulation (without any associated bleeding complications).

PITFALLS • Any sign of vascular compromise to the hand should be evaluated immediately. Amputation of digits is frequently the only treatment option available because ischemia is not noticed until tissue necrosis has occurred.

Diagnostic Studies Plain radiographs of the distal radius, wrist, and hand demonstrated no acute bony abnormalities. Upper extremity angiography was performed later in the patient’s hospital stay, and complete occlusion of the radial artery was demonstrated just proximal to the wrist. Furthermore, the ulnar artery was shown to provide little blood flow to the radial side of the hand. Some collateral flow was present coming from the ulnar arch, although no large vessels could be seen extending to the distal portion of the thumb or index finger.

Differential Diagnosis Radial artery thrombosis due to cannulation injury Embolic thrombosis of digital vessels Small vessel occlusion due to diabetes or a vasculitic disease Digital ischemia as a side effect of pharmacologic blood pressure support (e.g., Neo-Synephrine related vasoconstriction) Localized severe infection

Diagnosis Radial Artery Thrombosis Due to Cannulation Injury in a Patient with Radial Dominant Flow to the Hand Vascular complications due to cannulation or injection injuries can be devastating. It is important to know how radial artery cannulation injury occurs, not only because of the high frequency of radial artery use for placement of monitoring catheters, but also because of the extreme consequences of radial artery damage in select individuals. Understanding the arterial anatomy of the hand is key in accounting for cannulation injury. There are two main arches that support vascularity to the digits: the superficial palmar arch, which is an extension of the ulnar artery, and the deep palmar arch, which generally arises from the radial artery (Fig. 25–3). The superficial (ulnar) arch, which is

Proper Volar Digital Arteries

Common Volar Digital Arteries

Volar Metacarpal Artery I Ramus of the Superficial Arch Radial Artery

Volar Metacarpal Arteries II-IV Superficial Volar Arch Deep Volar Arch Ramus of the Deep Arch Ulnar Artery Volar Interosseous Artery

Figure 25–3. Vascular anatomy of the hand, demonstrating the deep and superficial arches and their typical communications. 153

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• Forcible extension of the digits or hyperextension of the wrist can produce blanching, causing a false-positive Allen’s test. • At least 11 pounds of pressure are required to occlude the radial or ulnar artery at the wrist when performing an Allen’s test. • Allen’s test must be modified when it is performed in unconscious patients. To perform the test for these patients, hand ischemia can be temporarily induced using an Esmarch bandage, and a reflow to the palmar arches can be assessed using a Doppler ultrasound device. • Catheters that are not irrigated will reliably produce radial artery thrombosis if left in place for more than 40 hours. Most authors recommend leaving the catheter in place for no more than 12 to 18 hours. • Pulse oximetry may provide normal values in the face of significantly compromised blood flow to the digits. It is therefore less valuable in identifying critical ischemia to the digits. • When a radial artery catheter is in place, it should not be ignored. The site should be examined periodically. Circumferential bandages (including hospital identification bracelets) should be removed, and hypotension, vasoconstrictive drugs, and hypothermia should be avoided if at all possible. Any signs of ischemia or inflammation, such as redness at the site, loss of capillary refill or normal tissue color distally, or change in pulses in the wrist or palm, should prompt immediate removal of the catheter. Any failure of local changes to reverse within 1 hour should make surgical exploration of the artery a serious consideration. 154

slightly more distal and palmar than the deep arch (radial arch), is the primary blood supply to the ulnar three digits through its connections with the volar digital arteries. The deep arch comes off the radial artery, where this vessel drops down through the anatomic snuffbox and branches into the princeps pollicis artery (to the thumb). This large vessel to the index finger terminates at the deep palmar arch. In the usual circumstance, both arches connect to each other. The ulnar arch often terminates as a smaller diameter vessel that connects to a superficial branch of the radial artery, and the deep radial arch usually terminates in the ulnar palm by connecting to the ulnar arch via collateral vessels. There can be, however, great variability in the specific vascular networking within any given hand. For example, the median artery, which is present in fetal development, can occasionally persist as a major vessel and contribute additional blood flow to the two main arches. More importantly, the two main arches may exist as “incomplete” patterns, in which there are minimal connections between the radial and ulnar derived vascular trees in the palm. It is thought that an incomplete ulnar arch exists in ~20% of hands, and in this scenario the thumb and index finger derive most, if not all, of their blood supply from the radial artery (Fig. 25–4). Identification of individuals at risk for radial artery cannulation injury, therefore, relies on noting the presence of incomplete arch vascular anatomy. Sometimes a history of cold intolerance in the hand provides a clue, although more commonly physical examination or vascular imaging is necessary. Simple physical examination can be remarkably helpful in identifying radial or ulnar artery dominance in the hand. The modified Allen’s test involves manually occluding both vessels in one hand after the patient makes a tight fist several times to pump blood out of the hand. Then, with the patient’s digits gently extended, the radial artery is released and the time

Radial Artery Ulnar Artery

Figure 25–4. An example of an “incomplete” vascular arch pattern, in which flow to the thumb and index finger are dependent on radial artery patency.

C A N N U L AT I O N I N J U R I E S

• Up to 30% of thrombi may form a day or more after the catheter is removed from the radial artery. Therefore, careful observation for hand ischemia must be pursued for several days after the catheter is removed.

required for the palm to regain its normal color is noted. The test is then repeated, noting the refill time when the ulnar is artery released. Normal refill time is between 2 and 3 seconds. A positive Allen’s test, or failure of palmar capillary refill in less than 4 or 5 seconds, is suggestive of incomplete arch vasculature. The vascular examination of the wrist and hand can be further worked up by a variety of more sophisticated methods, including Doppler ultrasound, pneumoplethysmography, and angiography. It should be noted, though, that the timed Allen is a remarkably simple and accurate screening test that can identify patients with incomplete palmar arches. In addition to vascular anatomy, there are several other factors that seem to influence development of ischemia after radial artery cannulation. A smaller catheter, such as a 20-gauge size, seems to be less likely to produce thrombosis than a larger one (18-gauge). Teflon catheters that are irrigated regularly seem to produce less thrombosis-producing irritation than heparin-coated polyethylene catheters. Duration of catheter presence is also an issue. The longer the catheter is present, the more likely it is to produce occlusion of the vessel. One study showed that in catheters present for more than 40 hours, thrombosis was present in 93% of patients, compared with 25% for catheters removed at 20 hours or less. In most cases, even if thrombosis of the radial artery occurs, the presence of complete vascular arches prevents critical ischemia from occurring in any particular part of the hand. Furthermore, in many cases, the thrombus is recanalized over time and does not cause any clinical symptoms. However, in patients with incomplete vascular arches, occlusion of the radial artery can produce total ischemia in one or several fingers (usually the thumb and index). Furthermore, medical conditions may be present that can further lower the threshold at which critical ischemia develops. Examples of such factors include hypotension, vasoconstrictive drugs, diabetes, peripheral vascular disease, coagulopathy, and Raynaud’s phenomenon. Some authors have found that pretreatment with aspirin may reduce the incidence of thrombosis following radial artery catheterization. In the clinical scenario described here, note that the patient was initially hypotensive, she received vasoconstrictive drugs, the catheter placed was an 18-gauge instead of a 20-gauge, and the catheter was in place for more than 3 days. All of these issues can have an impact on producing gangrene if the vascular arches are incomplete.

Surgical Management A protective splint was applied to the hand to prevent trauma to the compromised digits. One week later, when the patient had been medically stabilized, a thumb and index finger amputation was performed. No further progression of necrosis had occurred since the original assessment, and a transproximal phalanx amputation was performed for the thumb. The index finger was treated with an amputation through the distal portion of the middle phalanx. Digital neurectomies were performed at the amputation sites. No infection was present. Mid-lateral incisions were used and direct closure via a “fish-mouth” type wound was possible with well-vascularized local soft tissue.

Postoperative Management A forearm-based radial gutter splint was applied in the operating room and left in place for 1 week. Dressing change at that time demonstrated well-healing wounds with no evidence of infection or further soft tissue necrosis. Small individual dressings 155

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were applied to the thumb and index finger for 1 week. Occupational therapy was started with the first dressing change to aid in stump desensitization and proximal joint motion.

Alternative Treatment The compromised hand due to radial artery thrombosis usually attracts attention after irreversible ischemic necrosis has occurred; consequently, amputation of dead tissue is the only remaining treatment option. However, if hand ischemia is identified very early, alternative therapies may be helpful. Such interventions include use of intravenous heparin or low molecular weight dextran, intermittent sympathetic block, and intraarterial administration of reserpine or papaverine. Methods to improve cardiac output may also be helpful. Ultimately, surgical intervention via thrombectomy and repair of the injured vessel segment may be necessary to avert gangrene of the radial digits.

Suggested Readings Baker RJ, Chunpraprah B, Nyhus LM. Severe ischemia of the hand following radial artery catheterization. Surgery 1976;80:449–457. Bedford RF. Radial arterial function following percutaneous cannulation with 18 and 20 gauge catheters. Anesthesiology 1977;47:37–39. Bedford RF. Wrist circumference predicts the risk of radial-arterial occlusion after cannulation. Anesthesiology 1978;48:377–378. Bedford RF, Ashford TP. Aspirin pretreatment prevents post-cannulation radialartery thrombosis. Anesthesiology 1979;51:176–178. Bedford RF, Wollman H. Complications of percutaneous radial-artery cannulation. Anesthesiology 1973;38:228–236. Coleman SS, Anson BJ. Arterial patterns in the hand based upon a study of 650 specimens. Surg Gynecol Obstet 1961;113:409–424. Crossland SG, Neviaser RJ. Complications of radial artery catheterization. Hand 1977;9:287–290. Downs JB, Chapman RL, Hawkins IF. Prolonged radial artery catheterization. Arch Surg 1974;108:671–673. Downs JB, Rackstein AD, Klein EF, Hawkins IF. Hazards of radial-artery catheterization. Anesthesiology 1973;38:283–286. Ejrup B, Boguslav F, Wright IS. Clinical evaluation of blood flow to the hand. Circulation 1966;33:778–780. Falor WH, Hansel JR, Williams GB. Gangrene of the hand: a complication of radial artery cannulation. J Trauma 1976;16:713–715. Gelberman RH, Blasingame JP. The timed Allen test. J Trauma 1981;21:477–479. Katz AM, Birnbaum M, Moylan J, Pellett J. Gangrene of the hand and forearm: a complication of radial artery cannulation. Crit Care Med 1974;2:270–272. 156

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Lee KL, Miller JG, Laitung G. Hand ischemia following radial artery cannulation. J Hand Surg 1995;20B:493–495. Levinsohn DG, Gordon L, Sessler DI. The Allen’s test: analysis of four methods. J Hand Surg 1991;16A:279–282. Mandel MA, Dauchot PJ. Radial artery cannulation in 1,000 patients: precautions and complications. J Hand Surg 1997;2:482–485.

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26 Extravasation Injuries Leon S. Benson

History and Clinical Presentation

PEARLS • Fluid extravasation injuries that present with a diameter of less than 10 cm and have induration and redness as the primary findings are generally less severe and can often be treated with elevation and ice. • The incidence of doxorubicin hydrochloride (Adriamycin) extravasation injury is ~3% of those patients receiving the drug. The incidence of extravasation injury from any chemotherapy administration is ~6%. • The pain associated with a chemotherapy extravasation can be a significant long-term problem. Surgical excision of the affected area often greatly improves the patient’s quality of life, even for those individuals who are quite ill already. Excision also diminishes the likelihood or severity of joint stiffness and sympathetic dystrophy. • Because of their low osmolarity and less direct cytotoxicity, nonionic radiographic contrast agents (such as iohexol) are safer and better tolerated than traditional ionic agents (such as diatrizoate meglumine).

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After giving birth, a 26-year-old woman became acutely hypotensive from postpartum bleeding. Despite initial efforts at fluid resuscitation, she developed hypovolemic shock and subsequently was the recipient of massive volumes of intravenous fluids and blood to save her life. At one point an infusion pump was used to aid in rapid administration of electrolyte solution. Efforts to resuscitate her were successful and she was then transferred from the maternity ward to the intensive care unit (ICU). It was noted shortly after transfer to the ICU that her left forearm was swollen and discolored, but no further assessment of the extremity was performed at that time. Nursing notes indicated that despite the forearm appearance, peripheral pulse remained “good.” The patient was intubated and heavily sedated. About 8 hours after transfer to the ICU, it was noted that the patient’s left forearm and hand were massively swollen and blue. The hand surgery service was then consulted.

Physical Examination Massive swelling was noted from the left elbow to left hand with severe ecchymosis throughout the dorsal forearm. The patient was obtunded, and no pain responses could be elicited. Radial and ulnar pulses were easily palpable at the wrist. The entire forearm reflected “rock-hard” soft tissue tension. A hospital identification bracelet that had been around the left wrist was extremely tight and at this time was removed. Furthermore, an automatic blood pressure cuff had been placed at the left upper arm and had been cycling on and off every 20 minutes to check the patient’s blood pressure. This cuff was also removed and relocated elsewhere. It was also noted that an intravenous catheter (20-gauge) had been placed into the dorsal wrist to aid in rapid fluid replacement earlier in the day. This catheter was now removed and fluid could be seen leaking from the site. Later review of the catheter, IV tubing, and fluid bags revealed that epinephrine-containing solution had also been administered through this intravenous site.

Diagnostic Studies Plain radiographs of the elbow, forearm, and hand showed no fractures or other bony abnormalities. There was no gas or contrast media in the soft tissues. Compartment pressures of the dorsal and superficial volar forearm compartments were checked. The dorsal compartment pressure was 131 mm Hg and the volar compartment pressure was 125 mm Hg. Clear fluid began leaking from both puncture sites after compartment pressures were measured. No other diagnostic studies were pursued at that time.

E X T R AVA S AT I O N I N J U R I E S

PITFALLS • Intravenous infusion pumps can be particularly dangerous because they can inadvertently force fluid into an extravascular space, producing a compartment syndrome. Pediatric patients can be especially at risk for pump-related problems since the automatic shut off pressure of the pump may be gauged for adult physiology. • A specific protocol for administration of doxorubicin hydrochloride (Adriamycin) should be followed. Preventable problems have been identified as producing extravasation events, such as failure to release a proximal tourniquet, use of poor veins, or infusion administered under pressure. Small-diameter polyethylene catheters are better than sharp needles, which tend to puncture the posterior vessel wall. • Application of heat to an extravasation injury is not indicated. It will produce vasodilation, increased interstitial edema, increased swelling, and periarticular stiffness. Use of cool compresses and strict elevation is much better for immediate care.

Differential Diagnosis Forearm compartment syndrome due to intravenous extravasation Forearm compartment syndrome due to chronic compression Forearm ischemia due to proximal vascular occlusion Forearm muscle necrosis due to sepsis or localized infection

Diagnosis Forearm Compartment Syndrome Due to Intravenous Extravasation The prognosis for extravasation injuries can be characterized by four key variables: (1) the volume of material extravasated, (2) the type of material that has extravasated, (3) the amount of time that extravasated material has been present (also called the “necrosis interval”), and (4) the susceptibility of the host to injury. Loth et al (1991) have classified the severity of extravasation into three types (mild, moderate, and severe) based on the amount of extravasated agent. Mild extravasations present with minimal swelling and pain and represent small volume injuries. No blistering or redness is present and the patient can be treated with elevation of the extremity and a compression dressing. Moderate extravasations present with an area of soft tissue inflammation of 10 cm in diameter or less. Significant local tenderness and pain are present, although narcotics pain medication is rarely required. Some erythema may be present but blistering of the skin is absent. Moderate injuries are usually caused by extravasation volumes of 1 to 5 cc. Again, conservative measures such as elevation, cool compresses, and a compression dressing constitute the main form of treatment, although the patient may have residual symptoms for up to a month after injury. Severe extravasation injuries typically result from large volumes of agent and produce severe pain and local soft tissue changes, such as blistering, erythema, and dramatic swelling. Compartment syndrome may result, which would require immediate fasciotomy. In the absence of compartment syndrome or other vascular compromise, specific management of severe extravasations is influenced heavily by the type of extravasated agent involved. The type of extravasated agent constitutes the second major variable that influences prognosis for these injuries. Extravasated agents can be grouped into two main categories: vesicants and nonvesicants. Vesicants are materials that can produce local tissue necrosis. Chemotherapy drugs are an example of vesicants, with doxorubicin (Adriamycin) and mitomycin commonly producing dramatic local tissue necrosis. Calcium solutions, potassium solutions, fluorescein, sodium bicarbonate, and radiographic contrast media are also examples of vesicant agents. Some vesicant agents produce tissue necrosis via specific cellular mechanisms, such as inhibition of DNA synthesis, whereas other vesicants, such as electrolyte solutions, produce hyperosmolar states and cause cell death by fluid shifts or dramatic pH changes. Many vesicants are capable of producing a deep level of tissue necrosis that may take days or weeks to demarcate. Two particular vesicant agents merit special mention. Vasoconstrictor drugs that extravasate can be particularly dangerous, producing either a compartment syndrome or severe local ischemia and tissue death. Local injection of phentolamine may reverse ischemia and prevent disaster. Ultimately, surgical drainage may be required if ischemia cannot be reversed within 3 to 6 hours. Radiographic contrast is 159

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another common vesicant agent that can produce local tissue death. Obtaining a radiograph of the involved extremity can be helpful in delineating how much tissue is affected. In cases where more than 20 cc of contrast is involved, surgical decompression is usually indicated; postdrainage radiographs should be obtained to confirm satisfactory removal of the contrast material. Nonvesicant agents do not typically produce local tissue necrosis but do have the potential to cause significant inflammation; these agents are also sometimes called “irritants.” Examples of nonvesicant agents include blood products, Valium, methotrexate, and albumin. Most nonvesicant extravasations can be treated nonoperatively as long as circulation is not compromised and large volumes of agent are not involved. The necrosis interval has been described as the time between the moment of injury and the point at which irreversible tissue death occurs. Surgical drainage performed during this time interval can dramatically improve outcome, because the toxic agent will be removed before tissue necrosis has occurred. The necrosis for many chemotherapy drugs is 72 hours, whereas the necrosis interval for vasoconstricting drugs and radiographic contrast media can be as short as 4 to 6 hours. For those situations in which the patients first present after the necrosis interval has passed, surgical debridement is often better delayed. This is because nothing is gained by immediate debridement (because irreversible necrosis has already occurred) and the area of dead tissue often takes days or even weeks to clearly demarcate. Figures 26–1, 26–2, and 26–3 illustrate treatment algorithms for managing extravasation injuries due to chemotherapy agents, radiographic contrast materials, and vasoconstrictive drugs, respectively.

Figure 26–1. Treatment algorithm for chemotherapy agent extravasations. (With permission from Loth TS, Eversmann WW. Extravasation injuries in the upper extremity. Clin Orthop 1991;272:248–254.) 160

Figure 26–2. Treatment algorithm for radiographic contrast material extravasations. (With permission from Loth TS, Eversmann WW. Extravasation injuries in the upper extremity. Clin Orthop 1991;272:248–254.)

Figure 26–3. Treatment algorithm for vasoconstrictive agent extravasations. (With permission from Loth TS, Eversmann WW. Extravasation injuries in the upper extremity. Clin Orthop 1991;272:248–254.) 161

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Host factors also influence the prognosis of extravasation injuries. Advanced age, immune compromise, nutritional deficits, steroid dependency, and preexisting peripheral vascular disease are all common host factors that can greatly amplify the damage caused by any given extravasation event. Remember that the mainstay of conservative management is elevation, use of a cool compress, and a loosely wrapped splint to protect and rest the injured part. Although it may seem obvious, make sure that the offending intravenous catheter is removed so that no more agent can extravasate, and make sure that the affected extremity is not further compromised by tight circumferential items such as jewelry, hospital identification bracelets, or tight bandages. Application of heat to the affected area often makes the local swelling much worse and should be avoided. Mark the affected area of the limb with an ink marker so that improvement or worsening can be easily noted as time passes. Save whatever intravenous equipment and drug bags are present initially so that the offending agent and circumstances of extravasation can be clearly and thoughtfully assessed. Injection of antidote material into the affected area may be occasionally indicated for specific cases (i.e., hydrofluoric acid or powerful vasoconstrictor extravasations), but in most cases such injections should be avoided because they will only increase local tissue pressures, increase the likelihood of tissue death or vascular compromise, and inconsistently reach the offending agent. Surgical intervention is an immediate requirement if compartment syndrome or compromise of a major vessel is present. Surgical drainage and decompression of an extravasation injury is also helpful if large volumes of agent are involved, or if the offending agent is a vesicant and the necrosis interval has not yet expired. Once this interval has passed, surgical intervention may be better delayed until clear demarcation of dead tissue has occurred. After thorough debridement of dead tissue, flap coverage or other complex reconstructive procedures may be warranted based on the size of the remaining soft tissue defect.

Nonsurgical Management This patient presented with a severe, acute left forearm compartment syndrome. All circumferential appliances and intravenous lines were removed from the affected extremity, including the blood pressure cuff, hospital identification bracelet, and 20-gauge angiocatheter. This situation represented a surgical emergency, and all other immediate care required operative intervention.

Surgical Management The patient was taken to the operating room immediately for emergency fasciotomies. A dorsal, longitudinal incision was made from the lateral epicondyle to the mid-carpus, and the dorsal forearm fascia was completely released. A palmar incision was then performed, from the antecubital region to the mid-palm in the hand. The lacertus fibrosus was released, as well as the entire volar forearm fascia. The deep volar compartment was also explored and the fascia overlying the deep volar muscle layer was released. Distally, a carpal tunnel release was also performed (Figs. 26–4 and 26–5). Upon release of these compartments, ~250 cc of clear fluid was drained from the wounds. Laboratory analysis of this fluid suggested it was a mixture of plasma and 162

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Figure 26–4. The palmar surface of the left forearm immediately following fasciotomy.

Figure 26–5. The dorsal surface of the left forearm immediately following fasciotomy.

electrolyte solution. Neither the dorsal nor palmar forearm and wrist incisions could be closed primarily and no attempt was made to do so.

Postoperative Care The patient returned to the operating room multiple times over the next 3 weeks for wound debridements. After the swelling subsided and the wounds were stable, meshed full-thickness skin grafts were applied for soft tissue coverage.

Analysis of Case In the case history presented, the patient suffered a major extravasation injury from electrolyte solution intended to replace lost volume from bleeding. Several factors made this extravasation injury particularly severe. First, the patient had epinephrine infused with the electrolyte solution, which as an extravasant acted as a local vasoconstrictor and greatly worsened local ischemia. Second, because the patient was obtunded, recognition of the injury was significantly delayed and the patient developed a compartment syndrome, probably due both to the amount of fluid extravasated as well as to the vasoconstrictive nature of the agent. Third, the presence of constrictive devices around the extremity also contributed in some fashion to the severity of injury. Not only did the patient have a hospital identification band wrapped tightly around her wrist, the frequent blood pressures that were taken with an automatic cuff situated at the upper left arm may also have restricted venous outflow and added to congestion in the extremity. It is also noteworthy that an infusion pump was used, which can produce dramatic extravasation effects by forcing fluid into the extremity. All of these factors can add up and produce a more severe injury than would have otherwise occurred with intravenous fluid extravasation. This case also illustrates that the presence of peripheral pulses does not exclude a compartment syndrome or suggest that severe local soft tissue injury is not present. Furthermore, although it may seem obvious, the infusion should be turned off and the intravenous catheter removed immediately once a potential extravasation problem has been identified. Of note in this case presentation is that the patient may have received a significant additional amount of electrolyte and epinephrine solution for 163

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some period of time after abnormality first presented in the left forearm because no one bothered to turn off the intravenous line and move it to another location.

Suggested Readings Benson LS, Sathy MJ, Port RB. Forearm compartment syndrome due to automated injection of computed tomography contrast material. J Orthop Trauma 1996;10: 433–436. Bowers DG, Lynch JB. Adriamycin extravasation. Plast Reconstr Surg 1978;61: 86–92. Brown AS, Hoelzer DJ, Piercy SA. Skin necrosis from extravasation of intravenous fluids in children. Plast Reconstr Surg 1979;64:145–150. Gault DT. Extravasation injuries. Br J Plast Surg 1993;46:91–96. Larson DL. What is the appropriate management of tissue extravasation by antitumor agents? Plast Reconstr Surg 1985;75:397–402. Linder RM, Upton J, Osteen R. Management of extensive doxorubicin hydrochloride extravasation injuries. J Hand Surg 1983;8:32–38. Loth TS, Eversmann WW. Extravasation injuries in the upper extremity. Clin Orthop 1991;272:248–254. Loth TS, Eversmann WW. Treatment methods for extravasations of chemotherapeutic agents: a comparative study. J Hand Surg 1986;11A:388–396. Loth TS, Jones DEC. Extravasations of radiographic contrast material in the upper extremity. J Hand Surg 1998;13A:407–410. Luedke DW, Kennedy PS, Rietschel RL. Histopathogenesis of skin and subcutaneous injury induced by Adriamycin. Plast Reconstr Surg 1979;63:463–465. Mabee JR, Bostwick TL, Burke MK. Iatrogenic compartment syndrome from hypertonic saline injection in Bier block. J Emerg Med 1993;12:473–476. Scuderi N, Onesti MG. Antitumor agents: extravasation, management, and surgical treatment. Ann Plast Surg 1994;32:39–44. Seyfer AE. Injection and extravasation injuries. In: Hand Surgery Update. Rosemont, IL: American Academy of Orthopaedic Surgeons; 1996:405–411. Seyfer AE. Upper extremity injuries due to medications. J Hand Surg 1987;12A: 744–750. Seyfer AE, Solimando DA. Toxic lesions of the hand associated with chemotherapy. J Hand Surg 1983;8:39–42. Stanley D, Conolly WB. Iatrogenic injection injuries of the hand and upper limb. J Hand Surg 1992;17B:442–446.

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Section VI

Contractures

Dupuytren’s Contracture Jack Abboudi and David S. Zelouf

Stiff Joints Shelly M. Sailer

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27 Dupuytren’s Contracture Jack Abboudi and David S. Zelouf PEARLS • The tabletop test is positive when the patient cannot place his or her open hand flap onto a table surface due to flexion contractures. This finding may prompt consideration for surgical treatment. • Counsel patients with early disease as to your indications for operative treatment. This may help the patient seek reevaluation at an appropriate point for surgery before severe contractures form. • MP contracture correction tends to produce more satisfying results than PIP correction. • Cleland’s ligaments, the deep transverse metacarpal ligament, and the flexor tendon sheath are not involved in the disease.

PITFALLS • Procedures performed by “limited exposure” still require adequate visualization of the neurovascular structures that may be displaced from their normal location. • Neurovascular structures may be displaced superficially and toward the midline of the digit by the spiral cord and should not be assumed to be in their anatomic position. Generally, tracing the neurovascular structures is easier in a proximal to distal direction starting just distal to the transverse carpal ligament. • Neurovascular structures are displaced more toward the midline and more superficial with increasing PIP contracture.

History and Clinical Presentation A 51 year-old right hand dominant construction supervisor presented with a 2- to 3-year history of a progressive right ring finger contracture. He denies a history of trauma. He is of Scottish descent, and his father has undergone bilateral Dupuytren’s contracture releases. The patient denies a history of diabetes or other medical illnesses, and he is taking no medications.

Physical Examination A prominent cord is noted in the palm in line with the ring finger extending to the level of the proximal interphalangeal (PIP) flexion crease. There was a prominent nodule present over the palmar aspect of the proximal phalanx, with a 60-degree metacarpophalangeal (MP) contracture and a 10-degree PIP contracture (Fig. 27–1). The left hand exhibited early palmar disease with no contracture. No knuckle pads were noted, and there was no involvement of the plantar surfaces of the feet.

Radiographic Findings Plain x-rays of the right hand were unremarkable.

Differential Diagnosis Dupuytren’s contracture Joint flexion contracture Scar contracture Flexor tendon bowstring Tendon adhesions Tumor (i.e., fibrosarcoma)

Figure 27–1. Preoperative clinical photo. 167

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Diagnosis Dupuytren’s Contracture Dupuytren’s disease has been attributed to genetic lines of Viking heritage and northern European lineage with an autosomal-dominant pattern of inheritance. The condition presents most frequently in males and after the age of 40. Clinical features include painless palmar pitting, cords, and nodules frequently in line with the small and ring finger. Many structures, described as “ligaments” and “bands” in their normal state, are referred to as “cords” in the diseased state (Fig. 27–2). The spiral cord is a continuum of the diseased spiral band, lateral digital sheet, and Grayson’s ligament. The spiral cord is pulled to the midline with contracture, causing the neurovascular bundle to wrap around the straightening and tightening cord. The natatory cord can be palpated in the web space, and its contracture deviates the digit from the midline at the MP joint. See the suggested readings, later, for more comprehensive descriptions of the pathoanatomy. Disease progression generally leads to characteristic flexion deformities of the MP and the PIP joint. Associated findings include dorsal knuckle pads (Garrod’s nodules), thickening of plantar tissue in the foot (Lederhose’s disease), and penile fascia (Peyronie’s disease). Indications for surgical correction of Dupuytren’s contracture depend greatly on the impact of the deformity on the patient’s ability to perform activities of daily living and the ability and willingness of the patient to participate in the postoperative rehabilitation. Hard-and-fast, objective surgical indications are difficult to define. The “tabletop test” provides the earliest sign of significant flexion contracture, although this test alone is not always an indication for surgery. The test is positive when the patient cannot fully flatten his or her hand against a table surface. Generally, flexion deformities of the MP joints are better tolerated by the patient and are relatively easier to correct, as MP flexion is a relatively “safe” position that maintains

A

Figure 27–2. Anatomy of normal (A) and contractured (B) digits. 168

B

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collateral ligament length. On the other hand, PIP deformities interfere more with hand function and are more difficult to correct, as PIP flexion is a relatively “unsafe” position that allows for volar plate contracture. Therefore, PIP flexion deformities are stronger indications for surgery at earlier stages than are MP deformities. At the microscopic level, Dupuytren tissue demonstrates an abundance of normal fibroblastic and myofibroblastic cells. The local abundance of these cells explains some of the other molecular findings attributed to Dupuytren tissue such as increased amount of type III collagen. The fibroblastic and myofibroblastic proliferation has been localized around occluded microvessels, and seems to be a cellular response to local tissue ischemia. This may explain the association of Dupuytren’s contracture with conditions that predispose to tissue ischemia, such as alcohol use, smoking, and age. The myofibroblasts share cellular characteristics between fibroblasts and smooth muscle cells and are concentrated within the palmar nodules. The contractile elements of this cell type produce a progressive pull through the Dupuytren cords that leads to the characteristic flexion deformity. Residual myofibroblasts within the dermis and epidermis after surgical excision of diseased tissue have been implicated in the recurrence of the contracture. This notion is supported by the lower recurrence rate seen with palmar skin excision and full-thickness skin grafting after fasciectomy.

Surgical Management The patient was treated with a subtotal palmar and digital fasciectomy. He was brought to the operating room where, under axillary anesthesia, Brunner incisions were utilized to expose the pretendinous cord (Fig. 27–3). An early spiral cord was encountered at the level of the PIP joint. After both neurovascular bundles were identified and protected, the involved palmar fascia was excised and sent to the pathology laboratory for gross and histologic analysis. At the conclusion of the procedure, complete correction was obtained at both the MP and PIP joints. The tourniquet was deflated prior to closure, and brisk capillary refill was noted immediately. The wounds were closed with interrupted 5–0 nylon sutures, and a short arm plaster splint was placed, immobilizing the MP joints in 30 degrees of flexion, with the PIP joints comfortably extended.

Figure 27–3. Intraoperative photo demonstrating pretendinous cord. 169

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A

B

Figure 27–4. Three-month clinical follow-up demonstrating full extension (A) and flexion (B).

Postoperative Management A follow-up examination was done on the third postoperative day, at which time the patient’s dressing was removed. Inspection revealed minimal swelling, with wellvascularized flaps. A light dressing was applied and occupational therapy was instituted with a certified hand therapist, consisting of active, active assisted, and passive range-of-motion exercises. A resting night splint was fashioned with the ring finger in full extension, to be worn for 3 months. A follow-up visit at 3 months revealed an excellent early result, with full correction, and full flexion (Fig. 27–4).

Alternative Methods of Management There are no proven nonoperative modalities that can reverse or even halt the development of cords, nodules, and contractures. A significant number of patients develop progression of their flexion contractures and involvement of other digits, although the risk and the rate of progression are variable and difficult to predict. There are reports of rare cases of disease regression. Therefore, the unpredictable natural history of this disease may present a sense of “efficacy” to some patients who try nonoperative modalities, and they should at least be counseled accordingly. The future may hold promise for the treatment of Dupuytren’s contracture with collagenase injections into the diseased cords, and such protocols are currently under investigational study. Historically, radical palmar fasciectomy was performed as an attempt to rid the patient of all diseased tissue. However, recurrences were still noted, and this procedure has fallen out of favor due to associated wound complications and patient morbidity. Segmental fasciectomy has been described as a method of correcting the flexion contracture with segmental excision of diseased tissue through multiple incisions. Full-thickness skin grafting at these multiple incisions can theoretically prevent recurrence at those sites and provide “fire breaks” against full-length cord recurrence. Skin grafting techniques can also be done in conjunction with standard partial fasciectomy. Fasciotomy can be performed through a limited exposure to release the cords and provide correction of the contracture. This procedure does not attempt removal of diseased tissue; however, it does provide a method for contracture correction in the debilitated patient. 170

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Severe or recalcitrant deformities can ultimately be treated with amputation or ray resection. In such cases, all involved palmar skin should be excised and free skin grafting or dorsal skin should be used for flap closure if needed. Corrective osteotomies that change the arc of motion to a more functional zone and joint fusions have been utilized in problem cases as well. Correction of the contracture changes the lay of the palmar skin and may present areas not amenable to direct closure of the original incision lines. Different incisions and techniques related to wound closure have been described, and the surgeon should be familiar with each one and understand how to utilize them as the need arises. Generally, a standard Brunner zigzag incision is used for less severe contractures, and can be closed in V-Y fashion for added coverage. The transverse limb of the V-Y closure can be left open to relieve skin tension. In more severe contractures, a straight incision in line with the ray of the digit can be divided into multiple Z-plasty angles to provide exposure and to increase palmar skin length at closure. Ultimately, the finger can be flexed to gain direct closure, and small parts of the incision over the finger can be left to granulate, provided there is no direct exposure of bone, tendon, or neurovascular structures. There is extensive literature about an “open palm” technique that leaves the palmar part of the incision open to gain length. After surgery, the wound is cared for with daily dressing changes and closes via wound contracture over 3 to 5 weeks. Some have used the “open palm” technique routinely, and report a lower complication rate and better motion with this technique.

Complications Although most of the complications related to Dupuytren’s contractures are related to the surgical treatment of the disease, prolonged nonsurgical treatment of this condition can allow for severe contracture formation that makes salvage of the digit difficult if not impossible. Surgical complications of Dupuytren’s contracture fasciectomy are numerous, and many can be avoided or minimized with meticulous surgical technique. Vascular compromise of the digit is an immediate concern at the time of surgery. Meticulous technique and fine dissection of the neurovascular bundles prevent iatrogenic injury to those structures. Once the fasciectomy is complete, the tourniquet should be deflated. Vascular refill of the operated digits may lag behind the other digits, but should be normal within a few minutes. If, after observation, the finger is still blanched, flexion of the digit relieves tension from the neurovascular bundles that may have shortened with longstanding Dupuytren’s contracture. In such a situation, the digits need not be splinted in extension, as MP and PIP extension can be addressed with gradual postoperative therapy. Vasospasm may compromise vascular flow and can be alleviated by bathing the vessels with warm saline solution or with plain lidocaine. Hematoma formation can be minimized with meticulous hemostasis once the tourniquet is deflated after fasciectomy. Penrose drains can be placed as wick-type drains at multiple points along the closure. Some have advocated use of suction drainage that can be removed in the recovery room prior to discharge or at an early postoperative visit. The “open palm” technique provides a large surface for drainage, and hematoma formation is minimized with this technique. 171

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Skin sloughing is a concern due to the multiple thin flaps developed during the exposure. When designing the initial incision, the surgeon should survey the topography of the palmar skin for any particularly adherent areas. The dissection of these areas generally renders the skin particularly thin, and should not be planned at the base of the flaps where they may compromise the vascular supply of the whole flap. Rather, the incision should be planned through these troublesome spots. Loss of flexion can occur after Dupuytren’s contracture release, and can significantly restrict maximal grip strength, especially when involving the ring and small fingers. Preoperatively, virtually all patients with Dupuytren’s contractures have full flexion of the involved digits, barring any other underlying pathology. Postoperatively, the surgeon and patient are both quite focused on restoration of extension and should also be vigilant regarding maintenance of flexion. Recurrence of disease and extension of the disease to other digits are common after primary surgical treatment of Dupuytren’s contractures, and patients should be counseled about this preoperatively. These patients tend to present at a younger age with multiple digit and bilateral hand involvement. Surgical treatment of this subgroup is plagued with technical difficulties, higher recurrence rates, and prolonged postoperative recovery. Reflex sympathetic dystrophy has been reported in less than 10% of patients and requires prompt diagnosis and treatment.

Suggested Readings Badalamente MS, Hurst LC. The biochemistry of Dupuytren’s disease. Hand Clin 1999;15:35–42. Benson LS, Williams CS, Kahle M. Dupuytren’s contracture. J Am Acad Orthop Surg 1998;6:24–35. Boyer MI, Gelberman RH. Complications of the operative treatment of Dupuytren’s disease. Hand Clin 1999;15:161–166. Burge P. Genetics of Dupuytren’s disease. Hand Clin 1999;15:63–71. Crowley B, Tonkin MA. The proximal interphalangeal joint in Dupuytren’s disease. Hand Clin 1999;15:137–147. Elliot D. The early history of Dupuytren’s disease. Hand Clin 1999;15:1–19. Hurst LC. Dupuytren’s fasciectomy: zig-zag plasty technique. In: Blair WF, ed. Techniques in Hand Surgery. Baltimore: Williams & Wilkins; 1996:519–532. Hurst LC, Badalamente MA. Nonoperative treatment of Dupuytren’s disease. Hand Clin 1999;15:97–107. Jabaley ME. Surgical treatment of Dupuytren’s disease. Hand Clin 1999;15:109–126. Lubahn JD. Dupuytren’s fasciectomy: open palm technique. In: Blair WF, ed. Techniques in Hand Surgery. Baltimore: Williams & Wilkins; 1996:508–518. Lubahn JD. Open-palm technique and soft-tissue coverage in Dupuytren’s disease. Hand Clin 1999;15:127–136. Mullins PA. Postsurgical rehabilitation of Dupuytren’s disease. Hand Clin 1999;15: 167–174. 172

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Rayan GM. Clinical presentation and types of Dupuytren’s disease. Hand Clin 1999;15:87–96. Rayan GM. Palmar fascial complex anatomy and pathology in Dupuytren’s disease. Hand Clin 1999;15:73–86. Ross DC. Epidemiology of Dupuytren’s disease. Hand Clin 1999;15:53–62. Tomasek JJ, Vaughan MB, Haaksma CJ. Cellular structure and biology of Dupuytren’s disease. Hand Clin 1999;15:21–34. Tubiana R. Dupuytren’s disease of the radial side of the hand. Hand Clin 1999; 15:149–159. Yi IS, Johnson G, Moneim MS. Etiology of Dupuytren’s disease. Hand Clin 1999; 15:43–51.

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28 Stiff Joints Shelly M. Sailer

History and Clinical Presentation A 44-year-old right hand dominant cabinet maker presented to the emergency room after accidentally cutting the fingers of his right hand with a table saw.

Physical Examination The patient completely amputated his index finger through the middle phalanx just distal to the proximal interphalangeal (PIP) joint and his small finger through the proximal phalanx. The long and ring fingers were lacerated from the volar aspect through the flexor tendons and distal aspect of the proximal phalanges, but were held on by dorsal skin bridges. They were both avascular and insensate. The amputated portions of the index and small fingers were retrieved, but they were severely mangled and not amenable to replantation. He was taken to the operating room for immediate surgical management.

Diagnostic Studies Initial radiographs revealed traumatic amputation of the index finger through the middle phalanx, ring finger at the proximal phalanx, and small finger at the proxi-

PEARLS • Static-progressive and serial static splinting are very useful for resolving contractures with a “hard” end feel. • Dynamic splinting is most useful in resolving contractures with a “soft” end feel.

PITFALLS • Dynamic splinting forces are difficult to control, leading to poor splint compliance. • Dynamic splinting can cause inflammation of tissues when tension is placed too high. • Static splints do not allow for active motion while splinted, possibly contributing to tendon adhesions. 174

Figure 28–1. Anteroposterior (AP) view of the initial injury demonstrates complete amputations of the index and small fingers and near amputations of the long and ring fingers.

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Figure 28–2. Oblique view of the initial injury.

mal phalanx, and a unicortical defect of the long finger at the proximal phalanx (Figs. 28–1 and 28–2). Postoperative C-arm images demonstrate two Kirschner wires (K-wires) anatomically reducing the ring finger proximal phalanx fracture and extending through the PIP joint (Fig. 28–3). Radiographs taken 8 weeks postoperatively demonstrate union of the ring finger fracture and complete closure of the unicortical defect of the middle finger.

Figure 28–3. Postoperative C-arm image demonstrates fixation of the ring finger fracture. 175

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Surgical Management The ring finger proximal phalanx level amputation was stabilized with two 0.045inch crossed K-wires placed across the fracture site. Distally the pins extended through the PIP joint to provide better fixation of the short remaining distal fragment of the proximal phalanx. Despite near amputation, the long finger proximal phalanx fracture was found to be stable and did not require fixation. On both the ring and long fingers, the flexor digitorum profundus (FDP) tendons were repaired and the flexor digitorum superficialis (FDS) tendons were tenodesed to the FDP tendons. The radial and ulnar digital arteries and nerves were repaired. The extensor mechanism was intact in both long and ring fingers. Revision amputations of the index and small fingers were performed. A second surgery was ultimately required to regain full active range of motion. Five months after the initial injury this patient underwent a flexor tenolysis to the middle and ring fingers after passive range of motion was restored and the scars were soft and mature.

Postoperative Management Two weeks after initial surgery, the patient was referred to hand therapy to begin active motion of the thumb and wrist and only metacarpophalangeal (MP) motion of the fingers. The MP joints were stiff initially, flexing only 50 degrees, but progressed to 80 to 100 degrees within 4 weeks. Desensitization activities and compressive wraps were initiated for the index and small finger amputations. The volar wounds of the ring and long finger were slow to heal, but they finally healed by 6 weeks postoperatively. This case was complicated by the development of cellulitis in the ring finger 8 weeks postoperatively, which necessitated removal of the two percutaneous K-wires, and a short course of IV antibiotics followed by oral antibiotics. After the K-wires were removed, it was determined that the proximal phalanx fractures were stable enough to tolerate motion at the interphalangeal joints of the long and ring fingers. It was at this time that the severely stiff interphalangeal joints, the intrinsic tightness, and the lack of active flexor tendon function were brought to the forefront as a therapy challenge. Only 10 degrees of passive motion at the PIP joints was achieved on the first day of mobilization and was slow to improve with range-of-motion exercises

Figure 28–4. A metacarpophalangeal (MP) blocking splint used to facilitate active motion at the interphalangeal joints. 176

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Figure 28–5. A staticprogressive finger flexion splint used to impart lowload, long duration stress to lengthen shortened tissues.

alone. There was no active PIP or distal interphalangeal (DIP) flexion as the patient was now consistently contracting the lumbricals, which flexed the MP joints and extended the PIP joints. He could not isolate use of the FDS and FDP muscles as he had not used them functionally for weeks and they were adherent at the digit level. An MP blocking splint, which facilitated flexion at the PIP joints, was fabricated to retrain use of the long flexors (Fig. 28–4). A biofeedback unit was used to assist in training the patient to contract the long flexors and relax the lumbricals. Even though the patient had very little active motion, due to adhesions on the long flexors, it was important to maintain muscle strength and preserve independent function in preparation for a flexor tenolysis when appropriate. A static-progressive finger flexion splint was fabricated for the long and ring fingers (Fig. 28–5). Wearing time was increased slowly, monitoring for any extension lag. After 2 weeks, the patient had gained 30 degrees of PIP flexion, and had maintained full PIP extension. Wearing time was then increased to overnight (up to 8 hours) and range of motion steadily improved. By 4 months postinjury, the patient had nearly full passive PIP and DIP flexion, but only 30 degrees of active PIP flexion and 0 degrees at the DIP joints. A flexor tenolysis was required at 5 months postoperatively to restore active flexion. Immediate active motion was performed, and as postoperative edema decreased and the wounds healed, he was able to actively flex the middle and ring fingers to touch the palm (Fig. 28–6). This amount of flexion was adequate to grasp most objects for activities of daily living and tools for work.

Figure 28–6. Final outcome demonstrating excellent composite flexion of fingers. 177

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He returned slowly to his job as a cabinet maker after a course of strengthening and reconditioning. Some of his tool handles were adapted for improved grasp and custom gloves were required to accommodate the amputated digits.

Diagnosis Passive range-of-motion loss is the result of trauma and subsequent immobilization. Adaptive shortening of tissues and scar formation are the main sources of loss of joint flexibility and stiffness. All of these concepts apply in this case of near amputation with fractures and tendon lacerations. Besides exercises and stretching, several splinting techniques are available to provide prolonged stretch of shortened tissues. Splinting maintains the tissue elongation gained during therapy, home exercise programs, and functional use of the hand. Brand theorizes that the application of mechanical stress via splinting signals contracted tissue to “grow” or add cells while the body absorbs redundant tissue. Personal clinical experience and several studies have supported the use of low-load prolonged stress to apply load and stress to achieve permanent length changes in tissue, thereby increasing passive range of motion. Static-progressive splinting employs static positioning of a joint at the end range, at low tension for periods of time adequate to enact lengthening or growth of shortened tissues (Figs. 28–5 and 28–7). Because the components used in static-progressive tension lack the elasticity of those used in dynamic splinting, the appropriately set tension of the splint does not continue to stress the tissue beyond its current maximum length limit. It is well tolerated over long periods of time–overnight, for example. It is especially important with revascularized digits that tension be applied in a controlled fashion so as not to compromise blood flow. With the splint components used in this case, tension could be altered for comfort and vascular status, in minute degrees via the MERIT static-progressive component (UE TECH, Edwards, CO). A comfortable, well-tolerated splint with patient-controlled tension is typically able to produce the necessary elongation of adaptively shortened tissues, thereby regaining passive range of motion lost via trauma, immobilization, and scarring.

Alternative Methods of Management There are alternatives to the splinting program used to overcome stiff PIP joints. Table 28–1 describes the specific features of each and the advantages and disadvan-

Figure 28–7. Staticprogressive splinting is also used on larger joints such as the wrist. 178

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Table 28–1 Alternative Methods of Management Type of Management

Advantages

Disadvantages

Dynamic splinting: uses self-adjusting resilient components such as rubber bands, springs or elastic line to create the mobilizing force. Exerts tension upon one or more joints moving into ever increasing passive range of motion. Useful in resolving contractures with “soft” end feel.

Maximize adhesion length in either direction as patient can actively move while in splint; however, this ability to intermittently shorten tissue thwarts the purpose of the splint, which is to hold the joint at end range Allows active resistive motion in the opposite direction of the dynamic pull. Well tolerated over long periods of time because it holds tissue near the end of its elastic limit and does not stress beyond it. Provides low-load, end range positioning, which facilitates relaxation and lengthening of tissues. Pressure is distributed over a large surface area, which aids in comfort and vascular flow. Well tolerated over long periods of time because it holds tissue near the end of its elastic limit and does not stress beyond it. Provides low-load, end-range positioning, which facilitates relaxation and lengthening of tissues. Patient can make minute adjustments to splint tension to accommodate rangeof-motion changes and for comfort.

Forces difficult to control, which can lead to poor splint compliance and inadequate wearing time to achieve range-of-motion gains. Tension of splint continues even when tissue has reached its elastic limit, potentially causing inflammation of tissues.

Serial static splinting/serial casting: Statically positions joint near end of its elastic limit. Useful in resolving contractures with “hard” end-feel.

Static-progressive splinting: Involves the use of inelastic components such as Velcro tabs, progressive hinges, or screws to statically position joint(s). Useful in resolving contractures with “hard” or “soft” end-feel.

Splint or cast must be remolded or remade to accommodate increases in motion. Active motion is unavailable at casted joints; tendon adhesions may become denser as patient cannot remove cast for exercise. Motion may be lost in the opposite direction. Active motion not possible in the splint. Splint must be well made to distribute pressure appropriately to allow long wearing periods.

tages to consider when prescribing therapy for stiffness of any joint in the upper extremity.

Complications Surgical complications in this case, as discussed previously, included an infection of the ring finger at 8 weeks postoperatively and slow healing volar wounds, hindered by the patient’s heavy smoking habit. Therapy complications included flexor tendon adhesions, intrinsic tightness, inability to isolate lumbrical from long finger flexor function, and PIP joint stiffness. Other potential complications include tendon rupture and nonunion/malunion, but were not encountered in this case.

Suggested Readings Akeson WH, Ameil D, Avel M, et al. Effects of immobilization on joints. Clin Orthop 1987;219:28–37. 179

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Akeson WH, Ameil D, Woo SL-Y. Immobility effects on synovial joints. The pathomechanics of joint contracture. Biorheology 1980;17:95–110. Akeson WH, Ameil D, Woo SL-Y, et al. Collagen cross-linking alterations in joint contractures: changes in the reducible crosslinks in periarticular connective tissue collagen after nine weeks of immobilization. Connective Tissue Res 1977;5:15–19. Ameil K, Woo SL-Y, Harwood FL, et al. The effect of immobilization on collagen turnover in connective tissue: a biochemical-biomechanical correlation. Acta Orthop Scand 1982;53:325–332. Brand PW. Clinical Biomechanics of the Hand. St. Louis: CV Mosby; 1985. Bonutti PM, Windau JE, Abies BA, Miller FFI. Static progressive stretch to reestablish elbow range of motion. Clin Orthop 1994;303:128–134. Enneking WF, Horowitz M. The intra-articular effects of immobilization on the human knee. J Bone Joint Surg [Am] 1972;54A:973–985. Flowers KR, LaStayo P. Effect of total end range time on improving passive range of motion. J Hand Ther 1994;7:150–157. Flowers KR, Michlovitz SL. Assessment and management of loss of motion in orthopaedic dysfunction. In: Postgraduate Advances in Physical Therapy. Alexandria, VA: APTA, 1988. Light KE, Nuzik S, Personius W, Barstrom A. Low-load prolonged stretch versus high-load brief stretch in treating knee contractures. Phys Ther 1984;64:330–333. Schultz-Johnson KS. Splinting: a problem solving approach. In: Stanley BG, Tribuzi SM, eds. Concepts in Hand Rehabilitation. Philadelphia: FA Davis; 1992.

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Section VII

Tendon Injuries

A. Tenosynovitis Flexor Stenosing Tenosynovitis: Trigger Finger and Thumb Kevin D. Plancher

De Quervain’s Disease Kevin D. Plancher

Flexor Carpi Radialis Tunnel Syndrome Kevin D. Plancher

Flexar Carpi Ulnaris Calcific Tendinitis Richard W. Barth

B. Tendon Repair Acute Laceration of Flexor Tendons Mark S. Rekant

Delayed Treatment of Flexor Tendons: Staged Tendon Reconstruction Lawrence H. Schneider

Chronic Lacerations of Extensor Tendons Angela A. Wang and Michelle Gerwin Carlson

Avulsions of the Flexor Digitorum Profundus Donald M. Lewis and Randall W. Culp

FLEXOR STENOSING TENOSYNOVITIS: TRIGGER FINGER AND THUMB

29 Flexor Stenosing Tenosynovitis: Trigger Finger and Thumb Kevin D. Plancher

History and Clinical Presentation A 45-year-old right hand dominant woman was seen in the office because her right middle finger was stuck in her palm. She reported that her family physician gave her an injection in that finger 6 months ago for her symptoms of clicking and pain over the dorsal aspect of her proximal phalanx of her middle finger. She denies any symptoms of diabetes, rheumatoid arthritis, gout, or connective tissue disorders.

Physical Examination On examination the patient actively initiated extension of her middle finger but stopped with a short arc of motion because of pain. The patient withdrew her hand when passive extension was attempted because of pain. The hand and all digits have no signs of vascular compromise. The patient’s two-point sensory discrimination, as determined by the Weber two-point discrimination test, using a dull pointed eye caliper applied in the longitudinal axis of the digit without blanching the skin, is within normal limits. A tender, palpable nodule is noted over the palmar surface of the second metacarpophalangeal (MP) joint (Fig. 29–1).

Diagnostic Studies PEARLS • To avoid recurrence of a trigger finger, incise and excise a part of the annular pulley. • Early treatment and early motion in patients with RA and avoid releasing the A1 pulley. • Multiple trigger fingers may be a sign of flexor tenosynovitis associated with RA, so avoid releasing the A1 pulley.

PITFALLS • To avoid nerve injury to the thumb, utilize loupe dissection. • Avoid releasing the A1 pulley in patients with RA.

Anteroposterior (AP) and splay lateral radiographs reveal no osteophytes or evidence of osteoarthritis. No soft tissue masses are noted.

Figure 29–1. A palpable mass seen in the thumb pulley.

183

Figure 29–2. The digital flexor sheath contains five discrete “annular bands.”

Figure 29–3. The pathophysiology of the trigger finger.

Differential Diagnosis Tumors Mass Infection Osteoarthritis with osteophytes Trigger finger

Diagnosis Flexor Stenosing Tenosynovitis of the Right Middle Finger—“Trigger Finger” The digital flexor sheath contains five discrete “annular bands” (A1 through A5 pulley) (Fig. 29–2). These pulleys prevent bow-stringing of the flexor tendon and also maximize its efficiency in relation to digital motion. Nutrition of the flexor tendon sheath is dependent on perfusion from the surrounding tenosynovium rather than the vincula system, which perfuses the flexor tendon distally through a small network of vessels. The annular band and the tenosynovium are responsible for the pathophysiology of trigger fingers and thumbs (Fig. 29–3). When the normally thin flexor sheath becomes inflamed and thickened, it reduces the space that the tendon has to pass through. The tendon no longer glides freely and the tendon itself may swell up in a balloon-like mass and prevent passage of the tendon through the sheath. Forced movement at this point will drag the enlarged portion (Fig. 29–4) of the tendon through the sheath, producing a snapping

Figure 29–4. The forced movement drags the enlarged portion of the tendon through the sheath, producing a snapping sensation. This is also what can lead to the locking of the finger. 184

FLEXOR STENOSING TENOSYNOVITIS: TRIGGER FINGER AND THUMB

sensation and may lead to locking of the finger in flexion. The first annular pulley acts as a fulcrum about which the flexor tendon bends. This fulcrum has been postulated as causing focal tendon degeneration with sheath thickening and tendon nodule development.

Nonsurgical Management Conservative treatment includes modification of provocative activities in the workplace and personal hobbies. Oral nonsteroidal antiinflammatory drugs (NSAIDs), including cyclooxygenase (COX-II) inhibitors, and a steroid injection into the area of primary pathology is indicated. Contraindications to injections or NSAIDs include sensitivity to any of the materials or the presence of an infection. Using a 27-gauge, a 11⁄4-inch needle is used to inject 1.5 cc Celestone and 1.5 cc plain Marcaine/lidocaine without epinephrine into the area of the proximal flexor sheath and annular pulley. The needle should be placed at a 45-degree angle to the longitudinal axis of the metacarpal at the proximal-most extension of the fibro-osseous sheath, which is located just distal to the distal palmar crease (Fig. 29–5). The injection should not be forced, and if excessive force is required, then the needle should be repositioned. Patients are encouraged to use their finger in a normal fashion after the injection and should anticipate a decrease of triggering over the next 7 days. Gentle manipulation by the surgeon once the digit is anesthetized will ensure that the medication has moved proximally and distally throughout the fibro-osseous tunnel. A successful injection is always noted when a fluid wave can be palpated in the distal flexor sheath during the injection or when a “pop” is felt or heard with injection of the finger. The patient attends a supervised occupational therapy program for 6 weeks and schedules a follow-up appointment. If triggering occurs or if the finger becomes irreducibly locked, surgical intervention is prescribed.

Surgical Management Surgical management for a trigger finger is performed as an outpatient procedure under local anesthetic. The area over the A1 pulley is anesthetized using 3 cc of plain lidocaine solution. Limb exsanguination is maintained through an arm tourniquet inflated to 250 mm Hg. Surgical exposure is performed through a transverse incision at the distal palmar crease. Blunt dissection through the subcutaneous fat allows exposure of the proximal portion of the fibro-osseous sheath

Figure 29–5. The injection with the needle at 45 degrees to the longitudinal axis of the metacarpal at the proximalmost extension of the fibroosseous sheath. 185

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Figure 29–6. Intraoperative spreading to the sheath with scissors.

(Fig. 29–6), A1 pulley, as well as visualization of the radial and ulnar digital neurovascular bundles, which lie adjacent to the flexor sheath. The first annular pulley is released through a longitudinal incision and a small piece of the pulley is excised to avoid reformation of this pulley (Fig. 29–7). The distal border of the A1 pulley correlates with the anatomic landmark of the MP flexion crease. Release of the fibro-osseous sheath beyond this landmark jeopardizes the integrity of the second annular pulley, which can lead to flexor tendon bow-stringing and limitation in digital motion. Before wound closure, the patient is asked to actively extend and flex the finger to ensure complete sheath release. A dressing is applied to ensure wound protection but maintain digital motion. Multiple trigger fingers may be a sign of flexor tenosynovitis associated with rheumatoid arthritis. In these patients with secondary trigger fingers who do not respond to cortisone injection, flexor tenosynovectomy often is necessary. In the rheumatoid arthritis (RA) patient, release of the A1 pulley is not recommended because this enhances the biomechanical forces that are responsible for the finger deformity of RA, that is, volar subluxation and ulnar deviation of the digit at the MP joint. If flexor tenosynovectomy does not allow unrestricted gliding within the fibro-osseous sheath, resection of a slip of

Figure 29–7. The first annular pulley is released through a longitudinal incision. A small piece of the pulley should be excised to avoid reformation of this pulley. 186

FLEXOR STENOSING TENOSYNOVITIS: TRIGGER FINGER AND THUMB

the flexor digitorum superficialis tendon provides more room within the flexor sheath for the remaining slip of the superficialis and the flexor digitorum profundus tendon.

Complications Nerve Injury The most frequent surgical complication is digital nerve injury, which, if recognized, requires prompt nerve repair. The radial digital nerve is most often affected in a trigger thumb release as it lays 0.16 mm under the skin.

Bow-Stringing of the Flexor Tendon (Loss of Flexion) Release of the second annular pulley, in addition to the first annular pulley, may result in the loss of finger motion (an extensor lag). Taking care to release only the A1 pulley prevents this debilitating complication.

Scar Tenderness Scar massage and time generally relieve the tenderness.

Recurrence The condition can recur when the A1 pulley is only incised. Avoid this by excising the A1 pulley, not incising only a piece.

Joint Stiffness Avoid by prescribing supervised hand occupational therapy postoperatively.

Fibrous Nodule Formation Beneath the Scar Avoid by prescribing supervised hand occupational therapy postoperatively.

Suggested Readings Bonnici AV, Spencer JD. A survey of ‘trigger finger’ in adults. J Hand Surg [Br] 1988;15B:290–293. Freiberg A, Mulholland RS, Levine R. Nonoperative treatment of trigger fingers and thumbs. J Hand Surg [Am] 1989;14A:553–558. Marks MR, Gunter SF. Efficacy of cortisone injection in treatment of trigger fingers and thumbs. J Hand Surg [Am] 1989;14A:722–727. Otto N, Wehbe MA. Steroid injections for tenosynovitis in the hand. Orthop Rev 1986;15:290–293. Saldana MJ. Trigger digits: diagnosis and treatment. J Am Acad Orthop Surg 2001; 9:246–252. Turowski GA, Zdankiewicz PD, Thomson JG. The results of surgical treatment of trigger finger. J Hand Surg [Am] 1997;22A:145–149. 187

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Case 30 De Quervain’s Disease Kevin D. Plancher

History and Clinical Presentation A 45-year-old right hand dominant woman presents with wrist pain that is preventing her from doing activities at home. She spends a significant amount of time in her garden, and she has noticed increased wrist pain, especially when she uses her thumb. She reports that these symptoms do not improve with rest. She denies any history of trauma to her wrist and has not been diagnosed with rheumatoid arthritis.

Physical Examination

PEARLS • Initial management consists of a custom thumb spica splint and additional antiinflammatory medication and a possible corticosteroid injection • Careful attention to technique during injecting (needle angle and placement) • Longitudinal septum may divide the APL and the EPB in 20 to 30% of patients. • Necessary to identify and release both the EPB and APL before closure during surgery

PITFALLS • Unresponsiveness to corticosteroid injections and recurrent symptoms can occur because of the presence of the longitudinal septum • Injection not placed correctly will lead to recurrence of symptoms • Patient falling to follow conservative treatment regiment with hand therapy will in 5% of all patients necessitate surgical release 188

Pain and swelling are localized over the region of the radial styloid (Fig. 30–1). The pain radiates down to the thumb and a thickened fibrous sheath is palpable over the radial styloid. Maximum tenderness is noted over the radial styloid, and tenderness is also noted along the long abductor tendon and muscle. Pain is increased with extension and abduction of the thumb against resistance. A Finkelstein test is positive and produces significant pain (Fig. 30–2).

Diagnostic Studies Radiographs consisting of a posteroanterior (PA) and lateral view of the wrist as well as the important hyperpronated view or Robert’s view were within normal limits. No carpometacarpal (CMC) arthritis was evident on the Robert’s view.

Differential Diagnosis Scaphoid fracture Arthritis Flexor carpi radialis tendonitis Thumb carpometacarpal arthritis Intersection syndrome Wartenberg’s syndrome

Figure 30–1. Physical exam will localize pain and swelling over the region of the radial styloid.

D E Q U E R VA I N ’ S D I S E A S E

A

B

Figure 30–2. (A) Finkelstein test. (B) Physical exam on a patient.

Diagnosis De Quervain’s Tenosynovitis of the Right Wrist De Quervain’s disease may be caused by any condition that produces a swelling or a thickening of the tendons of the first dorsal compartment of the wrist (Fig. 30–3A). It is a stenosing tenosynovitis of the abductor pollicis longus (APL) and extensor pollicis brevis (EPB) tendons (Fig. 30–3B). This typically occurs in the third, fourth, and fifth decades of life and is 10 times more common in women. The cause is usually related to overuse and may be associated with rheumatoid arthritis. Overuse causes a chronic inflammation of the sheath that covers the long abductor and the short extensor tendons. The tendons of the APL and the EPB pass through a fibro-osseous tunnel formed by a groove in the radial styloid and overlying extensor retinaculum

A

B

Figure 30–3. De Quervain’s disease can have swelling or a thickening of the tendons of the first dorsal compartment. (A) The relationship of the compartments. (B) A close-up of the first dorsal compartment. 189

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Figure 30–4. The tendons of the abductor pollicis longus (APL) and the extensor pollicis brevis (EPB) pass through a fibro-osseous tunnel formed by a groove in the radial styloid and overlying extensor retinaculum.

(Fig. 30–4). The tendons deviate as they pass through the tunnel, and the angle increases with ulnar deviation of the wrist. Anatomic studies of the fibro-osseous canal have documented that in 94% of specimens the abductor pollicis tendon has two to four slips. Multiple EPB tendons are found in only 2%. Multiple subcompartments were recorded in 47% of patients and 75% of specimens. Multiple APL tendon slips and two subcompartments are the rule rather than the exception in normal anatomy. Despite the fact that many anatomy texts still suggest that the tendons of the EPB and APL are contained in a single compartment under the extensor retinaculum, several anatomic and surgical studies have convincingly demonstrated this to be true in less than 25% of operative cases. Accordingly, one should be certain to identify the EPB and APL tendons at the time of operation.

Nonoperative Management Negative radiographs and clinical examination determine conservative treatment, starting with a custom thumb spica splint (Fig. 30–5). In addition, antiinflammatory medications and a corticosteroid injection (Fig. 30–6) into the first dorsal compartment are important adjuvants. These are most successful within the first 6 weeks after injury. Some authors have reported a high rate of success with injections,

Figure 30–5. Conservative treatment starting with a custom thumb spica splint. 190

Figure 30–6. Corticosteroid injection into the first dorsal compartment.

D E Q U E R VA I N ’ S D I S E A S E

Figure 30–7. Cadaveric demonstration of the transverse incision for de Quervain’s tenosynovitis (ICM proximal to the radial styloid).

Figure 30–8. Cadaveric demonstration of the superficial radial nerve in relation to the first dorsal extensor compartment.

although a series of two injections may be necessary. Harvey et al reported that with an injection of steroids and local anesthetic into the tendon sheath, relief was seen in 80% of cases. However, when pain persists, surgical intervention is recommended.

Surgical Management The first dorsal compartment is exposed through a skin incision that runs from dorsal to volar in a transverse to oblique direction, parallel with the skin crease over the area of tenderness (Fig. 30–7). Dissection is continued through the dermis, avoiding branches of the superficial radial nerve (Fig. 30–8). A longitudinal incision is made through the entire length of the dorsal carpal ligament, exposing the tendons in the first dorsal compartment. With the thumb abducted and the wrist flexed, the APL and the EPB tendons are carefully lifted from the compartment (Fig. 30–9). Be sure that there is not an additional tendon in a separate sheath. In this case, the short extensor tendon of the thumb did not lie together with the long abductor tendon, but in a separate compartment. This compartment was opened and the fibrous partition between the two compartments was excised. One of the functions of the fibrous retinaculum covering the first extensor compartment is to prevent anterior displacement of the APL and EPB tendons during

Figure 30–9. Complete release (proximal and distal) of the tendons during testing with blunt resection. 191

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palmar flexion of the wrist. This function should be preserved by dividing the retinaculum near its dorsal line of attachment with the radius, thus preserving the ligament as a sling. Frequently, the APL and EPB may be located within separate spaces formed by an intracompartmental septum in the first compartment. Both tendons may also be duplicated; therefore, the first compartment may contain three or even four tendons in some individuals. Thus, it is important at the time of release to be sure that any intracompartmental septum has been divided. The surgeon should not assume that a complete release has been obtained when two tendons have been exposed. The skin is closed and a small pressure dressing is applied. The dressing is removed after 48 hours and a patch dressing is applied. Motion of the thumb and hand is encouraged and increased as tolerated.

Complications To avoid complications, careful attention to surgical technique at the initial release is essential. A common complication due to surgical technique is superficial radial nerve injury. Other complications include tendinous adhesions, which can cause neuritis and limit hand and wrist function, and volar tendon subluxation. Persistence of symptoms is also possible. If repeat cortisone injections fail to relieve symptoms, surgical reexploration may be necessary.

Suggested Readings Arons MS. De Quervain’s release in working women: a report of failures, complications, and associated diagnoses. J Hand Surg [Am] 1987;12A:540–544. Chow SP. Triggering due to de Quervain’s disease. Hand 1979;11:93–94. Finkelstein H. Stenosing tendovaginitis at the radial styloid process. J Bone Joint Surg [Am] 1930;12A:509–540. Harvey FJ, Harvey PM, Horsley MW. De Quervain’s disease: surgical or nonsurgical treatment. J Hand Surg [Am] 1990;15A:83–87. Jackson WT, Viegas SF, Coon TM. Anatomical variations in the first extensor compartment of the wrist. A clinical and anatomical study. J Bone Joint Surg [Am] 1986; 68A:923–926. McMahon M, Craig SM, Posner MA. Tendon subluxation after de Quervain’s release: treatment by brachioradialis tendon flap. J Hand Surg [Am] 1991;16A:30–32. Weiss AP, Akelman E, Tabatabai M. Treatment of de Quervain’s disease. J Hand Surg [Am] 1994;19A:595–598.

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FLEXOR CARPI RADIALIS TUNNEL SYNDROME

31 Flexor Carpi Radialis Tunnel Syndrome Kevin D. Plancher

History and Clinical Presentation A 45-year-old right hand dominant woman with a previous history of carpometacarpal (CMC) arthritis presents with swelling over the volar radial side of the wrist. The patient reports she played two sets of tennis and was unable to move her wrist back and forth.

Physical Examination The patient has tenderness directly over the flexor carpi radialis (FCR) at the wrist crease (Fig. 31–1). The Allen’s test was normal and a Tinel’s and nerve compression tests were negative.

PEARLS • Isolated FCR tendinitis is rare • FCR tendonitis is often seen secondary to CMC arthritis

PITFALLS • Be aware of possibility of intraarticular injection of Marcaine into radial artery • Rupture of the FCR tendon is possible with an injection. It can be avoided by using an orthoplast splint for 10 days postinjection.

Figure 31–1. Clinical hand that demonstrates location of tenderness over the flexor carpi radialis (FCR).

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Figure 31–2. Robert’s view of the carpometacarpal (CMC) joint demonstrating grade IV Eaton CMC arthritis.

Diagnostic Studies Anteroposterior (AP) and lateral oblique and Robert’s view (hyperpronated AP of the thumb) show abnormalities of the CMC joint (Fig. 31–2).

Differential Diagnosis Scaphotrapezial arthritis Scaphoid nonunions Basal joint arthritis of the thumb Linberg’s syndrome Volar ganglion FCR tendonitis

Diagnosis Flexor Carpi Radialis (FCR) Tendinitis Repetitive wrist motions experienced by some athletes can lead to a stenosis and synovitis within the fibro-osseous tunnel containing the FCR. The FCR passes through a synovial tunnel bordered by the scaphoid tuberosity, trapezial ridge, and the transverse carpal ligament (Fig. 31–3). Within the tunnel, the tendon occupies 90% of the available space. As the tendon enters this tunnel, it 194

FLEXOR CARPI RADIALIS TUNNEL SYNDROME

A

B

Figure 31–3. (A) The FCR passes through the scaphoid tubercle to insert on the second metacarpophalangeal joint. Note how CMC arthritis can lead to FCR tendinitis. (B) Synovitis of the FCR with pain on wrist motion. (Illustrations courtesy of The Indiana Hand Center and Gary Schnitz.)

deviates 30 degrees dorsally over the volar pole of the scaphoid to insert at the base of the second and third metacarpals and provides a slip to the trapezial ridge. Weeks has suggested that this angulation may create mechanical irritation and predispose the athlete to tenosynovitis. Athletes with FCR tendonitis have pain over the volar aspect of the wrist, proximal to the wrist crease and overlying the FCR tendon. Lister described a provocative test performed by abruptly extending a relaxed wrist to reproduce the pain. Pain also may be elicited on resisted flexion and radial deviation. Chronic synovitis and tendon ruptures may not allow active testing in some patients.

Nonsurgical Management Immobilization, antiinflammatory medication, and a corticosteroid injection may provide relief in the setting of a primary tendinitis (Fig. 31–4). Chronic processes may be resistant and often require decompression of the fibro-osseous tunnel. In the setting of an FCR rupture, simple debridement of the stump can provide effective pain relief. A wrist splint placed in neutral rotation often will alleviate all the pain.

Figure 31–4. Injection of the FCR tendinitis. 195

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A

B

Figure 31–5. (A) Note exposed anatomy of the FCR and radial artery and proximal cutaneous branch of the median nerve (PCBMN). (B) Probe placed in FCR tunnel prior to release.

Surgical Management Surgical treatment is rarely, if ever, needed and performed only in conjunction with CMC arthroplasty. If nonoperative treatment fails, the FCR tunnel can be decompressed. An incision is made radial to the FCR to prevent injury to the palmar cutaneous branch. The thenar muscles are reflected off the transverse carpal ligament and the tendon sheath is opened proximal to distal. The fibro-osseous tunnel along the ulnar border of the trapezium is released. The FCR should then be free to its insertion. Following surgery, range-of-motion exercises should be started early under the guidance of and occupational hand therapist (Fig. 31–5).

Complications Rupture of FCR tendon Intraarteriolar Marcaine injection

Suggested Readings Bishop AT, Gabel G, Carmichael SW. Flexor carpi radialis tendinitis I. Operative anatomy. J Bone Joint Surg [Am] 1994;76A:1009–1014. Fitton J, Shea FW, Goldie W. Lesion of the flexor carpi radialis tendon and sheath causing pain in the wrist. J Bone Joint Surg [Br] 1968;50B:359–363. Froimson A. Tenosynovitis and tennis elbow. In: Green DP, ed. Operative Hand Surgery. 3rd ed. New York: Churchill Livingstone; 1992:1989–2006. Gabel G, Bishop AT, Wood MB. Flexor carpi radialis tendinitis: II. Results of operative treatment. J Bone Joint Surg [Am] 1994;76A:1015–1018. Kiefhaber TR, Stern PJ. Upper extremity tendinitis and overuse syndromes in the athlete. Clin Sports Med 1992;11:39–55. Linburg RM, Comstock BE. Anomalous tendon slips from the flexor pollicis longus to the flexor digitorum profundus. J Hand Surg [Am] 1989;4A:79–83. 196

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Lister G. The Hand. 2nd ed. Edinburgh: Churchill Livingstone; 1984:244. Pyne JIB, Adams BD. Hand tendon injuries in athletics. Clin Sports Med 1992;11: 833–850. Stern PJ. Tendinitis, overuse syndromes, and tendon injuries. Hand Clin 1990;6: 467–476. Weeks PM. A cause of wrist pain: Non-specific tenosynovitis involving the flexor carpi radialis. Plast Reconstr Surg 1978;62:263–266.

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32 Flexor Carpi Ulnaris Calcific Tendinitis Richard W. Barth

History and Clinical Presentation A 46-year-old woman was well until the morning prior to presentation, when she awoke with significant pain in her right wrist. Aspirin initially helped alleviate her symptoms. She awoke on the day of presentation complaining of severe pain, redness, and limited motion. She denied systemic complaints or history of trauma or injury. Her past medical history was unremarkable and she took no medications.

Physical Examination The right wrist and forearm demonstrated 30 degrees of wrist flexion, 10 degrees of wrist extension, and significant swelling over the volar ulnar forearm. There was erythematous streaking extending from the wrist proximally into the forearm, but no regional lymphadenopathy. The flexor carpi ulnaris tendon was exquisitely tender to palpation just proximal to the pisiform. There was no sign of trauma and pulses were 2+ and symmetrical. The examination was otherwise unremarkable and the patient was afebrile.

A

Figure 32–1. Routine anteroposterior (AP) and lateral views of the wrist are normal. 198

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PEARLS • Awareness of the condition is the key to diagnosis. • Oblique radiographs may be necessary to demonstrate the calcific deposit. • Treatment is almost always nonoperative.

PITFALLS • Flexor carpi ulnaris calcific tendinitis can mimic infection.

Diagnostic Studies Routine anteroposterior and lateral radiographs of the right wrist were negative (Fig. 32–1). Oblique views demonstrated a small area of calcification just proximal to the pisiform (Fig. 32–2).

Differential Diagnosis Flexor carpiulnaris tendonitis Septic arthritis Septic tenosynovitis Cellulitis Inflammatory arthritis Crystalline disease

Diagnosis FCU Tendonitis The diagnosis is made by the history, characteristic physical findings, and radiographic findings. The most important factor in making the diagnosis is familiarity

Figure 32–2. An oblique radiograph demonstrates a small area of calcification just proximal to the pisiform. 199

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with the condition. The history is notable for the acute onset of severe pain, limited wrist motion, and swelling, but no systemic complaints suggesting infection. There is no history of penetrating injury and usually no recent trauma. The physical findings include swelling, loss of motion, and exquisite tenderness of the flexor carpi ulnaris tendon, often just proximal to the pisiform. There may be erythematous streaking extending into the forearm. The physical findings may mimic a septic joint or cellulitis with ascending lymphangitis, but there is no lymphadenopathy or fever. The radiographic findings are often pathognomonic. Often, there is a large fluffy calcific deposit in the region of the flexor carpi ulnaris tendon just proximal to the pisiform. The calcification may be subtle and visualized only on oblique radiographs as in this case. White count, differential, and sedimentation rate are almost always normal. The pathogenesis of calcium deposition in the soft tissues is unknown. It has been postulated that trauma induces an area of necrosis into which calcium is deposited. Symptoms are unrelated to the size of the calcium deposit. The actual deposit may be small and visible only with oblique radiographs. The calcium is released and causes a significant inflammatory response. The clinical picture is so much like an infectious process that many patients have been treated with antibiotics. Once the diagnosis is made, the treatment is straightforward. On follow-up radiographs, the calcium deposits have usually been resorbed within a few weeks.

Surgical Management Most patients respond to conservative measures. In patients who are refractory to conservative treatment, the calcific deposit may be surgically excised. This is accomplished by making a longitudinal incision in the flexor carpi ulnaris tendon, excising the offending material, and repairing the tendon. Use of intraoperative fluoroscopy or radiographs is recommended to ensure complete removal.

Postoperative Management A bulky compressive dressing is initially applied with a short arm splint. Range-ofmotion exercises are started 10 to 14 days postoperatively.

Alternate Methods of Management Treatment options include antiinflammatory medication by mouth or injection, splinting, and surgical excision. I have found these patients extremely disabled and have been gratified by the response to a corticosteroid injection. I attempt to needle the calcium deposit at the same time. Additionally, I use a wrist splint for several days until the symptoms resolve completely. A few patients have required a second steroid injection, but surgery is rarely necessary.

Complications The major complication of flexor carpi ulnaris calcific tendinitis is misdiagnosis. There are several reports in the literature of patients being treated with antibiotics and even admitted to the hospital with this condition. Complications of treatment 200

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of flexor carpi ulnaris calcific tendinitis are rare. Care must be taken to avoid injecting the ulnar nerve or artery. Depigmentation and subcutaneous fat atrophy can occur if the corticosteroid is injected into the subcutaneous tissue or skin itself. The ideal site of injection is adjacent to the flexor carpi ulnaris tendon. I also attempt to puncture the calcific deposit with the needle as well.

Suggested Readings Carroll RE, Sinton W, Garcia A. Acute calcium deposits in the hand. JAMA 1955; 157:422–426. Greene TL, Louis DS. Calcifying tendinitis in the hand. Ann Emerg Med 1980;9: 438–440. Moyer RA, Busch DC, Harrington TM. Acute calcific tendinitis of the hand and wrist: a report of 12 cases and a review of the literature. J Rheumatol 1989;16: 198–202. Phalen GS. Stenosing tenosynovitis: trigger fingers, trigger thumb, and de Quervain’s disease. Acute calcification in wrist and hand. In: Jupiter JB, ed. Flynn’s Hand Surgery. 4th ed. Baltimore: Williams & Wilkins; 1991:444–446. Wolfe SW. Tenosynovitis. In: Green DP, Hotchkiss RN, Pederson WC, eds. Green’s Operative Hand Surgery. 4th ed. Philadelphia: Churchill Livingstone; 1999:2026– 2027. Yelton CL, Dickey LE. Calcification around the hand and wrist. South Med J 1958;51:489–495.

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33 Acute Laceration of Flexor Tendons Mark S. Rekant

History and Clinical Presentation A 38-year-old right hand dominant musician presents to the office 4 days following a laceration to the volar surface of his right long finger sustained after a fall onto a broken piece of glass (Fig. 33–1). He complained of pain in the right long digit with inability to actively flex his finger. He also noted decreased sensation along the ulnar aspect of his finger. He had been working prior to the accident and wished to return to playing guitar as soon as possible. He denied any past medical history but did admit to smoking one pack of cigarettes per day. He had been seen previously at a local emergency room where his laceration was irrigated and loosely sutured. Tetanus booster and a dose of intravenous antibiotics were administered. He was discharged with a protective finger splint.

Physical Examination An oblique volar laceration was noted, beginning radially just proximal to the proximal interphalangeal joint extending ulnarly and distally 1 cm to the midaxial line of the right long finger. The patient demonstrated no active flexion of the proximal interphalangeal (PIP) or distal interphalangeal (DIP) joints. His two-point discrimination was greater than 15 mm along the ulnar border of that digit. The digit was warm, and had good color, turgor, and normal capillary refill.

PEARLS • Use fine instrumentation, atraumatic technique, and loupe magnification. • Ensure minimal gapping at the repair site with smooth juncture of tendon ends. • Provide sufficiently strong repair to permit and institute early controlled mobilization.

PITFALLS • Avoid excessive tendon handling during mobilization and repair. • Avoid disrupting pulley system, especially A2 and A4. • Avoid intruding or interfering with tendon vascularity. 202

Diagnostic Studies Anteroposterior and lateral radiographs of the injured hand or forearm should be evaluated to ensure that no bony injury is overlooked and to investigate the possibility of a retained foreign body. No fracture was appreciated.

Figure 33–1. Patient’s finger at presentation.

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Differential Diagnosis Laceration of both flexor digitorum superficialis and profundus and digital nerve Laceration of either flexor tendon singularly with inability to move secondary to pain No tendon laceration but unable to move secondary to pain No nerve laceration but rather contused/neuropraxic

Diagnosis Laceration of the Ring Finger Flexor Digitorum Profundus, Flexor Digitorum Superficialis, and Ulnar Digital Nerve to the Ring Finger The repair of lacerated flexor tendons of the hand and their return to appropriate function is one of the most difficult and challenging tasks for a surgeon to undertake. Lacerations within zone 2 are especially complex. Within this area of the fibro-osseous digital canal, the profundus and superficialis tendons interweave in an intricate and close relationship. Even minimal swelling of the epitenon is sufficient to impair free motion of both tendons. The margin for error in tendon repair is thus very small in this region. The necessity of minimizing adhesions can be a daunting charge. On the one hand, it requires nontraumatic treatment of the tendon, respecting the dorsally located blood support and, on the other, requires early motion, jeopardizing the continuity of sutures. This patient’s flexor tendons were repaired using a Tajimi technique with four strands of 4–0 polyester crossing the repair. Care was taken to avoid excessive handling of the tendons, with the tendon being grasped by forceps only once. Additionally, a 6–0 Prolene running epitendinous suture was used to minimize gapping and facilitate healing. The sheath was not repaired. No publication to date provides scientific evidence that sheath repair improves outcome. Although one may argue that reconstituting the sheath provides a barrier to adhesion formation, restores synovial fluid nutrition, and restores sheath mechanics, in practicality the synovial membranes are usually badly damaged and unsalvageable. Gapping at the repair site results in weakening and, potentially, adhesion formation. Each increase in suture caliber strengthens the repair, nevertheless, at the cost of additional material interference. This additional material may compromise tendon vascularity and/or precipitate adhesion formation. Biomechanically, core sutures placed dorsally strengthen the repair; yet there is a fine line, as sutures placed too dorsal may compromise the tendon’s blood supply. Early motion should be begun. Stressed tendons heal faster, gain tensile strength faster, form fewer adhesions, and demonstrate better excursions (Table 33–1). The surgeon must feel comfortable with his or her choice of techniques and suture material. These characteristics should lend themselves to easy placement of sutures in the tendon and the ability to place secure knots, afford minimal Table 33–1 Tensile Stress on Normally Repaired Flexor Tendons Passive motion 500 g Light grip 1500 g Strong grip 5000 g Tip pinch-index flexor digitorum profundus 9000 g 203

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Table 33–2 Repair Strength with Epitendinous Suture 0 Week Two strand Four strand Six strand

2500 g 4300 g 6000 g

1 Week (-50%) 1200 g 2150 g 3000 g

3 Weeks (-33%) 1700 g 2800 g 4000 g

6 Weeks (+20%) 2700 g 5200 g 7200 g

interference with tendon vascularity and gapping at the repair site, and provide sufficient strength throughout healing to permit the application of early motion stress to the tendon (Table 33–2).

Preoperative Management Initially, the wound was irrigated with 1 L of normal saline. A tetanus booster was administered. The laceration was loosely closed with 4–0 nylon suture in an interrupted fashion. The hand was immobilized with a volarly placed plaster splint maintaining the wrist in 45 degrees of extension, the metacarpophalangeal (MP) joints near 90 degrees of flexion with full extension of the proximal and distal interphalangeal joints.

Surgical Management The arm is exsanguinated with an Esmarch bandage and tourniquet inflated to 250 mm Hg. The use of 2 to 4 power loupe magnification greatly enhances one’s proficiency in performing flexor tendon repair, and small, precise instrumentation is a prerequisite for this type of surgical repair. As is necessary with every tendon laceration repair, the wound is extended in a Bruner type fashion both proximally and distally to provide a wide visibility of the injured area. Using midaxial extensions places the digital vessels and nerves at unnecessary risk unless a concomitant injury is suspected. The incisions are extended as needed to visualize the lacerated ends of the tendon or tendons. An adequate view of the surgical field must be created to avoid carrying out delicate surgical repairs within the confines of a small, cosmetic wound. Dissection begins midline, over the tendon sheath, and then proceeds with identification of the digital nerves and vessels. If these structures, too, have been severed, the ends are mobilized and brought into proximity for subsequent suturing. At this point, the laceration in the tendon sheath was identified at the C1 level (between A2 and A3). A window in the cruciate-sheath system is made by carefully excising this tissue. Additional windows may be necessary depending on the level of injury and positioning of the proximal and distal stumps. These should be fashioned as needed. However, great care is taken to preserve the annular components (especially A2 and A4), which are almost impossible to adequately repair. The distal stumps of the profundus and superficialis are delivered into the cruciate window by acutely flexing the DIP and PIP. Once the tendons are exposed in this manner, core sutures are placed in the superficialis and profundus and clamped for later usage (Fig. 33–2). 204

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Figure 33–2. After the tendons are exposed, core sutures are placed in the superficialis and profundus.

Retrieval of the proximal stumps may be difficult, and several techniques can facilitate their delivery into the repair site. The tendon ends may be “milked” in a proximal to distal fashion, again, with flexion, except this time at the wrist and MP joints. If not completely accessible at this point, a tendon retriever or grasper may be employed if the tendon(s) can be visualized in the sheath. The surgeon should be aware, however, that care must be taken when using this instrument, as repeated blind grasps down the tendon sheath may damage the delicate synovial lining of the pulleys and provoke adhesions. Additionally, two clever techniques may be employed. First, a skin hook may be used, as described by Morris and Martin. The hooked end is slid along the surface of the sheath until it is past the tendons, and then the hook is turned toward the tendons and pierced into the most superficial one. The instrument is pulled distally, with both tendons usually following. Second, a method described by Sourmelis and McGrouther can be used. A small catheter is passed from the distal wound into the palm (or vice versa) within the sheath. Through a midpalmar incision, the catheter is sutured to both tendons several centimeters proximal to the A1 pulley. The catheter is then pulled distally and freely delivers the tendon stumps for suturing. Regardless of the manner of proximal retrieval, once the tendon ends are brought into the cruciate window, a 25-gauge needle is used to maintain their position without unnecessary, repeated grasping of the tendons. Core sutures can then be placed in both the superficialis and profundus proximal ends to allow juxtapositioning with the distal ends of both (Fig. 33–3). Prior to final repair, it is necessary to ensure that the proper anatomic relationship between the superficialis and profundus is restored. It is worth a second look to verify that, indeed, the proximal end of the

Figure 33–3. Completed core suture placed in the profundus proximal end. 205

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Figure 33–4. The proximal end of the profundus, lying deep to the superficialis proximal to Camper’s chiasma.

Figure 33–5. Four core strands of 4–0 polyester are used in the repair of both the superficialis and the profundus.

profundus, lying deep to the superficialis proximal to Camper’s chiasma, is matched with its distal counterpart (Fig. 33–4). The repair of both the superficialis and profundus consisted of four core strands of 4–0 polyester (Fig. 33–5). An additional running horizontal locking stitch using 6–0 Prolene is placed in the peripheral epitendinous layer of each tendon. The flexor sheath was not repaired (Fig. 33–6). When the repair is completed the digit must be put through a full range of motion, passively extending the DIP point. This motion will test the strength of the repair. After the completion of the repair, the lacerated digital nerve was repaired using 9–0 nylon suture. Occasionally, both digital nerves and/or one or both arteries need repair as well. The skin was closed using 4–0 nylon in an interrupted fashion. A sterile dressing minimizing pressure between the digits was utilized. The finger was splinted with the wrist in 30 degrees of flexion. The MP joint flexed 45 degrees, and near extension of the PIP and DIP joints was noted.

Postoperative Management Understanding the healing stages of flexor tendons is helpful in guiding postoperative management. For days 1 to 3, tendon strength is equal to suture strength. From days 4 to 14, tendon strength decreases with the inflammatory response and weakening of collagen fibrils (the exudative phase). From days 15 to 28, tendon repair and strength begin to increase (the reparative phase) and passive motion helps con-

Figure 33–6. A running horizontal locking stitch of 6–0 Prolene is added in the peripheral epitendinous layer of each tendon. The flexor sheath was not repaired. 206

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vert longitudinal tensile forces to compression across the tendon-healing site. By day 28, the active phase of tendon healing is sufficiently underway to allow active motion. The flexor repair rehabilitation program is instituted 2 to 3 days postoperatively. It has been demonstrated that delicate active flexion performed with the wrist in extension should be relatively safe for tendons repaired with a four- or six-strand core suture technique enhanced by a strong running-locking epitendinous suture. This was the case with this patient’s repair. The program begins with the therapist instructing him to first passively flex all three long finger joints (MP, PIP, and DIP) while the wrist is maintained in flexion. Then, with the assistance of the therapist, he actively extends his wrist while maintaining or holding his digit in the flexed position. A resting splint is fashioned similar to a traditional dorsal blocking splint that positions the wrist in 30 degrees of palmar flexion, the MP joint in 45 degrees of flexion, and the interphalangeal joints in neutral. The splint is removed during therapy to allow assisted “place and hold” exercises. This protocol is followed for 4 weeks with individual adjustments made depending on the specific problems the patient may encounter, such as excessive pain, swelling, or joint stiffness. After 4 weeks, the repaired tendons should have regained sufficient strength to allow for progression or advancement of therapeutic modalities. Thus, at 4 weeks, active flexion and extension exercises of the digits and wrist are instituted with light muscle contraction. The patient is advised not to extend both the wrist and finger(s) simultaneously. The program continues to emphasize the “place and hold” technique incorporating passive digital flexion with the wrist flexed, followed by active maintenance of the flexion while the wrist is extended. Thereafter, the patient drops the wrist into flexion and extends the digit(s) to commence the tenodesis effect. The dorsal block splint is worn between exercise sessions. At 5 to 6 weeks, more vigorous exercises are permitted involving blocking exercises, isolated tendon excursion activities, and passive extension exercises. A strengthening program is begun at 8 weeks in a gradual, progressive manner. It should be emphasized that this protocol is not for everyone. Additionally, great success relies heavily on a well-trained therapist who thoroughly understands the rationale for an early motion rehabilitation program and its potential pitfalls.

Alternative Methods of Management In the event of tendon lacerations, nonoperative management is a less likely alternative. The consequences would result in the patient’s digit and hand being disabled. Options at that point are still not desirable. The patient would be left with permanent dysfunction or would have to choose surgical intervention. Yet at a later date the patient’s options may be more limited, such as tendon reconstruction or surgical amputation of the affected digit(s).

Complications Disruption of one or both flexor tendon repairs is a distressing complication. It may happen during therapy, subsequent to inadvertent strong gripping or lifting, or while a patient is asleep. Repaired tendons usually rupture through the suture material itself or through the knot. Ruptures, in cases after four-strand repairs, have been infrequent and generally are related to overzealous use of the injured hand because 207

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exemplary early motion fosters overconfidence in the strength of the healing tendon. If this does occur, the favored management is prompt reexploration and repeated repair. Reportedly, the most frequent late complication following an early mobilization protocol is development of flexion contractures at the PIP or DIP joints or both. Prompt recognition of the difficulty permits modification of the therapy program to allow greater extension along with judicious use of dynamic splints, which may help to avoid or overcome these deformities before they progress too far. The aim of all surgical intentions is return to full function and digital range of motion. Only meticulous technique, minimal operative trauma, and precise anastomosis will result in the restoration of the tendon’s gliding function and optimal range of motion.

Suggested Readings Bunnell S. Repair of tendons in the fingers. Surg Gynecol Obstet 1922;35:88–97. May EJ, Silverskiold KL, Sollerman CH. Controlled mobilization after flexor tendon repair in Zone II: A prospective comparison of three methods. J Hand Surg [Am] 1992;17A:942–952. Morris RJ, Martin DL. The use of skin hooks and hypodermic needles in tendon surgery. J Hand Surg [Am] 1993;18B:33–34. Sourmelis SG, McGrouther DA. Retrieval of the retracted flexor tendon. J Hand Surg [Am] 1987;12B:109–111. Strickland JW, ed. Flexor tendon repair—Indiana method. Indiana Hand Center Newsletter 1993;1:1–19. Strickland JW. Results of flexor tendon surgery in zone II. Hand Clin 1985;1: 167–179.

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34 Delayed Treatment of Flexor Tendons: Staged Tendon Reconstruction Lawrence H. Schneider

History and Clinical Presentation

PEARLS • The patient must demonstrate an ability to comply with a detailed rehabilitative program. • Staged reconstructions are not a perfect technique, but they are the only way to restore active motion at the interphalangeal joints of the finger in these difficult cases of flexor system disruption. • Never hesitate to build pulleys! Pulleys need to be strong. Although there are many techniques for pulley reconstruction, I prefer to wrap the tendon material around the proximal phalanx at A2 as was done in this case. At A4 I have most frequently used local tissue sutured over the implant, often with the addition of tendon material.

PITFALLS • Complications are not infrequent. • This is not a simple procedure for patient or surgeon. • Severe flexion contractures especially after stage 1 are poor prognostic signs. • Double digital nerve injury is a very poor preoperative sign. When present, it may be an indication for amputation or fusion (if the finger is in a nonfunctional position).

An 18-year-old student lacerated both flexor tendons in zone 2 of his right dominant index finger on broken glass. His primary treatment was by direct repair of both flexor tendons 3 days postinjury, and he was started on a mobilization program in a hand therapy unit. Unfortunately, this did not result in functional pull-through of his flexor tendons. He then underwent flexor tenolysis in an attempt to salvage function, a procedure that was also not successful. He was first seen on my hand surgery service at 4 months postoperative complaining of restricted motion in the operated finger.

Physical Examination The right hand showed no active flexor tendon function at either the flexor digitorum superficialis (FDS) or flexor digitorum profundus (FDP) of the right index finger (Fig. 34–1). Passive motion was almost full with only a mild flexion deformity

Figure 34–1. Right index finger held in extended position while attempted to make a full fist even after two operative procedures. 209

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at the proximal interphalangeal (PIP) joint. Sensory nerve function was intact. The skin was relatively pliable and soft considering that he had had an injury and two prior operations. The remainder of the hand was normal.

Diagnostic Studies Except for routine radiographs in cases with associated bone injury or arthritis, there are no diagnostic studies needed. Although there is some interest in the use of ultrasound and magnetic resonance imaging (MRI) in the evaluation of the flexor tendon system, I have not used these studies for these cases.

Diagnosis Flexor System Laceration of Right Index Finger, Status Postoperative Repair, and Tenolysis with Loss of Flexor Tendon Function Patients with injuries of the flexor system in which there has been marked scarring, disruption of the supporting pulley mechanism, and joint contracture not responsive to therapy measures often become candidates for tendon reconstruction using a staged approach. These patients often have a history of failed prior surgery, with adhesions preventing tendon gliding after a direct repair or tendon rupture after a tenolysis attempt. At the first stage, the scarred tendon is excised and the implant, attached only at its distal end, is placed in the flexor system of the finger. The implant as devised by Hunter and Salisbury consists of a Dacron woven tape encased in silicone rubber. The tape gives body to the implant to enhance its passive gliding and further provides a better hold for the distal sutures at its attachment to the profundus stump. Joint release, pulley reconstruction, skin revision, and nerve repair are performed at this first stage, as needed. Postoperatively the patient is placed in a passive exercise program to regain joint motion while allowing a smooth synoviallike sheath to form in response to the implant. Then at the second stage, performed 3 months later, the implant is replaced by a tendon graft. After this second stage an intense therapy program is initiated.

Nonsurgical Management Many of these patients present with joint contractures and may benefit from prereconstruction hand therapy to regain full passive motion in the finger preoperatively. This patient had almost full range of motion (ROM), so this therapy was not necessary here. There is no other nonsurgical management for this problem.

Surgical Management The patient was an appropriate candidate for exploration, with proposed staged flexor tendon reconstruction. As is common in our service, these operations are started under local anesthesia to see whether the repair can be salvaged by flexor tenolysis, and if not, as in this case, then a staged tendon reconstruction is undertaken with implant placement at this first stage. At exploration, it appeared that the repair had ruptured and the entire flexor system was involved in a heavy scar mass. Scarred tendon is sharply excised. Pulley 210

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destruction was noted at A2 and A3. Generally all remnants of the pulley system are saved, as even scar tissue can be used to support the implant. Even scarred pulleys are usable over the implant, but in this case A2 needed to be reconstructed. This was done by use of the technique where tendon material, which is generally available from the remnants of the discarded tendon, is wrapped two to three times around the proximal phalanx (Fig. 34–2). In reconstruction of A2, overlying the proximal phalanx, the tendon material is placed around the implant and deep (palmar) to the extensor mechanism. It is advantageous to carry out the pulley reconstruction over a temporary sizer tendon implant (Fig. 34–3). In this case the A1 pulley was preservable, and A4, although scarred, was salvageable. At completion of the pulley reconstruction, the sizer implant is removed and a new implant is broken out of its package, moistened in sterile solution, threaded into the flexor system, and attached distally to the stump of the profundus. In this passive program the proximal end of the implant is placed proximally in the distal forearm and not attached to any motor tendon but left free in the interval between the profundus and superficialis musculotendinous junctions in zone 5 (the distal forearm). At this first stage, scar excision and joint releases are performed as well as nerve repairs and skin revisions, as necessary. After the tourniquet is released and bleeding is controlled, wound closure is performed. The wound is dressed and the extremity is placed in a dorsal splint with the wrist in slight flexion, and the fingers in flexion at the MP joints and in extension for 1 week, at which time a passive mobilization program is begun. The interval between the two stages is devoted to regaining passive mobility of the involved joints while the soft tissues are healing and a synovial-like sheath is formed in response to the implant. The goal is to grade the finger up to a point

Figure 34–2. Exploration of the finger at stage 1 revealed loss of the A2 pulley. The sizer implant is in place and tendon material has been wrapped around the proximal phalanx and tendon implant to reconstruct the pulley. 211

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Figure 34–3. The pulley has been completed and rotated so that the sutures are lateral and will not be near the graft.

where it will accept a tendon graft at the second stage with a reasonable chance to succeed. Three months is sufficient to allow the sheath to form and the finger to heal completely. Stage 2, 3 months later, is actually a simplified tendon graft in that little dissection is needed or desired so as to do as little injury to the new sheath that has been created. The distal and proximal ends of the incision are opened to expose the ends of the implant. A long tendon graft is usually needed to bridge the gap between zones 1 and 5 and the palmaris longus is usually not long enough. The plantaris is excellent when available and can be removed through one incision at the medial ankle. If not present, and it is not possible to determine this without exploration, then the use of one of the toe extensors is a second choice. In this case the plantaris was used. It is sutured to the tendon implant and drawn into the sheath. The graft is attached distally to the distal phalanx and profundus stump using the Bunnell pullout technique and tied over a button on the nail. The tourniquet is released, bleeding controlled, and the distal (finger) wound closed. The tourniquet is reinflated and the proximal juncture performed in this case using the flexor digitorum profundus of the index finger as the motor. The suture technique is an interweave as described by Pulvertaft. When reconstructing the ulnar sided flexors the profundus mass of the third, fourth, and fifth fingers is usually used to motor the finger or fingers being reconstructed. A suture is placed in the fingernail for the postoperative mobilization program. The tourniquet is again removed and the proximal wound is closed. After the dressing is applied, a posterior molded splint is made with the wrist placed in flexion of 30 degrees, the fingers at 212

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70 degrees at the metacarpophalangeal (MP) joints, and the interphalangeal joints in extension. A protected mobilization program is started under the supervision of the hand therapist 2 or 3 days postoperative. Immobilization is continued for 3 to 4 weeks, and the pullout suture and button are removed at 4 weeks. Active flexion is started at 3 to 4 weeks with blocking techniques added as feasible but not before 4 weeks. Exercises are continued for ~12 weeks. Full resistance is allowed at ~8 to 12 weeks. Generally patients with good range of motion are protected from full resistance longer as they are more likely to rupture. This patient achieved an excellent recovery of active motion at 6 months after stage 2 tendon grafting (Fig. 34–4).

A

B

C

D

Figure 34–4. Range of motion achieved 6 months after stage 2 tendon grafting. 213

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Complications Complications of note include reaction to the implant at stage 1, which creates a synovial reaction with fluid building up in the forming sheath. This now rare reaction, synovitis, was thought to be secondary to contaminants or breakdown of the distal juncture. The fluid is sterile and is treated by slowing down the passive motion program. Other problems include infection, which, if not controllable by antibiotics, usually requires removing the implant and redoing the procedure in the future. Joint contractures that are persistent after stage 1 need to be treated by hand therapy protocols but portend a reduced prognosis. After stage 2, problems encountered include juncture ruptures, which are attributable to technical problems and resistant joint contractures. Rupture of a juncture should be treated by repair as soon as feasible. Although many of these reconstructions go smoothly, the most frequent problem seen is restricted motion secondary to adhesions, which, again, limit active pull-through of the tendon graft. The use of trained hand therapists helps keep this problem to a minimum.

Suggested Readings Byron P, Berger-Feldscher S. Post-operative therapy for flexor tendon repair. In: Taras JS, Schneider LH, eds. Atlas of Hand Clinics. Philadelphia: Saunders; 1996: 163–188. Hunter JM, Salisbury RE. Flexor tendon reconstruction in severely damaged hands, A two stage procedure using silicone Dacron reinforced gliding prosthesis prior to tendon grafting. J Bone Joint Surg [Am] 1971;53A:829–858. Mackin EJ. Therapist’s management of staged flexor tendon reconstruction. In: Hunter JM, Schneider LH, Mackin EJ, Callahan AD, eds. Rehabilitation of the Hand. 2nd ed. St. Louis: CV Mosby; 1984:314–323. Schneider LH. Staged flexor tendon reconstruction using the method of Hunter. Clin Orthop 1982;171:164–171. Schneider LH. Staged tendon reconstruction. Hand Clin 1985;1:109–120. Schneider LH. Complications in tendon injury and surgery. Hand Clin 1986;2: 361–371. Schneider LH. Flexor tendons—late reconstruction. In: Green DP, Hotchkiss RN, Pederson WC, eds. Green’s Operative Hand Surgery. New York: Churchill Livingstone; 1998:1898–1949. Wehbe MA, Hunter JM, Schneider LH, Goodwyn BL. Two-stage flexor-tendon reconstruction. Ten year experience. J Bone Joint Surg [Am] 1986;68A:752–763.

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35 Chronic Lacerations of Extensor Tendons Angela A. Wang and Michelle Gerwin Carlson

History and Clinical Presentation A 66-year-old right hand dominant man sustained a deep laceration to the dorsum of his right wrist when a plate glass mirror fell on it. He was evaluated at a local emergency room and was informed he would need surgery, but he wanted to be treated at another institution. Seventeen days later, he presented to the office with the complaint that he could not lift his fingers.

Physical Examination A well-healed 5-cm transverse laceration is noted on the dorsum of the right wrist just proximal to the edge of the extensor retinaculum. The patient lacked active extension of the index, long, and ring fingers at the metacarpophalangeal joints, as well as the thumb. In addition, he had a lack of extension of the wrist radially. The abductor pollicis longus, extensor pollicis brevis, and the small finger extensors were intact. Sensation in the distribution of the superficial radial nerve was intact (Fig. 35–1). PEARLS • Ultimate results are closely tied to postoperative care and rehabilitation. Careful attention to good splinting and controlled mobilization of the repaired tendon will yield better function when the tendon healing is complete.

PITFALLS • The ruptured tendon must be repaired under the proper tension. Although tendon reconstruction under excessive tension is to be avoided, the surgeon must fix the tendon at the proper length to provide adequate power. It should also be noted that repairs usually loosen over time.

Diagnostic Studies Radiographs of the right wrist were negative for bony pathology. No foreign bodies were present.

Figure 35–1. The patient under anesthesia preoperatively, with the wrist supported. Note the laceration on the dorsum of the wrist, and the lack of extension of the digits.

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Differential Diagnosis Extensor tendon laceration Rheumatoid arthritis synovitis Nerve injury

Diagnosis Laceration of the Second, Third, and Fourth Dorsal Compartments of the Right Wrist, Late Extensor tendon lacerations or ruptures that are treated in a delayed fashion may not be amenable to primary approximation and repair. Most tendon laceration and ruptures are best treated acutely; if this is not possible, the patient should be told that tendon reconstruction might be necessary. In cases of multiple tendon injuries, emphasis should be placed on recovering independent wrist and thumb extension, and mass extension of the fingers. Postoperative care plays an important role in recovery. Early controlled mobilization (passive digital extension with wrist flexion and active digital flexion with wrist extension) and dynamic splinting have been shown to have positive effects on tendon healing and ultimate function.

Surgical Management Four days later (3 weeks after the injury), the patient was brought to the operating room. Under regional anesthesia (an axillary block) with a tourniquet, an incision was made over the healed laceration and extended proximally and distally. The retinaculum was incised longitudinally over the fifth compartment, reflected back radially, and the dorsal compartments were identified and explored. The extensor carpi radialis brevis, extensor carpi radialis longus, extensor pollicis longus, extensor indicis proprius (EIP), and extensor digitorum communis (EDC) tendons were found to be lacerated. The extensor digitorum communis tendon had retracted proximally, and a large gap was present at the laceration site. The extensor carpi radialis brevis and extensor carpi radialis longus tendons were directly repaired with a 4-strand repair using a 4–0 nonabsorbable, nonbraided suture. Similarly, the extensor pollicis longus was primarily repaired. Due to the chronic nature of the injury, however, direct approximation of the EIP and EDC tendons created significant tension and did not allow the digit to be flexed with the wrist in neutral. The decision was made to perform a fractional lengthening of the EIP and EDC tendons at the musculotendinous junction cutting the tendinious portion of the musculotendinous junction, after which the wrist could be brought into the neutral position and the fingers could be passively flexed. The wound was closed in a layered fashion over a Penrose drain. The patient was then placed in a volar splint with the wrist in 30 degrees of dorsiflexion and the fingers in 20 degrees of flexion at the metacarpalphalangeal joints.

Postoperative Management On postoperative day 6, the patient was changed from his static splint to a dynamic outrigger extension splint, and began occupational therapy. The dynamic splint was 216

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Figure 35–2. Postoperatively, the patient is able to actively extend the digits fully.

Figure 35–3. Postoperatively, the patient is able to make a full fist, indicating proper tensioning of the repair.

discontinued at 3 weeks, whereupon the patient continued both active and passive range of motion exercises. He returned to work 9 weeks after the surgery, and by 3 months he had recovered full range of motion of the wrist and fingers, as well as good strength in the hand. (Figs. 35–2 and 35–3).

Alternative Methods of Management This patient underwent a combination of direct repair and repair using tendon lengthening. He was able to achieve a good result with maintenance of independent finger function. Alternative methods of tendon reconstruction in cases of late extensor tendon repair include tendon grafting and tendon transfer. Harvest sites for tendon grafting include the palmaris longus, or, in cases where the palmaris longus is absent, the toe extensors. If a single digit is injured, its tendon can be repaired in a side-to-side fashion with an adjacent digit. If this is not feasible, the EIP is often used for transfer; it is easily harvested, and leaves minimal deficit in the index finger if the EDC is intact. If several digits are affected, transfer of the superficial flexor tendons to the affected extensors can be performed. This method is particularly useful in cases of multiple chronic extensor tendon ruptures where direct repair is not possible (e.g., patients with rheumatoid arthritis). First described by Boyes in 1960, this procedure was modified by Nalebuff in 1973: the sublimis flexor tendon is rerouted around the radial or ulnar distal forearm. This transfer provides adequate power and excursion for transfer to an extensor surface without the need for extensive reeducation (Table 35–1).

Table 35–1 Alternative Methods of Management Type of Managemenent

Advantages

Disadvantages

Comments

Tendon lengthening Tendon grafting Tendon transfer

Technically easy For large gaps For large gaps

For short gaps only Donor deficit/incision Donor deficit/incision

No donor deficit Two tendon anastomosis sites More extensive dissection 217

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Complications Complications are more likely to occur in the more distal zones of repair. Scarring of the tendons can result in failure of gliding of the repair, which may manifest itself as either extensor lag or extrinsic extensor tendon tightness. To minimize this risk, the repair site should be away from the retinaculum and areas of previous scarring, and the completed transfers or repairs should be placed outside of the retinaculum, or the retinaculum opened over the repair. In addition, early controlled therapy and splinting should be initiated. Donor weakness of the transferred tendons can occur. If the EIP is used for transfer, presence of the EDC to the index is mandatory. Joint stiffness can result from immobilization. Careful attention to positioning of the small joints in the splint, as well as the aforementioned therapy, can help avoid this complication.

Suggested Readings Blair WF, Steyers CM. Extensor tendon injuries. Orthop Clin North Am 1992;23: 141–148. Chow JA, Dovelle S, Thomes LJ, et al. A comparison of results of extensor tendon repair followed by early controlled mobilization versus static immobilization. J Hand Surg [Br] 1989;14B:18–20. Lovett WL, McCalla MA. Management and rehabilitation of extensor tendon injuries. Orthop Clin North Am 1983;14:811–826. Nalebuff EA, Patel MR. Flexor digitorum sublimis transfer for multiple extensor tendon ruptures in rheumatoid arthritis. Plast Reconstr Surg 1973;52:531–533. Newport ML, Blair WF, Steyers CM. Long-term results of extensor tendon repair. J Hand Surg [Am] 1990;15A:961–966. Williamson SC, Feldon P. Extensor tendon ruptures in rheumatoid arthritis. Hand Clin 1995;11:449–459.

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36 Avulsions of the Flexor Digitorum Profundus Donald M. Lewis and Randall W. Culp

History and Clinical Presentation

PEARLS • The physical examination should check for active flexion and extension of the DIP, PIP, and MP joints separately to ensure the FDP, FDS, and extensors are intact. • The A2 and A4 pulleys should be preserved at all times to prevent bow-stringing. • If the bony fragment is too small or comminuted, it can be excised and the tendon repaired directly to the distal phalanx as in a type 1 or 2 injury.

PITFALLS • The tendon must be secured through or around the distal phalanx; fixation to the distal tendon remnant or periosteum is not secure. • The proximal tendon end must not be debrided or advanced more than 1.5 cm, to prevent tethering of the FDP and the quadrigia effect. • For type 1 and type 2 injuries, the PIP joint level must be explored before the palm, to prevent pulling the tendon proximally and converting a type 2 injury to a type 1 injury. This will rupture the long vinculum and its blood supply.

A 43-year-old right hand dominant air transportation specialist presented with pain in his left ring finger after an injury sustained at work. The patient reported pulling on the handle of a rototiller, which suddenly stopped, causing his finger to be forcibly hyperextended. He reported hearing a snap when this occurred and experienced immediate pain in his ring finger. He reports no prior injury to this area. This patient complained of pain at the level of the distal interphalangeal (DIP) joint of the ring finger.

Physical Examination The patient had volar swelling and tenderness, and could not actively flex his finger at the level of the DIP joint. Upon making a fist, he had a noticeable lack of flexion compared with the other digits (Fig. 36–1). The flexor digitorum profundi (FDP) to the other digits were intact as demonstrated by blocking the digits in extension at the level of the middle phalanx, and asking him to flex at the level of the DIP joints. The flexor digitorum superficialis (FDS) was intact in all fingers, as demonstrated by blocking the adjacent digits in extension at the level of the proximal interphalangeal (PIP) and DIP joints and asking the patient to actively flex at the level of the PIP joint in the examined finger. Active extension was possible at the metacarpophalangeal (MP), PIP, and DIP levels of all fingers. He had no complaints of numbness or tingling. He also had no complaints of pain in the palm, wrist, or forearm.

Figure 36–1. Presentation with ring finger unable to actively flex at the distal interphalangeal (DIP) joint.

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A

B

Figure 36–2. Radiographs of the distal phalanx bony avulsion.

Diagnostic Studies Individual radiographs of the left ring finger and hand were obtained. A small bony avulsion was seen at the volar proximal aspect of the distal phalanx of the affected finger (Fig. 36–2).

Differential Diagnosis Bony flexor digitorum profundus (FDP) avulsion Fracture/dislocation of the distal phalanx

Diagnosis The patient was diagnosed with bony flexor digitorum profundus avulsion. This is a classic history and presentation of an acute “jersey finger.” Four types of FDP avulsions have been described, as modified from Leddy’s original description: Type 1: Distal tendinous avulsion with proximal retraction into the palm Type 2: Distal tendinous avulsion with retraction to the PIP joint level Type 3: Distal bony avulsion with retraction to the A4 pulley Type 4: Distal bony avulsion with FDP avulsion from the bony fragment 220

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This case is an example of a type 3 or 4 avulsion injury diagnosed by radiographs and clinical examination. Surgical exploration differentiates types 3 and 4. The ring finger is the most common profundus tendon avulsion. A typical presentation is in sports injuries when the participant grabs the opponent’s jersey in a tackle, undergoing forced extension of the fingertip while the profundus is under maximal contraction. Thus the name “jersey” or “rugby” finger was coined. Type 1 and 2 injuries are defined by proximal retraction of the FDP tendon into the palm and finger respectively, with subsequent rupture of the short and possibly long vincula. Patients with a type 1 injury often have swelling, pain, and tenderness in the palm, and patients with a type 2 injury have swelling, pain, tenderness, and decreased motion at the level of the PIP joint. Sometimes a small fleck of bone is seen volarly at the level of the PIP joint on the lateral radiograph in type 2 injuries.

Surgical Management A comfortable ulnar gutter splint was applied to the patient with the ring and small fingers in the intrinsic-plus position. He was scheduled urgently for outpatient surgery that week. Type 1 injuries should be repaired within 7 to 10 days, as the tendon blood supply is theoretically compromised, due to rupture of the long and short vincula when the tendon retracts into the palm. Type 2, 3, and 4 injuries have a longer safety zone for repair, with successful reports greater than 2 months after injury. Earlier repair is recommended to facilitate rehabilitation, decrease morbidity, and prevent a possible conversion to a type 1 injury, with later rupture of the long vinculum and retraction into the palm. The next day, the patient was placed supine on the operating room table after obtaining general endotracheal anesthesia. Regional axillary block anesthesia is an acceptable alternative. The arm was placed on a hand table with a well-padded proximal arm tourniquet. After prep and drape, the limb was exsanguinated with an Esmarch bandage and the tourniquet inflated to 250 mm Hg. A volar zigzag incision was made at the level of the DIP joint on the ring finger, and exploration using loupe magnification was performed down to the flexor sheath. Hemostasis was meticulously maintained using bipolar electrocautery, and both neurovascular bundles were carefully protected throughout the procedure. The sheath was opened distal to the A4 pulley, taking care to preserve this pulley throughout the procedure to prevent bow-stringing of the tendon postoperatively (Fig. 36–3). A window between the C3 and A5 pulleys was opened to expose the distal bony avulsion fragment, and it was seen that the FDP tendon was still attached to this piece of the distal phalanx, indicating a type 3 injury. Hematoma and debris were curetted from the piece and from the avulsion site. The piece was reduced and held into position with a 0.035-inch Kirschner wire, and under fluoroscopy two 1.5-mm titanium self-tapping screws A3 pulley C2 pulley A4 pulley

Flexor digitorum C1 pulley superficialis A2 pulley A1 pulley

Flexor digitorum profundus

C3 pulley

Distal interphalangeal joint

Proximal interphalangeal joint

Metacarpal phalangeal joint

Figure 36–3. Anatomy of the flexor sheath. 221

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A

B

Figure 36–4. (A). Lateral radiograph and (B). a radiograph of a type 3 avulsion secured with two cortical screws.

were placed with bicortical purchase (Fig. 36–4). The fragment was seen to be stable with a range of motion. The tourniquet was deflated, hemostasis obtained, and saline irrigation performed. The skin was closed with 4–0 nylon simple sutures, a bulky dressing applied, and a dorsal blocking splint applied with the wrist in 30 degrees of flexion. The fingers were splinted in the intrinsic-plus position to relax the FDP tendon and prevent postoperative stiffness. Type 1 and 2 injuries necessitate exploration at the level of the PIP joint, where an additional palmar zigzag incision is used to expose the flexor sheath (Fig. 36–3). A transverse incision is made into the sheath just distal to the A2 pulley or through the C1 pulley. If the FDP tendon is not found at this level, then an additional incision is made in the palm and the flexor sheath is opened proximal to the A1 pulley. If the tendon is found at this level, it is classified a type 1 injury. The long and short vincula are ruptured, and the blood supply to the tendon is theoretically compromised. The tendon is retracted proximal to the flexor sheath, preventing this source of nutrition via intrasynovial diffusion. This necessitates earlier repair, within 7 to 10 days, to prevent possible necrosis and myostatic contracture that may develop. A 4–0 Prolene suture is placed as a core suture in the proximal tendon stump. An infant feeding gastrostomy tube or Swanson suture passer is placed in retrograde fashion from just distal to the A2 pulley (at the PIP level incision) through the flexor sheath. Care is taken to place the tube/suture passer through the flexor superficialis decussation and to exit proximal to the A1 pulley. The tube/suture passer is attached to the core suture, and the tendon is pulled distally to the level of the PIP joint. Next the tube/suture passer is fed retrograde under A4 (from the DIP level incision) and the tendon is pulled distally to the level of 222

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the avulsion at the distal phalanx. Care is taken to preserve the A2 and A4 pulleys to prevent bow-stringing postoperatively. A 25-gauge needle is used to spear the tendon at A4 to secure its position. A bone trough is created at the proximal volar aspect of the distal phalanx. Two heavy needles are drilled through the bony trough volarly, exiting dorsally and distally through the nail plate. The core suture ends are pulled through the eye of the needles and pulled through the distal phalanx and nail. They are pulled snug and tied securely over a button on top of the nail while flexing the finger. Any remaining stump of tendon at the base of the distal phalanx is sutured over this repair for additional security and healing potential. The sheath can be left open or repaired, depending on the surgeon’s philosophy. The closure and postoperative care are similar to the type 3 injury described before. The suture and button are removed at 6 weeks after surgery. If the tendon was initially found at the level of the PIP joint upon exploration, it is classified a type 2 injury. The long vinculum is assumed to be intact, providing a source of nutrition to the tendon and preventing further retraction of the tendon into the palm. The short vinculum from the distal end of the middle phalanx is ruptured. The tendon still lies within the flexor sheath and retains nutrition via intrasynovial diffusion. Due to these factors, the repairs have been reported more than 2 months after injury. A 4–0 Prolene core suture is placed in the distal tendon end, and pulled underneath A4 as described before. The suture is pulled through and tied to a button as described for a type 1 injury. If upon surgical exploration a type 4 injury is found, then reduction and fixation of the bony fragment would be performed with screws, as described before. The tendon avulsion from this bony fragment would then be repaired to the distal phalanx, as described for a type 1 or 2 injury.

Postoperative Management This patient was seen the following week and started on a flexor tendon zone 1 passive range of motion protocol, as described by Evans. A dorsal blocking splint was placed to keep the wrist in 30 degrees of flexion and the MP joints in 60 degrees of flexion. A second dorsal splint was applied to the digit to maintain 45 degrees of flexion at the DIP joint. Passive flexion of the digit was allowed out of the splint several times daily. A modified passive hook fist and passive PIP extension was allowed with the MP joints flexed. Place and holds were performed for the FDS. Wrist extension to 10 degrees was allowed with the fingers flexed under therapist supervision. Sutures were removed at 10 days and radiographs obtained at follow-up visits to ensure reduction of the fragment and progression of healing. At 21 days, active range of motion was instituted with a full fist place and hold, and the digital blocking splint was discontinued. At 28 days the patient was started with tenodesis wrist exercises, gentle isolated FDS exercises, and hook fisting. At 35 days, full DIP active motion was allowed, including extension. After bony union was confirmed radiographically and clinically, strengthening with resistance was started at 8 weeks; at 12 weeks the patient was allowed to return to full activity at work and in sports.

Alternative Methods of Management Alternatively, Bier block or local anesthesia can be used. Care must be taken with local anesthesia, as the palm may also need to be blocked in case of a missed or converted type 1 injury. A midlateral exposure can be used in the digit rather than a volar zigzag, depending on the surgeon’s preference. 223

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The tendon end can be secured to the distal phalanx by passing the core suture ends around the bone, rather than through it. It can still be secured over a button on the nail, as described before. Another method is to anchor the suture to the distal phalanx using a bone suture anchor. This leaves the nail bed and plate intact, and obviates the need for later suture removal. Chronic (>3 months) untreated cases can be left alone if asymptomatic. If there is bothersome instability or pain in the DIP joint, this can be treated by tenodesis or fusion. If the remaining proximal stump of the profundus tendon is tender, this can be excised from the palm. Another somewhat laborious approach would be to perform one- or two-stage tendon grafting through the superficialis, allowing active use of the DIP joint.

Complications Rerupture of the tendon can occur early or late. This should be repaired emergently as with the initial injury. Infection, skin slough, stiffness, and irritation at the wound and button site are infrequent. A slight loss of extension at the DIP joint commonly occurs. Nonunion or malunion of a bony fragment is a rare possibility, and can be prevented with careful attention to the bony reduction and fixation.

Suggested Readings Carroll RE, Match RM. Avulsion of the flexor profundus tendon insertion. J Trauma 1970;10:1109–1118. Eglseder WA, Russell JM. Type IV flexor digitorum profundus avulsion. J Hand Surg [Am] 1990;15A:735–739. Ehlert KJ, Gould JS, Black KP. A simultaneous distal phalanx avulsion fracture with profundus tendon avulsion: a case report and review of the literature. Clin Orthop 1992;283:265–269. Evans RB. A study of the zone I flexor tendon injury and implications for treatment. J Hand Ther 1990;133–148. Leddy JP. Avulsions of the flexor digitorum profundus. Hand Clin 1985;1:77–83. Leddy JP, Bechler J. Flexor tendon avulsion from the distal phalanx. In: Blair WF, ed. Techniques in Hand Surgery. Baltimore: Williams & Wilkins; 1996:120–128. Leddy JP, Packer JW. Avulsion of the profundus tendon insertion in athletes. J Hand Surg [Am] 1977;2A:66–69. Schneider LH. Fractures of the distal phalanx. Hand Clin 1988;4:537–547. Smith JH. Avulsion of a profundus tendon with simultaneous intraarticular fracture of the distal phalanx–Case report. J Hand Surg [Am] 1981;6A:600–601. Strickland JW. Flexor tendons–acute injuries. In: Green DP, Hotchkiss RN, Pederson WC, eds. Operative Hand Surgery, 4th ed. Philadelphia: Churchill Livingstone; 1999:1877–1883. Trumble TE, Vedder NB, Benirschke SK. Misleading fractures after profundus tendon avulsions: A report of six cases. J Hand Surg [Am] 1992;17A:902–906. 224

Section VIII

Fractures and Dislocations of the Hand

A. Phalanx Fractures Distal Phalangeal Fractures Kevin D. Plancher

Mallet Fractures Kevin D. Plancher

Proximal Phalangeal Shaft Fractures Kevin D. Plancher

Proximal Phalangeal Condylar Fractures Carrie R. Swigart

B. Metacarpal Fractures Metacarpal Neck Fractures Kostas J. Constantine and Thomas R. Kiefhaber

Metacarpal Shaft Fractures Robert J. Goitz, Sokratis Varitimidis, and Dean G. Sotereanos

Metacarpophalangeal Joint Injuries: Fractures (Intraarticular) at the Base of the Proximal Phalanx, An Arthroscopic Technique Joseph F. Slade III and John D. Mahoney

Metacarpal Head Fractures Paul R. Greenlaw and Mark R. Belsky

C. Dislocations: Phalanx and Metacarpals

Dorsal Dislocations of the Proximal Interphalangeal Joint Rosa L. Dell’Oca and Amy Ladd

Distal Interphalangeal Joint Dislocations John D. Wyrick

Dorsal Metacarpophalangeal Dislocations (Irreducible) Benjamin Chang and Mark Katz

Volar Metacarpophalangeal Dislocations (Irreducible) Benjamin Chang and Mark Katz

D. Thumb and Carpometacarpal Joint Ulnar Collateral Ligament Injuries: “Skier’s Thumb” Kevin D. Plancher

Carpometacarpal Joint Injuries: Bennett’s Fractures (Arthroscopic and Percutaneous Screw Technique) Joseph F. Slade III and John D. Mahoney

Carpometacarpal Joint Injuries: Bennett’s Fractures (Wire Technique) Michael Jablon

Complex Fractures at the Base of the Thumb: Rolando Patterns John A. Girotto, Shrika Sharma, Thomas J. Graham

Volar Dislocations of the Proximal Interphalangeal Joint

Carpometacarpal Joint Dislocation

Lisa L. Lattanza and Steven Z. Glickel

Andrew L. Haas and Kevin D. Plancher

Lateral Dislocations of the Proximal Interphalangeal Joint Christopher H. Martin and Steven Z. Glickel

D I S TA L P H A L A N G E A L F R A C T U R E S

37 Distal Phalangeal Fractures Kevin D. Plancher

History and Clinical Presentation A 35 year old carpenter was on the job using a table saw. He forgot to engage the safety and cut the tip of his finger. He presents to the emergency room with exposed bone at the tip of his finger after a transverse cut to his fingertip.

Physical Examination There is no soft tissue covering the end of the bone. Approximately 40% of the nail and nail matrix are present.

Diagnostic Studies Anteroposterior (AP), lateral, and oblique radiographs of the injured digit were obtained. The finger was assessed for foreign objects, joint dislocation, subluxation, and fractures.

Differential Diagnosis

PEARLS • Expect patients 50% of the time to have cold intolerance, hypersensitivity, and paresthesias. • Sew these flaps with chromic or catgut sutures. Suture to the nail should be absorbable to avoid painful removal in the office.

PITFALLS • Attention to detail in lifting the V-Y flap in the subcutaneous tissue will provide survival of the tissues. • Adequate incision and drainage with antibiotics will avoid infection in most cases.

Distal phalanx fracture Vascular injury Nerve injury Mallet fracture Distal phalanx (P3) dislocations

Diagnosis Open Distal Phalanx Fracture with Soft Tissue Loss The type of injury, the functional goal, and possible complications often determine the treatment of fingertip injuries. Factors to consider include finger sensitivity, a nontender finger, maximum length, nail appearance, normal joint movement, and cosmesis. On initial diagnosis, the viability of the tissues should be assessed to determine which tissue is unlikely to survive. It must also be determined what can be sacrificed and what must be preserved to maintain function. Transverse amputations are the easiest to repair. Treatment is determined by the coverage of the bone. The amount of nail following injury is also important in determining treatment. Depending on the level of amputation, blood vessel and nerve status must also be determined. In oblique dorsal amputations, if the nail is only partially injured, an attempt must be made to preserve it. The condition of the nail matrix is also important. Oblique palmar amputations are difficult to treat. Thenar flaps are an option. The goal of treatment in a palmar amputation is to provide a reconstructed pulp, which is sensitive and well cushioned. 227

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Surgical Treatment For this patient the volar V-Y flap or Atasoy technique was used to provide coverage of exposed bone with adequate padding. The patient was most concerned with fingertip tenderness and function of the finger. The finger was prepared and a lidocaine metacarpal block supplemented with bupivacaine provided anesthesia. A Penrose drain was placed on the digit to act as a tourniquet. The wound was irrigated and surgically cleaned, and debridement of the skin edges was performed. A pattern of the defect was transferred onto the palmar skin proximal to the defect. The skin pattern was made ~1 mm larger. The palmar skin incisions were marked from the lateral edges of the defect site to enclose the skin pattern and continued proximally and obliquely to meet in the midline of the finger at the distal crease (Fig. 37–1). The skin was incised through the dermis sharply and the flap was dissected from the periosteum and the flexor sheath. The Grayson’s and Cleland’s ligaments that surround the neurovascular bundles and connect the flap to surrounding tissues were bluntly dissected and divided with dissection scissors (Fig. 37–2). The flap was mobilized to allow advancement of the flap without tension (Fig. 37–3). Hemostasis was maintained with a bipolar cautery. The flap was then sutured to the nail with nonabsorbable sutures (Fig. 37–4). The apex of the V was closed with interrupted sutures, which were kept close to the

Figure 37–2. The Grayson’s and Cleland’s ligaments that surround the neurovascular bundles and connect the flap to surrounding tissues are bluntly dissected and divided with dissection scissors.

Figure 37–1. The palmar skin incisions are marked from the lateral edges of the defect site to enclose the skin pattern and continue proximally and obliquely to meet in the midline of the finger at the distal crease. 228

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Figure 37–3. The flap is mobilized to allow advancement of the flap without tension.

Figure 37–4. The flap is sutured to the nail with nonabsorbable sutures. 229

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Figure 37–5. The oblique incision is made from the palmar edge of the defect to intersect with the dorsal incision.

skin edge to avoid interference with the vascular supply. The tourniquet was deflated and blood supply to the flap was verified. The finger was treated with Xeroform, a light dressing, and a protective tip splint. The patient was instructed to keep the finger elevated for 2 days. The dressing was changed 5 days postoperatively and the patient was prescribed active exercises of the proximal interphalangeal (PIP) joint. Sutures were removed at 14 days postoperatively and the patient was instructed to keep the protective splint on for 4 to 6 weeks postoperatively.

Alternative Techniques The lateral V-Y flap technique uses flaps from the lateral side of the digit to close fingertip defects. Digital anesthesia is obtained with metacarpal block. The bone is debrided and the wound is irrigated. The dorsal incision is made from the amputation site to 2 mm lateral to the nail fold and continued proximally midway between the palmar and dorsal surfaces of the bone. The incision length is twice the width of the flap. The oblique incision is made from the palmar edge of the defect to intersect with the dorsal incision (Fig. 37–5). Advancement of the flaps requires complete release of the dorsal-lateral fibrous bands (Fig. 37–6). With tension on the distal aspect of the flap, the fibrous septum is dissected. The two flaps are advanced

Figure 37–6. Advancement of the flaps requires complete release of the dorsal-lateral fibrous bands. 230

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Figure 37–7. The two flaps are advanced toward each other and sutured together and to the nail bed.

toward each other and sutured together and to the nail bed (Fig. 37–7). Postoperative care is similar to the volar V-Y technique.

Complications Complications include infection, fingertip pain or stiffness, scar formation, and loss of motion. Most complications can be avoided with meticulous intraoperative technique, adequate postoperative care of the flap site, and early motion of the finger.

Suggested Readings Atasoy E, Ioakimidis E, Kasdan ML, Kutz JE, Kleinert HE. Reconstruction of the amputated fingertip with triangular volar flap. J Bone Joint Surg [Am] 1970;52A:921–926. Fisher RH. The Kulter method of repair of fingertip amputations. J Bone Joint Surg [Am] 1967;49A:317–321. Martin C, Gonzalez Del Pino J. Controversies in the treatment of fingertip amputations. Conservative versus surgical reconstruction. Clin Orthop 1998;353:63–73. Shepard GH. The use of lateral V-Y advancement flaps for fingertip reconstruction. J Hand Surg [Am] 1983;8A:254–259. Tupper J, Miller G. Sensitivity following volar V-Y plasty for fingertip amputations. J Hand Surg [Br] 1985;10B:183–184.

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38 Mallet Fractures Kevin D. Plancher

History and Clinical Presentation A 45-year-old left hand dominant professional squash player was lunging for a shot and fell, landing on his hand. He had sudden pain in his long finger with the inability to extend the tip of his finger. The patient reported no other injuries. He has no history of arthritis.

Physical Examination The patient is unable to extend the tip of his finger. There is swelling around the injury. The tip of the fingers is sitting at a 45-degree dropped position (Fig. 38–1). The finger has full vascular flow.

Diagnostic Studies Anteroposterior (AP), splay lateral, and oblique radiographs of the injured digit were obtained. The joint was assessed for joint dislocation, subluxation, and fractures (Fig. 38–2).

Differential Diagnosis Soft tissue mallet Dislocated distal interphalangeal (DIP) joint

Figure 38–1. Attitude of a finger with the inability to extend the tip sitting at 45 degrees.

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Figure 38–2. Radiograph, splay lateral, demonstrating a mallet of the ring finger of a different patient.

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PEARLS • Patient expectations of a straight finger upon healing is unrealistic. It is important to tell patient that half the “droop” will be a goal. • Do not underestimate the cosmetic emotional effect of a mallet finger on individual personalities.

PITFALLS • ORIF of a distal phalanx (P3) mallet is a technically demanding exercise. One drill hole is permitted with one pass only to avoid infection and damage to the articular surface. • Nonoperative treatment may lead to a splint that is too tight. Dorsal skin ulceration and maceration.

Figure 38–3. A type A mallet finger.

Diagnosis Mallet Fracture with Subluxation Mallet finger injuries range from pure tendon rupture to tendon rupture with a fracture of the base of the distal phalanx. A type A mallet finger is a tendon rupture (Fig. 38–3), a type B is a chip fracture, a type C is an avulsion fracture without displacement, a type D is an avulsion fracture with displacement of the fragment (Fig. 38–4), and a type E has displacement of the avulsion fracture with subluxation of the distal phalanx. Type E fractures often require operative intervention. Forceful hyperflexion usually results in pure tendon ruptures or tendon ruptures with a small bone fracture. In fractures involving articular surfaces, accurate anatomic reduction by surgery is usually required. For mallet fractures, satisfactory finger function may be regained despite mild arthrosis.

Nonoperative Management Nonoperative management is indicated for mallet fractures when the distal articular surface is congruous with the condyles of the middle phalanx and volar subluxation is not present (Fig. 38–5). However, in patients seen with acute injuries involving

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Figure 38–4. (A) Radiograph of a type D avulsion fracture with displacement of the fragment. (B) A type D avulsion fracture.

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Figure 38–5. (A) Lateral radiograph of middle phalanx with no volar subluxation present. (B) Mallet splint used for this type of fracture.

more than one third to one half of the joint space with volar subluxation present, open reduction and internal fixation (ORIF) have obtained good results.

Surgical Management Kirschner Wire Technique Regional or digital block anesthesia may be used. If digital block is used, 2% lidocaine is introduced either dorsally between the metacarpal heads or via a palmar approach. The anesthetic is injected on the radial and ulnar sides of each digit directly over the neurovascular bundle. It is very important to confirm that the injection has successfully anesthetized the dorsal cutaneous because it supplies the area of the incision. Using an H-shaped incision, dissection is made through the dorsal subcutaneous tissue. Most of the dorsal veins are sacrificed, although most of the radial and ulnar ones may be saved. Skin flaps are mobilized deep to the epitenon of the extensor mechanism to help avoid skin sloughing. The flaps are held by stay sutures and kept moist throughout the procedure using copious amounts of saline or lactated Ringer’s solution. The dorsal 30% of the radial ulnar collateral ligaments of the DIP joint can be taken down to mobilize the distal phalanx. Loupe or other magnification device may be used to adequately visualize the injury. The key to successful restoration of fracture and successful return to function in the long run rests on leaving the extensor mechanism intact and attached to the fracture fragment. The joint is copiously irrigated. Next, fracture fragment and any hematoma present are evacuated. Reduction is obtained by anatomic realignment of the dorsal cortex of the distal phalanx. Small instruments such as a dental probe, Freer elevator, and fine-tooth forceps are helpful in holding the reduction in place. A 0.028-inch Kirschner wire (K wire) is passed retrograde through the dorsal third of the fracture surface in the distal phalanx in such a way that the wire passes through the distal phalanx just below the sterile matrix of the nail bed and avoids the undersurface of the nail. Next, the dorsal fragment is anatomically reduced with the DIP joint in neutral position, and the pin is driven back across the fracture site. This secures both the fragment and the DIP joint. The second pin is passed through the fragment into the distal phalanx as an added stabilization force. This should be accomplished with extreme care because multiple attempts at fixation often result in comminution of the fracture and further compromises the possibility of achieving stabilization. If the fragment seems large for a K wire of the size suggested, a second wire may be added instead of using a larger wire. The additional wire adds torsional stability and is less likely to further break up the fragment. 234

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Anatomic reduction of the fragment is then confirmed by posteroanterior and splay lateral radiographs. The skin is then closed with nylon, and a bulky dressing and plaster splint are applied. The splint should immobilize the DIP joint and extend across the wrist to neutralize the flexor muscles.

Postoperative Management The first dressing change should be made between 24 and 48 hours. At that time, a smaller splint is applied to maintain stability of the DIP joint. Rehabilitation should begin following removal of the forearm splint at the first visit. Active motion of the metacarpophalangeal and proximal interphalangeal joints is crucial to maintaining good hand and finger function and must be started early. The patient should expect some discomfort but the importance of early rehabilitation cannot be overstated. At 4 to 6 weeks local tenderness at the site of the fracture should be assessed. If fracture healing has begun (as shown by minimal tenderness), the transarticular K wire should be removed. Active DIP joint flexion should then be instituted with blocking of the joint. When 2 or 3 additional weeks have passed, the remaining K wire is removed. At this time, more active motion with resistance can be started. Splinting may be reinstated if displacement is noted or discomfort begins. To avoid refracture, splinting should continue at night or during strenuous activity for at least 6 more weeks. Any wire at anytime that can be moved by gentle manipulation should always be removed to avoid the risk of infection secondary to a loose wire.

Alternative Technique Surgical Technique for Percutaneous Open Reduction and Internal Fixation (ORIF) After suitable antibiotics, the right arm is prepped and draped in the usual sterile fashion. A well-padded tourniquet is placed on the right upper arm and followed with exsanguinations and tourniquet up to 250 mm Hg. A mini C-arm is brought into the field and a small transverse incision, the size of a screw head, is made over the distal phalanx. The skin is cut through to the terminal tendon. Under fluoroscopy, use a reduction tool to verify that anatomic reduction is achieved (Fig. 38–6), and then again, using the C-arm, a spinal needle is

Figure 38–6. C-arm utilized intraoperatively to verify the anatomic reduction. 235

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Figure 38–7. (A) Intraoperative view of open reduction and internal fixation (ORIF) of the mallet fracture. (B) Lateral view of ORIF placement of the mallet fracture in the operating room.

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Figure 38–8. (A) Anteroposterior (AP) intraoperative view of screw fixation and Kirschner wire (K wire) placement. (B) Lateral intraoperative view to verify placement of screw and K wire.

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Figure 38–9. (A) AP radiograph 6 weeks postoperative and removal of K wire. (B) Lateral radiograph at 12-week follow-up. (C) AP radiograph at 12-week follow-up.

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placed to match an appropriate angle to place the screw into P3 (distal phalanx). Meticulous technique is used with a 1.1 mm drill bit while an assistant holds the hand, and then a self-tapping screw is usually used (8 mm) to transfix the fracture (Fig. 38–7). A longitudinal 0.35-inch K wire may be placed to allow screw protection while healing in the first 3 weeks (Fig. 38–8). Gentle active assisted rangeof-motion exercises are begun at 8 weeks with a protective splint (Fig. 38–9). Full passive and active exercises without restrictions can be performed at 12 weeks.

Complications Complications seen following mallet fracture surgery include deep joint infection, joint incongruity, and nail deformity.

Suggested Readings Casscells SW, Strange TH. Intramedullary wire fixation of mallet finger. J Bone Joint Surg [Am] 1983;65B:606–607. Darder-Prats A, Fernanadex-Garcia E, Fernanadex-Gabarda R, Darder-Garcia A. Treatment of mallet finger fractures by the extension-block K-wire technique. J Hand Surg [Br] 1998;23B:802–805. Gaberman SF, Diao E, Peimer CA. Mallet finger: results of early versus delayed closed treatment. J Hand Surg [Am] 1994;19A:850–852. Inoue G. Closed reduction of mallet fractures using extension-block Kirschner wire. J Orthop Trauma 1992;6:413–415. King HJ, Shin SJ, Kang ES. Complications of operative treatment for mallet fractures of the distal phalanx. J Hand Surg [Br] 2001;26B:28–31. Lubahn JD. Mallet finger fractures: a comparison of open and closed technique. J Hand Surg [Am] 1989;14A:394–396. Yamanaka K, Sasaki T. Treatment of mallet fractures using compression fixation pins. J Hand Surg [Br] 1999;24B:358–360.

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39 Proximal Phalangeal Shaft Fractures Kevin D. Plancher

History and Clinical Presentation A 37-year-old right hand dominant high school teacher and coach of the football team comes to the office because he got his finger caught in a football helmet during a drill. He said that he felt a crack and looked down and noticed his long finger on his right hand was pointing toward his thumb. He reports taking hold of it and pulling back straight and had the team trainer tape it to the index finger. He has no history of diabetes or vascular disease, and is presently not on any medications.

Physical Examination PEARLS Interosseous Wiring S TABLE F RACTURE PATTERNS (T RANSVERSE ) • Treat stable fracture pattern conservatively. • When a stable fracture pattern becomes unstable it needs to be surgically stabilized. • A K wire is utilized to stabilize the fracture after the interosseous wire is placed. • Preserve periosteum for closure. • Leave the twisted wire on the noncontact side of the finger. (Start wire from that side.) • Leave at least 5 mm bone bridge from fracture line to wire.

PITFALLS • Do not treat an unstable fracture pattern conservatively (spiral oblique). • If you leave prominent the twisted interosseous wire there will be soft tissue irritation. • Do not stabilize the fracture with K wire prior to tightening the stainless-steel wire when using the interosseous wire technique. 238

The tips of all fingers have good capillary refill and the patient’s two-point sensory discrimination, as determined by the Weber two-point discrimination test, using a dull pointed eye caliper applied in the longitudinal axis of the digit without blanching the skin, is within normal limits of all fingers. The hand and fingers show no sign of vascular compromise. Fingers are noted to be swollen with no obvious deformity and no open wounds. Patient was able to actively flex and extend all other fingers but felt pain in the little finger between the metacarpophalangeal (MP) and proximal interphalangeal (PIP) joints and was limited on his motion. He was sent for radiographs.

Diagnostic Studies Diagnostic studies include anteroposterior, splay lateral, and oblique radiographs of the hand. Oblique splay films are especially helpful in assessing intraarticular fractures and in removing the overlap from adjacent digits.

Differential Diagnosis Fracture of the phalanx Intraarticular Extraarticular Comminuted Tumor of proximal phalanx

Diagnosis Extraarticular Oblique Proximal Phalanx Fracture Many types of phalangeal fractures are seen, and the examining physician must note the resting posture of the injured hand in each case. When the fingers of the hand are flexed, a line should be drawn from the dorsal aspect of the PIP joint to the fingernail. This line should converge, not to a single fixed point, but rather directly

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PEARLS Screw Fixation • Fracture edges are inspected and the optimal position for screw fixation (perpendicular) is selected. • Anatomic reduction is ideal for maximal compression. • Ensure the fracture fragment is at least three times the thread diameter of the screw for fixation. • Long oblique and spiral fracture patterns may be fixed with 1.5-mm screws if the fracture is two to three times diameter of the phalanx. • Loupe magnification is helpful when using 1.1- or 1.5-mm screws.

PITFALLS Screw Fixation • Failure to clean and free fracture edges of soft tissue or hematoma will not allow anatomic reduction. • The screw head many irritate the soft tissues when prominent. • Early range-of-motion exercises without stable, rigid fixation will cause the loss of anatomic reduction and possible malalignment or malunion.

to the area of the scaphoid from the radial artery to the palmaris longus. One of the most common causes of malunion is a malrotation of a phalangeal fracture, and it is diagnosed by physical examination, not by x-ray (Fig. 39–1). Proximal phalanx fractures are often obvious, and local swelling along with the deformity are easy to identify. Recognition of rotational malalignment is essential. A complete sensory and motor evaluation should always be done, and the integrity of the dermis should be examined. The vascular integrity needs to be documented, and patency of collateral circulation should always be tested with an Allen’s test of the wrist and digit. Satisfactory physical examination may not be possible without local anesthetic, but the block should be provided only after a careful two-point sensory examination has been completed. Indications for operative intervention for phalangeal fractures are based on concerns about shortening or malrotation. Spiral and short oblique fractures are usually more susceptible to instability, and a few millimeters of shortening, although acceptable in the metacarpal, is not acceptable in the phalanx. Malrotation is never acceptable, and operative intervention is required for intraarticular fractures, open fractures, fractures with bone loss, and multiple phalangeal fractures that are associated with a neurovascular or tendon injury. Extensive soft tissue injury may require stable fixation to allow early mobilization and skin loss with hand fractures associated with polytrauma needs operative repair. Many factors determine the selection of treatment, including fracture location, intraarticular or extraarticular deformity, angulation, rotation, shortening, open or closed injury, associated neurovascular and soft tissue injuries, and the nature of the fracture (i.e., transverse, spiral, comminuted, or oblique). Additional considerations for operative reduction or internal fixation include the surgeon’s skill with the fixation device, the patient’s ability to work postoperatively with an appropriate plan, and the patient’s occupation. The operative goal is always to avoid prolonged immobilization because of the risk of permanent deformity and stiffness. However, soft tissue damage, infection, the need for a second procedure, and technique failure can occur when moving the fractures aggressively if fixation is not rigid. Operative fixation must ultimately have a better outcome than nonoperative management, and the risks and benefits must always be explained to the patient.

Figure 39–1. Intraoperative photo of malalignment of a fractured little finger (a different patient). 239

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Nonsurgical Treatment There are so many ways to treat phalangeal fractures that the choice of approach depends on the experience, expertise, and personal preference of the physician. No single method of treatment can be applied to all fractures of the phalanx, and a surgeon must be comfortable with multiple techniques. Fracture healing takes the same amount of time no matter which method is chosen, if treatment is performed correctly. Many fractures of the phalanges can be treated by closed reduction and cast immobilization. If the fracture pattern is stable (transverse), it can be treated nonsurgically. Fracture patterns that are inherently unstable (spiral oblique) will fall out of alignment and will usually require surgical stabilization. Soft tissue conditions with any neurovascular compromise or swelling may prevent nonoperative treatment. The position for immobilization is the intrinsic-plus position, with the MP joint in at least 70 degrees, if not 90 degrees, of flexion and the PIP and distal interphalangeal (DIP) joints in extension. A proximal phalanx dorsal blocking cast with an adjacent finger held in the cast can be applied when the hand is in the intrinsic-plus position, contracture is avoided, and the intrinsics are maintained in a relaxed position. This position also effectively immobilizes stable fractures of the proximal phalanx (Fig. 39–2).

Surgical Treatment Management of the soft tissue is paramount to a successful outcome when treating phalanx fractures. The ideal surgical exposure provides maximal visualization for

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C 240

B

Figure 39–2. Nonsurgical treatment of a proximal phalanx fracture of the long finger. This critically ill patient was treated using a distraction proximal interphalangeal (PIP) hinged splint. (A) Volar view. (B) Lateral view. (C) Dorsal view.

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the surgeon while preserving soft tissue gliding planes and minimizing surgical insult to the surrounding tendons. Exposure of the phalanges for fracture fixation is done primarily from a dorsal or lateral approach. Palmar exposures are discouraged, except when the PIP joint exposure is necessary for a volar plate arthroplasty. Exposure of the proximal and middle phalanx is accomplished through a dorsal longitudinal incision or a midaxial incision, with the terminal aspects of the incision curving toward the midline of the digit. The ends of the incision are incorporated into the dorsal skin creases allowing for adequate cosmesis. This extensile exposure allows access to the extensor hood, as well as access in the midaxial line. The extensor tendon must be retracted for exposure of the fracture when access to the middle phalanx is necessary. The periosteum should be incised at the midaxial line and raised as a flap, thereby preserving the gliding surface between the periosteum and the extensor tendon. Proximal phalanx fractures exposed through a dorsal longitudinal split in the extensor tendon have adequate exposure. The periosteum should be raised as a flap to allow exposure to the fracture and preservation of a gliding surface between the fracture plane and the extensor tendon.

Long Oblique Fracture: Open Reduction and Internal Fixation (ORIF) Screw fixation is used in the management of long oblique fractures. To manage fractures with screws alone, it is recommended that the length of the fracture be at least three times the width of the shaft. The choice of implant depends on skeletal size and fracture location. Low-profile implants are widely available now. In general, fractures of the phalanges are fixed with 1.0 mm to 2.0 mm screws. Self-tapping screws diminish the technical complexity of this technique. The technique of compression-screw fixation is usually done in a reproducible sequence of steps. Once the fracture has been opened, the fracture line is identified, and the fracture is anatomically reduced and held with either pointed reduction clamps or a small, smooth Kirschner wire (K wire). Ideally, the surgeon should try to minimize exposure of the skeleton, thereby limiting the devascularization. First, drill the near cortex with a 1.5-mm drill bit because this allows the screw to dynamically compress the fracture site. The technical point of this technique is to drill only the near cortex with this larger 1.5-mm drill bit. Then use a countersink to the near cortex to increase the contact pressure of the screw head. Place the drill guide into this near cortex drill hole and then drill the far cortex with a 1.1-mm drill bit. The drill sleeve is designed to fit in the near cortex and align the drilling of the far cortex. Measure the depth of the hole on the volar aspect to get the correct length screw and then tap with a 1.5-mm tap. Using a tap sleeve protects the surrounding soft tissues. Place the appropriate screw and follow with the second screw, and, if necessary, the third screw should be placed accordingly (Fig. 39–3).

Transverse Fracture: Interosseous Wiring The surgeon may choose from wrist blocks, intravenous regional or brachial block, or general anesthesia. The patient is placed supine, and, using a hand table, the arm and hand are extended onto the field. Using a dorsal longitudinal incision over the long proximal phalanx we make a lateral approach. We elevate the periosteum, and preserve it for later closure. The fracture site is exposed and the fracture hematoma is debrided. The cleaned two fracture ends are exposed, and a drill hole is made with a 0.035-inch K wire parallel to the transverse fracture, leaving a bridge of at least 241

B

A

Figure 39–3. (A) Proximal phalanx fracture. (B) Open reduction and internal fixation (ORIF) with screw fixation.

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C 242

B

Figure 39–4. (A) Transverse wiring of proximal phalanx fracture. (B) Intraoperative, prior to tightening the wire of a P2 fracture. (C) Intraoperative, after tightening the interosseous wiring of P2 fracture. Note: the Kirschner wire may be placed longitudinally or obliquely, according to surgeon preference.

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5 mm from the fracture line. A 26-gauge (No. 0) stainless-steel wire is then passed through the holes. Keep in mind that the side you want to leave the twisted wire on is the side you start on. This is usually best when left on the noncontact side. Load a smooth 0.035-inch K wire into your driver and place it obliquely out through the dorsal cortex until the tip protrudes slightly at the fracture site. Now reduce the fracture anatomically and then advance the wire into the proximal fragment and achieve cortical contact. The wires are then twisted around each other, and using the appropriate device (surgeon choice), are tightened. Secure the loop onto the bone. The twisted end is bent so that it is not prominent, to prevent soft tissue irritation. The periosteum is then restored and closed, followed by simple closure of the skin. The K wire remains in place and is trimmed to the appropriate length, and the tip protector is attached (Fig. 39–4).

Alternative Technique Plate fixation in the hand skeleton should be infrequent and should be reserved primarily for the metacarpals. Use of plates in the fingers is discouraged because of the frequent need for removal of hardware and tenolysis. However, highly comminuted fractures may require fixation with plates to allow adequate stability for early motion. For the phalanges, 1.5- and 2.0-mm plates are recommended. Their application requires an extensive exposure of the joint and precise placement of the implants (Fig. 39–5).

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Figure 39–5. (B) ORIF with double plates in complex gunshot injury to the proximal phalanx. (A) X-ray of complex plate fixation of a proximal phalanx fracture. 243

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Postoperative Postoperatively, have the patient try to achieve joint motion above and below the phalangeal fracture. Many factors determine the patient’s ability to proceed with early range of motion: the fracture geometry, the extent of soft tissue injury, and patient ability and reliability. A general rule with pins is that they should be removed no later than 4 weeks in phalangeal fractures. In stable and minimally displaced fracture patterns, the pin can safely be removed in 3 weeks to allow early active motion. Pins left in longer than 4 weeks are associated with permanent stiffness of the digit. Range of motion when plate or screw fixation is performed can be initiated after 4 to 5 days of soft tissue rest. Plate and screw fixation of the hand skeleton without the incorporation of a supervised early active range-of-motion program results in permanent stiffness of the hand. ORIF should be avoided in any patient who is unable to comply with an early active motion program.

Complications When malunion presents a functional problem, corrective osteotomies are effective in restoring motion. Nonunion is associated with percutaneous pinning of the fracture in distraction, and if this occurs, it is best managed with ORIF. Loss of motion is the most frequent complication when working with phalangeal fracture fixation. A supervised comprehensive hand therapy program, including active and passive range-of-motion exercises combined with dynamic splinting or progressive static splinting, is always recommended. After 3 to 4 months, tenolysis and capsulotomy of stiff joints are often helpful when supervised hand therapy has failed to restore acceptable motion. Infection is a frequent complication when working with the percutaneous pinning technique of phalangeal fractures. Most cases are self-limiting and respond rapidly to antibiotics and pin removal. Osteomyelitis secondary to complex open fractures can be particularly difficult to eradicate. Flexor or extensor tendon adhesions, with phalangeal fractures, may result from closed or operative treatment. A supervised progressive therapy program should be initiated. If supervised hand therapy for 3 months does not restore or improve motion, then a tenolysis may be indicated.

Suggested Readings Jupiter JB, Axelrod TS, Belsky MR. Fractures and dislocations of the hand. In: Browner BD, ed. Skeletal Trauma: Fractures, Dislocations, Ligamentous Injuries. 2nd ed. Philadelphia: WB Saunders, 1998:1294. Jupiter JF, Winters S. Open reduction internal fixation: phalangeal fractures. In: Strickland JW, ed. Master Techniques in Orthopaedic Surgery, The Hand. Philadelphia: Lippincott-Raven; 1998:41–48. McCue FC, Honner R, Johnson MC Jr, et al. Athletic injuries of the proximal interphalangeal joint requiring surgical treatment. J Bone Joint Surg [Am] 1970;54A: 937–956. McElfresh EC, Dobyns JH, O’Brien ET. Management of fracture-dislocation of the proximal interphalangeal joints with extension-block splinting. J Bone Joint Surg [Am] 1970;54A:1705–1711. 244

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Miller MD, Howard RF, Plancher KD. Treatment of Fractures of the Phalanges and Metacarpals. Surgical Atlas of Sports Medicine. Philadelphia: WB Saunders; 2003: 497–509. Stern PJ. Fractures of the metacarpals and phalanges. In: Green DP, Hotchkiss RN, Pederson WC, eds. Green’s Operative Hand Surgery, 4th ed. New York: Churchill Livingstone; 1999:711. Suzuki Y, Matsunaga T, Sato S, et al. The pins and rubbers traction system for treatment of comminuted intraarticular fractures and fracture-dislocations in the hand. J Hand Surg [Br] 1994;19B:98–107.

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40 Proximal Phalangeal Condylar Fractures Carrie R. Swigart

History and Clinical Presentation A 53-year-old right hand dominant man slipped and fell, striking his left fifth digit. He initially thought little of it, and it was not until later that day, while he was working with some tires and caught his left small finger, that he noticed pain and swelling of the digit. After initial consultation with an orthopedic surgeon, he was referred to a hand surgeon 6 days after injury.

Physical Examination There was circumferential swelling of the digit. The finger angulated dorsally at the level of the distal portion of the proximal phalanx. No rotation deformity was noted, although the patient was unable to completely flex the digit. Profundus and sublimis tendon function was intact, as was the neurovascular status. The patient was otherwise in good health. He had had cardiac bypass surgery, but had no current complaints of exertional angina. His only medication was Dilantin.

Diagnostic Studies Radiographs of the left small finger showed a comminuted fracture of the distal portion of the proximal phalanx. The fracture was slightly shortened and angulated dorsally ~35 degrees. There was no apparent intraarticular involvement (Fig. 40–1). PEARLS • Careful preparation and planning are mandatory for successful use of the minicondylar plate. • If rigid fixation is not likely to be attainable, closed or percutaneous methods must be considered.

PITFALLS • Careful attention to rotation alignment is critical. • The initial condylar K-wire placement has little to no margin for error. • Additional soft tissue disruption complicated by insufficient stability can be disastrous. 246

Diagnosis Unstable Comminuted Fracture of the Proximal Phalanx, Small Finger, Nondominant Hand This is an unstable fracture pattern due to both the comminution and the obliquity of the fracture. Comminuted, unstable fractures of the phalanges, especially about the proximal interphalangeal (PIP) joint, are difficult to treat and often result in limitations of motion and function, regardless of the treatment chosen. If open reduction is attempted, it is imperative that the fracture be rigidly fixed to allow for early range of motion. Operative fixation should be done on an urgent basis, ideally within the first 10 days to 2 weeks after the fracture.

Surgical Management After the physician reviewed the preoperative blood work, including the Dilantin level, the patient was taken to the operating room on an elective basis,

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Figure 40–1. Lateral (A) and anteroposterior (AP) (B) radiographs of the fracture showing marked apex palmar angulation and comminution.

11 days after sustaining the fracture. A Bier block anesthetic was used as a peripheral adjunct to general anesthesia. The patient was placed in the supine position with the left upper extremity on a hand table. The tourniquet, used for both the Bier block and hemostasis, was placed on the upper arm. It was inflated to 250 mm Hg. An ulnar straight midaxial incision, ~4 cm in length, was made. Careful dissection directly to the level of the bone was performed, achieving hemostasis with electrocautery. The dorsal sensory branches of the ulnar digital nerve were identified and preserved. The extensor apparatus was left intact and carefully elevated to expose the fracture beneath. Soft tissue and hematoma were removed using small curettes, and the fracture site was irrigated copiously. Due to the intercondylar fracture pattern, a minicondylar blade plate was selected as the implant. Because of the size of the phalanx, a 1.5-mm plate was chosen (Fig. 40–2). The first step in applying the plate was to pass a 0.045-inch Kirschner wire (K wire) distally across the condyles in the location of the future condylar screw (Fig. 40–3A). Its position was carefully checked in the anteroposterior (AP) and lateral planes with a minifluoroscopy unit. A preliminary reduction of the fracture was performed so that the appropriate length for the minicondylar plate could be assessed. This plate was then bent to match the lateral contour of the phalanx and trimmed to size. The blade of the plate was also trimmed to fit the AP dimension of the condyles. The blade of the plate was then 247

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Figure 40–2. A 1.5-mm titanium minicondylar blade plate.

inserted by first drilling a 1.5-mm hole adjacent and parallel to the K wire (Fig. 40–3B). The blade of the plate was then inserted, slipping the previously placed K wire through the hole for the condylar screw (Fig. 40–3C). The adjacent condylar screw was then placed, obtaining bicortical purchase (Fig. 40–3D). Once the condylar fragment was attached to the plate, the fracture was reduced. Due to the high degree of comminution, an anatomically keyed reduction could not be obtained. The fragments were aligned with maximal apposition of the fractured surfaces. Rotation was carefully checked during fragment alignment. The most proximal 1.5-mm screw was placed next, thus holding the fracture aligned and reduced with appropriate length of the proximal phalanx. The subsequent three screws were then carefully placed to rigidly stabilize the fracture (Fig. 40–3E). The wound was irrigated and closed with interrupted 5-0 nylon and 5-0 plain catgut sutures. Final radiographs were obtained, and a well-padded hand dressing was applied. The hand was immobilized with volar and dorsal plaster splints.

Postoperative Management A therapist saw the patient on the third postoperative day and the splint and dressing were removed. A custom-molded Orthoplast splint with the metacarpophalangeal (MP) joints flexed 40 degrees and the interphalangeal (IP) joints straight was fabricated to immobilize the affected and neighboring digit. Active range-of-motion exercises were begun out of the splint several times a day. The fracture healed uneventfully, and showed solid union on radiographs at 6 weeks

Figure 40–3. Application of the minicondylar blade plate begins with placement of a Kirschner wire across the condyles (A), followed by a drill hole parallel to this wire to position the blade (B). The blade is then inserted across the condyles (C), and they are further stabilized with the condylar screw (D). The fracture of the shaft is then reduced and the proximal screws placed (E). 248

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Figure 40–4. Lateral (A) and AP (B) radiographs of the fracture at 6 weeks postoperatively showing early healing and maintenance of the position of the hardware.

(Fig. 40–4). Despite initiation of early range-of-motion exercises, the digit motion at last follow-up examination, 3 months postoperatively, showed a 20-degree active extension lag at the PIP joint and a 15-degree extension lag at the distal interphalangeal (DIP) joint. PIP and DIP joint flexion were 70 and 75 degrees, respectively. The patient had returned to all activities without limitation and had no complaints of pain.

Alternative Methods of Management Alternative methods of management for this case are open reduction and fixation with another type of plate or with screws alone, or closed reduction and K-wire fixation (Table 40–1). Alternative plates would include any of the 1.5- or 2.0-mm minifragment plate systems. Because they are usually applied dorsally, these plates may be more bulky and can cause more problems with tendon gliding. Another disadvantage of these plates is that they lack the torsional stability afforded by the blade. Finally, it is difficult to attain rigid fixation of small condylar fragments with a simple dorsal plate. The principles of their application would be the same as for the blade plate, that is, fixation of the condyles first, followed by reduction and fixation of the shaft to the condyles. 249

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Table 40–1 Alternative Methods of Management Alternative Implants

Advantages

Disadvantages

Minicondylar blade plate (1.5 or 2.0 mm)

Provides excellent torsional stability and resistance to shear forces Easier to adjust the angle of the plate relative to the phalanx Interfragmentary compression

Potential for malreduction if the blade is not inserted in the correct plane

Technically easier, closed method

Does not allow for early active motion

Standard minifragment plate (2.0 mm T- or L-shaped plate) Lag screw fixation (1.5 or 2.0 mm) Kirschner wire fixation

Implant typically applied dorsally and may interfere with extensor mechanism Useful only in select fracture patterns

Either 1.5- or 2.0-mm screws can be used in isolation for selected fractures of the proximal and middle phalanges. Their use requires a fracture with minimal comminution and a long oblique or spiral pattern (i.e., in length at least 1.5 to 2 times the width of the base). Fixation with K wires, although perhaps technically easier, may lead to suboptimal results due to the inability to secure the fracture rigidly enough to allow for immediate motion of the digits. This method should be reserved for the case of the multiple digit injured hand when time allotted for fracture fixation is limited, or in a relatively simple fracture where minimal fixation is required.

Complications Plate fixation of phalanx fractures is associated with multiple potential complications. These include stiffness, malunion, nonunion, infection, and tendon rupture. Stiffness is the most common complication and is associated with complex fracture patterns requiring extensive soft tissue mobilization for fixation, and the failure to begin early postoperative motion. With certain fracture patterns, some amount of residual stiffness is inevitable, but this can be minimized by rigid fixation and early motion protocols. Malunion becomes significant when it interferes with hand function. The most common deformity is rotational, as this is the most difficult to judge clinically without being able to take the digit through a full range of motion. If the resulting rotational or angular malunion is sufficient to hinder hand function, osteotomy after fracture healing can be performed secondarily. Nonunion is associated with highly comminuted fractures resulting in bone loss, crush injuries, and open fractures. Nonunions can be treated effectively in most cases with internal fixation and bone graft. Infection may be classified as superficial and deep. Superficial infections may be successfully treated initially with oral antibiotics and local wound care. Deep infection must be addressed with aggressive debridement and irrigation and intravenous antibiotics. Occasionally, removal of the implant may be required and the digit can be stabilized temporarily with pins or a small external fixator.

Acknowledgment I would like to thank Dr. Scott Wolfe for providing this case, and for his assistance and advice in editing the manuscript. 250

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Suggested Readings Buchler U, Fischer T. Use of a minicondylar plate for metacarpal and phalangeal periarticular injuries. Clin Orthop 1987;214:53–58. Crawford GP. Screw fixation for certain fractures of the phalanges and metacarpals. J Bone Joint Surg [Am] 1976;58A:487–492. Hastings H. Unstable metacarpal and phalangeal fracture treatment with screws and plates. Clin Orthop 1987;214:38–52. McCue FC, Honner R, Johnson MC, Gieck JH. Athletic injuries of the proximal interphalangeal joint requiring surgical treatment. J Bone Joint Surg [Am] 1970; 52A:937–955. Page SM, Stern PJ. Complication and range of motion following plate fixation of metacarpal and phalangeal fractures. J Hand Surg [Am] 1998;23A:827–832. Stern PJ, Wieser MJ, Reilly DG. Complications of plate fixation in the hand skeleton. Clin Orthop 1987;214:59–65. Weiss APC, Hastings H. Distal unicondylar fractures of the proximal phalanx. J Hand Surg [Am] 1993;18A:594–599.

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41 Metacarpal Neck Fractures Kostas J. Constantine and Thomas R. Kiefhaber

History and Clinical Presentation A 20-year-old man was involved in a street brawl, in which he swung at but missed his opponent and struck a wall, causing immediate pain and swelling of his dominant right hand. Two days later, he presented to the emergency room complaining of continuing discomfort despite ice and elevation.

Physical Examination PEARLS • Acceptable reduction: 䡩 Index/long