ASSH Manual of Hand Surgery PDF

ASSH Manual
of Hand Surgery
FIRST EDITION
Warren C. Hammert, MD
Associate Professor of Orthopaedic Surgery and
Plastic Surgery
University of Rochester Medical Center
Rochester, New York
Ryan P. Calfee, MD
Assistant Professor of Orthopaedic Surgery
Washington University School of Medicine
St. Louis, Missouri
David J. Bozentka, MD
Chief Department of Orthopaedic Surgery
Pennsylvania Presbyterian Medical Center
Associate Professor Department of Orthopaedic Surgery
University of Pennsylvania Medical Center
Philadelphia, Pennsylvania
Martin I. Boyer, MD, FRCS(C)

Carol B and Jerome T Loeb Professor of
Orthopaedic Surgery
Washington University School of Medicine
St. Louis, Missouri
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Library of Congress Cataloging-in-Publication Data

ASSH manual of hand surgery / [edited by] Warren C. Hammert ... [et al.].
p. ; cm.
Other title: Manual of hand surgery
Includes bibliographical references and index.
ISBN 978-1-60547-212-6 (alk. paper)
1. Hand—Surgery—Handbooks, manuals, etc. I. Hammert, Warren C. II. American Society for
Surgery of the Hand. III. Title: Manual of hand surgery.
[DNLM: 1. Hand—surgery—Handbooks. 2. Hand Injuries—surgery—Handbooks. 3. Surgical
Procedures, Operative—methods—Handbooks. WE 39 A847 2010]
RD559.A825 2010
617.5'75059—dc22
2010000579
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To my family, for all of their support and encouragement.
—Ryan P. Calfee, MD
To my past, present, and future fellows,

residents and medical students.
—Martin I. Boyer, MD
To my wife, for her patience and support,

and the residents and fellows I have had the opportunity
to teach and learn from.
—Warren C. Hammert, MD
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Contents
Preface XVII
Section I General Concepts

1. Embryology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .03
AARON DAILUSKI
2. Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .07
A. BOBBY CHHABRA, CHEALON D. MILLER, AND LINDLEY WALL
3. Anesthesia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .29
J. MEGAN M. PATTERSON AND STEFAN LUCAS
4. Pharmacology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .35
MARK WILCZYNSKI
5. Arthroscopy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .44
MICHAEL S. BEDNAR AND CHARLES A. GOLDFARB
6. Amputations and Prosthetics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .58

WARREN C. HAMMERT
7. Techniques of Injections. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .65

MARTIN I. BOYER
8. Differential Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .71

CHAD R. MANKE AND PAUL F. NASSAB
Section II Specific Conditions

9. Chronic Pain Syndromes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .79
GEORGE D. CHLOROS, L. ANDREW KOMAN, ZHONGYU JOHN LI, AND THOMAS
L. SMITH
10. Tendon . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .93

JAMES CHANG, SHELLY NOLAND, JULIE E. ADAMS, DANIEL P. MASS, JOHN
G. SEILER III, JOHN S. TARAS, ANDREW TRUEBLOOD, MICHAEL J. BOTTE, DAVID
M. KALAINOV, RANDON C. JOHNSON, ANTHONY J. LAUDER, AND JENNIFER
MORIATIS WOLF
11. Tendon Transfers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .145

WARREN C. HAMMERT, ANN E. VAN HEEST, MICHELLE A. JAMES, CHRISTINE
KWAK, GEORGE S.M. DYER, BRANDON E. EARP, BARRY P. SIMMONS, AND
KIMBERLY L.Z. ACCARDI
12. Stiffness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .170

HILL HASTINGS II, JEFFRY B. WATSON, AND SURASAK JITPRAPAIKULSARN
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vi Contents
13. Fractures and Dislocations: Hand . . . . . . . . . . . . . . . . . . . . . . . . . . .186

ROBERT M. BALTERA, HILL HASTINGS II, KAVI SACHAR, AND SURASAK
JITPRAPAIKULSARN
14. Fractures and Dislocations: Wrist. . . . . . . . . . . . . . . . . . . . . . . . . . . .216

RYAN P. CALFEE, RICHARD BERGER, PEDRO K. BEREDJIKLIAN, DREW R. ENGLES,
JEFFREY A. GREENBERG, JONATHAN E. ISAACS, CANDICE MCDANIEL, TAMARA
D. ROZENTAL, PHIL BLAZER, AND OLIVIA PATE
15. Fractures and Dislocations: Forearm . . . . . . . . . . . . . . . . . . . . . . . . .255

SETH D. DODDS AND DAVID C. RING
16. Fractures and Dislocations: Elbow . . . . . . . . . . . . . . . . . . . . . . . . . . .264

MICHAEL DAROWISH, JESSE B. JUPITER, GRAHAM J.W. KING, KEVIN J. MALONE,
AND JEFFREY N. LAWTON
17. Nerve. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .294

JOHN ELFAR, JASON M. PETRUNGARO, RICHARD M. BRAUN, CHRISTINE J.
CHENG, RANJAN GUPTA, ADAM LABORE, AND JEFFREY E. WONG
18. Brachial Plexus. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .343

DONALD A. BAE AND TERRY MYCKATYN
19. Arthritis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .351

RICHARD A. BERNSTEIN, DOUGLAS M. SAMMER, MARCO RIZZO, CHARLES S. DAY,
LOUIS W. CATALANO III, BRIAN D. ADAMS, KARIM BAKRI, SETH D. DODDS, KEVIN
J. MALONE, STEVEN L. MORAN, AND CHRISTINA M. WARD
20. Skin and Soft Tissue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .393

L. SCOTT LEVIN, MARTIN I. BOYER, DAVID J. BOZENTKA, STEPHAN G. PILL, KODI
K. AZARI, NELSON CASTILLO, AND AMIT GUPTA
21. Acute Vascular Injuries of the Upper Extremity . . . . . . . . . . . . . . . . .424

JAMES P. HIGGINS
22. Vascular Conditions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .433

MICHAEL ALEXANDER MCCLINTON
23. Osteonecrosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .444

RAYMOND S. FRYREAR AND STEVEN L. MORAN
24. Dupuytren’s Disease. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .452

GHAZI M. RAYAN
25. Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .460

ED ATHANASIAN
26. Infections. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .471

THOMAS R. HUNT III, CHRISTOPHER ROBERT, MICHAEL MAKARY, AND
ALEXANDER M. MARCUS
27. Compartment Syndromes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .483

FRASER LEVERSEDGE
28. Injection Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .493

MARTIN I. BOYER
29. Extravasation Injuries. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .495

MARTIN I. BOYER
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Contents vii
30. Frostbite . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .497

KODI K. AZARI AND ROEE E. RUBINSTEIN
31. Thermal Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .502

KODI K. AZARI, CHRISTINE FISHER, AND GALEN S. WATCHMAN
32. Chemical Poisoning and Exposures . . . . . . . . . . . . . . . . . . . . . . . . . .507

KODI K. AZARI AND ROEE E. RUBENSTEIN
33. Bite Wounds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .511

KODI K. AZARI AND NELSON CASTILLO
Section III Other Conditions

34. Dermatologic Conditions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .519
LYNNE CORNELIUS AND KARA NUNLEY
35. Medicolegal Principles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .533

CHARLES CARROLL VI AND DAVID S. WELLMAN
36. Workers’ Compensation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .544

PAUL F. NASSAB
37. Clinical Trials and Hand Surgical Literature. . . . . . . . . . . . . . . . . . . .546

BRENT GRAHAM
38. Psychological Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .553

DAVID C. RING AND ANA-MARIA VRANCEANU
39. Splinting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .558

REBECCA VON DER HEYDE AND PATRICIA M. PAYTNER
40. Surgical Instrumentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .569

BETH PAIGE
41. Bone Grafting and Bone Graft Substitutes. . . . . . . . . . . . . . . . . . . . .591

DREW R. ENGLES AND ANDREW J. SCHOENFELD
42. Examination of the Severely Injured Hand . . . . . . . . . . . . . . . . . . . .599

DAVID J. BOZENTKA
Section IV Appendix
43. Definitions of Hand Surgery Terminology . . . . . . . . . . . . . . . . . . . . .609
KIMBERLY L.Z. ACCARDI AND WARREN C. HAMMERT
Index 617
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Boyer_FM.indd viii 2/22/2010 10:19:18 PM
Contributors
Kimberly L.Z. Accardi, MD, CPT, MC, Robert M. Baltera, MD

USAR The Indiana Hand Center
Philadelphia, Pennsylvania Assistant Clinical Professor
Orthopaedic Surgery Department
Brian D. Adams, MD Indiana University School of Medicine
Professor of Orthopaedic Surgery and Indianapolis, Indiana
Bioengineering
University of Iowa Michael S. Bednar, MD
Iowa City, Iowa Chief, Hand Surgery
Professor, Department of Orthopaedic
Julie E. Adams, MD, MS Surgery and Rehabilitation
Assistant Professor of Orthopaedic Surgery Stritch School of Medicine
Department of Orthopaedic Surgery Loyola University Chicago
University of Minnesota Medical School Chicago, Illinois
Minneapolis, Minnesota
Pedro K. Beredjiklian, MD
Associate Professor
Edward A. Athanasian, MD
Thomas Jefferson University School of
Associate Professor of Clinical
Medicine
Orthopaedic Surgery
Chief, Division of Hand Surgery
Weill Cornell Medical College
Rothman Institute
Hospital for Special Surgery
Philadelphia, Pennsylvania
Memorial Sloan-Kettering Cancer Center
New York, New York Richard A. Berger, MD, PhD
Professor
Kodi K. Azari, MD, FACS Department of Orthopaedic Surgery
Associate Professor of Orthopaedic Mayo Clinic
Surgery and Plastic Surgery Rochester, Minnesota
David Geffen School of Medicine at the
University of California at Los Angeles Richard A. Bernstein, MD
Los Angeles, California Assistant Clinical Professor
Department of Orthopaedic
Donald S. Bae, MD Yale University School of Medicine
Assistant Professor of Orthopaedic Hospital of Saint Raphael
Surgery
Harvard Medical School Michael Botte, MD
Associate in Orthopaedic Surgery Hand Surgeon
Children’s Hospital Boston Scripps Mercy Hospital
Boston, Massachusetts San Diego, California
Karim Bakri, MD Martin I. Boyer, MD

Resident Carol B and Jerome T Loeb Professor of
Department of Surgery Orthopaedic Surgery
Mayo Clinic Washington University School of Medicine
Rochester, Minnesota St. Louis, Missouri
ix
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x Contributors
David J. Bozentka, MD James Chang, MD

Chief, Department of Orthopaedic Professor and Chief of Plastic Surgery
Surgery Stanford University Medical Center
Penn Presbyterian Palo Alto, California
Chief, Surgical Section
Associate Professor, Department of A. Bobby Chhabra, MD
Orthopaedic Surgery Vice Chairman, Orthopaedic Surgery
University of Pennsylvania Medical Center Associate Professor of Orthopaedic and
Philadelphia, Pennsylvania Plastic Surgery
Division Head, Hand and Upper
Richard M. Braun, MD Extremity Surgery
Associate Clinical Professor of University of Virginia Health System
Orthopaedic Surgery Charlottesville, Virginia
University of California at San Diego
Active Medical Staff Christine J. Cheng, MD
Sharp Memorial Hospital Hand Surgeon
Active Medical Staff Overland Park, Kansas
Scripps Mercy Hospital
San Diego, California George D. Chloros, MD
Fellow
Ryan P. Calfee, MD Department of Orthopaedic Surgery
Assistant Professor Wake Forest University School of Medicine
Washington University School of Medicine Baptist Medical Center
Department of Orthopaedic Surgery Winston-Salem, North Carolina
Orthopaedic Surgeon
Barnes-Jewish Hospital Lynne Cornelius
St. Louis, Missouri Head, Department of Dermatology
Washington University
Charles Carroll IV, MD St. Louis, Maryland
Associate Professor of Clinical Orthopaedic
Surgery Aaron Dailuski, MD
Feinberg School of Medicine The Hospital for Special Surgery
Northwestern University New York, New York
Northwestern Orthopaedic Institute Michael Darowish, MD
Illinois Hand Center Fellow, Hand and Upper Extremity Surgery
Chicago, Illinois Cleveland Combined Hand Fellowship
Cleveland Clinic Foundation
Nelson Castillo, MD
Cleveland, Ohio
President, Department of Plastic
Surgery Charles S. Day, MD, MBA
University of Pittsburgh Medical Center Chief, Orthopaedic Hand Surgery
Pittsburgh, Pennsylvania Beth Israel Deaconess Medical Center
Assistant Professor of Orthopaedic Surgery
Louis W. Catalano III, MD Director of Orthopaedic Curriculum
Assistant Clinical Professor Harvard Medical School
Columbia University College of Boston, Massachusetts
Physicians and Surgeons
Attending Physician Seth D. Dodds, MD
C.V. Starr Hand Surgery Center The Hand Program at Yale-New Haven
Roosevelt Hospital Hospital
New York, New York New Haven, Connecticut
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Contributors xi
George S.M. Dyer, MD Jeffrey A. Greenberg, MD, MS

Instructor in Orthopaedic Surgery Orthopaedic Hand Surgeon
Harvard Medical School Indiana Hand Center
Brigham and Women’s Hospital Assistant Clinical Professor
Boston, Massachusetts Department of Orthopaedic Surgery
Indiana University Medical School
Brandon E. Earp, MD Indianapolis, Indiana
Instructor, Harvard Medical School
Attending Hand and Upper Extremity Ranjan Gupta, MD
Surgeon Chair, Department of Orthopaedic
Department of Orthopaedic Surgery Surgery
Brigham and Women’s Hospital Professor of Orthopaedic Surgery,
Boston, Massachusetts Anatomy & Neurobiology, and
John Elfar, MD Biomedical Engineering
Assistant Professor University of California, Irvine
Department of Orthopaedics Irvine, California
University of Rochester Medical Center Warren C. Hammert, MD
Rochester, New York Associate Professor of Orthopaedic
Drew R. Engles, MD Surgery and Plastic Surgery
Hand Surgery Specialist University of Rochester Medical
Hand and Microvascular Reconstructive Center
Surgery Rochester, New York
Summit Hand Center
Hill Hastings II, MD
Crystal Clinic, Inc.
Clinical Professor of Orthopaedic
Akron, Ohio
Surgery
Indiana University School of Medicine
Raymond S. Fryrear, MD Partner
Resident Physician The Indiana Hand Center
Department of Orthopaedics Indianapolis, Indiana
Mayo Clinic
Rochester, Minnesota James P. Higgins, MD
The Curtis National Hand Center
Christine Fisher, MD Union Memorial Hospital
Plastic Surgery Resident Baltimore, Maryland
University of Pittsburgh Medical Center
Thomas R. Hunt III, MD
Pittsburgh, Pennsylvania
John D. Sherrill Professor of Surgery
Director, UAB Hand and Upper
Charles A. Goldfarb, MD Extremity Fellowship
Associate Professor Director, Division of Orthopaedic
Washington University School of Surgery
Medicine/Barnes-Jewish Hospital University of Alabama
Department of Orthopaedic Surgery Birmingham, Alabama
St. Louis, Missouri
Jonathan E. Isaacs, MD
Brent Graham, MD Assistant Professor
Director, Hand Program Department of Orthopaedic
University Health Network Virginia Commonwealth University
University of Toronto Health System
Toronto, Ontario, Canada Richmond, Virginia
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xii Contributors
Michelle A. James, MD Adam LaBore, MD

Chief, Department of Orthopaedic Assistant Professor
Surgery Section of Physical Medicine and
Shriners Hospital for Children, Northern Rehabilitation
California Department of Orthopaedic Surgery
Chief, Division of Pediatric Orthopaedic Washington University School of
Professor of Clinical Orthopaedic Medicine
Surgery St. Louis, Missouri
University of California, Davis School of
Medicine Anthony J. Lauder, MD
Sacramento, California Assistant Professor
Hand and Upper Extremity Surgery
Surasak Jitprapaikulsarn, MD Department of Orthopaedic Surgery
Fellow University of Nebraska Medical Center
Indiana Hand Center Omaha, Nebraska
Indianapolis, Indiana
Jeffrey N. Lawton, MD
Randon C. Johnson, MD Hand and Upper Extremity Surgeon
Orthopaedic Surgeon Cleveland Clinic
Chicago Musculoskeletal Institute Cleveland, Ohio
Metro Orthopaedic
Chicago, Illinois Fraser J. Leversedge, MD
Assistant Professor
Jesse B. Jupiter, MD Department of Surgery/Division of
Hansjörg Wyss AO Professor of Orthopaedic Surgery
Orthopaedic Surgery Duke University
Harvard Medical School Durham, North Carolina
Chief, Hand and Upper Limb Service
Massachusetts General Hospital L. Scott Levin, MD, FACS
Boston, Massachusetts Chair, Department of Orthopaedic
Surgery
Graham J.W. King, MD, MSc, FRCSC Paul B. Magnuson
Chief of Orthopaedic Professor of Bone and Joint Surgery
Hand and Upper Limb Center University of Pennsylvania
St. Joseph’s Health Center Philadelphia, Pennsylvania
Professor, Department of Surgery
University of Western Ontario Zhongyu John Li, MD, PhD
London, Ontario, Canada Assistant Professor
Department of Orthopaedic Surgery
L. Andrew Koman, MD Wake Forest University School of
Professor and Chair Medicine
Department of Orthopaedic Surgery Winston-Salem, North Carolina
Wake Forest University School of
Medicine Stefan Lucas, MD
Winston-Salem, North Carolina Assistant Professor of Anesthesia
University of Rochester Medical Center
Christine Kwak, MD (URMC)
Department of Orthopaedic Chief of Anesthesia
Shriner’s Hospital of Northern California URMC Ambulatory Surgery Center at
University of California, Davis Sawgrass
Davis, California Rochester, New York
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Contributors xiii
Michael Makary, MD, MBA Paul F. Nassab, MD

Resident Physician Orthopaedic Surgeon
The University of Alabama at Birmingham North Kansas City, Missouri
Birmingham, Alabama
Shelly Noland, MD, BS
Kevin J. Malone, MD Resident in Plastic Surgery
Assistant Professor Stanford University
Department of Orthopaedic Surgery Palo Alto, California
Case Western Reserve University School
of Medicine Kara Nunley, MD
Metropolitan Medical Center Assistant Professor
Cleveland, Ohio Department of Dermatology
Chad R. Manke, MD St. Louis, Maryland
Hand Surgeon
Beth Paige, RN
Atlantic Orthopaedic Specialists
Barnes-Jewish Hospital
Virginia Beach, Virginia
St. Louis, Maryland
Alexander M. Marcus, MD J. Megan M. Patterson, MD
Orthopaedic Associates of Central Jersey, P.A. Assistant Professor of Orthopaedic
Edison, New Jersey UNC Department of Orthopaedic
Chapel Hill, North Carolina
Daniel P. Mass, MD
Professor of Surgery Patricia M. Paynter, OTRL/CHT
Section of Orthopaedic Surgery and Milliken Hand Rehabilitation Center
Rehabilitation Medicine The Rehabilitation Institute of St. Louis
University of Chicago Washington University School of Medicine
University of Chicago Hospitals Barnes-Jewish Hospital
Chicago, Illinois St. Louis, Missouri
Candice McDaniel, MD, MBA Jason M. Petrungaro, MD
Chief Resident Fellow, Hand and Upper Extremity Surgery
Medical College of Virginia Department of Orthopaedic Surgery
Richmond, Virginia University of Rochester School of Medicine
Rochester, New York
Chealon D. Miller, MD
Resident Physician Stephan G. Pill, MD, MSPT
University of Virginia Health System Resident, Department of Orthopaedic
Department of Orthopaedic Surgery Surgery
Charlottesville, Virginia University of Pennsylvania School of
Medicine
Steven L. Moran, MD Philadelphia, Pennsylvania
Professor of Plastic Surgery and
Orthopaedic Ghazi M. Rayan, MD
Mayo Clinic Clinical Professor of Orthopaedic Surgery
Rochester, Minnesota Adjunct Professor, Department of
Anatomy and Cell Biology
Terry Myckatyn, MD, FACS, FRCS(C) Director, Oklahoma Hand Fellowship
Assistant Professor Program
Plastic and Reconstructive Surgery Chair, Division of Hand Surgery
Washington University School of Medicine INTEGRIS Baptist Medical Center
St. Louis, Missouri Oklahoma City, Oklahoma
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xiv Contributors
David C. Ring, MD, PhD John G. Seiler III, MD

Medical Director and Director of Research Clinical Professor of Orthopaedic Surgery
Associate Professor of Orthopaedic Surgery Emory University
Department of Orthopaedic Surgery Atlanta, Georgia
Harvard Medical School
Barry P. Simmons, MD
Hand and Upper Extremity Service
Associate Professor of Orthopaedic Surgery
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts
Director, Hand and Upper Extremity
Marco Rizzo, MD Service
Associate Professor Brigham and Women’s Hospital
Department of Orthopaedic Surgery Boston, Massachusetts
Mayo Clinic
Thomas L. Smith, PhD
Rochester, Minnesota
Professor of Orthopaedic Surgery
Christopher Robert, MD Wake Forest University School of Medicine
Orthopaedic Resident Winston-Salem, North Carolina
University of Alabama at Birmingham
Birmingham, Alabama John S. Taras, MD
Associate Professor
Tamara D. Rozental, MD Department of Orthopaedic Surgery
Assistant Professor in Orthopaedic Thomas Jefferson University
Surgery Associate Professor and Chief
Harvard Medical School Division of Hand Surgery
Orthopaedic Surgeon Drexel University
Department of Orthopaedic Surgery Philadelphia, Pennsylvania
Beth Israel Deaconess Medical Center
Boston, Massachusetts Ann E. Van Heest, MD
Professor
Roee E. Rubinstein, MD Department of Orthopaedic Surgery
Chief Resident, Plastic and Reconstructive University of Minnesota
Surgery Minneapolis, Minnesota
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania Rebecca von der Heyde, PhD(C),
ORT/L, CHT
Kavi Sachar, MD
Assistant Professor of Occupational
Orthopaedic Surgeon
Therapy
Hand Surgery Associates
Maryville University
Denver, Colorado
Certified Hand Therapist
Douglas M. Sammer, MD Milliken Hand Rehabilitation Center
Assistant Professor of Surgery St. Louis, Missouri
Division of Plastic and Reconstructive
Surgery Ana-Maria Vranceanu, PhD
Washington University School of Medicine Instructor in Psychiatry
St. Louis, Missouri Harvard Medical School
Staff Psychologist
Andrew J. Schoenfeld, MD Behavioral Medicine Services
Clinical Fellow Department of Psychiatry
Department of Orthopaedic Surgery Behavioral Medicin e Specialist
Massachusetts General Hospital Department of Orthopaedic Surgery
Harvard Medical School Hand and Upper Extremity Services
Boston, Massachusetts Boston, Massachusetts
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Contributors xv
Galen S. Watchman, MD David S. Wellman, MD

Resident in Plastic and Reconstructive Resident Physician
Surgery Department of Orthopaedic Surgery
Division of Plastic and Reconstructive Northwester University Feinberg School
Surgery of Medicine
University of Pittsburgh School of Chicago, Illinois
Medicine
Pittsburgh, Pennsylvania Mark Wilczynski
Clinical Fellow in Hand Surgery
Lindley Wall, MD Washington University
Resident in Orthopaedic Surgery St. Louis, Maryland
St. Louis, Maryland Jennifer Moriatis Wolf, MD
Assistant Professor
Christina M. Ward, MD Department of Orthopaedic Surgery
Assistant Professor University of Colorado School
Department of Orthopaedic and of Medicine
Rehabilitation Denver, Colorado
University of Iowa
Iowa City, Iowa Jeffrey E. Wong, BA
Medical Student
Jeffry B. Watson, MD Department of Orthopaedic Surgery
Orthopaedic Surgeon University of California, Irvine School
Harvard Medical School of Medicine
Boston, Massachusetts Irvine, California
Boyer_FM.indd xv 8/21/2012 8:17:50 PM

Boyer_FM.indd xvi 2/22/2010 10:19:18 PM
Preface
The need for a pocket manual of hand surgery was articulated by the Governing
Council of the American Society of Surgery of the Hand during the Presidency of
Dr. David Lichtman and was set in motion during the Presidency of Dr. Richard
Gelberman. The goal of this pocket book, written by some of the brightest and most
clear-thinking minds in hand surgery today, is to provide an easy-to-use, complete,
ready reference for any student or practitioner who deals with hand surgical patients.
In addition to orthopaedic and plastic surgery residents, this book can prove to be a
valuable resource for medical students; residents in medicine, surgery, or emergency
medicine; fellows; practicing surgeons; occupational and physical therapists; hand
therapists; and occupational medicine physicians. In today’s era of rapidly accessible
electronic information, we wanted to assemble an even quicker reference for those
on the “front line” with their patients, those busy students, trainees, and practicing
doctors and therapists who do not have the time to go to a computer and “log in”
every time a question arises about diagnosis and management. We hope that this book
fulfills this purpose. We are grateful to all of our authors, as well as the work of the
editorial staff at Wolters Kluwer. Please let us know of any errors or inaccuracies that
are found.
Warren C. Hammert, MD
Martin I. Boyer, MD
David J. Bozentka, MD
Ryan P. Calfee, MD
xvii
Boyer_FM.indd xvii 2/22/2010 10:19:19 PM

Boyer_FM.indd xviii 2/22/2010 10:19:19 PM
I General Concepts
Boyer_Chap01.indd 1 2/13/2010 2:24:48 PM

Embryology
1
Aaron Dailuski
The development of the extremities requires precise temporal and spatial regulation of
multiple signaling pathways. Understanding of the basic molecular and developmental
events is helpful to understanding the pathoanatomy of congenital limb differences and
possible comorbid conditions in patients with other developmental anomalies.
I. Early Limb Formation
The upper limb buds first develop by day 26 following fertilization (fourth week of ges-
tation). Most of the critical patterning events occur between days 26 and 42 following
fertilization, making the first trimester the critical point for upper limb development.
When an interruption in the normal development process occurs, anomalies associated
with other structures developing during this time period may be seen, which explains
the occurrence of multiple anomalies.
Early limbs have a paddlelike shape and first have the proportional appearance of a
human extremity by the eighth week of gestation. Each limb has a core of mesenchymal
tissue from the somite (which develops into muscle) and the lateral plate (eventual con-
nective tissues of the limb) with an outer shell of ectoderm. After initial outgrowth, the
limbs rotate along their longitudinal axis to their final positions.
II. Molecular Events of Early Limb Development
Early limb development occurs with highly regulated molecular mechanisms control-
ling each of the three axes.
A. Longitudinal (proximodistal or PD) outgrowth, which controls overall limb
length.
B. Anteroposterior (AP) development occurs in the radioulnar plane.
C. Dorsoventral (DV) axis.
Although there are key regulators for each of these independent axes, coordination
between the three axes exists to ensure the development of an upper extremity with
proper proportions.
A. Proximodistal Growth
The key anatomic structure to early longitudinal growth of the limb is a ridge of ecto-
derm at the junction of the dorsal and ventral surfaces known as the apical ectodermal
ridge (AER). The tissue of the AER produces a signal, which is both necessary and
sufficient to promote longitudinal growth of the limb. The primary factors promoting
longitudinal growth produced by the AER are members of the fibroblast growth factor
family.

4 Section I • General Concepts
B. Anteroposterior Development
Identity of digits along the AP (radio-ulnar, pre-axial-postaxial) axis is crucial for normal
limb development and function. For example, the radial most digit, the thumb, has clear
morphologic differences from the remaining digits. The tissue responsible for setting
up AP axis in both the upper and lower limbs is a region of tissue along the posterior
margin of the limb paddle called the zone of polarizing activity (ZPA). The ZPA tissue
expresses the secreted signaling molecule sonic hedgehog (Shh), which alone can provide
the necessary signal for normal AP development. The primary function of Shh from
the ZPA is the coordination of AP development; however, its signal also affects develop-
ment along the PD and DV axes coordinating spatial growth along all three axes.
C. Dorsoventral Patterning
Dorsoventral patterning allows for normal development of the dorsal and ventral struc-
tures, including the normal flexion cascade of the digits. It is set up by the expression of
the signaling molecule Wnt7a in the dorsal ectoderm, which induces the transcription
factor Lmx1b in the dorsal mesoderm. The dorsal ectoderm appears to be the tissue
necessary for normal DV growth. The expression of the transcription factor Engrailed1
in the ventral ectoderm is necessary for normal ventral limb development.
Dorsal structures include nails, hair follicles, and extensor tendons whereas volar struc-
tures include flexor tendons and sweat glands. The nails first appear at 13 weeks gestation.
III. Limb Identity
Although the basic molecular machinery for early limb development is identical
between the upper and lower limbs, there are clear functional and morphologic differ-
ences between hands and feet. Though the details and human relevance have yet to be
fully determined, there are several upper and lower extremity–specific genes that have
been shown to participate in limb identity. The gene TBX5 is expressed specifically in
early upper extremity development and is involved with imparting identity to the upper
limb while the genes TBX4 and Pitx1 are expressed specifically in the lower extremity
and are involved with lower limb development.
IV. Later Events of Limb Development
Prior to the upper extremity taking on its typical morphological appearance, the specific
tissues that are necessary for normal hand development begin to form. As in early limb
development, coordination of development, both temporally and spatially, is necessary
to produce a functional limb. Although many of these specific tissues are formed by
separate molecular signals, parts of the molecular machinery used in early limb develop-
ment are conserved and used for these later events.
A. Skeletogenesis
Early mesenchymal condensation begins during the fifth week. The cellular aggregates
undergo chondrification forming the early cartilaginous anlagen. Lower oxygen tension
is thought to be a requirement for the development of the initial condensations and for
the conversion of these masses into cartilaginous anlagen. The cartilaginous anlagen
are then penetrated by blood vessels required for the initiation of ossification. By the
seventh week, ossified bone becomes apparent, initially in primary ossification centers
in the midpoints of long bones. The ossification of some of the bones of the upper

Chapter 1 • Embryology 5
extremity, such as the carpus, does not begin until the first postnatal year and continues
during childhood development.
Carpal ossification begins with the capitate during the first year of life and progress to
the hamate, triquetrum, lunate, scaphoid, trapezium, trapezoid, and pisiform by age 12.
Bone formation through endochondral ossification occurs at both ends of devel-
oping long bone from growth plates oriented at 180 degrees from each other. The
hedgehog signaling pathway, mediated by Indian hedgehog (closely related to Shh), is
a key regulator of growth plate chondrogenesis and ultimate growth of the long bone.
There are multiple additional signaling pathways that modulate and contribute to long
bone growth.
B. Development of Peripheral Nerves

The upper and lower limb buds initiate outgrowth at the level of the cervical and lumbar
regions, respectively. Sensory and motor nerves began migration into the limb during
the third week and become defined by the fifth week of development. Nerve ingrowth
progresses to the level of the elbow by week 5 and fingers by week 7. Dermatomes based
on each respective level are defined by region of skin and underlying tissue innervated
by a single spinal nerve level.
Sensory nerves are derived from neural crest tissue. Motor nerve development
requires contact and subsequent innervation of target muscle for neural survival. Nerves
not finding appropriate target muscles regress during development.
C. Vasculogenesis
The cardiovascular system is the earliest organ system developed in the embryo. The
early network of vessels within the limb is called the marginal sinus; it is amorphous
and does not have any recognizable resemblance to the adult upper extremity vascular
system. The process begins when the limb is paddle shaped and requires signaling from
the AER. The marginal sinus begins to degrade as cartilaginous blastema is formed in
the developing limb. Subsequent vasculogenesis occurs with early formation of vessels
starting in the fourth week.
Upper extremity vasculogenesis begins with formation of the brachial artery. The
median artery is the first major branch followed by the ulnar artery and the radial
artery, both of which occur later during limb development. The ulnar and radial arteries
continued to grow, becoming the dominant blood supply to the upper limb, while the
median and interosseous arteries regress.
D. Myogenesis
Muscle precursor cells condense during week 6 of development. Muscle blastema, as
opposed to developing cartilaginous precursors, requires higher oxygen tensions and
therefore, develops in a location distal to the formation of the chondrogenic blastema.
Muscle within the limb develops from the limb bud mesenchyme. The muscle
masses of the limb develop in discrete dorsal or ventral masses comprising the extensor
or flexor muscles of each of the upper and lower extremities.
V. Embryology and Development of Congenital Anomalies
The development of congenital differences arises either from an intrinsic molecular

abnormality or through external forces applied to the developing limb. Many candidate
genes instrumental for both early and late upper extremity development have been

elucidated through the use of genetic manipulation of animal models, especially in the
chicken and mouse. Information garnered through these experiments has been vital to
understanding limb development in humans. A surprisingly large number of molecular
signaling events are conserved between lower mammals and humans. Information from
these experiments has been critical in developing genetic testing for families. As impor-
tant, the molecular pathways crucial for the formation of specific tissues may lead to
possible treatments for tissue regeneration in adults.
Suggested Readings
Cohn MJ, Bright PE. Molecular control of vertebrate limb development, evolution and congeni-
tal malformations. Cell Tissue Res. 1999;296(1):3–17.
Daluiski A, Yi SE, Lyons KM. The molecular control of upper extremity development: Implica-
tions for congenital hand anomalies. J Hand Surg (Am). 2001;26(1):8–22.
Gupta A, Kay SPJ, Scheker LR. eds. Section 2: Birth, growth and development. In: The Growing
Hand. London, Harcourt Pub Ltd. 2000;25–56.
Johnson RL, Tabin CJ. Molecular models for vertebrate limb development. Cell.
1997;19;90(6):979–990.
Niswander L. Pattern formation: Old models out on a limb. Nat Rev Genet. 2003;4(2):
133–143.

Imaging
2
A. Bobby Chhabra, Chealon D. Miller, and
Lindley Wall
Standard radiographs of the hand and wrist include anterior-posterior (AP), lateral, and
oblique images. Computed topography (CT) may be used to improve visualization of
the articular surface and provide more detail of osseous structures. Magnetic resonance
imaging (MRI) is useful to evaluate soft tissue structures and is often used to evalu-
ate for occult fractures, osteonecrosis, injuries of the triangular fibrocartilage complex
(TFCC), and injuries of the scapholunate and lunotriquetral ligaments. Initial evalu-
ation of any hand and wrist pathology should begin with plain radiographic imaging
(x-rays). If initial x-rays are negative, advanced imaging is ordered based on physical
examination findings.
I. Hand and Wrist Anatomy
A. Bones of the hand and wrist (Fig. 2.1)

1. The hand is made up of five distal phalanges, four middle phalanges (the
thumb does not have a middle phalanx), five proximal phalanges, and five
metacarpals. The AP, lateral, and oblique radiographs are the most common
views used to diagnose pathology of the hand.
2. The wrist comprises eight carpal bones in two rows (Fig. 2.2). The wrist is
defined as the area beginning 3 cm proximal to the radiocarpal joint and
terminates at the carpometacarpal (CMC) joints. The bones of the hand and
wrist include the radius, ulna, scaphoid, lunate, triquetrum, pisiform, trape-
zium, trapezoid, capitate, and hamate. AP and lateral views are used most
often to evaluate wrist pathology.
B. Ligaments of the hand and wrist
1. The wrist joint comprises an articulation between the distal radius and the
distal ulna, and an articulation between the distal radius and ulna with
the bones of the carpus. There are extrinsic (originate or insert outside of the
carpus) and intrinsic (originate and insert within the carpus) ligaments that
support these joints.
2. The important extrinsic volar wrist ligaments form a double “V” pattern
and include the radioscaphocapitate ligament, and long and short radiolu-
nate ligaments ulnolunate, ulno-triquetral, (Fig. 2.3). Other ligaments on
the volar side include the triquetralcapitate, triquretralhamate, lunotriqure-
tral, scaphocapitate, scaphotrapezium, and capitotrapezoid. These liga-
ments are important from a clinical standpoint, but not from an imaging
standpoint.
3. The dorsal wrist also contains ligaments that are important for wrist stabil-
ity (Fig. 2.4). The major dorsal wrist ligaments are the dorsal intercarpal
ligament and the dorsal radiocarpal ligament. Similar to the volar wrist
ligaments, these are important clinically, but not from an imaging stand-
point.
7

Distal
phalanges
Middle
phalanges
Proximal
phalanges
Metacarpals
Carpals
Figure 2.1 Bones of the

hand.
3rd
metacarpal
4th
2nd metacarpal
metacarpal
1st 5th
metacarpal metacarpal
Trapezoid
Hamate
Trape m
zium tru
Capitate ique
Sc T r
(n ap
av ho Pisiform
icu id
lar
) Lunate
Radius Ulna
Figure 2.2 Bones of the

wrist.

Chapter 2 • Imaging 9
Figure 2.3 Extrinsic volar (palmar) wrist Figure 2.4 Extrinsic dorsal wrist
ligaments. ligaments.
Figure 2.5 T1 fat saturated MR arthrogram with normal scapholunate ligament (long
white arrow), lunotriquetral ligament ( grey arrow), and an area on the ulnar proximal
lunate indicating edema secondary to ulnocarpal impaction (short white arrow).
4. The intrinsic wrist ligaments are situated within the proximal and distal rows.
The scapholunate and lunotriquetral ligaments are the strongest ligaments
in the proximal row on the dorsal and volar aspects of the wrist, respectively.
The bones of the distal row are tightly linked to each other and to the meta-
carpals (Fig. 2.5).
5. The TFCC consists of an articular disk, meniscus homologue, ulnocarpal
ligament, dorsal and volar radioulnar ligament, and extensor carpi ulnaris

PALMAR
Ulnotriquetral ligament
Ulnolunate ligament
Ulnar capsule
Scaphoid
fossa
Prestyloid recess
Meniscus
Lunate fossa
homologue
Ulnar styloid
Articular disc
Dorsal DRUL
Radius Ulna superficial portion
Dorsal DRUL
DORSAL deep portion
Figure 2.6 Anatomy of the TFCC.
Ulnotriquetral
ligament
Lunotriquetral
ligament
Scapholunate
ligament
Triangular ligament
ulnar attachment Disc proper
Figure 2.7 TFCC on MRI.
sheath (Figs. 2.6 and 2.7). It originates from the medial border of the distal
radius and inserts into the base of the ulnar styloid. It separates the distal
radioulnar joint (DRUJ) from the radiocarpal joint.

Figure 2.8 Six extensor

compartments of the hand.
C. Muscles and tendons of the wrist and hand

1. There are six dorsal compartments of the wrist containing tendons that arise
from separate muscle bellies in the forearm (Fig. 2.8).
a) Extensor Compartment 1: Abductor pollicis longus and the extensor pol-
licis brevis (EPB)
b) Extensor Compartment 2: Extensor carpi radialis brevis and the extensor
carpi radialis longus.
c) Extensor Compartment 3: Extensor pollicis longus.
d) Extensor Compartment 4: Extensor digitorum comminus and the exten-
sor indicis propius.
e) Extensor Compartment 5: Extensor digiti minimi.
f ) Extensor Compartment 6: Extensor carpi ulnaris.
II. Anterior-Posterior and Posterior-Anterior Views of the Hand and Wrist
A. The AP view of the hand and wrist for the evaluation of hand and wrist injuries
is obtained with the volar surface of the hand facing the x-ray beam. The beam
passes from the volar surface to the dorsal surface.
B. The posterior-anterior (PA) view of the hand and wrist is obtained with the volar
surface of the hand facing the table (away from the x-ray beam). The beam passes
from the dorsal surface to the volar surface (Figs. 2.9 and 2.10).
C. The volar surfaces of most carpal bones are narrower. These bones are best pro-
filed with AP rather than PA views of the wrist because of improved alignment
of the periarticular cortices with the diverging x-ray beam.
D. The ulnar styloid is helpful in determining the direction in which the films were
obtained. In the standard AP view, the ulnar styloid is located centrally over the
distal ulna (because the view is taken with the forearm in supination), whereas
in the PA view of the wrist, the ulnar styloid is located ulnarly on the ulnar head
(because the forearm is in neutral rotation).

Figure 2.9 A: Technique for obtaining zero rotation. Note that the shoulder and the
forearm are the same distance from the floor. PA view of the hand. B: Radiograph for
PA view of the hand.

Figure 2.10 A: Technique for obtaining zero rotation PA view of wrist (note the shoulder
is abducted 90 degrees (parallel to the ground) and the elbow is flexed 90 degrees)

3
2
1
Figure 2.11. AP view of

wrist to assess Gilula’s lines.
E. A zero rotation view is used to determine the true ulnar variance. This is obtained
with the shoulder abducted 90 degrees, the elbow flexed 90 degress, and the
wrist in neutral position as illustrated in Fig 2.10A.
F. Gilula’s lines are seen on AP or PA views of the wrist. This wrist must be in neu-
tral radial ulnar deviation, and neutral flexion-extension. These lines represent
the borders of the carpal bones. Three lines are present: (1) along the proximal
margin of scaphoid, lunate, triquetrum; (2) distal margin of scaphoid, lunate,
and triquetrum; and (3) proximal margin of capitates and hamate. Disruption
in Gilula lines indicates dissociative ligamentous instability (Fig. 2.11).
III. Lateral View of the Hand and Wrist
A. The lateral view of the hand and wrist involves the x-ray beam passing in the
sagittal plane. The lateral view of the hand should provide visualization of the
phalanges and metacarpals.
B. The lateral view of the wrist should allow visualization of the metacarpals, lunate,
and radius in alignment (Fig. 2.12). An adequate lateral view of the wrist should
demonstrate the volar pisiform between the distal aspect of the scaphoid and the
palmar aspect of the head of the capitate.
C. A zero-rotation lateral view is obtained with shoulder adducted and the elbow
flexed 90 degrees. This will allow the best assessment of DRUJ congruency.
D. The lateral view of the wrist is the best view for the evaluation of the capitolu-
nate angle, the scapholunate angle and pathologies such as dorsal intercalated
segmental instability (DISI) and volar intercalated segmental instability (VISI).

Figure 2.12 A: Technique for obtaining

lateral view of the wrist. B: Lateral view
of the wrist. (Courtesy of Lou Gilula.)

Figure 2.13 DISI deformity seen on CT scan.
1. Normally the distal radius, lunate, capitate, and third metacarpal are colinear.
The scapholunate angle can be measured on lateral radiographs of the wrist
and the radiolunate angle exceeds 20 degrees of extension.
DISI (Fig. 2.13): In DISI deformity, the lunate is extended (dorsiflexed),
the scaphoid flexed, and the scapholunate angle measures more than 60°.
A DISI deformity results (normal 30-60°, mean 47°) from a scapholunate
ligament disruption, which if untreated can lead to wrist arthritis.
2. VISI: In VISI, the lunate is flexed in a volar direction in relation to the capi-
tate causing a zigzag deformity on the lateral radiograph (Fig. 2.14). VISI
can result from disruption of the lunotriquetral ligament and can cause
ulnar-sided wrist pain. It can also be a normal finding, and arise from a non-
dissociative instability.
IV. Radiographs of the Thumb
A. Radiographic assessment of the thumb is difficult to interpret on routine views

of the hand because the thumb is rotated out of the plane of the hand.
B. Roberts view is a true AP view of the thumb ray and is taken with the fore-
arm in maximal pronation and the dorsum of the thumb resting on the cassette
(Fig. 2.15). This view is often obtained to improve visualization of the first CMC
joint. It demonstrates arthritic changes of the CMC joint, and fractures or dis-
locations of the CMC joint.
C. Lateral view of the thumb and CMC joint is obtained with the forearm flat on
the table and the hand pronated 20 degrees with the thumb flat on the cassette

Figure 2.14 VISI deformity seen on plain radiograph.
Figure 2.15 Technique for obtaining Roberts view of the thumb.

(Fig. 2.16). The x-ray tube may be angled 10 degrees from vertical in distal to
proximal projection.
D. Stress views of the thumb can be used to evaluate the CMC joint and will allow the
visualization of five joints: trapeziometacarpal—thumb, trapeziometacarpal—
index scaphotrapezial, scaphotrapezoid, and trapeziotrapezoid. This view is
obtained with the hands pronated 60 degrees and the radial aspects of the distal
phalanges pressing together (Fig. 2.17).
Figure 2.16 Technique for obtaining lateral view of the thumb.
Figure 2.17 Radiograph for stress view of the thumb to evaluate CMC joint.

V. Special Views of the Hand and Wrist
General considerations: Isolated metacarpal views are difficult to obtain and rarely
attempted in the acute setting. To obtain improved visualization of the metacarpals and
digits, an oblique view of the hand is obtained. Views of the wrist in semisupination and
semipronation will allow for improved visualization of certain carpal bones as described
below. Thumb fractures are best visualized with a Roberts view as described above.
A. Oblique view of the hand (Fig. 2.18)
The hand rests on its ulnar border and tilts 40 to 45 degrees in palmar direc-
tion. The beam is directed toward the metacarpal phalangeal joints.
1. This view is used in addition to the AP and lateral views of the hand and is
used as part of the standard three-view hand series for hand trauma.
B. Pronated oblique view of the wrist (Fig. 2.19)
1. Technique: The hand rests on its ulnar border and tilts 40 to 45 degrees in a
volar direction; fingers are held in slight flexion and held together while the
central beam is directed to the center of the carpus.
2. This view is used to image the scaphoid, the triquetrum, body of the hamate,
scaphotriquetral, and trapezium-trapezoid joints. This view also allows
improved visualization of the fourth and fifth CMC joints.
Figure 2.19 A: Technique for obtaining

Figure 2.18 Radiograph for oblique view oblique view of the wirst. B: Radiograph
of the hand. for oblique view of the wrist.

C. Scaphoid view of the wrist (Fig. 2.20)

A scaphoid view is often obtained to cone down on the scaphoid. It is taken
with the wrist in 20 degrees of ulnar deviation (30 degrees of wrist extension
may also improve visualization) and is 64% sensitive in detecting scaphoid
pathology. It is also called a “PA ulnar deviation view” of the wrist.
D. Supinated oblique lateral view of the wrist (Fig. 2.21)
Figure 2.20 A: Technique for obtaining scaphoid view of the wrist. B: Radiograph for
scaphoid view of the wrist. (Courtesy of Lou Gilula.)

Figure 2.21 A: Technique for obtaining supinated oblique view of the wrist.
B: Radiograph for supinated oblique view of the wrist. (Courtesy of Lou Gilula.)

1. Technique: The hand rests on its ulnar border and tilts 30 to 35 degrees
dorsally into supination. The thumb should be slightly abducted to allow for
adequate visualization of desired structures. The central beam is once again
directed at the center of the carpus.
2. This view is used to image the pisiform and pisotriquetral joints.
E. Carpal tunnel view of the wrist (Fig. 2.22)
1. Technique: Hand is maximally extended. One can use the opposite hand or
a strap to provide extension. The volar surface of the wrist rests on the cas-
sette and a central beam is directed toward the base of the palm at about a
15-degree angle.
Figure 2.22 A: Technique for obtaining carpal tunnel view of the wrist. B: Radiograph
for carpal tunnel view of the wrist.

2. The carpal tunnel view is an axial view of the carpal canal and provides more
detailed information of the hook of the hamate and pisiform bone. A semisu-
pinated wrist view will also allow for a visualization of the hook of the hamate
(Fig. 2.23).
F. Clenched fist AP view of the wrist (Fig. 2.24)
1. Technique: Patient in same position as stated above for AP view. Before the
x-ray is taken, the patient clenches their fist as tightly as possible, and the
x-ray is taken with the patient’s hand clenched.
Figure 2.23 Technique for semisupinated view of the wrist.
Figure 2.24 Technique for obtaining clenched fist AP view of the wrist.

Figure 2.25 Radiograph

showing increased
scapholunate interval.
(Courtesy of David Rubin.)
2. The clenched fist view of the wrist is used to evaluate the scapholunate inter-
val and any widening that may be present. This view is useful in patients
suspected of having a scapholunate ligament disruption.
3. Clenching of the patient’s fist allows the capitate to pull proximally and
accentuates widening that may be present at the scapholunate interval.
A comparison view of the opposite hand is helpful in determining the normal
scapholunate interval.
4. Clenched fist views are best taken with the arm supinated and the wrist in
neutral.
5. Findings in scapholunate dissociation (Fig. 2.25)
a) A scapholunate interval of greater than 4 mm.
b) Cortical (signet) ring sign
c) Foreshortened scaphoid
VI. Arthrography of the Hand and Wrist
Arthrography has been used for the diagnosis of ligament tears seen with carpal instabil-
ity patterns and TFCC injuries, but, with improved diagnostic quality of MR imaging,
has been replaced by MR and MR arthrograms.
VII. Computed Topography
CT is often used to identify loose fragments and better define fracture patterns in frac-
tures difficult to assess by plain films. CT is also utilized to assess nonunion and fractures
of carpal bones that are suspected but not confirmed by plain radiographs or to define
architecture of fractured carpal bones (Figs. 2.26 and 2.27). As with plain radiographs,
CT uses ionizing radiation, but has the advantage of being formatted for three-dimen-
sional visualization of the carpal bones and the distal radius articular surface.
A. Technique: Images are obtained while the patient is prone and with the arm
stretched above the head. As with most CT scans, images are obtained in the
axial plane. The images are reformatted in the coronal and sagittal planes.

Figure 2.26 Sagittal CT scan showing a proximal scaphoid fracture with humpback
deformity and cyst formation at the nonunion site.
Figure 2.27 CT scan of wrist. Showing lunate osteonecrosis (Kienböck’s disease)

Three-dimensional reconstructions can also be formatted, which may improve

understanding of fracture patterns, particularly the distal radius.
CT scans of the wrist and hand are obtained to assess the nonunion of fractures (most
often scaphoid fractures), to better define difficult fracture patterns of the wrist, and for
assessment of subluxation/dislocation of the distal radio-ulnar joint. When evaluating
a scaphoid fracture/nonunion, the scan should be obtained in the longitudinal plane of
the scaphoid, rather than in the plane of the wrist.
VIII. Magnetic Resonance Imaging and Magnetic Resonance

Arthrography
Magnetic resonance imaging is an advanced imaging technique, often used to assess

ligaments and other soft tissues (Fig. 2.28). Circumstances in which MRI may initially
be beneficial: soft tissue injuries and injuries of the cartilage and ligaments; bone mar-
row abnormalities; carpal instability; osteonecrosis; and occult fractures (especially sca-
phoid fractures) (Fig. 2.29). MRI is also sensitive for diagnosing subtle physeal injuries
in children and for evaluating physeal bars and growth arrests. MR arthography is often
used to diagnose tears of the TFCC and the intercarpal ligaments of the proximal row.
A. Technique: The patient is placed prone and the affected extremity is placed
above the head with the forearm pronated. Alternatively, scanning may be per-
formed with the patient supine with the arm positioned at the patient’s side and
forearm in neutral.
Figure 2.28 MRI of the wrist.

B. Standard Pulse Sequences: T1, T2, and short tau inversion recovery (STIR).
MRI Sequence Fluid Bone Lipid
T1 Dark Bright Bright

T2 Bright Dark Bright
STIR Bright Dark Dark
C. T1-weighted images provide good anatomic detail and are useful for identifying
fat in lipomatous masses or atrophied muscles.
D. T2-weighted images are good for detecting pathologic conditions by accentuat-
ing the presence of abnormal fluid, edema, or hemorrhage related to traumatic
injury or an inflammatory process.
E. A fracture can be diagnosed when there is a linear area of low signal traversing
bone from cortex to cortex on the T1-weighted sequence with a corresponding
high signal on STIR sequence. Other sequences may be useful for ligamentous
pathology, muscle injury, or malignancy.
F. In patients with history and physical examinations highly suspicious for acute
scaphoid fractures with negative initial radiographic findings, MRI has been
found to be cost-effective early in diagnostic workup rather than the tradi-
tional approach of casting and waiting 10 to 14 days before repeat x-rays and
reevaluation.
G. Magnetic resonance arthrography (MR arthrography) is useful in the evaluation
of the scapholunate ligament, lunotriquetral ligament, and TFCC (Figs. 2.30
and 2.31).
H. MR arthrography can be performed with single, double, or triple compartment
(radiocarpal, intercarpal, and/or distal radioulnar compartment) injection of
contrast material.
Figure 2.29 Occult fracture of the scaphoid as seen on MRI. (Courtesy of David Rubin.)

Figure 2.30 Insertion of contrast under fluoroscopy in preparation for MR arthrogram.
Figure 2.31 MR arthrogram of the wrist (illustrating dye in

the radiocarpal joint).
1. Approximately 2 to 5 mL of contrast is administered under sterile technique

and fluoroscopic guidance. Fat-suppressed, T1-weighted images are then
taken in all three planes (see Fig. 2.30).
Suggested Readings
Hodge JC, Gilula LA. Imaging of the wrist and hand. J South Orthop Assoc. 1996;5(4):292–304.
Metz VM, Wunderbaldinger P, Gilula LA, Update on imaging techniques of the wrist and hand.
Clin Plast Surg. 1996;23(3):369–384.

Anesthesia
3
J. Megan M. Patterson and Stefan Lucas
Anesthesia for hand and upper extremity surgery can be provided by either general or
regional anesthesia. General anesthesia for upper extremity surgery is very similar to
that for surgery on other areas and will not be discussed in this chapter.
I. Brachial Plexus Anesthesia and Analgesia
Regional anesthesia for upper extremity surgery enjoys widespread practice in the
United States, albeit with a variety of approaches and philosophies. These blocks may
be performed as a sole anesthetic or in combination with sedation or general anesthesia.
Depending on the dosage of local anesthetic used, sensory “selectivity” or a complete
sensory and motor blockade can be achieved (Tables 3.1 and 3.2)
Onset time and duration of action may be subject to other additives (i.e., epineph-
rine), which help to prolong the duration of blockade, limit the peak plasma concentra-
tion, and act as a marker for intravascular injection (Table 3.3).
TABLE 3-1 Brachial plexus anesthesia
Block Brachial Plexus Best May Other

Approach Correlate Targeted for Miss Concerns
Interscalene Root/proximal Shoulder C8 and T1 Highest
approach trunk level surgery roots “ulnar incidence of
sparing” (really phrenic nerve
inferior trunk palsy, possible
sparing) seizure
Supraclavicular Distal trunk/ Mid-arm to Suprascapular Tradition-
approach division level hand nerve ally, highest
incidence of
pneumothorax
Infraclavicular Cord/proximal Mid-arm to Musculocutane- Deep block
approach branch level hand ous nerve, and
axillary nerve
Axillary Branch level Forearm Axillary nerve, Limb may not
approach and hand medial cutane- be akinetic
ous nerves (for surgical
of arm and anesthesia)
forearm, and
musculocuta-
neous
29

TABLE 3-2 Typical single-shot brachial plexus block durations
Duration of Duration of
Agent Onset Time Anesthesia Analgesia
Lidocaine 2%/ Very short ~3 h ~5–6 h
Mepivacaine 1.5% (5 min)
Lidocaine 1%/ Very short None to ~1.5 h ~3–4 h
Mepivacaine 0.75% (5 min)
Ropivacaine 0.5% Short ~4–5 h ~9–12 h
to 0.75% (8–12 min) (differential)
Bupivacaine 0.5% Delayed ~6–9 h ~10–16 h
(10–15 min)
Bupivacaine 0.25% Delayed ~3–4 h ~9–12 h
(10–20 min)
When performing nerve blocks at or distal to the elbow, we block each nerve indi-
vidually. For these peripheral nerve blocks, a 25 gauge 1.5 in needle is typically used.
II. Median Nerve
A. Anatomy
The median nerve contains fibers from the fifth cervical through the first thoracic nerve
roots and arises from the lateral and medial cords of the brachial plexus. It enters the
arm posterior to the pectoralis major muscle and descends anteromedial to the brachialis
muscle and posteromedial to the biceps brachii. In the upper arm, the median nerve lies
lateral to the brachial artery, crossing anterior to the artery to lie on its medial side at the
level of the insertion of the coracobrachialis.
In the antecubital fossa, the median nerve lies posterior to the lacertus fibrosis,
anterior to the brachialis, and medial to the brachial artery. It then enters the fore-
arm between the superficial and deep heads of the pronator teres muscle, and descends
the forearm between the flexor digitorum superficialis (FDS) and the flexor digitorum
profundus (FDP). Five centimeters above the wrist crease, the median nerve becomes
superficial and travels just radial to the palmaris longus (PL) tendon before entering the
carpal tunnel.
TABLE 3-3 Recommended maximum dosages
Maximum
Max Single Daily Dose
Max Single Dose Dose (with (with/without
Drug (Plain) Vasoconstrictor) Epinephrine)
Lidocaine 5 mg/kg 8 mg/kg 300/500 mg
Bupivacaine 2 mg/kg 3 mg/kg 400 mg
Despite considerable variability, these are accepted “maximums” for local anesthetics.

Chapter 3 • Anesthesia 31
1. The palmar cutaneous branch of the median nerve

This purely sensory branch of the median nerve provides sensation to the thenar palm.
It arises 5 to 7 cm above the wrist; however, it travels with the median nerve for 16 to
25 mm before diverging from the palmar-radial aspect of the median nerve. It then runs
distally along the ulnar border of the flexor carpi radialis (FCR) to the proximal margin
of the transverse carpal ligament (TCL). The palmar cutaneous branch of the median
nerve travels in a separate tunnel within the TCL, piercing the ligament in line with the
ring finger to enter the subcutaneous tissue. However, variation in the nerve’s anatomy
and location exist.
B. Median Nerve Block at the Elbow
The median nerve lies medial to the brachial artery at the elbow and can be anesthetized
by injecting 5 to 10 mL of local anesthetic just medial to the brachial artery and just
proximal to the line connecting the medial and lateral epicondyles.
C. Median Nerve Block at the Wrist
Several techniques can be used to block the median nerve at the wrist.
1. Local anesthetic is injected between the PL and the FCR at the level of the
proximal wrist crease. If no PL tendon is present, the needle is inserted just ulnar
to the FCR tendon. The patient should be instructed prior to needle placement
to advise the operator of any paresthesias or “electric shock” sensations in the
distribution of the median nerve. If these are encountered, the needle should be
repositioned prior to injection of anesthetic so that intraneural injection can be
avoided. This technique will provide adequate anesthesia to both the median
nerve and the palmar cutaneous branch of the median nerve.
2. A second method to provide anesthesia to the median nerve at the level of
the wrist is to perform a carpal tunnel injection of local anesthetic. The needle is
inserted into the carpal tunnel, starting from a point just ulnar to the PL tendon
and angling 30 degrees from the skin and slightly radial. Five to 7 mL of local
anesthetic is injected into the carpal tunnel, and again, if paresthesias are encoun-
tered the needle should be redirected more ulnar to avoid intraneural injection.
While this method will provide adequate anesthesia to the median nerve, it will
not provide anesthesia to the palmar cutaneous branch of the median nerve, and
a separate subcutaneous injection will need to be performed.
3. An additional method to inject the carpal tunnel with local anesthetic is through
the FCR tendon, angled distally and at 30 degrees in both the frontal and sagit-
tal planes toward the carpal tunnel. The needle is located deep to the median
nerve with this technique, and paresthesias are generally avoided.
III. Ulnar Nerve
A. Anatomy
The ulnar nerve is the terminal branch of the medial cord of the brachial plexus and
contains fibers from the eighth cervical and first thoracic nerve roots, with occasional
contributions from the seventh cervical nerve root. The ulnar nerve enters the arm
posterior to the pectoralis major and medial or posteromedial to the brachial artery. At
the level of the distal attachment of the coracobrachialis to the humerus, approximately
8 to 10 cm above the medial epicondyle, the ulnar nerve pierces the medial intermuscu-
lar septum to enter the posterior compartment of the arm. It continues to descend the
arm on the anterior surface of the medial head of the triceps.

At the elbow as the nerve passes through the cubital tunnel, it is bordered medial
by the elbow joint and laterally by the cubital tunnel retinaculum. The ulnar nerve then
passes between the two heads of the FCU and enters the anterior compartment of the
forearm. It travels down the forearm between the FCU and the FDP muscle bellies until
the distal third of the forearm where it becomes superficial and lies just radial to the
FCU muscle. The ulnar artery joins the ulnar nerve in the middle third of the forearm
and is lateral to the nerve as the two structures course distally. The palmar cutaneous
branch of the ulnar nerve, when present, arises at the junction of the middle and distal
third of the forearm, pierces the antebrachial fascia just above the distal wrist crease,
and supplies the skin of the hypothenar eminence. The dorsal cutaneous branch of the
ulnar nerve arises 5 to 7 cm proximal to the distal wrist crease, pierces the fascia 3 cm
proximal to the distal wrist crease, and courses subcutaneously dividing into as many as
nine branches to supply the skin on the dorsoulnar surface of the hand and wrist, the
small finger, and the ulnar half of the ring finger.
At the wrist, both the ulnar nerve and artery pass radial to the pisiform, ulnar to the
hamate hook, palmar to the TCL, and dorsal to the superficial palmar carpal ligament.
The ulnar nerve splits into its terminal branches at the level of the hypothenar eminence.
B. Ulnar Nerve Block at the Elbow

The ulnar nerve at the elbow can be easily anesthetized just posterior to the medial
epicondyle where it is easily palpable. Local anesthetic is injected, with care taken not
to inject anesthetic into the nerve or to impale the nerve on bone.
C. Ulnar Nerve Block at the Wrist

The ulnar nerve lies immediately radial to the FCU tendon, and ulnar to the ulnar artery.
The ulnar nerve is blocked at the wrist by injecting local anesthetic ulnar and deep (dor-
sal) to the FCU tendon at the level of the proximal wrist crease. A free flow of anesthetic
should be felt by the physician. A separate injection is necessary to block the dorsal sen-
sory branches of the ulnar nerve. Subcutaneous infiltration of local anesthetic beginning
from the site of the ulnar nerve block and extending dorsally to the midpoint of the wrist
will provide adequate anesthesia of the dorsal sensory branches of the ulnar nerve.
IV. Radial Nerve
A. Anatomy
The radial nerve arises from the posterior cord of the brachial plexus, receiving fibers
from the fifth through eighth cervical nerve roots. The radial nerve travels down the
arm in the posterior compartment, crossing from medial to lateral across the posterior
humerus at the level of the deltoid insertion. The radial nerve continues to travel dis-
tally, piercing the lateral intermuscular septum approximately 11 cm proximal to the
lateral epicondyle. The nerve then lies in the interval between the brachialis and the
brachioradialis muscles. As the radial nerve passes anterior to the lateral epicondyle and
enters the forearm, it divides into its terminal branches—the posterior interosseous
nerve (PIN) and the superficial branch of the radial nerve.
The superficial branch of the radial nerve passes anterior to the supinator and
descends the forearm on the deep surface of the brachioradialis muscle. It pierces the
fascia on the dorsal side of the tendon approximately 7 cm proximal to the wrist and
descends on the dorsoradial side of the wrist, branching and providing sensation to the
dorsoradial hand.

Chapter 3 • Anesthesia 33
The PIN provides innervation to the extensor muscles of the forearm as well as the
wrist capsule. It passes through the two heads of the supinator and crosses the proximal
radius to enter the extensor compartment of the forearm. The PIN initially descends
the forearm between the abductor pollicis longus, the extensor carpi ulnaris, and the
finger extensors and then courses through the muscle to lie on the posterior surface of
the interosseous membrane.
B. Radial Nerve Block at the Elbow
The radial nerve is blocked at the elbow at a point 3 to 4 cm above the lateral epicondyle.
C. Radial Nerve Block at the Wrist
The branches of the superficial branch of the radial nerve are best blocked by subcu-
taneous infiltration of local anesthetic. The injection should start at the level of the
radial styloid, just radial to the radial artery and extend dorsally around the wrist to the
midportion of the dorsum of the wrist.
V. Lateral Antebrachial Cutaneous Nerve
A. Anatomy
The lateral antebrachial cutaneous nerve (LABC) is the terminal branch of the mus-
culocutaneous nerve that originates from the lateral cord of the brachial plexus and
receives fibers from the fifth through the eighth cervical nerve roots.
The LABC becomes superficial at the anterolateral aspect of the elbow between the
biceps and the brachialis muscles and pierces the brachial fascia approximately 3 cm
proximal to the lateral epicondyle and 4.5 cm medial to the lateral epicondyle. It travels
down the forearm on the surface of the brachioradialis muscle belly and provides sensa-
tion to the lateral aspect of the forearm.
B. Lateral Antebrachial Cutaneous Nerve Block
The LABC can be effectively blocked at the elbow by a subcutaneous ring block around
the lateral and anterolateral aspect of the elbow.
VI. Digit
A digital block is administered either volarly or dorsally. The volar approach requires
that 3 to 5 cc of 0.5% Marcaine and 3 to 5 cc of 2% lidocaine (both without epineph-
rine) are injected into the flexor tendon sheath at the level of the metacarpo phalangeal
joint (MCP) flexion crease. This blocks both digital nerves by extravasation of the anes-
thetic out of the flexor sheath, and is good for fingertip anesthesia both dorsally and
volarly. The dorsal approach requires 10 cc total of anesthetic mixture, and is done by
infiltrating 4 cc at the radial volar base of the proximal phalanx of the digit in question,
as well as 2 to 3 cc of anesthetic dorsally over the base of the proximal phalanx. The
needle is withdrawn, and reinserted on the ulnar aspect of the base of the proximal
phalanx, where the remainder of the anesthetic is injected.
VII. Emergency Room Blocks
Fingertip/nail bed/distal or middle phalanx: Digital block

Palmar hand laceration: Median or ulnar (or both) nerve block

Boxer’s fracture: Ulnar nerve block

Distal radius fracture: Hematoma block as well as ulnar styloid block
VIII. Bier Block
Bier block is a form of intravenous regional anesthesia. It can allow for active motion
during the procedure. The person administering the anesthesia must make sure that
the tourniquet is functioning properly. If the tourniquet malfunctions and deflates pre-
maturely, a large volume of lidocaine will be released into the circulation and seizure
activity may occur.
A. Indications
1. Cases lasting less than 60 minutes.
2. Procedures involving the hand and wrist, or distal forearm, but typically is not
used for procedures around the elbow.
B. Technique
1. An IV is placed in the dorsal aspect of the hand to be operated on.
2. A double cuff tourniquet is placed on the arm.
3. The arm is exsanguinated and the proximal tourniquet is elevated.
4. 1% lidocaine is diluted with saline to 0.5% and injected at a dose of
0.5 mg/kg
5. The distal tourniquet is elevated and the proximal tourniquet can be deflated
following confirmation of the distal tourniquet inflation.
6. Upon completion of the case, the tourniquet can be cycled to allow slow release
of the lidocaine into the central circulation, minimizing the risk of systemic
toxicity. This is not necessary in cases lasting longer than 30 minutes as the
lidocaine is bound to the tissues in the forearm and will not be released into the
circulation.
IX. Hematoma Block
A hematoma block is a local block used most commonly to assist in the closed reduction
of distal radius fractures. As some anesthetic may extrude volarly around the median
nerve, neurologic function in the hand should be assessed prior to placing a hematoma
block. Utilizing a short acting anesthetic allows for more rapid return of median nerve
function.
A. Technique
1. Palpate for the fracture location along the dorsal distal radius.
2. Prepare the skin over the fracture with alcohol and betadine.
3. Inject 1 to 2 cc of 1% lidocaine with a 25 gauge or smaller needle making a
subcutaneous wheel at the site of the block.
4. Utilizing an 18 gauge needle on a 10 cc syringe penetrate through the wheel into
the fracture site. This is confirmed with aspiration of hematoma. The hematoma
may be largely evacuated at this point.
5. Inject through the same needle by exchanging the syringe for one filled with
10 cc of 1% lidocaine which is now injected into the fracture site.
6. The block should be set for fracture reduction in approximately 10 minutes.

Pharmacology
4
Mark Wilczynski
Many conditions affecting the hand and wrist are amendable to medical management.
Medications may be dispensed for therapeutic and prophylactic reasons; to aid in diag-
nosis; or to provide analgesia and anesthesia. The most common methods of adminis-
tering the medications include oral, intra-articular injection, extra-articular injection,
intramuscular injection, and intravenous injection. Prior to administration of medica-
tion, a thorough health history (i.e., additional health problems, current medications,
allergies, etc.) should be obtained to avoid potential adverse outcomes.
I. Local Anesthetics
Local anesthetics reversibly impede impulse conduction along axons and other excit-
able membranes that utilize voltage-gated sodium channels to generate action poten-
tials. Cocaine was the first local anesthetic to be isolated. Many other agents have
subsequently been developed. They may be grouped into esters or amides based upon
their chemical structure (Tables 4.1 and 4.2). Esters are more prone to hydrolysis and
therefore have a shorter duration of action; in addition, esters are more likely to cause
allergic reactions in susceptible patients. In general, the duration of analgesia can be
lengthened by the addition of a vasoconstrictive substance such as epinephrine. Clas-
sic teaching was that local anesthetics augmented with epinephrine should never be
used in the hand or fingers, but recent reports indicate that this may be safely used and
is being used with increasing frequency, initially in Canada and now throughout the
United States. If there is a concern about the perfusion following the use of epineph-
rine in a digit, 0.5% Phentolamine Mesylate can be injected to reverse the effect of
epinephrine, causing vasodilation and increased perfusion. It is administered by direct
injection at the site of infiltration.
Local anesthetics are used to prevent pain in well-defined regions of the body.
Desired duration of action should guide agent selection. In hand surgery, local anesthet-
ics are generally infiltrated into the operative field or injected near major nerve trunks
to provide anesthesia in their sensory distribution. Local anesthetics are neurotoxic at
high concentrations, and injection either directly into nerves or into the peripheral
circulation should be avoided. They may also be administered intravenously at a site
TABLE 4-1 Esters
Esters Duration of Action

Cocaine Medium
Procaine (Novocaine) Short
Tetracaine (Pontocaine) Long
35

TABLE 4-2 Amides
Amides Duration of Action

Lidocaine (Xylocaine) Medium
Mepivacaine Medium
Bupivacaine (Marcaine) Long
Etidocaine Long
Prilocaine Long
Ropivacaine Long
distal to an inflated tourniquet to provide regional anesthesia (Bier block). Techniques

for peripheral nerve blockade can be found in Chapter 3.
II. Antibiotics
Antibiotics are substances that inhibit microbial growth. They are used to prevent infec-
tion in the perioperative period as well as to treat existing infection. Antibiotic therapy
is most effective when it is directed against organisms likely to be encountered. In the
hand, the most common pathogen is Staphylococcus aureus. It is found in 50% to 80%
of hand infections. Other common organisms are Streptococcus and Gram-negative
species. Broad spectrum therapy for long periods of time can be detrimental.
There are four general mechanisms through which antibiotics are effective against
microbes.
A. Inhibition of cell wall synthesis
B. Increase in cell membrane permeability
C. Ribosomal inhibition
D. Interference with DNA metabolism
A. Inhibition of Cell Wall Synthesis

These antibiotics include the penicillins, cephalosporins, vancomycin, bacitracin,
aztreonam, and imipenem. Penicillins and cephalosporins prevent polysaccharide
cross-linking in the bacterial cell wall by inhibiting the transpeptidase enzyme activ-
ity. Cephalosporins have been divided into first, second, and third generations. First-
generation cephalosporins are largely antistaphylococcal drugs. Second-generation**
and third-generation cephalosporins have increasing Gram-negative coverage. Vanco-
mycin is active against Gram-positive microbes. It is primarily used to treat methicillin-
resistant S. aureus (MRSA) and Staphylococcus epidermidis. It is also used in those with
penicillin and/or cephalosporin hypersensitivity.
B. Increase in Cell Membrane Permeability

These agents bind to sterols in the cell membrane and disrupt its structural integrity.
Migration of ions and macromolecules into the cell causes cell death. These agents
include nystatin, amphotericin, and polymyxin. Nystatin and amphotericin are anti-
fungal agents. Polymyxin is active against some Gram-negative bacteria.

Chapter 4 • Pharmacology 37
C. Ribosomal Inhibition
These agents are bacteriostatic or bactericidal. Bacteriostatic drugs reversibly bind to
bacterial ribosomes inhibiting protein synthesis. In hand surgery, the most relevant
drugs in this category are the macrolides (clindamycin and erythromycin). Clindamycin
is effective against all anaerobes and most Gram-positive cocci. It is particularly useful
in the treatment of community-acquired MRSA. Erythromycin can be used to treat
S. aureus in penicillin-sensitive patients. Other bacteristatic drugs in this category
include chloramphenicol and tetracycline.
Bactericidal drugs bind to the 30s subunit causing mRNA to be misread. Agents
in this category include the aminoglycosides (gentamicin**, streptomycin, tobramycin,
amikacin, and neomycin). These drugs are particularly effective against Gram-negative
bacilli.
D. Interference with DNA Metabolism

These agents include the quinolones, rifampin, and metronidazole. Quinolones block
DNA gyrase, thereby inhibiting bacterial replication. Ciprofloxacin is probably the
most commonly used fluoroquinolone in the management of hand infections. It is
more effective against Gram-negative organisms than Gram-positive organisms. Equal
oral and intravenous (IV) bioavailabilities make ciprofloxacin a particularly attractive
drug. Achilles tendon ruptures have been reported following administration. Fluoro-
quinolones can damage the physis and should be avoided in the skeletally immature.
Rifampin blocks tRNA synthesis through inhibition of bacterial DNA-dependent
RNA polymerase. It offers broad coverage including Gram-positive organisms, Gram-
negative organisms, mycobacteria, and chlamydiae. Metronidazole forms oxygen free
radicals causing damage to DNA helical structure. It is particularly effective against
anaerobic organisms.
III. Analgesics
Narcotic analgesics are drugs derived from the opium poppy plant. They are useful
analgesics and are particularly effective in treating acute pain. They may be adminis-
tered via many routes: oral (PO), sublingual (SL), rectal (PR), transdermal, subcutane-
ous (SQ), IV, intramuscular (IM), epidural (E), and intrathecal (IT). Their properties
are mediated by opiate receptors in the central nervous system. In the spinal cord,
opiate receptors are present on presynaptic and postsynaptic neurons and function to
decrease pain transmission along neuronal pathways. Opiates are metabolized in the
liver. They may be metabolized to active intermediates that are then excreted by the
kidneys. The side effects of narcotics are predictable and include constipation, nausea,
sedation, pruritus, miosis, confusion, hallucinations, euphoria, hypotension, and respi-
ratory depression. Treatment of narcotic toxicity or overdose is with naloxone—an
opiate receptor antagonist.
A variety of natural and synthetic narcotic medications have been developed. These
include morphine sulfate (IM, IV, IT, PO, and PR), meperidine (E, IM, IV, and PO),
fentanyl (E, IV, PO, and transdermal), methadone (IM, IV, PO, and SQ), hydromor-
phone (IM, IV, PO, and PR), oxycodone (PO), propoxyphene (PO), codeine (IM
andPO), hydrocodone (PO), butorphanol (IM, IV, and nasal), and nalbuphine (IM,
IV, and PO).
Narcotic pain medication regimens are tailored for each individual patient’s
needs. Factors including method of administration, duration of action, and duration

of treatment should be considered. In general, severe or acute pain is treated with

parenteral medication. IV morphine sulfate and hydromorphone are commonly used.
Short-term pain such as that encountered in the postoperative period is well treated
with oral agents. Frequently, these medications combine acetaminophen with a narcotic
such as oxycodone, hydrocodone, or propoxyphene. When prescribing these medica-
tions, care should be taken not to exceed the maximal daily dose of acetaminophen,
as this may lead to hepatotoxicity. Pain of longer duration is frequently treated with
methadone or oral, extended release formulations of oxycodone or morphine. Long-
term use of opiates may lead to tolerance, whereby increasing levels of medication are
required to provide analgesia.
IV. Corticosteroids
Corticosteroids are naturally occurring compounds produced by the adrenal gland.

These lipophilic substances have the ability to cross the cell membrane and enter the
nucleus where they interact with DNA and RNA. They inhibit phospholipase A2 and
therefore secondarily inhibit the cyclooxygenase (COX) and lipoxygenase inflammatory
pathways that lead to the production of leukotrienes, prostaglandins, and thrombox-
anes. Their anti-inflammatory properties are used by hand surgeons to treat a variety of
musculoskeletal conditions. They are injected into joints, bursae, and tendon sheaths.
Injection into such enclosed spaces maximizes local effects and minimizes systemic
effects.
The steroid selected is largely driven by previous experience, as firm guidelines do
not exist. In general, short-acting compounds are used for acute conditions, whereas
long-acting compounds are used in chronic conditions.
Corticosteroid injections into the small joints of the hand and wrist are effective
adjunctive management for rheumatoid and osteoarthritis. Injection into the ten-
don sheath is effective in treating stenosing flexor tenosynovitis (trigger finger) as
well as de Quervain tenosynovitis. Instillation of corticosteroid formulations into the
subcutaneous tissues can cause local depigmentation as well as superficial dermal fat
necrosis.
Care must be taken to follow sterile technique to avoid the complication of iatro-
genic sepsis. Up to a third of patients may experience a transient, postinjection pain
flare. Furthermore, it may take up to a week after corticosteroid injection before maxi-
mal pain relief is achieved.
V. Nonsteroidal Anti-inflammatory Drugs
Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most frequently prescribed

medication in the United States. They are a heterogenous group of substances with anti-
inflammatory properties that exert their effects through the inhibition of COX and the
subsequent pro-inflammatory cascade responsible for the production of prostaglandins
and thromboxanes.
There are two isoforms of COX. COX-1 is constitutively expressed in many tissue
types including the gastric mucosa and kidneys. It is also important in platelet aggrega-
tion. COX-2 is an inducible enzyme expressed at sites of inflammation. Conventional
NSAIDs inhibit both COX-1 and COX-2. Many of their side effects are related to the
inhibition of COX-1. Conventional NSAIDs are known to cause peptic ulceration and
gastric bleeding as well as acute renal failure.

Conventional NSAIDS include aspirin, diclofenac, etodolac, ibuprofen,

indomethacin, ketoprofen, ketorolac, nabumetone, naproxen, oxaprozin, piroxicam,
salicylsalicylic acid, sodium salicylate, and sulindac.
A few of these medications merit discussion.
A. Aspirin
Aspirin was one of the first substances recognized for its anti-inflammatory and anal-
gesic properties. It is available without a prescription. It is an irreversible inhibitor of
platelet COX, and is frequently used as an antiplatelet drug. Its antiplatelet activity
effect lasts 8 to 10 days—the life of the platelet.
B. Ketorolac
Ketorolac is an NSAID used mainly for its analgesic effects rather than for its anti-
inflammatory properties. It is used to augment or replace narcotic analgesic. It is gen-
erally administered intravenously or intramuscularly. However, an oral formulation
is available. Renal toxicity is a common side effect so cumulative dosage should be
limited.
C. Etodolac
Although etodolac is a nonselective NSAID, it has 10 times more COX-2 activity than
COX-1. It also has good analgesic properties.
D. COX-2 Inhibitors
These medications inhibit only the COX-2 isoform of COX. They have no effect on
COX-1. Therefore, these medications act specifically at the site of inflammation but
avoid the side effects associated with COX-1 inhibition. As they have no effect on
platelet function, they are commonly used for preemptive analgesia prior to surgery.
They are also commonly used in those with a history of gastrointestinal bleeding.
Although these medications do offer some advantages over nonselective COX inhibi-
tors, they do carry significant side effects. Rofecoxib (Vioxx) and valdecoxib (Bextra)
are no longer available. Currently, the only available COX-2 inhibitor is celecoxib
(Celebrex).
VI. Rheumatoid Medications
Rheumatoid arthritis is a systemic autoimmune disorder causing joint inflammation

and destruction. Systemic corticosteroids have a long history in the treatment of rheu-
matoid arthritis. They have anti-inflammatory properties but they also slow the process
of joint destruction. Although they are effective disease modifying antirheumatic drugs
(DMARDs), the pitfalls of long-term, high-dose systemic corticosteroid therapy are
well documented. Other DMARDs have subsequently been developed.
A. Methotrexate is a first-line agent. It inhibits polymorphonuclear chemotaxis and
the function of macrophages and lymphocytes. The dosages used to treat rheu-
matoid arthritis are much lower than those required in cancer treatment.
B. Agents that block tumor necrosis factor-a (TNF-a) are also commonly used.
TNF-a is a cytokine that has a central role in joint destruction in rheumatoid
arthritis. It interacts with TNF cell surface receptors on T cells and macrophages,
thereby inhibiting their function. These medications include adalimumab
(Humira), infliximab (Remicade), and etanercept (Enbrel).

C. Leflunomide (Arava) is another common DMARD. It inhibits dihydro-orotate

dehydrogenase, resulting in the arrest of cell proliferation during the G1 phase of
the cell cycle. Rapidly proliferating T cells are inhibited.
D. Other available DMARDS include chlorambucil, cyclophosphamide,
cyclosporine, azathioprine, chloroquine, hydroxychloroquine, gold,
penicillamine, and sulfasalazine.
Many patients with rheumatoid arthritis are treated with a combination of medications.
Use of TNF-a blockers or leflunomide in conjunction with methotrexate and sys-
temic corticosteroid therapy is common. In addition, many patients with rheumatoid
arthritis use NSAIDs to help control inflammation.
Perioperative management of antirheumatoid medication is complex and should
be done in consultation with the patient’s rheumatologist. Patients on long-term corti-
costeroid therapy may have suppression of the pituitary-hypothalamic axis. Therefore,
they may have temporary elevated requirements to compensate for postsurgical physi-
ologic stress. Methotrexate should be continued throughout the perioperative period,
regardless of the procedure. TNF-a antagonists and leflunomide should be continued
for minor surgeries. However, they should be temporarily withheld for more involved
procedures.
VII. Other Common Medications Used by Hand Surgical Patients
A. Antihypertensives
Medications to lower resting systolic and diastolic blood pressure can be
categorized into four broad categories based upon their mechanism of action:
1. Diuretic medications—reduce blood pressure by reducing serum volume
2. Sympathoplegic agents—lower peripheral vascular resistance, alter cardiac
function, and increase venous capacitance
3. Vasodilators—relax vascular smooth muscle and decrease peripheral vascular
resistance
4. Angiotensin-converting enzyme inhibitors—inhibit angiotensin function
B. Anticholesterol medications
Medications used to treat hypercholesterolemia work through a variety of
mechanisms.
1. Statin drugs are common medications used in the treatment of hypercholes-
terolemia. They block the synthesis of cholesterol in the liver through inhi-
bition of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase. These
medications are well tolerated. Rare side effects include mild hepatitis, myo-
sitis, and gastrointestinal symptoms (e.g., nausea and flatulence). Common
statin medications include atorvastatin (lipitor), fluvastatin (lescol), lovasta-
tin (mevacol), parastatin (pravachol), rosuvastatin (crestor), and simvastatin
(zocor).
2. Bile acid sequestrants include cholestyramine and colestipol. Circulating
cholesterol is the stock material from which bile is made. These medications
bind bile in the gut and prevent its reuptake. Bile stores are replenished by
circulating cholesterol. These medications remain in the gut and are not
absorbed. Therefore, they are felt to be safe. However, patient compliance
tends to be poor secondary to abdominal discomfort and diarrhea.
3. Ezetimibe (zetia) is a relative new medication. It inhibits uptake of choles-
terol in the gut.

4. Nicotinic acid, or niacin, is another name for vitamin B3. It improves the
cholesterol profile predominantly by increasing HDL. It has a minor effect
on lowering LDL. “Flushing” is a common side effect.
C. Heart failure medications
Heart failure occurs when cardiac output fails to meet physiologic demand.
Chronic heart failure carries significant morbidity and mortality. Many medi-
cations used to treat chronic heart failure are also used to treat hypertension.
These medications include antiangiotensin agents, beta-blockers, vasodilators,
and diuretics. They diminish physiologic cardiac demand by lowering preload,
peripheral resistance, and heart rate.
Other medications used to treat heart failure increase the contractility of
the heart. These drugs are referred to as positive inotropic agents. They include
cardiac glycosides such as digoxin as well as bipyridines such as amrinone and
milrinone. Cardiac glycosides increase free intracellular calcium. This calcium is
free to interact with actin and myosin in the cardiac sarcomere causing increased
contractility. Likewise, bipyridines enhance cardiac contractility by increasing
free intracellular calcium. However, they also have an important vasodilatory
effect. Therefore, these medications increase the contractility of the heart and
decrease the resistance against which it must pump.
D. Antiplatelet medication
These medications inhibit platelet aggregation and thrombus formation. They
are particularly effective arterial anticoagulants. They are particularly common in
those with a history of coronary artery disease and stroke. They function through
a variety of mechanisms.
Aspirin, as previously mentioned, exerts its effect on COX and prevents
the formation of thromboxane A2, which causes platelet aggregation. It is a par-
ticularly useful medication following replantation. Postreplant patients may be
advised to take 81 to 325 mg once a day, at least for the period of intimal repair
(5 to 7 days) and often for longer periods of time.
Clopidogrel (Plavix) and ticlopidine (Ticlid) inhibit platelet aggregation by
irreversibly blocking the ADP platelet surface receptor protein. These drugs have
no effect on prostaglandin metabolism.
There is no clear consensus on the use of antiplatelet medication in the
perioperative period, in hand surgery. Many practitioners permit continued
therapy throughout the perioperative period without experiencing increased
intraoperative bleeding or postoperative hematoma. Furthermore, termination
of antiplatelet therapy perioperatively should only be done after discussion with
the patient and other physicians involved in the patient’s care.
E. Thyroid medication
Patients deficient in thyroid hormone must have it replaced. This is most
commonly accomplished with an oral formulation of the T4 enzyme called
levothyroxine. This medication should be continued in the perioperative
period.
F. Insulin and oral antihyperglycemic agents
The elevated blood glucose associated with diabetes mellitus is a result of
absent or inadequate production of insulin. In some situations, the physiologic
response to circulating insulin may also be impaired.
1. Type I diabetics have an inability to produce insulin secondary to B-islet
cell destruction in the pancreas. Insulin replacement therapy is the focus of
treatment for these individuals. To maintain tight control of blood glucose

levels, a variety of formulations of varying duration of action have been

developed.
a) Rapid-acting formulations (aspart or lispro) begin to work within 5 to
15 minutes and are active for about 3 to 4 hours.
b) Short-acting formulations (regular insulin) begin working within 30
minutes and are active for about 5 to 8 hours.
c) Intermediate-acting formulations (NPH or lente) begin working in 1 to
3 hours and are active for about 16 to 24 hours
d) Long-acting formulations (ultralente) begin working in 4 to 6 hours and
are active for about 24 to 28 hours.
e) Insulin glargine and insulin detemir begin working within 1 to 2 hours
and are active for about 24 hours.
f ) Mixtures of varying proportions of NPH and regular insulin have been
developed to help maintain tight control of blood glucose.
Insulin does not have an oral formulation. It is administered subcutaneously
or, in some instances, intravenously. Recently, the food and drug administration
approved an inhalational formulation called Exubera.
2. Type II diabetics become resistant to insulin. Although these patients may
have the ability to produce insulin, they do not secrete adequate amounts to
accomplish the desired physiologic response. Treatment in these patients is
focused upon increasing insulin secretion from the pancreas as well as height-
ening sensitivity to circulating insulin. There are four classes of oral antihy-
perglycemic agents:
a) Insulin secretagogues increase insulin release from the pancreas. They
include the sulfonylureas (e.g., glyburide, glipizide, and glimepiride),
the meglitinides (e.g., repaglinide and nateglinide), and d-phenylalanine
derivatives (e.g., nateglinide).
b) Biguanides such as metformin reduce blood glucose through a variety of
mechanisms. They stimulate tissue glycolysis, reduce hepatic and renal
gluconeogenesis, decrease GI absorption of glucose, and reduce plasma
glucagon levels.
c) The thiazolidinediones decrease insulin resistance by regulating genes
involved in glucose and lipid metabolism.
d) a-glucosidase inhibitors include acarbose and miglitol. They work in the
gut to prevent the breakdown of polysaccharides and starches into mono-
saccharides. Only monosaccharides such as glucose and fructose can be
absorbed from the intestinal lumen.
Patients who fast prior to surgery should discontinue their scheduled insu-
lin or oral antihyperglycemic medications to avoid iatrogenic hypoglycemia.
Instead, regular insulin should be administered as needed based upon a gradu-
ated scale of increasing hyperglycemia (sliding scale).
Suggested Readings
Abrams RA, Botte MJ. Hand infections: Treatment recommendations for specific types. J Am
Acad Orthop Surg. 1996;4(4):219–230.
Goldfarb CA, et al. Extra-articular steroid injection: Early patient response and the incidence of
flare reaction. J Hand Surg (Am). 2007;23(4):1513–1520.
Howe CR, Gardner GC, Kadel NJ. Perioperative medication management for the patient with
rheumatoid arthritis. J Am Acad Orthop Surg. 2006;14(9):544–551.

Katzung BG, ed. Basic and Clinical Pharmacology. 9th Ed. New York, NY: The McGraw-Hill
Companies; 2004.
Morris CD, Einhorn TA. Principles of orthopaedic pharmacology. In: Buckwalter JA, Einhorn
TA, Simon SR, eds. Orthopaedic Basic Science: Biology and Biomechanics of the Musculo-
skeletal System. 2nd Ed. Roosemont, IL: American Academy of Orthopaedic Surgeons;
2000:217–238.
Phillips WJ, Currier BL. Analgesic pharmacology II: Specific analgesics. J Am Acad Orthop Surg.
2004;12(4):221–233.

Arthroscopy
5
Michael S. Bednar and Charles A. Goldfarb
General Principles
I. Setup
Arthroscopy for the hand and wrist is performed with the patient in supine position
and the extremity on a stable arm table. A nonsterile tourniquet is placed and inflated
after exsanguination. A traction tower is utilized to allow the elbow and forearm to be
stabilized while the wrist or finger joints are distracted using weight applied through
finger-traps. For a wrist arthroscopy, either 2 or 4 finger-traps are applied to the digits;
for a thumb or finger arthroscopy, a single finger-trap is applied. The arthroscopy tower
is placed at the foot of the operating table for easiest viewing of the monitor. If a mini
fluoroscopy machine is utilized, it can be brought into the operative field from the
end of the arm table. Complications of the traction tower include over distraction of a
joint (limit traction to 10 lb) and heat or pressure injury from the metal traction tower
(assure tower is cool and pad extremity).
II. Equipment and General Guidelines (Fig. 5.1)
A. Wrist arthroscopy is performed using a 2.4 or 2.7 mm, 30-degree arthroscope.

B. Due to the close proximity of the cutaneous nerves, portals are created with a
skin incision only. A small curved clamp is used to dissect through the tissue to
the capsule of the joint
C. A blunt trochar in the arthroscope cannula is used to establish the viewing portal.
D. A shaver is utilized through the working portal. The shaver is typically 2.9 mm
in size, and the aggressiveness is dependent on the type of blade. Suction tubing
is attached to the shaver to remove the debris created in the shaving process.
E. Lactated Ringer fluid is used during arthroscopy. The fluid flows into the joint
through gravity (i.e., fluid pumps are not typically utilized).
F. A probe is used as a tool to evaluate the soft tissues of the joint including the
ligaments and the triangular fibrocartilage complex (TFCC). For arthroscopy
of the hand, these probes are also useful for reducing displaced ligaments. The
probes typically have a 2 to 3 mm curved tip for measurement and manipula-
tion purposes.
G. Toothed graspers are helpful for the removal of debris or loose bodies.
H. Suction punches allow biting of tissue and removal through suction tubing.
I. A 2.9 mm burr may be utilized for bone removal such as a distal ulna resection
or partial trapeziectomy.
J. A TFCC repair kit allows a minimally invasive technique for TFCC repair
with curved needles allowing the passage of suture and a snare to retrieve the
suture.
44

Chapter 5 • Arthroscopy 45
Shaver Power
Video Camera Monitor VCR
Pump Illuminator
Wrist Arthroscopy Tower
Figure 5.1 A: Diagram of OR setup for wrist/hand arthroscopy. The patient is in

supine position with the upper extremity on an arm board. The surgeon sits by
the patients head and should have clear visualization of the monitor. B: Example
of arthroscopy traction tower. The fingers are placed in finger-traps and the arm is
secured to the base of the tower.

K. Tuohy needles (blunt tip anesthesia needles) may also be used to repair TFCC
tears, especially ulnar-sided tears.
L. A suction trap may be placed in the suction tubing to “trap” shaved particles,
synovitis, and debris; the collected tissue can then be sent to the lab for analysis.
M. Small joint radiofrequency probes may be utilized for tissue removal or for heat
shrinkage applications such as scapholunate (SL) instability or carpometacarpal
(CMC) joint instability.
Hand Arthroscopy
I. Introduction
Arthroscopy of the hand is gaining popularity as it allows a minimally invasive tech-

nique for evaluation and treatment of selected joint-based problems. The joints most
amenable to arthroscopy are the thumb CMC joint, the thumb metacarpophalangeal
(MCP) joint, and the finger MCP joints. The principles of and setup for a hand arthros-
copy follow the guidelines summarized earlier in this chapter with a few caveats. First, a
2.4 or 2.7 mm arthroscope will provide excellent visualization but, in some patients, a
1.9 mm arthroscope may be more appropriate as the smaller size allows for easier mobil-
ity inside the joint (with a downside of increased fragility of the scope). And second,
while thermal devices may be utilized in the hand, care must be utilized given the close
proximity of the cutaneous nerves and the smaller fluid volume of the joints (the fluid
helps dissipate the heat).
II. Thumb CMC Joint Arthritis
A. The thumb CMC joint is the second most commonly arthritic joint in the hand
and postmenopausal women are the most frequently affected. Patients present
with localized pain and decreased function. When nonoperative treatment fails,
surgical intervention can be very helpful in alleviating symptoms. One surgical
option is the arthroscopic treatment of CMC arthritis.
B. Setup/portals (Fig. 5.2)
1. A high brachial tourniquet is used.
2. The patient is in supine position on the operating table with the arm on a
stable arm board.
3. The arm is exsanguinated, and the thumb is suspended in a traction tower
through a finger-trap with 8 to 10 lb of traction applied.
4. A needle is used to localize the joint (and insufflate with saline). A mini-
fluoroscopy machine may be used to confirm needle placement.
5. The 1U portal is established just ulnar to the extensor pollicis brevis (EPB)
tendon by incising the skin only and bluntly dissecting to and through the
joint capsule.
6. The small joint arthroscope is placed into the CMC joint.
7. Needle localization of the 1R portal (radial to abductor pollicis longus
[APL]) or the thenar portal (more volar and through thenar muscle bulk) is
performed to help establish a working portal.
8. Alternating the viewing and working portals will facilitate complete joint
evaluation and treatment.

MII
MI
MIII
1-R 1-U
Tm
r.a.
EPL
APL s.r.n
EPB
Figure 5.2 Diagram of portals for trapeziometacarpal arthroscopy. The 1R portal is

radial to the APL and the 1U portal is ulnar to the EPB. Care must be taken to avoid the
sensory branch (s.r.n) of the radial nerve in addition to branches of the radial artery (r.a).
C. Procedure
Arthroscopy allows a minimally invasive approach, and, when compared to open
procedures can offer equal effectiveness.
1. Arthroscopy allows joint evaluation, debridement (including loose body
removal), and synovectomy.
a) In patients with early stage disease, joint debridement may be combined
with an extra articular procedure such as a dorsal closing-wedge osteot-
omy of the metacarpal to change the loading pattern of the joint.
b) In patients with notable loss of cartilage, a partial trapeziectomy (3 mm
of distal trapezium) utilizing a 2.9 mm burr may be performed. A distrac-
tion pinning of the joint or a tendon interposition (most commonly the
palmaris longus tendon) can be performed.
D. Complications of this approach include the following:
1. Cutaneous nerve irritation from portal placement (the s-2 or s-3 branches of
the superficial branch of the radial nerve)
2. Injury to the radial artery (rare given it is several millimeters more proximal
at the scaphotrapezial trapezoid joint)

3. Interpositional graft extrusion (rare given small capsular opening for arthroscopy)
4. Failure to relieve pain
5. One benefit of the arthroscopic approach is that the larger, open procedure
may be performed if the minimally invasive procedure fails.
III. Thumb MP Joint Ulnar Collateral Ligament Injury
A. An injury to the ulnar collateral ligament (UCL) of the thumb MCP joint is
typically managed with cast or splint immobilization for 4 to 6 weeks. How-
ever, in patients with a complete ligament tear with retraction of the ligament
superficial to the adductor aponeurosis (Stener lesion), healing of the ligament
to bone cannot occur. Those patients with a Stener lesion typically have marked
MCP joint instability, and a risk of chronic instability at the thumb MCP joint
if not addressed. Open reduction of the UCL and reattachment to the base of
the proximal phalanx (often with suture anchor) is a reliable procedure.
B. An alternative treatment is an arthroscopic joint assessment and manipulation
of the UCL with a probe to allow it to assume its natural position deep to
the adductor aponeurosis. If the tendon can be restored to its normal posi-
tion adjacent to the base of the proximal phalanx, healing should occur reliably
with immobilization alone. This avoids the need for an open incision and hard-
ware placement. The setup is the same as for CMC arthroscopy. The portals are
established on the dorsal ulnar and radial aspect of the extensor mechanism.
IV. Idiopathic MCP Joint Synovitis
Rarely, one or more MCP joints may be affected with painful synovitis. Laboratory
evaluation including inflammatory labs may also be helpful in establishing a diagnosis.
Typically anti-inflammatory medications or a steroid injection will resolve the inflam-
mation. However, if these evaluations and treatments are unsuccessful in confirming a
diagnosis and improving symptoms, arthroscopy evaluation, debridement, and biopsy
may be helpful. The benefit of the arthroscopic approach is the avoidance of an open
incision with detachment (and repair) of the sagittal band. Arthroscopy allows a biopsy
of the tissue and a complete synovectomy with a 2.9 mm shaver.
Wrist Arthroscopy
I. Introduction
Diagnostic wrist arthroscopy provides a visual inspection of the articular surfaces, trian-
gular fibrocartilage complex, intra-articular portions of the intercarpal and intracarpal
ligaments, and wrist capsule of the radiocarpal and midcarpal joints.
Therapeutic wrist arthroscopy is used for
1. Synovial, ligamentous, cartilaginous, or loose body debridement
2. Arthroscopic assisted repairs of peripherial TFCC tears
3. Treatment of ulnocarpal impaction syndrome, including lunotriquetral (LT)
ligament debridement, central TFCC debridement, and distal ulnar resection
4. Ganglion excision
5. Reduction of intra-articular fractures

II. Diagnostic Wrist Arthroscopy
A. Portals (Fig. 5.3)

1. Radiocarpal
a) 1–2 portal is located in the anatomic snuffbox between the EPB and
extensor pollicis longus (EPL) tendon and is within 3 mm of the radial
artery and dorsal sensory branch of the radial nerve. This can be used as a
working portal for arthroscopic radial styloidectomy.
b) 3–4 portal is located between the EPL and extensor digitorum comminus
(EDC) tendons, 1 cm distal to Lister tubercle and just proximal to the SL
interval. It is used as the primary viewing portal, allowing visualization of
70% of the radiocarpal joint. There are no underlying vessels or nerves.
c) 4–5 portal is located between the EDC and extensor digitorum quinti
(EDQ) tendons at the insertion of TFCC into radius. There are no
underlying vessels or nerves. This is the primary portal for probing and
debridement and is used as a viewing portal to evaluate the LT ligament
and the ulnar aspect of the TFCC.
d) 6R portal is located between the EDQ and the extensor carpi ulnaris
(ECU), distal to the ulnar styloid. Branches of the dorsal sensory branch
of the ulnar nerve are near this portal. It can be used as a viewing portal
for visualization of the LT ligament, pisotriquetral recess, ulnotriquetral
(UT) ligament and ulnar aspect of the TFCC.
e) 6U portal is located ulnar to ECU tendon and the dorsal sensory branch
of the ulnar nerve is close to this portal. It is primarily used as an outflow
portal.
f ) Palmar—The palmar radiocarpal portal is located between the radiosca-
phocapitate and long radiolunate ligaments, approximately 3 mm from
radial artery and palmar cutaneous branch of the median nerve. The site
of this portal is visualized from 3–4 portal. A switching stick is placed
between ligaments and passed radial to the FCR to avoid injuring the
median nerve. A cannula is slid over switching stick to establish portal.
This gives visualization of palmar portion of SL ligament and dorsal
radiocarpal capsule. It is reported to facilitate arthroscopic assisted reduc-
tion of intra-articular distal radius fractures.
2. Midcarpal
a) Radial—The radial midcarpal is located 1 cm distal to 3–4 portal and
positions the scope between the scaphoid and proximal pole of capitate. It
allows the visualization of distal pole of scaphoid, scaphotrapezoid joint,
proximal pole of the capitate, and the SL articulation.
b) Ulnar—The ulnar midcarpal portal is located 1 cm distal to 4–5 portal,
between the LT and capitohamate joints. It allows visualization of the LT
articulation, triquetral hamate articulation, and the ulnar margin of capitate.
c) Scaphotrapeziotrapezoid (STT)—The STT portal is located at the ulnar
margin of EPL, between extensor carpi radialis longus (ECRL) and
extensor carpi radialis brevis (ECRB) tendons, in close proximity to the
dorsal sensory branches of the radial nerve.
3. Distal radioulnar
a) Proximal—proximal to ulnar head at sigmoid notch
b) Distal—between ulnar head and TFCC

EPL EDQ
8
2
6
4 7
1 9
3 5
10
11
ECU
ECRL
ECRB EDC
External Land Marks

1. 1R portal 7. 6R
2. STT portal 8. Triquetral hamate
3. 3-4 portal 9. 6U
4. RMC portal 10. DRUJ distal
5. 4-5 portal 11. DRUJ proximal
6. UMC portal
Figure 5.3 Diagram of portals for wrist arthroscopy. The radiocarpal portals are
named for their relationship to the extensor compartments. The 3–4 is the most
commonly used portal and is considered the working portal for most procedures.
The midcarpal portals are termed radial (scaphocapitate joint) and ulnar (the space
between the capitohamate and lunatotriquetral joints). The DRUJ portals are termed
proximal and distal.

B. Arthroscopic setup
1. Patient is in supine position with the arm on arm table with elbow in 90
degree of flexion. The arm strapped to arm table with care taken to pad the
cubital fossa. Distraction is used with overhead traction or free standing trac-
tion apparatus, with 10 lb of traction placed across wrist through finger-traps
applied to the middle and ring fingers.
C. Diagnostic arthroscopy
1. Radiocarpal joint
a) Establishing portals
1) An 18-gauge needle attached to a 20 cc saline filled syringe is inserted
into the 3–4 portal. The needle is angled with the inclination of the
radius: Approximately 22 degree in a volar direction and 12 degree in
the ulnar direction.
2) If there is not an intercarpal ligament or TFCC tear present, the joint
should fill with 5 to 7 cc of saline. If joint takes more than 10 cc,
palpate over midcarpal joint and distal radioulnar joint (DRUJ) to
determine site of the perforation.
3) The needle is withdrawn and only the skin is incised. Blunt dissection
is used to the depth of the wrist capsule and the arthroscopic blunt
trocar and sheath are inserted in the same direction as the needle.
4) A 2.7 mm arthroscope with 30 degree viewing angle inserted and irri-
gation inflow is initiated through the arthroscopic cannula, allowing
visualization of the prestyloid recess.
5) An 18-gauge needle is placed from 6U portal into the prestyloid recess
and is used as an outflow cannula.
6) An 18-gauge needle placed through 4–5 or 6R portal (surgeon’s choice):
The entry point should be distal to the capsular insertion of the TFCC
and the angle of portal should allow probing to radial styloid.
7) The skin over portal incised once proper placement is established and
blunt dissection to the capsule is completed prior to penetrating the
joint.
b) Viewing joint
1) The arthroscope is placed through the 3–4 portal and wrist is inspected
toward the radial aspect of the joint, visualizing the radial styloid and
scaphoid to the STT joint. Next, the arthroscope is advanced deeper
into the joint to allow the visualization of the radioscapholunate and
long radiolunate ligaments.
2) The scope is then withdrawn to allow visualization of the proximal
pole of scaphoid and then moved ulnar to membranous portion of the
SL ligament, looking for a perforation. The ligament is followed dis-
tally to the dorsal SL ligament. If a tear in the ligament is identified,
attempt “drive through” test, entering the midcarpal joint from the
radiocarpal portal.
3) Continue ulnarly to inspect the lunate and lunate facet of the radius.
4) Inspect the insertion of TFCC into the sigmoid notch; then move in
an ulnar direction inspecting the central TFCC, looking for degenera-
tive wear suggestive of ulnocarpal abutment syndrome. If a central
perforation is present, place scope into hole to inspect the ulnar head:
Pronation and supination of the forearm allow inspection of the entire
ulnar head.

5) Visualize the dorsal capsular insertion of the TFCC, looking for

synovitis, which may be suggestive of a peripheral TFCC tear. Next,
palpate the tension of the TFCC with a probe placed through the 4–5
or 6R portal looking for loss of the “trampoline effect,” diagnostic of
a peripheral TFCC tear.
6) Switch scope to 4–5 or 6R portal to allow better visualization of the
ulnar aspect of lunate, LT ligament, and triquetrum, looking for evi-
dence of ulnocarpal abutment syndrome. Inspect the ulnolunate (UL)
and UT ligaments.
7) The scope is then directed radially to look for neck of dorsal carpal
ganglion at distal edge of dorsal SL ligament.
2. Midcarpal joint
a) Establishing portal
1) An 18-gauge needle is inserted and saline is injected into the radial
midcarpal joint. If there is not a perforation of the SL or LT ligament,
the joint should fill with 3 to 5 cc of fluid. Following the skin incision
and blunt dissection to the capsule, a blunt trocar and cannula can be
inserted.
2) In osteoporotic individuals, trocar can enter the neck of the capitate
instead of the midcarpal joint.
b) Viewing joint
1) Inspect the STT joint, looking for degenerative changes. Then follow
the scaphocapitate joint proximally to the SL joint. Look for widening
of the joint, the tilt of the lunate and congruity of the concave surfaces
of the two bones. A probe may be placed in the SL interval.
2) SL dissociation can be described as classified by Geisler:
a. Grade I
i) Proximal membranous portion of SL ligament bulges
ii) No abnormalities from midcarpal portal
b. Grade II
i) Slight palmar flexion of scaphoid seen from radial midcarpal
joint
ii) Dorsal edge of scaphoid no longer aligns with lunate
iii) A 1 mm probe can enter the space, but not pass through it
c. Grade III
i) Interosseous spaces separates
ii) A 1 mm probe may be passed through the interosseous liga-
ment tear and twisted
d. Grade IV
i) Complete tear of dorsal and palmar SL ligaments
ii) 2.7 mm scope can be passed from midcarpal joint to radiocar-
pal joint
3) Continue ulnarly to assess the LT ligament (tears can be graded in
similar fashion to SL).
4) Determine if the lunate has an articulation with the hamate (type II
lunate) and if there is corresponding chondromalacia of the proximal
hamate.
5) If ulnar structures inadequately visualized or debridement required,
ulnar midcarpal portal made with an 18-gauge needle while visualized
from the radial midcarpal portal.

3. DRUJ arthroscopy
a) Establishing portal
1) To relax the dorsal capsule, place the forearm in supination. The prox-
imal portal is established with trocar aimed slightly distal. The distal
portal incision is preceded by insertion of an 18-gauge needle to avoid
damage to dorsal capsular insertion of the TFCC.
2) 1.7 or 2.0 mm scope easier to pass into distal portal
b) Viewing joint
1) From the proximal portal, assess articular cartilage of ulnar head and
sigmoid notch. From the distal portal, assess undersurface of TFCC,
ulnar head, and ulnocarpal ligaments.
III. Therapeutic Wrist Arthroscopy
A. Debridement
1. Synovium
a) Synovial biopsy can be performed with a biter/grasper or by collecting
specimens from the shaver.
b) Used to help diagnose
1) Rheumatoid arthtis
2) Crystalline arthritis (gout and pseudogout)
3) Pigmented villonodular synovitis
4) Infection
c) Complete synovectomy
1) Indicated in rheumatoid arthritis if
a. Well-preserved joints when medical management has not been
successful.
2) Contraindicated when
a. Dorsal tenosynovitis is present due to an increased risk of tendon
rupture
b. Very thin skin due to increased risk of skin avulsion from finger-traps
2. Ligament
a) Debridement of partial SL or LT ligament tear may decrease symptoms
of joint irritation from the ligament stump. The membranous portion of
the ligament is usually debrided.
b) Switch scope and shaver between 3–4 and 4–5/6R portals from proper
viewing and shaving.
3. Cartilage
a) Common sites
1) Proximal pole of hamate
2) Distal pole of scaphoid
3) Ulnar side of lunate
4) Proximal pole of scaphoid
b) Grade (derived from Outerbridge)
1) Grade I—softening of cartilaginous surface
2) Grade II—fibrillation and flattening of surface
3) Grade III—fibrillations to varying depths and poorly attached seg-
ments of cartilage (“crabmeat”)
4) Grade IV—full thickness loss of cartilage with visible sclerotic
subchondral bone

c) Treatment—Dependent upon grade and size of lesion

1) Grades I to III
a. Debride synovitis and surface fibrillation to normal cartilage
2) Grade IV
a. Debride cartilage to stable rim. Drill holes into subchondral bone
to stimulate bleeding.
b. May resect 1 to 2 mm depth of bone with bur from central crater
to stimulate fibrocartilage (chondroplasty).
B. Peripheral TFCC repair
1. TFCC anatomy
a) Central disc
1) The TFCC is considered to be a U shaped structure, with the bottom
of the U attached to the ulnar styloid and the open arms of the U
attached to the palmar and dorsal rims of the sigmoid notch of the
radius, the central disc is the open space between the arms of the U,
which attaches to the ulnar rim of the sigmoid notch
2) Avascular collagen is arranged in random, wavelike pattern
b) Peripheral TFCC
1) Well vascularized, linearly arranged collagen bundles that begin at the
ulnar fovea and styloid and attach to the palmar and dorsal rims of the
sigmoid notch of the radius, also attach to the UL and UT ligaments
palmarly and the wrist capsule under the fifth and sixth compartments
dorsally
2) Major stabilizer of DRUJ in forearm rotation
2. Classification of traumatic TFCC tears (Palmer)
a) IA
1) Central tear—occurs 2 to 3 mm from attachment of central TFCC to
sigmoid notch
b) IB
1) Peripheral tear, from origin at ulnar styloid, with or without styloid
fracture
2) Many dorsal tears of the TFCC from the fifth and sixth compartment
capsule also considered to be of this type.
c) IC
1) Peripheral tear along the volar margin along the attachments of the UL
and UT ligaments
2) Least common type of TFCC tear
d) ID
1) Peripheral tear with avulsion of TFCC from insertion into sigmoid
notch
2) Most commonly occurs following distal radius fracture
3. Diagnosis
a) Pain over ulnar wrist
1) Point tenderness between ulnar styloid and flexor carpi ulnaris (FCU)
tendon at ulnocarpal joint line (foveal region)
2) Instability and pain with stressing DRUJ in neutral, pronation, and
supination
b) Radiographic
1) X-ray—Determine ulnar variance and assess for ulnocarpal abutment
syndrome if ulnar variance positive

2) MRI
a. Best for detecting radial and central TFCC tears
b. Lacks sensitivity to detect ulnar-sided TFCC tears
c) Arthroscopic
1) Loss of trampoline effect
a. Probe placed through 4–5/6R portal
b. Loss of tension of TFCC when probe is pushed against it
2) Synovitis
a. At dorsoulnar insertion of TFCC into capsule
b. Need to remove to find TFCC detachment from capsule
4. Technique
a) The scope is placed in the 3–4 portal and the shaver in 4–5/6R
b) Debride synovitis and rim of TFCC to stimulate bleeding
c) Make a 1-cm incision over fifth dorsal compartment
d) Retract EDQ and/or ECU tendon
e) Place two long 16-gauge needles across capsule and into TFCC
f ) Wire loop is placed through one needle to capture a 2–0 monofilament,
absorbable suture
g) 2–4 sutures are placed across the TFCC tear
h) All sutures are tied over the wrist capsule with care taken not to entrap
tendon or a branch of the dorsal sensory branch of the ulnar nerve
i) Post-operative rehabilitation
1) Long arm/Munster cast for 4 to 6 weeks
2) Begin forearm rotation at 4 to 6 weeks
3) Begin strengthening at 6 to 8 weeks
C. TFCC debridment
1. Classification of degenerative TFCC lesions (Palmer)
a) IIA—Wearing of TFCC without perforation or chondromalacia
b) IIB—Wearing of TFCC with chondromalacia of the lunate or ulna
c) IIC—Perforation of the TFCC with lunate chondromalacia
d) IID
1) Perforation of the TFCC with lunate and/or ulna chondromalacia
2) LT ligament perforation without static carpal instability
e) IIE
1) TFCC perforation
2) Ulnocarpal arthritis
2. Technique
a) Similar to TFCC repair
b) Debride with combination of 2.0 to 3.0 full radius shaver, suction punch,
biters, arthroscopic knives, and electrocautery probes
c) Remove only unstable central TFCC
1) Do not incise/excise dorsal or palmar DRUJ ligaments.
2) Do not remove more than central two third of the TFCC.
d) Post-operative rehabilitation
1) Splint for comfort for 1 week.
2) Intermittent splinting and restriction of forceful grasping and repeti-
tive activities for 1 month.
D. Distal ulna resection
1. Indications
a) Palmer IIC and D lesions

b) If static carpal instability is present, consider ulnar shortening osteotomy

to tighten UL and UT ligaments
2. Technique
a) Debride central TFCC perforation as described until ulnar head is
visualized.
b) Rotating forearm allows the visualization of entire head.
c) 4 mm burr placed, burr in one location until sheath stops further debri-
dement by burr (~2 to 3 mm).
d) Slowly rotate forearm to level entire head to this depth of resection.
e) Shaver placed in distal DRUJ portal to remove rim of bone next to sig-
moid notch.
f ) Check adequacy of resection with fluoroscopy.
g) Post-operative rehabilitation
1) Long arm splint for 1 week
2) Begin range of motion at 1 week
3) Begin strengthening at 4 to 6 weeks
4) Expect tenderness over distal ulna for 2 to 3 months
E. Dorsal carpal ganglion excision
1. Indications
a) Not responsive to aspiration, with or without cortisone
b) Painful or cosmetically unappealing
2. Technique
a) Scope placed through 4–5/6R portal and the dorsal SL ligament is visual-
ized. A pear shaped stalk visible in two third of wrists. If stalk is not seen,
assume origin of DCG is from dorsal capsule. A needle is placed through
skin into the ganglion sac to reach the stalk. This will be in the region of
the 3–4 portal. A 1 cm area of dorsal capsule is removed at origin of stalk
with shaver or suction punch, taking care to avoid dorsal SL ligament in
resection. Decompress any remaining fluid in the ganglion sac. If the sac
is large, it can be excised by extending arthroscopic portal.
b) Post-operative rehabilitation
1. Splint for 1 week
2. Begin range of motion
3. Delay full activities for 6 weeks
F. Arthroscopic-assisted reduction of distal radius intra-articular fractures
1. Indications
a) Articular displacement greater than 2 mm
b) Best for aligning radial styloid fractures
c) May be used to determine adequacy of reduction of dye-punch fractures.
d) Assess intracarpal ligament pathology.
2. Technique
a) Best performed 3 to 7 days after fracture as it is difficult to see past acute
bleeding before 3 days and difficult to manipulate fracture fragments after
7 days
b) The forearm is wrapped with elastic bandage to limit fluid extravasation
through the fracture and into forearm. The scope placed through 3–4
portal and outflow is established through 6U portal. The joint is flushed
with irrigation solution through gravity feed only. The shaver is placed
through 4–5 or 6R portal to remove clot.

c) The fracture is reduced using 0.0625 K-wires placed into fracture

fragments. The articular surfaces are aligned under arthroscopic visualiza-
tion and the K-wires are advanced across fracture. The wires may be sup-
plemented with cannulated screws or plates if desired for more definitive
fixation.
d) For radial styloid fractures, assess SL interval for ligament tear and SL
instability.
G. Arthroscopic-assisted reduction of scaphoid fractures
1. Indications
a) Displaced but reducible scaphoid fractures
b) Assess adequacy of reduction
2. Technique
a) Scope placed through radial midcarpal portal and the scaphoid is reduced
with joysicks placed in the distal and proximal poles to facilitate reduc-
tion. The K-wire for a cannulated screw is placed in the long axis of the
scaphoid while maintaining reduction and the compression screw is
inserted.
Suggested Readings
Badia A. Arthroscopy of the trapeziometacarpal and metacarpophalangeal joints. J Hand Surg.

2007;32(A):707–724.
Bettinger PC, et al. An anatomical study of the stabilizing ligaments of the trapezium and
trapeziometacarpal joint (gross and arthroscopic). J Hand Surg. 1999;24(a):786–798.
Corso SJ, et al. Arthroscopic repair of peripheral avulsions of the triangular fibrocartilage complex
of the wrist: A multicenter study. Arthroscopy. 1997;13:78–84.
Culp RW, Ostermann AL, Kaufmann RA. Wrist arthroscopy: Operative procedures. In: Green
DP, Hotchkiss RN, Pederson WC, Wolfe SW, eds. Green’s Operative Hand Surgery. 5th Ed.
Philadelphia, PA: Elsevier, Churchill Livingstone; 2005:781–803.
Ekman EF, Poehling GG. Principles of arthroscopy and wrist arthroscopy equipment. Hand Clin.
1994;10(4):557–566.
Hofmeister EP, et al. The role of midcarpal arthroscopy in the diagnosis of disorders of the wrist. J
Hand Surg (Am). 2001;26:407–414.
Osterman AL, Raphael J. Arthroscopic resection of dorsal ganglion of the wrist. Hand Clin North
Am. 1995;11:7–12.
Palmer AK. Triangular fibrocartilage complex lesions: A classification. J Hand Surg (Am)
1989;14:594–606.
Ruch DS, Poehling GG. Wrist arthroscopy: anatomy and diagnosis. In: Green DP, Hotchkiss RN,
Pederson WC, Wolfe SW, eds. Green’s Operative Hand Surgery. 5th Ed. Philadelphia, PA:
Elsevier, Churchill Livingstone; 2005:769–779.
Walsh EF, et al. Thumb carpometacarpal arthroscopy: A topographic, anatomic study of the thenar
portal. J Hand Surg. 2005;30(A):373–379.
Whipple TL, et al. Wrist arthroscopy. Instr Course Lect. 1995;44:139–145.

Amputations and Prosthetics
6
Warren C. Hammert
Amputations in the upper extremity differ significantly from those in the lower
extremity. Sensation is more important in the hand as its absence prevents activity
without direct vision. Patients with lower extremity amputations tend to function fairly
well in comparison to those of the upper extremity at comparable levels. For example, a
below knee amputee tends to have less difficulty with daily activities in comparison to a
below elbow amputee. Fortunately, upper extremity amputations are less common than
those involving the lower extremity and often are at a more distal level.
Upper extremity amputations can result from a number of conditions, including
trauma, congenital deformities, such as vascular malformations, and acquired condi-
tions, such as tumors or chronic vascular disorders.
I. Goals of Amputation
Regardless of the cause, certain points are important to maximize function and mini-
mize morbidity following amputations.
1. Preservation of functional length
2. Provide durable coverage
3. Maintain sensibility and minimize symptomatic neuromas
4. Early return to work and activities
5. Early fitting of prosthetics when applicable
Fingertip injuries and soft tissue flaps for their reconstruction will be covered in the
chapter on soft tissue coverage.
II. General Principles
A. Management of the Neurovascular Bundle

The nerve and artery should be separated. Any transection of a nerve will result in a
neuroma. The goal of nerve management during amputation is to place the nerve stump
in a well-padded area away from the surgical scar. This can be accomplished by placing
gentle traction on the nerve, sharply transecting it, and allowing it to retract proximally
under healthy soft tissue with minimal mechanical contact. The artery should be cau-
terized and allowed to retract proximally away from the surgical scar.
B. Management of Tendons
As a general rule, both flexor and extensor tendons are pulled distally, transected, and
allowed to retract proximally. The extensors will retract much less than the flexors due
to attachments to other structures (i.e., lateral bands, sagittal bands, and adjacent exten-
sor tendons via juncturae). They should never be pulled distally, or sutured together to
58

Chapter 6 • Amputations and Prosthetics 59
act as a source for coverage of exposed bone, as this will prevent the normal excursion of
both tendons and compromise the function of the remaining digits.
C. Management of Bone
Bone ends should be trimmed and smoothed so that there are no sharp areas or spikes,
which may be sensitive or tender following healing. When the amputation is through
the joint and cartilage is present, the condyles are trimmed, creating a smooth, rounded
contour. Often, the central portion of the cartilaginous surface can be left in place,
creating a smooth tip.
D. Management of Soft Tissue

The goal of soft tissue coverage should be to provide well-padded coverage of the ampu-
tation stump without tension on the skin closure. This can be completed with local soft
tissue flaps or regional flaps, if necessary to preserve functional length. Skin grafts over
exposed bone are not durable and often tender when the patient attempts to touch the
end of the injured finger.
E. Management of the Thumb

Amputations through the thumb require special consideration because of the impor-
tance of the pinch, grasp, and gripping activities. The maintenance of length is also
important. Amputations involving the distal phalanx will typically result in a functional
thumb. Effort should be undertaken to provide durable sensate soft tissue coverage with
the liberal use of flaps. In addition, greater efforts should be taken to replant a thumb
when possible. Amputations proximal to the IP joint should be managed so that future
reconstructive options are available.
Local soft tissue coverage can often be obtained by the use of a Moberg flap. This
involves making midaxial incisions on the radial and ulnar aspects of the thumb,
and elevating the volar skin containing both neurovascular bundles. The flap is then
advanced distally, allowing closure of wounds up to 2 cm in length. This technique
involves flexion of the IP joint requiring therapy to regain extension and some patients
may be left with an IP joint flexion contracture. Slight further advancement can be
obtained with a transverse skin incision at the level of the MP joint flexion crease. This
creates a proximal defect, which typically is skin grafted. Alternatively, it can be left to
heal secondarily, but this increases the risk of development of a contracture. This tech-
nique is reliable in the thumb due to the independent dorsal blood supply, but poses a
risk in the fingers, as dorsal skin necrosis may occur.
III. Digital Amputations
A. Distal Phalanx
Amputations of the distal phalanx can often be managed by trimming the bone below
the soft tissue, so it is not exposed and covering with local flaps or allowing healing by
secondary intention. If the amputation is proximal to the lunula of the nail, there in
no advantage to trying to maintain the nail, and the nail matrix can be ablated at the
time of amputation revision. The maintenance of the DIP joint is advantageous if the
FDP and terminal extensor tendon insertions are intact. This will allow for greater grip
strength and better overall hand function. If the tendon insertions cannot be main-
tained, amputation can be completed at the level of the DIP joint, as there is no advan-
tage in maintaining a small remnant of the distal phalanx.

B. DIP Joint
Amputations though the DIP joint are managed by rounding the condyles, removing the
volar plate, and providing a smooth contour to the middle phalangeal head. Alternatively,
there may be some merit in maintaining the volar plate and suturing the FDP tendon to
the volar plate. This will maintain the proper length and tension on the FDP, increasing
the power grip, and decreasing the chance of developing a lumbrical plus finger.
C. Middle Phalanx
Amputations through the middle phalanx can be shortened to allow adequate local soft
tissue coverage, as long as the insertion of the FDS and central slip is maintained. This
will not only help with flexion of the PIP joint but will also increase MP joint flexion
by approximately 50% (from 45 to 90 degrees). When the index finger is involved,
patients will bypass this digit and use the middle finger for pinch and grasp. If the FDS
insertion has not been maintained, there is not a significant advantage to maintaining
the middle phalanx, as this joint will not flex. Although the additional length may be
advantageous from a cosmetic standpoint, the lack of functional benefit will usually
result in an amputation at the PIP joint.
D. PIP Joint
Amputations through the PIP joint are managed in the same manner as those through
the DIP joint. Since MP joint flexion will rely solely on the intrinsics, anticipated
motion will be approximately 45 degrees.
E. Proximal Phalanx
The remaining proximal phalanx will flex through the intrinsics and extend through the
extrinsic extensors. This will typically allow about 45 degrees of motion. If there is good
length of the proximal phalanx, this will prevent objects from falling out of the hand. As
the amount of proximal phalanx decreases, the advantage of maintaining this decreases,
as there will be minimal motion. In this case, consideration is given to a ray resection,
but this is typically not done in an acute traumatic setting.
F. MP Joint
Because there are not prominent condyles, amputations at the MP joint level require
little bony work. This can typically be easily performed in the acute setting. Unfortu-
nately, these typically produce suboptimal results. Amputations in the index and small
fingers leave a prominence, which can often cause difficulty when placing the hand in a
confined space, such as a pocket or a purse. Amputations of the middle and ring finger
create a space in the central aspect of the hand, making it difficult to hold small objects,
such as coins, allowing them to fall from the patient’s hand. In the traumatic setting,
the tissues are allowed to heal and ray amputation is performed at a latter time. When
performing amputations for other reasons, such as tumor resection, ray resection can be
performed at the time of the initial amputation.
IV. Ray Amputations
A. Index Finger
An elliptical skin incision is created. The common digital nerve to the ulnar side of the index
and radial aspect of the middle finger is isolated and divided distal to the middle finger radial
branch. The digital vessels are cauterized and transected. The flexor tendons are divided and
allowed to retract. The extensor tendons are divided, including the juncturae between the

EDC to the index and middle fingers. Subperiosteal dissection is completed around the
bone and an oblique cut is made distal to the insertion of the ECRL tendon. The oblique
cut is made with the distal portion along the ulnar and volar aspect, so it will not be palpable.
The digital nerves are buried in the periosteal tube created when the metacarpal was exposed
or in the first dorsal interosseous muscle belly. The tendon of the first dorsal interosseous
muscle is attached to the radial base of the proximal phalanx of the long finger.
B. Middle Finger
The middle finger ray amputation is performed in the same basic manner as the index
finger with the following exceptions. Mere excision will create a significant gap between
the index and ring fingers. This can be managed with two different procedures:
1. Closure of the space distally by approximating the deep intermetacapal
ligament
2. Creation of an osteotomy at the base of the index metacarpal and transpos-
ing this to the base of the middle metacarpal. This requires internal fixation,
typically with plates and screws, but can result in a very good functional and
aesthetic result.
C. Ring Finger
The procedure is similar to the index and middle fingers with one exception. There are
no tendinous attachments to the base of the metacarpal, so the entire metacarpal can be
excised. The potential space can be closed by approximation of the deep intermetcarpal
ligament and allowing the base to slide in a radial direction. No formal soft tissue release
of the fifth CMC joint is necessary for this to occur.
D. Small Finger
This is treated similar to the index finger, with transection distal to the insertion of the
ECU tendon.
V. Multiple Digits
When more than one digit is involved, the preservation of length becomes more impor-
tant. Other important issues are optimizing sensation with innervated flaps if necessary
and maintaining a deep first web space.
VI. Proximal Amputations
With more proximal amputations, it is generally best to maintain as much length as

possible and allow the patient to function. Ultimately, a more proximal level may be
required for prosthetic fitting (a distal forearm amputation allows for better prosthe-
sis fitting and use than an amputation through the carpus. As the level of amputa-
tion moves from the wrist to the proximal forearm, the degree of pronation and
supination is decreased. The incision is curvilinear shaped from radial to ulnar. The
nerves are transected and buried in the muscle bellies proximally. The bone edges are
transected and rounded so as not to create pressure on the skin following closure.
The flexor tendons are sutured together with horizontal mattress sutures. In a similar
fashion, the extensor tendons are sutured together and then the groups of flexor and
extensor tendons are sutured together to provide soft tissue bulk over the amputation
stump.

Elbow disarticulation and above elbow amputations are managed in a similar fash-
ion, with smoothing of the osseous structures and coverage of the bone with approxi-
mation of the flexor and extensor tendons.
VII. Post Operative Management
A. Rehabilitation/Hand Therapy
Following amputation surgery, the wound is covered with a nonadhearant dressing and
a plaster splint. The patient is seen in the office around a week for a wound evaluation
and rehabilitation is begun. Goals of hand rehabilitation include local wound care, an
early range of motion exercises. Often, a protective splint is useful during the early heal-
ing process. As healing progresses, modalities such as edema control, scar massage, and
tip desensitization are useful.
VIII. Adverse Outcomes
A. Neuroma Management
By definition, any transection of a nerve will result in a neuroma. One of the goals of
amputation surgery is to minimize the chance of developing symptomatic neuromas. It
is preferable to prevent a nerve injury from becoming symptomatic, rather than treating
it after the fact. Transecting the nerve and allowing it to retract away from the wound
margins will minimize the chance of developing a symptomatic neuroma. This will
avoid the nerve resting in a superficial location where it is apt to be easily traumatized.
Multiple techniques have been described to prevent and treat symptomatic neuromas.
These include burying the nerve in muscle, bone, suturing two nerves ends together,
and covering the nerve ends with silastic caps. There are no good studies illustrating any
one technique is better than another.
Treatment of a symptomatic neuroma is typically quoted as successful 75% of the
time, with each subsequent treatment successful 75% of the time, so eventually, revision
of the neuroma should be successful at resolving the symptoms.
B. Quadrigia
This is a term originally used by Verdan to describe an imbalance of the flexor tendons.
The origin of this term is from the Roman chariot drawn by four horses. Although each
of the horses had their own reigns, the driver could not control the reigns individually
and still use one hand to fight, so the reigns were wrapped around one hand. The ten-
sion had to be equal on each of the reigns for the horses to pull in a coordinated fashion.
In a similar manner, the FDP tendons to the middle, ring, and small fingers have a
common muscle belly and contract as a single unit. When the tension is altered on one
tendon, such as would be seen when a FDP tendon is pulled distally to cover bone, or
when it is tensioned too tightly prior to suturing it to the volar plate, the normal tension
is disturbed, resulting in the inability to fully flex the uninjured digits.
C. Lumbrical Plus Finger

When the FDP tendon is transected in zone I, as occurs with an amputation through
the DIP joint or middle phalanx distal to the FDS insertion and the tendon retracts
proximally, excessive tension can occur on the extensor mechanism at the level of the
central slip. This occurs via the lumbrical muscle, whose origin is on the FDP tendon in
the palm. The proximal pull of the FDP creates tension on the lumbrical whose distal

insertion is along the lateral band and acts through the central slip to extend the PIP
joint. Thus, effort to flex the PIP joint results in further proximal retraction of the FDP,
tightening the lumbrical, and paradoxically extending the PIP joint.
Management involves transection of the distal lumbrical tendon in the region of
the lateral band. This will remove the tension on the central slip and allow the digit to
flex at the PIP joint.
D. Cold Intolerance
Injured digits will almost always have some degree of cold sensitivity, which is obviously
a greater problem in the northern climates. This probably improves to some degree
with time, but will always be present and is a result of the initial injury, rather than any
reconstructive effort.
E. Phantom Pain
This becomes more of a problem with more proximal amputations. The assistance of a
pain management specialist as well as a psychiatrist or psychologist can be helpful and
aid in the patient recovery.
IX. Prosthetics
A. Digital
The use of digital prosthetics is mainly for aesthetic purposes, but can be helpful with
keyboard use. They are most commonly used in women who desire the appearance of a
digit. In the long term, many patients initially fitted for a prosthetic do not use it.
B. Below the Elbow

Below elbow amputees are good candidates for prosthesis. Early fitting of the prosthesis
will help the patient return to activities and adjust to the amputation. The successful
fitting and use require a minimum of about 2 in of bony tissue distal to the elbow.
There are two types currently widely used: Body powered and myoelectric prosthesis.
These patients should be followed routinely to check for proper fitting, as adjustments
will be required, especially early in the process.
C. Body-powered Prosthesis
This as a prosthesis contains a strap that is harnessed around the contralateral shoulder.
A cable is attached distally to hooks, and the device is powered by flexing the shoulder
to allow the device to open. The relaxation of the shoulder allows the device to close,
based on rubber band around the hooks, which pulls the ends together. Alternative
designs include a closing device as well as a prosthetic hand, which is typically created
as a closing device.
D. Myoelectric Prosthesis
These mechanical devises require voluntary control of the forearm musculature, are
more expensive and less durable, but can provide greater force when activated. They do
not require a strap around the opposite shoulder and can be activated with the shoulder
in any position.
E. Passive Cosmetic Prosthesis

If the patient is not interested in a functional device, a passive suction fitted prosthesis
can be fabricated.

Suggested Readings
Alison A, Mackinnon SE. Evaluation of digital prosthesis. J Hand Surg (Am). 1992;17(5):
923–926.
Brown PW. Less than ten—surgeons with amputated fingers. J Hand Surg (Am).
1982;7(1):31–37.
Chow SP, Ng C.Hand function after digital amputation. J Hand Surg (Br). 1999;18(1):125–128.
Peimer CA, et al. Hand function following single ray amputation. J Hand Surg (Am).
1999;24(6):1245–1248.
Steichen JB, Idler RS. Results of central ray resection without bony transposition. J Hand Surg (Am).
1986;11(4):466–474.

Techniques of Injections
7
Martin I. Boyer
I. Setup (Fig. 7.1)
All injections to the hand and wrist can be completed with the same formulation of
local anesthetic and corticosteroid:
A. 1 cc of 0.5% Marcaine
B. 1 cc of 2% lidocaine
C. 1 cc of 40 mg/mL of DepoMedrol
Other steroid or local anesthetic mixtures can be used if desired, but this is the preferred
mixture of the author.
D. A 3 cc syringe is used, and a 30 gauge 0.5 in needle is utilized as well for all
injections except those into the carpal tunnel. For those injections, a 25 gauge
1.5 in needle is used.
E. An iodine-impregnated swab stick is used for preparation of the injection site,
and sterile gloves are utilized. A moist 4 × 4 gauze pad (either isopropyl alco-
hol or normal saline) is used to wipe out any blood or prep solution from the
injection site, and a dry 4 × 4 gauze pad is used to clean the saline or alcohol. A
band-aid is used to cover the injection site; it can be removed safely after a few
hours.
II. Carpal Tunnel
A. Trans-FCR (Fig. 7.2)

The needle is introduced through the flexor carpi radialis (FCR) tendon, angled
approximately 20 degrees in the frontal plane (aiming ulnarly) and 45 degrees in the
sagittal plane. The needle is advanced slowly, taking care to redirect the needle should
paresthesias be felt by the patient. The floor of the carpal tunnel is reached, and the
needle is withdrawn slightly before injection is begun. A free flow of injectate should
occur. Following completion of the injection, some patients may complain of persistent
numbness in the median nerve distribution, although this is rare.
B. Carpal Tunnel: Ulnar Side (Fig. 7.3)

The needle is introduced at the wrist crease just ulnar to the palmaris longus tendon,
angles approximately 30 degrees in the sagittal plane and no more than 20 degrees in
the frontal plane (aiming radially). The needle is advanced slowly, taking care to redirect
the needle if paresthesias are felt by the patient. The floor of the carpal tunnel is reached,
and the needle is withdrawn slightly before injection is begun. A free flow of injectate
should occur. Following completion of the injection, some patients may complain of
persistent numbness in the median nerve distribution, although this is rare.
65

Figure 7.1 Setup.
Figure 7.2 Trans-FCR.
Figure 7.3 Carpal tunnel: ulnar side.

Chapter 7 • Techniques of Injections 67
III. CMC Thumb Injection (Fig. 7.4)
Traction is applied to the thumb ray, and the joint space of the CMC is palpated dor-
sally. Slight passive flexion and extension of the thumb are useful to palpate the dorsal
aspect of the base of the metacarpal (between the tendons of the first and third dorsal
compartments) moving distal to the fixed distal edge of the trapezium. The needle is
advanced slowly, and a slight “pop” is felt when the capsule is breached. The solution is
injected slowly, as the rapid filling of a nondistensible joint space can cause tremendous
pain. Often only 1 to 2 cc is injected.
IV. de Quervain Syndrome Injection (Fig. 7.5)
The radial styloid is palpated volar to a line extended proximally from the thumb meta-
carpal. The point of maximal tenderness at the first dorsal compartment is palpated,
and the needle is introduced. The floor of the compartment is reached, and the needle
Figure 7.4 CMC thumb injection.
Figure 7.5 de Quervain syndrome injection.

is withdrawn slightly. Injection proceeds slowly while the surgeon palpates along the
sheath of the APL and the EPB to feel for filling. A small “pop” may be felt by both
the surgeon and the patient proximal to the compartment when the sheath has been
filled maximally. The location of the radial artery is kept in mind during this injection
(slightly distal, and deep to the tendons at the proximal edge of the anatomic snuffbox).
Subcutaneous injection should be avoided, as the risk of skin depigmentation as well as
the risk of fat necrosis over the styloid is increased.
V. Intersection Syndrome (Fig. 7.6)
The point of maximal tenderness is palpated approximately 6 cm proximal to the radial

styolid, in line with the tendons of both the first and second dorsal compartments. The
needle is introduced slowly, taking care to redirect the needle should paresthesias be felt
by the patient in the distribution of the sensory branch of the radial nerve. The radius
is reached by the tip of the needle, withdrawn slightly, and injection can proceed. The
physician should feel free flow of the injectate.
VI. Radiocarpal/Scapholunate Injection (Fig. 7.7)
Lister’s tubercle is palpated while the patient holds his hand in the vertical position.
One centimeter distal to Lister is a depression that can be felt by the surgeon, which
locates the patient’s point of maximal tenderness. Occasionally a slight fullness is felt
in this area, potentially signifying an occult dorsal ganglion. The needle is introduced
and directed slightly proximal to coincide with the volar slope of the dorsal aspect of
the distal radius. Once the joint is entered, the injection should proceed with minimum
resistance.
Figure 7.6 Intersection syndrome.

Chapter 7 • Techniques of Injections 69
Figure 7.7 Radiocarpal/scapholunate injection.
Figure 7.8 Trigger finger injection.
VII. Trigger Finger Injection (Fig. 7.8)
The volar MCP flexion crease is palpated (distal edge of the A1 pulley), and the needle
is introduced slowly until the bone of the proximal phalanx is reached. The needle is
withdrawn slightly, and injection proceeds slowly. The surgeon may palpate proximally
and distally over the flexor sheath in order to feel the injectate filling the sheath; addi-
tionally, a gentle “pop” can be felt by both patient and surgeon when the sheath has
been filled maximally. Subcutaneous injection of trigger digits has not been shown to be
of substantial detriment in terms of efficacy.

Figure 7.9 Trigger thumb injection.
Figure 7.10 Ulnocarpal injection.
VIII. Trigger Thumb Injection (Fig. 7.9)
The injection is similar to the trigger finger injection, except that the point of entry of
the needle is over the diaphysis of the proximal phalanx, where the sheath can be felt
easily deep to the skin.
IX. Ulnocarpal Injection (Fig. 7.10)
The ulnar styloid is palpated while the patient holds his hand in the vertical position.
Just distal to the ulnar styloid, a depression can be felt that signifies the ulnocarpal joint;
distally the ulnar aspect of the triquetrum can be felt. The needle is directed transversely
and slightly proximal, toward the lunate facet of the distal radius, and the injection
should proceed with minimum resistance.

Differential Diagnosis
8
Chad R. Manke and Paul F. Nassab
Introduction
This chapter is intended to give the reader a list for common problems to be considered
when a patients has a general complaint—localized pain, numbness, etc. The specific
conditions are discussed in more detail in the chapter on the specific topic.
I. Ulnar-Sided Wrist Pain
A. Trifibrocartilage complex tear—may be traumatic or degenerative (degenerative

commonly associated with ulnar carpal impaction and LT ligament injuries)
1. Diagnosis: Positive foveal sign (point tenderness over the ulnar aspect of the
wrist where the TFCC inserts into the ulna), reproducible discomfort with
stress to the dorsal or palmar radioulnar ligaments.
2. Imaging: MRI, MR arthrography, arthroscopy, and arthrogram (not rou-
tinely done with improved qualities of MR).
3. Treatment
a) Conservative—Splinting, anti-inflammatory medications, and steroid
injections.
b) Operative—Wrist arthroscopy with debridement and arthroscopic or
open TFCC repair for type IB and IC injuries. Type II injuries may
require additional procedures, such as wafer or ulnar shortening osteot-
omy, with open or arthroscopic TFCC repair
B. DRUJ instability
1. Diagnosis: Instability of the DRUJ in supination, neutral, or pronation.
2. Imaging: Plain x-ray; CT scan in neutral, pronation, and supination; MRI to
evaluate the TFCC.
3. Treatment: Acute instability may be amenable to TFCC repair. Chronic
instability will require reconstruction.
C. Ulnocarpal abutment/impaction
1. Diagnosis: Pain with ulnar deviation or ulnar-sided loading, radiographic
changes in ulnar head or lunate/triquetrum, associated with ulnar positive
variance.
2. Imaging: Zero rotation plain x-rays and MRI with changes in the proximal
ulnar corner of the lunate (to differentiate from Keinbocks, when the entire
lunate is involved). Dynamic ulnocarpal impaction may be seen and is best
imaged with a pronated grip view radiograph.
3. Treatment: Ulnar shortening (wafer vs. osteotomy).
D. Extensor carpi ulnaris (ECU) tendonitis/instability
1. Diagnosis: Pain over the ECU tendon, pain with resisted wrist extension and
ulnar deviation over the ECU, painful snapping (instability) of the ECU
with supination/pronation.
71

2. Treatment: Bracing, activity modification, anti-inflammatories, injection,

ECU debridement, sixth compartment retinacular reconstruction.
E. Flexor carpi ulnaris (FCU) tendonitis
1. Diagnosis: Pain over the FCU tendon, pain with resisted wrist flexion over
the FCU tendon.
2. Treatment: Bracing, anti-inflammatories, injection, and surgical debridement
F. Pisotriquetral arthritis
1. Diagnosis: Positive pisotriquetral grind sign
2. Imaging: Carpal tunnel view x-ray or 30 degree supinated view of wrist
demonstrates pisotriquetral arthritic changes
3. Treatment: Bracing, anti-inflammatories, steroid injection, and pisiform
excision
G. Lunotriquetral ligament tear
1. Diagnosis: Lunotriquetral shuck, pain over lunotriquetral ligament, may be
associated with ulnar carpal impaction in chronic cases.
2. Imaging: MRI or MR arthrography—often difficult to diagnosis without
arthroscopy.
3. Treatment: bracing, anti-inflammatories, injection, arthroscopic debridement,
pinning, ligament reconstruction, lunotriquetral fusion, 4 corner fusion.
H. Hook of the hamate fracture
1. Diagnosis: Pain to palpation of the hamate and history of trauma
2. Imaging: Carpal tunnel view x-ray and CT scan
3. Treatment: Immobilization, open reduction internal fixation, and excision
I. Hypothenar hammer syndrome
1. Diagnosis: History of repeated trauma to the hypothenar base, pain and
numbness of ulnar-sided digits, cold intolerance, and ulcerations
2. Imaging: Angiogram, MR angiogram, or CT angiogram
3. Treatment: Activity modification, bracing, smoking cessation,
anti-inflammatories, calcium channel blockers, thrombolytics, and surgical
reconstruction
II. Radial-Sided Wrist Pain
A. Thumb basal joint arthritis

1. Diagnosis: Pain and swelling over first CMC joint, positive CMC grind
sign
2. Imaging: x-ray with arthritic changes the trapezium, can involve only the
thumb CMC joint alone, or with the STT joint
3. Treatment: Bracing, anti-inflammatories, injection of steroids, hyaluronate
injection, joint debridement (open or arthroscopic), first metacarpal osteot-
omy, trapeiometacarpal fusion, trapeziectomy ± ligament reconstruction ±
tendon interposition, and implant arthroplasty
B. Scaphotrapeziotrapezoid arthritis
1. Diagnosis: Swelling over the dorsoradial aspect of the wrist, loss of wrist
flexion/extension, pain to palpation over the STT joint
2. Imaging: x-ray with arthritic changes of STT joint
3. Treatment: Bracing, activity modification, anti-inflammatories, injection,
STT fusion, trapezium excision with or without ligament reconstruction,
and interposition

Chapter 8 • Differential Diagnosis 73
C. Radioscaphoid arthritis
1. Diagnosis: History of remote wrist trauma, pain at the radial styloid or snuff
box region, pain with radial deviation of the wrist, radiographs with arthritic
changes of radioscaphoid joint. Typically occurs as a late sequella of scaphol-
unate (SL) ligament injury or scaphoid nonunion
2. Imaging: x-ray with radioscaphoid joint space sclerosis and narrowing
3. Treatment: Bracing, anti-inflammatories, injection of steroids, radial sty-
loidectomy, scaphoidectomy, and partial wrist fusion
D. de Quervain stenosing tenosynovitis
1. Diagnosis: Pain and swelling over first dorsal compartment, positive Finkel-
stein test, pain with resisted palmar abduction of the thumb
2. Treatment: Bracing, anti-inflammatories, injection of steroids, first dorsal
compartment release
E. Intersection syndrome
1. Diagnosis: Pain ± crepitus over the second dorsal compartment, located 4 cm
proximal to radial styloid, and discomfort with repetitive wrist flexion and
extension
2. Treatment: Bracing, anti-inflammatories, injection, and longitudinal release
of the second dorsal compartment
F. Occult scaphoid fracture/nonunion
1. Diagnosis: History of remote trauma, pain with palpation of the scaphoid,
and loss of wrist motion
2. Imaging: x-ray, MRI
3. Treatment: Immobilization (for acute fractures only), open reduction internal
fixation, nonvascularized or vascularized bone grafting, and ± bone stimulator
G. Tumors
1. Diagnosis: Direct palpation about the wrist, palpable mass, which transil-
luminates, clinical suspicion for occult ganglia
2. Imaging: MRI
3. Treatment: Observation, splinting, aspiration, and excision
H. Wartenberg syndrome (sensory radial nerve compression)
1. Diagnosis: pain and parasthesias over dorsal-radial aspect of hand, history
of compressive jewelry about the wrist, Tinel sign over nerve branches, and
diagnostic wrist injection.
2. Treatment: Removal of compression about wrist, neurolysis in some severe cases
I. Scaphoid avascular necrosis (primary = Preiser’s disease, secondary to scaphoid
nonunion—much more common):
1. Diagnosis: Pain in snuff box
2. Imaging: x-ray—fragmentation of proximal pole, MRI
3. Treatment: Surgical revascularizaion or salvage procedures—scaphoidectomy
and partial wrist fusion, proximal row carpectomy
III. Dorsal Wrist Pain
A. Intersection syndrome
1. Diagnosis: Pain ± crepitus over the second dorsal compartment, located 4 cm
proximal to the radial styloid, and discomfort with repetitive wrist flexion
and extension
2. Treatment: Bracing, anti-inflammatories, injection, longitudinal release of
the second dorsal

B. Extensor tendon synovitis

1. Diagnosis: Tenderness to palpation over the specific extensor compartment
and pain with resisted extension of specific extensor tendon
2. Treatment: Bracing, anti-inflammatories, and steroid injection
C. Kienbock’s disease
1. Diagnosis: Pain over the lunate, swelling over dorsal aspect of wrist, loss of
wrist motion, and high clinical suspicion in early stages
2. Imaging: x-ray and MRI
3. Treatment: Bracing, anti-inflammatories, steroid injection, radial osteot-
omy, capitate osteotomy, revascularization with vascularized bone graft-
ing, methaphyseal core decompression, proximal row carpectomy, wrist
fusion
D. Scapholunate ligament tear
1. Diagnosis: History of trauma, pain with palpation over SL ligament, and
positive scaphoid shift sign
2. Imaging: x-rays, clenched fist/grip view, MRI, MR arthrography, and
arthroscopy
3. Treatment: Immobization of partial tears, direct repair of acute tears, SL liga-
ment reconstruction dorsal wrist capsulodesis
E. Occult ganglion
1. Diagnosis: Direct palpation about the wrist and clinical suspicion for occult
ganglia
2. Imaging: MRI
3. Treatment: Bracing, anti-inflammatories, aspiration, and excision
F. Radiocarpal arthritis
1. Diagnosis: Pain and swelling over dorsal aspect of wrist, loss of range
of motion, most commonly occurs as late sequella of SL ligament injury,
scaphoid nonunion, or intraarticular distal radius fracture
2. Imaging: Plain x-ray
3. Treatment: Bracing, anti-inflammatories, activity modification, injection of
cortisone
a) If lunate fossa is involved: Radioscapholunate fusion with excision of
distal pole of the scaphoid, total wrist fusion
b) If lunate fossa is spared: Proximal row carpectomy, scaphoid excision and
four-bone fusion, total wrist fusion
IV. Numbness and Tingling
A. Thumb and index finger

1. Wartenberg syndrome (sensory radial nerve compression)
a) Diagnosis: pain and parasthesias over dorsal-radial aspect of hand, history
of compressive jewelry about the wrist, Tinel sign over nerve branches,
and diagnostic wrist injection.
b) Treatment: Removal of compression about wrist and neurolysis in severe
cases
2. Carpal tunnel syndrome
a) Diagnosis: Tinel sign over median nerve, positive carpal tunnel compres-
sion test, Phalen sign, Semmes-Weinstein monofilaments, and nighttime
pain/awakening

Chapter 8 • Differential Diagnosis 75
b) Ancillary studies: Electrodiagnostic studies (nerve conduction velocities

and electromyography)
c) Treatment: Bracing, anti-inflammatories, injection, and carpal tunnel
release
3. Pronator syndrome = proximal median nerve compression
a) Diagnosis: Absence of provocative maneuvers for carpal tunnel syndrome,
pain with resisted pronation, positive Tinel over proximal median nerve,
and numbness in distribution of palmar cutaneous branch of median
nerve in addition to digits in median nerve distribution
b) Ancillary studies: Electrodiagnostic studies
c) Proximal median nerve decompression
4. Radiculopathy (C6)
a) Diagnosis: Diminished brachioradialis reflex, positive Spurling sign, and
weakness of wrist extension
b) Ancillary studies: Electrodiagnostic studies and MRI of C-spine
c) Treatment: Anti-inflammatory medications, traction, oral steroids, epi-
dural steroids, anterior cervical diskectomy, and fusion
B. Numbness and tingling of the middle finger
1. Carpal tunnel syndrome—as above
a) Diagnosis: Diminished triceps reflex, positive Spurling sign, and weak-
ness of wrist extension
b) Ancillary studies: Electrodiagnostic studies, MRI of C-spine
dural steroids, anterior cervical diskectomy, and fusion
C. Numbness and tingling of the ring and small finger
1. Cubital tunnel syndrome
a) Diagnosis: Tinel sign over the ulnar nerve at the elbow and positive elbow
flexion test
b) Ancillary studies: Electrodiagnostic studies
c) Treatment: Splinting, anti-inflammatories, ulnar nerve decompression
with or without transposition, and medial epicondylecctomy
2. Ulnar nerve compression at Guyon canal
a) Diagnosis: Tinel sign over Guyon canal and normal sensation in dorsal
cutaneus branch of ulnar nerve distribution
b) Ancillary studies: Electrodiagnostic studies, possible MRI to evaluate for
ganglion or space occupying lesion, and MRA for ulnar artery aneurysm/
thrombosis
c) Treatment: Bracing, anti-inflammatories, and decompression of Guyon
canal
a) Diagnosis: Normal reflexes, positive Spurling sign, weakness of hand
intrinsics
b) Ancillary studies: Electrodiagnostic studies, MRI of C-spine
dural steroids, anterior cervical discectomy, and fusion
4. Hypothenar hammer syndrome
a) Diagnosis: History of repeated trauma to the hypothenar base, pain and
numbness of ulnar-sided digits, cold intolerance, ulcerations, and Allen test
with diminished or absent filling of the hand through the ulnar artery.

b) Ancillary studies: Arteriogram, MR arteriogram, or CT arteriogram

c) Treatment: Activity modification, bracing, smoking cessation, anti-
inflammatories, calcium channel blockers, thrombolytics, and surgical
ligation with or without reconstruction
5. Lower trunk compression
a) CXR required to evaluate for pancoast tumor
b) Evaluate for ipsilateral unilateral mydriasis (Horner’s Syndrome)
V. Miscellaneous
A. Complex regional pain syndrome

1. Type I—No identifiable nerve injury
2. Type II—Identifiable nerve injury
a) Diagnosis: Pain out of proportion to level of injury, burning pain, discol-
oration, and autonomic dysfunction
b) Ancillary studies: three-phase bone scan, osteopenia on plain radiograph,
response to phentolamine mesylate, laser Doppler fluxmetry, and nerve
conduction study
c) Treatment: Hand therapy, peripheral nerve decompression, calcium chan-
nel blockers, stellate ganglion block, surgical sympathectomy, and dorsal
column and periventricular gray matter stimulators
VI. Dorsal Hand Mass
A. Dorsal carpal ganglion

B. Extensor tenosynovitis
C. Wrist synovitis
D. Extensor digiti brevis manus
E. Carpometacarpal boss
F. CMC dislocation
G. Malignancy (epithelioid sarcoma, synovial sarcoma)
H. Giant cell tumor of the tendon sheath
VII. Acute Loss of Active Digital Motion
A. Fracture/dislocation
B. Sagittal band rupture
C. Extensor tendon rupture
D. Locked trigger finger (PIP)
E. AIN or PIN paresis
F. Trapped collateral ligament (MCP)
VIII. A “Clunking” Wrist
A. ECU tendon subluxation

B. Midcarpal instability
C. DRUJ subluxation/instability
D. SL instability

II Specific Conditions

Chronic Pain Syndromes
9
George D. Chloros, L. Andrew Koman,
Zhongyu John Li, and Thomas L. Smith
I. Introduction
A. Pain is defined as “an unpleasant sensory and emotional experience associated with
actual or potential tissue damage” by the International Association for the Study
of Pain (IASP). Chronic extremity pain, which persists in the absence of ongoing
cellular injury or compromise and extends beyond the injured area or distribu-
tion of the involved nerve, is termed complex regional pain syndrome (CRPS).
It is a clinical syndrome without a pathognomonic marker.
B. There are three types of CRPS
1. Type 1—previously termed reflex sympathetic dystrophy (RSD)—includes
the clinical manifestations of pain, functional impairment, autonomic dys-
function, and/or dystrophic changes without an identifiable nerve lesion.
2. Type 2—previously termed Causalgia—is defined by pain, functional impair-
ment, autonomic dysfunction, dystrophic changes with an identifiable nerve
lesion.
3. Type 3—are other pain dysfunction problems and are not discussed in this
chapter except as part of the differential diagnosis.
CRPS types I and II may be sympathetically maintained or sympa-
thetically independent, as defined by pain relief from a sympatholytic inter-
vention such as intravenous phentolamine of a stellate ganglion block. Many
oral medications have a sympatholytic effect.
C. Terminology
1. Nociceptive pain originates from a mechanical source. A nociceptive origin or
component of CRPS is common.
2. Neuropathic pain emanates from an injury or malfunction of a peripheral
nerve. CRPS is one manifestation of neuropathic pain. For example, pain
from a neuroma or a neuroma-in-continuity that is localized to the injured
nerve or phantom-limb pain is neuropathic but not CRPS.
3. Sympathetically maintained pain (SMP) is defined as pain, which is amelio-
rated by blocking sympathetic receptors. Drugs, which have this property are
termed sympatholytic.
II. Complex Regional Pain syndrome
A. CRPS is a clinical entity defined by pain, autonomic dysfunction, trophic

change, and functional impairment. There is no pathognomonic marker or
test.
B. In the absence of pain, the process is no longer CRPS. However, residual con-
tracture, deformity, and stiffness are considered the sequelae of CRPS.
79

80 Section II • Specific Conditions
C. Incidence and prevalence is

1. Unknown in most locals.
2. In Olmsted County, the incidence was reported as 5.5 per 100,000 and the
prevalence as 20.7 per 100,000 in 2003.
3. The incidence after fracture of the distal radius varies from 4% to 39% in
prospective series.
4. Smoking is a significant risk factor.
D. Synonyms—there are over 40. Some of the most common are
1. Algodystrophy
2. RSD
3. Causalgia
4. Major causalgia
5. Minor causalgia
6. Minor traumatic dystrophy
7. Major traumatic dystrophy
8. Shoulder-hand syndrome
9. Sympathetic-maintained pain syndrome (SMPS)
III. Anatomy and Physiology of Pain
A. Pain is initiated in the periphery, potentiated by local reflexes and humeral fac-
tors, relayed via peripheral nerves to the dorsal horn of the spinal cord (wide
dynamic range neurons), amplified and modified in the spinal cord; and trans-
mitted to cortical centers.
B. Within the spinal cord, the pain signal is modified and modulated. The magni-
tude of pain depends upon the mechanism of initiating event; afferent informa-
tion transmitted; efferent modulation; and CNS interpretation.
C. Painful (nociceptive) information is activated peripherally (transduction) by
mechanical, thermal, chemical, or ischemic events and transmitted by small
myelinated (A-D) and small unmyelinated C afferent peripheral nerve fibers to
spinal cord.
D. The perception and physiologic consequences are related to a complex interplay
of physiologic events and psychological factors.
E. Pathophysiology—Proposed mechanisms fall into two large groups
1. Peripheral abnormalities include alterations in vasomotor tone with enhanced
nociceptor activity; abnormal sympathetic activity; abnormal stimulation
of somatic sensory axons following partial nerve injury; increased sensory
afferent impulses; local demyelination with “sprout” outgrowth resulting
in increased nociceptor sensitivity; damage to peripheral nerve; damage to
mixed motor/sensory nerves; peripheral microvascular shunting and second-
ary to abnormal sympathetic tone
2. Central neurologic dysfunction
These include abnormalities of the “internuncial pool”; increased
activity within the substantia gelatinosa; abnormal modulation of wide-
dynamic-range neurons; abnormal modulation of afferent signals in higher
cortical centers of the brain; and/or cortical adaptations and changes.
3. True pathophysiology is probably a combination of peripheral and central
mechanisms.
4. CRPS is conceptually an exaggeration or abnormal prolongation of the “nor-
mal” pathophysiologic events following injury.

Chapter 9 • Chronic Pain Syndromes 81
IV. Natural History
A. Observations and prognosis

CRPS type 1 and 2 is a departure from the orderly and predictable response
of an extremity to a traumatic or surgical insult. There is persistence of neuro-
pathic pain with an inappropriate intensity combined with absence of impeding
or ongoing tissue damage.
1. It may either represent multiple pathophysiologic subgroups or have a com-
mon etiology; however, the exact pathophysiologic cause is not defined.
2. A transient dystrophic response (abnormal physiology) to injury or trauma is a
normal phenomenon. Abnormal prolongation of this response and inability of
the patient to modulate or control the pain cycle appears to be the best expla-
nation of RSD. A cascade of reversible and irreversible events then ensues.
3. The natural history is poorly defined and is altered by treatment.
4. CRPS is not a psychogenic condition, and the emotional suffering is the
result, and not the cause of CRPS.
5. In general, diagnosis and initiation of treatment within 6 to 12 months of
onset result in significant improvement.
6. However, patients with CRPS and fracture of the distal radius have a poorer
prognosis; stiffness, and “poor finger function” at 3 months correlate with
10 year morbidity
7. Some patients in spite of early and appropriate treatment do poorly with
long-term functional impairment, chronic pain, deformity, or any combina-
tion thereof.
8. CRPS may result in irreversible end-organ dysfunction, including loss of
normal arteriovenous (AV) shunt mechanism and permanent alterations in
central neurologic responses.
9. Swelling occurs early, and stiffness and atrophy are present in later stages;
pain at any stage is associated with AV shunting and nutritional deprivation
(relative ischemia).
10. Eighty percent of those treated within 1 year of injury show subjective
improvement; only 50% of those treated after one year improve.
11. The most effective aspect of treatment of RSD is early recognition—best results
occur if diagnosis and active management are initiated before 6 months.
B. Clinical characteristics
1. Pain is unremitting, “out of proportion to the injury” and does not depend
on the magnitude of the inciting effect; often described as “tearing”, “burn-
ing”. Some CRPS patients may fearfully withdraw the limb from the exam-
iner and develop avoidance patterns. Pain on exposure to cold is frequent.
Pain is not significantly improved with the use of narcotic analgesics, but it
will frequently respond to sympatholytic medications. Difficulty sleeping,
restlessness, and anxiety are common complaints. Pain may be assessed using
standardized and/or validated instruments (e.g., visual analog scale, Short-
Form 36, self-administered questionnaires). Cold sensitivity may be assessed
using the McCabe scale.
Pain includes
a) Allodynia (painful response to a nonpainful stimulus)
b) Hyperpathia (increased pain sensitivity)
c) Hyperalgesia
2. Stiffness of fingers, wrist, and shoulder is common.

3. Functional deficit is secondary to pain swelling and stiffness.

4. Trophic changes (autonomic dysfunction) include sudomotor dysfunction,
temperature, swelling, diffuse osteopenia, and skin alterations.
V. Diagnosis/Clinical Presentation
A. Extremely variable in history, physical findings, and diagnostic workup.

B. History almost always includes surgical or traumatic insult; however, it may have
been very mild.
C. Clinical diagnosis is made if pain is intense or unduly prolonged; and two or
more of the following are noted: Stiffness; delayed functional recovery; trophic
changes and/or autonomic dysfunction.
D. Autonomic dysfunction is almost always present in some form and includes
vasomotor instability; pseudomotor abnormality; thermoregulatory changes;
and abnormal nutritional flow with aberrant AV shunting.
E. Presentation—usually presents after trauma—major or trivial. Women are more
frequently affected than men. Children and adolescents are afflicted rarely but
can have severe involvement. Upper and lower extremity involvement is approxi-
mately equal. An identifiable mechanical trigger or etiologic component (e.g.,
entrapped nerve) is present in less than 50% of cases.
F. Signs and symptoms are pain; swelling; stiffness; dry skin; hair loss; abnormal
sweating; and /or discoloration.
G. Diagnostic tests
1. Plain x-rays may be normal but often show osteoporosis with subchondral
resorption. Classic CRPS roentgenograms demonstrate osteopenia with peri-
articular and subchondral resorption (Sudeck atrophy), but changes appear
late and therefore radiographs are not a useful screening tool. As many as
30% of patients have no x-ray abnormalities.
2. Bone scans may be characteristic and confirmatory for CRPS, but are not
pathognomonic. Three phase scans are utilized but are insufficiently sensi-
tive. First and second phase bone scans may demonstrate asymmetry of flow
dynamics and quantify vasomotor instability and abnormal autonomic flow.
Third phase scans—when positive—demonstrate increased periarticular
uptakes in involved and uninvolved joints.
3. A positive third phase bone scan adds credence to the clinical diagnosis; iden-
tifies a recognizable subgroup of CRPS; has no prognostic significance; and
does not correlate with thermoregulatory or vasomotor states.
Kozin MacKinnon Werner
Specificity 75%–85% 96% 92%

Sensitivity <60% 98% 50%
4. Thermoregulatory and nutritional blood flow testing help to quantitate and

quantify distal extremity autonomic function as reflected in thermoregulatory
and nutritional blood. A form of stress—thermal or emotional—improves
reliability and reproducibility (Fig. 9.1).
Isolated cold stress test has been described to assess dynamic sympa-
thetic response of an extremity to changes in environmental temperature.

Figure 9.1 The common underlying mechanism is deprivation of nutritional flow and
resulting in pain via abnormal AV control through arteriovenous anastomoses (AVA).
This is true in either a hot swollen hand with increased total flow, or a cold, stiff hand
with decreased total flow. (From Koman LA, ed. Bowman Gray Orthopaedic Manual.
Winston-Salem, NC: Orthopaedic Press; 1996.)
It permits the measurement of skin surface temperature of the digit, which

is a reflection of total blood flow. It is highly sensitive to vasomotor distur-
bances that occur in 80% to 90% of patients with RSD. It is not specific
for CRPS.
Laser Doppler Fluximetry (LDF) measures total blood flow to a
depth of 1 to 1.5 mm. As part of a stress test, it measures the velocity
of moving red blood cells by the Doppler shift of a single wavelength of
light reflected by the red cells; correlates with flow (i.e., volume of red
cells in motion); provides dynamic information about vasomotion. Laser
Doppler flux, or the total blood flow in the superficial portion of the
digit, directly correlates with nutritional blood flow to the digit, which
can be adequate even when rotal blood flow and thus, temperature, is
decreased.
5. Vital capillaroscopy is a technique for measuring nutritional blood flow in
the nail fold of hand and foot. It was developed by Fagrell in mid-1970s at
the Karolinska Institute in Sweden and allows measurement of nutritional

capillary blood flow by direct observation through a compound microscope.

Patients with RSD have reduced nutritional flow and inability to modulate
flow when compared to normal patients. In addition, vital capillaroscopy
suggests that patients with long-standing RSD have irreversibly reduced cap-
illary blood flow to soft tissues, which is unresponsive to sympathetic or local
modulation.
6. Pseudomotor function may be evaluated by quantitative and qualitative eval-
uation of sweat production. This may be accomplished by measuring
a) Resting sweat output (RSO), as described by Chelimsky in 1955, mea-
sures sweat production after a sympathetic block. To date this test has
been used as a research tool. Prolonged improvement correlates with short
duration of arm pain and elevated RSO.
b) Quantitative pseudomotor axon reflex (QSART): The QSART correlates
highly with the RSO. When the RSO and the QSART are combined,
they correlate with the clinical diagnosis.
7. Endurance testing is an effective technique for documenting subtle func-
tional deficits and is performed using computerized equipment (e.g., similar
to those used in a functional capacity evaluation). The use of these tech-
niques permits the demonstration of objective signs of weakness and fatigue
not possible with using static testing. Endurance testing, which is extremely
accurate and difficult to falsify, may demonstrate functional impairment that
would otherwise be missed.
8. Diagnostic procedures include stellate ganglion blocks and intravenous
phentolamine—which blocks a1 and a2 receptors—affecting a sympatho-
lytic effect. Relief suggests SMPS. Therefore, a positive response (relief of
symptoms) supports SMPS and a negative response suggests an alterna-
tive diagnosis or irreversible peripheral changes with or without central
pain.
9. Peripheral nerve conduction velocities and electromyography may be utilized
to identify neuropathic conditions.
VI. Classification and Staging
Classifications are discussed but generally do not suggest specific interventions or

provide prognostic significance. Classifications have been suggested by de Takats in
1937, Costen in 1955, and Steinbrocker in 1958. Although multiple authors, including
the IASP, have attmpted to implement criteria for CRPS, these are predominantly for
research purposes and there is not a “gold standard” for diagnosis and thus, there are of
limited use to clinicians. The modified Mayo RSD score may be helpful. Staging and
severity may be of benefit; however, since most patients are treated inadvertently before
definitive diagnosis, classifications based upon temporal (time in weeks or months) are
inconsistent and clinically irrelevant.
Therefore, a different approach may be more relevant for the clinician: CRPS may
be functionally and physiologically classified as (i) Hot, swollen stage (increased total
flow, but decreased nutritional flow) and (ii) Cold, stiff stage (both total and nutri-
tional flow are decreased). The distinction of SMP—better prognosis—versus sym-
pathetically independent pain—worse prognosis—is important. Management of the
latter is complex and beyond the scope of this review.

VII. Treatment
A. Early recognition of possible CRPS and the initiation of treatment are essential
for optimal outcomes. However, diagnosis before 6 to 12 weeks is not common,
especially in milder variants of CRPS.
B. Treatment is aided by a determination of (i) physiologic staging—the amount
of total flow (increased or decreased); the extent of AV shunting and the degree
of nutritional deprivation (i.e., “hot” versus “cold” stage) (Tables 9.1 and 9.2);
(ii) if the pain is sympathetically maintained or independent; and (iii) the pres-
ence of an identifiable nociceptive injury.
C. Management choices include therapy, vitamins, oral medications, parenteral
medications, and/or surgery:
1. Therapy and modalities that are usually combined with oral medications.
These include hand therapy with active and passive range of motion exer-
cises (within limits of pain); splints; contrast baths (alternating heat and
cold); and transcutaneous nerve stimulators; H wave therapy has been
beneficial; stress loading may ameliorate symptoms in many (Watson,
1987).
2. Oral pharmacologic interventions, which provide a sympatholytic effect,
are used in the treatment of CRPS (Table 9.3). None are labeled by the
Food and Drug Administration for use in CRPS, and their use has been
derived from general experience in the management of neuropathic pain.
They are used on a trial-and-error basis. Multiple classes of drugs are
appropriate and include
a) Antidepressants
b) Anticonvulsants
c) Membrane-stabilizing agents
d) Adrenergic agents
e) NSAIDs and steroids
f ) Observations and cautions
TABLE 9-1 The two states of microvascular perfusion associated with

CRPS
Two states of microvascular perfusion associated with CRPS

• Increased total flow • Decreased total flow
• Decreased nutritional flow • Decreased nutritional flow
Symptoms Hot, swollen Cold, stiff
Signs • Edema Atrophic
• Increased sweating
Pain • With hyperalgesia Hyperalgesia
• Without hyperalgesia
• With cold intolerance Cold
• Without cold tolerance
Source: Reproduced from Koman LA, ed. Bowman Gray Orthopaedic Manual. Winston-Salem,
NC: Orthopaedic Press; 1997, with permission.

86
Boyer_Chap09.indd 86
TABLE 9-2 Management of a “hot swollen,” CRPS
Modality Effect Action Example

Immobilization with Decrease pain
splints or casts Prevent progression to contracture
Section II • Specific Conditions
Avoid tight casts

Compressive dressings Decrease edema
and elevation of the limb Avoid tight dressing
Hand therapy Decrease pain Active ROM (esp. PIP joints)
Helps prevent arthrofibrosis/ isometric exercises if active
contracture ROM causes too much pain
minimize passive ROM
Stress loading activities Decrease pain/edema
Other modalities:
cryotherapy and TENS
Contrast baths Decrease pain
NSAIDs Decrease nonneuropathic pain Important to control pain
Control edema related to ongoing cell and
tissue damage. Little effect on
the neuropathic SMP of CRPS.
Narcotics Decrease nonneuropathic pain
2/16/2010 8:35:31 PM
Calcium channel blockers Decrease edema and increase Increase nutritional flow (by Amlodipine (Norvasc) 2.5–5
nutritional flow diminishing the increased mg/day po, Nifedipine
Help to prevent arthrofibrosis shunting via AV anastomoses) (Adalat, Procardia) 10–30
mg tid or 30–90 mg qid
sustained
Steroids Decrease inflammation 10 mg/day po
Tricyclic antidepressant Decrease pain Amytriptylene (Elavil),
Sympatholytic action 25–75 mg tid
Selective serotonin Fluoxetine (Prozac),
reuptake inhibitor 20–80 mg/day
Anticonvulsant Gabapentin (Neurontin),
600–800 mg tid
Adrenergic agent Improves edema and hyperalgesia Presynaptic α2 agonist Clonidine (Catapres), 1-mg/h
patch, weekly or 1 mg pot id
initially
Continuous autonomic Decreases pain and sympathetic
blockade of the stellate nervous system influence
ganglion
Source: Reproduced from Koman LA, ed. Bowman Gray Orthopaedic Manual. Winston-Salem, NC: Orthopaedic Press; 2007, with permission.
Chapter 9 • Chronic Pain Syndromes
87
2/16/2010 8:35:31 PM
88
TABLE 9-3 Oral medications for CRPS
Major Short-term
Disadvantage or Side
Drug Usual Dosage Mechanism Effects Contraindications
Amitriptyline hydrochloride 25 mg tid or 50 mg qhs. Inhibits amine Drowsiness With guanethidine

(Elavil hydrochloride) pump-decreased NE sulfate
(norepinephrine) uptake
Pregabalin (Lyrica) 50–200 mg tid Antinociceptive–binding Dizziness
alpha 2-delta subunit Somnolence
Peripheral edema
Gabapentin (neurotin) 300–600 mg tid Blocks calcium channels Dizziness
Peripheral edema
Asthenia
Fluoxetine (Prozac) 20 mg/day AM Serotonin inhibitor Minimal drowsiness
Phenytoin (Dilantin) 100 mg tid Decreases resting mem- Minimal drowsiness
brane potentials; inhibits
amine pump; stabilizes
synaptic membrane
3/8/2010 8:58:51 PM
Phenoxybenzamine 40–120 mg/day Al-receptor blocking Orthostatic hypertension
hydrochloride (Dibenzyline) agent
Nifedipine (Procardia) 10 mg tid may increase Ca++ channel block- Headache
slowly to 30 mg tid. ing agent; prevents AV Postural hypotension
shunting; increases
nutritional flow
Amlodipine (Norvasc) 5–10 mg qd Ca++ channel block- Headache
ing agent; prevents AV Postural hypotension
shunting; increases
nutritional flow
Corticosteroids 20–80 mg/day; Stabilize membranes; Adrenal suppression;
prednisone equivalents × increase nutritional flow; Avascular necrosis (dose
5–40 days decrease inflammatory related)
pain
Chapter 9 • Chronic Pain Syndromes
89
2/16/2010 8:35:31 PM
The most common oral agents are amitriptyline, gabapentin, pregabalin, clonidine,
and nifedipine.
No oral medications are approved by the FDA for CRPS. The table, provided is a brief
summary and is not sufficient as a guide for the off-label use of these powerful drugs. It is
imperative that the practitioner understand all the risks and potential benefits; the potential
drug interactions and the side effects before prescribing. The mention of these drugs neither
advocates nor endorses their use.
3. Vitamin C, at a dose of 500 mg per day, has been demonstrated to decrease
the incidence of CRPS after distal radius fracture. The role of other vitamins
is unclear.
4. Parenteral agents are often administered by anesthesiologists
a) Intravenous agents administered with or without tourniquet include
1) Guanethidine
2) Clonidine
3) Phentolamine
4) Cortisone sulfate
5) Reserpine
6) Bretylium
b) Agents administered by injection using lidocaine, marcaine, and ropiva-
caine by Stellate ganglion blocks—single or continuous; axillary; brachial;
infraclavicular; scalene; and/or epidural catheter.
c) Calcitonin, bisphosphonates (show benefits in double-blinded trials of
CRPS) and recently N-methyl-d-aspartate (NMDA) antagonists (ket-
amine, memantine) have been used with success.
d) Continuous autonomic block may be achieved by indwelling catheters
in the epidural space or contiguous to the brachial plexus or peripheral
nerves.
e) Peripheral nerves or the brachial plexus.
D. Surgical and ablative therapies
1. Release of sites of compression of peripheral nerves (such as carpal or cubital
tunnel releases) can be done in the setting of CRPS type 2 following hand
surgical procedures.
2. Surgical correction of neuropathic or nociceptive sites is important and may
be done early if the dystrophy can be controlled chemically.
3. Sympathectomy at the cervicothoracic and periarterial level is reported.
However, ablative and irreversible cervicothoracic sympathectomy produces
upregulation of adrenergic and other receptors and should be avoided. Phe-
nol and radiofrequency sympathectomy do not have this effect.
4. Neurolytic blockade of peripheral nerves may be efficacious in selected
patients; it is accomplished by chemical neurotemesis using phenol or
alcohol.
5. Implantable peripheral nerve stimulators are valuable in selected patients.
6. Dorsal column stimulators have been shown to be efficacious and cost
effective for refractory CRPS but have a high complication rate.
7. Neurosurgical procedures suitable for CRPS include thalamic stimulators,
gray matter stimulators, and cingulotomy.
E. Psychotropic therapy
1. Techniques employed include counseling; biofeedback; adaptive therapy

F. Prevention. The most effective treatment of RSD is the prevention of progres-

sion by careful technique and initiation of early intervention.
1. Avoid tight casts.
2. Avoid laceration or entrapment of nerves. That is known to produce severe
pain and disability, which increase dystrophic response acutely.
3. Superficial radial nerve, dorsal cutaneous ulnar nerve, and palmar cutaneous
branch of the median nerve are involved most commonly.
4. A few moments identifying and avoiding at-risk nerves during surgery will
significantly reduce the risk of development of postoperative RSD.
5. Postoperative discomfort “out-of proportion” to traumatic insult, especially
if manifested by “burning,” restlessness, and difficulty in sleeping, should be
treated to interrupt the “dystrophic cycle.”
6. Prophylactic vitamin C is supported in the literature, is inexpensive and
without side effects.
G. Late management of CRPS extremity manifestations
1. Surgery on extremities with CRPS is appropriate if the pain can be managed
by medications—administered by continuous block, orally or both.
2. Assuming adequate perioperative control is possible by sympatholytic inter-
ventions, nociceptive and neuropathic foci may be managed by
a) Neurolysis of compressed nerves
b) Correction of mechanical lesion
c) Decompression of the site of peripheral nerve compression Carpal tunnel
release (CTR), Cubital tunnel release (CUTR)
3. Similarly treatment of deformity and contracture may be addressed
surgically
a) Release of contracted MP or PIP joints
b) Release of contracted intrinsic muscles
c) Osteotomy to correct malunion
d) Treatment of nonunion
VIII. Summary
A. Complex pathologic entity; characterized by persistent pain, functional deficit,

trophic changes, and vasomotor abnormalities.
B. Treatment with a combination of therapeutic approaches aims at decreasing
sympathetic hyperactivity and improving nutritional microvascular blood flow.
C. Most important factor in the clinical approach to RSD—prompt recognition
and aggressive management
D. Treatment protocols should include
1. One or more use of nonoperative therapeutic options to address SMP, edema,
and functional impairment.
2. Delineation of primary cause if possible and its correction or alleviation if
possible.
3. Local surgical intervention, after control of dystrophic response, to correct
primary or secondary mechanical problems (e.g., nerve entrapment).
4. Surgical sympathectomy should be employed only if all other techniques
have failed.

Suggested Readings
Eisenberg E, Geller R, Brill S. Pharmacotherapy options for complex regional pain syndrome.
Expert Rev Neurother. 2007;7:521–531.
Koman LA, et al. Complex regional pain syndrome. In: Green D, Hotchkiss R, Pederson W, Wolfe
S (eds). Green’s Operative Hand Surgery. 5th Ed. Philadelphia, PA: Churchill Livingstone;
2005:2015–2044.
Merritt WH. The challenge to manage reflex sympathetic dystrophy/complex regional pain syn-
drome. Clin Plast Surg. 2005;32:575–604
Placzek JD, et al. Nerve decompression for complex regional pain syndrome type II following
upper extremity surgery. J Hand Surg (Am). 2005;30:69–74.
Sandroni P, et al. Complex regional pain syndrome type I: Incidence and prevalence in Olmsted
county, a population-based study. Pain. 2003;103(1–2):199–207.
Veldman PH, et al. Signs and symptoms of reflex sympathetic dystrophy: Prospective study of 829
patients. Lancet. 1993;342:1012–1016.
Watson HK, Carlson L. Treatment of reflex sympathetic dystrophy of the hand with an active
“stress loading”program. J Hand Surg (Am). 1987;12:779–785.
Zollinger PE, et al. Can vitamin C prevent complex regional pain syndrome in patients with wrist
fractures? A randomized, controlled, multicenter dose-response study. J Bone Joint Surg Am.
2007;89:1424–1431.

Tendon
10
James Chang, Shelly Noland, Julie E. Adams,
Daniel P. Mass, John G. Seiler III, John S. Taras,
Andrew Trueblood, Michael J. Botte, David M.
Kalainov, Randon C. Johnson, Anthony J. Lauder,
and Jennifer Moriatis Wolf
Flexor Tendon Biology
Flexor tendons I the hand are intrasynovial and are formed by bundles of collagen
fascicles that can be subdivided into radial and ulnar halves and volar and dorsal com-
ponents. The dorsal portion of the tendon receives its blood supply from two vinculae,
which are supplied by branches of the radial and ulnar digital arteries. In contrast, the
volar portion of the tendon receives minimal direct blood supply. Synovial diffusion
allows nutrients to supply the avascular portions of the tendon. The flexor tendons are
covered by a thin epitenon layer and run through a tight fibro-osseous sheath in Zone
II. This fibro-osseous sheath makes the repair of flexor tendons challenging as adhesion
and scar formation can inhibit gliding and hinder postoperative range of motion and
rehabilitation.
I. Flexor Tendon Healing
Flexor tendon wound healing can be divided into intrinsic and extrinsic components.
A. Intrinsic healing involves the tenocytes within the tendon and on the epitenon
layer.
B. Extrinsic healing involves the inflammatory cells and fibroblasts from the over-
lying sheath. Extrinsic healing may result in the formation of adhesions between
the tendon and its sheath, which interferes with the necessary gliding of the
tendon through the sheath.
II. Wound Healing
Like other types of wound healing, there are four phases of tendon wound healing:
hemostatic (immediate), inflammatory (0 to 7 days), proliferative (2 to 28 days), and
remodeling (starting at sixth week).
A. The hemostatic phase is characterized by vasoconstriction, platelet deposition,
and fibrin clot formation.
B. During the inflammatory phase, inflammatory cells from the surrounding tis-
sues migrate into the area of injury and phagocytize necrotic tissue and clot.
There is also deposition of the extracellular matrix including fibronectin, which
is used as scaffolding for collagen deposition and vascular ingrowth.
C. The proliferative phase is characterized by an increase in the number of
fibroblasts, collagen deposition, and vascular ingrowth along the collagen/
fibronectin scaffolding.
93

D. During the remodeling phase, the strength of the tendon repair increases.
Collagen fibers become parallel with uninjured tendons. Throughout the
process of tendon healing, active and passive range of motion is necessary to
prevent adhesion formation and promote tendon gliding and repair strength.
III. Growth Factors
Multiple studies have been performed to evaluate the molecular basis of tendon healing
and to identify potential growth factors that may be involved. These include vascular
endothelial growth factor (VEGF), insulinlike growth factor (IGF), platelet-derived
growth factor (PDGF), basic fibroblast growth factor (bFGF), and transforming growth
factor b (TGF-b).
A. VEGF has a known role in tumor angiogenesis and also promotes angiogenesis
in tissues after injury, including tendons. Its mRNA levels peak 7 to 10 days
after repair and return to baseline by day 14.
B. IGF-1 has been found to promote wound healing, and its presence can reverse
the negative effects of steroids. It potentiates cell proliferation and thus possibly
tenocyte proliferation. It improves tendon healing by stimulating the prolif-
eration of cells and collagen, by decreasing the size of the injured area, and by
increasing the strength of the tendon.
C. bFGF is increased for 8 weeks postrepair of a tendon injury. Its effects include
increasing the number of tendon fibroblasts and increasing the amount of col-
lagen type III.
D. PDGF is expressed very quickly after tissue injury. It plays a role in fibroblast
proliferation, collagen deposition, and angiogenesis. It has been found to be
increased in healing tendons where it increases the production of collagen, pro-
teoglycan, IGF-1, and DNA synthesis in tenocytes.
E. TGF-b is a ubiquitous growth factor that is secreted by many cells in the
body. It has been found to be increased in tendons and sheaths after injury.
It increases collagen production by tenocytes. This causes increased scar for-
mation and fibrosis. Research has investigated the possibility of inhibiting
its role to prevent adhesion and scar formation and improve tendon repair.
Inhibitors that have been investigated include TGF-b antibodies and the
molecules decorin and mannose-6-phosphate. Studies have indicated that
the supplementation of decorin and mannose-6-phosphate may reduce TGF-
b-induced collagen production. The intraoperative application of mannose-
6-phosphate has been shown to significantly increase postoperative range of
motion.
IV. Future Directions
Recent advances in flexor tendon repair and rehabilitation include the use of multi-
strand repair techniques and early active motion protocols. While these have led to
better outcomes in terms of improved repair strength and range of motion, there is
still a need for further advances for this difficult problem. An understanding of the
biomolecular cascade of growth factors in flexor tendon wound healing will have sig-
nificant clinical implications. In the future, manipulation of growth factors will allow
the acceleration of tendon healing and/or inhibition of excessive healing and adhesion
formation.
Boyer_Chap10.indd 94 2/22/2010 10:25:18 AM

Chapter 10 • Tendon 95
Acute Flexor Tendon Injuries
Acute injuries to the flexor tendons are common. Treatment and prognosis depend on
the location and extent of the injury.
I. Anatomy
Zones:
The flexor tendon system of the hand is divided into five zones (Fig. 10.1).
Zone I is the area distal to the flexor digitorum superficialis (FDS) insertion at the
mid-middle phalanx. This area is distal to the FDS insertion; thus only the flexor digi-
torum profundus (FDP) is injured in lacerations within this zone.
Zone II represents the area from the FDS insertion at mid-middle phalanx proxi-
mally to the A1 pulley at approximately the level of the distal palmar crease, comprising
the proximal portion of the digital sheath. Topographically, this is the area from the
distal palmar crease to the midregion of the middle phalanx.
Zone III comprises the area between the proximal aspect of the A1 pulley and the
proximal aspect of the origin of the lumbrical muscles from the FDP tendons. Topo-
graphically, this represents the region from the distal portion of the transverse carpal
ligament (TCL) and the distal palmar crease.
Zone IV represents the region within the carpal tunnel.
Zone V extends from the musculotendinous junction distally to the proximal edge
of the TCL.
Figure 10.1 The flexor tendon system of the hand.

A. FDS
1. The FDS flexes the proximal interphalangeal (PIP) joints.
2. The median nerve innervates the FDS.
3. The FDS has two heads of origin.
a) The ulnar head originates from the medial epicondyle, the medial col-
lateral ligament, and the proximal ulna.
b) The radial head originates from the proximal radius distal to the supina-
tor insertion.
4. The FDS courses superficial to the median and ulnar nerves and separates the
deep muscle group of the forearm (FDP, flexor pollicis longus [FPL], prona-
tor quadratus) from the superficial layer (pronator teres, flexor carpi radialis
[FCR], palmaris longus, flexor carpi ulnaris [FCU]).
5. In the midforearm, the FDS muscle divides into superficial and deep layers,
which give rise to 4 tendons that course under the flexor retinaculum in a
specific configuration: The border digit tendons (index and small) run dorsal
to the central digit tendons (middle and ring). In 25% of cases, the FDS to
the small finger is absent.
B. FDP
1. The FDP flexes the distal interphalangeal (DIP) and the PIP joints.
2. The FDP to the index and middle fingers is innervated by the median nerve,
and the FDP to the ring and little fingers is supplied by the ulnar nerve.
3. The FDP originates from the proximal ulna and interosseous membrane and
courses in the deep layer of flexor muscles.
4. The FDP of the index finger often arises from a separate muscle belly, allow-
ing more independent motion.
5. The four FDP tendons course deep to the FDS tendons through the flexor
retinaculum and the carpal tunnel.
6. In the digits, the flexor tendons traverse through fibro-osseous sheaths lined
with synovium. A series of five annular and three cruciate pulleys are formed
from condensations of the sheath.
7. Five strong annular pulley bands allow for close apposition of the tendon
to bone, while the thinner three cruciform pulleys collapse to assist in full
digital flexion.
8. The pulleys are ordered from proximal to distal (Fig. 10.2).
a) A1 originates from the palmar plate of the metacarpophalangeal (MCP) joint.
b) A2 arises from the periosteum of the proximal region of the proximal
phalanx.
c) C1 lies between the A2 and A3 pulleys.
d) A3 originates from the palmar plate of the PIP joint.
e) C2 lies just between the A3 and A4 pulleys.
f ) A4 originates from the periosteum in the middle of the middle phalanx.
g) C3 is located between the A4 and A5 pulleys.
h) A5 originates from the palmar plate of the DIP joint.
C. At the entrance to the fibro-osseous sheath, the FDS tendons lie superficial to the
FDP tendons.
D. Subsequently, the FDS tendon divides into two slips that wrap around the FDP
tendon such that the FDP becomes volar to the FDS as the two slips rejoin via
fibers of Camper chiasma (Fig. 10.3).
E. The FDS slips insert on the mid-middle phalanx, while the FDP continues
through the fibro-osseous sheath to insert on the volar base of the distal phalanx.

Figure 10.2 The digital pulley system.
II. Examination
A. The patient with a suspected tendon injury should be examined before administering
local or regional analgesics to determine the extent of injury. The distal neurovascu-
lar status is assessed by two-point discrimination and capillary refill.
B. The location and extent of laceration are documented, as is the resting posture
of the hand and digits. In the presence of a flexor tendon laceration, the digits
assume an extended posture at the DIP and PIP joints. Wrist extension does not
change this position, in contrast to the tenodesis effect resulting in obligatory
finger flexion with wrist extension in the intact hand.
Proximal Distal
Figure 10.3 FDS tendon divides into two slips that wrap around the FDP tendon such that
the FDP becomes volar to the FDS as the two slips rejoin via fibers of Camper chiasma.

Figure 10.4 A: Assessment of FDS function;

B: Assessment of FDP function.
C. The location of injury should be assessed to determine which tendon(s) have

been compromised.
1. FDS continuity can be tested by examining for isolated PIP flexion of each
digit with the other digits held in full extension at the MCP, PIP, and DIP
joints. The patient is asked to flex the free digit actively at the PIP joint. Pres-
ence of active flexion indicates continuity of the FDS to that digit, although
a partial laceration cannot be excluded (Fig. 10.4A).
2. The continuity of the FDP is assessed by asking the patient to flex the DIP
joint while the PIP joint is held in extension (Fig. 10.4B).
D. Radiographs should be examined to exclude bony injuries.
E. Treatment is based upon the zone of injury and injured structures. Delayed treat-
ment of injuries is described in the reconstruction section.
III. Zone of Injury
A. Zone I
1. Zone I is the area distal to the FDS insertion at the mid-middle phalanx.
Because this area is distal to the insertion of the FDS, only the FDP is injured
in lacerations of this zone. Avulsion injuries are also possible within Zone I.
2. A Jersey finger is an avulsion of the tendon from the distal phalanx or from a
fracture of the base of the distal phalanx.

a) Classically the ring finger is involved, and the mechanism of injury is

a sudden hyperextension moment applied to a finger with the FDP in
maximal contraction.
b) Leddy described three types of Zone I flexor tendon injuries (Fig. 10.5).
1) Type I: The proximal tendon is retracted into the palm. Disruption of
the vincular blood supply and proximal musculotendinous retraction
indicate that early repair may be of benefit.
2) Type II: The tendon is retracted to the PIP joint. Repair is possible for
as long as musculotendinous compliance allows.
3) Type III: Avulsion of the tendon with a bony fragment. The bony
fragment usually is entrapped by the distal edge of the A4 pulley,
which prevents retraction. Delayed repair is usually possible.
a) Under brachial tourniquet control in the operating room, the FDP
insertion site at the distal phalanx and the A4 pulley are exposed
through a volar zigzag or midaxial incision.
b) The tendon is sutured and is prepared for attachment to bone. The
stitch is passed through or around the bone to exit dorsally and
distal to the lunula through the nail plate and sterile matrix (to
avoid nail growth abnormalities). The ends can then be tied dor-
sally. Suture anchors have also been used successfully. Larger bony
avulsions usually require fixation with pins or screws.
3. Lacerations
a) The proximal tendon is exposed either locally in the bed of the wound or
retrieved via techniques described for Zone II below. If the tendon retracts
proximally, passing the tendon through the A4 pulley may require sequen-
tial dilatation of the A4 pulley and trimming of the tendon stump.
b) If the distal limb of the laceration is less than 1 cm, advancement of the
tendon and primary repair to bone may be considered. More than 1 cm
of shortening is not advised due to the development of a quadregia effect,
and tendon-to-tendon repair is needed. Primary tendon-to-tendon repair
is described below.
B. Zone II
1. Zone II is the area from the FDS insertion at mid-middle phalanx proximally
to the A1 pulley, comprising the digital sheath. Topographically, this is the
area from the distal palmar crease to the midregion of the middle phalanx.
Figure 10.5 Zone I flexor tendon injuries as described

by Leddy.

2. Lacerations in this area may involve both the FDS and the FDP. This area
is known as, “no man’s land,” as historically results of tendon repair in this
region had poor results.
3. Tendon repair
a) Empiric data suggest that primary repair be undertaken if more than 60%
of the tendon cross-sectional area is disrupted. If less than 60% of the
tendon is disrupted, then it may be sufficient to debride the cut edges to
prevent tendon catching at the pulleys.
b) Contraindications to primary repair include tendon disruption in the setting
of purulent infection, extensive contamination, or soft tissue deficiency.
c) Timing of repair may be dictated by concomitant injuries such as vascular
insufficiency, but in the setting of an isolated tendon injury, early repair
is ideal. Repair can typically be completed up to three weeks following
injury. Results of direct repair after a delay in treatment of more than
3 weeks are less satisfactory.
d) If the repair is not performed emergently, the wound should be irrigated
and the skin loosely closed in the emergency department. Appropriate
antibiotics and tetanus prophylaxis should be given. The patient should
be placed in a dorsal splint.
e) Repair should be performed under brachial tourniquet control in the oper-
ating theatre. If concomitant nerve or vessel injuries are to be repaired,
this work should be undertaken before tendon work as the flexed posture
of the digit after tendon repair may make further surgery difficult.
f ) The tendon ends are exposed using midlateral incisions or zigzag incisions
incorporating the lacerations. The sheath may be opened via radial or ulnar-
based flaps between the A2 and A4 pulleys. The annular pulleys should be
preserved, but it is often necessary to open the C2 or C1 pulleys.
g) The tendon ends may be captured and held for repair by 25-gauge nee-
dles. This helps to minimize tendon trauma. The ends are minimally deb-
rided to prepare for suturing.
h) The proximal tendon stump may be visible in the fibro-osseous sheath and
can be retrieved using gentle pressure to milk the tendon from proximal to
distal. If the tendon has retracted proximally to the palm, then a red rubber
catheter tube may be passed retrograde from the wound into the palm. An
incision is then made in the palm, and the tube is sutured to the tendons. The
tube is pulled back out of the distal wound, carrying the tendons with it.
i) The distal tendon stumps can usually be delivered into the wound by
flexing the DIP and PIP joints. If less than 1 cm of the tendon can be
delivered by this technique, it may be necessary to incise the next distal
cruciate pulley to gain sufficient working length.
j) It is critical to restore the anatomic relationship of the FDS and FDP such
that the FDP is passed through the FDS slips at the decussation. Repair
of the lacerated FDS slips may require smaller sutures (4-0 or 5-0) to
decrease trauma to the small slips and reduce bulkiness.
k) In most cases, repair of both the FDS and the FDP is indicated. In cases
where the bulk of the repair does not allow gliding within the flexor sheath,
one slip of the FDS can be excised. If the tendon stumps are contaminated
or frayed, repair of the FDP alone with excision of the FDS tendon can be
considered. Caution should be used in choosing this option because it limits
future procedures should repair fail.

l) Repair strength is proportional to the number of core sutures crossing

the repair. Historically, most repairs were performed with 2 core strands,
but most authors currently recommend a minimum of 4 core sutures to
cross the site. Additional strands of core suture increase repair strength,
but must be balanced against the surgeon’s ability to suture the tendon
atraumatically and between bulk and gliding of the repaired tendon.
m) 3-0 or 4-0 nonabsorbable braided polyester or fiberwire suture is typically
utilized for the core suture.
n) Suture method depends on the surgeon’s preference (Fig. 10.6).
o) Epitendinous sutures decrease gap formation, improve contour, and
improve strength of the construct between 10% and 40% of ultimate ten-
sile strength. Typically, 6-0 running Prolene suture is preferred (Fig. 10.7).
p) Before closure, tendon gliding through the A2 and A4 pulleys should be
assessed with passive flexion. Gentle pulley dilatation as indicated may be
required.
q) The tourniquet is released, hemostasis is obtained, and the wound is
closed. The hand should be immobilized with a dorsal plaster slab extend-
ing from the forearm to the fingertips of all the digits. The wrist should be
positioned in 30 degrees of palmar flexion, the MP joints in 60 degrees of
flexion, and the PIP and DIP joints in full extension.
Seiler 4 strand Single-Cross Grasp Figure 10.6 A-E Techniques for flexor tendon
E repair

Figure 10.7 Epitendinous suture methods.
IV. Zone III
Zone III injuries are usually complex, due to the proximity of flexor tendons to other
critical structures including the common digital nerves, the superficial arch, the motor
branch of the median nerve, and the lumbrical muscles.
A. Wounds are extended proximally and distally in Bruner fashion; then they are
thoroughly explored, irrigated, and debrided.
1. Injuries to the deep structures of the palm, that is, the deep motor branch
of the ulnar nerve and the deep palmar arch, are repaired prior to addressing
flexor tendons.
B. Usually, a lumbrical muscle tethers cut flexor tendons and prevent them from
retracting from the wound bed.
1. If the proximal end cannot be identified, a second longitudinal incision is
made in the forearm and the tendon is identified at this level.
a) A short whip stitch is placed in the proximal tendon end and then used
to pass the tendon through the carpal tunnel and into the distal surgical
wound.
b) The tendon is then repaired in the usual fashion.
C. The decision to repair an injured lumbrical muscle depends on the extent of
tissue loss.
1. Repair without advancement: Repair fosters return to normal function and
also improves blood supply to the tendon repair site.
2. Excessive advancement will result in paradoxical IP joint extension with
attempted forceful flexion (lumbrical plus finger).
D. Following tendon repair, microsurgical repair of superficial neurovascular
structures may proceed.

V. Zone IV
Zone IV injuries are rare because of the protection provided by the TCL and carpal
bones. Injuries to this depth commonly involve the median nerve, as it is the most
superficial structure in the carpal tunnel.
A. The wound is extended into the palm and forearm, in line with the long axis of
the ring finger.
B. Skin flaps are retracted and the soft tissues are irrigated and debrided.
C. If possible, cut tendons should be repaired either proximal or distal to the carpal
tunnel without releasing the TCL.
D. In cases where the median nerve is lacerated, however, the carpal tunnel must be
fully released.
1. TCL is step-cut
Begin radially through the proximal ligament, then transversely through the
body of the ligament, and completing through the ulnar half of the distal
portion.
E. Hemorrhagic tenosynovium is thoroughly debrided and proximal and distal ten-
don ends are matched and repaired.
1. A four-stranded, locked-cruciate core stitch with a running epitendinous
stitch is used.
2. The median nerve should be repaired after all tendons are repaired.
F. The step-cut TCL ends are then sutured with 3-0 absorbable suture in the
Z-lengthened position.
1. Repair of the TCL is done for prevention of bowstringing during rehabilita-
tion.
2. In cases where the TCL is irreparable due to injury, the palmaris longus
tendon or a long toe extensor may be harvested and used to reconstruct
the ligament. The graft is woven through remaining tissue and sutured to
itself.
3. Postoperative rehabilitation is not altered by TCL reconstruction.
VI. Zone V
Acute injuries to flexor tendons and the flexor musculature in Zone V may be repaired
within 3 weeks of the time of injury. After 3 weeks, permanent musculotendinous unit
shortening occurs and secondary reconstruction or tendon transfers may be required
to correct the defect. If the injury is more than 7 days old, the surgeon should also be
prepared to perform nerve grafting for median nerve injuries.
A. The traumatic wound should be extended proximally and distally, and the
wound should be carefully explored, irrigated, and debrided.
1. The presence of hematoma within a tissue plane gives the surgeon an indica-
tion of the depth of the wound.
2. Hemorrhagic synovium in particular should be debrided, examining for
injured tendons that may have retracted into the muscle belly.
B. The volar antebrachial fascia is incised to improve exposure, but the investing
fascia of each individual muscle should be preserved whenever possible to facili-
tate suture repairs.
1. A muscle will not hold suture, but its fascia will.
C. The proximal and distal ends of the cut tendons are then matched.

1. If distal tendon ends have retracted into the carpal tunnel, then the TCL
should be released to allow adequate exposure.
a) The TCL is step-cut, beginning radially through the proximal ligament,
continuing transversely through the body of the ligament, and complet-
ing through the ulnar half of the distal portion.
b) The TCL is repaired in a lengthened position at closure to prevent bow-
stringing of tendons during rehabilitation.
2. Traction is applied to the distal tendon to identify its corresponding digit.
a) Due to interconnections between flexor tendons and their synovial
sheaths, more than one digit may flex.
b) The principle digit supplied by a tendon may be identified by comparing
the force of flexion exerted at the digital pads during traction.
3. Four cues are checked to identify the proximal tendons.
a) First, tendons are provisionally identified by their position in the forearm.
b) General appearance:
1) Profundus tendons are flat and multistranded
2) Superficialis, FPL, and the index finger profundus are oval.
c) Angles of laceration
d) Cross-section size and shape
4. Final check of tendon matching:
Tendon ends are brought to apposition and secured with a transfixing hypo-
dermic needle.
When all tendons are connected, the normal flexion cascade of the
fingers should be recreated.
D. Repair
1. Profundus tendons are repaired first, followed by the FPL and the superficia-
lis tendons.
2. Tendon-tendon repair: 3-0 Ethibond (or 3-0 or 4-0 looped Supramid suture)
using a locked four-stranded core stitch and the repair site “tidied” with a 6-0
nylon, running epitenon stitch.
3. Muscle-tendon repair: Interrupted 3-0 Ethibond, Kessler stitch with a run-
ning nylon epitendinous stitch.
4. Intramuscular injury: horizontal mattress stitches with 0 and 2-0 absorbable
suture are placed through the investing fascia to approximate the lacerated
ends.
After tendon repair, whether in zones III, IV, or V, flexor tendon tension
should be uniform and the cascade of resting fingers returned to normal with
tenodesis intact. This is the final check before wound closure.
VII. Segmental Tendon Defects in Zones III to V
The advancement of profundus tendons in the presence of a segmental tendon defect

should be avoided. In such cases, direct end-to-end repair will result in shortening of
the FDP. Because the profundus tendons share a common muscle belly, the shortened
tendon will decrease the excursion of the other tendons and thus result in the loss of
terminal flexion at all fingers. This is commonly called the “quadrigia” effect.
Specific conditions:
A. End-to-end repair of the profundus is not possible: The distal end is sutured to
the adjacent profundus.

B. End-to-end repair of the superficialis is not possible: Tendon is not repaired and
the patient is left with a profundus finger.
C. Interposition tendon grafts may also be considered to fill in tendon substance
defects.
1. Palmaris and toe extensor tendons are the most commonly used grafts.
VIII. Partial Tendon Laceration
Although the injured tendon maintains some measure of continuity, management of

partial lacerations of flexor tendons poses a significant challenge for clinical judgment.
Primary concerns are predicting the tendon’s capacity to tolerate loads and avoid late
rupture and the prevention of limited range of motion due to tendon entrapment and
“triggering.” Secondary rupture is uncommon.
A. Although repair of partial lacerations of more than 60% of the flexor tendon is
commonly advocated, as little as 25% of the flexor tendon may provide adequate
strength for unrestricted active range of motion.
1. Repairs are done in the usual fashion—a core stitch of 3-0 braided suture
with a running epitenon repair with 6-0 nylon.
B. Lacerations involving 33% to 60% can typically be treated with an epitendinous
suture only.
C. Lacerations involving less that one third of the tendon substance are best treated
with debridement of the tendon ends. The lowest resistance to gliding results
from trimming of the flexor tendon to a smooth contour.
1. This showed no adverse effects on tendon strength.
2. Partial sheath excision may also improve tendon gliding in the digital
sheath.
a) The A2 and A4 pulleys should be preserved.
IX. Flexor Tendon Rehabilitation Principles
Despite technical improvements in flexor tendon repair, particularly in Zone II, out-
comes are fair to poor in 7% and 20% of cases and secondary surgeries including ten-
olysis and joint capsular release are often performed. Rupture has been reported in
up to 6% of repairs, most often due to poor patient compliance with postoperative
limitations but also resulting from technical errors and overly aggressive therapy. Appro-
priately directed therapy, matched to patient needs and disposition, is crucial for the
avoidance of complications and the optimization of outcomes.
A. Tendon healing (see earlier portion of the chapter on Tendon Biology)
1. While the extrinsic healing response has the potential for greater and more
rapid collagen deposition at the repair site than the intrinsic, it carries the
disadvantage of forming restrictive adhesions.
2. These adhesions limit tendon excursion, resulting in loss of active flexion
and/or the loss of differential motion at the PIP and DIP or differential
motion between digits.
3. Activity restrictions must reflect the predicted strength of the tendon repair
as it relates to the time from surgery. Tendon repairs weaken for the first
4 weeks after surgery if immobilized, but have been shown to maintain time
zero repair site strength for the first 3 weeks postoperatively if mobilized
using a clinically relevant place-and-hold synergistic wrist protocol.

a) At the end of the first postoperative week, repair strength is 50% less than
that of the original repair if immobilized. If the tendon is mobilized pas-
sively during this time, no loss of time zero repair site strength occurs.
b) At 3 weeks, strength is decreased by 30% if immobilized. The intact (gap
£3 mm) repair site begins to accrue ultimate strength beginning at three
weeks.
c) By the end of the sixth postoperative week, the tendon repair is 20%
stronger than at the time of surgery. If mobilized using a synergistic wrist
protocol, then repair site strength can increase by a factor of two or more
during weeks 4 to 6 postoperatively.
B. Adhesion prevention
1. Modern rehabilitation protocols are based on the use of controlled mechani-
cal loading and tendon excursion to mechanically inhibit the formation of
extrinsic tendon adhesions.
a) Although up to 9 cm of flexor tendon excursion is needed to achieve
full, combined wrist and finger flexion, only 3 to 4 mm of intrasynovial
tendon glide is needed to prevent adhesion formation.
2. Tension in excess of the tendon repair site’s force of gapping may cause gaps
in excess of 3 mm, if not overt rupture.
a) Increased tendon gapping does not directly result in loss of range of
motion, but delays the development of tendon strength and may contrib-
ute to late tendon rupture as the demands of therapy increase.
3. There are a variety of rehabilitation protocols used in modern practice. Some
place more stress on the tendon repair site than others. Some require greater
patient adherence to activity limitations and tolerance for discomfort than
others. Careful matching of patient characteristics to the rehabilitation regi-
men is necessary to optimize patient performance and satisfaction.
C. Edema control
1. Tendon motion during the first 5 postoperative days has been shown to
increase the tensile strength of repairs when compared with similar tendons
treated with immobilization.
a) Edema in the repaired tendon and its surrounding soft tissues increases
the resistance to finger flexion during this same period. The additional
work required to flex the digit may exceed the force-to-gapping of the
tendon repair, resulting in a weakened or even ruptured tendon.
Recommendation:
1) Short-term restriction of flexion, lasting no more than 3 days, while
aggressive edema control consisting of elevation and digital wrapping
is begun.
2) Extension stretching with the goal of achieving full PIP extension may
begin immediately after surgery.
X. Flexor Tendon Rehabilitation Programs
A. Passive range of motion (Duran protocol)

1. Passive exercises performed under therapist’s supervision.
2. Postoperative splint: Extension block splint with IP’s extended, MCPs flexed
70 degrees, and the wrist flexed 10 degrees.
a) Passive flexion and active extension exercises are allowed in the splint.

b) Passive extension is allowed in isolated joints, with all other joints in

maximal flexion.
3. At three weeks, the wrist splint is reheated and the wrist is extended to zero
degrees.
4. At one month, “active motion” in the form of place-and-hold exercises is
begun.
a) The digit is placed in a fully flexed position and the patient voluntarily
holds it in this position.
5. At 6 weeks, the patient is weaned from splinting and active motion begins
under therapist supervision.
a) Blocking exercises at the DIP and PIP are used to provide differential
flexion between FDS and FDP from this point on.
6. Ten weeks after surgery, resisted strengthening exercises begin.
7. All activity restrictions are lifted at 16 weeks.
B. Kleinert modification of passive motion protocol
1. Elastic bands are attached to the digit’s nail and pass under a palmar hand
pulley to the wrist.
a) The palmar pulley maximizes DIP and PIP flexion compared to models
that attach directly to the wrist.
2. Active finger flexion is restricted, but fingers are passively flexed by the elastic
bands. This maintains a protected position and allows for active extension
exercises.
3. This protocol results in a higher incidence of flexion contractures at the PIP
than is seen in the Duran protocol.
4. Rubber bands should be removed at night and the hand returned to a resting
position with the IP’s extended.
C. Active motion protocols
1. All controlled motion protocols are designed to provide tendon excursion
without the creation of nonfunctional gaps. Passive motion protocols avoid
active tensioning of the repair site and instead rely on externally applied
forces to produce tendon gliding, preventing adhesions.
2. Proponents of active motion protocols, however, argue that true proximal
migration of the repair site depends on tension from the musculotendinous
unit.
a) Externally applied forces may buckle or roll the tendon during joint
motion rather than cause the tendon to glide through its surrounding
tissues.
1) At least 300 g of intrinsic tension is required at the repair site to achieve
predictable tendon excursions with passive motion of the digits.
3. Improved suture materials and techniques using four or more suture strands
crossing the repair site have been employed to resist unacceptable gapping
and repair site rupture during active motion.
4. The most commonly employed protocol of this type was popularized by
Strickland.
D. Strickland protocol
1. Tendon repaired with at least a four-stranded core suture and an epitendi-
nous stitch.
2. Two splints are employed.
a) The first is a conventional dorsal blocking splint: IP’s extended, MCPs
50 degrees flexed, and wrist 10 to 15 degrees flexed.

b) The second splint, a hinged “tenodesis” orthosis, is provided. This allows

the wrist to be fixed anywhere from full flexion to 30 degrees of exten-
sion, allowing for an increased tendon excursion with synergistic wrist
extension and finger flexion. MCPs are maintained in 60 to 70 degrees of
flexion to decrease forces on flexor tendons.
3. Therapy is begun within the first 48 hours after surgery and combines edema
control with range of motion exercises.
4. The patient is then instructed in “place and hold” exercises.
a) Here, the wrist is extended 30 degrees and the fingers fully flexed passively.
1) The “hold” component involves the patient actively holding the digit
in this flexed position for at least 5 seconds.
b) When not exercising, the patient returns to their dorsal blocking splint.
5. After one month, the patient may discontinue use of the tenodesis splint and
begins to place and hold at progressively greater MCP extensions.
6. At 6 weeks, the resting splint is discontinued and active finger flexion begun.
Joint blocking at the PIP and DIP increases tendon excursion and favors dif-
ferential flexor movement.
7. At two months, light strengthening may be instituted.
8. Full, unrestricted activity is allowed at 14 weeks.
E. Early active motion
1. Postoperative splinting: Patient placed in extension block splint with IPs
extended, MCPs flexed 70 degrees, and the wrist extended 20 degrees.
2. Active extension of the fingers is allowed from the time of surgery.
3. Controlled active flexion is begun with limited repetitions at 24 to 48 hours
and is repeated every four hours throughout the day.
a) Two repetitions of passive flexion to the palm are followed by two active
hold exercises that place the PIP at 30 degrees and the DIP at 5 to
10 degrees of flexion in the first week.
4. Flexion is advanced gradually to 80 to 90 degrees of PIP flexion and 50 to
60 degrees of DIP flexion by the fourth postoperative week.
5. Light strengthening begins at 8 weeks.
6. All postoperative limitations are lifted at 14 weeks.
F. Zones III to V injuries
1. Protected motion is needed to optimize results in all zones.
2. Either passive, active, or early active motion protocols may be employed at
the clinician’s discretion. The choice of protocol depends primarily on the
predicted strength of the tendon repair and patient’s perceived motivation
and ability to understand and comply with activity restrictions.
3. Loss of differential digital motion is common in zones IV and V, where
repaired tendons lie in close proximity to one another and intertendinous
adhesions may form.
XI. The Pediatric Patient
Children less than 10 years old and patients with developmental or psychosocial limitations
that predict for inability to comply with activity limitations should be casted in 20 degrees
of wrist extension and full MCP flexion with fingers fully extended. Immobilization for
3 to 4 weeks is followed by hand therapy to regain active and passive flexion. Tenolysis and/
or surgical release of joint contractures may be needed once the tendon repair matures.

Flexor Tendon Reconstruction
I. Rupture Repair
A. Repair site rupture can be caused by multiple factors after flexor tendon repair
1. Patient non-compliance with the aftercare regimen
2. Non-availability of skilled hand therapy
3. Formation of peritendinous adhesions
4. Complex injury
5. Repair method
B. Patient assessment
1. Loss of flexor tone
Assess the flexor cascade and look for loss of appropriate flexor cascade as a sign
of repair site rupture. Digits that are swollen can be very difficult to examine.
2. Loss of tenodesis
If the examiner is skilled, remove the splint and slowly move the wrist from
palmar flexion to wrist extension. If the repair is intact and gliding, there
should be some increase in digital flexion
3. Loss of tendon flicker
If the examiner is skilled, remove the splint and ask the patient to demon-
strate tendon function with a flicker of active motion
4. If the examiner is skilled and a multistrand, multigrasp suture method was
used to repair the tendon, then place the fingers into flexion, and ask the
patient to hold them in that position. Inability to hold the fingers may sug-
gest repair site rupture
C. Diagnosis
1. The diagnosis of repair site rupture is based on clinical findings
2. Ultrasound may be helpful in differentiating adhesion formation from ten-
don rupture
D. Early detection of repair site rupture
1. Assess risks for repair site rupture
2. Treatment alternatives
a) Re-repair
b) Preparation for tendon grafting
c) Nonsurgical strategies: Range of motion exercises and buddy straps
E. Late detection of repair site rupture
1. Assess the risks for repair site rupture
2. Preparation for tendon grafting
a) Recover full passive range of motion in both flexion and extension
b) Allow soft tissues to stabilize
c) Schedule tendon grafting when the patient has the time and the desire to
participate in an intensive hand therapy rehabilitation program
3. Interphalangeal (IP) joint fusion
4. Amputation Ray/resection
5. Nonsurgical strategies: Range of motion exercises and buddy straps
F. Patient education
Often the results from re-repair are not as good as the results of successful pri-
mary tendon repair.

II. Tenolysis
A. Tenolysis is the procedure that is recommended and performed to remove

peritendinous adhesions around the repair site and along the tendon surfaces in
order to restore normal tendon gliding and improve digital range of motion.
B. At 3 to 4 months following tendon repair, patients have recovered approximately
90% of their ultimate range of motion.
C. Tenolysis can be an effective strategy to improve range of motion when several
criteria are met.
1. The patient has recovered full passive range of motion in both flexion and
extension.
2. The tendon repair is intact.
3. The soft tissues have stabilized.
4. The patient is motivated and desires to participate in an intensive therapy
program.
5. Hand therapy is available to the patient.
D. Operative procedure
1. The patient should undertake the procedure when they have sufficient time
and access to undergo appropriate rehabilitation.
2. If the procedure is done under IV regional anesthesia, the intraoperative
range of motion can be demonstrated to the patient.
3. Extensile digital exposure is necessary.
a) The old incision
b) Midaxial incision may be useful to avoid placing the suture line over the
flexor tendon sheath.
4. Remove all peritendinous adhesions
a) Initially assess the repair site and remove adhesions from this area.
b) Secondarily remove any other adhesions that have formed. Small angled
beaver blades may be useful for reaching beneath crucial pulleys.
c) Work within windows in the flexor tendon sheath to restore full tendon
excursions.
d) Manipulate or release any residual joint contracture.
E. Begin intensive hand therapy on the first postoperative day.
III. Tendon Grafts
A. Introduction
1. Tendon grafting is a procedure that uses a free autogenous tendon graft,
which is harvested from a distant site, and used to re-establish the continuity
of the flexor tendon unit.
2. Most commonly, the procedure is done to restore the function of the FDP
muscle tendon unit.
B. History of flexor tendon grafting
1. Until the 1970s, flexor tendon grafting for reconstruction of Zone II injuries
was the preferred method of treatment for patients with laceration of the
flexor tendons.
2. With the advent of successful flexor tendon repair, the indications for flexor
tendon grafting have substantially decreased.
3. The results of tendon grafting have improved over time with the introduction
of rehabilitative methods that employ digital range of motion and improved

methods for care of associated injuries to the skin, nerve, and skeleton.
The choice of the donor tendon may also improve the outcome following
tendon grafting.
C. Indications for surgery
1. Neglected digital laceration with flexor tendon transection.
2. Failed flexor tendon repair
3. Severe crushing injury with segmental tendon loss
D. Findings on Physical Examination
1. Loss of normal finger cascade
2. Absent FDP function on clinical examination
3. Absent FDS function on clinical examination
4. Alteration of two-point discrimination on either side of the finger.
5. Vascular supply of the finger:
a) Digital Allen testing
b) Assessment of capillary refill
c) Assessment of venous congestion
6. Piability and softness of the skin and subcutaneous tissues.
7. Pulley function; fixed PIP and DIP flexion deformity if A2 and A4 pulleys are
incompetent respectively.
8. Carefully assess the patient for the presence of the desired donor tendon.
E. Radiological assessment
1. Plain radiographs should be done to ensure that the skeleton is stable.
2. Additional imaging is usually not necessary.
F. Timing for surgery
1. Procedure is done electively.
2. In unusual circumstances, tendon grafting may be done for acute reconstruc-
tion in the setting of severe trauma.
3. In general, the procedure should be done when
a) The soft tissues are mature.
b) The skeleton is stable.
c) Full passive range of motion has been recovered.
G. Single-stage and multiple-stage tendon grafting
1. Single-stage tendon grafting
For single-stage tendon grafting, the finger is examined and if the sheath is
sufficient, the tendon graft is harvested and inserted in a single operation.
Often this requires dilation of the pulleys and to ensure that the graft will
be freely mobile when placed in the sheath. This method of tendon graft-
ing has the advantage of requiring a single operation; it shortens the course
of treatment and has outcomes similar to multiple-stage tendon grafting.
It requires that the flexor tendon sheath be suitable to immediate tendon
passage.
2. Multiple-stage tendon grafting
When the tendon sheath is not suitable for single-stage grafting, a sili-
cone rod is secured distally and placed into the tendon sheath to facilitate
re-formation of a suitable tendon sheath. If needed, pulleys may be recon-
structed over the rod. This method requires a second procedure for tendon
graft insertion and may have complications related to the silicone rod itself
(synovitis and infection). Typically, the second stage (tendon graft insertion)
is done approximately 6 weeks later and can be done through smaller inci-
sions. Participation in hand therapy is crucial during both stages, as passive
digital range of motion must be maintained.

3. Paneva-Holevich technique
FDS to FDP coaptation repair combined with Hunter tendon rod can be
attempted. Main difficulties are due to a bulky tenorrhaphy in the palm fol-
lowing the first stage, and the difficulty in tensioning the graft on repair to
the distal phalanx during the second stage.
H. Technical aspects of tendon grafting surgery
1. Patient preparation
The patient must understand that the procedure will be more complicated
than primary repair and may require multiple procedures to obtain the maxi-
mum range of motion. The therapy that is required after the procedure is
extensive and necessary. If the patient is unwilling/unable to participate in an
organized therapy program then tendon grafting is NOT a good alternative.
2. Surgical preparation
a) Supine position.
b) Brachial tourniquet.
c) Preoperative antibiotics are usually indicated.
d) Preparation of a distal site for donor tendon graft harvest if necessary.
3. Choice of the incision
a) Mid-axial incision
b) Bruner type of incision (zigzag)
c) Combined incision incorporating original wound
d) Mini proximal and distal incisions
These incisions are used for the second of two stages and allow the graft to be
passed without the need for dissection of the entire finger.
4. For single-stage grafting, confirm the nature of the tendon injury and per-
form tenolysis and/or tendon excision as necessary. Annular pulleys may need
dilation with a pediatric uterine sound
5. Assess the need for any other procedures
a) Pulley reconstruction
b) Nerve repair/grafting
c) Z-plasty or other skin rearrangement
6. Choice of the donor tendon (for autogenous donor tendons)
a) Palmaris longus
1) Extrasynovial donor tendon
2) Most common graft used today
3) Minimal donor morbidity from uncomplicated harvest
4) May be unilateral or absent on both forearms
5) Does not reach distal forearm
b) Plantaris
2) Requires leg dissection for harvest
c) Toe extensors
2) Requires leg dissection
d) Flexor digitorum longus
1) Intrasynovial donor tendon
2) Usually the second toe is used
7. Choice of the distal repair site
a) Tendon to bone interface
b) Base of the distal phalanx is most common

8. Choice of the proximal repair site

a) “In the palm” or just distal to the lumbrical origin in the palm of the
hand
b) In the forearm proximal to the TCL—requires a longer tendon graft
9. Verification of presence of the critical annular pulleys
a) A2
b) A4
10. Insertion of the tendon graft
a) Pass a chilled pediatric feeding tube or similar device through the flexor
tendon sheath (chilled so that the tube is more rigid, and can pass through
the pulley system more easily).
b) Sew the graft to the feeding tube with a loose suture near the site of the
proximal juncture.
c) Pull the feeding tube distally and pass the graft through the sheath behind
the tube.
d) Secure the graft at each end of the tendon sheath so that the graft is not
pulled into the sheath with repositioning of the finger.
11. Distal repair (done first, to allow easier tensioning of the tendon during
performance of the proximal weave)
a) Tendon to bone preferred
b) Usually done first with the proximal repair done second
c) Pull out suture methods
1) Prolene (or other monofilament sutures)
2) Around the bone
3) Through the bone
4) Out the fingertip
d) Suture anchor methods
1) Mini anchor(s) placed at the site of graft insertion
2) Sliding suture placed to allow the graft to be slid into position on the
distal phalanx as the suture is secured
e) Common features
1) Small bone trough or cortical roughening to which the tendon can be
sewn
2) Good contact between the graft and the point of repair
12. Proximal repair
a) Location
The proximal repair may be done in the palm or in the distal forearm.
The location of the proximal repair does not influence the outcome of
digital flexion. If the proximal repair is done in the palm, it should be
done distal to the origin of the lumbrical muscle.
b) Usually the second of the two repairs
c) Method of tendon repair
1) Pulvertaft tendon weave
2) Two passes of the tendon graft through the proximal tendon when
possible
3) Secured with 3-0 braided Dacron, Supramid, Fiberwire or other
synthetic suture material
13. Setting the tension
a) Set the tension of the graft to create a finger cascade that shows slightly
increased flexion for the grafted finger.

b) In general, it is easier to set the tension of the graft in the proximal repair
site.
14. Wound closure
a) The wound is closed with a fine nylon suture.
b) A sterile, nonadherant, antibiotic-impregnated dressing is applied to the
wound sites.
15. Splint application
After application of the dressing to the finger and hand, the patient should be
placed in a dorsal protective shell with the wrist in approximately 35 degrees
of flexion, the MP joint flexed to approximately 50 degrees, and the IP joint
at 10 degrees of flexion.
IV. Care After the Procedure
Patients are started on a program of occupational therapy as soon after the procedure as
possible. We start passive range of motion for the fingers immediately. Other therapy
interventions are made based on the complexity of the reconstruction and the compli-
ance and understanding of the patient.
V. Pulley Reconstruction
A. Pulley reconstruction
Pulley reconstruction is the procedure that is done to restore tendon position in
the flexor tendon sheath.
B. Pulley rupture
Pulley rupture of the crucial annular pulleys is an uncommon injury but does
occur after open injuries and in elite sporting events (NFL football and rock
climbers). After pulley rupture, the flexor apparatus falls away from the phalanx.
This change in the position of the tendon can cause PIP joint flexion and loss of
distal joint flexion (or flexion strength).
1. With rupture of the A2 pulley, patients usually present with a fixed flexion
deformity of the PIP joint.
2. Diagnostic imaging
a) Plain radiographs are usually normal.
b) MR imaging is effective and demonstrates palmar translation of the
flexor tendon. Comparison with the adjacent normal digits can be very
helpful.
C. Treatment alternatives
1. Nonsurgical strategies
Nonsurgical strategies can be effective; especially if they are implemented
within the first 4 weeks following injury and before a fixed deformity
develops. A pulley ring, molded by a hand therapist, will help hold the ten-
dons in position while the soft tissues heal. A PIP joint extension splint may
also be necessary.
2. Surgical strategies
a) Reconstruction materials
1) Autogenous tendon graft
a. Extrasynovial donor tendon
i) Palmaris longus

ii) Extensor indicus proprius

iii) Extensor digitorum longus
b. Intrasynovial donor tendon
i) Flexor digitorum longus
2) Extensor retinaculum
3) Hemi-slip of FDS
b) Methods of reconstruction
1) Belt loop methods
The belt loop method is technically straightforward and the tension
is easy to adjust. For the A2 pulley, reconstruct a pulley length of
at least 5 mm and pass the reconstruction material deep to the
extensor mechanism. Tension the repair with a Pulvertaft weave
method so that the FDS and FDP tendons are in an appropriate
position in the digital sheath. After the reconstruction is complete,
check to ensure that there is full tendon excursion and no signifi-
cant residual tendon bow stringing. For the A4 pulley, the recon-
struction may be passed over the top (dorsal) of the extensor
mechanism.
2) Trans-osseous reconstructions
3) Use of the “ever present” rim of the pulley
c) Goals of reconstruction
1) To restore the position of the flexor tendons in the tendon sheath.
2) To create a reconstruction that is of sufficient length and tension to
hold the tendons near the bone but not restrict excursion of the
tendons.
I. Anatomy (FIG 10.8)
A. Extrinsic Muscles
The extrinsic muscle-tendon units arise from the lateral elbow, radius, ulna, and forearm
interosseous membrane. The wrist extensor muscles include the extensor carpi radia-
lis longus (ECRL), the extensor carpi radialis brevis (ECRB), and the extensor carpi
ulnaris (ECU). The thumb and finger extensor muscles include the abductor pollicis
longus (APL), the extensor pollicis brevis (EPB), the extensor pollicis longus (EPL),
the extensor indicis proprius (EIP), the extensor digitorum communis (EDC), and the
extensor digiti minimi (EDM).
The wrist and finger extensor tendons pass through six retinacular compartments
along the dorsal aspect of the wrist. The first extensor compartment contains the APL
and EPB tendons, which insert onto the bases of the first metacarpal and thumb proxi-
mal phalanx, respectively. The ECRL and ECRB tendons course through the second
extensor compartment and attach to the bases of the second and third metacarpals,
respectively. The EPL tendon courses through the third extensor compartment and
inserts onto the dorsal base of the thumb distal phalanx.
The EIP and EDC tendons pass through the fourth extensor compartment, the
EDM tendon passes through the fifth extensor compartment, and the ECU tendon
passes through the sixth extensor compartment. The EIP, EDC, and EDM tendons
join the finger extensor apparatuses, whereas the ECU tendon inserts onto the base
of the fifth metacarpal. The relationship of the EIP and the EDC of the index finger

Figure 10.8 Anatomy of the extensor mechanism of the digit. (Reprinted from Doyle
JR. Dorsal hand. In: Doyle JR, Botte MJ, eds. Surgical Anatomy of the Hand and
Upper Extremity. Philadelphia, PA: Lippincott Williams & Wilkins; 2003:653.)
usually puts the EIP ulnar and deep to the EDC. In addition, the muscle belly of the
EIP extends more distally. Juncturae tendinum are filamentous and tendinous bands
that interconnect the extensor tendons of the index, long, ring, and small fingers at the
dorsum of the hand.
B. Intrinsic Muscles
The intrinsic muscle-tendon units include seven interossei (three palmar and four dor-
sal) and four lumbricals. The interossei muscles originate on the finger metacarpals with
distal attachments to the extensor apparatuses and the bases of the proximal phalanges:
four are dorsal that assist with abduction of the index, middle, and ring fingers, and three
are palmar that assist with adduction of the index, ring and small fingers. The lumbrical
muscles originate on the FDP tendons and insert into the radial lateral bands distally.
The combined intrinsic muscle-tendon units course volar to the axis of rotation of MCP

joint and dorsal to the axes of rotation of PIP and DIP joint. This anatomic arrangement
leads to MCP joint flexion and IP joint extension with muscle contraction.
C. Extensor Apparatus
The finger extensor apparatus is comprised of the extrinsic and intrinsic tendons and
soft-tissue-stabilizing structures. The extrinsic tendon contribution to each finger passes
dorsally over the MCP joint before trifurcating into a central slip, which continues
and inserts into the dorsal base of the middle phalanx, and two lateral slips (radial and
ulnar). The interosseous and lumbrical tendons form a lateral band on each side of the
digit. These lateral bands join with the lateral slips of the extrinsic extensor tendon at
the level of the PIP joint to form the conjoined lateral bands. The two conjoined lateral
bands converge dorsally and insert at the base of the distal phalanx as the terminal
extensor tendon.
Structures stabilizing the finger extensor apparatus and coordinating joint move-
ment include the sagittal bands (connect the extrinsic extensor tendons to the MCP
joint volar plate), the transverse retinacular ligaments (connect the lateral bands to the
PIP joint volar plate), and the triangular ligament (connect the conjoined lateral bands
over the middle phalanx). The oblique retinacular ligaments are variably present and
assist with linking IP joint motion (active DIP joint flexion leads to tightening of the
ORL and concurrent PIP flexion, whereas active PIP joint extension leads to tighten-
ing of the ORL and concurrent DIP extension). The ORL arises from the palmar plate
of the PIP joint and flexor tendon sheath and inserts onto the dorsal base of the distal
phalanx with the terminal extensor tendon.
The thumb extensor apparatus is less complex. The EPL tendon is necessary for
strong thumb retropulsion and IP joint hyperextension. The EPL tendon passes over
the MCP joint stabilized by two sagittal bands, and attaches directly to the dorsal base
of the distal phalanx. The EPB tendon courses radial to the EPL tendon and inserts
onto the dorsal base of the proximal phalanx to assist with MCP joint extension. Two
intrinsic thumb muscles (abductor pollicis brevis [APB], flexor pollicis brevis [FPB]),
and the adductor pollicis weakly contribute to thumb extension via attachments to the
extensor apparatus.
D. Anatomic Variations
An extensor digitorum brevis manus muscle is present in 3% of hands and can be con-
fused with a dorsal wrist ganglion cyst. The EIP tendon is normally positioned ulnar
to the index finger EDC tendon, and the EDM tendon is normally positioned ulnar to
the small finger EDC tendon. Infrequently, the EIP tendon courses radial to the index
finger EDC tendon. The small finger EDC tendon is absent frequently, and the EPB
tendon is absent in approximately 5% of individuals. The APL tendon is composed of
two or more tendon slips and the EPB is often located in a separate dorsal subcompart-
ment within the first dorsal compartment. There are often duplicate EDC tendon slips
to the ring and small fingers.
II. Zones of Injury
There are nine zones described for wrist and finger extensor tendon injuries and five
zones described for thumb extensor tendon injuries. The odd numbered zones are
positioned over the joints.

A. Finger and Wrist Injuries

The soft tissue envelope is inspected, the neurovascular status is assessed, and active
as well as passive (with and without wrist flexion tenodesis) wrist and finger motions
are observed. Independent extension of either the long or ring finger requires intact
EDC tendon slips. Autonomous extension of the index and small fingers requires func-
tional EIP and EDM tendons, respectively. Weakness of extension against resistance
may imply a partial tendon injury. Auxiliary imaging with an ultrasound or MRI may
confirm a suspected partial or complete tendon laceration.
1. Zones I and II (mallet finger). Closed tendinous ruptures or small dorsal lip
fractures are immobilized with a DIP joint extension splint for a minimum of 6
weeks. Open tendon injuries are repaired and consideration may be given toward
reflecting a conjoined lateral band distally if there is loss of tendon substance.
Closed mallet fractures involving more than 50% of the joint surface with DIP
joint subluxation are managed by operative treatment; the goal is to establish a
reduced, congruous joint. Numerous surgical techniques have been described
(e.g., extension block pinning). Irrespective of treatment method, a small DIP
joint prominence, a terminal joint extensor lag, and a swan-neck deformity may
persist.
2. Zone III (Boutonniere). The boutonniere finger deformity denotes a flexion
posture of the PIP joint with concurrent hyperextension of the DIP joint. This
abnormality results from disruption of the central slip attachment to the dorsal
base of the middle phalanx, as well as disruption of the triangular ligament across
the dorsal aspect of the middle phalanx. Initially, the lateral bands remain dorsal
to the PIP joint axis of rotation and maintain the PIP joint in extension. If left
untreated, the lateral bands migrate volarly, leading to PIP joint flexion and
increased tension on the conjoined lateral bands with development of a DIP
joint hyperextension deformity.
Early management is predicated upon recognition of the central slip injury.
Weak PIP joint extension and/or a supple PIP joint extensor lag are patho-
nemonic findings. Closed tendinous or small central slip avulsion injuries may
be treated by splinting. Open tendinous injuries, and PIP joint dislocations with
a residual extensor deficit of 30 degrees or greater, are best managed with central
slip repair. Loss of tendinous substance can be addressed by reflecting a portion
of the central slip distally (Snow procedure), or centralizing dorsal strips of the
lateral bands (Aiche procedure). A displaced fracture at the dorsal base of the
middle phalanx may require fracture repair or excision of the bone fragment and
reattachment of the central slip. In all cases, the PIP joint is immobilized in full
extension for 3 to 6 weeks and early active motion exercises of the MCP and DIP
joints are encouraged. Closed PIP transarticular pinning with the joint in full
extension can be considered.
3. Pseudoboutonniere. A PIP joint sprain with damage to the volar plate may
lead to the development of a PIP joint flexion contracture without DIP joint
hyperextension. Unlike an acute boutonniere deformity, the flexed PIP joint in a
pseudoboutonniere deformity is stiff and the DIP joint is not hyperextended.
Treatment of a pseudoboutonniere deformity involves splinting or serial
casting of the PIP joint into extension. Failure to obtain partial correction of
the joint contracture may relate to a concomitant injury to the flexor tendon
sheath with tendon bowstringing or Dupuytren disease. Surgery to correct a
pseudoboutonniere deformity is considered if the PIP joint flexion contracture

persists beyond 30 degrees and interferes with hand function. A PIP joint
contracture greater than 50 degrees is often associated with attenuation of
the central slip, which may impede efforts at rebalancing the digit following
release.
4. Zone IV. A laceration involving less than 50% of the tendon width is managed by
the immobilization of both IP joints in extension for 3 to 6 weeks, with or without
inclusion of the MCP joint. An injury including more than 50% of the tendon
width is typically repaired and the digit is immobilized in a comparable manner.
5. Zone V (sagittal band rupture, fight bite). A partial or complete laceration
of the EDC tendon over the MCP joint is repaired. Postoperatively, the wrist
is immobilized in extension, the MCP joint is immobilized in neutral to slight
flexion, and the finger IP joints are positioned in neutral.
Disruption of one or both sagittal bands may occur in the absence of EDC
tendon injury. Disruption of the radial sagittal band is more common than dis-
ruption of the ulnar saggital band, with a propensity for involvement of the long
finger. Closed injuries less than 3 weeks old are best managed by immobilization
of the MCP joint in extension for 4 to 6 weeks. Closed injuries greater than
3 weeks in duration may require repair of the torn sagittal band and/or release
of the contralateral sagittal band. Open sagittal band injuries with damage to
greater than two third of the structure, and sagittal band injuries leading to
divergent extensor tendon subluxation in the index and small fingers should be
repaired surgically.
A fight bite over the MCP joint often includes damage to the EDC tendon
and one or both sagittal bands. A partial or complete EDC tendon laceration
can be overlooked as the tendon will retract proximally with finger extension.
To avoid missing this injury, the wound should be explored with the MP and
IP joints in flexion as well as full extension. Initial management of a fight bite
involves copious wound irrigation and debridement of foreign material. The
articular cartilage of the MC head is inspected directly. Antibiotics are adminis-
tered, the tetanus vaccination status is assessed, and serological testing for HIV
and hepatitis is entertained. Definitive repairs of the tendon and sagittal band(s)
injuries may be delayed in the presence of gross contamination.
6. Zone VI. Extensor tendon and junctura tendinum injuries proximal to the MCP
joint are repaired. A single tendon laceration at this level can be masked by an
intact junctura. A tendinous defect may require bridging with junctura tendi-
num or an autogenous tendon graft. Postoperatively, the wrist is immobilized
in extension, the finger MCP joints of the digit involved as well as the adjacent
two digits (if injury proximal to junctura) are immobilized in neutral to slight
flexion, and the finger IP joints are positioned in full extension.
7. Zone VII. The extensor tendon(s) is repaired and consideration is given toward
partial or complete repair of the overlying extensor retinaculum to prevent ten-
don bowstringing. Postoperatively, the wrist is immobilized in extension and
the finger MCP joints are positioned in neutral to slight flexion. If only wrist
extensor tendons have been injured, the fingers are not immobilized.
8. Zones VIII and IX. Injured muscle-tendon units in the proximal forearm are
repaired with figure-eight sutures. A side-to-side tendon transfer is indicated, if
there is loss of muscle and/or tendon tissue. Extensor tendon ruptures caused
by abrasion due to dorsally placed distal radius fixation plates or rheumatoid
arthritis of the radiocarpal or the ulnocarpal joints will often be irreparable. They
would need either an intercalary tendon graft or tendon transfer to motor MCP

extension of the finger(s) involved. Postoperatively, the wrist is immobilized in

extension and the finger MCP joints are positioned in neutral to slight flexion.
If only wrist extensor muscle-tendon units have been injured, the fingers are not
included in the splint.
B. Thumb Injuries
Hyperextension of the thumb IP joint necessitates an intact EPL tendon. Incom-
plete IP joint extension may be possible following disruption of the EPL tendon,
if the thumb intrinsic muscles are intact.
1. Zones TI and TII (mallet thumb). Closed tendinous and small avulsion frac-
tures are immobilized with an IP joint extension splint for a minimum of 6
weeks. Open injuries are repaired and the IP joint is splinted or pinned in exten-
sion for a comparable period of time. Loss of tendon substance may necessi-
tate intercalary tendon grafting (e.g., palmaris longus tendon). A forearm-based
thumb spica splint is preferred after surgery in Zone TII: The thumb sagittal
bands are not substantial enough to prevent excess tension across the repair in
this zone.
2. Zones TIII to TV. A closed, nondisplaced EPB tendon avulsion injury is treated
by application of a forearm-based, thumb spica splint with the thumb MCP
joint in full extension for 6 weeks. Open disruption of the EPB tendon may
necessitate tendon repair to prevent development of a boutonniere deformity
(MCP joint flexion and IP joint hyperextension). Active IP joint motion is per-
mitted in both cases.
Lacerations of the APL and/or EPL tendons are repaired and the thumb is
immobilized for 6 weeks in a forearm-based, thumb spica splint. The MCP joint
is included in the splint after APL tendon repair, whereas both the MCP and
IP joints are incorporated after EPL tendon repair. If a thumb extensor tendon
injury occurs beneath the extensor retinaculum and requires repair, the respective
extensor compartment is released to permit unrestricted tendon gliding.
III. Rehabilitation
The goal of rehabilitation is to regain tendon excursion without gapping or rupture

of the tendon repair. Assistance from a trained hand therapist is an integral compo-
nent of postoperative management. The initial splint is removed after several days.
Continued immobilization in a splint or cast for 6 weeks or greater is preferred after
surgical repair of wrist extensor tendon injuries, thumb extensor tendon injuries, and
finger extensor tendon injuries in Zones I, II, VIII, and IX. Finger extensor tendon
repairs in Zones III to VII may be treated by additional immobilization or early
protected finger motion.
The potential for early mobilization and loading depends on the quality of
the tendon repair, associated bone and soft tissue injuries, and patient compliance.
Early motion (4 to 5 mm of tendon excursion) will increase the tensile strength of a
tendon repair and improve tendon-gliding properties. Varied techniques have been
described, including controlled passive motion, short arc active motion, dynamic
extension splint treatment, and relative motion splint treatment. Full composite
wrist and finger motion and resisted extension across the repair site are avoided for
approximately 6 weeks.

Chronic Extensor Tendon Disorders
I. Boutonniere Deformity (FIG. 10.9)
A. Definition
A boutonnière deformity of a digit is characterized by flexion at the PIP joint and
hyperextension of the DIP joint. It results from and initial loss of extensor force
at the PIP joint, with subsequent palmar migration of the conjoined lateral band
of the extensor mechanism secondary to triangular ligament insufficiency, and
increased or concentrated extensor force at the DIP joint. In a chronic condi-
tion, the digit may be stiff and the deformity fixed, that is, it cannot be actively
or passively correctable.
B. Etiology
1. A boutonnière deformity is caused by imbalance of the extensor mechanism,
usually initiated by loss of extensor mechanism’s attachment at the middle
phalanx (central slip).
2. The central slip can be injured by
a) Laceration
b) Closed avulsion
1) Direct blow to the distal end of the outstretched digit, forcing the PIP
joint into flexion while there is tension on the central slip (thus
avulsing the central slip off of the middle phalanx)
c) Attrition by weakening from chronic inflammation at the PIP joint
1) Rheumatoid arthritis
2) Other chronic inflammatory afflictions
d) Burns
3. The loss of the central slip results in active loss of extension at the PIP
joint.
4. Unopposed motion of the digital flexors (flexor digitorum sublimis and pro-
fundus) will result in the PIP joint assuming a flexed position.
5. Progressive palmar migration of the adjacent portions of the extensor mecha-
nism (lateral conjoined bands) at the PIP joint results in further PIP joint
flexion.
6. The extensor force becomes concentrated at the distal phalanx, resulting in
hyperextension of the DIP joint due to the conjoined lateral bands remain-
ing dorsal to the axis of rotation of the DIP joint. This is accompanied by
shortening and contracture of the oblique retinacular ligament.
7. In the chronic state, the deformity is not passively correctable
8. In long-standing conditions, the chronic, fixed contractures at the PIP (or
DIP) joint can lead to secondary arthrosis and associated joint pain.
C. Clinical problems and patients’ complaints
1. Patients will usually have complaints regarding inability to flex DIP joint and
inability to fully extend the PIP joint.
2. Often, the fixed hyperextension at the DIP joint is the main complaint, since
it interferes with the DIP joint flexion needed for grasping objects.
3. In the chronic state, there is usually little or no associated pain or tenderness
at the central slip.
4. In the chronic state, if arthrosis develops at the PIP joint, associated joint
pain and swelling will usually occur.

Figure 10.9 Formation of the boutonnière deformity. (Reprinted from Doyle JR. Dorsal
hand. In: Doyle JR, Botte MJ, eds. Surgical Anatomy of the Hand and Upper Extremity.
Philadelphia, PA: Lippincott Williams & Wilkins; 2003:653.)
D. Physical examination
1. In the acute situation, the digit should be anesthetized and the PIP joint
extended passively to full extension. The patient is then asked to keep the
PIP fully extended in an active fashion—if the patient cannot maintain active
extension, incompetence of the triangular ligament is diagnosed and simple
splinting or PIP pinning will not lead to reliable active PIP extension at the
completion of treatment.
2. On inspection, the digit will have the visible classic boutonnière deformity of
flexion at the PIP joint and hyperextension at the DIP joint.
3. The sensate pad of the pulp of the digit is not utilized for object grasp.
4. If mild and passively correctible, the digit will reassume the position of PIP
flexion and DIP hyperextension when passive correction is released.
5. In the advanced or chronic condition, the deformity may be stiff and fixed.
It will not be passively correctible.
6. Secondary arthrosis at the PIP (or DIP) joint leads to painful attempted
motion, and/or further loss of function.
E. Treatment of boutonnière deformity
1. Conservative (nonoperative)
a) Hand therapy for passive stretching, combined with corrective splint-
ing, may increase mobility and flexibility at both the DIP and PIP
joints.
b) In the chronic state, achieving true correction may not be possible with-
out surgery.
c) However, stretching and splinting that increase mobility may facilitate
surgical correction.

2. Operative management
a) To address the hyperextension at the DIP joint, surgical lengthening of
the terminal tendon is performed (Fowler procedure).
b) Lengthening of the terminal tendon decreases the hyperextension force,
and also can potentially allow some of the extensor force to be transferred
to the PIP joint, and the flexion deformity may be decreased.
c) To address the flexion at the PIP joint, multiple procedures may be
necessary. These included mobilization and dorsal repositioning of the
subluxated lateral tendons; and repair, tightening, or tendon grafting of
the central slip (Littler procedure). Tendon transfers have also been used
(Matev), using the lateral bands.
d) Contracture release of the palmar aspect of the PIP joint (volar plate
release) may be required if full passive correction cannot be achieved.
Palmar release and dorsal reconstruction would usually occur in two
stages temporally separated by three months.
e) If PIP or DIP joint arthrosis has developed, arthrodesis (fusion) or arthro-
plasty may be performed, along with repositioning of the lateral tendons
and rebalancing the extensor mechanism.
F. Complications of treatment
1. Boutonnière deformity is considered one of the more difficult hand deformi-
ties to correct. Often the surgical results are less than optimal, leaving the
patient with a residual deformity.
2. Postoperative complications include
a) Incomplete correction of deformity
b) Recurrence of deformity
c) Overcorrection of the DIP joint, resulting in residual flexion at the DIP joint
d) Residual stiffness at the PIP joint; loss of flexion
e) Chronic pain at the PIP joint secondary to joint arthrosis
II. Swan—Neck Deformity
A. Definition
A swan neck deformity of a digit is characterized by flexion at the DIP joint
and hyperextension at the PIP joint. It results from imbalance of the extensor
mechanism of the digit, from either laceration or incompetence (stretch) of the
extrinsic tendon force on the distal phalanx, or from over-pull of the extensor
mechanism (intrinsic and extrinsic) at the PIP joint.
Initially the deformity may be flexible and passively correctable. In the
chronic condition, the deformity may become fixed.
B. Etiology
1. The swan neck deformity develops from either loss of extension force at the
distal phalanx, or from over-pull of extensor force on the proximal phalanx.
Several conditions can initiate a swan neck deformity.
2. The swan neck deformity can develop initially from loss of the extensor ten-
don at the terminal tendon at the distal phalanx, resulting in extensor force
transferred to the proximal phalanx.
3. The terminal tendon can be injured initially by
a) Closed avulsion from direct blow on the distal phalanx of the outstretched
digit, forcing the distal phalanx into flexion and rupturing or stretching
the taught extensor tendon (mallet finger).

b) Open laceration of the terminal tendon

c) Attrition by weakening from chronic inflammation at the DIP joint,
along with extensor tendon subluxation and intrinsic tightness
1) Rheumatoid arthritis
2) Other inflammatory conditions
4. The swan neck deformity can also develop at the PIP joint, from over-pull of
the intrinsic muscles and increased pull at the central slip
a) Rheumatoid arthritis.
b) Spasticity from traumatic brain injury or stroke.
c) Intrinsic tightness. The Bunnell intrinsic tightness test is performed to
compare the tightness of the PIP joints when the MP joint is extended
and the MP joint is flexed. If the PIP joint is tighter with the MP joints
extended, this is an indication of intrinsic tightness and should be
addressed when addressing the swan neck deformity.
5. Volar subluxation of the MCP joints in inflammatory conditions such
as rheumatoid arthritis can also lead to an increased pull on the central
slip through the tethered common extensor and produce the swan neck
deformity.
6. Loss of the pull of the FDS (laceration, closed rupture, or iatrogenic tendon
harvest) can also initiate the swan neck deformity.
7. Congenital laxity of the volar plate of the PIP joint may lead to joint hyper-
extension, and have a role in the development of swan neck deformity.
7. The deformity, in an advanced or chronic state, is accompanied by stretch or
rupture of the volar plate of the PIP joint.
8. In the chronic condition
a) The deformity may develop secondary fixed joint contractures.
b) Chronic hyperextension at the PIP joint (or flexion at the DIP joints) leads
to abnormal mechanical stresses of the joints and secondary degenerative
arthrosis. Associated pain at the PIP (or DIP) joint usually develops.
C. Clinical problems and patients’ complaints
1. Patients usually complain of inability to flex the PIP joint actively.
2. The digits may become “locked” in hyperextension at the PIP joint, and,
to initiate digital flexion, the patient must manually bring the digit out of
hyperextension with the contralateral hand.
3. Grasp is weak from inability to flex the PIP joint.
D. Physical examination
1. On inspection, the digit will have the visible classic swan neck deformity of
hyperextension at the PIP joint and flexion at the DIP joint.
2. In the early stages, there may be varying degrees of flexibility, that is, active or
passive motion. If passively correctible, the digit will reassume the deformity
position when full active digital extension is attempted.
3. To initiate PIP flexion, the patient often uses the contralateral hand to bring
the PIP joint out of locked hyperextension. Once the joint is out of hyperex-
tension, active flexion of the joint is often possible.
4. In the advanced or chronic condition, the deformity may be stiff and fixed.
It will not be passively correctible.
5. Secondary degenerative arthrosis at the PIP joint leads to joint pain and/or
further loss of motion.
E. Treatment of chronic swan neck deformity
1. Conservative (non-operative)

a) Even in the chronic condition, hand therapy for passive stretching

combined with corrective splinting may increase mobility and flexibility
at both the DIP and PIP joints.
b) Extension block splints will help correct or manage hyperextension at the
PIP joint.
c) Progressive extension splinting at the DIP joint will help correct the flex-
ion deformity.
d) In the severe or long-standing condition, achieving true correction is usu-
ally not possible without surgery.
e) However, stretching and splinting that increase mobility may facilitate
operative correction.
a) Since there are many initiating causes of the swan neck deformity, many
surgical procedures have been described. Different procedures address
different causes.
b) Hyperextension at the PIP joint can be addressed by lengthening the
central slip. If intrinsic tightness is present, lengthening or release of the
intrinsic muscle contributing to the central slip is performed.
c) Hyperextension at the PIP joint may also be addressed from the volar
aspect of the joint, by tethering the joint in partial flexion using the FDS
tendon (FDS tenodesis), re-thinking a lateral bond (Tonkin) or removing
an ellipse of skin on the volar aspect of the joint (dermodesis). (Both of
these procedures are directed to creating a mild resting flexion contracture
at the PIP joint)
d) In the chronic state, if PIP (or DIP) arthrosis is present, joint fusion
(arthrodesis) or replacement (arthroplasty) may be indicated. Soft tissue
rebalancing is also necessary.
e) If there are accompanying associated problems such as MCP subluxation
from arthritis, these joints are addressed as well (usually including MCP
arthroplasty).
F. Complications of treatment
1. Like the chronic boutonnière deformity, chronic swan neck deformity is
difficult to correct.
2. Postoperative complications include
a) Incomplete correction of deformity.
b) Recurrence of deformity.
c) Residual stiffness at the PIP joint.
d) Tenodesis or dermodesis at the PIP joint result in a flexion contracture at
the joint (which is still, however, preferable to hyperextension deformity)
as long as DIP hyperextension does not develop secondarily.
e) Residual or chronic pain at the PIP or DIP joint secondary to joint arthrosis.
f ) Persistent loss of extension at the DIP joint due to over correction.
III. Chronic EPL Rupture
A. Definition
The EPL can rupture, from either trauma or attritional weakening at a point
where it slides against Lister tubercle. Inflammatory conditions contribute to the
risk of rupture by weakening the tendon from chronic synovitis and associated
tendon erosions. Chronic inflammatory arthritis and synovitis also lead to bone

erosion and irregularities at Lister tubercle, further increasing the risk of rupture.
Rupture of the EPL results in loss of active hyperextension of the IP joint of the
thumb, along with weakness of extension and retropulsion at the MCP joints
and carpometacarpal (CMC) joints.
B. Anatomy
The EPL is the principal extrinsic hyperextensor of the thumb. It originates from
the dorsal surface of the ulnar diaphysis and the interosseous membrane and
inserts on the base of the distal phalanx of the thumb. It provides hyperextension
to the distal phalanx of the thumb and assists in extension and retropulsion of
the proximal phalanx and metacarpal of the thumb.
In its course across the distal forearm, it is in close continuity with the dorsal
surface of the distal radius. At the level of the distal radius, it passes deep to the
extensor retinaculum in the third dorsal compartment and continues to pass
against a boney prominence, Lister is tubercle. Lister’s tubercle serves as a pulley
or point to redirect the tendon radially toward the thumb. The tubercle is usu-
ally smooth on its surface where the tendon passes. The tendon then continues
distally to reach the base of the thumb distal phalanx.
C. Etiology
1. The EPL is at risk for rupture as it passes Lister’s tubercle, where there is fric-
tion of the tendon against the bone.
2. Inflammatory disorders such as rheumatoid arthritis produce chronic teno-
synovitis at the wrist level. The chronic inflammation can weaken the EPL,
and produce attritional ruptures.
3. The chronic tenosynovitis or chronic osteoarthritis can also lead to bone
irregularities or erosions, producing a rough surface on Lister tubercle, fur-
ther contributing to attrition of the EPL. Additional carpal irregularities
from carpal subluxation or instability will further risk tendon injury.
4. A history of fracture of the distal radius (usually nondisplaced) can increase
the risk of an attritional rupture.
5. Retained hardware, such as plates or screws on the dorsal distal radius where
the EPL passes, also increases risk for tendon rupture.
6. Acute rupture, from closed trauma or laceration, can partially or completely
disrupt the EPL. If not treated, these injuries will lead to chronic tendon
dysfunction.
D. Clinical problems and patients’ complaints
1. There is often a history of preceding dorsal wrist pain, secondary to preexist-
ing dorsal wrist synovitis.
2. At the time of rupture, the patient may feel a “pop” or giving way, as the
rupture is complete.
3. Besides loss of extension at the IP joint, there is usually associated weakness
to extension at the MCP and CMC joints.
4. The patient may have difficulty in attempting to pinch, since it will be dif-
ficult to retropose the thumb and place it in the plane of the fingers
5. Long-standing loss of the EPL can lead to a fixed, hyperflexion deformity at
the IP joint.
6. Chronic flexion with abnormal stress on the IP joint can lead to secondary
joint arthrosis.
E. Physical examination
1. The thumb may assume a position of flexion at the IP joint, due to unop-
posed pull from the FPL.

2. Active IP extension is absent or weak. (Note: The intrinsic muscles of the

thumb, APB, and FPB may produce some IP joint extension, through
their insertion into the extensor mechanism. Acuate IP hyperextension is
absent).
3. In inflammatory conditions, there may be associated synovitis and swelling
on the dorsal wrist, with accompanying wrist tenderness, loss of motion, or
crepitus.
4. There may be some tenderness at the specific ruptured tendon ends.
5. Long-standing loss of the EPL can lead to a fixed, hyperflexed IP joint. If
secondary joint arthrosis develops, there will be tenderness or painful passive
motion at the IP joint.
F. Treatment of chronic EPL ruptures
1. Nonoperative
a) In long-standing EPL ruptures with IP joint stiffness, hand therapy prior
to operative management may be performed to maximize active and pas-
sive motion prior to tendon reconstruction.
a) In the chronic, long-standing EPL ruptures, the tendon ends will retract,
or will be eroded by synovitis, and there may be a large gap (intercalary
defect) between the tendon ends.
b) Operative end-to-end repair of the tendons is not possible.
c) An intercalary defect can be bridged and the tendons ends repaired using
a tendon graft, harvested from the expendable palmaris longus or planta-
ris tendon.
d) Alternatively, thumb extension can be restored by tendon transfer of the
EIP to the distal end to the EPL. (The EIP to the index finger is an
expendable extensor tendon, index finger extension is preserved by the
EDC tendon.)
e) Synovectomy and smoothing or excision of irregular bone surfaces is also
often done to prevent further ruptures in the future.
f ) If there is a fixed deformity of the IP joint, soft tissue release may be con-
sidered.
g) If there is associated IP joint arthrosis, arthrodesis may be warranted.
G. Complications of EPL reconstruction
1. Residual weakness of thumb extension.
2. Rerupture of the grafted repair or transferred tendon.
3. If the tendon repair or graft is too tight, loss of thumb flexion and palmar
abduction can occur.
IV. Chronic ECU Rupture
A. Definition
The ECU tendon is one of the principal extensors of the wrist. It provides both
wrist extension as well as ulnar deviation. It can rupture, usually at the level of the
wrist, from either trauma or attritional weakening. It is at risk for rupture as it passes
through a shallow groove in the head of the ulna. Inflammatory conditions contrib-
ute to the rupture from chronic synovitis surrounding the tendon and associated
tendon erosions. Chronic inflammatory arthritis and synovitis also lead to bone ero-
sion and irregularities of the head of the ulna. The tendon gliding against the rough
bone surface contributes to the rupture. Rupture of the ECU results in loss of active

wrist extension in ulnar deviation. Wrist extension will still be possible but will tend
to deviate radially due to the radial wrist extensors (ECRL and ECRB).
B. Anatomy
The ECU is one of the principal wrist extensors (along with the ECRB and
ECRL). It originates from the common extensor origin at the lateral epicondyle
of the humerus and the posterior border of the ulna. It inserts on the base of the
fifth metacarpal. It provides wrist extension and ulnar deviation.
In its course across the distal forearm, it is in close continuity with the dorsal
surface of the ulna. At the level of the distal ulna, it passes deep to the extensor
retinaculum in a slight groove in the head of the ulna to form the sixth dorsal
compartment.
C. Etiology
1. The ECU is at risk for rupture as it passes through the groove on the head
of the ulna in the sixth dorsal compartment. It is in contact with bone on
its deep surface and in contact with the extensor retinaculum on its dorsal
surface.
synovitis at the wrist level. The chronic inflammation can weaken the ECU,
and lead to attritional ruptures.
irregularities or erosions, producing a rough surface on the head of the ulna,
further contributing to attrition of the ECU. Additional carpal irregulari-
ties from subluxation or instability contribute to the risk tendon injury.
4. Instability of the distal ulna from chronic inflammatory conditions can result
in dorsal subluxation of the distal ulna, and concomitant palmar migra-
tion of the ECU tendon (caput ulna syndrome). The migration of the ECU
diminishes its extensor efficiency, places the tendon under further abnormal
stresses and increased risk of rupture.
5. Acute rupture, from closed trauma or laceration, can partially or completely
disrupt the ECU. If not treated, these injuries can lead to chronic dysfunction.
1. In slow, progressive attritional ruptures of the ECU, patients may note pro-
gressive weakness of wrist extension, especially in ulnar deviation.
2. With wrist extension, there will be a tendency for the wrist to deviate radially,
due to the influence of the ECRL and ECRB.
3. There is often a history of preceding dorsal ulnar wrist pain or dorsal sublux-
ation of the head of the ulna, secondary to preexisting chronic inflammation
and dorsal wrist synovitis.
4. As in other extensor tendon ruptures, at the time of rupture, the patient may
feel a “pop” or giving way, as the rupture is complete.
1. Wrist extension will be weak, especially in ulnar deviation.
2. The wrist will tend to deviate radially during extension due to unopposed
pull of the radial wrist extensors (ECRL and ECRB).
3. In inflammatory disorders, there may be tenderness over the dorsal wrist in
the area of the rupture due to tenosynovitis, arthritis, or to sensitivity of the
ruptured tendon ends. Tenosynovitis may present with a boggy mass on the
dorsal wrist.
4. The distal ulna may be prominent due to dorsal subluxation (from instability
caused by chronic inflammation).

F. Treatment of ECU rupture

1. Conservative (nonoperative) treatment
a) Nonoperative treatment cannot restore ECU tendon function.
b) However, hand therapy to regain passive motion may be beneficial prior
to operative reconstruction, especially if stiffness has developed.
c) Protective splinting will help prevent further tendon injury, especially to
any adjacent, partially attenuated tendons.
d) Aggressive active exercises should be avoided to prevent further damage to
adjacent attenuated extensor tendons.
a) In chronic, long-standing ECU ruptures, the tendon ends will be retracted
or attenuated, and direct end-to-end repair of the tendon is not possible.
b) The intercalary defect (gap) can be repaired with a free tendon graft using
the palmaris or plantaris (both of which are expendable donor tendons).
c) Alternatively, if the tendon is irreconstructable, then tendon transfer can
then be considered.
d) The EIP or ECRL can be transferred to the ECU, thus helping to balance
the tendency for radial deviation. Wrist extensor strength, however, will
not necessarily be improved.
e) The FCU and FCR can also be used for a transfer, but are usually not
sacrificed unless wrist extension is extremely weak.
f ) Synovectomy and smoothing or excision of irregular bone surfaces is
often also done to prevent rupture. Stabilization of the distal ulna, or
excision of the ulnar head (Darrach procedure) may also be indicated as
prophylaxis against future ruptures.
g) In some patients, there is little disability with loss of the ECU function,
and the rupture is well tolerated; nonoperative care can be given.
G. Complications of ECU reconstruction
1. Residual weakness of wrist extension
2. Rerupture of the grafted or transferred tendon
3. Over-tightness of the grafted or transferred tendon, resulting in difficulty in
fully flexing the wrist
V. Chronic Rupture EDQ
A. Definition
The EDQ is an extrinsic extensor muscle to the small finger. It works with the
EDC to provide extension of the small digit. Similar to the ECU, the site of rup-
ture of the EDQ is usually at the level of the wrist, from either trauma or from
attritional weakening. It is at risk for rupture as it passes dorsal and adjacent to
head of the ulna. Inflammatory conditions contribute to rupture from chronic
synovitis, tendons erosions, and associated tendon weakening. Chronic inflam-
matory arthritis and synovitis also lead to bone erosion and irregularities of the
head of the ulna. The tendon gliding against the rough bone surface further
contributes to risks of rupture. Rupture of the EDQ results in weakness of digital
extension of the small finger.
B. Anatomy
The EDQ tendon assists the EDC to provide digital extension of the small
finger. In some patients, the EDC is congenitally absent, and the EDQ is the
primary extensor of the small finger. The EDQ is a relatively small muscle. It

originates from the common extensor origin of the lateral epicondyle of the
humerus and the intermuscular septum. It inserts into the extensor mechanism
of the small finger. It assists with extension of the small finger, and contributes
weakly to wrist extension.
In its course across the distal forearm, the EDQ is in close continuity with
the dorsal surface of the ulna. At the level of the distal ulna, it passes deep to
the extensor retinaculum just radial to the ECU tendon to form the fifth dorsal
compartment.
C. Etiology
1. Similar to the ECU tendon, the EDQ is at risk for gradual attenuation and
chronic rupture as it passes in close continuity to the head of the ulna in the
fifth dorsal compartment. It is in contact with bone on its palmar surface and
in contact with the extensor retinaculum on its dorsal surface.
synovitis at the wrist level. The chronic inflammation, including synovitis
of the distal radioulnar joint, can weaken the EDQ and lead to attritional
ruptures.
further contributing to attrition of the EDQ. Additional carpal irregularities
from subluxation or instability contribute to the risk of tendon injury.
4. Instability of the distal ulna from chronic inflammation can result in dorsal
migration of the distal ulna (caput ulna syndrome), placing further abnormal
stresses on the EDQ and increasing risk of rupture.
5. Osteoarthritis can also produce osteophytes and irregularities of the ulnar
head, and risk tendon rupture.
6. Acute rupture, from closed trauma or laceration, can partially or com-
pletely disrupt the EDQ. If not treated, these injuries can lead to chronic
dysfunction.
1. The patient will note weakness of digital extension of the small finger.
2. If the EDC is congenitally absent, loss of the EDQ will result in complete
loss of extrinsic extension.
3. The digit will be held in flexion at the MCP (and possibly at the PIP and
DIP) joints.
4. Active extension at the MCP joint will be absent.
5. There may be residual active extension at the PIP and DIP joints, secondary
to the intrinsic muscles (interossei and lumbricals).
1. The small digit will assume a position of flexion at the MCP joint.
2. MCP extension will be weak or absent.
3. There may be boggy swelling and tenderness of the dorsal wrist secondary to
synovitis and or injury to the tendon.
4. Dorsal subluxation of the head of the ulna may be present.
F. Treatment
1. Conservative (nonoperative) management
a) Similar to the ECU and EPL chronic rupture, nonoperative treatment
cannot restore the chronic ruptured tendon.
b) However, hand therapy to regain passive motion may be beneficial prior
to operative reconstruction if secondary contractures have developed.

c) Protective splinting will help prevent further tendon injury, especially to

any adjacent, partially attenuated tendon.
d) Aggressive active exercises should be avoided to prevent further damage to
adjacent attenuated extensor tendons.
a) In chronic, long-standing ruptures, the tendon ends will be retracted
or attenuated, and direct end-to-end repair of the tendon is not pos-
sible.
b) The intercalary defect (gap) can be repaired with a free tendon graft
using the palmaris or plantaris (both of which are expendable donor
tendons).
c) Alternatively, if tendon attenuation is severe, or there is longitudinal dam-
age to the remaining tendon, grafting may be less optimal; tendon trans-
fer can then be considered.
d) Tendon transfer can be accomplished by side-to-side suture of the distal
ruptured at the end of the EDQ to the adjacent EDC to the ring.
e) The EIP can also be transferred to the EDQ.
f ) Synovectomy and smoothing or excision of irregular bone surfaces is
performed to prevent further ruptures in the future. Stabilization of the
distal ulna or excision of the ulnar head (Darrach procedure) may also be
necessary as prophylaxis against future ruptures.
g) In some patients, there is little disability with loss of the EDQ function.
If the rupture is well tolerated, operative treatment may not necessarily be
warranted.
G. Complications of EDQ reconstruction
1. Residual weakness of digital extension.
2. Rerupture of the grafted or transferred tendon.
3. Over-tightness of the grafted or transferred tendon, resulting in difficulty in
fully flexing the digit.
VI. Chronic EDC Ruptures
Chronic EDC ruptures most often occur as a result of proliferative tenosynocvitis, often
seen in conjunction with rheumatoid arthritis.
A. Definition
The EDC are the extrinsic extensors to the index through small fingers. They
work in conjunction with the EIP and EDQ to provide extension of the index
and small digit and in isolation to provide extension to the middle and ring
digits. Similar to the ECU and EDQ, the site of rupture of the EDC is usually
at the level of the wrist, from either trauma or from attritional weakening and
typically begins with the ulnar most digit and progresses in a radial direction.
It is at risk for rupture as it passes dorsal and adjacent to head of the ulna.
Inflammatory conditions contribute to rupture from chronic synovitis, tendons
erosions, and associated tendon weakening. Chronic inflammatory arthritis and
synovitis also lead to bone erosion and irregularities of the head of the ulna.
The tendon gliding against the rough bone surface further contributes to risks
of rupture. Rupture of the EDC results in weakness or loss of digital extension
of the fingers.

B. Etiology
1. Similar to the ECU and EDQ tendons, the EDC tendons are at risk for
gradual attenuation as they passes in close continuity to the head of the
ulna in the fourth dorsal compartment. They are in contact with bone on
its palmar surface and in contact with the extensor retinaculum on its dorsal
surface.
synovitis at the wrist level. The chronic inflammation, including synovitis
of the distal radioulnar joint, can weaken the EDC, and lead to attritional
ruptures, beginning with the small finger and progressing to involve the ring,
middle, and index fingers.
further contributing to attrition of the EDC. Additional carpal irregularities
from subluxation or instability contribute to the risk of tendon injury.
4. Instability of the distal ulna from chronic inflammation can result in dorsal
migration of the distal ulna (caput ulna syndrome), placing further abnormal
stresses on the EDQ and EDC and increasing risk of rupture.
5. Osteoarthritis can also produce osteophytes and irregularities of the ulnar
head, and risk tendon rupture.
6. Acute rupture, from closed trauma or laceration, can partially or com-
pletely disrupt the EDC. If not treated, these injuries can lead to chronic
dysfunction.
1. The patient will note weakness or inability to extend the fingers.
2. The digit will be held in flexion at the MCP (and possibly at the PIP and
DIP) joints.
3. Active extension at the MCP joint will be absent. (the finger will “droop”)
4. There may be residual active extension at the PIP and DIP joints, secondary
to the intrinsic muscles (interossei and lumbricals).
5. This will begin in the small finger and may progress in a radial direction to
include the ring, middle, and index.
1. The digit or digits will assume a position of flexion at the MCP joint.
2. Active MCP extension will be weak or absent.
3. There may be boggy swelling and tenderness of the dorsal wrist secondary to
synovitis and or to injury to the tendon.
4. Dorsal subluxation of the head of the ulna may be present.
F. Treatment
1. Conservative (nonoperative) management
a) Similar to other chronic attritional ruptures, nonoperative treatment
cannot restore the chronic ruptured tendon.
b) Surgical treatment should be performed to prevent further tendon
ruptures, especially if all tendons are not ruptures.
c) Intact tendons can serve as a source for transfer to restore lost function.
a) The underlying source must be addressed. If there is synovitis, arthritis, or
instability at the DRUJ contributing to the tendon rupture, this must be
addressed. At minimum, a synovectomy should be performed and often a
distal ulnar resection (Darrach resection) is performed.

b) Isolated small finger rupture can be treated with end to side transfer of the
small to the ring or EIP to EDC small transfer.
c) When ring and small EDC tendons are ruptures, an end-to-side transfer
from middle to ring and EIP to EDC small can be used to restore digital
extension.
d) When three or four extensor tendons are ruptured, the remaining EDC
or EIP tendons are not strong enough to allow for extension of all fingers
and transfer of FDS tendons from the middle and ring can be used. This
is an ‘out-of-phase’ transfer (see Chapter 11), so it will require therapy
to relearn how to extend the fingers. The transfer can be through the
interosseous membrane (which allows the straightest line of pull, but
scarring can occur at this level), or around the radial aspect of the wrist.
e) Tendon transfers are secured using a Pulvertaft type of weave.
G. Complications of EDC reconstruction
1. Residual weakness of digital extension.
2. Rerupture of the grafted or transferred tendon.
3. Tightness of the grafted or transferred tendon, resulting in difficulty in fully
flexing the digit.
4. Scaring of the transferred tendons, preventing adequate excursion and thus,
limiting extension or flexion.
Tendinopathy
I. Trigger Digits
A. Definition
A tenosynovitis of the flexor tendons in the hand that leads to tendon entrap-
ment and a “catching” or “popping” as the digit flexes and extends.
B. Anatomy
1. The FDP and FDS enter the hand deep to the flexor retinaculum (transverse
carpal ligament) in the common flexor synovial sheath. The tendons fan out
to their respective digits and enter their respective digital synovial sheaths.
Each digit has a strong ligamentous tunnel containing the flexor tendon and
the tendon synovial sheath, known as the fibrous digital sheath. This sheath
runs from the metacarpal head to the base of the distal phalanx. Thickenings
of the fibrous digital sheath are known as pulleys.
2. There are five annular pulleys and three cruciate pulleys. The A1 pulley, the
pulley most commonly involved in trigger digits, lies over the volar surface of
the metacarpal head. The sheath system of the thumb consists of the A1 and
A2 pulleys separated by an oblique pulley.
C. Pathogenesis
1. Trigger digits occur as the likely result of a size discrepancy between the flexor
tendon and the tendon sheath, specifically, the A1 pulley. Both the tendons
and the A1 pulley undergo pathologic changes including fibrocartilaginous
metaplasia. Histologic changes specific to the tendons include fraying and
degeneration on the volar (avascular) side.
2. Changes in the A1 pulley, which are often the most significant, include gross
hypertrophy, degeneration, chondrocyte metaplasia, and type III collagen
proliferation.

D. Etiology/demographics
Trigger digits, one of the most common causes of hand pain, occur more
frequently in women than men.
1. The most commonly affected digits are the thumb and the ring finger.
2. Trigger digits often present as a primary condition.
3. They may be also seen as a secondary condition in patients with diabetes
mellitus, rheumatoid arthritis, or other rheumatologic conditions.
E. Clinical findings and diagnosis
Patients present with pain and a “locking, catching, or popping” of the proximal
interphalageal joint of the affected digit or the IP joint of the thumb. A palpable
nodule may be present within the flexor tendon just proximal to the A1 pulley.
Applying pressure over this nodule may cause tenderness and may exaggerate
the triggering. Many classification systems of trigger digits have been created;
however, no single one is commonly accepted.
1. The differential diagnosis of trigger digits includes PIP joint sprain, pseudobou-
tonniere, sesamoiditis, Dupuytren disease, subluxation of the long extensor tendon
over the metacarpal head, MCP joint arthritis, and locking of the MCP joint.
F. Treatment
1. Treatments of trigger digits include both conservative and surgical methods.
a) Nonoperative methods of management include observation, nonsteroidal
anti-inflammatory medications (NSAIDs), corticosteroid injections, and
splinting.
1) With corticosteroid injections, the hand is sterilely prepared over
the pulley of the affected digit. Using a preparation of lidocaine
without epinephrine plus a soluble corticosteroid, an injection into
the affected flexor tendon sheath is performed at the level of the
metacarpal head. The corticosteroid preparation is injected slowly.
One study demon-strated that 93% of patients were symptom free at
3 months after injections. A second injection can be offered if the first
dose does not completely resolve symptoms. Injections are less
effective in diabetic patients, especially those with poor chronic blood
glucose control.
2) When splinting is utilized, the affected digit is splinted in extension
during sleep. With this technique, the enlarged portion of the tendon
can theoretically expand the overlying tendon sheath. Splinting is a
useful alternative in patients reluctant to undergo corticosteroid
injection. Although results are less reliable than with other techniques,
Patel and Bassini reported 66% of patients who underwent splinting
to be symptomfree at 1 year.
b) Surgical treatment of trigger digits involves release of the A1 pulley.
1) In open release, the A1 pulley is surgically exposed with care being
taken to protect the nearby digital nerves and vessels. Following
exposure, the pulley is divided longitudinally under direct visualization.
Complications of this technique include injury to the digital nerve,
incisional tenderness, inadvertent sectioning of the A2 pulley, and
recurrence. Iatrogenic injury to the A2 pulley will result in bowstringing
and decreased flexion of the digit.
G. Postoperative care
Patients are encouraged to begin immediate active and gentle passive range of
motion. Sutures are removed at 2 weeks and patients are then allowed to advance

activities as tolerated. Some patients, especially diabetics, may require a short

course of occupational therapy to alleviate swelling and stiffness.
II. de Quervain Syndrome
A. Definition
de Quervain’s disease is a stenosing tenosynovitis of the the APL and the EPB
tendons in the first dorsal compartment of the wrist. The disease results in radial
wrist pain exacerbated with motion.
B. Anatomy
1. The extensor retinaculum of the wrist covers the dorsal surface and contains six
synovial sheaths, producing six dorsal compartments. The first dorsal compart-
ment contains the EPB and APL tendons. The APL normally has more than
one tendon slip in the compartment and the EPB is often located in a separate
dorsal subcompartment. If muscle is seen in the first dorsal compartment then
it represents the EPB as its myotendinous junction extends more distal than the
APL’s.
2. The first dorsal compartment represents a fibro-osseous tunnel, with part of
the compartment being formed by soft tissues (the extensor retinaculum)
and the floor being formed by bone (the radius). In one third of patients, the
compartment is divided by a septum, which may be the underlying cause of
the tenosynovitis.
C. Pathogenesis
Shear forces produce inflammation with resultant thickening of the extensor
retinaculum of the first dorsal compartment. The forces involved in producing
the disease include thumb adduction with concomitant ulnar deviation of the
wrist. Since the first dorsal compartment represents a fibro-osseous tunnel, the
thickening of the dorsal structures results in significant narrowing of the first
dorsal compartment, such that motion of the tendons through the compartment
produces pain.
D. Etiology/demographics
de Quervain’s tenosynovitis has been reported to occur up to six times more
frequently in women, often immediately antepartum or postpartum. Many
etiologies for this disorder have been theorized including repetitive motion and
overuse, trauma, anatomic variations, biomechanical compression, systemic
inflammatory diseases, and increased volume states. Of specific interest are the
anatomic variations of the first dorsal compartment. Anatomic studies have shown
the presence of multiple tendon slips of APL. The presence of a separate dorsal
compartment within the first dorsal compartment may exist in some patients,
dividing the multiple APL tendon slips from the dorsally situated EPB tendon.
E. Clinical findings and diagnosis
Patients with de Quervain’s tenosynovitis report pain and tenderness along the
radial side of the wrist. The symptoms are worsened with the grasping and lift-
ing of objects. On examination, patients have tenderness to palpation of the first
dorsal compartment over the radial styloid.
1. Two provocative tests have been described in the diagnosis of de Quervain
disease.
a) In the Finkelstein test, the examiner grasps the patient’s thumb and
ulnarly deviates the hand and wrist. Reproduction of the patient’s pain
indicates a positive test.

b) In the Eichoff maneuver, the patient grasps his or her thumb inside of a
clenched fist and deviates the wrist ulnarly. Again, the result is positive if
the maneuver reproduces the patient’s pain.
2. The differential diagnosis of de Quervain’s disease includes intersection syn-
drome, fracture of the radial styloid, radioscaphoid arthrosis, scaphoid frac-
ture, basilar arthritis of the thumb, SIT arthrosis giant cell tumor of the distal
radius and radial sensory neuritis.
F. Treatment
1. Initial treatment of de Quervain tenosynovitis is nonsurgical. Conservative
therapies include rest, splinting, and NSAIDs, and injections.
a) Splinting allows for rest of the involved tendons. A radial thumb spica
extension splint holds the wrist in neutral and positions the thumb
30 degrees of flexion and 30 degrees of abduction. Some studies have
shown an 80% failure rate with this modality.
b) Corticosteroid injection is more effective than splinting with approxi-
mately 60% of patients getting long-term relief.
1) The technique for injection involves positioning the wrist in slight
ulnar deviation. The APL and EPB tendons are then palpated. A prep-
aration of corticosteroid and lidocaine without epinephrine is injected
into the tendon sheath with the needle positioned parallel to the ten-
dons. The corticosteroid preparation is injected slowly, following
attempted suction to be sure that the radial artery is avoided.
2) Complications of corticosteroid injection include subcutaneous fat atro-
phy, hypopigmentation of the skin, weakening or rupture of the ten-
dons, postinjection flare of symptoms, and radial sensory nerve injury.
2. Surgery is indicated when nonoperative management fails to provide relief.
Surgical treatment involves the open release of the dorsal retinaculum of the
first dorsal compartment, and radial sensory nerve injury.
a) In the procedure, an incision is made on the radial side of the wrist overly-
ing the radial styloid. Blunt dissection is performed parallel to the course
of the tendons (longitudinal) with care being taken to identify and pro-
tect the radial sensory nerve and its branches. The dorsal retinaculum of
the first dorsal compartment is identified and sharply incised longitudi-
nally along the dorsal border. The tendons are then examined, and any
intracompartmental septae are released.
b) Complications of surgery include injury to the radial sensory nerve,
incomplete decompression of the compartment, volar subluxation of the
tendons, and complex regional pain syndrome.
G. Postoperative care
Patients are kept in a thumb spica splint for 2 to 3 weeks postoperatively. After
2 to 3 weeks, mark sutures are removed and activities are advanced as tolerated.
Some will require a removable splint for several weeks after suture removal for
pain and edema control.
III. Intersection Syndrome
A. Definition
A tenosynovitis associated with the ECRB and ECRL in the second dorsal com-
partment of the wrist. The name is somewhat a misnomer as the tenosynovitis

occurs at a site distal to the intersection where the first dorsal compartment (APL
and EPB) crosses over the second dorsal compartment.
B. Anatomy
Approximately 6 cm proximal to the carpus, the first dorsal compartment ten-
dons (APL and EPB) traverse the tendons of the second dorsal compartment.
This is the area of pain and swelling that can be seen with intersection syndrome.
Branches of the superficial radial nerve cross over the first dorsal compartment
just proximal to the extensor retinaculum.
C. Pathogenesis
The pathologic process of intersection syndrome likely involves entrapment of
the tendons in the second dorsal compartment and chronic irritation at the point
where the first compartment tendons cross the second compartment tendons.
D. Clinical findings and diagnosis
Patients will present with pain and swelling at a site approximately 4 to 6 cm
proximal to the radial styloid. Interestingly, although the site of physical findings
lies directly over the APL and EPB the true tenosynovitis is located distal to this
area in the synovial sheath of the second dorsal compartment under the extensor
retinaculum. The condition is often found in athletes involved in activities that
require repetitive wrist extension. Such activities include kayaking, rowing, and
weightlifting. Furthermore, this condition has also been called “bugaboo” wrist,
as the term “bugaboo” is another name for deep powder skiing. Deep powder
skiing requires frequent wrist extension and that can often lead to intersection
syndrome. One of the hallmarks of this condition is the sensation of “footprints
on freshly packed snow” when the examiner palpates the tendinous intersection
involved.
E. Treatment
1. The mainstay of treatment is conservative management with activity modi-
fication, anti-inflammatory medications (NSAIDs), thermoplast splinting
with the wrist in slight extension, and occasional steroid injections into the
second dorsal compartment. These measures will be beneficial in the vast
majority of patients.
2. Surgical release should be considered in the recalcitrant case. The second dor-
sal compartment is approached with a longitudinal incision beginning just
proximal to the radial styloid and continuing to the area of swelling and pain
over the first dorsal compartment. The sensory branch of the radial nerve is
identified and protected. The retinaculum over the ECRB and ECRL should
be released on the ulnar side to avoid the theoretical complication of palmar
dislocation of the tendons. The area of diseased tenosynovium should then
be dissected from the tendons. The retinaculum should not be closed.
F. Postoperative care
The wrist is splinted in slight extension for 10 to 14 days. After the first post-
operative visit, a removable splint is applied and patients are allowed to begin
slowly advancing activities as tolerated.
IV. Extensor Carpi Ulnaris Tendonitis
A. Definition
A tenosynovitis associated with the ECU as it courses through the sixth dorsal
compartment and its own fibro-osseous tendon sheath.

B. Pathogenesis
1. Tendonitis—A traumatic twisting event is usually the inciting event that
leads to the inflammation and pain associated with ECU tendonitis. The
ECU is predisposed to tendonitis because of its deep fibro-osseous tunnel
(of which the tendon occupies 90%). Furthermore, the course of the ECU
at the distal ulna is angled in the ulnar direction as it enters a groove on the
dorsal surface of the ulnar head. Finally, the subsheath of the ECU over the
distal ulna is an important stabilizer of the DRUJ and as such is vulnerable
to injury and inflammation after an injury to the triangular fibrocartilage
complex (TFCC).
2. Subluxation can occur with disruption of the ECU subsheath when the sixth
compartment remains intact. The ECU tendon snaps as it moves out of the
ECU groove on the ulnar head, as the forearm is pronated. The tendon again
snaps as it moves back into the groove during supination.
C. Clinical findings and diagnosis
Most patients will present with ulnar-sided wrist pain and swelling stemming
from a traumatic (normally twisting) injury. Nocturnal pain is also frequent.
Tenderness will often be noted over the fibro-osseous tunnel and distally to the
tendon’s insertion on the base of the fifth metacarpal. Increased pain will be elic-
ited with resisted extension and ulnar deviation and passive flexion and radial
deviation of the wrist. However, patients will often have pain with any wrist
motion. Some patients will complain of dorsal hand paresthesias as the dorsal
sensory branch of the ulnar nerve courses over the distal ulna and the ECU.
Patients may complain of audible and palpable snapping over the ulnar head if
the ECU is allowed to subluxate out of its groove because of a sheath tear. This is
best appreciated in a hypersupinated wrist that is taken from extension into ulnar
deviation and flexion. Complete relief of pain after a lidocaine injection confirms
the diagnosis. Radiographs can be helpful to rule out other conditions that can
cause ulnar-sided wrist pain including DRUJ arthritis, ulnar styloid fractures,
TFCC injuries, and ulnocarpal impaction syndrome. MRI can help identify the
inflammation surrounding the ECU as well as any associated TFCC tears.
D. Treatment
1. Initial measures for treating ECU tendonitis include activity modification,
splinting (in slight extension), anti-inflammatory medications (NSAIDs),
physical therapy, and corticosteroid injections. Intratendinous injections are
to be avoided as they can lead to tendon rupture.
2. Surgical intervention is warranted when conservative treatment fails to allevi-
ate symptoms. A dorsal curvilinear incision can be made paralleling the dorsal
sensory branch of the ulnar nerve. The incision should begin 2 to 3 cm proxi-
mal to ulnar styloid and continue out toward the base of the fifth metacarpal.
Careful dissection must be performed to protect the dorsal sensory branches
of the ulnar nerve. The sheath and tunnel are then completely released and
the tendon is debrided of any proliferative tenosynovium. Postoperative sub-
luxation of the ECU is a risk, and the sheath should be repaired.
3. Cases involving preoperative subluxation of the ECU require reconstruction
of the subsheath and can be completed using a slip of the extensor retinacu-
lum to stabilize the tendon in its tunnel.
E. Postoperative care
Patients are splinted for 10 to 14 days in slight extension and ulnar deviation.
Sutures are removed at 2 weeks and patients are allowed to begin gentle,

nonresistive activities. Activities are slowly advanced as tolerated once soft tissue
healing has occurred.
V. Flexor Carpi Radialis Tendonitis
A. Definition
A stenosing tenosynovitis of the FCR as it courses over the carpus at the wrist
crease and travels toward its insertion on the floor of the volar hand at the base
of the second metacarpal.
B. Anatomy
The tendon of the FCR begins approximately 8 cm proximal to the radiocarpal
joint. Its synovial sheath extends from the origin of the tendon to its insertion
at the base of the second metacarpal. At 4 to 5 cm proximal to the radiocarpal
joint, the tendon is covered with thick fibers from the antebrachial fascia. The
tendon enters a thick fibro-osseous tunnel at the proximal aspect of the trape-
zium. The tendon occupies 90% of the available space within the fibro-osseous
tunnel and is encircled by the tubercle of the trapezium. As the FCR crosses
the trapezial ridge, it angles sharply dorsally to insert on the second metacarpal.
Along its course, only 1 mm separates the tendon from the scaphoid tubercle,
the trapezium, and the scaphoid-trapezium-trapezoid (STT) joint.
C. Pathogenesis
Due to its close proximity to other structures of the volar radial wrist, the FCR
can be predisposed to tenosynovitis. Although FCR tendonitis can be a result of
trauma, it is more commonly due to overuse. The tight fibro-osseous tunnel and
sharp angulation of the FCR over the ridge of the trapezium make it surprising
that more cases of flexor carpi radialis tendonitis are not identified. FCR tendon-
itis can also be secondary to pathology in the surrounding structures that are in
close proximity. This includes scaphoid fractures, arthritic conditions of the STT
joints or CMC joint of the thumb, and ganglion cysts arising from the carpus.
D. Clinical findings and diagnosis
Patients with FCR tendonitis will present with volar radial wrist pain often cen-
tered over the scaphoid tubercle or base of the trapezium.
1. Increased pain with resisted wrist flexion and radial deviation is considered
pathognomonic by some authors. Passive extension and ulnar deviation of
the wrist will often also elicit increasing pain. Pain relief with lidocaine injec-
tion into the FCR sheath is confirmatory for the diagnosis.
2. Importantly, this is a diagnosis of exclusion and other various conditions
must be ruled out. Other conditions that must be included in the differ-
ential for volar radial wrist pain include scaphoid fractures, STT arthritis,
thumb CMC joint arthritis, ganglia, de Quervain tenosynovitis, and Linberg
syndrome (an anomalous intertendinous connection between the tendon of
the FPL and that of the FDP). With this multitude of other diagnoses, it is
critical that a thorough history be obtained documenting prior trauma, pain,
and surgeries.
3. Radiographs (anteroposterior, oblique, and lateral) should be obtained to rule
out a secondary tendonitis stemming from pathologic conditions of adjacent
osseous structures.
4. An MRI can also be obtained to identify any underlying cysts or occult
fractures.

E. Treatment
1. Treatment should initially consist of nonoperative measures in the scenario
of primary FCR tenosynovitis. Modalities such as ice, anti-inflammatory
medications (NSAIDs), splinting, physical therapy, and occasional steroid
injections can all be implemented. Steroid injections can cause tendon rupture
(if this eventuality occurs, it often leads to the resolution of symptoms).
2. Surgical intervention should be entertained in cases that do not respond to
conservative measures. In secondary tendonitis, tendon fraying and ultimately
rupture can occur rapidly if not addressed in a timely manner.
a) For primary FCR tendonitis, a 3 to 4 cm longitudinal incision is made over
the course of the FCR starting proximal to the wrist crease and extend-
ing to the base of the thenar eminence. Care must be taken during this
approach to avoid injury to the palmar cutaneous branch of the median
nerve, which lies just ulnar to the FCR. Thenar branches of the radial
sensory nerve and terminal branches of the lateral antebrachial cutaneous
nerve coursing over the thenar eminence are identified and protected at
the distal extent of the incision. The FCR release is started proximal to
the start of its fibro-osseous tunnel as it courses over the scaphoid and is
continued to a point just distal to the tubercle of the trapezium. Frayed
fibers of the tendon should be excised and the trapezial groove inspected
for any spurs or sharp edges, which can be removed with a rongeur. After
debridement, the sheath should not be closed.
b) In cases of secondary tendonitis, the underlying cause of the inflammation
should be addressed. Success with operative treatment approaches 90%.
The wrist is splinted for 10 to 14 days after surgery. At the first postoperative
visit, sutures are removed and patients are allowed to slowly advance activities
as tolerated.
VI. Epicondylitis
Lateral and medial epicondylitis represent insertional tendinopathies of the extensor

and flexor muscle groups at the elbow. Lateral epicondylitis, or tennis elbow, is three
times more common as medial epicondylitis (also known as golfer’s elbow). Studies of
pathologic tissue from surgery have shown that epicondylitis represents a degenerative
tendinosis, rather than an inflammatory process.
A. Presentation
1. The incidence is equal for males and females with the dominant arm affected
most frequently.
2. Peak incidence is in fifth decade of life (age range 35 to 55 years)
3. Pain is typically located at or just distal to the lateral (or medial) epicondyle.
4. Pain exacerbated by lifting, particularly with the arm in neutral rotation or
in pronation. Lateral epicondylitis is aggravated by activities involving active
wrist extension while symptoms of medial epicondylitis are brought on by
active wrist flexion.
5. Lateral epicondylitis, differential diagnosis includes
a) Radial tunnel syndrome
b) Intra-articular elbow pathology such as synovial plica

c) Radial head chondrosis

d) Herpes zoster (C6 root)
6. Medial epicondylitis, examiner should evaluate for
a) Medial collateral ligament injury
b) Ulnar neuritis or nerve compression
c) Triceps tendinitis
d) Herper zoster (c8 root)
B. Pathologic anatomy
1. Lateral epicondylitis: Studies have shown that the ECRB origin is the
primary tendon affected in lateral epicondylitis. The ECRB lies deep
to the ECRL and the extensor aponeurosis, the origin of the EDC and
ECU.
2. Medial epicondylitis: The flexor pronator origin, specifically the medial
conjoint tendon (MCT), is thought to be the site of pathology in medial
epicondylitis. The MCT lies just anterior to the anterior oblique ligament
and originates from the anterior inferior medial epicondyle. The flexor carpi
radialis and pronator teres have origin attachments to the MCT, as do the
palmaris longus and the FCU.
C. Physical examination
1. Patients note tenderness with palpation over the involved epicondyle and
over its tendinous attachments
2. There is generally minimal pain with range of motion except in the severe
stages
3. Lateral epicondylitis—resisted wrist extension causes pain over lateral epi-
condyle
4. Medial epicondylitis—resisted wrist flexion and pronation cause pain over
medial epicondyle
D. Radiology
1. Plain x-rays may show insertional calcifications at the epicondyle, but add
little to diagnostic accuracy.
2. MRI is not necessary to make the diagnosis, but when obtained, will usually
show a partial tear of the extensor or flexor insertion.
3. Ultrasound will also show areas consistent with a partial tendon insertion
tear. It has moderate sensitivity and variable specificity.
E. Treatment
Most of the clinical studies of epicondylitis focus on patients with lateral epicon-
dylitis, due to its increased prevalence. However, most principles of treatment
can be applied to patients with medial epicondylitis, except where noted.
1. Conservative treatment
a) The use of counterforce braces (tennis elbow pads) and short arm splints
at night have been shown to decrease pain with a short-term effect.
b) Occupational therapy for stretching and massage can be a helpful adjunct
in epicondylitis.
3. Ultrasound and corticosteroid iontophoresis have not been shown to be
more effective than placebo in randomized trials, although pain levels
generally decrease with their use.
c) Corticosteroid injections have been shown to improve pain in the short
term, but placebo-controlled trials have not shown steroid injections to
be superior to placebo at long-term follow-up.

d) Newer modalities such as botulinum toxin, autologous blood injection,

nitric oxide patches will require more study before their use is recom-
mended.
e) Modification of activities should be reviewed with each patient. In general,
activities that exacerbate the symptoms should be altered. For example,
patients with lateral epicondylitis should lift with their arms supinated
and close to their body.
f ) Observation (“wait and see”) has been suggested with the thought that
symptoms will resolve over time.
1) Studies in the European literature have shown equivalent outcomes results
at 1 year in groups treated with injection, therapy, or observation.
2) A recent study in Canada showed equivalent results between therapy
and observation at 1 year.
2. Operative treatment
Epicondylitis should be treated non-operatively, reserving surgical options for
those patients who have failed at least 6 months of nonoperative measures.
a) Lateral epicondylitis—operative options include open and arthroscopic
debridement of the tendon origin. Percutaneous release of the extensor
mass has been described in limited studies.
1) Open debridement of the lateral epicondyle—“Nirschl procedure”
a. The incision is based on the lateral epicondyle.
b. The extensor fascia is opened and the interval between the ECRL
and EDC is split to expose the ECRB origin.
c. Do not dissect too posteriorly on the lateral epicondyle; this risks
injury to the lateral ulnar collateral ligament (LUCL).
d. Devitalized tissue, which appears opalescent, grey, shiny, and
abnormal, is excised at the ECRB origin. Pathological examination
will reveal chondromyxoid metaplasia of the ECRB tendon.
e. A small portion of the lateral epicondyle is excised either with a ron-
geur or a small osteotome; alternatively, some authors favor drilling the
epicondyle, all with the goal of stimulating blood flow to the surgical
site and providing a raw bleeding surface for the tendon repair.
f. The EDC and ECRL tendons are repaired over the roughened
epicondyle using a resorbable suture.
2) Arthroscopic debridement of the lateral epicondyle
a. After establishing standard anterolateral and proximal anteromedial
portals, the lesion is identified with the arthroscope in the proximal
anteromedial portal and the shaver in the anterolateral portal.
b. Usually, the pathologic lesion is seen as fraying of the undersurface
of the ECRB following resection of the subjacent elbow capsule.
c. Distinction must be made between the LUCL and the ECRB to
protect the LUCL from injury; keeping resection above the midpoint
of the capitellum and radial head helps prevent LUCL damage.
d. Abnormal or degenerative tissue at the ECRB origin is removed
with a shaver, and the lateral epicondyle is then decorticated.
b) Medial epicondylitis
1) Open treatment of medial epicondylitis
a. An incision is placed just anterior to the medial epicondyle.
b. The flexor pronator fascia is identified and opened, leaving a small
cuff of tissue for repairing the fascia to the epicondyle.

c. The flexor pronator muscle is elevated, and the elbow capsule is

identified.
d. The abnormal nidus of tissue is usually identified at the MCT, and
a 1 to 2 cm portion of the MCT septum is removed.
e. The medial epicondyle is either shaved or drilled to stimulate
bleeding.
f. The flexor pronator mass is repaired back to the epicondyle using the
preserved cuff of flexor pronator tissue using a resorbable suture.
Suggested Readings
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Tendon Transfers
11
Warren C. Hammert, Ann E. van Heest, Michelle A.
James, Christine Kwak, George S.M. Dyer, Brandon E.
Earp, Barry P. Simmons, and Kimberly L.Z. Accardi
Basic Principles
Tendon transfers involve using a functional muscle tendon unit to replace a lost function.
This loss of function can be due to a peripheral nerve injury, spinal cord injury, stroke,
traumatic brain injury, cerebral palsy, or any other cause. The more closely the tendon
to be transferred resembles the nonfunctioning muscle tendon unit, the more likely
it will be successful. Several principles should be considered prior to beginning the
transfer and all these variables play an important role in determining the most optimal
transfer.
I. Correction of Contracture
All joints should be supple with full passive motion prior to tendon transfer, as post-
operative active motion will not be greater than preoperative passive motion. If the
joint does not have full passive motion, this is corrected prior to tendon transfer by
contracture release.
II. Tissue Equilibrium
The optimal time should not be until the scars are mature, the joints are supple, and the
edema has resolved. Every effort should be made to place the transfers in healthy tissue,
even if this means performing a different transfer. When a bed of healthy tissue is not
present, consideration should be given to resurfacing with vascularized fasciocutaneous
flaps prior to tendon transfer.
III. Straight Line of Pull
The most efficient tendon transfer is one that passes in a straight-line from its origin to
the site of insertion.
IV. One Tendon—One Function
It is obvious that a tendon cannot be used for two different functions (digital flexion
and extension), but the effectiveness of the transfer is reduced when trying to provide
two similar functions (digital extension and thumb extension), as the transfer will only
effectively move the joint to which it is most tightly attached.
145

V. Strength
The tendon chosen for transfer must have adequate strength to perform its new
function. A muscle loses roughly one MRC grade of strength following transfer,
i.e., a muscle graded at 5/5 might decrease to 4+/5 following transfer. As a general rule,
muscles that have been denervated and have subsequently recovered are not good donor
muscles. In order to successfully perform tendon transfers, an understanding of the rela-
tive strengths of the muscles in the forearm and hand should be obtained (Table 11.1).
When choosing a muscle to transfer, one would prefer to have a muscle of the same or
greater strength as the donor.
VI. Amplitude of Motion
It is difficult for a muscle to replace one with a greater excursion. By rough estimation,
tendons that insert at the wrist level have 30 mm of total excursion, the digital extensors
have 50 mm of excursion, and the digital flexors have 70 mm of excursion (Table 11. 2).
It can also be stated that muscles attaching at the wrist have about 30 mm excur-
sion, muscles attaching around the metacarpophalangeal (MP®MCP) joints have 50
mm of excursion, and muscles attaching nearer the finger tips have about 70 mm of
excursion. These are general rules and the specific excursions are slightly different for
the flexor pollicis longus (FPL) and the flexor digitorum superficialis (FDS) tendons.
To increase the amplitude of a given muscle, a transfer can incorporate more than
one joint to allow the tenodesis effect to augment amplitude. This occurs when a wrist
TABLE 11-1 Relative strength of muscles available for transfer
BR and FCU Ρελατιϖε στρενγτη = 2

Wrist extensors (ECRB, ECRL, ECU), digital Ρελατιϖε στρενγτη = 1
flexors (FPL, FDS, FDP), PT, and FCR
Digital extensors (EDC, EIP, EDQ) Ρελατιϖε στρενγτη = 0.5
1. This classification does not include the shoulder. It is a guide to the forearm and hand only.
Determination of patient suitability for posterior deltoid-to-triceps transfer or biceps-to-triceps
transfer is considered separately.
2. The need for triceps reconstruction is stated separately. It may be required in order to make
BR transfers function properly (see text).
3. There is a sensory component to the classification. Afferent input is recorded using the method
described by Moberg and precedes the motor classification. Both ocular and cutaneous input
should be documented. When vision is the only afferent available, the designation is “Oculo”
(abbreviated O). Assuming there is 10 mm or less two-point discrimination in the thumb and
index finger, the correct classification would be Cu, indicating that the patient has adequate
cutaneous sensibility. If two-point discrimination is greater than 10 mm (meaning inadequate
cutaneous sensibility), the designation O would precede the motor group (example, O 2).
4. Motor grouping assumes that all listed muscles are grade 4 (MRC) or better and a new
muscle is added for each group; for example, a group 3 patient will have BR, ECRL, and
ECRB rated at least grade 4 (MRC).
Source: Reprinted with permission from McDowell CL, Moberg EA, House JH: The Second
International Conference on Surgical Rehabilitation of the Upper Limb in Tetraplegia
(Quadriplegia). J Hand Surg (Am). 1986;11:604–608.

Chapter 11 • Tendon Transfers 147
TABLE 11-2 Excursion muscles available for transfer
Wrist extensors and flexors 30 mm excursion (ECRL, ECRB, ECU,

FCR, FCU)
Digital extensors 50 mm excursion (EDC, EIP, EDQ, EPL)
Digital flexors 70 mm excursion (FDS)
flexor is transferred to a digital extensor. The wrist flexor has an amplitude around
30 mm, but this can be used to restore motion in a muscle, which normally has 50 mm
excursion by flexing the wrist and allowing the digital extension to be augmented
through tenodesis.
VII. Synergy
A transfer will be more effective and easier for the patient to use if the action of the
transferred muscle is synergistic to the one it is replacing. Since wrist extension is syn-
ergistic with digital flexion and wrist flexion with digital extension, these reciprocal
actions are to be kept in mind when performing a transfer.
VIII. Expendable Donor
The transfer of a tendon should not result in loss of a function. Therefore, at least one
wrist flexor and extensor should be maintained.
IX. Arthrodesis
It is generally best to avoid arthrodesis to stabilize a joint as patients can use a mobile
joint to their advantage, even if there is limited voluntary control of the joint. For
example, a patient with a supple wrist may have minimal wrist control, but can supinate
the forearm, allowing for wrist extension through gravity and attendant digital flexion
via tenodesis to help with grasp.
X. Classification
Peripheral nerve injuries are generally classified as high (elbow level) or low (wrist level).
They are also classified a single nerve injuries or combined (more than one) nerve injuries.
XI. Operative Technique
In tendon transfer surgery, the functional muscle tendon unit is repaired to the non-
functional tendon using a strong weave to connect the tendons and decrease the chance
for separation of the two tendons. This is commonly completed with three Pulvertaft
weaves, in which one tendon is passed through the substance of the second tendon,
interlocking the tendons and securing them to each other, creating a strong repair. The
tension is set so as to allow for some slight postoperative stretch, as it is rare to create

a transfer that is too tight. The postoperative program varies, depending on the type
of transfer, but generally involves a period of three weeks’ immobilization, followed by
active and passive mobilization.
Peripheral Nerve
I. Radial Nerve Palsy
Radial nerve palsy can be divided into high and low injuries. A high radial nerve palsy
involves the radial nerve proper whereas the low palsy involves only the posterior
interosseous nerve (PIN) (both of these are near the level of the elbow).
The importance in the difference in high and low high and low radial nerve palsies
is in the presence or absence of active wrist extension. The radial nerve proper will
innervate the brachioradialis (BR), extensor carpi radialis longus, and brevis (ECRL
and ECRB) prior to dividing into the PIN and the radial sensory nerve and thus, a
patient with a high radial nerve palsy will lack wrist extension, thumb extension, and
digital extension.
With radial nerve injuries, three functions are lost and must be replaced:
Thumb extension
Finger extension
In high nerve palsies, wrist extension
A. Low Radial Nerve Transfers
Thumb extension PL-EPL

Digital extension Brand—FCR-EDC
Jones—FCU-EDC
Modified Boyes—FDS ring-EDC
Each of these transfers for digital extension can be used successfully. The disadvan-
tage of the flexor carpi ulnaris (FCU) transfer lies in sacrificing the strongest wrist flexor
and its importance in hammering or the “dart throwing” motion. The disadvantage
in the FDS ring transfer is the lack of synergism and although EDC excursion is best
replicated by the FDS transfer, it is more difficult for the patient to retrain a muscle
traditionally used for digital flexion to provide digital extension.
B. High Radial Nerve Transfers (in Addition to the Low Radial Nerve
Transfers)
Wrist extension PT-ECRB

Pronator teres (PT) is almost always used to restore wrist extension and is trans-
ferred to the most central radial wrist extensor—ECRB.
II. Median Nerve Palsy
A. Low median nerve transfers

The functional deficit resulting from low median nerve palsy is the loss of palmar
abduction of the thumb. Therefore, tendon transfers for low median nerve palsies

are transfers to a muscle along the course of the ABP muscle (roughly), the plane
between the pisiform and the MP joint of the thumb. Transfers distal to the pisi-
form allow more thumb flexion and better opposition. Transfers proximal to the
pisiform allow more thumb abduction so that the patient can move the thumb out
of the plane of the palm, but do not provide pronation necessary for opposition.
There are four transfers typically used for low median nerve palsies:
FDS ring, extensor indicis proprius (EIP), palmaris longus (PL), and Abduc-
tor digiti minimi (ADM). The tendon to be transferred is inserted near the level
of the MP joint of the thumb, typically along the radial aspect near the site of
the insertion of the abductor pollicis brevis (APB), but other sites have been
described.
1. Opposition/abduction
a) FDS ring (Riordan). This transfer requires the creation of a pulley to
recreate the direction of the ABP. This is typically in the region of the
pisiform, either by creation of a hole in the palmar fascia or with a distally
based loop of the FCU.
b) EIP (Burkhalter). This transfer is completed by routing the EIP around
the ulnar aspect of the forearm and inserting the tendon at the insertion
of the APB. Distal harvest of the EIP is undertaken to assure the surgeon
of adequate length.
c) Palmaris longus (Camitz). This transfer functions as an abductor trans-
fer rather than a true opposition transfer. It is most commonly used in
patients with long standing carpal tunnel syndrome who have difficulty
moving the thumb out of the plane of the palm. The palmaris longus is
harvested with a distal extension to include a strip of palmar fascia and
transposed through a subcutaneous tunnel to the insertion of the APB.
d) ADM (Huber). This transfer is most commonly used for reconstruction
in congenital thumb hypoplasia. The muscle is detached from the inser-
tion on the small finger proximal phalanx and turned on itself to insert at
the level of the APB.
B. High median nerve transfers
In addition to the loss of thumb opposition, patients with high median nerve
palsies lack thumb, index, and middle finger flexion due to paralysis of the FPL
and flexor digitorum profundus (FDP) to the index and middle fingers.
1. Thumb flexion BR–FPL
2. Index/middle finger flexion. FDP (ring and small)–FDP (index and middle)
side-to -side transfer
III. Ulnar Nerve Palsy
A. Low ulnar nerve palsies. The ulnar nerve innervates the majority of the intrin-
sic muscles in the hand. Loss of ulnar nerve function in the hand causes loss
of power pinch (Jeanne and Froment signs), digital clawing, asynchronous
digital flexion, and persistent abduction of the small finger at the MCP joint
(Wartenberg sign).
1. Power pinch is a result of contraction of the adductor pollicis and the first
dorsal interosseous, allowing the thumb to contract against the stabilized
index finger. With loss of the ulnar-innervated intrinsics, the MP and inter-
phalangeal (IP) joints are controlled by the extrinsic flexors and extensors.

The extensor pollicis longus (EPL) normally functions as a secondary

adductor of the thumb, but now becomes the only thumb adductor. Pinch
is achieved with contraction volar to the axis of rotation of the MCR joint
in order to stabilise the MCP joint. The FPL moment at the IP joint then
exceeds the EPL moment at the IP joint, resulting in IP joint flexion FPL
(Froment sign).
2. Clawing. Flexion begins with the intrinsic muscles’ initiation of MP joint
flexion, followed by DIP and PIP flexion due to the combined action of
the extrinsic flexors (FDS and FDP). When the intrinsic muscles become
paralyzed, clawing (MP extension with PIP flexion) occurs due to the
contraction of the extrinsic digital flexor and extensor muscles without the
balancing force of the intrinsics. The extrinsic extensors cause extension
at the MP joint while the extrinsic flexors cause flexion at the DIP and
PIP joints. In low ulnar palsy, clawing is seen in the ring and small finger
since the lumbricals to the index and middle finger are innervated by the
median nerve. For clawing to be present, the FDP must cause active PIP
and DIP flexion, and is therefore substantially diminished in the ring and
small fingers in high ulnar nerve palsy.
3. Wartenberg sign. Paralysis of the third volar interossei combined with the
abduction force of the PIN innervated extensor digiti minimi (EDM) causes
an abduction of the small finger known as Wartenberg sign.
B. Low ulnar nerve transfers
Transfers for low ulnar nerve palsies are directed at the prevention of
clawing, the restoration of power pinch, and restoration of adduction of the
small finger.
1. Power pinch
a) ECRB with graft to adductor pollicis
The ECRB is detached from its insertion and pulled proximal to the
extensor retinaculum. It is extended with a graft, passed between the
index and middle metacarpals and then passed subcutaneously to insert
into the ulnar aspect of the base of the proximal phalanx of the thumb.
This transfer benefits from the synergy between wrist extension and active
pinch, making it straightforward for the patient to learn to activate the
transfer.
b) FDS ring to adductor pollicis
The FDS is transferred subcutaneously to the adductor pollicis, using
the palmar fascia as a pulley. This transfer is not synergistic, as pinch will
occur with wrist flexion rather than extension, so it is not as intuitive as
the ECRB transfer and requires more training to use the transfer.
2. Clawing
a) FDS ring to lateral bands (proximal phalanx)
The ring finger FDS is transected distally and removed from the flexor
sheath, split longitudinally and then inserted into the radial lateral band
of the ring and small finger under enough tension to produce MP joint
flexion and PIP joint extension. Some surgeons prefer to attach the FDS
into the radial aspect of the proximal phalanx to prevent the tendon trans-
fer from stretching out.
b) Zancolli lasso procedure
This procedure involves harvest of the FDS passing it through a win-
dow created between the A1 and A2 pulleys, and suturing it to the A1

pulley, creating a static tenodesis causing a MP joint flexion contracture

and allowing PIP joint extension through the extrinsic extensor tendon
insertion in the central slip.
c) ECRB with graft to intrinsics
Brand described transferring the ECRB, with an intercalary graft, to
the ring and small fingers for isolated ulnar nerve palsies or to all four
fingers in combined low median and ulnar nerve palsies. The tendon is
transected at its insertion and pulled proximal to the extensor retinacu-
lum. It is extended with a two-tailed graft, passed dorsal to the retinacu-
lum, through the intermetacarpal space and palmar to the deep intervolar
plate ligament (through the lumbrical canal) to insert into the lateral
bands of the ring and small fingers.
3. Correction of Wartenberg deformity
This can be accomplished be transferring the ulnar slip of the EDM to
the radial aspect of the MP joint and inserting it into the radial collateral
ligament.
C. High ulnar nerve palsy
The primary difference between the high and low ulnar nerve palsies lies in the
loss of function of the ulnar 2 slips of the FDP in the high palsy. This lack of
extrinsic flexion mitigates against clawing. Transfers for high ulnar nerve palsies
are directed at the restoration of power pinch and flexion of the ring and small
fingers. Subsequent transfers to prevent clawing may be necessary.
1. Power pinch
This transfer is the ECRB with graft as previously described. The use of the
ring FDS in contraindicated due to absence of the ring finger FDP.
2. Digital flexion
Ring and small finger flexion is obtained by transferring the ring/ small to the
index/ middle FDP in a side-to-side fashion. This is the same principle that is
used in high median nerve injuries where the two functioning FDP tendons
are used to power the two paralyzed muscles.
IV. Combined Median and Ulnar Nerve Palsies
Motors for transfer are limited to muscles innervated by the radial nerve.
A. Combined Low Median and Ulnar Nerve Transfers

Thumb adduction is typically achieved by ECRB to adductor pollicis with a graft as
described for low ulnar nerve palsies. Thumb opposition is achieved with EIP around
the ulnar aspect of the wrist as described for low median nerve palsies. Clawing is pre-
vented by transferring the FDS from the middle to the index and middle lateral bands
and the FDS from the ring to the ring and small lateral bands.
B. Combined High Median and Ulnar Nerve Transfers

In addition to the pinch, opposition and clawing transfers used for low combined
median and ulnar nerve palsies, the ECRL is transferred to all four FDP tendons
to restore digital flexion and BR to FPL for thumb flexion. Preservation of wrist
motion to assist with grasp and pinch through tenodesis will greatly improve
function.

V. Musculocutaneous Nerve Palsies
The functional loss from this injury is elbow flexion. As experience with nerve transfers
continues to improve (Oberlin transfer and MacKinnon double fascicular transfer),
the number of patients requiring tendon transfer to restore elbow flexion will decrease.
Patients who can benefit from these transfers include those who have had failed nerve
repair or reconstruction, those in whom an excessive period of time has elapsed between
injury and presentation, and those with irreparable plexus injuries wherein sources of
nerve grafts or nerve transfers are not available.
A. Pectoralis Major Transfer

The pectoralis major has a dual innervation. The lateral pectoral nerve is derived
from the lateral cord of the brachial plexus (C5, C6, and C7) and supplies the
clavicular portion of the muscle. The medial pectoral nerve arises from the medial
cord, containing fibers from C8 and T1 and is spared in upper trunk brachial plexus
lesions. The medial pectoral nerve supplies the sternocostal portion of the muscle
and this portion can be used to restore elbow flexion. The muscle can be detached
from its insertion on the humerus and the distal aspect of the muscle is transferred to
the biceps tendon. Elongation with a fascia lata autograft is necessary. Alternatively,
the humeral insertion can be transferred to coracoid process of the scapula. This is
a technically demanding procedure and the postoperative appearance is bothersome
to some patients, but does produce good strength and leaves minimal functional
deficit.
B. Latissimus Dorsi Transfer

The latissimus is innervated from the thoracodorsal nerve, from the posterior cord (C6,
C7, and C8). Similar to the pectoralis major transfer, the latissimus can be transferred
by leaving the origin on the humerus intact, but generally it is transfered anteriorly to
the coracoid process of the clavicle or the acromion, creating a vector similar to that
of the biceps. The distal aspect of the muscle is transferred to the distal biceps tendon.
Although this is technically more difficult, the aesthetic results are superior to the pec-
toralis major transfer. It can be transferred with a skin paddle to allow for the bulk of
the muscle and it still provides strong elbow flexion.
C. Steindler Flexorplasty
This procedure involves transfer of the origin of the flexor pronator mass (innervated by
the median nerve) proximally 5 cm, and affixing it to the anterior humeral shaft.
D. Triceps Transfer
This procedure may involve the sacrifice of elbow extension strength for elbow flexion,
allowing gravity to assist in elbow extension. The triceps is detached distally and trans-
ferred around the lateral aspect of the humerus and secured to the distal biceps tendon.
This procedure is not routinely used due to loss of active elbow extension.
VI. Axillary Nerve Palsies
Axillary nerve palsies, similar to musculocutaneous nerve palsies, typically result from
upper trunk brachial plexus injuries rather than isolated nerve injuries and paralysis of
the deltoid and rotator cuff from axillary nerve injury often accompanies paralysis or

weakness of elbow flexion. The problems resulting from axillary nerve injury include
lack of external rotation and abduction of the shoulder. External rotation is required
to bring the hand above the level of shoulder and reach the mouth. The intact internal
rotators of the shoulder (pectoralis major and latisssimus dorsi) cause the humerus
to rotate internally to the chest. When elbow flexion is restored, the humerus will be
displaced proximally if the shoulder is not stable. The goals of the tendon transfers
for axillary nerve palsies are to stabilize the shoulder by restoring muscle balance.
Alternatively, shoulder stability can be obtained from arthrodesis. The transfer most
commonly used for shoulder stability is the latissimus dorsi, either alone or with the
teres major.
L’Episcipo Procedure
The tendons of insertion on the latissimus dorsi and the teres major are transferred
posteriolaterally on the humerus, converting internal rotators to external rotators. The
shoulder must have passive external rotation for this to be successful, so if a contracture
of the shoulder joint is present, it must be released simultaneously. In addition, a rota-
tional osteotomy of the proximal humerus can improve arm position.
Cerebral Palsy
I. Introduction
A. Cerebral palsy is a central nervous system (CNS) insult causing an upper motor
neuron injury; the normal inhibitory control of tone is lost and the resultant
peripheral manifestation is spasticity. Muscle spasticity causes muscle imbalance
across joints with resultant loss of function. With growth, secondary skeletal
changes can occur as well.
B. Cerebral palsy has the added complexity that the CNS injury occurs in the
perinatal period so that the effect of spasticity on the immature skeleton must
be considered as well.
C. In the upper extremity, the typical pattern of spastic joint deformities includes
shoulder internal rotation, elbow flexion, forearm pronation, wrist flexion
and ulnar deviation, thumb-in-palm and finger swan neck or clenched fist
deformities.
D. Although this pattern of deformity is the most common, the particular pattern
and severity are specific for each patient based on the extent and area of the
underlying CNS disorder.
E. Motor involvement can take the form of spasticity (increased tone), flaccidity
(decreased tone), or athetosis (lack of or poor control of tone).
II. Patient Evaluation
A. Assessment of the patient with spastic cerebral palsy starts with the history and
physical examination.
B. Because cerebral palsy is associated with low birth weight and prematurity, asso-
ciated medical problems should be noted, particularly seizures and mental retar-
dation as indicators of more global CNS involvement.
C. Physical examination for passive range of motion of the shoulder, elbow, fore-
arm, wrist, and hand is performed to evaluate for joint and/or contractures.

Passive range of motion needs to be done slowly to overcome muscle spasticity

with gentle sustained resistance.
D. Active range of motion is assessed next, including specific muscle testing for
voluntary motor control of antagonist muscles. This is particularly important
for muscles that are considered for tendon transfer such as the pronator teres
(for PT re-routing); the FCU, extensor carpi ulnaris (ECU), or the BR (for wrist
extension); the extensor pollicus longus (for EPL re-routing); and the extensor
pollicis brevis (EPB) and abductor pollicis longus for control of antagonists to
the thumb-in-palm deformity.
E. Appropriate consultation and/or multispecialty approach to care should be con-
sidered prior to considering surgical intervention.
III. Surgical Planning
A. Several alternatives to surgical intervention exist and should be considered.

Exploration of the treatment pros and cons may require discussions that include
the rehabilitation physicians, neurologists, and/or neurosurgeons to adequately
explore the options of tone-reducing medications (valium and baclofen), tone-
reducing injections (botulinum toxin and phenol), tone-reducing neurosurgery
interventions (selective dorsal rhizotomy), or therapy interventions (splinting
and stretching programs).
B. Initial treatment includes splinting, stretching, and therapy interventions.
C. A patient may be a possible candidate for surgical intervention, if the patient is
not a candidate for alternative treatments listed above or if that the treatments
listed above did not resolve this patient’s upper limb dysfunction.
D. Usually a child needs to be at least 7 years of age to consistently cooperate with a
preoperative assessment of muscle tone and control, as well as with postoperative
therapy protocols imperative to a successful result.
E. Preoperative decisions
1. What muscles are spastic and cause a joint imbalance leading to limb dys-
function? The spastic muscles may need to be released or weakened by
lengthening.
2. What muscles are flaccid or have poor motor control, leading to joint imbal-
ance with resultant limb dysfunction? The flaccid or poorly control muscles
need to be augmented usually through tendon transfer.
3. What muscles are under good voluntary control, and are available for tendon
transfer? The muscles with good voluntary control are best for good results
with tendon transfer.
4. Is there significant athetosis or poor coordination? In general, athetosis has
poor results with surgical intervention.
F. Treatment of the hand dysfunction centers on improving muscle balance to max-
imize hand function consistent with the quality of voluntary control retained.
The primary lesion in the brain is not treated and remains the limiting factor to
the success of the surgery. The goal is not normalization of hand use, but rather
to improve joint positioning to maximize assistive hand function. Surgical treat-
ment is indicated in patients with spastic deformity and contractures, unrespon-
sive to nonsurgical treatment, which produce specific functional impairment
and could be improved by better joint positioning.

IV. Surgical Treatment
A. Elbow flexion deformity

1. Release or lengthen the spastic muscle(s):
a) Biceps lengthening
b) Brachialis lengthening
c) BR origin release
B. Forearm pronation deformity
a) PT release
b) Pronator quadratus release
2. Augment the weak or flaccid muscle (tendon transfers):
a) PT rerouting
C. Wrist flexion deformity
a) Fractional lengthening of the FCU or flexor carpi radialis (FCR) at
musculotendinous junction
b) Flexor pronator slide off origin of medial epicondyle
a) BR to ECRB tendon transfer to increase wrist extension
b) ECU to ECRB tendon transfer to centralize ECU tendon, decreasing
ulnar deviation
c) FCU to ECRB tendon transfer (classic Green transfer) is the most com-
mon wrist tendon transfer.
d) FCU to EDC tendon transfer to improve active finger extension
3. Stabilize the joint for severe instability or contracture:
a) Proximal row carpectomy to improve passive wrist extension in wrist joint
contracture
b) Wrist fusion if skeletally mature, particularly for very low functioning
patients.
D. Thumb-in-palm deformity
a) Adductor pollicis origin release if the thumb ray is adducted.
b) Flexor pollicis brevis origin release if the thumb metacarpal-phalangeal
joint is flexed.
c) FPL lengthening if the thumb IP joint is flexed.
a) Donors: BR, FCR (if FCU not transferred), PL, and FDS
b) Recipients: AbPL, EPB (if MCP joint is stable), and EPL
c) Rerouting: EPL
a) MCP joint fusion or volar capsulodesis
b) IP joint fusion
E. Finger swan neck deformity
a) Intrinsic slide
b) Ulnar motor neurectomy
a) Lateral band rerouting


a) FDS PIP joint tenodesis
F. Post-operative management
1. Cast for complete immobilization for 4 to 6 weeks.
2. After the cast is removed, a custom splint is worn full time, with the splint
off three to five times per day for active range of motion and light activities
of daily living (showers, eating).
3. At 8 to 10 weeks postoperative, the splint is worn only at night and for pro-
tection during high-risk activities (recess, gym, and play), and strengthening
exercises commence.
V. Complications and Their Management
1. Overcorrection.
2. Undercorrection.
3. Recurrence with skeletal growth.
4. Avoid arthrodesis; lose tenodesis effect.
5. Lack of improved function despite better position.
6. Balance is the key, and it can be difficult to obtain and maintain.
VI. Outcomes of Treatment
1. Using the House Upper Extremity Functional Use classification, in another

review of all upper extremity surgical procedures, Van Heest and House reported
an average improvement of function so that the limb improved from a poor pas-
sive assist to a good active assist.
2. New measurement outcome tools such as the SHUEE (Shriner’s Hospital Upper
Extremity Evaluation) have been developed to measure outcomes specifically in
cerebral palsy.
Spinal Cord Injury
I. Introduction
A. Epidemiology
1. In the United States, spinal cord injuries have an annual incidence estimated
at 12,000 cases annually.
2. The most common causes are motor vehicle accidents and falls from a height.
Fifty-five percent occur in patients 16 to 30 years old, and 80% are men.
B. Anatomy
1. The hand surgeon is not as concerned with the specific vertebral level of
cervical injury as much as the specific strength of each muscle in the upper
limb.
2. The classification (Table 11.3) used in this chapter was developed by an
international group of tetraplegic hand surgeons in 1978 in Edinburgh and
modified in 1984 at Giens, France.
3. By using manual muscle testing, the most helpful evaluation of the tetraple-
gic patient is to make a working list of what the patient has (grade 4 strength

TABLE 11-3 International classification for surgery of the hand in

tetraplegia
Sensibility Motor Description

O or Cu Group Characteristics Function
0 No muscle below elbow Flexion and supination
suitable for transfer of the elbow
1 BR
2 ECRL Extension of the wrist
(weak or strong)
3* ECRB Extension of the wrist
4 PT Extension and pronation
of the wrist
5 FCR Flexion of the wrist
6 Finger extensors Extrinsic extension of
the fingers (partial or
complete)
7 Thumb extensor Extrinsic extension of
the thumb
8 Partial digital flexors Extrinsic flexion of the
fingers (weak)
9 Lacks only intrinsics Extrinsic flexion of the
fingers
X Exceptions
Source: Edinburgh 1978, Modified—Giens, 1984.
or higher), as shown in Table 11.3, and what the patient needs (grade 1
strength or lower), as shown in Table 11.3. Lastly, one must determine what
muscles are available for transfer and which muscles best match to the
patient’s needs using tendon transfer principles of work capacity, amplitude,
and direction of pull combined with other surgical adjuncts of arthrodesis
and tenodesis.
C. Historical review
1. Before the 1960s, the poor prognosis and poor survival rate of patients with
spinal cord injury precluded the need for upper extremity reconstruction.
2. The advancements in tendon transfer surgery, initiated by Bunnell,
were applied to the tetraplegic patient by Moberg, Lamb, Zancolli, and
Freehafer.
3. Studies show that patients with spinal cord injury are underserved so that
only 14% of patients, eligible for care, are actually receiving reconstruction.
4. Lack of coordination and relationships between the rehabilitation physicians
and hand surgeons is the major cited reason for the lack of treatment in
spinal cord injury.

II. Surgical Planning
A. Evaluation
1. Physical examination would include sensory and motor testing to establish their
group (0 to 9) using the International Classification as shown in Table 11.1, by
establishing which muscles the patient has over grade 4 strength.
2. Evaluate passive range of motion to evaluate joint/muscle contractures, teno-
desis effect, and resting posture of the hand.
3. Determine which muscles are available for transfer.
4. Timing of these transfers is not until there is no further documented improve-
ment in motor strength following serial examinations.
B. Pertinent anatomy
1. Nerve deficits cause a predictable pattern of injury.
2. The pattern seen with a spinal cord injury is based on segmental innervation;
this concept means that the anterior horn cells in the spinal cord that are
injured occur in a predictable pattern from cephalad to caudad position.
3. When a spinal cord injury occurs, the motor nuclei cephalad to the injury
will be functional; the motor nuclei at or caudad to the level of the injury will
be nonfunctional.
C. Classification (Table 11.1)
1. The International Classification for Surgery of the Hand in Tetraplegia
(ICSHT) groups characterize the most common patterns of presentation,
based on the strength of muscles below the elbow. Groups are based on the
number of muscles (below the elbow) and at least grade 4 strength on manual
muscle testing based on segmental innervation patterns of injury.
D. Surgical indications—cervical spinal injury with upper limb partial paralysis
1. Stabilized motor recovery (12 months postinjury)
2. Preoperative workup compatible with functional improvement with surgical
reconstruction
3. Medically stable (blood pressure, bowel and bladder function)
4. Infection free (decubitus ulcers, bladder)
5. Full passive range of motion
6. Realistic goals with good motivation/desire
7. Personal and social stability to carry out rehabilitation and staged procedures
(if necessary)
E. Surgical contraindications
Significant spasticity and psychological problems are two factors that have had a
uniformly adverse effect on results of surgical treatment.
III. Tendon Transfer Surgery by Level
A. Elbow extension tendon transfers

Two options exist for reconstruction: deltoid to triceps and biceps to triceps
transfers.
1. Posterior deltoid to triceps tendon transfer
a) The posterior deltoid to triceps transfer uses the posterior third and the
posterior half of the middle third of the deltoid muscle as a donor. An
interposition tendon graft is used, and the triceps tendon serves as the
insertion.

b) Posterior deltoid to triceps transfers are compromised by the prolonged

shoulder and elbow immobilization required postoperatively, as well as
tendon graft elongation over time.
2. Biceps to triceps tendon transfer
a) The biceps to triceps tendon transfer can be performed using a medial
routing technique.
b) Expected outcome for biceps to triceps transfer is continued improvement
in strength over at least 1 year and significant improvement in activities of
daily living such as overhead reaching and driving activities.
c) A randomized prospective comparison of posterior deltoid to biceps ver-
sus biceps to triceps with medial routing tendon transfer reported that
at 2 years, seven of eight arms treated with biceps to triceps transfer had
antigravity use of the arm, whereas only one of eight arms treated with
posterior deltoid to triceps had antigravity use of the arm.
B. Forearm pronation
1. Pronation is important to patients who have active wrist extension only
because if the hand cannot be pronated, gravity cannot be used to provide a
tenodesis effect.
2. Biceps rerouting converts the biceps from a supinator into a pronator, as
described by Zancolli.
IV. Tendon Transfer by IFSHT Group Level
A. Group 0
Patients in this group have no muscle groups below their elbow with grade 4
strength.
1. Group 0’ patients may be candidates for elbow extension transfers, as already
described.
2. May be a candidate for BR to ECRL tendon transfer A few group 0 patients
may have both a weak BR and a weak ECRL. Transfer of the BR to the radial
wrist extensors may provide sufficient strength to extend the wrist against
resistance.
3. May be candidate for functional electrical stimulation under research
protocol.
a) BR to ECRB tendon transfer
Indications
1) Group 1 patient with greater than grade 4 strength BR with less than
grade 4 strength of wrist extension
2) Group 0 patient with grade 3 strength BR and less than grade 4
strength wrist extension
B. Group 1
Patients in this group have BR with grade 4 or greater strength, and all other mus-
cles groups below the elbow have less than grade 4 strength (see Table 11.3).
1. Two procedures are necessary for group 1 patients, and both can be done
simultaneously, if desired:
a) BR to ECRB tendon transfer.
b) Passive key pinch reconstruction.
1) Stabilization of the thumb IP joint by pin fixation, fusion, or split FPL
transfer.

2) FPL tenodesis to the distal radius for the correct tension for lateral
pinch.
3) Stabilization of the MP joint. If greater than 45 degrees of flexion is
present, use EPB and EPL tenodesis to the dorsal first metacarpal with
a bone anchor suture; if greater than 10 degrees of passive hyperexten-
sion is present, use a volar capsulodesis or an MP arthrodesis.
2. Many authors have reported fairly uniformly good results using this proce-
dure with a typical series with an average final pinch strength of 0.7 kg.
C. Groups 2 and 3
Patients in these groups have BR and wrist extension with grade 4 or greater
strength, and all other muscles groups below the elbow have less than grade 4.
1. It may be difficult to determine the differential strength of ECRL (group 2)
and ECRB (group 3), in order to avoid loss of wrist extensor strength.
2. For the patients in groups 2 and 3, the BR is always available for transfer and
has been used in a variety of ways.
3. For group 2 and 3 patients, House’s one-stage active key pinch reconstruc-
tion consists of
a) CMC fusion.
b) BR to FPL tendon transfer.
c) EPL tenodesis.
d) Split FPL transfer for stabilization of the thumb IP joint.
e) If the index finger does not flex enough to be a base for key pinch, then a
lasso procedure.
D. Groups 4 and 5
Patients in this group have BR and wrist extension (ECRL and ECRB) as
well as PT (group 4) and FCR (group 5) with grade 4 or greater strength,
and all other muscles groups below the elbow have less than grade 4 strength
(see Table 11.1).
1. In patients in group 4, the PT is strong enough to consider for transfer.
2. In patients in group 5, the addition of wrist flexion strength improves antag-
onist power for the wrist extension-driven tenodesis function of the fingers.
3. In groups 4 and 5, the BR, ECR, and the PT muscles are available for trans-
fer. The ECRB and the FCR are left in place to preserve good wrist control.
4. Because there are more muscles available in patients in groups 4 and 5, the
surgeon most commonly would choose a two-stage reconstruction of grasp
(flexor phase) and release (extensor phase).
Two-stage grasp, pinch, and release
Stage 1: Extensor Phase
a) CMC fusion
b) EPL and EDC tenodeses
Option: BR to EPL/EDC tendon transfer.
Stage 2: Flexor Phase
a) ECRL to FDP tendon transfer
b) BR to FPL tendon transfer
Option: PT to FPL tendon transfer
E. Groups 6 and 7
Patients in these groups have at least grade 4 strength of the BR, ECRL, ECRB,
PT, and FCR. Additionally, at least grade 4 strength of the EDC is present in
group 6, and also of EPL in group 7 (see Table 11.3).

1. Because some degree of finger/thumb extension is present for these patients,

a separate extensor phase is not required.
2. Reconstruction for these groups of patients consists of a flexor phase only.
3. For the group 6 patients, the finger extensors are strong but EPL function
is either absent or too weak to extend the thumb and an EPL tenodesis is
necessary.
4. For the group 7 patients, both finger and thumb extensors are strong, so the
flexor phase alone is performed.
Surgical technique of group 6 and 7 reconstructions
1. ECRL to FDP for active finger flexion
2. BR or PT to FPL for active pinch
3. Thumb control options
a) The CMC joint can be fused to provide key pinch positioning.
b) The MP can be fused if unstable, using a capsulodesis technique or a
sesamoid fusion.
c) The IP joint can be controlled from hyperflexion (Froment sign) using
the “split FPL” technique.
F. Group 8
Patients in this group have weak finger flexion and lack intrinsic function. Usu-
ally, the long flexors to the ulnar digits (ring and small fingers) are stronger than
those to the thumb, index, and long fingers.
1. Flexion of the index and long fingers can be improved or strengthened by
connecting all four profundus tendons together using a FDP side-to-side
transfer.
G. Group 9
Patients in group 9 have functioning superficialis muscles, as well as all the other
extrinsic finger and thumb flexors and extensors, but do not have intrinsic mus-
cle innervation.
1. This is the smallest group in patients with tetraplegia and in many ways
can be treated much like a patient with a combined low median, and ulnar
peripheral nerve palsy.
2. These patients will benefit most from opponensplasty and from intrinsic
reconstructions, tailored to the intrinsic imbalance present, such as a lasso
reconstruction.
V. Intrinsic Reconstruction
A. Tendon transfer surgery in patients with spinal cord injury has focused pri-
marily on the reconstruction of extrinsic muscle function for grasp, pinch, and
release.
B. After spinal cord injury, loss of intrinsic and extrinsic control leads to varying
degrees of muscle imbalance, influenced by the level of motor control, flaccid
paralysis, spasticity, and ligamentous laxity, as well as different postinjury splint-
ing protocols.
C. Intrinsic reconstruction procedures are an adjunct to extrinsic reconstructions
and serve to improve the results of extrinsic procedures. Intrinsic reconstructive
procedures are tendon transfers or tenodeses designed to improve intrinsic bal-
ance in the fingers and/or thumb.

D. The most common intrinsic imbalances and their recommended treatments

include the following:
1. Hyperflexion of the thumb IP joint (Froment sign) treated with split FPL
transfer. This involves splitting the FPL in a longitudinal fashion from the
insertion in the distal phalanx to the level of the A1 pulley. The radial slip is
transferred subcutaneously to the EPL, balancing the pull between the flexor
and the extensor.
2. Clawing of the digits with MP hyperextension of the fingers and PIP flex-
ion with early digital “roll-up” treated with Zancolli lasso procedure. The
Zancolli lasso procedure helps initiate MP flexion as the first stage of digital
roll-up followed by PIP and DIP flexion, which makes large cylindrical grasp
more effective.
3. PIP flexion deformity due to central slip deficiency treated with intrinsic
tenodesis free grafts EPL distally.
VI. Conclusion
A. Hand reconstruction is only one facet of the medical care and support services
necessary for rehabilitation after spinal cord injury.
B. Assessment of outcomes for tetraplegic hand reconstruction continues to improve
and allow for comparison of interventions.
C. The most useful evaluation of the tetraplegic patient is to make a working list of
what the patient has (grade 4 strength or higher), as shown in Table 11.3 what
the patient needs, and lastly, one must determine what muscles are available for
transfer and which muscles best match the patient’s needs using tendon transfer
principles of work capacity, amplitude, and direction of pull, combined with
other surgical adjuncts of arthrodesis and tenodesis.
Stroke
I. Introduction
Although most stroke victims survive the cerebrovascular insult, many are left with cogni-
tive and/or motor impairment. Stroke is the primary cause of hemiplegia, which causes
significant functional disability. During the weeks following a stroke, motor involvement
of the upper extremity progresses from flaccid paralysis to increased muscle tone or spastic-
ity. This progression may be accompanied by severe pain, and may interfere with hygiene
when spasticity makes positioning of the upper extremity difficult. Contractures and joint
subluxations develop due to the imbalance of muscle tone in the arm, leading to further
difficulty in maintaining function and hygiene. The spastic shoulder is internally rotated
and adducted. The elbow is flexed with the forearm pronated, and the wrist is flexed with
the fingers either flexed or extended, and a thumb-in-palm deformity is present.
II. Evaluating Patients with Acquired Hemiplegia
Initial evaluation of the stroke patient includes motor and sensory assessment. Motor
evaluation includes assessing, for the entire upper extremity, motor tone, strength, vol-
untary control, and contractures. Increased tone, or spasticity, may masquerade as a
fixed contracture. Using various techniques such as nerve blocks and EMG, voluntary

contractions can be elicited, the contributions of specific muscle groups can be isolated,
and fixed joint contractures can be diagnosed.
Sensory evaluation is also important in the assessment of the poststroke patient. Pain,
temperature, light touch, proprioception, and two point discrimination are assessed. The
patient’s kinesthetic awareness of the extremity in space indicates the potential for regain-
ing control and use of the arm. The neglected upper extremity, which lacks voluntary con-
trol, has poor rehabilitation potential. Treatment is then directed at improving hygiene.
III. Non-operative Management of the Hemiplegic Upper Extremity
A. Splinting may help with pain and spasticity, but recent studies have shown that
splinting may not be as beneficial in preventing fixed joint contractures as previ-
ously thought.
B. Physical and occupational therapy, including an aggressive range of motion and
stretching protocol, may reduce contracture formation and help relieve pain.
C. Muscle relaxants may help relieve pain associated with increased muscle tone.
D. Lidocaine and/or phenol nerve blocks reduce tone locally, and the pain associ-
ated with it.
E. Botulinum toxin reduces spasticity temporarily and may reduce contractures and
pain when used in conjunction with an exercise therapy program.
IV. Surgery for the Hemiplegic Upper Extremity
Voluntary control should be thoroughly evaluated preoperatively. Local anesthetic blocks

or botulinum toxin injections may be necessary to reduce tone enough to discern voluntary
control in less affected muscles. Other preoperative considerations include assessment of pro-
prioception, two point discrimination, patient motivation, and cognitive function. Surgery
is more likely to improve function when the patient is motivated and has good cognition,
voluntary control of the extremity, good proprioception, and two point discrimination less
than 10 mm. These criteria are less important when the primary indication for surgery is to
improve hygiene by improving access to the palm, volar wrist, antecubital fossa, or axilla.
In general, surgical management is considered when nonoperative management is
unsuccessful or not feasible, and when the clinical status of the patient has stabilized.
A. The hand
1. Finger extension is limited.
a) Surgical release of spastic finger flexors may enhance release (by improv-
ing finger extension) as well as provide access to palmar skin for hygiene.
Flexor tendons may be lengthened en masse or individually. Usually
both FDS and FDP tendons are spastic and both must be lengthened to
improve finger extension. This can be accomplished by Z-lengthening or
fractional lengthening (detaching the tendon from surrounding muscle at
the musculotendinous junction). Lengthening the extrinsic finger flexors
decreases finger flexion strength, which weakens grip. In order to avoid
excessive weakening, it is recommended that the tendon be lengthened
approximately one half the distance of the extension lag (the difference
between active extension and normal extension).
b) The FDS tendons can be transected as far distally as possible in the
forearm, and transferred to the FDP tendons (which are transected as
far proximally as possible, to gain length) in order to release a severe
clenched fist deformity. This operation causes significant weakening

of grasp, and should be used primarily for hygiene in the minimally

functional hand.
2. Thumb-in-palm deformity
a) Thumb extension may be limited by a spastic adductor pollicis and/or
FPL. Release of the adductor at either its insertion on the proximal pha-
lanx of the thumb or at its origin on the floor of the palm can improve
thumb abduction without loss of key pinch strength or instability of the
MP joint. Z-lengthening or fractional lengthening of the FPL in the mid-
forearm will allow extension of the thumb IP joint; arthrodesis of this
joint provides pinch stability.
B. The wrist
1. The flexed wrist position can be corrected by Z-lengthening the wrist flex-
ors, which include the FCR, FCU, and palmaris longus. Electromyographic
studies are helpful in distinguishing the activity of each specific muscle group
with various wrist and hand positions. In the presence of voluntary control,
which can be identified with nerve blocks, surgical lengthening can restore
better control over wrist extension. With severe contractures and deformity,
lengthening as well as bony procedures such as proximal row carpectomy and
radiocarpal arthrodesis are necessary.
2. Surgical release of the flexor pronator mass reduces the pronation and wrist
flexion deformity. This requires an extensive dissection at the elbow, and risks
a supination deformity. Alternatively, the PT can be released from its insertion,
and the wrist flexors lengthened using a Z-lengthening technique as above.
C. The elbow
1. The elbow is flexed secondary to spasticity in the BR, biceps, and in some
cases, the brachialis muscles. The persistently flexed elbow leaves the hand in
an unfavorable position, and impairs hygiene by causing skin maceration in
the antecubital fossa and impeding daily activities such as putting on clothes.
Fractional lengthening or release of the BR and brachialis, and Z-lengthening
of the biceps reliably improve elbow position and function.
D. The shoulder
1. Spasticity of the shoulder girdle muscles typically involves the latissimus
dorsi, teres major, pectoralis major, and subscapularis, adducting and inter-
nally rotating the shoulder. Axillary hygiene becomes difficult in this posi-
tion, and daily activities such as dressing are challenging due to inability
to abduct the shoulder. Muscle imbalance causes shoulder contracture and
posterior glenohumeral subluxation. Fractional lengthening of the involved
muscles or releasing the tendinous insertions of the muscles can improve
shoulder abduction. This is typically done through an anterior approach to
the shoulder using the deltopectoral incision.
Rheumatoid Arthritis
I. General Principles
Rupture of the extensor or flexor tendons among patients with rheumatoid arthritis
may occur in patients with advanced or uncontrolled disease. Fortunately, this compli-
cation, along with other manifestations of advanced rheumatoid disease, is also becom-
ing less common as the medical management of inflammatory arthritis continues to
improve. Tenosynovitis refractory to medical therapy may be an indication for early

tenosynovectomy, even in the absence of rupture. Currently, most surgeons will delay
surgical intervention for 3 to 6 months following any change in medication to allow
adequate time to evaluate the clinical effect.
It is common for a patient’s first tendon rupture to be treated as a near-emergency
by the treating rheumatologist or internist, and the patient will be urgently referred to a
hand surgeon. Although the actual rupture does not necessitate emergent management,
the first rupture should be considered as a sentinel event, signaling the need for timely
surgery to prevent further ruptures.
II. Extensor Tendon Ruptures
A. Anatomy
The most commonly ruptured tendons are the digital extensors of the small finger and
ring finger. The typical site of rupture is at the wrist near the DRUJ and ulnar head.
B. Evaluation and management overview
1. Rheumatoid arthritis severe enough to cause tendon ruptures is also likely
to create significant deformity throughout the hand, wrist, and elbow. The
whole limb should therefore be approached systematically. In the rheumatoid
patient, an apparent tendon rupture may actually reflect a different manifes-
tation of the disease.
a) A PIN or an AIN palsy may be caused by synovitis or an effusion at the
elbow, and may mimic an extensor or flexor tendon rupture. The tenod-
esis examination and a detailed evaluation of all extrinsic tendons in the
hand can be helpful in making the distinction.
b) Tendon subluxation may also prevent active extension from a flexed pos-
ture, but without a tendon rupture, patients will be able to maintain joint
extension once passively placed in that position.
c) Indications for surgery include pain loss of function, and deformity.
1) Evaluation of the tendons. Perform tenosynovectomy of the affected
tendon, and all compartments adjacent to it. This may be the most
significant and beneficial aspect of the patient’s intervention. It is
much better to prevent a rupture than to reconstruct one.
2) Evaluation of the distal ulna. Dorsal subluxation and synovitis are
typically present (caput ulna). These may result in a bony spur over
which the extensor tendon can progressively fray and then rupture.
The gold standard for management of the distal ulna has been simply
to resect it (the Darrach procedure). Other options include hemi-in-
terposition arthroplasty, or matched distal ulnar resection arthroplasty.
Sauvé-Kapandji distal ulnar arthrodesis can be done if ulnar transloca-
tion of the lunate is noted. These procedures provide pain relief, reduce
subluxation, and minimize future injury to the overlying tendons.
Currently, DRUJ prosthetic arthroplasty is evolving, but its role in
rheumatoid arthritis has yet to be defined.
3) Evaluation of the radio-carpal joint and the carpus. If the joint is
painful, but without significant arthritis, the patient may benefit from
wrist synovectomy alone. If there is radiographic evidence of
degeneration, and the patient is symptomatic, a limited or complete
wrist fusion is beneficial. However, radiographic arthritis, in the
absence of clinical symptoms, is not an indication for surgery. The role
of wrist arthroplasty with simultaneous tendon transfer or repair is

unclear. Patients may express a clear preference for a wrist with motion,
as long as it is adequately stable and free of pain. Recently a new
generation of promising total wrist implants have become available,
which may minimize the problems of loosing or breakage.
4) Evaluation of the hand. When wrist disease, MCP disease, and extensor
ruptures coexist then the order of management should be as follows:
Reconstruction of the wrist and thumb, including tenosynovectomy and
tendon transfers, followed by staged treatment of the digital joints.
C. Extensor transfers
1. Like tendon transfers for other conditions, reconstructive transfers in the
rheumatoid hand are selected considering what donor tendons are available,
expendable, and appropriately matched in power, excursion, and phase with
the ruptured tendon.
2. Classic transfers for extensor ruptures of the small and ring include EIP to
small finger extensor and EDC of the ring finger to the long finger. In cases
involving rupture of three digital extensors, the FDS of the ring finger can be
used, either passed through the interosseous membrane, or around the radius
or ulna. For EPL reconstruction, the standard transfer is the EIP when it is
available.
III. Flexor Tendons
A. The FPL ruptures most commonly. It characteristically ruptures near the sca-
phoid tubercle (Mannerfelt lesion). The other digital flexors may rupture at the
wrist, in the palm or digits. The FPL can also rupture in the sheath. Ruptures
within the sheaths of either the digits or the thumb are considered unreconstruc-
table, and appropriate arthrodeses can be performed. Flexor tenosynovectomy
can be very effective in the digits as well as in the hand or wrist, decreasing
pain and improving function. If passive motion is significantly better than active
motion, tenosynovectomy can be considered.
B. Similar to extensor ruptures, the whole hand and wrist of the rheumatoid patient
with flexor tendon ruptures should be evaluated, and flexor repair or transfer
should be considered part of an overall management strategy for the patient.
In the thumb, the IP joint should be evaluated. If it demonstrates significant
articular destruction or instability, fusion may be the best option. In some cases,
direct repair is feasible (direct repair is not commonly used due to the attritional
nature of the rupture and quality of the ruptured tendon, but when possible,
works better with flexors than extensors). Reconstruction with a tendon graft,
most commonly the palmaris longus, can be performed or alternatively, transfer
of the ring FDS if it is not affected.
Brachial Plexus
I. Goals
The goals of treatment following brachial plexus injury are

1. To improve the position and control of the shoulder, thereby improving posi-
tion of the arm and hand,
2. To improve active elbow flexion so that the hand may be brought to the mouth,
3. To restore pinch, grasp, and release functions of the hand

II. Principles
A. Therapy: Maintenance of range of motion in the shoulder, elbow, and hand.

Therapy should first optimize strength of the shoulder prior to addressing the
elbow and the hand.
B. An appropriate sequence of surgeries is planned. The hand is operated prior to
the elbow, which itself is operated prior to the shoulder. This facilitates patient
positioning in the operating room (it would be difficult to operate using a hand
table after the shoulder is fused in a position of abduction and flexion.)
C. Surgical treatment is carried out once the full extent of the neurological injury
has been diagnosed and has shown to stabilize.
III. Shoulder
A. Options for the surgical management of the shoulder include the following:
Arthodesis of the scapulothoracic joint or glenohumeral joint, trapezius muscle
transfer, Latissimus dorsi and teres major (L’Episcipo procedure), and external
rotation osteotomy of the humerus.
B. Therapy is used to maintain joint range of motion prior to surgical intervention.
C. Arthrodesis is indicated for patients with paralysis of the deltoid and supraspi-
natus as well as good function of the elbow and hand. Active voluntary control
of the trapezius, levator scapulae, serratus anterior, and rhomboids is evaluated
preoperatively, as these muscles will motor the scapulothoracic joint actively fol-
lowing glenohumeral arthrodesis. Position for shoulder arthrodesis is 30 degrees
of abduction, 30 degrees of forward flexion, and 30 degrees of internal rotation.
Position can be modified based on the body habitus of the patient.
D. Tendon transfers to improve external rotation include transposition of the terres
major and/or the latissimus dorsi, known as the L’Episcipo procedure. If passive
external rotation is limited secondary to articular or capsular constraints, a cap-
sular release can be performed.
IV. Elbow
Options for the surgical management of the elbow include nerve transfers and muscle-
tendon transfers.
A. The purpose of muscle or tendon transfer is to improve elbow flexion; thereby
allowing the patient to bring his hand to his face. Options include transfer of local
muscles, transfer of “shoulder” muscles, and free innervated muscle transfer.
1. Local Transfers include triceps to biceps or transposition of flexors/extensors
of the forearm.
a) Triceps to biceps transfer is indicated in patients with full strength of the tri-
ceps; patients with cocontraction of the triceps and biceps; and in patients
for whom active extension of the elbow is less essential.
b) Transposition of flexors/extensors of the forearm (also referred to transpo-
sition of the medial or lateral epicondyle) is indicated for patients with
triceps paralysis combined with full strength of the forearm flexors or
extensors. Transposition of the medial epicondyle has the disadvantage of
mixed elbow flexion with pronation.
B. Transfer of latissimus dorsi or pectoralis major can improve elbow flexion
in patients with paralysis of the triceps, forearm flexors, and extensor. The

pectoralis major transfer can either be unipolar (transfer of the tendinous inser-
tion from the humerus to the radial tuberosity after grafting with a stout tube
of fascia lata autograft) or bipolar (transfer of the tendinous insertion from the
humerus to the shoulder and the muscle to the proximal radius). Sternomastoid
transfers with fascia lata autograft have been described, as have pectoralis minor
transfers.
C. Free muscle transfers are indicated in patients with paralysis of the triceps,
forearm flexors and extensors, latissimus dorsi and pectoralis major. The most
commonly utilized muscle for transfer is the innervated gracilis flap.
V. Wrist and Hand
A. Wrist and hand function should be addressed prior to stabilization of the shoul-
der and restoration of elbow function.
B. Options for addressing wrist and hand function include selective arthrodeses and
tendon transfers.
C. Tendon transfers can be used to restore pinch, grasp, and release functions of
the thumb, digits, and wrist.
D. Selective arthrodesis of small joints of the hand (CMC thumb, PIP index
through small, DIP joints and others) can improve hand function. Arthrodeses
can be done in conjunction with tendon transfers.
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Stiffness
12
Hill Hastings II, Jeffry B. Watson, and
Surasak Jitprapaikulsarn
Digital Stiffness
Congruent articular surfaces, tendon mobility, muscular strength, and a pliable soft
tissue envelope are prerequisites to digital motion. Digital stiffness results from pro-
cesses that compromise one or more of these factors. The etiology of digital stiffness is
wide ranging and includes Dupuytren contracture, central or peripheral nervous system
disorders, congenital disorders such as camptodactyly or arthrogryposis, and posttrau-
matic or rheumatologic alteration in regional bone morphology or joint stability.
This chapter will focus on stiffness resulting from trauma, swelling, or immobiliza-
tion without change in periarticular bone morphology.
I. Pathoanatomy
Hand stiffness commonly results from a combination of prolonged edema, ischemic

muscle contracture, and direct tendon scarring.
Contractures typically become fixed with the MP joints in extension, the interpha-
langeal joints in flexion, and the thumb metacarpal in adduction.
A. MP joint
1. The metacarpal head is trapezoidal with a wider palmar than dorsal surface.
2. As the MP collateral ligaments originate in the retrocondylar recess, passing
volarly to insert on the palmar aspect of the proximal phalanx, the collateral
ligaments are taut in flexion. This “cam” effect results in greater stability of
the MP joint in flexion (coupled with a larger joint surface contact area).
3. Provided greater joint laxity in extension, the patient with an edematous
digit will most comfortably rest in MP extension. Over time, the collateral
ligaments become fixed and are unable to lengthen as necessary to permit MP
flexion.
B. PIP joint
1. Unlike the MP joint, the PIP joint has no “cam” effect and the fluid capac-
ity of the joint is similar in flexion and extension. Also, the PIP volar plate
is thicker, less pliable, and does not “telescope” in length like the MP volar
plate.
2. The tendency for the PIP joint to become stiff in flexion is explained by the
relative increased tension in the extrinsic flexors due to the MP joint exten-
sion. Chronically, the volar plate and contracted collaterals can contribute to
the inability to extend the PIP joint.
3. In addition to losing terminal extension, PIP joints also tend to lose terminal
flexion. Extremes of flexion are sacrificed with persistent dorsal soft tissue
edema. Normally, the dorsal PIP joint skin requires 12 mm of lengthening
to obtain 90 degrees of flexion. With 5 mm of edema over the joint, the
170

Chapter 12 • Stiffness 171
same degree of flexion requires 19 mm of lengthening in skin that is now less

pliable. Over time, skin, collateral ligament, and dorsal capsule contractures
combine to create fixed contractures that limit PIP flexion as well.
C. DIP joint
1. DIP joint structure is similar to that of the PIP joint, with broad articular
contact area, a central articular groove, and equal collateral ligament tension
throughout the arc of motion.
2. The volar plate is different from that of the PIP joint due to the absence of
checkrein ligaments to prevent hyperextension.
D. Extensor mechanism
The digital extensor mechanism is divided into the intrinsic and extrinsic
components.
1. Extrinsic extensors (EIP, EDQ, and EDC) originate proximal to the wrist.
These tendons cross the dorsal midline of the MP joint to become the central
extensor slip inserting at the PIP joint. Note that the extrinsic extensors are
the sole mechanism for MP extension by means of their action through
their attachment to the volar plate through the sagittal bands. Short, direct
fiber attachments from the undersurface of the tendon to the dorsal capsule
and dorsal phalangeal base are described, but these do not have constant effect
on MP extension. Further distal, the long extrinsic extensor sends off two
lateral slips to merge with the lateral bands of the intrinsic system in the distal
portion of the proximal phalanx to form the conjoined lateral band.
2. Intrinsic extensor mechanism
a) The intrinsic extensors comprise seven interosseous (four dorsal and three
volar) muscles and four lumbricals. The deep motor branch of the ulnar
nerve innervates all interossei and the lumbricals to the ring and small fingers.
The long and index lumbricals are median nerve innervated (via fibers ema-
nating from the common digital nerves to the first and second webspaces).
1) Interossei—Flex the MP and extend the IP joints (the “intrinsic plus”
posture).
a. Dorsal interossei abduct the digits from the middle finger.
b. Volar interossei adduct the digits toward the middle finger.
i) The superficial head of the dorsal interossei inserts on the
proximal phalanx providing abduction and secondarily MP
flexion. The deep head of the dorsal interossei pass dorsal to
the deep transverse metacarpal ligament (DTML) (but volar to
the axis of rotation of the MCP joints) to insert into the lateral
bands, which immediately send transverse fibers dorsally
toward the central extensor tendon to contribute to MP flex-
ion. Just distally, the oblique fibers arch distally and dorsal to
insert alongside the central slip on the dorsal lateral tubercles
of the middle phalangeal base to effect PIP extension.
ii) The lateral bands are joined by the lumbricals (which have just
passed palmar to the DTML) on the radial aspect of each digit
and lateral slips of the central extensor tendon to form the
conjoined lateral band. The conjoined lateral bands from each
side of the digit merge over the middle phalanx to form the
terminal tendon, which extends the DIP joint.
iii) The volar interossei have no direct attachment to the proximal
phalanx and form the lateral band on the opposite side of the

digit from the lateral band formed by the dorsal interossei,

with identical contributions of transverse and oblique fibers.
iv) Contracture of the interosseous muscles limits simultaneous
MP extension and IP flexion. This “intrinsic tightness” is a
frequent occurrence following prolonged edema in the hand or
in situations following vascular compromise, such as a com-
partment syndrome.
b) The lumbricals
1) The four lumbricals originate on the FDP tendons in Zone 3 of the
palm, with the index and long (median innervated) arising only from
the FDP to those fingers and the ring and small (ulnar innervated)
arising from the FDP tendons from the adjacent digits as well. Unlike
the interosseous tendons, the lumbrical tendons pass palmar to the
DTML before joining the lateral band to become the conjoined ten-
don. Lumbrical contraction relaxes the FDP tendon (its origin and
antagonist) while creating tension in the lateral band to extend the IP
joints. The volar position of the tendon relative to the DTML at the
MP joint further contributes to MP flexion.
2) Any abnormal tension of the lumbricals will affect IP joint motion. As
with the interossei, this can result from muscle ischemia, decreasing
the excursion of the lumbrical muscle-tendon unit. Direct scarring of
the lateral band tendon to the bone (often seen following phalangeal
fracture) will also limit lateral band excursion and IP motion. The
tendon of the lumbrical has also been known to scar down to the
interosseous tendon, forming an adhesion that “straddles” the DTML
and limits excursion of both.
E. Flexor tendons
The retraction of avulsed or unrepaired FDP tendon can also result in limited
flexion of the PIP joint, despite the FDS tendon being intact. As the FDP retracts,
the lumbrical origin is moved proximally, increasing the lumbrical’s resting ten-
sion. Attempted flexion results in further FDP retraction and tension through the
“pretensioned” lumbrical tendon, placing a paradoxial extension moment at the
PIP (because of the lateral bands situated dorsal to the axis of rotation of the PI
joint) and resisting flexion from the FDS. This is known as the lumbrical plus
deformity.
F. Skin
The skin of the hand and digit contributes to stiffness in several ways. Acutely,
edematous skin necessitates an increased force to accomplish motion. Chronically,
skin becomes contracted around stiff joints contributing to contracture. Traumatic
and surgical wounds can also produce joint contractures or scar to flexor and exten-
sor mechanisms to limit motion.
II. Evaluation of the Stiff Digit
A. This discussion assumes that all skeletal issues such as phalangeal nonunion or
malunion, intraarticular incongruity, and periarticular bony blocks to motion
have been corrected.
B. Barriers to flexion include dorsal capsular contracture, contracted collateral
ligaments, adherent extensor tendons, dorsal skin contracture (such as wounds
allowed to heal by secondary intention), and intrinsic tightness.

C. Flexor tendon adhesions, rupture or excessive repair site gap will impair active
flexion while still allowing passive flexion.
D. Extension blocks include volar capsule (volar plate) contracture, palmar skin
contractures, and adherent flexor tendons.
E. Insufficiency or scarring of extrinsic extensor motor units will impair active
while still permitting passive extension.
F. Identification of all components limiting active joint motion may occur only
after fixed joint contractures are resolved, allowing assessment of the integrity of
the flexor and extensor motor tendon units.
G. Evaluation begins with comparison of active motion versus passive motion of
both the PIP and MP joints.
1. If passive motion is greater, then the most limiting problem is outside of the
joint itself. Specifically, the flexor or extensor motor unit is either denervated,
incompetent or tethered by scar.
2. Similarly, if passive motion changes with the position of surrounding joints,
the etiology is outside of the joint itself.
3. When the intrinsics have a normal degree of elasticity and excursion without
other factors blocking MP or PIP motion, one can easily assume the intrinsic
minus position of full MP extension and IP flexion.
4. When there is diminished excursion of the intrinsics, they cannot stretch
enough to allow for the full intrinsic minus position. That is, PIP flexion can
only be achieved through compromise of MP extension, and MP extension
can only occur if the PIP is extended. This is referred to as intrinsic tightness.
Tightness of the lumbricals relative to the interossei can further be differentiated
by passively flexing the PIP joint and DIP joint together. If resistance is noted
with passive DIP flexion despite facile PIP flexion during the Bunnell intrinsic
tightness test, the lumbrical muscle may be the contracted component.
5. Extrinsic tightness occurs when there is diminished passive excursion of the
EDC, EIP, or EDQ muscle-tendon units. The most common cause of this is
when the tendon is adherent to surrounding structures following trauma. In
this situation, simultaneous flexion of the MP and PIP joints is limited. The
differentiation of extrinsic versus intrinsic tightness blocking flexion is key to
developing any treatment plan.
6. Oblique retinacular ligament contracture is detected by passive simultaneous
extension of the DIP and flexion of the PIP joints (Boutonniere). This struc-
ture acts as a passive link for simultaneous flexion and extension of the PIP
and DIP joints. If the ligament is contracted, DIP flexion will only occur with
some degree of PIP flexion to relax the ligament.
III. Treatment
A. Nonoperative therapeutic options should be exhausted prior to consideration for

surgical treatment.
B. The results of a sustained progression through splinting and motion are gener-
ally enduring with less potential morbidity.
1. Splinting regimens that stretch contracted joints or tissues operate on the prin-
ciple that sustained tension changes tissues elasticity and cell proliferation.
a) Dynamic splints apply stretch through springs or elastic bands against
contracted tissues while still allowing for some motion.

b) Static splints maintain the joint in one position without applying force,
and serial static splints hold the joint in one position while applying stretch
to contracted tissues. As the contracted tissues relax in response, the serial
static splint is remolded or changed to continually apply stretch against
the contracture while being worn. Static progressive splints operate on the
same principle, but they have some component (such as a gear or ratchet)
that allows the splint position to be modified without custom molding.
c) Treatment goals should be individualized for the digit and the patient.
Some patients may be able to function without full digital flexion of both
hands and are less willing to undergo extreme or prolonged measures
to obtain that. Furthermore, the ulnar-sided digits generally require a
greater arc of motion than the long and index fingers, whose tasks are
mostly performed in conjunction with the thumb and require only mod-
erate degrees of flexion.
1) As noted above, MP joints should be immobilized in flexion. However,
if stiff in extension, a program of dynamic and static progressive splint-
ing combined with aggressive hand therapy usually results in signifi-
cant improvement of motion.
2) Depending on the initiating pathology, the PIP joint can exhibit
limited flexion, extension, or both. Regimens of daytime dynamic
splinting with nighttime serial static splinting and stretching exercises
frequently result in improvement.
d) Surgical release can be considered when nonoperative results have
plateaued and are not adequate for function. Furthermore, several key
criteria must be satisfied.
1) All soft tissue swelling and inflammation should be resolved.
2) Wounds should be healed or covered beforehand.
3) Articular surfaces should be stable and congruent. Release of a non-
congruent joint usually results in temporary instability followed by
stiffness.
4) Finally, the patient needs to be fully informed and committed to a
prearranged aggressive postoperative motion therapy regimen that
begins from postoperative day two or three. Only if these conditions
are met should surgical release be scheduled.
After determining the amount of active and passive motion in
each direction at each joint, Boyer and colleagues have outlined a sys-
tematic operative approach for six combinations of stiffness based on
physical examination findings.
1) No passive flexion or extension. This suggests both dorsal and volar
pathology.
a. Dorsal joint contracture, contracture of dorsal portion of collate ral
ligaments, or extensor adhesions can inhibit gliding of these struc-
tures and limit joint flexion.
b. On the palmar aspect, accessory collateral ligament contracture,
volar plate checkrein ligament contracture, skin contracture, and
flexor tendon adhesions will limit passive extension.
c. Dorsal and volar procedures performed during the same anesthetic
are not advisable, as flap necrosis or prohibitive pain and swelling
often result and undermine intraoperative gains. Therefore, the volar
aspect is usually addressed first in a progressive sequence as below.

i) Two or four flap Z-plasties in skin

ii) Checkrein ligament, accessory collateral release
iii) Palmar or complete collateral release
iv) Provision of stable gliding skin surface
d. Following restoration of full passive extension and subsidence of post-
operative swelling and inflammation, dorsal release can be pursued to
restore passive flexion and also the active component of extension.
e. Recalling the preoperative assessment to check for intrinsic versus
extrinsic extensor tightness.
i) If intrinsic tightness is present, an intrinsic release will need to
be performed by resecting a wedge of tendon from the lateral
bands on each side of the digit.
ii) In the setting of extrinsic tightness or dorsal joint contracture,
sequential dorsal release is needed. Working on either side of the
central slip tendon (it does not need to be disrupted), the dorsal
joint capsule is resected, and any adhesions between the bone
and the extensor tendon are excised. Next, the dorsal portion of
the collateral ligament origins should be resected, followed by the
remainder of the origins if passive flexion is still incomplete.
iii) Complete collateral ligament resection can be performed with-
out resultant instability if the articular surfaces are congruent
and there is a stable central slip insertion and volar plate.
f. Once passive flexion is restored, the presence of active flexion can-
not be determined in the anesthetized patient unless a proximal
volar counter incision is made to allow for manual traction on the
flexor tendons. If manual traction on the flexor tendons does not
result in joint flexion, exploration of the flexor system will become
necessary on a delayed basis.
2. No passive flexion, no active extension, full passive extension. In this situ-
ation, there are dorsal extensor tendon adhesions and probably a tight dorsal
joint capsule. Flexor tendon adhesions may be present, but this is unusual
and cannot be detected preoperatively owing to lack of passive flexion. These
differ from Type 1 fingers in that a volar soft tissue contracture is absent.
a. A dorsal release of the joint capsule and extensor tendon adhesions
should restore passive flexion and, most likely, active extension.
Neurolept anesthesia (sedation with local field block that avoids
prolonged muscle paralysis) is beneficial. Once the suspected teth-
ered components are addressed and the patient has been given
adequate local anesthetic, he or she can participate in attempted
active motion to assess the adequacy of dorsal extensor release and
potential for flexor tenolysis on a delayed basis.
3. No active flexion, no passive extension, intact passive flexion. These digits
have no extensor tendon adhesions or dorsal capsuloligamentous tightness
(evidenced by full passive flexion), but are tethered by palmar pathology. This
may be from skin contracture or deficiency (healed burn scar) or contracted
volar plate and ligaments. Also, the lack of active flexion indicates either flexor
tendon adhesions or discontinuity.
a. First, a supple palmar soft tissue envelope and passive motion must
be restored. A palmar skin contracture release or burn scar excision
(requires Z-plasty or coverage procedure) could be combined with

a volar checkrein and accessory collateral release to restore full

passive extension. The collateral ligament origins may also have to
be released. This can be done without resultant instability.
i) The flexor tendon must be explored to determine if scarred
within the sheath, elongated, or ruptured.
1. If the tendon is bound by adhesions, tenolyse, and mobiliza-
tion immediately.
2. If ruptured, either primary repair or grafting will be required.
Primary repair is possible only if the proximal stump has
adequate excursion for repair without excessive tension.
Again, however, a stable, supple layer of palmar soft tissue
and restored passive motion are needed before any tendon
repair or reconstructive procedures.
3. If there are insufficient A2 and A4 pulleys or the tendon glid-
ing sheath is in poor condition, staged grafting with place-
ment of a silicone rod and pulley reconstruction will be
needed. This will require a second stage to exchange the rod
for tendon graft, and perhaps a third for subsequent tenoly-
sis. Allow enough time between each of these procedures to
achieve soft tissue stability, as this is a considerable undertak-
ing and commitment for surgeon and patient.
4. If the FDS is intact but the FDP ruptured, it is reasonable to
restore an FDS-only digit through tenolysis and consider
later DIP fusion in slight flexion.
4. No active flexion or active extension. Full passive with no active motion
suggests incompetence of both the flexor and extensor mechanisms, either
from tendon adhesions or discontinuity.
a. Reconstruction of each side must be done separately, as the proto-
cols for protective motion of one side would jeopardize the other.
i) Reconstruction of the extensor side first is favored in the radial
digits, whereas reconstruction of the flexor side is preferred in
the ulnar digits.
5. No passive extension, full active flexion. This is usually simply due to con-
tracted palmar structures, such as skin or volar plate.
a. Release skin, volar plate checkrein, and collateral ligament as needed.
6. Full active extension, full passive flexion, no active flexion. With full pas-
sive flexion and active extension, the dorsal tissues are in continuity and glid-
ing. Furthermore, the palmar tissues are not contracted.
a. Flexor tendons are either encased in adhesions, gapped or rup-
tured. At exploration the need for tenolysis, repair, primary graft,
or staged reconstruction can be determined.
b. If a patient demonstrates only intrinsic tightness with supple joints
(demonstrated by Bunnell intrinsic tightness test described above),
an intrinsic release may be required.
Wrist Stiffness
The minimum functional range of motion for most activities of daily living has been
described as 30 degrees of extension, 5 degrees of flexion, 10 degrees of radial deviation,
15 degrees of ulnar deviation, 50 degrees of supination, and 50 degrees of pronation.

Although motion in any plane may be diminished, limitation of extension and supina-
tion are the most disabling and attract more patient concern. Less has been written on
the management of wrist contractures in the English literature than on digital con-
tractures. However, this brief section will review some of the principles and known
approaches to the management of problematic wrist stiffness.
I. Evaluation
As arthrofibrosis is the limitation of motion due to loss of capsular compliance, other

causes should be ruled out. Clinical and radiographic assessments are directed at other
potential etiologies such as nonunion, malunion, carpal instability, avascular necrosis,
neuromuscular spasticity, and cutaneous contractures. For the DRUJ, comparison CT
scans of both wrists may be required to detect subtle subluxation or instability. Motion
measurements are made in all three planes, and the character of the end points (hard
or soft) is noted.
II. Treatment
As for digital contractures, an ounce of prevention is worth a pound of cure. Early stiff-
ness in the flexion-extension plane often responds to diligent active and passive motion
exercises and dynamic or static progressive splinting. Intra-articular steroid injections
have shown some benefit in the treatment of shoulder adhesive capsulitis and may be a
useful adjunct if no progress occurs with the above regimen.
A. Operative treatment can be considered when progress has plateaued and motion
is still unsatisfactory following at least 6 months of therapy.
1. Rigidity in the flexion-extension plane may result from intra-articular adhe-
sions in the midcarpal or radiocarpal joints, or may result from thickening
and fibrosis of the wrist capsule. Intra-articular adhesions are amenable to
arthroscopic management through standard dorsal and ulnar wrist portals
in the radiocarpal and midcarpal joints. Dorsal adhesions may require
the use of a palmar radial portal placed through the flexor carpi radialis
subsheath.
2. Extra-articular capsular adhesions that do not respond to therapy may be
addressed through open or arthroscopic methods. Contractures limiting flex-
ion can be approached with open dorsal incisions through windows in the
extensor compartments.
a) Complete dorsal capsulotomy, including the DRC ligament, should
restore wrist flexion. However, fluoroscopic evaluation should then be
performed to confirm that the joint is not “hinging” open dorsally sec-
ondary to fibrotic volar radiocarpal capsule.
b) If this occurs, volar capsulotomy can be performed through an extended
carpal tunnel incision. The thickened volar capsule can then be transected
while avoiding direct section of the extrinsic volar ligaments.
c) Likewise, if wrist extension is limited, volar capsulotomy can be per-
formed and followed by dorsal release if fluoroscopy suggests dorsal hing-
ing with wrist extension.
3. Arthroscopic release of the capsule has also been described by Verhellen and
Bain through standard dorsal working portals with a hooked electrocautery
device. While dorsal and volar radiocarpal ligaments can be divided, the

authors emphasize avoiding sectioning of the ulnocarpal, dorsal radioulnar,

and volar radioulnar ligaments in order to avoid instability.
4. As noted above, loss of supination results from fibrotic thickening of the volar
DRUJ capsule. This may be alleviated through open volar DRUJ capsular
release. The volar capsule is excised proximal to the TFC. A dorsal DRUJ
capsulectomy may be performed to address loss of pronation, although this is
infrequent.
Elbow Stiffness
The elbow serves as the most important joint that allows placement of the hand within
a large volume of space. Any loss of elbow motion will compromise placement of the
hand and thereby inflict a disability to overall upper extremity function.
Most activities of daily living require a 100 degrees arc of flexion/extension (30 to
130 degrees) and 100 degrees of forearm rotation (50 degree pronation and 50 degree
supination). Deficient elbow and forearm motion will lead to awkward postural adap-
tations such as flexion of the wrist and neck for placement of the hand to mouth, or
flexion of hip and knee for reaching to the feet or ground.
I. Anatomy
A. Osseous anatomy
The elbow joint is one of the most inherently congruous joint in the human
body. The ulnohumeral joint acts as a hinge allowing flexion and extension.
1. It comprises the trochlea on the humeral side with two surfaces separated by a
sulcus. The trochlear notch of the ulna has a reciprocal longitudinal ridge and
subtends a circumference of approximately 190 degrees. This feature makes it
highly constrained.
2. A nonarticular transverse groove separates the proximal ulna into the coro-
noid anteriorly and the olecranon posteriorly. The coronoid process provides
an anterior buttress to resist posteriorly directed forces. The anteromedial
facet of the coronoid process is a crucial stabilizer against varus and rotational
stress.
The olecranon process also contributes to varus-valgus stability. Incre-
mental excision leads to a linear decrease in valgus stability.
3. The radiocapitellar joint and proximal radioulnar joint (PRUJ) acts as a pivot
allowing axial forearm rotation. The radial head has a slightly elliptical shape
and articulates with capitellum, lesser sigmoid notch of the ulna, and lateral
lip of the trochlea. It serves as the secondary stabilizer to valgus stress and
posterolateral rotatory instability, contributes to axial stability of the radius,
and transmits loads (up to 60%) across the elbow.
B. Soft tissue anatomy
1. The medial collateral ligament complex is made up of three components:
Anterior, posterior, and transverse bundles. The anterior bundle, the thick-
est and primary restraint to valgus stress, originates from anteroinferior
aspect of the medial epicondyle and inserts on the sublime tubercle of the
ulna.
2. The lateral collateral ligament (LCL) complex is composed of the LCL, the
annular ligament, and extensor/supinator origin. Fibers of the LCL blend

with those of the annular ligament to insert broadly over the supinator crest
of the ulna. The complex provides the primary restraint to posterolateral
rotatory instability.
3. The anterior capsule plays little role in elbow stability unless all the other
primary and secondary stabilizers have been lost.
4. Muscles crossing the elbow provide dynamic stability to the joint and include
the flexor/pronator and extensor/supinator origins. The biceps, brachialis,
and triceps stabilize the elbow by compressing the constrained joint surfaces
together.
II. Cause
The elbow is inherently predisposed to stiffness due to

A. Its highly congruous and conformed articulation
B. The sensitivity of the capsule to react to trauma
C. The susceptibility of the brachialis muscle when injured to form heterotopic
bone and
D. Contracture and scarring of injured structures after injury when mobilization is
delayed
E. Elbow contractures have many causes including
1. Trauma including fracture, dislocation, soft tissue injury
2. Previous elbow surgery
3. Ectopic ossification (EO)
4. Congenital conditions such as arthrogryposis (most common), Larsen
syndrome, Meiten syndrome, and congenital contractural arachnodactyly
5. Spasticity from neural axis injury, cerebral vascular accident (CVA), and
cerebral palsy
6. Burns
III. Classification
Based on anatomic location of the pathology, elbow contractures are classified as

A. Extrinsic contracture—contracture of capsule, collateral ligaments or sur-
rounding muscles, EO, and extra-articular malunion
B. Intrinsic contracture—intra-articular adhesions, articular malalignment, loose
bodies, and articular cartilage loss
In general, intrinsic contractures usually have an extrinsic component. Extrinsic con-
tracture can be addressed by therapy intervention or surgical resection of the pathology.
In contrast, intrinsic contracture cannot be treated effectively with therapy and usually
require surgical correction of the articular deformity.
IV. Evaluation
A. Age on the patient

The most favorable outcomes of treatment are usually achieved in young adult
patients.

1. Due to lack of maturity that may limit postoperative therapy cooperation,

surgical treatment in the very young patient should be judiciously selected.
2. Older patients may present medical comorbidity or associated problems of
the hands and shoulders that at times may negatively impact their ability to
maintain operative gains in elbow motion.
B. History
The medical history should include the cause and duration of contracture,
previous treatment, progression or improvement with therapy, and the patient’s
perceived functional deficits relating to occupational, recreational, and daily liv-
ing requirements.
The stiff elbow is usually painless throughout the zone of limited motion
except at the end range. Differential diagnosis of painful stiff elbow include
1. Internal derangement from intra-articular incongruity or arthrosis
2. Neuropathic pain from ulnar nerve involvement
3. Impingement of osteophytes
4. Excessive forceful manipulation and
5. Early stage of ectopic bone formation
C. Physical examination
The measurement of arc of flexion/extension, pronation/supination, and
quality of endpoint should be documented. Soft endpoint implies soft tissue
contracture whereas hard endpoint implies bony block. The quality of soft
tissue and location of previous scar should be noted. Skin that blanches with
stretch should be suspected as a component of contracture. Neurologic status
especially ulnar nerve must be carefully examined. Muscles passing across the
elbow should be tested for tightness and strength.
D. Radiologic evaluation should include
1. Anteroposterior (AP) view of distal humerus.
2. AP view of proximal ulna.
3. Lateral view of elbow, coronoid view, and radiocapitellar view. In most
instances, these radiographs provide all the needed information.
4. CT scan may be required for the evaluation of articular surfaces, loose bodies,
and the exact location and extent of bony spur or EO.
V. Management
A. Nonsurgical treatment
In most of stiff elbows, rehabilitation treatment should be used as an initial
treatment. The goal is to improve motion by increasing tissue extensibility with
plastic elongation of soft tissue. The modality options include
1. Physical agents including any forms of therapeutic heat
2. Strengthening exercise
3. Static progressive splinting such as turnbuckle splints
4. Dynamic splinting such as dynamic hinged elbow splint with rubber-band
traction or with spring-loaded hinged dynamic splints
Manipulation under anesthesia is usually contraindicated because of
poor response of the elbow to passive manipulation and potential for peri-
articular fracture and tearing of muscles, which may lead to additional scar
or ectopic bone.
B. Surgical treatment

1. Indication for surgery

a) Surgery is indicated in patients who have persistent functional deficit
after appropriately applied nonsurgical treatment and sufficient motiva-
tion to complete a rigorous postoperative program.
b) Most patients require surgical treatment when flexion contracture exceeds
30 to 40 degrees and maximal flexion is less than 110 degrees.
c) However, some patients may require nearly full motion for specific voca-
tional or recreational activities. Full extension is usually needed by gym-
nasts, throwing athletes, and certain musicians.
2. Timing for surgery
The optimal timing is based upon cause of contracture, failure of physical
therapy, and status of the soft tissues.
a) In patients with failed internal fixation, nonunion of distal humerus,
loose bodies, or obviously impinging osteophytes, early surgery may be
indicated.
b) For other extrinsic causes, contractures of more than 6 month’s duration
usually do not respond to nonsurgical treatment.
c) When ectopic bone is present, surgical excision and contracture release
may be undertaken as soon as it can be well defined radiographically, usu-
ally after the third month following trauma.
3. Surgical methods of contracture release
Method of surgical correction is individualized based upon
a) Cause of contracture
b) Severity
c) Quality of articular surface and
d) Age and status of patient. The patients should be informed about the
possibility of secondary procedures such as open release if arthroscopic
release proves ineffective or too time-consuming, dual approach to the
joint or application of hinged external fixation.
4. Anesthesia
For simple contractures, a brachial plexus block is preferred. In complex
contractures affecting both flexion and extension, a continuous indwelling
catheter brachial plexus block can be used in order to facilitate rehabilitation
with continuous passive motion (CPM). The indwelling catheter is removed
after the third day.
5. Open contracture release
a) Anterior approach
1) Advantage—Provides direct exposure to the anterior capsule and ante-
rior ectopic bone.
2) Disadvantage—Requires exposure of the anterior neurovascular
structures, may lead to additional anterior soft tissue scarring, and
cannot address pathology of the olecranon process and olecranon
fossa.
b) Lateral approach-LCL sparing technique
1) Advantage
a. Allows for anterior and posterior exposure to the joint
b. Preserves joint stability allowing unrestricted rehabilitation
c. Allows PRUJ and radial head exposure and possibility of radial
head arthrolysis or excision in the patients with restricted forearm
rotation

d. The incision is in the neutral axis of flexion-extension, avoids

exposure of anterior neurovascular structures, and limits additional
anterior scarring.
2) Disadvantage
a. Requires additional medial incision in the patient who needs ulnar
nerve decompression
b. Difficult to access posteromedial aspect of the joint
3) Surgical technique
a. Kocher incision to the elbow (anconeus-ECU interval)
b. Expose anterior joint by elevating the ECRL origin from humerus.
Retract the ECRL and brachialis anteriorly and excise the anterior
capsule.
c. Perform anterior debridement
d. Restore coronoid fossa
e. Excise loose bodies, scar tissue, and bony fragment
f. Partially excise enlarged coronoid process particularly medial coronoid
g. Expose posterior joint by reflecting triceps and proximal part of
anconeus posteriorly
h. Perform posterior debridement
i. Excise scar tissue and bony fragment from olecranon fossa
j. Partially excise enlarged olecranon process including medial and/or
lateral gutter osteophytes.
c) Medial over-the-top approach
1) Advantage
a. Enables decompression and transposition of ulnar nerve
b. Allows for easiest exposure of the anterior coronoid process
2) Disadvantage
a. More difficult to address radiocapitellar joint
b. Does not allow surgical exposure and treatment of the PRUJ
3) Surgical technique
a. Curved skin incision posterior to the medial epicondyle
b. Identify and mobilize ulnar nerve
c. Elevate anterior two thirds of flexor-pronator group from medial
humerus and retract brachialis away from anterior capsule
d. Perform anterior capsulectomy and anterior debridement
e. Reflect triceps posteriorly, and then perform posterior capsulotomy
and posterior debridement
If the contracture remains after release through one approach,
additional exposure and release on the opposite side of the elbow can
be helpful.
6. Arthroscopic contracture release
Arthroscopic release and debridement is an alternative but can be more
time-consuming and should be undertaken only by surgeons with consid-
erable elbow arthroscopy experience. It is particularly attractive in simpler
contractures, young athletes and those with mainly intrinsic pathology such
as loose bodies and small impinging osteophytes. Several studies have docu-
mented the efficacy of this procedure in the patients with more severe con-
tractures. However, contracture associated with extensive bony impingement
or required ulnar nerve transposition are difficult to manage by arthroscopy,
and open release is advised.

a) Ulnar nerve management

Ulnar nerve decompression with or without transposition shoulder be
considered in patients with
1) Preoperative ulnar nerve symptoms.
2) Severe contracture with less than 90 degree flexion preoperatively.
Even without preoperative nerve symptoms, ulnar nerve symptoms are
likely as marked elbow motion may be restored in these cases.
3) Tendency of the ulnar nerve to subluxate. Lengthy arthroscopic sur-
gery with severe swelling about the elbow may require in situ cubital
tunnel release to avoid postoperative ulnar nerve compression.
b) Hinged external fixation
1) Indication
a. Unstable elbow after extensive release in severe contracture
b. Extensive myostatic contracture (usually from the brachialis and
biceps) in long-standing contracture
c. Distraction arthroplasty
c) Distraction arthroplasty with or without interposition
1) Indication
a. Intra-articular malunion
b. 50% or more loss of the articular cartilage
c. Extensive intra-articular adhesions
7. Special circumstance
a) Heterotopic ossification
Ectopic ossification (EO) is defined as the formation of mature lamel-
lar bone in nonosseous tissues.
1) Predisposing factor—Bony or soft tissue injuries around the elbows:
The incidence is proportionate to severity of injury (more common in
fracture-dislocation than in pure dislocation)
a. Neural axis trauma
b. Burns
c. Forceful manipulation of the elbow
d. Multiple surgeries especially within first 2 weeks after trauma
e. Certain surgical approaches such as Boyd approach to the elbow
f. History of EO elsewhere
g. Ankylosing spondylitis, DISH, and Paget disease
2) Clinical assessment
EO formation typically begins within 12 weeks of trauma. Localized
soft tissue swelling, hyperemia, and pain with tenderness are presented
the early stage. This condition may be mistaken for infection. As the
process progresses, erythema, tenderness, and swelling resolve and
elbow motion progressively diminishes. Foci of EO may become
palpable. The endpoint changes from soft to more rigid.
a. Laboratory tests and serial bone scan are no longer used.
b. Serial plain radiography is the most useful modality to establish the
diagnosis, locate its position, and follow its progression. The well-
demarcated margin with trabeculation is referred to as mature,
commonly takes up to 9 months to develop.
3) Prophylaxis
a. Indicated in patients with severe elbow trauma and predisposing
factor(s)

b. Includes (i) NSAID within 5 days after inciting event (indomethacin

is used commonly), (ii) low-dose radiation within 3 days after incit-
ing event, and (iii) early active mobilization
4) Treatment
Nonoperative treatment including exercise program and corrective
splinting should be initiated to improve motion. Surgical treatment is
indicated only for patients with functional impairment. Surgical inter-
vention at 3 to 5 months after elbow trauma can be safely performed.
The desire to delay surgery for metabolically quiescent HO, neuro-
logic recovery in head injury, or local tissue stability in burn must be
balanced against the risks of progressive contracture and prolonged
infirmity. In very young skeletally immature individuals, however, EO
has occasionally been observed to resolve, and a delay in surgical treat-
ment is reasonable.
The surgical approach is based on the location of HO, previous
elbow incision, plane(s) of contracture, and need for nerve
decompression.
b) Elbow contracture following burn
The surgical treatments are dependent on the type and location of
burn scar. The recommended procedures are
1) Z-plasty, local flap or excision, and skin graft for a longitudinal hyper-
trophic scar band limited to antecubital area
2) Release and skin graft for a longitudinal hypertrophic scar band that
extends across the antecubital fossa to the axilla or wrist
3) Scar excision and skin flap coverage (usually regional pedicle flaps) for
extensive antecubital scarring without linear band.
c) Elbow contracture in nonunion of distal humerus
1) This condition is technically challenging due to many reasons includ-
ing extensive scar and adhesions, difficulty in achieving realignment,
poor purchase of devices in osteopenic bone, and overstress to the
reconstruction if contracture still remains.
2) Extensile approach, release of capsular structures, intra-articular
anatomical reduction and extra-articular realignment, rigid internal
fixation, and bone grafting are usually required.
3) Total elbow replacement may be indicated in low-level distal humeral
nonunion in elderly patient with poor bone quality.
8. Postoperative care
The extremity is elevated for the first 24 hours. Motion is then initiated by
the use of CPM device while the brachial block is still effective. The CPM is
continued until the patient is easily capable of achieving the desired machine
limits. Active and passive range of motion exercises are used of the CPM
devise six times a day. Splints are usually mandatory for 2 to 3 months after
surgery. Static progressive splints (such as turnbuckle splint) are generally
better tolerated than dynamic splints in the perioperative period. Strengthen-
ing exercises begin at 4 weeks.
9. Complication
a) Wound complication (hematoma and seroma): This problem can
be prevented by secure hemostasis before closure and drain placement.
If they present, aspiration or surgical evacuation should be considered
because of the tendency to interfere with motion and to be infected.

b) Infection: The risk factors are previous surgery, poor soft tissue coverage,
poorly vascularized bone, and use of hinged external fixator.
c) Nerve palsies: These usually are transient and completely resolve.
Arthroscopic release is considered to have a higher risk of nerve injury
than with open release.
d) Complete failure to improve motion: Fortunately, this condition is
uncommon. It usually is seen with significant articular cartilage destruc-
tion or intra-articular malunion deformity.
Suggested Readings
Cohen MS, Hastings H. Post-traumatic contracture of the elbow: Operative release using a lateral
collateral ligament sparing approach. J Bone Joint Surg (Br). 1998;80:805–812.
Hotchkiss RN. Treatment of the stiff elbow. In: Green DP, ed. Green’s Operative Hand Surgery. 5th
Ed. Philadelphia: Elsevier Churchill Livingstone, 2005:939–958.
Jupiter JB, O’Driscoll SW, Cohen MS. The assessment and management of the stiff elbow. Instr
Course Lect. 2003;52:93–111.
Morrey BF. The posttraumatic stiff elbow. Clin Orthop Relat Res. 2005;431:26–35.
Savoie F. Arthroscopic treatment of the arthritic elbow. J Bone Joint Surg (Am). 2005;87:
2113–2121.
Ball CM, Galatz LM, Yamaguchi K. Elbow instability: Treatment strategies and emerging concepts.
Instr Course Lect. 2002;51:53–61.
Davila SA, Johnston-Jones K. Managing the stiff elbow: Operative, nonoperative, and postopera-
tive techniques. J Hand Ther. 2006;19(2):268–281.
Jupiter JB, et al. Posttraumatic reconstruction in the hand. J Bone Joint Surg (Am). 2007;89:
428–435.
Kleinman WB: DRUJ contracture release. Tech Hand Up Extrem Surg. 1999;3(1):13–22.
Lee SK, Gargano F, Hausman MR. Wrist arthrofibrosis. Hand Clin. 2006;22:529–538.
Shin AY, Amadio PC. Stiff finger joints. In Green, Hotchkiss, Pederson, Wolfe (eds): Green’s Opera-
tive Hand Surgery. 5th Ed. Philadelphia, PA: Elsevier, Churchill Livingstone, 2005:417–438.
Smith RJ. Non-ischemic contractures of the intrinsic muscles of the hand. J Bone Joint Surg Am.
1971;53:1313–1331.
Young VR, Wray RC, Weeks PM. The surgical management of stiff joints in the hand. Plast Recon-
str Surg. 1978;62:835–841.

Fractures and
Dislocations: Hand
13
Robert M. Baltera, Hill Hastings II, Kavi Sachar,
and Surasak Jitprapaikulsarn
I. Open Fractures/Antibiotics
Open fractures of the distal phalanx in an immunocompetent host with intact circula-
tion can be treated with irrigation and debridement alone. Open fractures of other
bones in the hand should be treated with antibiotics in addition to irrigation and deb-
ridement. Betadine has been shown to interfere with osteoblastic function in labora-
tory models. Fractures that are delayed greater than 24 hours in treatment, which are
grossly contaminated, or present in a host with multiple systemic diseases (particularly
diabetes, peripheral vascular disease, cancer patients undergoing treatment, and various
infectious disease states, i.e., AIDS) should be treated with a third-generation cepha-
losporin. An aminoglycoside should be added for crush injuries, and penicillin should
be added for farm injuries and bite wounds.
II. Distal Phalanx Fractures
Distal phalanx fractures can be separated into those involving the distal tuft, the shaft,
and the articular surface of the DIP joint.
A. Tuft fractures can be classified as either simple (single fracture line) or commi-
nuted (multiple fracture planes). Tuft fractures that are nondisplaced, regard-
less of the amount of comminution, can be treated with splinting alone, as
even a fibrous union can give stability for the nail bed. Rarely, these fractures
require fixation with small guage Kirschner wires (K-wires) to provide a stable
bed for an associated nail bed repair. Tuft fractures that involve an open wound
do not require any antibiotics and can be treated with aggressive debridement
alone.
B. Nail bed injuries
The nail bed is composed of the germinal matrix, the distal extent of which
can be identified by the white lunula visible under the proximal aspect of the
nail, and the sterile matrix, the red tissue visible under the remaining aspect
of the nail. The germinal matrix provides 90% of the nail growth, while the
sterile matrix is mainly responsible for adherence of the nail. The proximal nail
is covered by the eponychium, the tissue overlying the lunula (Fig. 13.1). The
eponychium, or roof of the nail fold, provides the cells that produce the shine of
the nail. The hyponychium is the area of keratinized skin at the distal edge of
the nail, providing a barrier against infection. The paronychium is the folds
of skin overlying the lateral edges of the nail. This is the area most susceptible
for infection.
Any displaced tuft fracture or nail avulsion is an indication of a nail bed
injury and should be explored surgically with removal of the nail and repair
186

Chapter 13 • Fractures and Dislocations: Hand 187
Figure 13.1 Anatomy of the nail bed and fingertip.
under loupe magnification with fine resorbable suture. Repair of the nail bed
often facilitates reduction of the underlying bony fragments and vice versa.
The germinal matrix can be better visualized if necessary by 1-cm incisions
starting at the proximal lateral nail fold and angled perpendicular to the nail
fold (Fig. 13.2). After repair, the placement of a nonadherent dressing in the nail
fold prevents adherence of the germinal matrix to the roof of the nail fold. This
Figure 13.2 Incisions extending proximally from the radial and ulnar corners of the
proximal lateral nail fold for exposure of the germinal matrix.

dressing can be left in place, allowing the new nail to force out the gauze over
time. If the nail plate is available, it can be placed back into the nail fold after
nail bed repair to act as a splint for the underlying fracture as well as a spacer to
keep the nail fold open.
C. Subungal hematomas, unless accompanied by nail avulsion from the nail fold or
displaced fracture, can be treated nonoperatively. Cautery or a large bore needle
through the nail plate can be used for symptomatic relief but is not necessary. A
subungual hematoma involving greater than 50% of the nail may require nail
plate removal and repair of the nail bed injury.
D. Distal phalanx shaft fractures
1. Fractures of the shaft are classified by their direction, either longitudinal or
transverse, and their nature, either stable or unstable. Unstable fracture, i.e.,
those in which the displacement or angulation cannot be corrected with
closed reduction, should be treated with small gauge K-wires, either two
0.028 in or one 0.035 in, preferably not crossing the DIP joint.
2. Bony mallet fractures
Fractures of the dorsal base of the proximal aspect of the distal phalanx can
occasionally lead to subluxation of the distal phalanx volarly. Closed reduc-
tion and percutaneous transarticular K-wire fixation of the subluxated distal
phalanx to the middle phalanx is recommended. Anatomic reduction of the
displaced fragment is possible with fracture fixation or extension block print-
ing. Open reduction is required infrequently when treated acutely. If there is
no subluxation of the distal phalanx, closed splinting is adequate.
E. Fractures of the DIP
Fractures of the middle phalanx extending into the DIP joint have been classified
by London into three grades. (Fig. 13.3) Grade I is a nondisplaced unicondylar
fracture. Grade II is a displaced unicondylar fracture, and Grade III is a bicon-
dylar comminuted fracture. Grade I fractures can be treated in a splint for 3
weeks followed closely with weekly x-rays. The splint is then discontinued and
protected motion, i.e., buddy-taped to the adjacent digit, for an additional 2
to 3 weeks. Grade II injuries are by definition displaced and should be reduced
and fixed with K-wires or screws. Grade III injuries are comminuted, bicondylar
fractures. They are usually the result of direct trauma, and the degree of com-
minution often makes anatomic reconstruction impossible.
Figure 13.3 London’s classification of P2 condylar fractures.

III. Middle Phalanx Shaft Fractures
Fractures of the middle phalanx shaft are classified by their stability and fracture geometry,
i.e., transverse or oblique. Nondisplaced fractures and fractures that are stable after reduc-
tion can be treated with a short period, i.e., 3 weeks, of immobilization of the proximal
interphalangeal (PIP)/DIP joints leaving the MP joint free. They should be followed with
weekly radiographs to ensure that alignment is maintained. Protected range of motion is
then instituted for an additional 2 weeks by buddy-taping to an adjacent digit. Acceptable
parameters for nonoperative treatment include no clinical malrotation of the digit and
no angulation greater than 10 degrees in any plane. Rotation is best determined clinically
with the digit in full flexion. Digital block should be used for pain control as needed in the
office to permit evaluation for rotational malalignment with active flexion.
Oblique fractures tend to be unstable and to shorten, even after a good reduction
is obtained. Very little shortening is tolerated at this level because the extensor mecha-
nism cannot adjust, leading to an extensor lag at the DIP joint. Treatment of oblique,
comminuted, and open fractures involves internal fixation. While crossed K-wires can
often be done without open reduction, it is difficult to mobilize the finger because of
tethering of soft tissue until the K-wires are removed, often at 3 weeks after surgery. Lag
screws and plate fixation allow earlier range of motion, but the hardware can irritate
the tendons, and an additional surgery may be required to remove the hardware and/
or release adhesions. Decreased range of motion, however, is reported in over 50% of
all fractures, regardless of fixation techniques. Early motion, then, is essential to a good
outcome; and stable fixation is necessary to allow immediate mobilization.
IV. Fracture and Dislocation of the Proximal Interphalangeal Joint
PIP joint stiffness or ankylosis is poorly tolerated and significantly impairs grasp and
activities that require fine dexterity. Injuries to the PIP joint are challenging to treat due
to technical difficulties in handling small articular fragments, the tendency for stiffness
following injury and surgery, and residual controversies regarding optimal treatment.
A. Anatomy and biomechanics
1. Bony anatomy
The PIP joint is a hinge joint allowing 100 to 110 degrees of motion in the
sagittal plane and minimal motion in the axial and frontal planes.
a) The head of proximal phalanx is composed of two concentric asymmetric
condyles separated by an intercondylar sulcus. The dorsal margin of each
condyle is roughly half the width of the volar margin. The ulnar condyle
projects further distal than the radial condyle in small finger, is shorter in the
index and middle fingers, and both condyles are of nearly equal length in
the ring finger. The longer projecting condyles have a greater radius of cur-
vature. In the coronal plane, the articular surfaces tilt away from the second
web space. These features provide a rotational component to the motion of
each finger, allowing the tips to converge toward each other in flexion.
b) The base of middle phalanx consists of biconcave articular surfaces sepa-
rated by a central ridge. The radius of curvature of the surface is slightly
greater than that of the reciprocal proximal phalangeal surface imparting
a small degree of sloppiness to the hinge.
The volar aspect of the base has two thickened lateral corners and two
lateral tubercles to which portions of the collateral ligaments attach.

The palmar base of the middle phalanx is critical for joint stability
and provides buttressing support to resist dorsal subluxation.
2. Soft tissue structures
a) The Volar plate is a swallow tail-like (tapering in two limbs proximally)
strong fibrocartilaginous structure covering the volar aspect of the joint.
1) Origin—Thin attachment continuous with the periosteum of proxi-
mal phalanx, synovial reflection, C1 pulley, and A2 pulley
2) Insertion—Thicker strong lateral fibers attach to the lateral corner of
the base of middle phalanx. Thinner central fibers blend with the volar
periosteum
3) Function
a. First restraint to hyperextension
b. Second restraint to lateral stability
c. Provides mechanical advantage to the flexor tendons by increasing
their moment arm
b) Collateral ligaments
1) Proper collateral ligament
a. Origin—The pit on the lateral side of head of proximal phalanx
b. Insertion—The thickened lateral corner of the base of middle pha-
lanx along its entire volar 40%, volar plate (only most volar fiber)
c. Function—First restraint to lateral stability
2) Accessory collateral ligament
a. Origin—Lateral side of the head of proximal phalanx palmar to the
proper collateral ligament origin
b. Insertion—Lateral edge of volar plate
c. Function—Very little role in joint stability. Prevents the volar plate
from redundancy and allows the base of middle phalanx to move
along the corresponding surface as the joint flexes.
The volar plate and the two collateral ligaments form a “box” or
“chariot” configuration acting in concert to provide PIP joint stability.
Dislocation can occur if this complex fails at least two planes.
B. Injuries to PIP joint
1. Dislocation with or without fracture
a) Dorsal dislocation
b) Volar dislocation
c) Lateral dislocation
2. Isolated fracture
a) Fracture of head of proximal phalanx (detailed under Proximal Phalangeal
Fracture section)
b) Intra-articular fracture of base of middle phalanx
1) Dorsal base fracture
2) Volar base fracture
3) Avulsion of collateral ligament insertion
4) Volar lateral plateau compression fracture
5) Pilon fracture
3. General treatment principles
The PIP joint has great propensity to develop stiffness following injury,
surgery, and prolonged immobilization (especially >3 weeks). Inappropriate
or delayed treatment usually results in stiffness, chronic pain, and posttrau-
matic arthritis.

Re-establishing and maintaining the concentric stable reduction and early

mobilization are the crucial factors for the good functional outcomes. If tech-
nically feasible, anatomical reduction of articular surface should be obtained.
4. Dorsal dislocation
Most common joint dislocation of the hand
Mechanism of injury—combination of hyperextension and some degree
of axial load
a) Classification
1) Type I—Hyperextension injury— Partial or complete avulsion of
volar plate (usually from distal insertion)
2) Type II—Pure dorsal dislocation—Avulsion of volar plate and bilat-
eral splitting of collateral ligaments
3) Type III—Fracture-dislocation—dislocation with volar base frac-
ture
b) Kiefhaber modification of Hastings classification
1) Stable fracture-dislocation
Less than 30% articular base of middle phalanx
Congruent through full range of motion
2) Tenuous
30% to 50% articular base of middle phalanx, reduces with less than
30 degrees flexion
3) Unstable
Mote than 50% of A-P diameter or less than 50% but requires more
than 30 degrees PIP flexion to maintain reduction
b) Diagnosis
AP and lateral views of the entire finger are obtained. On the perfect
lateral x-ray, the two condyles of the proximal phalanx should be super-
imposed upon each other. In fractures, partially pronated and supinated
obliques should also be obtained.
Subtle subluxation can be missed easily. The features on the lateral
view that confirm a perfect concentric reduction are
1) Absence of dorsal “V sign” (divergence of dorsal articular surface)
2) The center of head of proximal phalanx is aligned with the axis of
middle phalanx in all positions
c) Treatment
1) Hyperextension injury
a. Acute injury Extension block splint in slightly flexed position 1 to
2 weeks
b. Chronic injury—Presenting with PIP hyperextension or swan neck
deformity in the absence of chronic mallet finger
i. Treatment—Volar plate reattachment or flexor digitorum super-
ficialis (FDS) tenodesis
2) Pure dorsal dislocation
Closed reduction and immobilization in slightly flexed position 1 to 2
weeks
3) Dorsal Fracture-Dislocation
The important factors for determination of treatment are
a. Size of volar fragment; Less than 30% of A-P diameter implies
stable; more than 50% of A-P diameter implies unstable
b. Comminution of volar fragment

c. Degree of PIP flexion required to maintain reduction (>30-45

degrees)
d. Treatment options
i) Stable and tenuous stability
Extension block splinting—Motion of PIP and DIP joints can
be initiated immediately. The wrist is splinted in 20 to 30
degree extension, the metacarpophalangeal (MCP) joint in
slight flexion, and the PIP joint blocked in 10 to 20 degrees
greater flexion than the point of demonstrated instability. It is
critical to secure the proximal phalanx up to the splint to pre-
vent its sag, which effectively will lead to PIP extension.
1. Advantage—Easy to do, monitor, and convert to another
form of treatment
2. Complications are mostly salvageable
3. Disadvantage—Difficult to apply in too short, small, or
swollen digits
4. Complication—resubluxation, late flexion contracture
ii) Unstable
Extension block pinning—Extension block pinning can be use
in the short, small, or swollen digit that precludes application
of extension block splint
iii) Transarticular pinning
Simple technique—Difficult to determine its efficacy because
of a small number of cases reported
iv) Open reduction and internal fixation
1. Indication—Unstable fracture-dislocation with simple
fragments large enough to accommodate implant devices
2. Surgical approach—Both volar and dorsal approaches have
been described
3. Implant devices—Miniscrew (1.1-1.5mm), K-wire, tension
band wire
4. Nearly full restoration of motion possibile
5. Complication—Stiffness, flexion contracture, posttrau-
matic arthritis, and infection
v) External fixation
A variety of devices in both static and dynamic modes include
wire fixator such as Agee force-couple, push traction; pin and
rubber band or pin and spring traction systems such as Suzuki
traction; the customized external fixator; the commercial
external fixator
1. Principle—Provide distraction force across joint
2. Reduce fracture fragments via ligamentotaxis
3. Provide volar-directed force on the middle phalanx in
certain systems
4. Allow immediate PIP motion
5. Do not reduce depressed articular fragments (especially
central fragments)
6. Indication—Unstable fracture-dislocation with single frag-
ment or comminuted fracture. Can be used as adjunct to
internal fixation

7. Contraindication—Fracture of head of the proximal

phalanx
Satisfactory results can be expected in acute injuries
with precise application of the fixator, concentric reduc-
tion, and early range of motion.
8. Complication
i. Loss of reduction upon fixator removal
ii. Pin traction infection
iii. Joint stiffness
iv. Articular incongruity
vi) Volar plate arthroplasty
1. Principle—Resurface the damaged articular surface of the
middle phalanx with vascularized fibrocartilaginous tissue
and provide a volar buttress to maintain joint stability.
To be successful, the volar plate should be adequately filled
with the volar defect to prevent recurrent subluxation
2. Indications—Acute unstable fracture-dislocation especially
with comminuted or impacted volar fragment
3. Chronic fracture-dislocation of PIP joint
Certain cases of osteoarthritis (OA) with a viable dorsal
articular surface
Many series reported satisfactory results from this pro-
cedure especially in acute injuries. With greater than 40%
articular involvement, results are unpredictable.
4. Complication
i. Recurrent subluxation; One of the causes is articular
involvement exceeding 40% and residual volar defect
inadequately filled by the volar plate. Consider hemi-
hamate resurfacing arthroplasty (HHRA) or filling the
residual bony defect with a slip of FDS or bone graft in
acute cases, or osteotomy in chronic cases.
ii. Flexion contracture—most common complication
iii. DIP stiffness
iv. Angular deformity
vii) HHRA
1. Principle—Restore an osteocartilaginous buttress and
replacement to the palmar base of middle phalanx with a
contour-matched portion of the ipsilateral dorsal hamate
2. Indications
i. Acute unstable fracture-dislocation especially with
comminuted or impacted volar fragment
ii. Chronic fracture-dislocation of PIP joint
iii. Comminuted lateral plateau fracture of the base of
middle phalanx
iv. Salvage after failure of previous surgery
v. Severe injuries involving >50% of the articular surface,
in which volar plate arthroplasty is unfeasible
3. Contraindication—Fracture of dorsal articular surface.
4. Reported satisfactory results in a few intermediated-term
studies

5. This is an attractive procedure for the treatment of this

difficult fracture-dislocation.
5. Volar dislocations
These are uncommon injuries but can lead to late deformities because of
unrecognized diagnosis. Central slip injury is relatively common in volar
dislocation of PIP joint. It can be easily missed and then lead to late bouton-
niere deformity. In the patient presenting with semiflexion of PIP joint after
trauma, the differential diagnosis should be included for central slip rupture
and volar plate injury.
Injuries can be classified into
a) Simple volar dislocation
1) Pathology—Bilateral disruption of collateral ligaments, volar plate,
and occasionally rupture of central slip
2) Treatment
a. Closed reduction
i) Reducible
No extension lag of PIP joint: Short-time immobilization
Extension lag of PIP joint (usually unstable): Open repair of
central slip
ii) Irreducible: Open reduction
The obstacles to reduction usually are interposed central slip
or collateral ligament
b) Volar fracture-dislocation
The factors that determine the treatment are
1) The size of dorsal fragment and
2) Fracture displacement
Volar fracture-dislocation with small dorsal fragment (<20% of articu-
lar surface) and less than 2 mm displacement can be treated with PIP
joint splinting as in closed boutonniere injury.
Volar fracture-dislocation with large dorsal fragment (>20% of
articular surface) or more than 2 mm displacement can be treated with
open reduction and screw or wire fixation. Internal fixation may be
supplemented by external fixation when fixation is tenuous and insta-
bility is substantial.
c) Volar rotatory dislocation
1) Pathology
Rupture of volar plate and a collateral ligament
A condyle of head of proximal phalanx is encircled between the
central slip and the lateral band
2) Treatment
a. Closed reduction
i) Reducible
No extension lag of PIP joint: Short-term immobilization
Extension lag of PIP joint: Splinting as in closed boutonniere
injury
ii) Irreducible—Open reduction and central slip repair
6. Lateral dislocation
a) Rare injury of PIP joint
The injury involves the rupture of a collateral ligament and volar plate
b) Treatment

Lateral dislocation usually reduces spontaneously or is easily reduced by

closed means. Finger buddy splint with early motion is recommended
Open repair or reconstruction of collateral ligament may be consid-
ered in certain high-performance patients such as athletes, manual labor-
ers, or cases with chronic painful PIP instability
7. Isolated dorsal base fracture
a) An avulsion involves the insertion of central slip
As in volar dislocation, missed or untreated injuries may be a prelude to
boutonniere deformity
b) Treatment
1) Small fragment (<20% of articular surface) and less than 2 mm
displacement: Splint as in closed boutonniere injury
2) Large fragment (>20% of articular surface) or more than 2 mm
displacement → open reduction and screw or wire fixation
8. Isolated volar base fracture
a) An avulsion involves the insertion of volar plate into the base of middle
phalanx
Usually less than 10% of articular surface
b) Treatment
Finger buddy splint with early motion is enough
If the PIP joint represents the tendency to hyperextend, extension block
splint in neutral is recommended (as the treatment of hyperextension injury)
9. Avulsion of collateral ligament insertion
Treatment—Nonoperative treatment with finger buddy splint for less than
3 weeks is preferred for nondisplaced fracture
For the prevention of late lateral stability in significantly displaced
fracture, ORIF with miniscrews, K-wires, or tension band wire should be
considered.
10. Volar lateral plateau compression fracture
Result of an eccentric axial load that causes articular depression and meta-
physeal impaction—The A-P and lateral x-ray may miss the articular depres-
sion. An oblique view can usually show this depression.
Treatment—Nonoperative treatment may result in angular deformity
and residual pain
Recommended treatment is ORIF with K-wires or screws and bone grafting
11. Comminuted intra-articular fracture (pilon fracture)
From axial loading injury, depressed and comminuted central articular surface
and complete seperation of volar and dorsal articular surfaces from diaphysis.
Treatment
a) The goal of treatment is to reassociate the overall architecture of the base
of middle phalanx, realign the axis of middle phalanx on proximal pha-
lanx both sagittal and coronal planes, and allow early motion. Anatomical
reduction is usually infeasible and less important.
The patient should be informed about inevitable stiffness and post-
traumatic arthritis.
b) Nonoperative treatment usually results in suboptimal outcome.
c) Operative treatments include
1) Dynamic external fixation (in any forms of traction devices)
2) ORIF with or without bone grafting
3) Combination of external and internal fixations

Based on available data, the results of external fixation are comparable

to ORIF, but the complication rate is higher in ORIF.
V. Fracture of Proximal Phalanx
Fractures of the proximal phalanx are common; however, inappropriate treatment

may result in extensor tendon adhesions, joint stiffness, malunion, and decreased
function.
A. Normal anatomy
The proximal phalanx has a straight to slightly convex dorsal cortex that
is thicker than the concave volar cortex. Longitudinal crests on the medial and
lateral margins of the volar surface correspond to A2 pulley insertion on each
side.
The proximal phalanx is totally surrounded by mobile tendons except over
a small volar lateral area. The close relationship of the extensor mechanism
provides support for fractures but is also prone to extensor adhesions by its
coverage.
B. Pathoanatomy and pathophysiology
Unstable in metaphyseal and diaphyseal proximal phalangeal fractures generally
angulate palmarly. The proximal fragment is flexed by interosseous attachments,
while the distal fragment is extended by the extensor central slip. This defor-
mity relatively lengthens the extensor mechanism resulting in a PIP extension
lag (the extensor mechanism can compensate for 2 to 6 mm of relative lengthen-
ing before an extension lag occurs). One millimeter of bone-tendon discrepancy
translates to 12 degrees of extension lag and due to close proximity of extensor
mechanism and bone, tendon adhesion after injury or surgery may contribute
to extension lag as well.
The fracture configuration will determine the type of deformities that may
occur: Angular deformity usually results from transverse fracture, whereas short-
ening is caused by comminuted, long oblique, or spiral fractures. Malrotation
typically occurs from long oblique or spiral fracture.
C. Principles of treatment
The aims of treatment of proximal phalangeal fracture include
1. Anatomical (or nearly anatomical) reduction to alleviate deformity and to
restore equilibrium of flexor and extensor forces
2. Maintenance of reduction in a way sufficient for initiation of early range of
motion
3. Early mobilization to maximize tension band effect of the extensor mecha-
nism and to minimize complications of tendon adhesion and joint stiffness
D. Nonoperative treatment
Nondisplaced closed fractures usually can be treated by nonoperative means.
Buddy splinting to adjacent finger is enough.
The criteria for accepted alignment after fracture reduction include
1. At least 50% apposition
2. No clinical malrotation
3. Less than 15 degrees of frontal or sagittal plane angulation
4. Less than 4 mm of shortening
5. Full ROM after reduction

Closed displaced fractures should be reduced by digital traction then flexion

of the MCP joint to 70 to 90 degrees. A short arm cast is applied holding
the wrist in 30 degrees of flexion with a dorsal block splint extension to
hold the MCP joint in flexion, and the interphalangeal joints in extension.
Within this splint, early active flexion of the PIP joint is initiated.
Prolonged immobilization (i.e., >3 weeks) should be avoided. Maintaining
the MCP joint in this position and initiating early active PIP motion will
help maintain reduction by providing a tension band effect through the
extensor mechanism.
E. Operative treatment
1. Indications for surgery
a) Unstable fracture after reduction
b) Irreducible fracture
c) Most long oblique or spiral fractures with rotational malalignment
d) Fracture associated with skin, neurovascular, or tendon injuries
e) Multiple fractures of the hand or digit
2. In operative planning, emphasis should be placed on the following:
a) Mechanical strength of the constructs
b) Profile of implants for limited soft tissue volume and extensibility
c) Soft tissue management and handling
d) Adequacy of functional aftercare
The ideal fixation device is low profile to minimize interference with ten-
don gliding, and rigid enough to facilitate early mobilization.
3. Surgical options
a) K-wire fixation
1) Indications—unstable transverse fracture after reduction, long oblique,
or spiral fractures
2) Advantages—simple technique, keeping soft tissue sleeve undisturbed
(in percutaneous pinning), readily available devices
3) Disadvantages—relatively weak implants (in some configurations),
complications of soft tissue(tendon) tethering and pin loosening,
reported unfavorable outcome in comminuted fracture, open fracture,
and associated soft tissue injuries
b) Percutaneous transmetacarpal pinning
Either a single or two K-wires are inserted across the flexed MCP joint
and down the intramedullary canal of the proximal phalanx. The PIP
joint is left free for active motion. Rotational alignment is secured by
flexion of the PIP joints of the injured and adjacent digits during pin
insertion.
c) Intramedullary K-wires
As in the use of flexible nails fixation for another long bones, this tech-
nique can minimize soft tissue/implant interference and can provide
stability sufficient for early motion. It is not suitable for spiral or com-
minuted fractures since subsequent shortening may still occur.
d) Multiple parallel K-wires for long oblique or spiral fractures
e) Crossed K-wires
Technically, this configuration of fixation usually requires open reduc-
tion. Strength of the fracture construct is enhanced when combined with
tension band wire or intraosseous wires.

f ) Intrafocal pinning
This method can be considered in irreducible fracture especially in juxta-
articular area (neck and base of the phalanx)
g) Intraosseous wiring
1) Indication—Transverse shaft fracture that requires open reduction
2) Advantages—Limited exposure, readily available devices
3) Disadvantages—Relatively weak implant
4) Preferred configurations for increasing strength—two parallel loops,
90 to 90 wires, wiring with K-wire supplement
h) Screw fixation
1) Indication—Long oblique or spiral fractures, intra-articular marginal
fracture of the base, intra-articular condylar fracture
2) Prerequisite
a. Large enough fragments to accommodate screw(s)
b. The fracture line greater than 2.5 times the diameter of the bone
in long oblique or spiral fractures
i) Plate fixation
1) Indications—Comminuted fracture of shaft or periarticular area with
segmental defect
Open fracture with concomitant soft tissue injuries especially ten-
don laceration
2) Advantages—Most rigid construct in several biomechanical studies
3) Disadvantages
More extensive surgical exposure
—Potential interference with tendon gliding, predisposing to adhe-
sions, technically demanding
—High complication rate following fractures with associated soft tis-
sue injury.
—May be difficult to close periosteum to achieve a gliding surface for
the overlying tendons.
—Either a lateral plate (less-disruptive surgical approach and undis-
turbed dorsal extensor mechanism) or a dorsal plate can be utilized.
j) External fixation
1) Indications—Open fracture (with or without bone loss) with associ-
ated soft tissue injuries (skin, neurovascular structure)
2) Closed fracture (especially comminuted fracture) with severe soft tis-
sue injuries
3) Advantages
—Maintaining an intact soft tissue envelope
—Adjustability of alignment
—Facilitation of further soft tissue assessment and reconstruction
4) Disadvantage
—Soft tissue impaling and tethering that may hinder active motion
—Both dorsal and lateral applications of external fixators have been
described.
F. Type of fracture
Based on anatomical location, proximal phalangeal fractures are divided into
a) Base fracture
b) Extra-articular
c) Intra-articular

d) Neck fracture
e) Shaft fracture
f ) Head fracture
1. Fracture base of proximal phalanx
a) Dorsal comminution is the most common cause of instability after reduc-
tion.
Acceptable sagittal plane angulation is less than 25 degrees (lateral
view)
b) Treatment
1) Extrainticular
Stable fracture after reduction—Extension block splinting
Unstable following reduction—Percutaneous K-wire fixation
Irreducible—ORIF
2) Intra-articular
Goal is anatomic reduction with early motion—typically requires
ORIF
In rare cases, a hemiarthroplasty may be the best solution
2. Fracture shaft of proximal phalanx
a) Treatment
1) Stable fracture after reduction: Short arm cast incorporating extension
block splinting of digit
2) Unstable following reduction or long oblique or spiral fracture:
Percutaneous K-wires or ORIF
3) Comminuted fracture and/or severe soft tissue injury—External
fixation
4) Transverse—Percutaneous K-wire fixation or ORIF
5) Irreducible: ORIF
3. Fracture neck of proximal phalanx
a) Relative ratio in adults and children is about 1:10.
b) The most common fracture pattern is dorsal displacement with partial
contact
c) Treatment
1) Partial displacement—Percutaneous K-wire fixation
2) Complete displacement—ORIF
3) Avascular necrosis of phalangeal head has been reported after open
reduction
4. Fracture head of proximal phalanx
Some fracture patterns of the condyles may be easily missed if proper radio-
graphs are not obtained. Operative treatment is challenging because of han-
dling with small articular fragment and frequent comminution.
5. Unicondylar fracture
These fractures are the most common patterns of fracture head and are clas-
sified into four types (Weiss and Hastings)
—Type I oblique volar
—Type II long sagittal
—Type III dorsal coronal
—Type IV volar coronal
a) Most of these fractures, even when nondisplaced, are substantially
unstable.
b) Treatment

1) Nondisplaced fracture—Splinting or percutaneous K-wire fixation

2) Displaced fracture—Closed reduction and percutaneous K-wire fixa-
tion, ORIF (need two implants to prevent rotational instability)
3) Bicondylar fracture
i) Most of these difficult fractures require open reduction.
ii) Implants: Minicondylar plate with lateral application
iii) Miniscrew in each condyle
iv) Oblique tension band wires
v) Multiple K-wires
4) Other uncommon fractures
Triplane fracture: This fracture presents with cleavage lines in the
sagittal, coronal, and transverse planes. Treatments is by ORIF with
miniscrews or by open reduction and external fixation
5) Osteochondral shearing fracture
This condition is usually associated with PIP dislocation and char-
acterized by thin layer of subchondral bone attached to articular
cartilage. A few operative treatments have been conducted including
fibrin glue fixation and K-wire with composite figure-of-eight
wire.
G. Complications
1. Loss of motion
The most common complication is loss of motion. Predisposing factors
include prolonged immobilization, an associated joint injury, soft tissue inju-
ries from initial trauma, surgical dissection, and fixation devices.
Rehabilitation including edema control, motion exercises and dynamic
splinting is initiated. Surgical treatment can be considered when the motion
gains reached a plateau short of what is needed. The components of stiffness
dictate the surgical techniques used.
2. Malunion
a) Extra-articular malunion
Deformities include malrotation, angulation (volar and lateral), and
shortening. Surgery is indicated in the patients with functional impair-
ment associated with malunion.
The factors that determine surgical treatment are
1) Type of the deformity
2) Severity
3) The presence of tendon adhesion, joint contracture, or bone loss
4) Presence or absence of a viable and stable soft tissue sleeve
b) Surgical options
1) Corrective osteotomy at malunion site (almost always preferred)
i) Advantage—Allows for multiplanar correction, capsulectomy, and
tenolysis
Greatest potential for correction
ii) Disadvantage—Increasing risk of postoperative adhesion from
both surgical exposure and implants
iii) Transverse or step-cut osteotomies are preferred for isolated malro-
tation
iv) Wedge (either opening or closing) osteotomy is used for isolated
angular deformity or combined malrotation and angulation. If

shortening is contributed to be the component of the deformity,

opening wedge is recommended.
2) Metacarpal osteotomy
i) Advantage—Keeping the soft tissue of proximal phalanx
undisturbed
ii) Disadvantage—Limited degrees of correction, produces a “Z”
deformity (digit may have suitable rotation in full flexion, but will
have appearance of malrotation in extension), tenolysis at the frac-
ture site done concurrently may be necessary
c) Intra-articular malunion
Condylar malunion of head of proximal phalanx may cause pain, angular
deformity, PIP stiffness, or posttraumatic arthritis.
1) Surgical options
a. Intra-articular osteotomy; the advantage of restoration of articular
contour should be balanced with technical difficulty and the risks
of motion loss and osteonecrosis.
b. Extra-articular osteotomy: This technique corrects overall align-
ment of PIP joint and avoids the risks of intra-articular surgery. It
provides a satisfactory outcome in a few published series.
c. Salvage procedures—PIP arthroplasty, arthrodesis
d. Frontal and sagittal correction is possible, but restoration of full
motion may be difficult.
3. Nonunion
Phalangeal nonunion is uncommon. Most nonunions are atrophic and have
contributing factors including neurovascular injuries, bone loss, and infec-
tion. Nonunion is most often complicated by associated tendon dysfunction
and joint stiffness.
a) Surgical options
1) Resection of the nonunion, plate fixation, bone grafting with tenoly-
sis and capsulectomy.
2) Ray amputation or PIP fusion for unsalvageable situation
VI. MCP Dislocations
A. Dorsal MCP dislocation—Volar plate ruptures and if it displaces into the joint,
it results in complex dislocation. If it does not displace into the joint, it results in
simple subluxation
1. Simple subluxation
a) Volar plate not interposed in joint
b) Can be treated with closed reduction
1) Flex wrist to relax flexor tendons
2) Push proximal phalanx dorsal to volar without axial traction
3) Axial traction may convert to complex dislocation by pulling volar
plate into joint
c) Once reduced, treat with early ROM and extension block splint for 2 weeks
2. Complex dislocation (skin dimpling overlying the dislocation, metacarpal,
and proximal phalanx are collinear)
a) Volar plate is interposed in joint

b) In index finger, flexor tendon displaces ulnarly and lumbrical displaces

radially and these tighten around metacarpal neck when closed reduction
is attempted, preventing the reduction
c) In small finger, the flexor tendons and lumbrical displace radially and
the abductor digiti minimi and flexor digiti minimi ulnarly, again
tightening around the metacarpal neck when closed reduction is
attempted
d) Dorsal surgical approach
1) Split extensor tendon to expose joint
2) Can occasionally push volar plate out of with freer elevator
3) Usually must split volar plate longitudinally and then push volar out
of joint using a freer elevator
e) Volar surgical approach
1) Digital nerves are tented just beneath skin and are at risk with skin
incision
2) Release A1 pulley to expose volar plate
3) Volar plate can be pulled out once nerves are protected
3. Volar MCP dislocations
a) Rare
1) Interposing structures include
a. Dorsal capsule
b. Volar plate
c. Collateral ligament
d. Junctura tendinum
2) Attempt closed reduction
3) Open reduction through dorsal approach
B. Gamekeeper’s thumb
1. Eponym: “Skier’s thumb”
2. Mechanism of injury: Fall onto outstretched hand with thumb held in ante-
position, hyperabduction of the thumb at MCP joint causes acute injury to
he ulnar collateral ligament (UCL)
3. Ecchymosis, swelling, tenderness along the course of the UCL and the volar
plate
4. Clinically evident mass may be present to palpation proximal to the thumb-
index web space (‘Stener’ lesion)
5. Ligament avulsed from the base of the proximal phalanx most frequently
a) Occasional small bony fragments accompany avulsed ligament
b) CAUTION: Displaced fracture of the proximal phalanx does not auto-
matically imply/confer instability
1) Bony fragments usually noted to be more malrotated than appreciated
on radiographs
6. PA and lateral radiographs of the thumb are obtained
7. Stress views: Obtained in clinical setting where instability is sought prior to
surgical repair
a) Instillation of 1-2 ml of 1% lidocaine by intra-articular injection into the
MCP joint may be required for adequate relaxation
b) Comparison to contralateral side
c) Proper collateral only: Instability in MCP 30° flexion only
d) Proper and accessory collateral tear: Instability in both MCP flexion and
extension

e) Radiographic note: Observe extent of frontal plane shift of the base of the
proximal phalanx radially, and compare to the contralateral side
8. Surgical repair if instability noted
a) UCL that is retracted proximally and lies superficial and proximal to the
leading edge of the Adductor aponeurosis will not heal to the base of the
proximal phalanx
b) The ligament is identified, replaced deep to the Adductor (‘flipped back
into place’) and affixed to its insertion
c) Immobilization for a period of time sufficient for soft tissue healing to
bone to occur – approximately 6 weeks
d) K-wire can be placed across MP joint after repair at surgeon’s discretion
e) Internal fixation or K-wire fixation if a fracture fragment of suitable size
is attached to the avulsed ligament
9. Chronic injury
a) Risk of instability and weakness in side pinch and tip pinch
b) OA of MCP may result
c) Splint may be required
d) Surgical Rx: ligament reconstruction with tendon graft, MCP arthrod-
esis, or reconstruction with local tissue combined with an advancement
of the adductor insertion along the ulnar aspect of the proximal phalanx
(Neviaser)
C. Radial collateral ligament (RCL) tear of thumb MCP
1. Less frequently appreciated than acute UCL rupture
2. Often accompanied with a tear of the dorsal-radial MCP joint capsule
3. Ecchymosis, swelling, tenderness along the course of the RCL and the dorsal
aspect of the MCP
4. Clinically evident mass not present
5. Site of ligament tear ( proximal, midsubstance or distal) is more evenly dis-
tributed than UCL tears.
6. PA and lateral radiographs are obtained
a) See volar subluxation of the proximal phalanx on the lateral view
b) C/w contralateral side to see difference on lateral view
c) Fracture of the radial base of the proximal phalanx seen less frequently
d) Avulsion of the dorsal capsule seen occasionally
e) Stress views required infrequently
7. Surgical repair usually performed if clinical and/or radiographic instability
noted
a) Frequent sequelae of MCP joint pain along radial and dorsal joint line
noted if left unrepaired/unreduced
This needs to be added to the section on Thumb MCP dislocations.
Please have a look, append/edit as necessary and send it to India. Thanks.
VII. Metacarpal Fractures: Diagnosis
Metacarpal fractures can be divided into fractures of the metarpal head, neck, shaft,
and base. The treatment varies based on which metacarpal is involved and its location.
Important parameters in evaluation include angulation, shortening, and malrotation.
The acceptable amount of angulation varies by location and patient considerations. In
general, no degree of malrotation is acceptable.

Metacarpal fractures, fracture dislocations

A. History of trauma
1. Direct blow or rotational injury with axial load.
2. High energy injuries (i.e., automobile) may result in multiple fractures.
3. Wounds (i.e., bites) may result in open fractures or infection.
B. Physical examination
1. Inspection for open wounds and associated injuries
a) Any fight wounds over the MCP joint are open joints until proven
otherwise.
1) Extensor tendon can be lacerated and retracted.
b) Dorsal wounds over metacarpal fractures are almost always open
fractures.
c) Volar wounds with metacarpal fractures may be lacerations without frac-
ture communication.
2. Deformity indicates location
a) Deformity at metacarpal base may indicate CMC dislocation.
b) MCP joint deformity may indicate MCP dislocation.
c) A prominence over the shaft indicates angulation.
d) Shortening can be assessed by comparing to the opposite side.
e) Malrotation assessed by lining up fingernail in partial flexion and full
flexion if possible. Compare to opposite side.
3. Motor examination
a) Difficult to assess due to pain
b) Typically no motor deficits unless open wounds
c) With open dorsal wounds, check extensor tendon function
d) With open volar wounds, check flexor tendon function
4. Neurovascular examination
a) Typically only affected with open wounds
b) Dorsal wounds may affect dorsal sensory branches of radial or ulnar
nerve
c) Volar wounds can involve digital nerves
5. Compartment syndrome
a) Be suspicious in closed injuries with multiple fractures or dislocations and
massive swelling, and with closed crush injuries
C. Imaging
1. Radiographs mandatory
a) PA, lateral, oblique
b) Brewerton view for metacarpal head fractures
c) 30 to 45 degree oblique views for CMC joints
d) Roberts view for thumb CMC joint
2. CAT scan
a) For inconclusive radiographs of CMC fractures/dislocations
b) For multiple CMC dislocations
c) For complex metacarpal head fractures
D. General assessment
1. Determine which bone is fractured/dislocated in which location
2. Divide injuries into
a) Bone fractured
b) Location

1) MCP joint
2) Metacarpal head
3) Metacarpal neck
4) Metacarpal shaft
5) Metarcarpal base
3. Treatment is dependent on above assessment.
Metacarpal head fractures
A. Basic principles of articular reduction apply
B. No degree of articular displacement is acceptable
C. Requires surgical fixation
D. Surgical approach
1. Dorsal incision
2. Either centrally split extensor apparatus or release and repair sagittal band
3. Capsule is either incised longitudinally and peeled off the MC head and
proximal phalanx or a transverse capsulotomy is made over the dorsal joint.
4. Hardware cannot protrude from joint surface
a) Fix with multiple small screws in collateral recess, headless screws, or
K-wires
5. Ideal fixation secure enough to allow for early motion
E. Severely comminuted head fractures
1. Consider external fixation
2. MCP joint replacement is an option understanding the possibility of loosen-
ing and instability
F. Stiffness is most common complication, so early motion is critical
G. MCP fusion or arthroplasty are options for late arthritis
Metacarpal Neck Fractures
A. Treatment depends on which bone is involved
1. Acceptable degrees of apex dorsal angulation vary with different studies
a) Index: 10 to 15 degrees
b) Middle: 10 to 15 degrees
c) Ring: 20 to 40 degrees
d) Small: 20 to 60 degrees
2. An acceptable amount of angulation may vary between patients, depending
on occupation, avocations, and preferences
3. If left with a deformity, patient must understand the deformity and its
clinical significance
4. Patient will have loss of appearance of knuckle, with a proximal prominence
along the dorsal aspect of the metacarpal and a bump in the palm
5. The deformity will likely not result in any functional limitations
6. Pseudoclawing (compensatory MCP hyperextension and PIP flexion)
requires reduction
7. Cast immobilization
a) Immobilize MCP joints in 70 to 90 degrees flexion to stretch collateral
ligaments, leave PIP joints free
b) Cast for 4 weeks
c) May consider functional bracing or taping
8. Closed reduction
a) Median nerve block, ulnar nerve block, or Bier block
b) Reduction maneuver: Jahss technique

1) 90 degrees MCP flexion, dorsal pressure through proximal phalanx

while stabilizing metacarpal shaft
c) Immobilize, follow with serial radiographs
9. Indications for operative treatment
a) Open fractures
b) Fight bites require I and D but no internal fixation until wound is stable
c) Unacceptable angulation
d) Any malrotation
e) If cast immobilization is contraindicated (i.e., multitrauma setting)
a) Unstable fractures
b) Failed closed reduction
c) Any clinically important malrotation
d) Unacceptable angulation
e) Technique
1) Closed reduction percutaneous pinning (CRPP) with the MCPs flexed
in order to ensure that rotational alignment is correct
a. Anterograde
i) Through metacarpal base
b. Retrograde
i) Through collateral recess
ii) Put pins in with MCP flexed to avoid collateral contractures
c. Encourage PIP motion
d. Remove pins 4 weeks
2) ORIF
a. Perform if cannot get reduction for CRPP
b. Reduce fracture and pin as with CRPP (MCPs flexed for rotational
alignment)
c. Difficult to plate because limited bone for distal fixation
VIII. Metacarpal Shaft Fractures
A. Treatment depends on which bone is involved

1. Acceptable degrees of angulation
a) Index: less than 10 degrees
b) Middle: less than 10 degrees
c) Ring: 20 degrees
d) Small: 20-30 degrees
2. No malrotation is acceptable
3. Shortening does not cause functional problems but may be aesthetically
unacceptable
4. Cast immobilization
a) Immobilize MCP joints in 70 to 90 degrees flexion to stretch collateral
ligaments, leave PIP joints free
b) Cast for 4 weeks
5. Closed reduction
a) Median nerve, ulnar nerve, or bier block
b) Correct angular deformity with PIP flexed and pressure through proximal
phalynx

c) Cast as above with serial radiographs

d) Immobilze for 4 weeks
6. Indications for operative treatment
a) Open fractures
b) Unacceptable angulation
c) Any malrotation
d) Multiple fractures
e) If cast immobilization is contraindicated
a) K-wires
1) Place retrograde through metacarpal base or anterograde through
collateral recess
2) Allow for MCP and PIP motion
3) Remove in 4 weeks
b) Plate/screw fixation
1) Can use multiple lag screws for long spiral fractures
a. Try to get at least two lag screws
2) Plate fixation for transverse fractures
a. Try to cover plate with periosteum to prevent tendon irritation
b. Begin early motion to prevent tendon adhesions
3) External fixation for comminuted fractures, segmental bone loss, and
soft tissue loss
IX. Metacarpal Base Fractures
A. Extra-articular
1. Treat similar to metacarpal shaft fractures
a) K-wires
1) Place across fracture and CMC joint into carpus
3. Plate fixation
a) Will require T type plate to maximize proximal fixation
b) Avoid joint penetration with proximal screws
B. Intra-articular
1. Requires anatomic reduction
2. Often associated with dislocations
3. Consider CT scan to assess preoperatively
4. Treat with ORIF or CRPP
5. Hard to assess quality of reduction without ORIF
6. Usually fix with multiple K-wires or lag screw fixation depending on frag-
ment size
X. Thumb Extra-articular Metacarpal Base Fracture
A. Occurs at metaphyseal/diaphyseal junction

B. Apex dorsal angulation with adduction, flexion, and supination of distal
fragment

C. Acceptable angulation:
1. 20 to 30 degrees
2. Increased angulation decreases breadth of the thumb web space and causes
compensatory MCP hyperextension
D. Closed reduction
1. Longitudinal traction, pronation, and extension
2. Difficult to hold in cast
3. Difficult to assess reduction with radiographs
4. Consider assessing reduction with fluoroscopy
5. Best view is true lateral of metacarpal
E. Surgical fixation
1. Above closed reduction maneuver with K-wires across CMC joint for 4 to
6 weeks
2. Open reduction rarely needed for acute fractures, but may be required with
delayed presentation
a) Follow with K-wire fixation
The Carpometacarpal Joints

The carpometacarpal (CMC) joints are a diverse grouping of articulations that share the
commonality of linking the digital components of the hand with the carpus. They pos-
sess, however, very different roles in hand function. Their position within the hand,
their distinctly different morphology, and adjacent myotendinous structures affect not
only their actions but also their potential risk for injury.
While isolated dislocations are possible, frequently CMC injuries are fracture dislo-
cations with varying degrees of osseous involvement. It is perhaps best to think of these
injuries as three distinct subgroups: Thumb or preaxial (first CMC joint), central (second
and third CMC joints), and ulnar or postaxial (fourth and fifth CMC joints) injuries.
Thumb Carpometacarpal Joint

A. Anatomy—The thumb CMC joint possesses a unique articulation where
each opposing surface is composed of a convexity and a concavity oriented
orthogonally. This has been very accurately described as an inverted “horse
saddle” sitting atop a second “horse saddle.” The stability of this joint is
conferred by both these matching boney contours and the supporting soft
tissues. Several authors believe that the most important ligament is the anterior
oblique ligament that tethers the base of the metacarpal with the trapezium.
Dorsally the capsule is confluent with the extensor/abductor mechanism and
thus these structures work in unison to support the joint. While this joint, as a
result of these undulating surfaces, enjoys a generous range of motion, it does
come at a price. Of all the CMC joints, this is the one most likely to develop
symptomatic osteoarthritis.
B. Thumb metacarpal fractures—Extra-articular fractures of the base of the first
metacarpal are frequently apex dorsally angulated. Thirty degrees of angulation
can be accepted. Excessive angulation should be addressed so that a compen-
satory hyperextension deformity does not develop at the metacarpophalangeal
(MCP) joint.
1. Nondisplaced fractures are treated with cast immobilization.
2. For displaced or angulated fractures treatment options include closed
reduction and casting (often satisfactory in pediatric patients where there is a
robust periosteal sleeve), closed reduction and percutaneous pin fixation, or

open reduction and fixation. While a variety of implant options are available,
percutaneously placed Kirschner wires (K-wires) are the most commonly
utilized due to their ease of insertion, ease of removal, and their ability to
stabilize fracture components that may be too small or too comminuted for
fragment specific screw fixation.
C. In 1910, Rolando described a series of comminuted intra-articular fractures
at the base of the thumb. They include either “T” or “Y” type fracture patterns.
He believed patients did poorly whether they were treated with cast or skeletal
traction. More recently, authors have described a variety of operative procedures,
which tailor treatment to the degree of comminution present. Corresponding
fractures of the trapezium are quite rare. When the fracture fragments are large
and sufficiently preserved, open reduction and plate fixation can be employed.
For severely comminuted fractures, where fragment specific fixation cannot be
obtained, skeletal traction via an outrigger can be employed, as described by
Gelberman or a quadrilateral external fixator, spanning the first and second
metacarpals.
D. Thumb CMC fracture dislocations—The eponymous Bennett fracture, first
described in 1882, is the prototypical CMC fracture dislocation. Because of
its more isolated position and as a result, greater ease of radiographic imaging,
the treating physician more readily recognizes intra-articular incongruence and
subluxation of the distal fragment. Typically, the fracture dislocation is well
visualized on standard radiographic series. The fracture typically consists of two
components: The smaller volar fragment, which remains attached to the trape-
zium via the anterior oblique ligament, and the second fragment that typically
has the greater percentage of articular surface and is attached to the metacarpal
shaft. As the shaft component is attached to the long thumb abductor (APL)
and the thumb adductor (adductor pollicis), it typically migrates proximally,
dorsally, and radially. Optimal treatment, including the importance of precise
intra-articular reduction, remains debated. The restoration of concentric articu-
lar surfaces is a requisite component of joint stability and that the importance
of the congruency of articular fragments is proportional to the percentage of the
joint surface that is involved.
1. Thumb CMC fracture dislocation treatment—Because of the inherent insta-
bility of the Bennett fracture components, closed treatment alone is rarely
employed. Surgical options include closed reduction and pin fixation as well
as open reduction and internal fixation (ORIF).
a) Percutaneous fixation: Fracture reduction is obtained via longitudinal
traction, dorsal to volar compression of the basilar fragments and
slight pronation of the thumb. Percutaneous fixation is then obtained
by either employing dual K-wire placement with one pin transfix-
ing the major fragment and smaller volar fragment and the second
transfixing the major fragment to the trapezium. An alternative per-
cutaneous technique employs transmetacarpal pin fixation. In this
technique, after reduction is obtained, two K-wires are placed trans-
fixing the first and second metacarpals. Pins are typically left in place
for four to 6 weeks or until clinical and radiograph evidence of heal-
ing is present. Splint immobilization is used in conjunction with pin
fixation and typically continues until 6 weeks postoperatively. Once
the pins are removed, active range of motion exercises are begun. Pas-
sive range of motion exercises are initiated at 6 weeks postoperatively

and strengthening is added at 8 weeks postoperatively if clinically

indicated.
b) ORIF is utilized for irreducible fractures or per physician preference.
The Wagner approach, which incorporates a longitudinal incision
along the axis of the thumb metacarpal between the glabrous and
nonglabrous skin, is conjoined with a smaller transverse limb proxi-
mally ending at the flexor carpi radialis (FCR) tendon. The deeper
dissection requires subperiosteal reflection of the thenar musculature
off of the metacarpal and identification of the CMC capsule. If intact,
the capsule is then incised to allow for visualization of the articular
fragments. Anatomic reduction is coupled with K-wire fixation. If the
fracture fragments are large enough, screw fixation is performed (1.5
to 2.7 mm). If the fragments are too small or comminuted, K-wires
alone may be employed. The K-wires can be placed either percutane-
ously if placed dorsoradial to volar-ulnar or cut and buried subcutane-
ously. At closure, the capsule is repaired and can be imbricated if it was
found to be patulous upon initial inspection. The aftercare is similar
to that for percutaneous treatment except that active range of motion
can begin at the first postoperative visit when screw fixation has been
utilized.
c) Supplemental cancellous distal radius bone graft can be used, if necessary,
to support the articular fragments.
d) Complications include injury to the nearby radial sensory nerve
branches, typically due to retraction during exposure via the Wagner
approach. Pin tract infections may occur. Late complications include
posttraumatic arthritis that may be the result of residual incongruence
or simply a function of initial chondral trauma. Nascent malunions,
which show no evidence of arthritic change, can be treated by intra-
articular osteotomy and fixation. Malunions with arthritic change
are better addressed with either arthrodesis or arthroplasty. The
choice of salvage procedure is dependent upon patient and surgeon
preferences.
E. Dislocations—Isolated dislocations of the thumb CMC joint are quite rare.
Dislocations are invariably dorsal. Unfortunately, capsular ligamentous injuries
with less-dramatic clinical and radiographic findings are more common and
often missed or under treated. These may go on to develop capsular laxity and
symptomatic instability.
1. On clinical examination, there may be dorsal subluxation that reduces with
direct pressure or thumb extension. The involved thumb often has greater
translation in both the anterior posterior (AP) and radial to ulnar planes.
Stress radiographs, in which both thumbs are imaged in the posterior
anterior projection while the radial borders of the thumb proximal phalanges
are pressed against one another, are often helpful in assessing instability. An
incompetent CMC joint capsule will allow the metacarpal base to subluxate
radially off of the trapezium. True lateral radiographs of the thumb may
show dorsal subluxation of the metacarpal base, also a sign of ligamentous
insufficiency.
2. Thumb CMC dislocation closed treatment—While nonoperative treatment
of first CMC joint dislocations can be done, results are unreliable in terms of
restoring stability.

3. In most instances, open treatment with ligament reconstruction is pre-

ferred. The technique has been described by Eaton and Littler.
a) The same Wagner approach previously described is utilized. The joint
capsule, if intact, is then split parallel to the articular surfaces. The FCR
tendon is identified and is mobilized from the wrist crease to the mid
trapezium. An AP tunnel is created from the volar metacarpal flare (just
distal to the anterior oblique ligament insertion) emerging in the dorsal
metacarpal metaphysis. This tunnel should be parallel to the joint surface.
Using the thumbnail as a guide, the dorsal hole is situated in the mid-
sagittal axis of the metacarpal. The radial half of the FCR tendon is then
harvested. A distally based tendon graft 6 to 8 cm in length is typically
harvested.
b) As the tendon spirals in its orientation, cutting the ulnar half proximally
yields a graft attached radially at the second metacarpal base. The lig-
ament is reconstructed by passing the tendon from volar to dorsal
through the boney tunnel. The metacarpal base is reduced and the
FCR graft is then tensioned. The tendon is then secured to the adja-
cent periosteum with nonabsorbable sutures. The FCR graft is then
passed dorsal to volar (in the sagittal axis of the thumb) between the
extensor pollicis brevis and the abductor pollicis longus (APL). The
tendon is then looped around the intact distal FCR from posterior
to anterior (in the sagittal axis of the wrist). It is then tensioned and
sewn or woven into the distal APL aponeurosis. If there is any con-
cern regarding stability or compliance, a supplemental transarticular
K-wire can be added.
c) Forearm-based thumb spica immobilization is continued for
4 weeks. At this point, the patient is converted to a removable
splint. If a transarticular K-wire was utilized, this is also removed.
The remainder of the rehabilitation is identical to that for closed
treatment.
Central Carpometacarpal Joints

A. Anatomy—The index and middle digit CMC joints enjoy very stable
articulations with the trapezoid and the capitate. This is a function of their
geometry, position in the center of the hand, strong interosseous ligaments,
and the expansive attachment of extrinsic wrist tendons. This robust soft
tissue support structure makes fracture dislocations more likely than isolated
dislocations.
1. Because injuries to the CMC joints are often poorly visualized on standard
posterior-anterior (PA) radiographs, particular attention must be paid to lat-
eral and oblique images. Dorsal prominence of a metacarpal base or marked
angulation of an individual metacarpal shaft should raise the suspicion of a
fracture dislocation or dislocation.
2. Some individuals have preexisting carpal bosses, which should not be mis-
taken for fractures. These are best seen on a “carpal boss view” radiograph.
This is a lateral view radiograph of the hand and wrist with slight supination
and slight wrist flexion. Often both wrists are imaged on the same cassette to
allow for comparison.
B. Central CMC fractures—Intra-articular fractures of the second and third
metacarpal bases are relatively uncommon. Diaphyseal and distal metaphyseal

injuries are more prevalent. Suspicion for other occult carpal injuries should be
high owing to the significant force required to injure these well-protected articu-
lations.
1. Nonoperative fracture treatment—Nondisplaced fractures can be treated
by cast immobilization. Casts should include both the MCP joints distally
and the wrist proximally.
2. Operative fracture treatment. Unstable but reducible fractures can be
treated with closed reduction and K-wire fixation. Care should be taken to
avoid accidental injury to the terminal radial artery when placing implants in
the second metacarpal base. When open reduction is required, the metacar-
pal bases are approached via a longitudinal incision centered over the meta-
carpal. When both metacarpals are injured, an incision centered between the
metacarpals allows access to both bases. Cast or splint protection is necessary
for 6 weeks following initiation of treatment. If rigid fixation is achieved,
early active range of motion exercises can be instituted with interval splinting
to decrease joint stiffness.
C. Central CMC fracture dislocations—Fracture dislocations, when present are
invariably dorsally displaced. Diaphyseal fractures of adjacent metacarpals may
allow for the requisite leverage to allow a fracture dislocation of these otherwise
well-protected joints.
1. Fracture dislocation treatment—While fracture dislocations treated acutely
may reduce easily, they are often unstable. Supplemental K-wire fixation is
often recommended.
2. For irreducible fracture dislocations or late-presenting injuries, open reduc-
tion and fixation are often requisite. This can be achieved by transarticular
fixation, transmetacarpal fixation, or both. When large fracture fragments of
the articulating carpal bones are involved, ORIF may be required to repair
the intercarpal architecture as well.
D. Central CMC pure dislocations are rare injuries. Difficulties in detection and
thus late presentation may be seen.
1. Dislocation—Treatment and aftercare are essentially identical to that for
fracture dislocations. Because the metacarpal bases have an inverted trapezoi-
dal shape, satisfactory reduction and anatomic dorsal contour can be assessed
directly.
2. As these joints have little intrinsic capacity for motion, stiffness is rarely
an issue at the CMC level in the index and middle digits. For chronic
dislocations, especially those with arthritic change, primary arthrodesis can
be considered. However, arthrodesis is not recommended for acute injuries
and should be reserved as a salvage procedure.
XI. Ulnar Carpometacarpal Joints
A. Anatomy—The fourth and fifth metacarpal bases articulate with the distal
surface of the hamate. While the fourth metacarpal also enjoys small
articulating surfaces (and corresponding sturdy interosseous ligaments) with
its neighboring metacarpals, the volar ulnar border of the fifth metacarpal
is stabilized by the pisometacarpal ligament. Additionally, the fourth and
especially the fifth CMC joints enjoy more range of motion than the central
CMC joints. This is due in part to the more saucerlike articulation between

the fifth metacarpal and the hamate. The convex fifth metacarpal base more
readily pivots in shallow concavity of the distal hamate. Their position on
the lateral border of the hand leaves them less protected and hence more
susceptible to injury. Of all the CMC joints, the fifth is the most commonly
injured. As a result of the pull of the extensor carpi ulnaris (ECU) tendon,
proximal migration of the fifth metacarpal base frequently occurs with
injuries to this joint.
1. Ulnar CMC fractures—Both extra-articular and intra-articular fractures of
the base of the fifth metacarpal are seen routinely. Nondisplaced fractures
may be treated with immobilization alone. Operative treatment is other-
wise identical to that employed on the other aforementioned periarticular or
intra-articular fractures. Unlike the thumb metacarpal, mild residual angula-
tion (in the flexion extension plane) is better tolerated and less likely to result
in a compensatory MCP joint hyperextension deformity.
B. Ulnar CMC fracture dislocations—As with the other CMC articulations, frac-
ture dislocations are more common than pure dislocations.
1. The Reverse Bennett fracture is an injury analogous to the Bennett fracture
of the first CMC joint in which there is an intra-articular fracture of the
fifth metacarpal base that dislocates or subluxates proximally and dorsally.
It has also been called a Busby fracture. At times, fifth CMC joint injuries
are associated with a fracture or fracture dislocation of the fourth meta-
carpal base. Unlike the thumb where trapezium fractures are rare, often
the fracture pattern involves the hamate rather than either of the opposed
metacarpal bases.
a) Radiographs of this injury can be quite deceptive in that the articula-
tion between the hamate and the fifth metacarpal base remains normal in
appearance. However, close analysis of the radiographs reveals shortening
of the fifth metacarpal. Visually this shortening is manifested in the loss of
metacarpal length as measured off of a tangential line abutting the third
through fifth metacarpal heads in a PA radiograph.
b) On a lateral radiograph, the fourth and fifth CMC joints are usually
obscured by the superimposed second and third metacarpals. However,
on a 30 degree pronated lateral view these articulations are seen in pro-
file without being obscured by the central metacarpals. When there is a
concern regarding the status of the associated carpal fractures, computer-
ized axial tomography can be helpful.
2. Ulnar CMC fracture dislocation treatment. As is common to CMC injuries,
acute treatment consisting of closed reduction and immobilization can be
attempted but there is a high risk of redisplacement within a cast or splint;
therefore, the threshold for supplemental K-wire fixation is quite low. It
is often difficult to assess the fourth and fifth CMC joints for the quality
of closed reduction using fluoroscopic techniques. The threshold for open
reduction of the joints is low as well.
a) Open reduction and fixation is employed for irreducible dislocations or
delayed presentation.
b) The fifth CMC joint can be exposed through a longitudinal incision just
ulnar to the fifth extensor compartment. The dorsal cutaneous branch of
the ulnar nerve is identified and protected. If the fourth and fifth CMC
joints are both involved, a longitudinal incision can be placed between
the fourth and fifth metacarpal axes.

c) A K-wire is typically placed across the fifth CMC joint and a sec-
ond transmetacarpal K-wire is placed from the fifth into the fourth
metacarpal.
d) If both ulnar CMC joints are injured the transmetacarpal K-wire can also
penetrate the third metacarpal. A third K-wire can be utilized if there is
any question regarding the rigidity of the construct.
e) Additionally, when large hamate fractures are present or when the hamate
fracture is in the coronal plane of the wrist, screw fixation is preferable.
One or two (1.5 to 2.7 mm) screws can be placed from dorsal to palmer
within the hamate. As the fifth and possibly the fourth metacarpals have
been dissociated from the remaining metacarpals, once again transmeta-
carpal K-wire fixation is recommended to the intermetacarpal component
of these injuries.
f ) If presentation is late, ORIF is not recommended. Early mobilization
with late arthrodesis is performed if needed based on patient symp-
toms.
C. Ulnar CMC pure dislocations are rare owing to the robust ligamentous enve-
lope. Volar dislocations have been reported but the vast majority of injuries
result in dorsal displacement.
1. Complex injuries. Multiple dislocations, involving all four CMC joints, are
rare but do occur. They are typically the result of high-energy injuries such
as motorcycle accidents. Patients with these injuries may have other more
life-threatening injuries. As a result, these hand injuries may not be immedi-
ately recognized or may require definitive care after the patient is stabilized.
Divergent dislocations can also occur. These can occur between any of the
metacarpals.
2. Ulnar CMC dislocation treatment is similar to that for the second and third
CMC dislocations. The majority of these injuries treated acutely are amena-
ble to closed reduction and percutaneous K-wire fixation. Irreducible injuries
are treated with open reduction and pinning.
3. Chronic dislocation treatment. There are multiple salvage treatment options
available for chronic dislocations with arthritic change. Most commonly
arthrodesis is performed. Alternatively, tendon interposition arthroplasty
and silastic implant arthroplasty have been described. The latter two salvage
options allow for the preservation of flexion and extension at the recon-
structed fifth CMC joint.
Suggested Readings
Badia A, et al. Dynamic intradigital external fixation for proximal interphalangeal joint fracture-
dislocations. J Hand Surg. 2005;30A:154–160.
Dias J. Intraarticular injuries of the distal and proximal interphalangeal joints. In: Berger RA,
Weiss AP, ed. Hand Surgery. Philadelphia, PA: Lippincott Williams & Wilkins;2004:153–174.
Ellis SJ, et al. Treatment of proximal interphalangeal dorsal fracture-dislocation injuries with
dynamic external fixation: A pins and rubber band system. J Hand Surg. 2007;32A:
1242–1250.
Glickel SZ, Barron OA, Catalano LW. Dislocations and ligament injuries in the digits. In: Green
DP, ed. Green’s Operative Hand Surgery. 5th Ed. Philadelphia, PA: Elsevier, Churchill Living-
stone; 2005:343–388.
Kang R, Stern PJ. Fracture dislocation of the proximal interphalangeal joint. J Am Suc Surg Hand.
2002;2:47–59.

Stern P. Fractures of the metacarpals and phalynges. In: Green DP, pederson WC, Hotchkiss
RN and wolfe SW, eds. Green’s Operative Hand Surgery. 5th Ed. Philadelphia PA 2005:
277–301.
Page SM, Stern PJ. Complications and range of motion following plate fixation of metacarpal and
phalangeal fractures. J Hand Surg. 1998;23A(5):827–832.
Suprock MD, Hood JM, Lubahn JD. Role of antibiotics in open fractures of the finger. J Hand
Surg. 1990;15A(5):761–764.
William RMM, et al. Treatment of unstable dorsal proximal interphalangeal fracture/dislocation
using a hemi-hamate autograft. J Hand Surg. 2003;28A:856–865.
Zook EG. Anatomy and physiology of the perionychium. Hand Clin. 2002;18:556.

Fractures and
Dislocations: Wrist
14
Ryan P. Calfee, Richard Berger, Pedro K.
Beredjiklian, Drew R. Engles, Jeffrey A. Greenberg,
Jonathan E. Isaacs, Candice McDaniel, Tamara D.
Rozental, Phil Blazer, and Olivia Pate
I. Anatomy of the Carpus
A. The wrist consists of eight carpal (wrist) bones interposed between the forearm
(radius and ulna) and the five metacarpal bones. The carpal bones may be divided
into two rows of four bones each.
1. The proximal carpal row is composed of (from radial to ulnar) the scaphoid,
lunate, triquetrum, and pisiform.
2. The distal carpal row is composed of (from radial to ulnar) the trapezium,
trapezoid, capitate, and hamate.
3. Provided minimal bony constraint, the carpus is supported by the intrinsic
(originate and insert within the carpus) and extrinsic (originate or insert out-
side the carpus) ligaments.
4. Within each row, adjacent bones are held together with intrinsic interosseous
ligaments, while the rows of bones are connected by large capsular radiocar-
pal and intercarpal ligaments.
5. The specific ligaments comprising the proximal row interosseous ligaments
are the scapholunate and lunotriquetral interosseous ligaments. Each is “C”
shaped, covering the dorsal, proximal, and palmar regions of the respective
joints.
a) The interosseous ligaments can be divided into three regions, each with
unique gross and histologic as well as mechanical characteristics.
b) The dorsal region of the scapholunate interosseous ligament is a true liga-
ment. It is the thickest and strongest region and constrains translation
between the scaphoid and the lunate.
c) The palmar region of the lunotriqeutral ligament shares these characteris-
tics.
d) The palmar region of the scapholunate interosseous ligament is also a true
ligament. It is thin and constrains rotation (flexion-extension, pronation-
supination) between the scaphoid and the lunate. The dorsal region of the
lunotriquetral interosseous ligament shares these characteristics.
e) The proximal regions of the scapholunate and lunotriquetral ligaments
are composed of fibrocartilage and are believed to function as menisci,
absorbing compressive loads along the proximal rims of the articulations.
6. Extrinsic ligaments
a) Along the volar side of the wrist from radial to ulnar, the ligamentous
elements include radioscaphoid and long and short radiolunate ligaments.
These ligaments extend from the radial side of the radius and extend obliquely
ulnarward to attach to elements of the proximal and distal carpal row.
216

Chapter 14 • Fractures and Dislocations: Wrist 217
b) The dorsal extrinsic ligament (the counterpart of the palmar ligaments) is

the dorsal radiotriquetral (dorsal radiocarpal) ligament, which originates
at the junctional raphe between the scaphoid and lunate fossa and extends
obliquely across to attach to the lunate and triquetrum. This ligament
shares a common attachment on the triquetrum with the dorsal, intrinsic,
scaphotriquetral ligament (dorsal intercarpal ligament).
c) Palmarly and ulnarly there is a relatively superficial ligament, the ulno-
capitate, which arises near the fovea and extends obliquely to the side of
the capitate. Two ligaments arise from the volar limbus of the triangu-
lar fibrocartilage complex (TFCC), the so-called ulno-lunate and ulno-
triquetral ligaments.
d) These ligamentous elements form dorsal and palmar V-shaped ligaments
that support the carpus and are directly perpendicular to forces that favor
carpal dissociation from the radius. The arrangement of these ligaments
puts them in a position to act as a supportive sling for the carpus, and resist
translation under load especially with the arm in an extended position and
with the forearm in neutral rotation. This is the position in which most
power activities are performed. When the supportive sling mechanism is
lost, radiocarpal dislocation can occur. The dislocations may be purely
ligamentous; however, avulsion fractures that contain ligament origins
off the dorsal or volar radial rim of the radius are commonly present.
II. Carpal Kinematics
A. The wrist and distal radioulnar joint (DRUJ) combine to form essentially a uni-
versal joint, normally capable of stable motion with six degrees of freedom in the
cardinal planes (flexion, extension, radial deviation, ulnar deviation, pronation, and
supination). Combining these motions results in circumduction. Many consider
the “dart throw” axis as the most functional motion in the wrist, which combines
radial deviation and extension through ulnar deviation and flexion. In general
terms, the center of rotation can be thought of as being in the head of the capitate.
1. Overall, the bones of the distal carpal row are tightly bound to each other,
creating essentially a single functional unit.
2. The bones of the distal row move with the hand through all six degrees of
freedom.
3. The proximal carpal row behaves differently.
a) First, there is significant motion between adjacent bones as the entire row
moves in generally the same direction. This is similar to the behavior of
train cars traveling as a group down a railroad track, but exhibiting some
independent motion through their couplings.
b) The proximal carpal row bones move with the distal row bones during
flexion and extension of the wrist (adjunct rotation) but continue to
experience flexion and extension during radial and ulnar deviation of the
wrist, respectively (conjunct motion). This occurs because the scaphoid
is shaped and positioned within the wrist such that any extrinsic loading
will induce flexion.
c) The triquetrum, on the opposite side of the proximal row, will experience
extension when loaded.
d) The lunate simply moves with the dominant direction of its neighbors, as
long as the intrinsic interosseous ligaments are intact.

e) Wrist radial deviation is accomplished with flexion of the proximal carpal

row as the scaphoid flexes allow wrist to deviate without distraction of the
ulnar carpal articulations.
f ) Wrist ulnar deviation comprises primarily of proximal row extension with
engagement of the hamate in the triquetrum and extension of the sca-
phoid as the trapezium and trapezoid move away from the distal radius.
Scaphoid Fracture and Fracture Nonunion
I. Introduction
Scaphoid fractures are often the result a fall onto an outstretched hand. Fractures of the
waist or middle third are most common in adults, while distal third fractures are more
common in children.
A. Associated injuries may include fractures of the distal radius and radial head.
Scaphoid fractures may also be seen in perilunate injury patterns. When a sca-
phoid fracture is present in association with lunocapitate and lunatotriquetral
instability, the injury is termed trans-scaphoid perilunate instability. Similarly,
when a scaphoid fracture is present in association with a capitate fracture and
triquetrolunate instability, the injury is termed trans-scaphoid, trans-capitate
perilunate instability or scaphocapitate syndrome.
B. Fracture nonunion and avascular necrosis (AVN) is more common in proximal
pole fractures, given the retrograde blood supply to the proximal aspect of the
scaphoid.
II. Scaphoid Anatomy
A. The scaphoid occupies a position in both the proximal and distal carpal rows. It
is almost completely covered in articular cartilage and has no tendinous attach-
ments.
B. Morphologically it can be divided into proximal and distal thirds (poles), and a
central third termed the waist.
C. The blood supply to the scaphoid can be divided into two main anatomic regions.
1. The dorsal scaphoid branches of the radial artery enter the bone through
the nonarticular dorsal ridge and the distal tubercle, supplying 70% to 80%
of the bone, including the proximal pole. As a result, the blood supply to the
proximal pole of the scaphoid is retrograde, which is the main reason why
the more proximal fractures are susceptible to developing AVN following a
fracture.
2. A second group of vessels arising from the volar scaphoid branches of the
radial artery enters via the scaphoid tubercle to supply the distal 20% to 30%
of the bone. This flow is typically anterograde, which explains why the more
distal fractures have a tendency to heal uneventfully.
III. Evaluation
A. Patients typically present with wrist pain that is localizable to the anatomic
snuffbox on physical examination. Careful attention should be paid to the radial
head in the elbow and the distal radius to rule out any associated injuries.

B. The radiographic evaluation should include PA, lateral, and ulnar devia-
tion (scaphoid) views of the wrist. For evaluation of the distal pole, a carpal
tunnel view or a semisupinated lateral view can be helpful. The sensitivity of
fracture detection with the standard radiographic series in the acute setting
is moderate, and pronation and supination oblique views may increase this
sensitivity.
C. Patients with a history and clinical examination suggestive of fracture but nega-
tive initial radiographs should be treated empirically in a thumb spica splint
or cast, followed by repeat radiographs in 7 to 10 days. If repeat films are also
negative and the clinical suspicion for a fracture remains, further studies such
as computerized tomography (CT) or magnetic resonance imaging (MRI)
should be considered.
D. Assessment of fracture healing can also be problematic. CT scans are a valuable
adjunct obtained prior to the discontinuation of immobilization if union is in
question.
IV. Classification
A. Classification: Scaphoid fractures can be classified by location and chronicity, as

both have significant implications with regard to prognosis. Fracture pattern also
has some prognostic significance, as oblique or vertical fractures are known to be
more difficult to treat than their horizontal counterparts.
B. Scaphoid fractures are broadly considered unstable if
1. Fracture displacement of greater than 1 mm is present
2. Fracture angulation—scapholunate angle greater than 60 degrees (normally
30 to 60 degrees), or radiolunate or capitolunate angle greater than 15 degrees
(normally −25 to +10 and 0 to 15 degrees, respectively) is present and/or
3. Fracture comminution is present
4. the intrascaphoid angle is greater than 45 degrees, and
5. there is an associated intercarpal ligament tear (i.e., trans-scaphoid perilunate
fracture dislocation)
V. Treatment
The treatment of scaphoid fractures is dictated by the stability and anatomic location
of the fracture.
A. Stable distal pole fractures should be immobilized in a short- or long-arm
thumb spica cast for about 6 weeks, at which time radiographic union is often
observed.
B. Stable waist fractures can be managed in a long-arm thumb spica cast for
6 weeks followed by short-arm thumb spica casting for another 6 weeks or until
radiographic union is achieved. The long-arm cast prevents forearm rotation and
felt to decrease healing time.
C. Stable proximal pole fractures are difficult to treat in a closed manner, and may
require as long as 20 weeks to heal without operative intervention.
D. Stable fractures in which the diagnosis has been delayed but which do not dis-
play evidence of nonunion may be treated with a trial of cast immobilization.
E. Any fractures treated with immobilization should not be considered healed until
there is definite evidence of osseous bridging, which is best assessed with CT scan.

F. Unstable or displaced fractures typically require surgical fixation. Surgical

options include closed reduction and percutaneous pinning, closed reduction
and percutaneous headless compression screw fixation, and ORIF with a head-
less compression screw.
G. Distal pole fractures are best approached volarly, while proximal pole fractures
are best approached dorsally. Fractures of the waist of the scaphoid can be
approached from either dorsal or volar (or both). Union is most predictably
achieved with a single compression screw placed beneath the articular surface.
H. Arthroscopic assisted or open reduction may be required depending on displace-
ment and comminution. Primary bone grafting should be considered in com-
minuted fractures. Surgical fixation and bone grafting should be considered for
fractures not healed after 3 to 4 months of closed treatment.
I. Recently, surgical fixation of stable or nondisplaced scaphoid waist fractures has
been advocated, although to date the outcomes of nonoperative and operative
treatment of nondisplaced scaphoid fractures appear similar, with each method
having advantages and disadvantages.
J. With proper management, nearly 100% of distal pole fractures, 80% to 90% of
waist fractures, and 60% to 70% of proximal pole fractures go on to bony union.
Delay in diagnosis by more than 1 month is associated with a higher incidence
of nonunion.
VI. Fracture Nonunion
Due to several anatomic factors including a tenuous blood supply, scaphoid fracture
nonunion with or without development of AVN of the proximal pole is encountered
frequently in clinical practice.
A. Patients with fracture nonunion typically present with wrist pain with or without
a specific history of trauma.
B. Radiographically, nonunion is characterized by sclerosis, cyst formation, flexion
(humpback) deformity of the scaphoid due to the flexed posture of the distal
fragment, and dorsal intercalated segment instability (DISI) deformity of the
wrist in the more chronic cases. This change in carpal mechanics as a result of
scaphoid nonunion leads to a recognizable pattern of articular degeneration of
the wrist joint termed the SNAC (scaphoid nonunion advanced collapse) wrist.
C. Establishing the presence of proximal pole AVN can be difficult preoperatively.
Vascularity of the proximal pole can be assessed preoperatively with gadolinium-
enhanced MRI scans or intraoperatively by assessing the presence of punctate
bleeding from the proximal pole.
D. Symptomatic fracture nonunions can be treated with cancellous, corticocancellous,
or vascularized bone grafting in conjunction with internal fixation (headless
compression screw).
1. Nondisplaced nonunions can be treated with corticocancellous grafting from
a volar approach (Russe technique)
2. Displaced nonunions with a humpback deformity require the placement of
a corticocancellous volar wedge graft from a volar approach to correct the
humpback deformity.
3. For proximal nonunions or those in which the proximal fragment has devel-
oped AVN, volar grafting techniques are contraindicated. In the absence
of fragmentation and presence of structural integrity of the proximal pole

at the time of surgery, reconstruction in the form of ORIF and bone

grafting should be attempted. With the use of ORIF and conventional
bone grafts, only about half of scaphoid nonunions with proximal pole
AVN will go on to heal. Local vascularized bone grafts can be used
for the treatment of scaphoid nonunions complicated by AVN. The dis-
tal radius vascularized bone graft based on the 1,2 intercompartmental
supraretinacular artery is used commonly. Other grafts that have been
described include
a) A vascular pedicle originating from the second dorsal intermetacarpal vas-
cular bundle, which is directly implanted into the nonunion site.
b) Vascularized bone grafts from the distal radius based on a pronator
quadratus pedicle, among others. While vascularized bone grafting ini-
tially generated great interest, results of longer-term follow-up of non-
unions treated with this technique remain less than ideal.
c) Vascularized free graft from the medical femoral condyle
4. In the presence of fragmentation and absence of structural integrity of the
proximal pole at the time of surgery, salvage procedures such as fragment
excision with intercarpal arthrodeses, or proximal row carpectomy are typi-
cally recommended.
I. Carpal Instability
Carpal instability has been described in numerous fashions. It is important to under-

stand the traditional nomenclature of instability patterns as well as additional qualities/
descriptors that can assist in treatment decisions as Larsen et al. (1995) detailed.
A. Types of instability
1. Carpal instability dissociative refers to instability within a carpal row; sca-
pholunate or lunotriquetral ligament tears. This involves an intrinsic liga-
ment injury, and leads to counterrotation between the radial and ulnar
components of the carpal row.
2. Carpal instability nondissociative (CIND) occurs when the bones within
each carpal row are normally constrained but support has been lost either
between the rows or between a row and its neighboring structure (i.e., mid-
carpal instability). Extrinsic ligaments are most likely injured in this case.
3. Carpal instability complex incorporates each of the above elements and
denotes marked loss of ligamentous support (i.e., perilunate dislocation).
4. Carpal instability adaptive describes the unstable carpus occurring as a result
of pathology proximal or distal to the carpus itself (i.e., a malunited distal
radius fracture).
B. Degree of instability
1. Static: When the carpus is malaligned (i.e., scaphoid excessively flexed) on
resting radiographs, the ligamentous injury has likely compromised both pri-
mary and secondary restraints at a given joint.
2. Dynamic: When resting radiographs are normal but stress views demon-
strate intercarpal widening (i.e., scapholunate diastasis on grip radiograph) a
dynamic instability is diagnosed.
3. Predynamic: In the predynamic state, patients report pain or tenderness that
corresponds to an injured ligament but all imaging is normal (i.e., pain over
the scapholunate ligament but normal resting and grip radiographs).

C. Lunate posture
1. Dorsal intercalated segmental instability (DISI) refers to abnormal lunate
extension seen on lateral radiographs. This most commonly is associated with
scapholunate ligament tears, which free the lunate from the flexion moment
that the scaphoid imparts.
2. Volar intercalated segmental instability (VISI) describes abnormal flexion of the
lunate on lateral radiographs. This most commonly occurs with disruption of the
lunotriquetral ligament, which releases the lunate to flex with the scaphoid, and
can also occur with generalized ligamentous laxity leading to a CIND pattern.
3. Ulnar translocation and dorsal translocation of the carpus involve displace-
ment of the carpus as a unit with the lunate moving in the direction specified.
D. Force transmission
1. Greater arc injuries involve an arc of injury that is transmitted through, and
fractures, the involved carpal bone (i.e., trans-scaphoid perilunate dislocation).
2. Lesser arc injuries involved purely soft tissue injury and can disrupt multiple
ligamentous structures without fracture.
E. Chronicity
1. Acute (<1 week)
2. Subacute (1 to 6 weeks)
3. Chronic (>6 weeks): Primary ligament healing unlikely
F. Etiology
1. Traumatic
a) Indirect forces applied to the outstretched, extended hand are most com-
monly responsible for carpal instability.
b) Mayfield et al. (1980) described the accepted sequence of perilunar insta-
bility
1) Stage 1: Scapholunate ligament tear or scaphoid fracture
2) Stage 2: Capitolunate dissociation
3) Stage 3: Lunotriquetral ligament tear or triquetral fracture
4) Stage 4: Dislocation of the lunate
2. Nontraumatic (i.e., chronic inflammatory arthritic degeneration as in rheu-
matoid arthritis)
II. Diagnosis
A. History: Patients with carpal instability can present with wrist pain, weakness,
or loss of motion. Some experience a high energy trauma to the upper extremity
while others with subtle instability often recount a lower energy injury that may
have involved a seemingly benign fracture (Chauffeur-type, or distal radius styloid
fracture).
B. Physical examination: A detailed wrist examination is performed bilaterally as
the asymptomatic wrist offers an excellent control for the comparison of motion,
joint laxity, and symptoms produced on provocative testing (up to 20% of
asymptomatic wrists demonstrate a clunk on scaphoid shift test).
1. Inspection for malalignment or signs of acute trauma (swelling and
ecchymosis).
2. Assess forearm, wrist, and digital motion. “Clicks” or crepitus should always
be correlated with pain reproduction.
3. Note degree of ligamentous laxity (i.e., elbow/digit hyperextension).

4. Grip and pinch strength

5. Palpate ligaments of wrist
6. Selective provocative testing
a) Scaphoid (Watson) shift test (for scapholunate ligament tear)
1) Place examiner’s thumb on the palmar surface of the patient’s distal
pole of the scaphoid
2) Place the examiner’s index finger over the dorsal surface of the
scapholunate joint
3) Passively move the patient’s wrist from ulnar deviation to radial deviation
while applying a dorsally directed force on the distal pole of the scaphoid
4) A positive response is dorsal pain with detection of dorsal subluxation
of the proximal pole of the scaphoid.
b) Lunotriquetral shuck (Regan and Linscheid): Grasp the pisotriquetral
column between the examiner’s thumb and index finger with one hand,
and stabilize the lunate with the other hand. Translate the pisotrique-
tral column anteriorly and posteriorly, estimating the magnitude of
translation.
c) Lunotriquetral shear (Kleinman): Grasp the pisotriquetral column
between the examiner’s thumb and index finger with one hand and pas-
sively move the wrist through radial/ulnar deviation with the other, look-
ing for assymetrical displacement patterns of the triquetrum.
d) Lunotriquetral compression (Linscheid): Apply compression (medial to
lateral) across the LT joint, assessing for pain.
e) Lichtman test: To diagnose midcarpal instability, axial compression is
applied to the hand and the wrist is brought from radial deviation into
ulnar deviation. As this occurs, the proximal row produces a clunk as it
rapidly attains the extended posture that it failed to gradually obtain dur-
ing the motion (“catch up” clunk).
III. Imaging
A. Imaging is helpful, but must be interpreted carefully, knowing that a spectrum

of normal conditions exist.
1. Posteroanterior and lateral radiographs of the wrist are absolutely necessary, and
most useful when combined with comparison views of the contralateral wrist.
2. Both must be taken in a standard position, such that the third metacarpal is
collinear with the longitudinal axis of the radius.
3. Calculation of specific angles on lateral radiographs can be determined by
use of the axis of the specific carpal bone as demonstrated in Figure 14.1 and
Table 14.1.
B. On the PA radiograph (in neutral radial-ulnar deviation and with the hand and
wrist flat on the x-ray plate), one should look for the disruption of Gilula lines,
defined as the normally continuous arches created by connecting the images of
the subchondral lines of the proximal surfaces of the proximal carpal row, the
distal surfaces of the proximal carpal row, and the proximal surface of the distal
carpal row.
1. Gaps between adjacent bones may be significant if asymmetrical.
2. Additionally, dynamic changes may be created with motion of the wrist or
application of load through grip.

A B
C
C D
Scapholunate
Angle
Radioscaphoid
Angle
E F
Figure 14.1 Method for determining carpal angles from lateral radiograph: A: The scaphoid
is outlined along the volar aspect with a line between the most volar portion of the proximal
and distal poles. B: The axis of the lunate is determined by a line perpendicular to the line
connecting the dorsal and volar distal aspects. C: The axis of the capitate is determined by
a line connecting the center of the proximal and distal articular surfaces. D: The radius
is determined by a line perpendicular to its distal third. Commonly used carpal angles:
E: Scapholunate F: Radioscaphoid. (Reprinted with permission from Glickel SZ, Barron
OA, Catalano LW III. Green’s Operative Hand Surgery, 5th Ed. Philadelphia, PA: Elsevier,
Churchill Livingstone; 2005, Fig. 14–12, p. 537.)

TABLE 14-1 Normal measurements for intercarpal angles
Joint Normal Standard Deviation

Relationship (degrees) (degrees)
Radiolunate 0 ±10
Radioscaphoid 47 ±32
Scapholunate 47 ±32
3. Other imaging may be of use on a case-specific basis, including arthrography,

MRI (with or without a gadolinium arthrogram component), live fluoros-
copy, radionuclide scintigraphy, and ultrasound.
C. Arthroscopy offers a unique opportunity for evaluation of the status of the car-
pus and, most typically necessitate observation in both the radiocarpal and
midcarpal joints. Geissler et al. (1996) have devised a classification scheme
(Table 14.2) based upon the midcarpal appearance of the proximal row joint
clefts and have correlated these features with grades of ligament disruption.
Care must be taken, however, to view these findings in the light of normal
laxity.
D. Computed tomography may identify subtle avulsion fractures.
E. MRI is of variable sensitivity and specificity for identifying carpal ligamentous
injury with usefulness that varies both with the quality of the scanner and inter-
pretive experience of the surgeon and radiologist.
F. MRI arthrography may increase the test’s accuracy.
TABLE 14-2 Arthroscopic classification for intercarpal (scapholunate and

lunatotriquetral) ligament injuries
Scapholunate Interosseous
Ligament Status Congruity
Geisler (Radiocarpal Joint (Midcarpal Standard Probe Behavior
Grade Perspective) Perspective) (Midcarpal Perspective)
I Hemorrhage, No step-off Probe not admitted into SL
otherwise intact or LT joint cleft
II Torn, disrupted Slight step-off Probe admitted into SL or
LT joint cleft, but cannot
be twisted
III Torn, disrupted Step-off Probe admitted into SL or
LT joint cleft and can be
wrist 360 degrees
IV Torn, disrupted Step-off and “Drive through” lesion—a
static gap 2.7 mm arthroscope can
be passed between the
radiocarpal and midcarpal
joint through the joint cleft

IV. Scapholunate Dissociation
A. Scapholunate dissociation (SLD)

1. Dissociation of the scaphoid and lunate represents the most common form
of carpal instability.
2. This injury occurs most commonly as the result of axial loading in a wrist
positioned in dorsiflexion, ulnar deviation, and intercarpal supination.
3. Patients often have pain over the scapholunate ligament palpated 1 cm
distal to Lister tubercle. The Watson shift test may be positive in acute
cases.
4. Once uncoupled, the scaphoid tends to excessively flex and the lunate extends
(DISI) resulting in an increased scapholunate angle and a “cortical ring sign”
on a PA radiograph as the distal scaphoid is now being imaged in line with its
longitudinal axis. Additionally, radiographs may show a diastasis greater than
3 mm between the scaphoid and lunate, implying dorsal intercarpal ligament
separation from the lunate.
5. Power grip radiographs may identify dynamic instability produced by rupture
of the scapholunate interosseous ligament with preservation of secondary
stabilizers.
6. Chronic scapholunate diastatis produces progressive arthritic degeneration
termed scapholunate advanced collapse (SLAC).
a) Stage 1: arthritis at the radial styloid
b) Stage 2: arthritis of the entire scaphoid fossa of the distal radius
c) Stage 3: arthritis of the capitolunate articulation
7. Treatment
a) Acutely diagnosed tears of the scapholunate interosseous ligament are
treated surgically. A dorsal ligament repair through bone tunnels or with
suture anchors can be performed and supplemented by K-wire fixation of
the scapholunate and scaphocapitate joints. Generally, protective fixation
is maintained for 2 to 3 months.
b) Partial tears not responding to conservative treatment may be debrided
arthroscopically.
c) Chronic injuries are generally less amenable to direct ligament repair and
are approached with either a dorsal capsulodesis (especially with dynamic
instability, but less reliably in cases of fixed instability), a tenodesis (such
as the Brunelli reconstruction using the FCR), bone-ligament-bone
reconstruction, or limited carpal arthrodesis (i.e., scaphotrapezial and
scaphocapitate).
d) Once arthritic changes are present at the radial syloid-scaphoid joint,
a radial styloidectomy may be considered (Stage 1 SLAC) while more
advanced arthritis often necessitates proximal row carpectomy, scaphoid
excision and four corner fusion, total wrist fusion, or total wrist arthro-
plasty.
B. Specific x-ray findings
1. It is important to recognize that dynamic SLD may appear normal under
standard static x-ray examination.
2. Motion series or grip views of the wrist may unmask a dynamic subluxation
of the scaphoid or a diastasis between the scaphoid and the lunate. Fluoros-
copy may also be useful to detect dynamic instability patterns.

TABLE 14-3 Treatment for scapholunate ligament injuries based on

arthroscopic grading
Geisler Grade SLAC

I II III IV I II III
Pins + (1) + (1) + (2) + (2)
Direct repair + (3) + (3) + (4)
Reconstruction + (2) + (3) + (4)
Augmentation + (5) + (5) + (5,6) + (5,6)
Partial arthrodesis + + (7) + + +
Salvage + (7) + +
3. As the severity of the dissociation increases, more static changes can be

detected radiographically.
4. The scaphoid can assume a more flexed (or vertical) posture. This results in
an increasingly exaggerated radioscaphoid and scapholunate angle on lateral
radiographs.
a) The scaphoid will appear foreshortened in a PA x-ray, and a “cortical ring
sign” may appear where the cortex of the vertical scaphoid appears more
radiodense.
b) In advanced SLD, the lunate may be extended in an otherwise neutrally
positioned wrist, and the carpus may have collapsed height due to the
capitate migrating proximally and dorsally on the extended lunate.
5. The lunate may be excessively ulnarly translated, where over 50% of the
proximal surface may be located ulnar to the level of the lunate fossa.
C. Treatment (Table 14.3)
1. Optional
2. As part of additional procedure
3. Only if scapholunate relationship is easily reducible
4. Accompanied by very limited radial styloidectomy, if painful
5. Some prefer adding capsulodesis to any approach for SLD
6. Higher-grade SLD treatment may be augmented with the insertion of a
headless screw across the scapholunate joint (Reduction and Association of
Sacphoid and Lunate (RASL) procedure) or dorsal ligamentoplasty using a
strip of tethered dorsal intercarpal ligament.
7. If scapholunate relationship is difficult to reduce
V. Lunotriquetral Dissociation
A. Lunotriquetral dissociation
1. Lunotriquetral ligament injuries occur less commonly than scapholunate
ligament injuries and occur as a result of a fall axial loading in a wrist posi-
tioned in dorsiflexion, radial deviation, and intercarpal pronation.

2. Patients may present with pain on the ulnar side of the carpus and demonstrate
positive provocative signs as described previously.
3. Radiographs may be normal or demonstrate a VISI posture of the lunate.
More subtle findings may include the disruption of Gilula lines.
4. Wrist arthroscopy greatly aids in diagnosing lunotriquetral injuries with the mid-
carpal portals allowing a clear assessment of any dissociation between the bones.
5. Lunotriquetral ligament injures have been treated in a variety of fashions.
The ligament has been repaired, reconstructed, and the lunotriquetral articu-
lation arthrodesed. Shin et al. (2001) reported superior results for ligament
repair and reconstruction compared to arthrodesis.
Dynamic instability, which by definition requires provocation to be prob-
lematic, most likely occurs with disruption of only the lunatotriquetral ligament.
Static instability, which has fixed radiographic features of scaphoid and lunate
flexion and/or triquetral dorsiflexion (VISI deformity) implies lunotriquetral
ligament disruption and dissociation of the dorsal radiocarpal ligament from
the lunate.
B. Diagnosis
1. Examination
In advanced cases, there may be subluxation of the ulnar aspect of the wrist
relative to the forearm. Pain and tenderness in the region of the lunotrique-
tral joint are nearly universally present. This region can be easily located by
palpating the dorsal tubercle of the triquetrum distal to the dorsal promi-
nence of the ulnar head. It is possible many times to aggravate the symptoms
of LTD with one or more provocative maneuvers described previously. Each
maneuver should be carried out as a comparative examination between the
symptomatic and asymptomatic contralateral wrist.
a) Lunotriquetral shuck
b) Lunotriquetral shear
c) Lunotriquetral compression
2. Specific x-ray findings
It is important to recognize that dynamic LTD may appear normal under
standard static x-ray examination. Motion series or grip views of the wrist
may unmask a dynamic shift between the lunate and the triquetrum. Fluo-
roscopy may also be useful to detect dynamic instability patterns. As the
severity of the dissociation increases, more static changes can be detected
radiographically. It is difficult to detect changes in the orientation of the tri-
quetrum in standard PA and lateral radiographs due to its shape and lack of
easily recognizable landmarks. In advanced LTD, the triquetrum may appear
statically shifted distal to the lunate. A disastasis between the lunate and the
triquetrum is not likely to be seen. The lunate may be volarflexed in an oth-
erwise neutrally positioned wrist.
C. Treatment
The treatment algorithm below can serve as a guideline for treatment, but
patient conditions and surgeon preferences are currently the most important
factors (Table 14.4).
1. Optional
2. As part of additional procedure
3. Only if lunotriquetral relationship is easily reducible
4. If lunotriquetral relationship is difficult to reduce

TABLE 14-4 Treatment for lunatotriquetral ligament injuries based on

arthroscopic classification
Geisler Grade
I II III IV
Pins + (1) + + (2) + (2)
Direct repair + (3) + (3)
Reconstruction + (3) + (3)
Partial arthrodesis + + (4)
Salvage + (4)
VI. Perilunate Dislocation
A. Perilunar instability
1. Resulting from high-energy trauma, perilunate instability involves the rup-
ture of multiple ligaments and can result in the frank dislocation of the lunate
(generally volarly, preserving the short radiolunate ligament).
2. Perilunate dislocations are named according to the direction of the displaced
carpus with dorsal perilunate dislocations being the most common. In peri-
lunate dislocations, the lunate remains in its radius fossa whereas in lunate
dislocations the lunate itself is dislocated.
3. Up to 25% of perilunate dislocations may be missed during initial
evaluation.
4. Patients generally present with grossly swollen hands. Lateral radiographs
most readily identify the carpal pathology.
5. Initial treatment consists of closed reduction combining axial traction, wrist
extension, and a thumb stabilizing the volar lunate before flexing the hand
back over the lunate to reduce the dorsal perilunate dislocation. Patients
should be examined for signs of acute carpal tunnel syndrome.
6. Acute injuries are then treated through either dorsal or combined dorsal and
volar approaches with K-wires placed across the scapholunate, scaphocapi-
tate, and lunotriquetral joints. Capsular-ligamentous ruptures and the
scapholunate/lunotriquetral ligaments may be repaired. Fixation is generally
maintained for 10 to 12 weeks.
7. Greater arc injuries including the trans-scaphoid perilunate dislocation are
ideally treated with ORIF of the fractured carpal bone in conjunction with
necessary K-wire fixation of ruptured ligaments. However, when commi-
nuted, contaminated by open wounds, or when occurring in older individuals,
proximal row carpectomy or wrist fusion may best serve the patient.
VII. Midcarpal Instability
A. Often atraumatic, midcarpal instability may present with painful clunking when
radial/ulnarly deviating the wrist, decreased motion, weakness, or an ulnar-sided
midcarpal sag.

B. More likely to be seen in association with chronic laxity, patients are initially
treated with NSAIDs, immobilization, activity modification, and steroid
injections.
1. Failing conservative management, operative options include capsulodesis or
limited wrist arthrodeses (triquetrohamate or four corner).
2. When midcarpal collapse occurs secondary to a distal radius malunion, a
corrective osteotomy of the radius generally results in good outcomes.
VIII. Axial Carpal Dislocations
A. These injuries longitudinally disrupt the carpus and are the result of severe, high-
energy injuries such as crush or blast injuries.
B. Axial dislocations are classified by the direction of instability (axial-ulnar, axial-
radial, combined).
C. Treatment consists of debridement of nonviable tissue and K-wire fixation of the
injured structures. Outcomes are most closely linked to the severity of associated
nerve, artery, and tendon injuries.
Radiocarpal Dislocations
Radiocarpal dislocations refer to entities in which the carpus, namely, the proximal car-
pal row, dissociates from the distal radius. Radiocarpal dislocations are usually the result
of high-energy injuries and are frequently associated with small avulsion fractures off
of the distal end of the radius. This is an uncommon injury, with fewer than 100 cases
reported. The dislocation can be in volar or dorsal direction and is associated with con-
comitant intercarpal ligament injuries. Early detection and treatment are necessary to
avoid neurovascular complications and late wrist dysfunction.
I. Anatomy (see section at beginning of this chapter)
II. Diagnosis
History: The history obtained by someone who has sustained a radiocarpal dislocation
is usually fairly straightforward. Radiocarpal dislocations occur as a result of high-energy
injuries. The position of the hand, the position of the forearm, and the direction of the
force applied to the hand determine the shear force that is applied to the distal radius. If the
shear force is significant enough to fracture elements of the distal radius that contain the
extrinsic ligamentous attachments to the carpus, then a radiocarpal dislocation can occur.
III. Examination
A gross deformity is usually present in patients with radiocarpal dislocations as the

alignment and relationship of the carpus relative to the radius is distorted. Since patients
with radiocarpal dislocations have sustained a high-energy injury, it is essential to look
for associated injuries of the hand or upper extremity. It is very important to ensure that
there is no vascular compromise and a neurological exam is done to identify peripheral
nerve injuries. All of these findings on examination should be clearly documented so
that they can be compared to postoperative exam assessments. It is frequently difficult

to make any assessment of wrist range of motion due to significant pain at the time of
injury. With complete radiocarpal dislocations, range of motion is frequently minimal.
Digital motion, however, should be accurately assessed.
IV. Radiographs
Radiographic findings in radiocarpal dislocations are significant. There is malalignment

of the carpus relative to the distal radius, with the lunate translated in an ulnar direction
following reduction of the dislocation. The AP view or PA view frequently shows overlap
of the carpal elements with the radius proximally as the carpus is in a proximal position
relative to the radius. On the lateral x-ray, the malposition of the carpus is seen fre-
quently. Carpal elements are in a palmar or dorsal position. The colinearity between the
radius, lunate, and capitate is disrupted. Frequently, small avulsion fractures off the volar
or dorsal rim of the radius are seen. These fragments are significant in that the ligamen-
tous elements that stabilize the radiocarpal joint are contained on these fragments.
V. Classification
In the Mayo Clinic Classification scheme, radiocarpal dislocations without associated

intercarpal pathology are CIND types, carpal instability—non-dissociative. In the
Fernandez Classification of distal radius fractures, radiocarpal dislocations are Type IV.
These are avulsion fractures with radiocarpal dislocations. In the Universal Classifica-
tion, radiocarpal dislocations are frequently IV-D injuries.
VI. Treatment
Radiocarpal dislocations are unstable injuries even if radiocarpal alignment can be

achieved with closed reduction. Some authors and surgeons advocate closed reduc-
tion and immobilization; however, these injuries may frequently remain unstable. The
first line of treatment is the restoration of radiocarpal alignment. Reduction should
be achieved as quickly as possible. Splint immobilization and compressive dressing to
control edema should be applied. Once reduction is achieved, postreduction radio-
graphs are obtained. Unrecognized avulsion fragments, or any additional occult frac-
tures that may not have been recognized on initial injury radiographs, are identified.
Despite anatomic reductions, these injuries are unstable and operative stabilization is
recommended. If large fracture fragments are present, traditional screw and/or buttress
plating methods are appropriate. Frequently fracture fragments are small and creative
techniques for operative intervention usually need to be considered. Small, independent
screws and wiring techniques are frequently necessary to stabilize these elements. Rarely,
pure ligamentous injuries occur and techniques to reattach ligament avulsions using
wire techniques and/or suture anchors can be employed.
VII. Summary
Radiocarpal dissociation is an infrequent condition that is seen posttraumatically. Both volar

and dorsal radio-carpal dislocations can occur. They are frequently associated with distal
radial rim avulsion fractures that contain extrinsic dorsal and volar wrist ligament origins.
Recognition of these injuries is important to prevent neurovascular compromise and late
radiocarpal arthrosis. Prompt reduction and operative stabilization are recommended.

Triangular Fibrocartilage
I. Introduction
Patients will present with ulnar-sided wrist pain after acute injuries, subacutely after
trauma or changes in avocational or vocational activities and frequently will present
with complaints that develop insidiously without any inciting or preexisting event.
The differential diagnosis for lesions that cause ulnar-sided wrist pain is extensive
(Table 14.5).
II. Anatomy of the TFCC
A. The DRUJ is a synovial joint.

B. Minimal bony constraints.
TABLE 14-5 Differential diagnosis of ulnar sided wrist pain
Location Diagnosis
Extra-articular ECU Tendonitis
ECU instability
DSBrU neuritis
Space occupying lesions
Periarticular Impaction
Impingement
TFC tears
ECU subsheath
Disc-carpal ligament injuries
LT ligament injuries
synovitis
Articular DRUJ arthrosis
DRUJ instability
LT arthrosis
CMC (hamate/metacarpal)
Piso-triquetral arthrosis
Hamate arthrosis
midcarpal instability
Loose bodies
Ulnar chondrosis
Lunate chondrosis
Lunatomalacia (Kienbock’s)

C. Rotational as well as translational movement of the radioulnar articulation.

1. Translation in a dorsal volar as well as proximal distal plane.
D. Bony elements of the joint do not provide stability so, therefore, stability is pro-
vided by the surrounding soft tissue elements.
E. TFCC refers to soft tissue elements that surround and stabilize the DRUJ. TFC
is a wedge-shaped disk of fibrocartilage that has a very dense cartilaginous attach-
ment along the sigmoid notch of the radius (Fig. 14.2).
1. Histologic studies show that the articular disc is relatively avascular.
a) Peripheral (ulnar) attachment of the TFC is richly vascularized.
b) Vascularity diminishes as one progresses from the ulnar to the radial side.
2. Dorsal radioulnar ligaments (DRUL) and volar radioulnar ligaments (VRUL)
bridge the sigmoid notch to the fovea of the ulna
a) Dorsal and palmar thickenings of the TFC
b) Complex attachment to the distal ulna
1) Superficial component to the midpoint of the styloid
2) Deep attachment to the fovea (Fig. 14.3)
3. Disc-carpal ligaments (Fig. 14.3)
a) Thickened areas of the wrist capsule
b) Extend distally to attach to carpal elements
c) Ulno-lunate and ulno-triquetral ligaments
d) Names of these ligaments are misnomers since the ligamentous attach-
ment emanates from the limbus and not from the ulna
e) Discrete named capsular thickenings are not present dorsally
F. TFCC
1. TFC plus other elements
a) VRUL and DRUL
b) Disc-carpal and ulno-capitate ligaments
c) Meniscal homologue
1) Function is ill defined
2) Vascularized tissue between the ulnar capsule, TFC, and triquetrum
d) ECU tendon
e) Subsheath of the ECU
Central TFC
TFC Superficial Portion
(styloid insertion)
TFC Deep portion

Ligamentum
Subcruentum
(foveal insertion)
Figure 14.2 TFCC showing superficial and deep components of radioulnar ligaments
and central articular disc (TFC).

Disc-carpal Triquetrum
ligaments
TFCC Lunate
superficial portion
(styloid insertion)
Ligamentum subcruentum
(foveal insertion)
Ulna Radius
Figure 14.3 Foveal (deep) attachment of TFCC and disc carpal ligaments.
1) Intimate with the dorsal ulnar aspect of the TFC

2) Tears of this subsheath are frequently encountered with peripheral
TFC tears
III. Diagnosis
A. History
1. May be a sudden, rotational traumatic event that brought on the pain.
a) Racquet sports with sudden, abrupt supination
b) Baseball players will associate their pain during hitting
c) High-speed vehicular injuries associated with a forceful twisting of the
forearm, usually in association with gripping or grasping of a steering
wheel.
2. May be insidious and non-traumatic.
a) Pain with activities that require forearm rotation
1) Gripping and twisting doorknobs or trying to open lids on jars.
b) Described as deep, aching discomfort.
c) It is usually activity related.
d) It may be associated with mechanical elements such as locking, clicking,
or catching.
e) Firm gripping activities are painful, especially in patients with dynamic
ulnar impaction.
B. Examination
Examination of the ulnar wrist is best performed with the patient seated on the
opposite of a table on which they can rest both of their elbows with their hands
up toward the ceiling. This position enables the examiner to access all parts of
the affected wrist and the normal. It enables the examiner to place the wrist
in any position of forearm rotation. It enables the examiner to examine, for
comparison, the opposite, uninvolved wrist.
1. Inspection

a) Usually there is no visible deformity.

b) Subtle fullness or swelling about the ulnar wrist may be identified.
c) Visible swelling may be evident in patients with synovitis of the ulno-carpal
joint.
2. Palpation
a) Most important element of the examination.
b) Essential to accurately localize the area of maximal tenderness.
1) Many anatomic elements in close proximity
c) Prior to palpation, the patient is asked to localize the area of maximal
tenderness with a single finger or a small object such as a pencil eraser.
d) Examiner palpation follows the patient’s identification of maximal
tenderness.
1) Pisotriquetral articulation
2) Lunotriquetral articulation
3) Soft tissue elements
a. ECU
b. Dorsal sensory branch of the ulnar nerve
4) Foveal tenderness
a. Most common finding in patients with TFC pathology (Berger).
b. Soft spot on the ulnar side of the wrist between the FCU and
ECU.
i) The only structure that is deep to the examiner’s finger is the
ulnar capsule and just below this is the TFC.
c. Different components of the TFC can be brought to the examiner’s
finger by varying the position of forearm rotation (dorsal portion
delivered with the forearm in pronation, volar portion with the
forearm in supination).
3. Provocative maneuvers
a) Assess stability of the DRUJ.
1) TFC lesions frequently not associated with instability
2) Solid DRUJ at the extreme of pronation and supination
a. Symmetric to the opposite side.
b. Midrange instability is normal, but should be symmetric.
c. If provocative tests for instability reproduce discomfort, it is likely
that TFC pathology is present.
d. Ulnocarpal stress test (rotation while wrist positioned in ulnar
deviation) suggestive of TFC pathology (ulnocarpal impaction).
e. Rule out coexisting pisotriquetral or lunotriquetral abnormalities.
i) Pisotriquetral shear maneuver
ii) Lunatotriquetral shear maneuvers
Positive responses to these provocative tests may indicate coex-
isting pathologies.
f. ECU instability.
i) ECU should be stable within the groove
ii) Forearm rotation with the wrist flexed will elicit ECU
instability
C. Imaging
1. Plain x-rays
a) Initial screening tool
b) Standard: PA neutral forearm zero rotation view (Fig. 14.4)

Zero PA Zero Lat.
A B
Figure 14.4 Proper technique for obtaining zero rotation radiographs to assess the ulnar
variance. A: PA view is obtained with shoulder abducted to 90 degrees and elbow flexed
90 degrees. B: Lateral is obtained with shoulder adducted and elbow flexed 90 degrees.
1) Details of the DRUJ

2) Ulnar variance
a. Ulnar positive: Higher incidence of ulnar impaction and TFC tears.
b. Static zero rotation views give a baseline measurement of ulnar
variance.
c. Grip zero view for dynamic ulnar impaction (Freidman and Palmar).
d. Assess the morphology of the volar ulnar portion of the lunate as
patients with chronic ulnar impaction can have significant abnor-
malities (Fig. 14.5).
D. Advanced imaging
1. In the majority of cases, a diagnosis can be made based on history, physical
examination, and plain radiography. From these, a treatment plan can be for-
mulated. Occasionally the diagnosis remains questionable or unclear or the
differential diagnosis contains many elements and more advanced imaging is
necessary.
2. MRI evaluation of the ulnar wrist (with or without intravenous or intra-
articular administration of contrast medium) can provide imaging of the soft
tissue elements of the TFCC. An MRI with a gadolinium-enhanced arthro-
gram can provide data regarding perforations or tears of the TFC that allow
fluid flow. Many studies have shown that there are asymptomatic patients
with perforations and tears so that all findings diagnosed with advanced imag-
ing techniques MUST be correlated with historical and physical findings.
MRI has been useful in diagnosing partial deep tears of the fibrocartilage and
impaction lesions of the lunate. It can also help distinguish impaction lesions
from osteonecrosis.
3. Plain arthrography, three-compartment cinearthrography, plain tomography,
computed tomography, and computed tomography coupled with arthrogra-
phy are imaging techniques that do not provide much diagnostic value when
compared with MR arthrography.
E. Arthroscopy
1. Useful as an adjunct to history and physical examination
a) Considered both diagnostic and therapeutic.
b) Arthroscopy can confirm and quantify lesions of the articular disk.

Figure 14.5 Plain radiograph (A) and (B) MRI demonstrating changes in lunate
consistent with ulnar carpal impaction—note the lucency in the proximal ulnar aspect
of the lunate and corresponding changes on MRI.

c) Detects peripheral tears of the TFC.

d) Detects lesions of the disk-lunate and disk-triquetral ligaments.
e) Quantifies extent of lunate impaction cartilage defects.
f) Identification and treatment of intra-articular loose bodies.
g) Treatment at time of arthroscopy: Repairs, debridements, and tissue
ablation.
F. Classification
In 1989, Palmer proposed a classification scheme for disorders of the TFC. The
basis of this scheme splits disorders of the TFC into traumatic (Type I) and
atraumatic (Type II) lesions.
A. Type I: traumatic (Fig. 14.6)
a) 1A: Central lesions
b) 1B: Peripheral tears with or without an associated styloid fracture
c) 1C: Volar or distal
d) 1D: Sigmoid notch (radial) avulsion with or without an associated sig-
moid notch fracture
B. Type II: Acquired lesions with a progression of degenerative change
a) 2A: TFC wear but no TFC tear
b) 2B: TFC wear with lunate or ulnar head chrondromalacia.
c) 2C: 2B with a TFC perforation
d) 2D: 2C with ulnocarpal arthrosis
G. Treatment
1. Type I TFC Lesions
a) In general, traumatic lesions that do not have instability can usually be
treated conservatively initially. Long-arm splinting with the forearm in a
semisupinated position is recommended with repeat clinical evaluation
after about 4 to 6 weeks of conservative care. With symptom resolution
and clinical improvement, conservative care can be continued; however,
if symptoms persist and clinical findings on examination are still present
then proceeding to operative intervention with proposed repair of injured
structures can be done.
1C
1D
1B
1A
Figure 14.6 Location of traumatic (Type I) TFCC lesions: 1A—central tear,

1B—peripheral tear along ulnar insertion into fovea, 1C—tear of ulno carpal ligaments,
and 1D—tear of radial attachments at region of sigmoid notch.

TABLE 14-6 Diagnosis and treatment for TFCC injuries
Lesion Symptoms Treatment

1A • Pain, mechanical clicking Debridement of torn, irregular por-
tion of articular disk to stable rim.
Usually arthroscopic.
1B • Painful forearm rotation Arthroscopy frequently confirms
diagnosis
• Large tears may be asso- Arthroscopic repairs (small tears)
ciated with instability Open repairs—Large tears
• May be associated with
—Subsurface tears
styloid fracture
—Large styloid fracture
1C • Least frequent Open/arthroscopic repair
• Painful rotation
• May be associated with
1B tear
1D • May be associated with Open/arthroscopic repair
distal radius fracture Consider debridement for small
• May include both radioul- tears
nar ligaments
• Tear is in the avascular
zone of TFC
b) Acute traumatic lesions with instability can be managed conservatively

if the DRUJ and the ulnocarpal relationship can be reduced absolutely
concentrically. Patients with these lesions should be managed with
long-arm casting with their forearm held fully supinated. It is impera-
tive to ensure a concentric reduction during immobilization. Patients
should be cautioned that despite a period of conservative care, persistent
symptoms of pain and instability are possible and delayed operative inter-
vention may still be recommended. After casting is completed, a 6-week
period of long-arm splinting with gradual return to activities is recom-
mended. If patients do experience pain following immobilization and
gradual return to activities, then operative intervention and stabilization
are recommended.
Recommendations for the treatment of traumatic (Type I) lesion of
the TFC that continue to be symptomatic despite conservative treatment
are summarized in Table 14.6.
2. Type II lesions
Patients usually present with an insidious pattern of symptom onset.
a) Conservative treatment
1) Activity modification.
2) Elimination of offending activities.
3) Long-arm splinting to control forearm rotation.
4) Wrist immobilization splints that do not control forearm rotation may
not be effective.

5) Elastic compression strap may help, especially in working patients

who may fi nd full-time long-arm splinting cumbersome and
impractical.
6) Steroid injections: Diagnostic and therapeutic (usually temporary
relief )
a. Most useful in clinical situations with associated synovitis
b) Arthroscopy
1) Essential adjunctive tool in treatment of Type II and chronic Type I
injuries.
2) Better visualization of the entire articular disk than one sees with an
open, ulnocarpal approach.
3) Allows visualization of the entire proximal carpal row.
4) Allows visualization of interosseous and extrinsic ligaments that is not
seen with arthrotomy.
5) Operative arthroscopy is especially useful for the Type II lesions.
c) Arthroscopic treatment
1) Once conservative measures have failed, arthroscopic management is
recommended.
a. Central tears of the TFC (avascular zone) can be debrided using
i) Mechanical small joint arthroscopic shavers
ii) Suction punches
iii) Radiofrequency ablation probes
iv) Laser ablation devices.
b. Coexisting pathology can be addressed
i) Removal of loose bodies
ii) Debridement of fragmented, unstable cartilage 3. Lesions of the
proximal carpal row can be evaluated and treated
iii) Debridement/repair interosseous ligaments lesions
iv) Decision regarding adjunctive treatment (open vs. arthroscopic)
H. Joint levelling
In the ulnar neutral or ulnar negative variant, debridement and/or repair of the
TFC tear and addressing adjunctive pathology is associated with good clinical relief
of symptoms. However, in the patient with ulnar positive variance, either static or
dynamic, concomitant ulnar variance needs to be addressed. Less-favorable results
have been noted in patients with TFC tears and ulnar positivity that have not had
their ulnar variance addressed. Correction of ulnar variance is the recommended
treatment in patients with ulnar impaction in the absence of a TFC tear.
1. Options for correcting ulnar variance
a) Open limited distal ulnar head resections (wafer procedure)
b) Arthroscopic wafer procedure
c) Arthroscopic distal ulnar resection can be performed through a central
TFC tear
d) Open diaphyseal ulnar shortening
e) Distal osteochondral closing wedge shortening
I. Summary
Lesions of the TFC and associated components are common causes of ulnar-
sided wrist pain. A directed history and focused physical examination lead to
the majority of diagnoses. Basic and advanced imaging techniques are adjuncts.
One should develop familiarity with arthroscopic techniques as many lesions
of this complex structure are successfully treated using these techniques.

Distal Radioulnar Joint
I. Anatomy of the DRUJ
The DRUJ comprises the distal ulna and radius articulating at the concave sigmoid
notch of the radius with the convex ulnar seat. The sigmoid notch articulates with
60 to 80 degrees of the ulna’s 230 degrees articulating portion of the head in midrange,
but less than 30 degrees of the head in the extremes of pronation and supination. The
sigmoid notch is cartilage covered and continuous with the lunate facet of the radius.
These two surfaces are separated by the TFC attachment to the radius.
The TFC attaches to the ulna styloid near the base. The ulnocarpal ligament com-
plex (lunocapitate, ulnolunate, and ulnotriquetral ligaments) attaches at the ulnar styloid
hilar area and to the volar surfaces of the lunate and triquetrum. The DRUL and VRUL
run along the edges of the TFC and are the two main stabilizers of the DRUJ. Secondary
stabilizers include the pronator quadratus muscle and the interosseus membrane. The
TFC, the ulnocarpal ligament complex, the DRUL and VRUL, the ECU tendon sheath
and subsheath, and the meniscus homologue all make up the “TFCC” (Fig. 14.7).
II. ECU Tendon Dislocation/Subluxation
A. The ECU tendon originates at the lateral epicondyle and mid–third of the
dorsum of the ulna and inserts on the dorsum of the base of the fifth metacarpal.
It runs in a grove along the dorsal ulnar aspect of the ulna and through the sixth
extensor compartment.
B. The tendon normally acts to extend and ulnarly deviate the wrist. The ECU has
some normal play in the ulna groove and a painless snapping sensation is not
Ulnar carpal
ligament
ECU in
sheath
Central
TFC
Ulna
Radius
Figure 14.7 Anatomy of DRUJ and stabilizing structures (TFCC).

necessarily pathologic. The sixth compartment can become torn as a result of

blunt or twisting trauma and this “snapping sensation” can become much more
exaggerated and painful.
C. On physical examination, the patient should be point tender to the sixth exten-
sor compartment, may have swelling, and ulnar deviation of the wrist with the
forearm in supination that will reproduce the painful subluxation or dislocation
of the tendon.
D. Treatment in the acute setting should include 6 weeks of bracing or casting in
a pronated/radially deviated position to allow healing of the tendon sheath. If
this fails or the process is already chronic, then the primary surgical option is to
create a new stabilizing loop of tissue using a flap of extensor retinaculum.
III. Volar Ulnar Dislocation of the DRUJ
A. Volar dislocations occur less often than dorsal dislocations and are the result of
forced supination or a direct blow to the ulna.
B. The patient presents with pain, swelling at the DRUJ, loss of pronation, and a
tender volar mass (the ulnar head).
C. Treatment: Closed reduction and immobilization in a neutral long-arm cast for
3 to 4 weeks, if stable.
D. If the DRUJ is unstable (DRUJ shuck test in neutral and at extremes of pronation/
supination), then repair of the articular disc (and the VRUL and DRUL) or fractured
ulnar styloid is required. DRUJ instability is determined by “shucking” the joint with
translation of the ulna volarly and dorsally while stabilizing the radius, carpus, and
hand. There should be an equivalent amount of play in neutral to the contra-lateral
wrist and firm end points at the extremes of supination and pronation.
1. Repair of the TFCC can be done through a dorsal approach through the fifth
extensor compartment with an upside down “L”-shaped capsular flap. The
avulsed TFCC insertion can be secured down to its insertion into the fovea
using small bone tunnels or with a bone anchor.
IV. Dorsal Ulnar Dislocation of the DRUJ
A. Dorsal dislocation of the ulna can result from a fall onto the hand with the fore-
arm hyperpronated and wrist in extension.
B. The patient presents with swelling, pain loss of supination, and a tender dorsal
mass (the ulnar head).
C. Reduction is achieved through supination of the forearm while direct pressure is
applied over the distal ulna. Inability to reduce the dislocation may require open
reduction to remove an entrapped ECU tendon or interposed DRUJ capsule.
D. If stable after closed reduction, immobilization in a neutral long-arm cast for
3 to 4 weeks should be adequate. If unstable, consideration should be give to
repairing the TFC as above.
V. DRUJ Instability
DRUJ instability is the result of trauma and is often associated with distal radius frac-
ture with significant shortening, basilar ulnar styloid fracture, and angulated radial
shaft fractures (Galeazzi fractures). Acutely, the diagnosis is based on radiographic signs

(see below) or on examination of DRUJ (shuck test) immediately after stabilization of

associated radius fracture. Chronically, (after associated injuries have healed and patient
is trying to return to normal activities), patient typically has pain at DRUJ and TFCC
insertion (ulna fovea), and pain ± “clunking” with pronation/supination. The radioul-
nar ligaments (and secondary stabilizers) are mostly at risk of tearing with greater than
5 to 7 mm of radial shortening or significant radial shaft angulation.
A. Imaging
1. Plain films: Signs of DRUJ instability may include
a) Widening of the radioulnar joint on an AP view
b) Fracture at the base of the ulnar styloid (often not a real indicator of
DRUJ instability)
c) Unstable fracture at rim of sigmoid notch (typically dorsal fragment of
lunate fossa)
d) Significant shortening of the radius
e) Radial or ulnar shaft malalignment
f ) Dislocation of the ulna on a lateral view of the wrist in neutral (the
scaphophisocapitale (SPC) lateral)
2. Although the diagnosis can routinely be made with clinical examination and
plain x-rays, CT or MR scans have been used to access more subtle instabil-
ity. Both wrists are imaged simulataneously (for comparison) and evalua-
tion should be performed in three postions: Neutral, full supination, and full
pronation.
B. Acute instability
1. Radioulnar ligamants can only tolerate 5 to 7 mm shortening of the radius
before one or both of the distal radioulnar ligaments tear at the ulna attach-
ment. With fracture of radiual diaphysis, prognostic factors for ongoing DRUJ
instability include significant radial shortening or angulation and an initially
widened DRUJ. Galeazzi fracture dislocations are associated with a high rate
of TFCC injury. Fractures at the base of the styloid can be problematic if they
are displaced, as the TFC and the luno-triquetral-ulnar ligament attach there.
2. Treatment
a) If after stabilization/fixation of the distal radius fracture and reduc-
tion of the DRUJ, the joint is felt to be stable, further treatment is not
necessary.
b) If the joint is unstable in neutral or in the extremes of pronation/supination,
open TFCC repair will create an anatomic reconstruction. Alternatively,
percutaneous pinning across the radius and ulna use a 6.2 K-wire or larger,
parallel and proximal to the DRUJ while holding the joint reduced (leave
the pin out of the radial and ulnar cortices to facilitate removal if pin breaks)
will often allow enough soft tissue healing to create a stable DRUJ.
c) If there is a fracture at the base of the ulnar styloid, at the site of inser-
tion of the deep fibers of the TFCC, the TFCC fibers are often attached
to the ulnar styloid fragment and ORIF of fracture at the base of ulnar
styloid will produce good stabilization of the DRUJ. Pinning alone of the
styloid (without an associate tension band wire construct) is usually not
adequate alone and will require immobilization for healing. Fixation of
these fractures can restore stability by stabilizing the insertion points of
the TFCC.
d) Ulnar styloid tip fractures are not typically associated with instability and base
fractures that are not associated with instability do not need to be fixed.

C. Chronic instability
1. Ongoing instability of the DRUJ that is symptomatic is seen after malunited
radius (or ulna) fractures, under treated acute DRUJ instability, or a combi-
nation of both.
2. Treatment depends on the presence of arthritis, patient demands, and associ-
ated disorders.
a) In the absence of arthritic changes
1) Any malalignment of the radius (or ulna) must be corrected with
osteotomy (± bone grafting) and fixation.
2) The sigmoid notch may also require corrective osteotomy to restore rim
contours if abnormally flat. “Flat” notch can be an anatomic variant or the
result of malunion following injury. However, addressing this issue in con-
junction with definitive ligament reconstruction may improve results.
3) Joint leveling by lengthening osteotomy of the radius (usually in con-
juction with correction of angulation) or shortening of the ulna is
necessary for successful ligament repair or reconstruction.
4) The distal radioulnar ligaments are repaired if possible and augmented
with ligamentous reconstruction using tendon graft. Several tech-
niques have been described.
b) When arthritic changes are present
1) Symptomatic treatment can include splinting and activity modifications.
If this fails to relieve symptoms, then surgical options should not include
ligamentous reconstruction as this will exacerbate arthritic pain.
2) Distal ulna resection (Darrach procedure) can be performed in the
very low demand patient. Stabilization of the ulnar stump (using slips
of the ECU ± FCU and the pronator quadratus) will help prevent
dorsal/ ulnar instability, but radioulnar impingement can still be prob-
lematic.
3) Fusion of the DRUJ joint with proximal bone resection and pseudo-
arthrosis formation (to allow rotation) (Sauve-Kapanji) is another rea-
sonable strategy. This also can be complicated by ulnar stump instabil-
ity and painful impingement against the radius.
4) DRUJ replacements are now available but there are limited long-term
outcome data available.
Distal Radius Fractures
I. Anatomy of the Distal Radius
A. The distal aspect of the radius is a plateau that articulates with the carpal bones
of the wrist and the ulnar head.
B. The articular surface of the distal radius has three concavities that correspond to
the sites of articulation with the scaphoid, lunate, and ulna.
C. Supporting ligaments originate at the distal radius and insert within the car-
pus. In addition, there are ulnar-based ligaments (the TFCC) that maintain the
relationship of the radius to the ulna and allow the radius and hand to articulate
with, and rotate around the ulna.
D. The surface anatomy is notable for Lister tubercle, which is palpated on the
dorsal aspect of the distal radius and acts as a fulcrum for the extensor pollicis

longus. There is also a tubercle or bare spot between the first and second
dorsal extensor compartments that is a location often used for placement of
percutaneous pin fixation.
E. The distal articular surface of the radius has a radial inclination averaging
22 degrees and a palmar tilt averaging 11 degrees. Radial inclination is measured
as the angle formed by a line drawn tangential to the distal radius articular sur-
face on PA projection and a line perpendicular to the longitudinal axis of the
radius. Palmar tilt is measured as the angle formed by a line drawn tangential
to the distal articular surface on a lateral view and a line perpendicular to the
longitudinal axis on the radius. Ulnar variance is measured on the PA view as
the difference in length between the radius and ulna. The ulnar variance should
be compared to the contralateral side.
II. Pathogenesis
A. Fractures of the distal radius can be seen in all age groups. Younger patients are
often from high-energy injuries and may have other associated injuries. Older
patients often sustain distal radius fractures from an isolated fall.
B. Concomitant soft tissue injuries are common and may include TFCC tears, sca-
pholunate interosseous ligament tears, and lunotriquetral ligament tears.
III. Radiography
A. Obtain true PA and lateral views of the wrist without plaster. Pronation and
supination oblique views are helpful at delineating the fracture pattern.
B. For particularly comminuted intra-articular fractures, CT scans are helpful to
delineate amount of displacement and location of fragments. The studies often
alter treatment decisions. Three-dimensional CT scan reconstructions have been
advocated for some complex intra-articular fractures.
C. Tilt views are obtained to provide a tangential view of the articular surface and
improve assessment of hardware adjacent to the joint surface.
1. The lateral tilt view is obtained by elevating the forearm equal to the radial
inclination to limit the overlap of the radial styloid with the articular surface.
2. The PA tilt view is obtained by elevating the forearm equal to the radial tilt
to limit the overlap of the dorsal or volar cortex with the articular surface.
3. The 45 degree pronated view improves assessment of subchondral screw
placement.
IV. Classification
Multiple classification schemes are described, including Frykman (Table 14.7), Melone,
and Mayo. The key distinctions that determine fracture stability for the clinician are
described below:
A. Displaced versus non-displaced: Displaced fractures following reduction will
tend to move toward the position of initial injury and may be unstable.
B. Intra-articular versus extra-articular fractures
1. Intra-articular fractures include any injury involving the articular surface of
the distal radius. These fractures tend to be more unstable than extra-articular
injuries. It is important to note whether the radiocarpal, ulnocarpal, or DRUJs
(or a combination) are involved.

TABLE 14-7 Frykman classification
No Distal Associated Distal

Ulna Fracture Ulna Fracture
Extra-articular I II
Intra-articular into radiocarpal III IV
joint (RC)
Intra-articular into DRUJ V VI
Intra-articular into RC and VII VIII
DRUJ
2. Extra-articular fractures are metaphyseal fractures that spare the articular

surface.
C. Quality of bone is an important factor. Osteopenic bone is more likely to collapse
with closed treatment.
D. The greater the degree of comminution or fragmentation, the more unstable
the fracture pattern.
E. Position of distal fragment relative to radial shaft involving angulation and
displacement is considered.
F. Related injuries such as soft tissue injuries, carpal fractures, etc., lead to unstable
injuries
G. Eponyms
1. Colles fracture—refers to simple, metaphyseal distal radial fracture with open
volar angulation and dorsal displacement of distal fragment, loss of radial
height, and dorsal tilt of the articular surface.
2. Barton fracture—intra-articular fracture, seen best on lateral x-ray, in which
the volar margin of the distal radius is broken, allowing the carpus to sub-
luxate volarly along with the fracture fragment. A reverse or dorsal Barton
fracture involves a dorsal intra-articular sheer injury. These fracture patterns
are unstable injuries.
3. Smith fracture—metaphysical distal radial fracture with apex dorsal angula-
tion and volar displacement.
4. Chauffeur fracture is an intra-articular fracture in which the radial styloid has
displaced in one large fragment. Scapholunate ligament tears are frequently
associated.
H. Ulnar styloid fracture treatment is controversial. Operative fixation is generally
not considered unless the DRUJ is unstable on clinical examination following
fixation of the distal radius fracture. DRUJ instability is more common when the
fracture includes the base of the ulnar styloid.
V. Functional Classification Scheme
The presence or absence of a fracture by itself is not enough to determine whether

a fracture should be treated by any specific method. Other factors to be considered
include the patient’s age and needs, the degree of fragmentation at fracture site, skin/
soft tissue condition, stability of fracture fragments after reduction and stability after

a few days of immobilization. Bone quality is an essential modifier to a distal radius

facture, as osteopenia increases the difficulty in maintaining reduction and/or fixation.
VI. Physical Examination
A. Condition of skin, local nerve, and vascular and tendon function in addition to
the elbow, shoulder, and fingers should all be assessed.
B. Most patients present with a “dinner fork” deformity. This occurs as a result of
dorsal displacement of distal fragment.
C. Extension of energy to or from radius can result in major soft tissue injury.
Tears of scapholunate and other intercarpal ligaments may occur. Fractures of
the radial styloid are associated with scapholunate injury.
D. Distal radius fractures can also lead to compartment syndrome, particularly in high-
energy trauma. Patients with distal radius fractures may develop acute carpal tunnel
symptoms. Numbness may be related to a nerve contusion in which the symptoms
develop soon after the injury and are nonprogressive. An acute carpal tunnel syn-
drome causes pain, progressive numbness, and median nerve dysfunction.
VII. Treatment
A. Closed reduction
If the fracture is significantly displaced or angulated, acute closed reduction
is required. Acceptable alignment is dependent on multiple factors including
functional demand, physiologic not chronologic age. Indications for the reduc-
tion of a Colles fracture are generally a loss of radial height greater than 5-mm,
10 degrees or more of dorsal tilt as well as residual articular incongruity (Knirk
and Jupiter).
1. Goal of acute reduction is decompression of muscle and nerve tissue, suf-
ficient fracture stability to allow finger motion, and stabilization of forearm
rotation.
2. Reduction is accomplished via traction and manipulation and may be aided
by the use of finger traps. Finger traps overcome the forces of forearm mus-
cles in spasm and help realign smaller, intra-articular fragments.
3. Anesthesia for reduction under the form of a hematoma block with 1% lido-
caine is often all that is required. Conscious sedation may be required for
some reductions.
4. Dorsally displaced distal radius fractures can be reduced by initially repro-
ducing the mechanism of injury by extending the wrist to disengage the
fracture fragments followed by distraction and a volar-directed and prona-
tion-directed force on the distal fragment. The wrist is splinted in 20 degrees
of ulnar deviation and 20 degrees of flexion. Excessive flexion should be
avoided as it can lead to acute carpal tunnel syndrome.
5. Whether or not manipulation is required, the wrist requires immobilization.
A sugar-tong splint or short-arm cast is recommended. The function of the
cast or splint is to maintain fracture alignment while allowing the thumb and
digits to move freely at the MCP joints.
6. Postreduction x-rays should be obtained to confirm adequate reduction.
7. Patients should be instructed to maintain strict elevation.

8. Factors associated with instability are excessive comminution, initial loss of

more than 15 mm in radial height, initial dorsal tilt greater than 20 degrees,
comminution of dorsal and/ or volar cortices seen on postreduction films,
articular displacement, radio-carpal instability–associated ulna fracture or
DRUJ dislocation.
9. Patients should return for follow-up at 7 days after manipulation to deter-
mine whether the fracture reduction has been maintained.
10. Acceptable reduction: Shortening of less than 5 mm, frontal plane distal
radial angle greater than 10 degrees, dorsal tilt less than 10 degrees.
B. Operative fixation
If bone quality or fracture pattern precludes stable, nonoperative treatment, opera-
tive fixation should be considered. This includes displaced, intra-articular fractures.
1. Several techniques are utilized and optimal method of fixation is based on
fracture pattern and surgeon preference.
2. The choice of operative treatment depends on fracture configuration, sta-
bility of fracture and DRUJ, articular involvement, soft tissue injury, etc.
Choices include
a) Open reduction internal fixation, including volar and/or dorsal plating.
These approaches often allow early mobilization.
1) Volar, or FCR, approach is based on the interval between the FCR
tendon (median nerve) and the radial artery. Incision is made directly
over the distal course of the FCR tendon.
2) Dorsal approach allows access to distal radius between the third and
fourth dorsal compartments.
3) Fragment specific fixation utilizing a combination of these approaches.
b) External fixation
1) Considered for severely comminuted fractures not amenable to ORIF,
and open fractures with significant soft tissue injury.
2) In the majority of cases, external fixation is accompanied by adjuvant
percutaneous fixation or ORIF, depending on degree of comminution,
articular involvement, and stability of fracture reduction.
3) Dorsally displaced fractures are reduced by distraction and volar trans-
lation. Longitudinal distraction alone will lead to dorsal tilt of the
articular fragment due to the pull of the volar extrinsic ligaments.
c) Closed reduction and percutaneous pin fixation using K-wires. Patients
will typically be immobolized for following this procedure.
3. If the ulnar styloid is fractured and the DRUJ is grossly unstable, then
stabilization of the ulnar styoid fragment and thus, the TFCC should be
performed. Ulnar styloid fractures without DRUJ instability are treated
nonoperatively.
4. Bone graft is considered in cases of bone loss, severe comminution, metaphy-
seal impaction for support of the subchondral surface. This is not routinely
required when using volar locking plates.
VIII. Complications
A. Acute
1. Median nerve dysfunction
2. Ulnar nerve injury

3. Radial sensory nerve injury with percutaneous fixation

4. Instability of DRUJ
5. Pin tract infection with percutaneous and external fixation
6. Compartment syndrome
B. Late
1. Posttraumatic arthritis following intra-articular fractures
2. Malunion: A dorsally angulated malunion leads to the loss of wrist flexion
and rotation and may require corrective osteotomy
3. Tendon rupture
a) EPL rupture may occur in minimally displace fractures treated nonopera-
tively related to mechanical irritation or ischemia from hematoma at the
extensor retinaculum. Treatment typically involves EIP to EPL transfer.
b) Flexor or extensor tendon attritional rupture may occur related to hard-
ware adjacent to tendons.
4. Stiffness of the wrist is common following distal radius fractures. It is
important to monitor shoulder, elbow, and digital range of motion during
treatment of the wrist injury.
5. Chronic regional pain syndrome (CRPS)
Distal Ulna Injuries
I. Anatomy of the Distal Ulna
The ulnar shaft flares distally and forms the ulnar neck. Arising from the ulnar neck are
the two distal most structures of the ulna: The ulnar head and the styloid process.
A. The head of the ulna is lateral, rounded, and distally and laterally is covered by
articular cartilage. Distally, it articulates with the TFCC and ulnocarpal ligaments.
The lateral, anterior, and medial surfaces of the head articulate with the distal
radius at the sigmoid notch of the radius and form the DRUJ. The DRUJ is the
joint about which pronation and supination of the forearm occur.
B. The styloid process is a postero-medial, narrow, and nonarticular structure. It is the
most distal part of the ulna. The groove between the ulnar head and the ulnar styloid
is called the fovea. It serves as an insertion point for the TFCC at the base of the
styloid. The ulnar styloid is also an attachment point for the ulnocarpal ligaments.
Distal to the TFCC from the ulna is the triquetrum of the carpus bones. A groove for
the ECU runs between the ulnar head and the styloid dorsally.
II. Examination
A. Begin with inspection, looking for swelling, deformity, ecchymosis, and skin
lesions, which may indicate an open fracture of the distal radius or ulna.
1. In many open distal radius fractures, the skin lesion will be on the ulnar side.
B. Palpation of the distal radius and ulna may reveal deformity, tenderness, and/or
crepitus. The DRUJ should be examined for instability and tenderness.
C. The ulnar styloid should also be examined for tenderness. Tenderness dorsally
between the ulnar styloid and the carpus may be an indication of TFCC injury.
D. Range of motion should be assessed by comparison to the contralateral side if
possible. Range of motion may be limited acutely by pain and swelling.

E. A neurovascular examination is performed.

1. Pulses should be palpated or checked with a Doppler. Areas of mottling or
pallor should be noted indicating possible vascular compromise.
2. Venous flow is also important and venous congestion may cause blue or pur-
ple discoloration.
3. Sensory examination of the hand and fingers may delineate a peripheral nerve
injury. The integrity of the radial, ulnar, and median nerves should be exam-
ined in all injuries. An acute carpal tunnel syndrome may be precipitated by
swelling.
III. Imaging
A. The distal ulna should be examined by a zero rotation posteroanterior and true
lateral views of the wrist. A true lateral of the wrist should demonstrate the
palmar cortices of the scaphoid, pisiform, and capitate in order from volar to
dorsal.
B. Ulnar variance can be measured from a true PA film with the wrist in neutral
rotation. The ulnar variance is then measured as the distance between a trans-
verse line at the level of the lunate fossa and a transverse line at the level of the
ulnar head. With neutral variance, 80% of the axial load is supported by the
radius and 20% is supported by the ulna.
C. A CT scan of the wrist may better elucidate fracture patterns and involvement of
the DRUJ and is the definitive study to assess for DRUJ dislocation.
IV. Isolated Ulnar Fractures
A. Distal nightstick
This is an isolated fracture of the distal diaphysis of the ulna and most often
caused by a direct trauma to the forearm as when the forearm is raised to block
a blow.
1. Those who are displaced less than 50% and have less than 10 to 15 degrees of
angulation are deemed to be stable. The periosteum and interossseous mem-
brane are intact, preventing rotational movement and helping to stabilize the
fracture. These injuries can be treated by a below-elbow cast or a brace for
6 weeks, allowing for wrist and elbow movement.
2. An attempt should be made at closed reduction if there is greater than 50%
displacement or more than 10 to 15 degrees of angulation. In this situation,
the periosteum and interosseus membrane are likely disrupted causing insta-
bility of the fracture site through pronation and supination of the forearm.
These fractures can be managed nonoperatively through long-arm casting for
6 weeks if they can be reduced.
3. However if closed reduction fails they should be managed surgically with
ORIF with a 3.5-limited contact dynamic compression plate.
B. Styloid
1. Avulsion fractures of small portions the ulnar styloid will not cause instability
of the DRUJ. These may be treated nonoperatively in a long-arm posterior
splint with the arm in neutral rotation.
2. An ulnar styloid fracture at the base of the styloid that is displaced may dis-
rupt the TFCC and may lead to instability of the DRUJ. This fracture should
be fixed internally.

3. Ulnar styloid fractures are at high risk for nonunion, approximately 26%.
These are often asymptomatic and therefore do not need intervention. How-
ever, these nonunions can be a cause of ulnar-sided wrist pain especially with
an unstable DRUJ or a TFCC injury. These can be treated by open reduc-
tion, internal fixation of the fragment, or subperiosteal excision of the frag-
ment if the DRUJ is stable.
V. Distal Ulnar Fractures in Association with Distal Radius Fractures
A. Ulnar styloid
Approximately 51% to 65% of distal radius fractures have an associated ulnar
styloid fracture. The size, location, and amount of displacement in ulnar styloid
fractures may be predictors of DRUJ instability and therefore of functional out-
come. Larger fracture fragments, fractures at the base of the styloid, and greater
displacement are at risk for DRUJ instability. DRUJ instability can also occur
in the absence of an ulnar styloid fracture. Treatment options are as mentioned
above, with closed reduction and pinning, open reduction internal fixation, or
with excision and reattachment of the TFCC to the remaining distal ulna.
B. Ulnar head and neck
1. Ulnar head and neck fractures result in a small, metaphyseal fracture frag-
ment, which is covered by 270 degrees of articular surface. These factors
make internal fixation very challenging. Many of these fractures, however, do
not need or benefit from fixation as they become well aligned and stable after
realignment and stabilization of the distal radius.
2. However some of these fractures remain malaligned or unstable even after
addressing the distal radius, and may lead to decreased DRUJ function,
decreased stability of the forearm, and increased risk of nonunion. Other
complications include cross union and chronic pain.
3. When internal fixation is required, typically fixed angle fixation devices are uti-
lized. The soft tissue anatomy, ECU sheath, dorsal ulnar cutaneous nerve, and
TFCC must all be carefully considered and respected in the surgical approach.
C. Distal diaphyseal fractures of the radius and ulna
1. Distal both bone fractures in adults are usually displaced and unstable. These
fractures are usually treated with ORIF with plating of the radius and ulna.
These should be fixed early, before the onset of swelling. Nonunion in the
forearm after surgical treatment is rare.
2. Forearm compartment syndrome may develop preoperatively or postopera-
tively with these fractures. Pain out of proportion to the injury and pain with
passive flexion or extension of the fingers are important early clinical indica-
tors. Measurement of compartment pressures of the forearm can confirm the
diagnosis and can be helpful in uncooperative patients.
VI. Pediatric Considerations
The ulnar epiphysis is cartilaginous at birth. An ossification center appears at the ulnar
head at approximately age 4 and extends into the ulnar styloid, which is the last area of
the distal wrist to ossify. The distal epiphysis of the ulna closes at approximately age 20.
Children have the ability to correct angulation in the plane of joint movement by
growth and remodeling, therefore they respond well to closed reduction and casting.

A. Distal both bone fractures

1. Pediatric ulnar fractures are often associated with radius fractures, as bone
both forearm fractures. Distal third fractures account for 75% of pediatric
radius and ulna shaft fractures and are able to remodel more than middle
or proximal third injuries. Rotational deformity and encroachment of the
interosseous space cannot be corrected by growth and remodeling; there-
fore, significant deformity requires ORIF or closed reduction and pinning.
2. After closed reduction, assessment of pronation and supination should be
performed. Distal third fractures may be more stable when immobilized in
pronation. In patients less than 6 years old, up to 15 degrees of angulation
and 5 degrees of rotation are acceptable. Between the ages of 6 and 10,
there should be less than 15 degrees of angulation; however, if the reduc-
tion allows adequate pronation and supination, more angulation may be
preferable to surgical fixation. About 10 degrees of angulation should
remodel in this age group. Over 12 years of age, no angular or rotational
deformity is acceptable and these patients should be treated similar to
adults, with ORIF.
B. Greenstick fractures
1. Children may sustain incomplete fracture of the ulna with cortex failure on
one side and plastic deformation on the other side with or without an incom-
plete or complete fracture of the radius.
2. With an isolated ulnar shaft greenstick fracture, tenderness of the radial head
may indicate a Monteggia fracture equivalent. Up to 30 degrees of angulation
in an infant and up to 15 degrees in a child are acceptable.
3. If there is significant angular deformity, the fracture should be reduced
and may require overcorrecting the fracture and completion of the fracture
through the plastically deformed cortex in order to prevent recurrence or
worsening of the deformity.
C. Distal ulna physeal injuries
1. These are much less common than physeal injuries of the distal radius; how-
ever, these have a higher incidence of growth arrest. About 70% to 80% of the
longitudinal growth of the ulna is derived from the distal physis. Therefore,
growth arrest here can cause significant ulnar shortening. The rate of distal
ulnar growth arrest is probably less than 10%. Specific acceptable amount of
physeal displacement is unknown; however, 30% physeal displacement has
been shown to heal readily.
2. Salter-Harris Types I and II injuries usually can be managed with closed
reduction and casting.
3. Salter–Harris Types III and IV may require ORIF to restore anatomic align-
ment of the joints surfaces and physeal surfaces.
4. Salter-Harris Types V and VI are the most likely to result in partial or com-
plete growth arrest and may require surgical procedures to prevent or correct
deformity.
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Fractures and Dislocations:
Forearm
15
Seth D. Dodds and David C. Ring
Forearm
I. Introduction
A. The rotary movements (pronation/supination) provided by the unique two

bone, dual intra-articulation structure of the forearm greatly expand the variety
of ways in which objects can be positioned and manipulated by the hand.
B. Loss of this motion as a result of malunion, prolonged immobilization, and/or
proximal or distal radioulnar joint (DRUJ) incongruity following trauma to the
adult forearm can be disabling.
C. The gradual improvement in functional outcomes and decrease in the rate of
complications associated with the management of forearm fractures during this
century parallel the history of the development of sound, stable techniques of
internal skeletal fixation, which permit mobility while assuring the maintenance
of skeletal alignment during fracture union.
D. Forearm fractures are often the sequelae of high-energy injury and a relatively
large percentage are open fractures.
E. Injury and treatment-related complications include compartment syndrome,
neurovascular injury, soft tissue loss, bone loss, refracture after plate removal,
and posttraumatic radioulnar synostosis. Infection is unusual, even in the case
of an open fracture due in part to the relative ease of wound debridement as well
as the well-perfused forearm musculature.
II. Anatomy
A. There is a slight apex posterior bow along the entire length of the ulna as seen
on a lateral radiograph.
B. The ulna is triangular in cross section through the majority of its midportion,
becoming cylindrical distally. The laterally directed apex of the triangle cor-
responds with the insertion of the interosseous ligament. The posterior apex
remains essentially subcutaneous as it divides the flexor and extensor muscula-
ture on the ulnar border of the forearm, and is palpable along the entire length
of the bone.
C. The radius has a double curvature in both the anteroposterior and lateral
planes.
D. The large ulnar concavity of the distal curvature of the radius allows for over-
riding of the ulna without restriction of pronation. Loss of this “radial bow” is
associated with limitation in both forearm rotation and grip strength.
E. The radius rotates about the relatively stationary ulna along an axis that passes
roughly through the center of the radial head proximally and the fovea of the
ulnar head distally.
255

F. Rotation of the radius occurs via axial rotation of the radial head at the proximal
radioulnar joint (PRUJ), whereas distally, the motion is a combination of axial
rotation and translation of the radius relative to the ulna.
G. The association of the radius and ulna is maintained by ligamentous structures
at the proximal and DRUJs as well as by the interosseous ligament, a ligamen-
tous sheet interconnecting the two bones along their midportion that extends
from radial-proximal to ulnar-distal.
H. The PRUJ is stabilized by the annular and quadrate ligaments proximally, and
the interosseous ligament.
I. The distal radioulnar articulation is stabilized by the triangular fibrocartilage
complex (TFCC). The complex represents a combination of structures that are
inseparable in anatomic dissections including the articular disc, the dorsal and
volar radioulnar ligaments, the ulnar collateral ligament, and the sheath of the
extensor carpi ulnaris.
III. Operative Exposures
A. Ulna
1. The posterior apex of the ulnar shaft defines the plane between the extensor
forearm musculature innervated by the radial nerve and the flexor muscula-
ture innervated by the ulnar nerve.
2. Elevate the muscle, extraperiosteally from only one side of the bone. Extra-
periosteal means that you leave the periosteum on the bone, only elevate the
muscle.
B. Radius
1. Dorsal or thompson exposure
a) The dorsal (or Thompson) approach has waned in popularity as a result
of the potential of injury to the posterior interosseous nerve, which must
be dissected from the substance of the supinator and protected.
b) A straight longitudinal skin incision is made along the line connecting the
lateral epicondyle at the elbow with Lister tubercle at the wrist while the
elbow is at 90 degrees of flexion and the forearm is in neutral rotation.
c) The internervous interval between the extensor digitorum communis
(supplied by the posterior interosseous nerve) and the extensor carpi
radialis brevis (supplied by the radial nerve) is most easily identified by
locating the point at which the abductor pollicis longus and extensor pol-
licis brevis emerge from between the mobile wad and dorsal compartment
musculature in the distal half of the forearm.
d) The deep fascia is incised directly adjacent to this interval and the mus-
cles are separated in a distal to proximal direction until their common
aponeurosis is encountered. The supinator muscle covering the proximal
radius is thereby exposed.
e) Utilization of the proximal portion of the dorsal surface of the radius for
plate fixation requires identification and mobilization of the posterior
interosseous nerve as this nerve may lie almost directly adjacent to the bone
at this level and could potentially be trapped beneath a plate. The posterior
interosseous nerve emerges from between the superficial and deep heads
of the supinator muscle approximately 1 cm proximal to the distal limit
of this muscle. It can be identified at this point and then dissected free
from the muscle being careful to preserve its muscular branches. Following

Chapter 15 • Fractures and Dislocations: Forearm 257
sufficiently proximal mobilization of the nerve, exposure of the radial shaft

can be performed by rotating the radius into full supination and detaching
the insertion of the supinator from the anterior aspect of the radius.
f ) Exposure of the midportion of the bone is facilitated by mobilization and
retraction of the crossing abductor pollicis longus and extensor pollicis
brevis muscles. Exposure of the radius distal to the extensor pollicis brevis
is performed in the interval between the radial wrist extensors (extensor
carpi radialis brevis and longus muscles) and the extensor pollicis longus
muscle, which ultimately produce the tendons occupying the third and
second dorsal extensor compartments, respectively.
2. Anterior or Henry exposure
a) Exposure of the anterior surface of the radius is both safer and more
extensile than a dorsal exposure.
b) A straight longitudinal incision along a line between the lateral margin of
the biceps tendon at the elbow and the radial styloid process at the wrist
will afford access to the plane between the mobile wad and the flexor
musculature of the forearm.
c) The deep fascia is incised adjacent to the medial border of the brachio-
radialis and a plane is developed between this radial nerve–innervated
muscle and the median nerve–innervated flexor carpi radialis and prona-
tor teres muscles. Dissection is initiated distally and proceeds proximally
following the course of the radial artery.
d) Arterial branches to the brachioradialis and the recurrent radial artery
arising near the elbow are ligated and the radial artery is mobilized and
retracted medially with the flexor carpi radialis muscle.
e) The superficial radial nerve is encountered on the undersurface of the
brachioradialis and remains lateral with this muscle.
f ) Deep dissection is initiated proximally where the biceps tendon is fol-
lowed toward its insertion on the bicipital tuberosity of the radius. Full
supination of the forearm displaces the posterior interosseous nerve
laterally and brings the insertion of the supinator muscle anterior. The
insertion of the supinator muscle is identified by deepening the muscular
plane along the lateral aspect of the biceps tendon. Here one may encoun-
ter a bursa between the biceps tendon and the supinator, which further
facilitates this dissection.
g) The posterior interosseous nerve remains well protected within the sub-
stance of the supinator muscle during elevation of its insertion from the
radius, provided that excessive lateral traction is not applied and the fore-
arm is held in supination.
h) The insertion of the pronator teres can be detached or the plate can be placed
directly on top of the insertion. The body of the flexor digitorum superficia-
lis must be elevated in order to expose the midportion of the radius.
i) In the distal portion of the wound, the pronator quadratus and the flexor
pollicis longus are also elevated from the bone, usually extraperiosteally.
IV. Forearm Compartment Release
A. Fascial release for compartment syndrome can be performed through the standard
volar Henry type exposure in the setting of a forearm fracture, or through a straight
ulnar McConnell type incision when exposure of the bones is not required.

B. Unlike the leg, the three compartments in the forearm (volar, dorsal, and mobile
wad) arm are interrelated and release of the volar compartment usually releases
the other compartments. Release of the lacertus fibrosis and the carpal tunnel
should be done routinely as part of the decompression.
V. Treatment
Despite numerous descriptions of the relevant anatomy and proper methods of reduc-
ing forearm fractures, which appeared early in the twentieth century these fractures
remained “problem” fractures and attracted a variety of early attempts at operative
treatment.
A. Early attempts at internal fixation, although sufficient to hold open reduc-
tions, did not preclude the need for external immobilization, resulting in
comparably poor function outcomes in fractures treated by open or closed
methods.
B. The development of larger, corrosion-resistant, compression plates led to
a dramatic decrease in the rate of fracture nonunion while simultaneously
providing sufficient stability for confident early mobilization of the forearm.
The dynamic compression plates and the emphasis on immediate mobi-
lization of the limb developed by the AO/ASIF in particular made open
reduction and internal fixation a predictable treatment for diaphyseal fore-
arm fractures with a rate of nonunion below 5% and excellent functional
results.
C. A 3.5-mm limited contact dynamic compression plate or the equivalent
should be used—recon plates and third or semitubular plates are too weak. A
minimum of three screws should be placed proximal and distal to the fracture
site.
D. Intramedullary implants continue to be reintroduced periodically, but have
inherent weaknesses including difficulty maintaining rotational alignment, dif-
ficulty restoring the anatomic radial bow, the need for supplemental immobi-
lization, a high nonunion rate, and the technical difficulty of device insertion
with frequent splitting of the cortex and protrusion of the nail through the
cortex or into a joint.
E. The results of intramedullary nailing of forearm fractures have improved mod-
estly following the introduction of nails of square and triangular cross section
intended to better control rotation, improved nail design and insertion tech-
niques intended to restore the anatomic radial bow, and closed nailing under
fluoroscopic guidance. However, despite these improvements, intramedullary
nailing continues to lack the predictability and stability of modern plate and
screw fixation that have essentially solved the “problem” of forearm fractures and
made plate fixation the treatment of choice.
F. Isolated fractures of the ulna without associated radioulnar instability (the so-
called nightstick fracture) usually heal with nonoperative treatment. Operative
treatment is considered when there is greater than 50% translation or greater
than 10 degrees of angulation of the fracture fragments.
G. Isolated fractures of the radius are common. These benefit from plate fixation
unless they are nondisplaced. The DRUJ should be carefully evaluated after
stabilization of the radius.

VI. Open Fractures
A. Immediate plate fixation of all but the most complex and contaminated forearm
fractures is associated with an acceptably low rate of infection in open fore-
arm fractures treated by immediate plate and screw fixation (0% to 3%) when
perioperative antibiotics, thorough wound debridement, and delayed primary
closure of the traumatic wounds is performed.
B. When infection occurs, its eradication is not necessarily dependent upon
implant removal. As long as all bone fragments and soft tissues are well vascular-
ized, stable internal fixation will facilitate wound care and help maintain length
and alignment, as well as range of motion and overall function, without hinder-
ing treatment of the infection.
VII. Fracture-Dislocations of the Forearm (Galeazzi, Monteggia,

and Essex-Lopresti Lesions and their Variants)
A. The Galeazzi fracture is a fracture of the radial diaphysis (often the distal third)
in association with dislocation of the DRUJ.
B. The Monteggia fracture and its variants represent a fracture of the proxi-
mal ulna associated with PRUJ disruption and radiocapitellar subluxation or
dislocation.
C. The Essex-Lopresti lesion is a fracture of the radial head with rupture of the
interossesous ligament of the forearm.
D. Bipolar forearm fracture-dislocations or radioulnar dissociation represents a
more complex injury with associated disruption of the interosseous ligament.
E. Clinical and anatomic investigations have determined a number of clues indi-
cating DRUJ disruption, which can be detected on radiographs: (i) Fracture of
the ulnar styloid at its base, (ii) Widening of the DRUJ space, (iii) Dislocation
of the radius relative to the ulna seen on a true lateral radiograph, and (iv) Short-
ening of the radius beyond 5 mm relative to the distal ulna under a constant
applied load.
F. Proximally, the radio-humeral-ulnar joint is dislocated if a line through the
radial shaft and head does not bisect the capitellum in all positions of flexion/
extension.
G. Galeazzi fracture-dislocations are treated with anatomic reduction and plate
and screw fixation. If the ulnar styloid is fractured at its base, it should be
repaired. The DRUJ is usually stable and the forearm can be mobilized imme-
diately postoperatively. If the DRUJ remains unstable, forearm can be immo-
bilized in midsupination for four weeks, occasionally with transfixion of the
distal ulna to the radius with one or two stout smooth Kirschner wires (not
transarticular).
H. Anterior and lateral Monteggia fractures (Bado Types 1, 3, and 4 [indicating a
fracture of both bones with anterior or lateral dislocation of the radial head from
the PRUJ]) are usually treated with anatomical reduction and internal fixation
of the ulna and early mobilization. Instability or incomplete reduction of the
radial head is most commonly a result of ulnar malalignment, and the annu-
lar ligament should rarely need to be explored or repaired. Posteior Monteggia
lesions (Bado Type 2) are more complex and best considered along with elbow
fracture-dislocations.

I. With Essex-Lopresti and bipolar fracture-dislocations, the treatment principles

include stable anatomic reduction of all fractures, preservation of radiocapitellar
contact with operative fixation or prosthetic replacement, and addressing the
soft-tissue injury either with direct repair or immobilization in a reduced posi-
tion (with or without cross-pinning).
VIII. Refracture
A. Initially the AO/ASIF recommended removal of all implants following fracture

healing; however, because the removal of forearm plates has been associated
with a risk of refracture (either through the old fracture site or a screw hole), in
addition to the risks of a second operation (injury to the posterior interosseous
nerve in particular), most surgeons no longer remove the plates unless they are
causing definable problems. This is true in athletes as well.
B. The risk of refracture following plate removal is believed to result from
a combination of incomplete healing and the osteoporosis, which occurs
under a plate as a result of some combination of disruption of the vascular
supply to the bone and stress shielding. Risk factors for refracture follow-
ing plate removal include fracture comminution or inability to gain com-
pression of fracture fragments, implant size (less likely following removal of
3.5 mm than 4.5 mm plates), implant removal earlier than one year postin-
jury, radiolucency beneath the plate, and inadequate protection following
plate removal.
Interosseous Membrane
The interosseous membrane (IOM) supports the architecture of the forearm. The
radius, ulna, and IOM create a mobile, oblong ring sustained by the proximal and
DRUJs. Pronation and supination occur as the radius rotates over the stationary ulna.
During physiologic forearm rotation, the IOM endures relatively low strains. The shape
and structure of the radius and ulna (along with the DRUJ and PRUJ) provide inherent
stability to the forearm joint. It is not until the forearm joint has been disrupted that
the IOM becomes a significantly functional entity.
I. Anatomy
A. The IOM is a quadrangular, ligamentous membrane that extends from the

radius proximally to the ulna distally, filling the space between and linking the
two bones of the forearm.
1. It separates the anterior and the posterior compartments of the forearm.
Proximally and distally, the membrane is not continuous and is perforated by
the posterior and anterior interosseous vessels. It is arranged in a continuous
fashion volarly and is discontinuous dorsally.
2. This ligament of the forearm consists of multiple bands; for example, the
central band is considered the primary restraint to proximal migration of
the radius (Fig. 15.1). It is the most consistent and dominant portion of the
IOM, spanning obliquely from the interosseous tubercle on the radius to a
broad attachment on the ulna.

Figure 15.1 The IOM is composed of multiple distinct bundles. The central band
of fibers (marked *) comprises the thickest and most stout portion of this composite
ligament between the radius and the ulna. (From Poitevin LA. Anatomy and
biomechanics of the interosseous membrane: Its importance in the longitudinal
stability of the forearm. Hand Clin. 2001;17(1):97–110, vii.)
3. Muscles originating from the IOM include the FDP, FPL, EPB, APL, EIP,
and EPL. Histologically, the IOM is primarily composed of collagen arranged
in fibrils surrounded by elastin.
II. Biomechanics
A. Researchers have theorized several functions for the IOM: Force transfer from the
radius to the ulna, origin for several flexor and extensor muscles, maintenance of

longitudinal and transverse forearm stability, and support during pronation and
supination.
B. Due to the obliquity of the attachment of its fibers, the central bundles of the
IOM relax when the radius is distracted. When the radius is compressed or axi-
ally loaded, these same bundles tighten.
C. The biomechanics of the IOM allow it to transfer forces from the radius to the
ulna.
1. At the level of the DRUJ, the radius bears about 80% of a compressive load
and the ulna about 20%.
2. At the level of the PRUJ, the radius bears 60% of the load and the ulna
40%.
3. This distal to proximal load transfer from radius to ulna takes the burden
from the radiocarpal joint and distributes it more equally at the level
of the elbow. When the integrity of the forearm “ring” has been com-
promised by injury or surgical intervention (such as with radial head
excision), the strain in the IOM increases. After radial head excision,
this strain is further increased as the forearm rotates from supination to
pronation.
III. Pathology
A. An Essex-Lopresti injury or longitudinal radioulnar dissociation consists of

1. Fracture of the radial head
2. Rupture of the IOM
3. Disruption of the DRUJ with or without tearing of the TFCC.
4. It is an injury that is typically difficult to diagnose and even harder to treat.
This type of radioulnar dissociation is usually a result of a high-energy fall
onto an outstretched hand, creating a longitudinal compression force on the
wrist, forearm, and ultimately the elbow.
5. Frequently, attention by the medical personnel is initially focused on posi-
tive elbow radiographs. Often, the radial head fracture provides sufficient
elbow pain that patients are distracted from any symptoms in the forearm or
wrist. However, in these severe injuries, the forearm is rendered unstable by
the loss of continuity of the IOM. The radius migrates proximally, resulting
in decreased motion, weakness, and increased forearm and wrist pain over
time.
6. The key to Essex-Lopresti injuries is early diagnosis with appropriate history,
physical examination, and radiographs of the forearm and wrist. Treatment is
guided by the discovery of this injury.
B. The successful treatment of a radioulnar dissociation or an Essex Lopresti
injury is incumbent on the maintenance of forearm length. Forearm length
is dependent on operative repair (open reduction and internal fixation) or
replacement of the radial head. Repair of the TFCC and/or the dorsal and
volar distal radioulnar ligaments may be required.
1. With the restoration of forearm length and stability at the DRUJ, direct open
repair or reconstruction of the IOM central band is not needed. In general,
the treatment of radioulnar dissociation is more effective when the diagnosis
is made within the first week of injury and before definitive management of
the radial head fracture.

Suggested Readings
Anderson LD, et al. Compression-plate fixation in acute diaphyseal fractures of the radius and
ulna. J Bone Joint Surg Am. 1975;57(3):287–287.
Chapman MW, Gordon JE, Zissimos AG. Compression-plate fixation of acute fractures of the
diaphyses of the radius and ulna. J Bone Joint Surg Am. 1989;71(2):159–169.
Essex-Lopresti P. Fractures of the radial head with distal radio-ulnar dislocation; report of two
cases. J Bone Joint Surg Br. 1951;33B(2):244–247.
Hotchkiss RN, et al. An anatomic and mechanical study of the interosseous membrane of the
forearm: Pathomechanics of proximal migration of the radius. J Hand Surg (Am). 1989;14(2
Pt 1):256–261.
McGinley JC, Kozin SH. Interosseous membrane anatomy and functional mechanics. Clin Orthop
Relat Res. 2001;383:108–122.
Poitevin LA. Anatomy and biomechanics of the interosseous membrane: Its importance in the
longitudinal stability of the forearm. Hand Clin. 2001;17(1):97–110.
Rettig M, Raskin K. Galeazzi fracture-dislocation: A new treatment-oriented classification. J Hand
Surg (Am) 2001;26:228–235.
Richards RR. Chronic disorders of the forearm. J Bone Joint Surg Am. 1996;78(6):916–930.
Ring D, Jupiter JB, Simpson NS. Monteggia fractures in adults. J Bone Joint Surg. 1998;80A:
1733–1744.
Schemitsch EH, Richards RR. The effect of malunion on functional outcome after plate fixa-
tion of fractures of both bones of the forearm in adults. J Bone Joint Surg Am. 1992;74(7):
1068–1678.
Skahen JR III, et al. The interosseous membrane of the forearm: Anatomy and function. J Hand
Surg (Am). 1997;22(6):981–985.

Fractures and Dislocations:
Elbow
16
Michael Darowish, Jesse B. Jupiter, Graham J.W. King,
Kevin J. Malone, and Jeffrey N. Lawton
The stability of the elbow joint is a result of primarily the bony anatomy. There are two
articulations at the elbow and as a result, there are two arcs of motion.
1. The ulnohumeral joint resembles a hinge joint and permits flexion and exten-
sion at the elbow.
2. The radiohumeral and proximal radioulnar joints allow for axial rotation that
results in pronation and supination of the forearm.
I. Functional Anatomy (Fig. 16.1)
A. Osseous components
1. The ulnohumeral is one of the most confined and inherently stable joints in the
body.
2. The trochlea is surrounded 180 degrees by the trochlear notch.
3. The distal humerus tilts 30 degrees anteriorly and the trochlear notch tilts
posteriorly in the sagittal plane. This relationship has implications for stabil-
ity and motion:
a) The coronoid process resists posterior translation of the forearm in both
flexion and extension.
b) Elbow flexion is enhanced.
c) The relatively large width of the trochlea and the olecranon enhance varus
and valgus stability.
4. The radial head articulates with the proximal ulna forming the proximal
radial ulnar joint (PRUJ).
5. The radial head resists both posterior translation of the forearm and resists
valgus stress.
B. Capsuloligamentous components
1. The medial collateral ligament (MCL) and the lateral collateral ligament
(LCL) are the main capsuloligamentous stabilizers of the elbow.
2. The MCL complex has three discrete components.
a) The posterior bundle originates from the inferior aspect of the medial
humeral epicondyle and courses distally to the medial joint line along the
sigmoid notch of the ulna (essentially a thickening of the joint capsule).
b) The anterior bundle is the most distinct and structurally important com-
ponent. It also originates from the inferior aspect of the medial humeral
epicondyle. It courses distally and anteriorly to insert on the medial aspect
of the coronoid on the sublime tubercle. This bundle is tight in extension
and is an important stabilizing structure of the medial elbow against the
type of valgus stress that is created in an overhead throwing motion or a
fall onto an extended elbow.
264

Chapter 16 • Fractures and Dislocations: Elbow 265
Humerus Olecranon fossa
Olecranon Lateral epicondyle
Origin of lateral ulnar

collateral ligament
Medial
epicondyle
Capitellum
Supinator crest
Sulcus for (attachment of annular
ulnar nerve and lateral collateral
ligaments)
Head
Ulna
Neck
Radial tuberosity
Radius
B
Figure 16.1 A and B Morphlogy of the elbow. Anterior and posterior view of osseous
anatomy of the elbow. (Courtesy of Leversedge FJ, Goldfarb CA, Boyer MI, and Lin M.)

c) The transverse component is the least important part of the MCL

complex. It is a capsular thickening that runs from the medial border of
the coronoid to the medial aspect of the olecranon.
3. The LCL complex is made up of the radial collateral ligament, the annular
ligament, and the lateral ulnar collateral ligament. The LCL arises from the
lateral humeral condyle at a point through which the axis of rotation passes.
Because of this, it maintains a uniform tension throughout the arc of motion.
It bifurcates as it extends distally.
a) The anterior portion is called the radial collateral ligament, and it blends
with the annular ligament around the radial head.
b) The posterior portion is called the lateral ulnar collateral ligament and
inserts onto the lateral portion of the ulna at the supinator crest. This liga-
ment is the primary lateral stabilizer of the elbow and its compromise will
result in the posterior sagging of the radial head and lateral aspect of the
sigmoid notch of the ulna with respect to the capitellum and trochlea of
the humerus. This condition is called posterolateral rotatory instability.
4. The anterior capsule and the collateral ligament complexes act as important
secondary dynamic stabilizers, and contribute to resisting valgus stress.
C. Musculotendinous components
1. The biceps, brachialis, and tricep muscles help maintain the trochlea in the
trochlear notch.
2. Together the muscles provide dynamic stability to the elbow.
D. Nerve relationships
1. The ulnar nerve runs posterior to the medial epicondyle and lies medial and
deep to the olecranon process. It may be at risk by anterior and ulnar penetra-
tion of the cortex by Kirschner wires (K-wires) in a tension band technique.
2. The radial nerve runs along the lateral aspect, anterior to the lateral epicon-
dyle and crosses anterior to the radiocapitellar joint.
3. The median nerve runs medial to the brachial artery, which lies medial to
the biceps tendon. The mnemonic MAT can be used to remember this ori-
entation from medial to lateral.
Elbow Fractures and Dislocations: Simple Elbow Dislocations
I. Anatomy
(See section on elbow anatomy at the beginning of this chapter.)
II. Definition
A “simple” elbow dislocation involves dislocation of the ulnohumeral joint without

associated fractures to the radial head, olecranon, or coronoid. When these other inju-
ries are present, the injury is termed “complex” and the treatment protocol differs.
While “simple” dislocations are primarily soft tissue injuries with disruption of the
secondary stabilizers, postreduction radiographs reveal periarticular fractures in up to
60% of cases and operative exploration reveals osteochondral injuries in nearly 100%
of acute elbow dislocations. Without the injuries seen in the complex patterns, the pri-
mary joint stabilizers remain intact and allow for nonoperative management.

III. Incidence
Acute elbow dislocations account for 10% to 25% of all injuries to the elbow. The
mechanism of injury is typically a fall onto an outstretched hand with the elbow
extended and the arm abducted away from the body. The proposed sequence of
events based on laboratory studies is that a combination of valgus, supination, and
axial forces applied to the elbow results in a sequential failure of the soft tissues, pro-
gressing from the LCL to the anterior and posterior capsules, and finally the MCL
This sequence of events has not been universally supported by clinical studies. This
is typically an injury of the young adult with the median age for the injury around
30 years.
IV. Evaluation and Initial Treatment
Evaluation should include a complete assessment of the arm with particular attention
to the neurovascular status.
1. Arterial injury or occlusion has been reported.
2. The motor and sensory examination of the median, ulnar, and radial nerves is
determined and documented.
3. The wrist and shoulder are assessed for deformity or pain, as concomitant upper
extremity injuries have been reported to occur in up to 15% of cases.
4. Radiographs in two planes should be assessed to determine the direction of the
dislocation. These injuries are described by the position of the ulna in relation
to the distal humerus. Approximately 90% of dislocations occur with posterior
or posterolateral displacement of the ulna. The radiographs should be evaluated
for associated periarticular fractures.
5. Attempts at closed reduction typically require adequate muscle relaxation and
analgesia. There are many different described maneuvers but they all include
correction of medial/lateral displacement and then application of longitudinal
traction with the elbow extended followed by elbow flexion. This will allow
the coronoid to be brought around the trochlea. Reduction should produce a
palpable clunk.
6. Immediately following reduction, the elbow should be assessed for stability.
It will typically demonstrate instability to valgus stress and in full exten-
sion. The neurovascular status of the arm following reduction is reassessed.
Although the distal pulses may be diminished on initial examination, they
often return to normal after reduction. There is a higher incidence of brachial
artery lacerations with open dislocations and with complex elbow disloca-
tions. A pulseless arm after reduction is an indication for immediate explora-
tion. Similarly, nerve injuries are rare with simple elbow dislocations. The
ulnar nerve is most commonly involved and usually resolves with time. If
there is a brachial artery injury, there may be a median nerve injury as well
because of their proximity.
7. Postreduction radiographs should be assessed for concentric reduction of the
ulnohumeral, radioulnar, and radiocapitellar joints. Joint space widening may
be an indication of entrapped chondral fragments or soft tissue in the joint and
is an indication for exploration.

8. There are few indications for open reduction or immediate exploration. Open
dislocations and dislocations with associated brachial artery laceration should
be explored. The other indications include a joint that must be maintained
beyond 50 to 60 degrees of flexion to remain reduced and a joint with suspected
entrapped fragments following reduction. In the setting of persistent instabil-
ity without evidence of disruption of the bony anatomy, the medial and/or the
LCL complexes need to be repaired or reconstructed. Typically, the ligaments
are avulsed from their humeral origin.
V. Postreduction Management
1. If the joint is stable following reduction and radiographs confirm concentric

reduction, the elbow is placed into a splint in approximately 90 degree flexion
and the forearm in full pronation (to allow healing of the LCL).
2. The immobilization should be discontinued in approximately 1 week and
elbow motion initiated. Immobilization for longer than 3 weeks has been
associated with long-term stiffness. Radiographs should be taken at 1 week
to confirm maintained reduction. If the joint is still reduced, the patient can
begin range of motion exercises with intermittent splinting for protection and
comfort. Radiographic follow-up will typically show calcification within the
anterior capsule or along the collateral ligaments, but rarely is the cause of
limited motion.
VI. Results
Flexion returns first, with maximum improvement usually seen by 12 weeks. Return of
extension can continue to show improvement for up to 5 months following injury. Loss
of extension is the most common sequela of this injury as patients will typically lose
10 to 15 degrees of extension. As clinical studies have shown the relationship between
period of immobilization and final range of motion, many authors are encouraging an
earlier motion program. Despite the trend for shorter immobilization, there has not
been an increase in the rate of redislocation or early instability.
Long-term follow-up studies conducted at 3 years and 24 years after injury have
shown that elbow discomfort is present in up to 50% of the cases. Average flexion
contracture was 12 degrees at 24 years. Greater degrees of flexion contractures were
associated with longer periods of immobilization. Radiographs showed minimal post-
traumatic changes with no loss of joint space.
Coronoid Fractures
I. Anatomy (see additional information at beginning of chapter)
The coronoid is the anterior projection of the greater sigmoid notch of the proximal
ulna (Fig. 16.2) It consists of a tip, body, anterolateral, and anteromedial facets. At the
base of the anteromedial facet, the sublime tubercle provides the insertion site for the
anterior bundle of the MCL. The coronoid is an important stabilizer against posterior,
varus, and posteromedial rotatory instability of the elbow. Larger coronoid fractures
have a greater influence on elbow stability.

Figure 16.2 Morphology of the coronoid. The coronoid consists of a tip, body,
anterolateral, and anteromedial facets. At the base of the anteromedial facet, the sublime
tubercle provides the insertion site for the anterior bundle of the MCL.
II. Incidence
Coronoid fractures do not occur in isolation; consequently, their incidence is poorly

documented. They are usually associated with radial head fractures, elbow dislocations,
ligament injuries, or transolecranon fracture-dislocations.
III. Classification
A. There are two commonly employed classification systems outlining the patterns
of coronoid fractures.
1. The Regan and Morrey system is based on the height of the coronoid
fragment (Fig. 16.3).
a) Type I: Small “avulsion” of the tip of the coronoid process (typically <10%)
b) Type II: Includes up to 50% of the coronoid.
c) Type III: Involves greater than 50% of the coronoid.
The system of O’Driscoll is based on the location of the fracture (Fig. 16.4).
The coronoid is divided into the tip, the anteromedial facet, and the base.
a) Coronoid tip fractures are divided into fragments that are less than or
greater than 2 mm in size.
b) Fractures of the anteromedial facet are divided into three subtypes.
1) Subtype 1 anteromedial facet fractures involve the rim. They begin just
medial to the tip of the coronoid and extend toward the sublime tuber-
cle but do not involve it.
2) Subtype 2 fractures involve the rim of the anteromedial facet and the
tip of the coronoid.

Figure 16.3 Regan and Morrey classification. A type I fracture is a small “avulsion” of
the tip of the coronoid process (typically <10%). A type II fracture includes up to 50%
of the coronoid. A type III involves greater than 50% of the coronoid.
3) Subtype 3 fractures involve the sublime tubercle and also the rim with
or without involvement of the tip of the coronoid.
c) Basal coronoid fractures consist of a fracture through the body of the
coronoid and involve at least 50% of the coronoid height.
1) Subtype 1 involves only the coronoid
2) Subtype 2 is a coronoid body fracture in association with a fracture
through the olecranon.
IV. Clinical Evaluation
A history of fall on outstretched arm is typical; however, some have a higher energy
mechanism. Careful examination of both collateral ligaments and the DRUJ is needed
to evaluate for associated injuries. Anteroposterior and lateral radiographs of the elbow
are essential. Positive fat pad sign for a hemarthrosis may be the only radiographic
finding if the coronoid fracture is small or nondisplaced. A double crescent sign is asso-
ciated with anteromedial coronoid fractures. Supplementary oblique views can more
accurately define the anatomy, displacement of the fracture, and any associated injuries.
CT imaging is recommended for all coronoid fractures as it is difficult to visualize the
pattern and magnitude of injury with standard radiographs. 3D reconstructions can
assist with preoperative planning.
V. Management
The treatment of coronoid fractures is dependant on the size and pattern of fracture and
the presence and severity of associated osseous and ligament injuries.

Figure 16.4 O’Driscoll classification. The coronoid is divided into the tip, the
anteromedial facet, and the base. A: Fractures of the anteromedial facet are divided
into three subtypes. Subtype 1 anteromedial facet fractures involve the rim. They begin
just medial to the tip of the coronoid and extend toward the sublime tubercle but do
not involve it. Subtype 2 fractures involve the rim of the anteromedial facet and the
tip of the coronoid. Subtype 3 fractures involve the sublime tubercle and also the rim
with or without involvement of the tip of the coronoid. B: Basal coronoid fractures
consist of a fracture through the body of the coronoid and involve at least 50% of the
coronoid height. Subtype 1 involves only the coronoid while subtype 2 is a coronoid
body fracture in association with a fracture through the olecranon.

A. Nonoperative
Indicated for small fractures of the tip of the coronoid without associated elbow
instability. The arm can be splinted for comfort for 1 week and then active range
of motion exercises are initiated using a collar and cuff or splint at 90 degrees for
support during the first 3 to 4 weeks. Follow-up should include clinical examina-
tion and radiographs to ensure that the range of motion progressively recovers
and the elbow remains congruously reduced. If stiffness is a problem, early refer-
ral should be considered for physical therapy, with or without splinting.
B. Open reduction and internal fixation (ORIF).
Larger coronoid fractures should be treated with ORIF. Fixation options include
suture fixation, compression screws, and headless compression screws and plates.
The fixation technique chosen depends on the size the fragment(s), the pattern
of injury, and the presence of comminution and osteopenia. Suture fixation is
used for small, comminuted fragments while buttress plate fixation is preferred
for anteromedial coronoid fractures.
C. Surgical approach
The surgical approach depends on the size and location of the fragment and the
presence of associated injuries.
1. If there is a concomitant fracture of the radial head, which is to be replaced,
the coronoid can be well visualized and fixed from a lateral surgical approach.
Sutures or screws can be placed though the subcutaneous border of the ulna.
2. If the radial head is intact, fixation of the coronoid is often still possible by
subluxing the elbow to obtain an adequate view.
3. If visualization from a lateral exposure is not adequate or if an anteromedial
coronoid fracture is present, a medial approach should be employed.
4. Smaller coronoid fractures can be approached by splitting the common flexor
origin after identifying and protecting the ulnar nerve while larger ones can
be approached by working through the floor of the flexor carpi ulnaris (FCU)
after transposition of the ulnar nerve, or lifting up the whole flexor pronator
group off the medial elbow, as for a submuscular ulnar nerve transposition.
Basal fractures with an associated olecranon fracture can often be repaired
working through the exposure afforded by the olecranon fracture, with fixa-
tion achieved with lag screws placed through the plate.
VI. Rehabilitation
Immobilization of the elbow for 1 week following the initial injury or postoperatively
is often helpful to control pain and swelling. Active motion of the elbow should then
be initiated within a safe arc of motion. If there are associated injuries such as an elbow
dislocation or collateral ligament injury, terminal extension should be avoided until
muscle tone improves. Passive stretching should be avoided for 6 weeks due to a risk of
heterotopic ossification. Strengthening is initiated after fracture healing is secure, typi-
cally 6 to 8 weeks postoperatively. Nighttime static progressive extension splinting can
be helpful to regain terminal elbow extension.
VII. Outcome
The limited data available regarding the outcome of coronoid fractures are compli-
cated by the presence and management of associated osseous and ligamentous injuries.
Nonoperative treatment of anteromedial coronoid fractures has been documented to

have a high incidence of elbow instability and posttraumatic arthritis while ORIF has a
favorable outcome. Similarly, larger coronoid fractures treated nonoperatively are com-
plicated by a high incidence of elbow instability and arthritis. ORIF effectively restores
elbow stability and good functional outcome in most patients.
VIII. Complications
Instability and stiffness are the most frequent complications following fractures of the
coronoid. Late osteoarthritis is not uncommon, likely due to chondral injuries from the
associated elbow dislocation and due to residual instability. Heterotopic ossification seems
to be more common with repeated surgical procedures, and with associated dislocations.
Radial Head Fractures
I. Anatomy and Biomechanics (see additional information at the

beginning of this chapter)
The radial head is elliptical and variably offset from the radial neck, with an articular
dish that is circular and shallower than the capitellum, allowing for translation during
rotation (Fig. 16.5). The articular portion is flattened with thick cartilage while the
nonarticular portion is more rounded with thin or absent cartilage. About two thirds
of the circumference of the head articulates with the PRUJ. The blood supply is from
Figure 16.5 Morphology of the proximal radius. The radial head is offset from the
radial shaft and contains both articulating and nonarticulating portions. The articular
dish is concave, allowing for articulation with the capitellum.

capsular perforators at the head-neck junction, and through the medullary canal. Over
half of the load transfer across the elbow is through the radial head, and it contributes
substantially to the axial, valgus, and posterolateral rotatory stability of the elbow.
II. Incidence
These are the most common fractures of the elbow. Radial neck fractures are more
frequent in children, whereas head fractures are more common in adults. Displaced
fractures usually have associated injuries of the collateral ligaments. Fractures of the cor-
onoid, capitellum and olecranon, elbow dislocations, and ruptures of the interosseous
membrane are seen concurrently with higher energy injuries.
III. Classification
A modified Mason classification most commonly employed.

Type I: Undisplaced or less than 2 mm displacement.
Type II: Displaced fracture of the head or neck without comminution.
Type III: Displaced and comminuted.
Type IV: Associated elbow dislocation.
IV. Clinical Evaluation
A history of a fall on an outstretched arm is typical; however, some may have a higher
energy mechanism. Patients typically present with elbow pain, limited extension and/
or rotation, and tenderness over the radial head. Careful examination of collateral
ligaments and DRUJ is needed to evaluate for associated injuries. Anteroposterior and
lateral radiographs of the elbow may demonstrate a positive fat pad sign, indicating
hemarthrosis (Fig. 16.6). This may be the only radiographic finding in an undisplaced
Anterior Hemoarthrosis
Posterior
fat pad
fat pad
Synovial
fluid
Figure 16.6 Fat pad sign. A hemarthrosis as a consequence of a radial head fracture
elevates the anterior and posterior fat pads of the elbow such that they become visible
on a lateral radiograph.

Figure 16.7 Technique for aspiration and local anesthetic injection into the elbow.
A needle is inserted into the elbow at the centre of a triangle formed by the lateral
epicondyle, the tip of the olecranon, and the radial head. After aspirating the
hematoma, local anesthesia is injected into the elbow and the range of motion is re-
evaluated.
fracture. Supplementary oblique views and CT imaging can more accurately define
the anatomy, displacement of the fracture, and any associated injuries. If forearm
rotation is restricted, a local anesthetic injection should be performed to rule out a
mechanical cause of stiffness that is not evident on radiographs. Under sterile tech-
nique, a needle is inserted into the lateral elbow at the centre of a triangle formed by
the lateral epicondyle, the tip of the olecranon, and the radial head. After aspirating
the hematoma, 10 cc of local anesthesia is injected into the elbow and the motion is
re-evaluated (Fig. 16.7).
V. Management
A. Nonoperative
Indicated for undisplaced or minimally displaced fractures without a block to forearm
rotation. The arm splinted for comfort for a few days, and then active range of motion
exercises are initiated using a collar and cuff for support for the first three to 4 weeks.
Follow-up should include clinical examination and radiographs to ensure that the range
of motion progressively recovers and the fracture does not displace. If stiffness is a

problem, early physical therapy should be considered, with or without splinting (either
static progressive or dynamic).
B. Fragment Excision
Displaced radial head fractures, which interfere with forearm rotation and are too small,
comminuted or osteopenic to reliably treat with ORIF should be treated by excision
of the fragment if it comprises less than 25% of the radial head and does not articulate
with the proximal radioulnar joint.
C. Open Reduction and Internal Fixation

Fractures that are displaced greater than 2 mm and involve one third or more of the
radial head should be considered for ORIF; however, the indications for operative man-
agement remain poorly defined. Smaller fractures that interfere with forearm rotation
should also be treated with ORIF if technically possible. In general, ORIF is preferred
if the fracture fragments are larger, not excessively comminuted and the bone is of suffi-
cient quality to allow for stable fixation and early motion. Fractures involving the whole
head with disruption of the periosteal blood supply at the radial neck have an increased
incidence of nonunion and avascular necrosis. Fixation options include bioabsorbable
pins, small countersunk compression screws, headless compression screws, and standard
or precontoured plates.
D. Radial Head Excision

Excision of the radial head can be employed in the setting of displaced comminuted
fractures of the radial head that cannot be repaired with ORIF due to small fragment
size, osteopenia, poor vascularity, or gross contamination from compound injuries. Pre-
requisites to radial head excision are the absence of associated injuries to the collateral
ligaments, interosseous membrane, and the DRUJ (the so-called Essex-Lopresti lesion)
or an elbow dislocation. Since the incidence of associated soft tissue injuries is between
75% and 100% in most series of comminuted radial head fractures, the circumstances
where radial head excision is performed without replacement are uncommon. Further-
more, since the associated soft tissue injuries are difficult to diagnose, routine radial
head replacement following radial head excision should be considered.
E. Radial Head Arthroplasty

Radial head replacement is indicated for displaced comminuted fractures, which cannot
be reliably treated with ORIF due to comminution, osteopenia, or compromised vascu-
larity. Radial head replacement should be routinely performed in the setting of known
or probable associated soft tissue or osseous injuries of the elbow. A metallic radial head
arthroplasty is typically used; however, the optimal implant design is unknown due to
a lack of comparative studies.
VI. Surgical Approach
The radial head can be approached using either a posterior or a lateral skin incision.
1. In patients with an associated LCL disruption, the radial head can be fixed or
replaced through the soft tissue injury.
2. In the circumstances of an intact lateral ligament, the interval between the
anconeus and extensor carpi ulnaris (Kocher approach) can be employed.

3. Alternatively a more anterior approach, splitting the common extensor tendon

is useful, as it allow access to the more anterior portion of the radial head,
the typical location of partial articular fractures. This interval is anterior to the
lateral ulnar collateral ligament, which is at risk of injury with more posterior
exposures. If the dissection extends distal to the radial neck, the forearm should
be maintained in pronation to protect the posterior interosseous nerve. This
will place the PIN anterior to the field of dissection. Care should be taken when
placing retractors anterior to the radial neck to avoid a compressive neurapraxia.
Careful repair of the annular ligament and the LCL following radial head sur-
gery is done to maintain the stability of the elbow.
VII. Rehabilitation
Immobilization of the elbow for 1 week following the initial injury or postoperatively
is often helpful to control pain and swelling. Active motion of the elbow should then
be initiated within a safe arc of motion. If there are associated injuries such as an elbow
dislocation or collateral ligament injury, terminal extension should be avoided until
muscle tone improves. Passive stretching should be avoided for 6 weeks due to the risk
of heterotopic ossification. Strengthening is initiated after fracture healing in secure,
typically 6 to 8 weeks postoperatively. Nighttime static progressive extension splinting
can be helpful to regain terminal elbow extension.
VIII. Outcome
The functional results of radial head fractures are dependant on the nature of the
fracture, the presence of associated injuries, and their management. Mason I fractures
have an excellent outcome in the majority of patients with a low incidence of late
displacement, stiffness, pain, or osteoarthritis. Displaced Mason II fractures without
a block to motion often do well with nonoperative management with a low incidence
of residual symptoms; however, radiocapitellar osteoarthritis is seen commonly at
long-term follow-up. Other authors have reported improved outcomes with ORIF of
displaced radial head fractures when compared to nonoperative management. There
are no randomized clinical trials to provide guidance on the optimal management of
Mason II fractures. Similarly, Mason III fractures treated with ORIF or radial head
arthroplasty have varying results reported in the literature. In general, metallic radial
head arthroplasty has been more reliable than ORIF of comminuted fractures; how-
ever, the outcome is highly dependent on the presence of associated injuries and their
management.
IX. Complications
Stiffness is the most frequent complication following radial head fractures, par-
ticularly the loss of terminal extension. Avascular necrosis and nonunion are more
commonly seen with ORIF of comminuted fractures. Late osteoarthritis is not
uncommon, particularly with residual articular incongruity or following radial
head excision. Heterotopic ossification seems to be more common with repeated
surgical procedures, with associated dislocations, and in patients with concomitant

head injuries. Radial head prostheses can develop symptomatic loosening and
capitellar wear.
Olecranon Fractures
Olecranon fractures are common in adults and span a wide spectrum of complexity
from simple nondisplaced fractures to fracture-dislocations of the elbow. By defini-
tion, all olecranon fractures are intra-articular and typically require operative interven-
tion in order to restore anatomic alignment of the joint and to restore the extensor
mechanism. Important in the understanding of olecranon fractures is recognizing the
complexity of the fracture pattern and matching it with the appropriate treatment
option and surgical technique. Treatment options include nonoperative therapy, frag-
ment excision, tension-band wiring, intramedullary screw fixation, and plate and screw
fixation. The goal of treatment is to restore the extensor mechanism, to prevent stiff-
ness by allowing early motion, and to prevent degenerative changes by maintaining a
congruous joint.
I. Anatomy
(See section on anatomy at the beginning of this chapter.)
II. Mechanism and Associated Injuries
A. The majority of olecranon fractures are isolated and result from a low-energy
fall, particularly in older patients with osteoporotic bone.
B. Fractures can occur from direct trauma or from avulsion by pull of the
triceps.
C. Higher energy fractures with comminution are seen in younger patients, usually
in motor vehicle or motorcycle accidents.
D. Radial head and coronoid process fractures, Monteggia-type injuries (radial
head dislocation).
E. Open injuries are uncommon.
F. High-energy injuries can be associated with forearm compartment syndrome.
G. Fracture-dislocations may be associated with ulnar nerve injury.
III. Initial Evaluation
A. As in any trauma situation, the patient should be evaluated according to the

Advanced Trauma Life Support protocol.
B. In low-energy falls, especially in older patients, the mechanism of injury
should be thoroughly evaluated to ensure that there is no underlying medi-
cal cause (e.g., syncope). Associated injuries such as distal radius fractures,
cervical spine injuries, and hip fractures should also be considered in this
population.
C. The skin should be examined for open injuries. If a splint is on, it must be
removed. Typically, there is a significant amount of subcutaneous swelling and
bruising. A depression at the fracture site can sometimes be appreciated.

D. In all injuries, particularly the higher energy injuries, a thorough and

well-documented neurovascular examination should be performed. Specific
attention should be given to ulnar nerve and anterior interosseus nerve function
(seen in Monteggia injuries).
E. Initial radiographs are often limited due to pain. The personality of the fracture
and other possible associated injuries can be assessed, typically on the lateral
projection.
F. Postmanipulation radiographs or a CT scan may provide additional informa-
tion for fracture-dislocations or when radial head or coronoid process fractures
are suspected.
IV. Fracture Classification and Patterns of Injury
There are several classifications systems used for olecranon, as well as proximal ulna and
radial fractures. No one classification is universally used:
A. AO classification
1. Type A: Extra-articualar fractures at the metadiaphysis level.
2. Type B: Intra-articular fractures of either the radius or ulna.
B1: An olecranon fracture.
3. Type C: Complex fractures of both the proximal radius and ulna.
B. Schatzker classification
1. Transverse fracture through the deepest point of the trochlear notch usually
resulting from sudden pull of the triceps.
2. Complex transverse fracture with comminution or central, articular impac-
tion from a direct force.
3. Oblique fracture usually from hyperextension.
4. Comminuted fracture with associated fracture of the coronoid process.
5. Oblique fracture distal to the midpoint of the trochlear notch. (Tension
band fixation is inadequate.)
6. Olecranon fracture with associated radial head fracture and possibly MCL
injury.
C. Mayo classification
1. Type I: Nondisplaced fractures. The fracture may be either noncomminuted
(Type IA) or comminuted (Type IB).
2. Type II: Displaced, stable fractures. The proximal fracture fragment is
displaced more than 3 mm, but the collateral ligaments are intact, and
there is no elbow instability. The fracture may be either noncomminuted
(Type IIA) or comminuted (Type IIB).
3. Type III: Displaced, unstable fractures: The proximal fracture fragment is
displaced and the forearm is unstable in relation to the humerus. This is a
fracture-dislocation. It also may be either noncomminuted (Type IIIA) or
comminuted (Type IIIB).
V. Treatment Options
A. Nonoperative
1. Nondisplaced fractures in which the extensor mechanism is intact may be
treated without surgery.
2. The elbow should be immobilized in 30 degrees of flexion for 6 weeks.

3. Repeat radiographs should be obtained at 1 week to look for displacement of

the fracture.
4. Nonoperative treatment is uncommon because of the length of immobiliza-
tion required and the risk of elbow stiffness.
B. Operative
1. Surgical planning
a) The patient can be positioned either supine with the arm across the
chest or lateral decubitus/prone with the arm draped over a padded
support.
b) Either a sterile or nonsterile tourniquet applied at the upper arm can be
used.
c) General or regional anesthesia (e.g., axillary block) can be utilized.
d) A midline posterior skin incision is utilized, incorporating open wounds
if present. A curvilinear approach that does not pass directly over the
olecranon can be used but may cross more cutaneous nerves.
e) The ulnar nerve usually does not need to be isolated.
2. Surgical techniques
a) Tension band wiring
1) Used for simple fractures at the level of the transverse groove
2) Failure to recognize distal extension or more complex injury will lead
to fixation failure.
3) After inspection to rule out more extensive comminution and after
reduction, two parallel 0.062 or 0.045-in K-wires are passed through
the fracture site and through the anterior cortex distal to coronoid
process
4) One or two holes are drilled transversely across the ulna distal to the
fracture site.
5) One 18-gauge or two 22-gauge stainless steel wires are passed through
the holes and placed in a figure-of-eight configuration. The proximal
part of the wire is passed through the insertion of the tricep. The wires
are tensioned with two loops on both sides of the figure-of-eight con-
figuration.
6) This technique converts tension forces into compression forces at the
fracture site.
b) Intramedullary screw technique
1) Can be used in lieu of tension band wiring for simple fractures.
2) A large 6.5 mm cancellous screw is placed down the shaft of the ulna
to grab the distal cortex.
3) Complications include malreduction and distal ulna fracture.
4) A tension band can supplement screw fixation.
c) Plate and screw fixation
1) Used for comminuted fractures, Monteggia fractures, and olecranon
fracture-dislocations (discussed in the next section).
2) Dynamic compression plates are used. One-third tubular plates are not
adequate for fixation.
3) Plates can be placed dorsally, medially, or laterally.
4) The plate should contour around the proximal ulna to increase the
number of screws that can be placed proximally.
5) The triceps insertion can be incised longitudinally to place the plate
directly on bone.

6) Anatomic restoration of the coronoid and olecranon processes is

critical and the remaining comminution can be bridged.
d) Excision and triceps advancement
1) This technique is rarely indicated as primary treatment.
2) It may be used in significantly comminuted, osteopenic bone for
infirm, older patients with low functional demands.
3) This technique is contraindicated with collateral ligament, radial head,
or coronoid process injury.
4) After excision of the fragments, the triceps is attached with large
grasping sutures through drill holes just below the articular
margin.
5) Excision of larger pieces has greater potential for elbow instability.
3. Postoperative management
a) Active range of motion should be initiated the day after surgery.
b) Resistive exercises should be delayed until early healing is seen at 6 to
8 weeks.
c) Tenuous fixation or excision and triceps advancement should be immobi-
lized for 4 to 6 weeks before exercises are started.
VI. Complications
A. Hardware failure
1. Occurs in up to 5% of patients.
2. Tension bands fail if used for comminuted or complex factures.
3. Plates may fail if not properly contoured or when placed either medially or
laterally.
B. Hardware prominence
1. Up to 80% of patients may experience symptoms from hardware.
2. This can be prevented by seating the K-wires in the olecranon, position-
ing the twisted wire loops away from the skin, and longitudinally incising
the triceps tendon to place a plate directly on bone.
C. Infection
1. Infections are unusual and occur in more complex injuries.
D. Nonunion
1. Nonunions are unusual, especially for simple fractures.
E. Ulnar neuropathy
1. May occur in up to 5% of cases.
2. Usually resolves with conservative management.
3. Symptoms may develop as late as 4 to 6 weeks in which case the neuropathy
may benefit from a release.
F. Heterotopic ossification and stiffness
1. Stiffness is common in elbow injuries, but it is uncommon in olecranon
fractures.
2. Stiffness increases with complexity of the fracture.
3. Heterotopic ossification may occur and has been reported in up to 13% of
cases.
G. Arthrosis
1. Severe arthrosis is uncommon.
2. Some level of arthrosis may be seen in up to 20% of patients.

Anterior Column
Coronoid Process
Brachialis Muscle
Anterior Aspect of Capsule
Lateral Column Medial Column

Radial Head Medial Collateral Ligament
Capitellum Coronoid Process
Lateral Collateral Ligament Medial Condyle Epicondyle
Complex
Posterior Column
Olecranon Process
Triceps Muscle
Posterior Aspect of Capsule
Figure 16.8 Stabilizing osseous, musculotendinous, and ligamentous structures of the

elbow. Disruption of any one of these elements can cause elbow instability. (Reproduced
with permission from Ring D, Jupiter JB. Current concepts review: Fracture-dislocation
of the elbow. J Bone Joint Surg Am. 1998;80:566–580.)
Proximal Radius and Ulna Injuries: Complex Elbow Instability (Fig. 16.8)
By definition, a complex elbow dislocation differs from a simple ulnohumeral

elbow dislocation by having an associated fracture of a major bony stabilizer: Distal
humerus, radial head, proximal ulna, or coronoid process. These fractures make the
injury inherently unstable and necessitate operative intervention to restore anatomic
alignment and elbow stability. The risk of recurrent instability and arthrosis increases
with the complexity of the injury. Critical to understanding how to evaluate and treat
these injuries is knowing the importance, function, and relationship of each major
element of bony and ligamentous anatomy and its relative contribution to elbow
stability.
I. Functional Anatomy
(See section on anatomy at the beginning of this chapter.)
II. Mechanism of Injury
A. Most complex dislocations occur from a high-energy fall on an outstretched

hand or a motor vehicle accident (MVA). The force causes the trochlea to
be levered out of the proximal ulna causing capsuloligamentous, musculo-
tendinous, and bony injury to the olecranon, coronoid process, or radial
head.

B. Most commonly, the injury is a combination of valgus-, supination-, and

axial-directed forces.
C. Sequential and predictable injury starts from the lateral side and moves anteri-
orly and posteriorly to the medial side.
D. Anterior or transolecranon fracture-dislocations occur with a direct blow to the
elbow in flexion.
E. Posterior Monteggia injuries are usually low-energy falls in older, osteopenic
women.
III. Clinical Evaluation
A. As in all fractures, especially high-energy elbow fracture-dislocations, the patient

should be first evaluated according to the Advanced Trauma Life Support guide-
lines.
B. Head trauma will specifically have an effect on management and outcome of the
elbow due to increased incidence of heterotopic bone formation.
C. The skin should be evaluated for open wounds.
D. A thorough neurovascular examination is done before any manipulation and
repeated afterward for any change.
E. Forearm compartment syndrome should be considered in high-energy injuries.
F. Anteroposterior and lateral radiographs of the elbow are necessary.
G. 2D and 3D reformatted CT scans are often needed for the fixation of coronoid,
radial head, or olecranon fractures.
IV. Classification and Pattern of Injury
A. Ligamentous injury with radial head fractures.

B. Ligamentous injury with radial head and coronoid process fractures (“terrible
triad injuries”).
C. Ligamentous injury with radial head, coronoid process, and olecranon process
fractures.
D. Anterior or transolecranon fracture-dislocation.
E. Posterior Monteggia injuries.
V. Ligamentous Injury with Radial Head Fracture
A. The addition of a radial head fracture to a simple dislocation implies a higher

energy injury, more challenging treatment, and ultimately worse outcomes.
B. Mason I fractures that restrict motion and some Mason II fractures require fixa-
tion; nonrepairable Mason II fractures and Mason III fractures require metallic
head replacements to restore valgus stability.
C. The radial head should not be resected (and not replaced with a metallic arthro-
plasty) in the setting of complex elbow dislocations in order to allow the liga-
ments to heal at the correct length and tension.
D. After radial head fixation or replacement, LCL and wrist extensor musculoten-
dinous origin repair may be necessary if there is disruption or persistent poste-
rolateral rotatory instability.
E. MCL evaluation and repair may be necessary with continued valgus instability.

F. In the unusual event of persistent instability despite radial head fixation and
LCL and MCL repair, a hinged external fixator should be applied to maintain
elbow stability and motion.
VI. Ligamentous Injury with Radial Head and Coronoid Fracture

(Terrible Triad)
A. Increased chances of acute and chronic instability as well as elbow arthrosis.

B. CT scans are particularly helpful in preoperative planning, specifically for evalu-
ating coronoid fractures.
C. Regardless of size, the coronoid fragment should be fixed by either suture repair
of the anterior capsule, screw fixation, or plating to recreate anterior buttress.
D. The LCL should be repaired, usually at the lateral epicondyle attachment site.
E. Again, a hinged external fixator may be necessary if instability persists.
VII. Ligamentous Injury with Radial Head, Coronoid, and Olecranon

Fractures
A. There is complete disruption of all four elements of the structural ring of the
elbow (see Fig. 16.8).
B. In addition to the treatment used for terrible triad injuries, the trochlear notch
must be anatomically restored. Dorsal plating of the ulna is typically required
(refer to “Olecranon Fractures” section).
C. Coronoid fractures are typically large.
VIII. Anterior or Transolecranon Fracture Dislocations
A. The injury is defined by a complex olecranon or proximal ulna facture with

anterior dislocation of the forearm with maintenance of the PRUJ.
B. Though these are high-energy injuries, outcomes after surgical fixation are bet-
ter than terrible triad injuries.
C. The injury is distinct from anterior Monteggia fractures (refer to the chapter
Fractures and Dislocations: Forearm) because of maintenance of the PRUJ.
D. Treatment consists of dorsal plating of the proximal ulna fracture usually with-
out need for ligament repair.
E. Postoperative instability and arthrosis are uncommon.
IX. Posterior Monteggia Fracture
A. The injury is usually seen in older osteopenic women after a low-energy fall onto
the elbow.
B. A posterior radial head dislocation is present in combination with a proximal
ulna fracture, and possibly a large coronoid fracture with ulnohumeral
instability.
C. The radial head may be fractured and the LCL may be injured, but the MCL is
typically spared.
D. Classification of posterior Monteggia injuries

1. Type A: Fractures including the coronoid process

2. Type B: Fractures at the metaphysis
3. Type C: Fractures at the diaphysis (refer to the chapter Fractures and
Dislocations: Forearm)
4. Type D: Complex, comminuted fractures of the entire proximal ulna
E. Successful treatment involves both recognition and repair of the coronoid, radial
head, and LCL injuries. However, anatomic reduction of the ulna appears to be
the most important factor for successful treatment.
F. A distractor may be helpful in reducing the fracture as well as temporarily pin-
ning the proximal ulnar piece to the humerus.
G. A plate applied dorsally to the proximal ulna is an ideal fixation method.
X. Complications
A. Recurrent instability
1. Failure to recognize or treat a fracture/ligament injury is the most common
cause of recurrent instability.
2. Salvage may involve the reconstruction of disrupted or attenuated ligamen-
tous structures, osteotomies or grafting for osseous malunions or bone loss
and hinged external fixation.
B. Heterotopic ossification
1. Increased with higher level of injury and soft tissue damage, closed head
injury, and burns.
2. Seen both anteriorly between the capsule and brachialis as well as posteriorly
between the capsule and triceps.
3. May be resected when trabeculae are seen on plain radiographs (no consensus
on ideal timing).
4. Prophylaxis with Indomethacin or radiation therapy is recommended after
resection.
C. Stiffness
1. Some loss of motion after elbow fracture-dislocation is expected.
2. Typically, extension is lost more than flexion.
3. The amount of stiffness increases with energy of the initial injury, the amount
of heterotopic bone formed, and delay of motion after repair.
4. Treatment includes static progressive or dynamic splinting, heterotopic bone
excision, and capsular release.
D. Posttraumatic arthritis
1. Common after high-energy injuries and with recurrent instability.
2. Fascial arthroplasty is an option for younger patients while total elbow
replacement is an option for less active patients.
E. Neurologic injury
1. May be seen after manipulation of the fracture or fixation.
2. Typically the injury is a neurapraxia and will recover.
F. Vascular injury
1. Very rare, but the brachial artery is mostly at risk.
2. Reperfusion usually occurs after manipulation.
3. Angiography may be needed to evaluate.
G. Compartment syndrome
1. Rare, but may be seen in high-energy fracture-dislocations.

Distal Humerus Fractures
I. Epidemiology
There is a bimodal distribution curve, with peaks occurring in men aged 12 to 19 (MVA
or athletic injuries) and women over 80 (falls). The incidence in men decreases from
age 19 until rising again at age 70, whereas the incidence in women increases over time
after age 20. From 1970 to 1995, the age-adjusted incidence in women above 60 has
doubled. Additionally, there has been a nearly threefold increase in women from 1970
to 1995; this is anticipated to nearly double again by 2030.
II. Anatomy (see section on anatomy at the beginning of this chapter)
The distal humerus can be thought of as a triangle, where the medial and lateral col-
umns are supporting struts, connected by the trochlea. The trochlea is positioned in
94 to 98 degrees of valgus, and is 3 to 8 degrees externally rotated. The medial column
ends 1 cm proximal to the trochlear articular surface and diverges at 45 degrees to the
humeral shaft; the lateral column ends at the distal aspect of the trochlea and diverges at
25 degrees to the humeral shaft. The central portion between the columns is thin, with
the coronoid fossa anteriorly, and the olecranon fossa posteriorly; 6% of patients have
a frank fenestration of this area.
The medial and lateral epicondyles are the origins of the flexor and extensor masses,
respectively. The distal epicondyles also serve as the origins of the MCL and LCL.
III. Evaluation of a Patient with an Elbow/Distal Humerus Fracture
A. Physical Examination
Skin integrity should be evaluated, as up to 50% of high-energy bicolumn fractures are
open. A neurovascular examination should be performed.
B. Radiographic Evaluation
All elbow fractures should be evaluated with AP and lateral radiographs, ideally prior to
splint application to avoid obscuring fracture detail. In all but the most simple fracture
patterns, computed tomography with 3D reconstructions should be obtained preop-
eratively; this can help to better elucidate fracture patterns and evaluate comminution
to help with operative planning. In polytraumatized or unstable patients, the physician
should consider obtaining traction views in the operating room to better evaluate frag-
ments and look for intra-articular injury, especially fractures through the trochlea and
capitellum in the sagittal plane (coronal shear factures). Provisional treatment of open
injuries or simultaneous treatment of other long bone injuries can be performed and
the distal humerus temporized; definitive fixation can be delayed until later time when
appropriate radiographic evaluation can be obtained.
IV. Classification
Several systems for organizing and classifying distal humerus fractures exist; however, none is
universally adopted. We will discuss these fractures taking into account multiple factors, based
on anatomic location and description of fracture pattern rather than any specific system.

A. Extra-articular/supracondylar
These injuries will be considered in the discussion of humeral shaft fractures.
B. Intra-articular
1. Single column
a) These injuries are very rare in adults. They typically occur due to a varus
or valgus stress applied to the elbow. Lateral column injuries are more
common than medial. These injuries are considered “high” if fractured
fragment includes the majority of the trochlea, or “low” if the majority of
the trochlea remains with the intact humerus.
b) In high fractures, the ulna and radius follow the displacement of the frac-
tured column. Clinically, these are more unstable injuries, and are associ-
ated with collateral ligament injuries. Almost all require ORIF.
c) Treatment of low fractures depends on displacement. Those with less than
2 mm displacement can be treated with brief immobilization. The arm
should be positioned to relax the musculature originating off the column
(lateral column ® supination; medial column ® pronation). Consider
ORIF to allow earlier mobilization. In those fractures with more than 2 mm
displacement, ORIF allows earlier motion and better outcome than
closed management
2. Bicolumnar
These fractures may be due to either a direct blow or axial load. Being high-
er-energy injuries, particularly in the younger patient population, 20% to
50% are associated with open injuries. Each component of the triangle is
disrupted, making these more difficult injuries to treat
C. Special considerations
1. Lateral epicondyle
In adults, these fractures are usually associated with elbow dislocation. While
the fragment usually reduces with reduction of elbow joint, the elbow joint
must be carefully evaluated for asymmetric reduction and/or incarcerated
fragments.
2. Medial epicondyle
Fractures of the medial epicondyle may be secondary to direct injury or
due to avulsion. If the fracture fragment is small and minimally displaced
(<1 cm), it can be treated closed. However, if the fragment is displaced, of
a large size, or caught within the ulnotrochlear joint, this requires ORIF via
open approach to protect the nearby ulnar nerve.
3. Capitellar and coronal shear fractures
The clinician must have a high level of suspicion to carefully look for these
injuries. The lateral radiograph may demonstrate the “double arc sign”; CT
scan can help with diagnosis and operative planning for these fractures.
V. Positioning for ORIF
A. Prone
1. Advantages: Excellent exposure of posterior elbow, access to posterior iliac
crest
2. Disadvantages: Difficult to flex elbow; airway not immediately accessible to
anesthesiologist, requires general anesthesia with endotracheal intubation,
facial swelling in dependent position with prolonged cases

B. Lateral decubitus
1. Advantages: Excellent access to posterior elbow, allows gravity to assist with
reduction, allows for elbow flexion, access to anterior or posterior iliac crest
2. Disadvantages: Patient facing away from anesthesiologist
C. Supine with arm across the chest
1. Advantages: Allows access to anterior and posterior elbow, allows elbow joint
to be hyperflexed, small bump behind the scapula helps to rotate the opera-
tive arm forward, optimum for regional anesthesia
2. Disadvantages: Gravity causes shortening of fracture, second assistant helpful
to position arm in space
VI. Surgical Approaches to the Distal Humerus for Fixation of

Bicondylar Fractures
A. Ulnar Nerve Identification and Dissection

Every approach to the distal humerus, save direct lateral approaches, should begin with
identification and protection of the ulnar nerve. This portion of the case is performed
under tourniquet. The ulnar nerve should be identified and mobilized from the inter-
muscular septum to the first motor branch to the FCU. The nerve is then mobilized
and placed anteriorly in a moistened sponge to protect it during fracture fixation. At the
conclusion of the case, the nerve can either be transposed anteriorly or returned to its
normal anatomic location. If hardware is placed in a position that will irritate the ulnar
nerve, transposition should be performed. It should be noted that some authors suggest
transposition is not necessary in every case.
B. Triceps Sleeve
The triceps sleeve approach is indicated for extra-articular supracondylar fractures.
The triceps is identified, and medial and lateral windows are created on either side
of the triceps. Medially the ulnar nerve is identified between the two heads of the
FCU and followed proximally to the Arcade of Struthers. Laterally the radial nerve
is identified between the triceps and brachialis. The radial nerve lies on the lateral
humeral shaft approximately 14 cm proximal to the joint surface. In fractures of the
distal humerus, however, this distance will be lesser secondary to shortening of the
arm. Once both nerves are identified and protected, the triceps can be dissected medi-
ally and laterally and mobilized to either side to allow for exposure of the humeral
cortex.
C. Triceps Splitting
The triceps splitting approach is indicated for extra-articular fracture fixation; no
intraarticular visualization is afforded. Proximal extension of this approach is possible,
following identification of the radial nerve directly posterior in the spiral groove at the
level of the inferior margin of the deltoid tuberosity. In order to improve distal visual-
ization, the medial 75% of the triceps insertion can be sharply elevated from the ulna.
Additionally, the most proximal, nonarticular portion of the olecranon can be osteoto-
mized, taking care to not remove too much and create instability.
D. Triceps Tongue
The triceps tongue allows for intra-articular visualization of the distal humerus
while avoiding olecranon osteotomy and maintaining the native triceps insertion.

The tendinous portion of the distal triceps is identified and cleared of overlying soft
tissue. The entire length of the triceps tendon is then incised as a distally based tongue,
taking care to leave tendinous margins for later repair. The triceps tendon is elevated
off the underlying muscle fibers and reflected distally. The underlying muscle fibers are
divided in line with the fibers through the depth of the muscle down to the humerus.
The triceps belly can be retracted medially and laterally; distal subperiosteal elevation
medially and laterally can aid in complete visualization of the articular surface.
E. TRAP
Another alternative to olecranon osteotomy for intra-articular visualization is the Triceps
Reflecting Anconeus Pedicle (TRAP) approach. The patient is positioned supine to
allow for elbow hyperflexion. The triceps insertion is elevated subperiosteally, taking
down Sharpey’s fibers, from ulnar to radial; the anconeus is elevated in a continuous
layer. To improve visualization, the distal tip of the olecranon is excised, again tak-
ing care not to remove too much and cause instability. Intra-articular visualization is
achieved by hyperflexing the elbow. If further visualization is needed, partial MCL and
LCL subperiosteal releases can be performed, with reattachment through bone tunnels
at the conclusion of the case.
F. Olecranon Osteotomy
The olecranon osteotomy is historically considered the gold standard for intra-articular
visualization of the distal humerus, though it does require iatrogenically creating an
intra-articular osteotomy. After identification and mobilization of the ulnar nerve, the
proximal aspect of the olecranon is osteotomized to allow for proximal retraction of
the olecranon and triceps and visualization of the distal humerus. Some authors advo-
cate elevation of the anconeus as a flap prior to osteotomy to avoid denervation of the
anconeus. The osteotomy can be performed either extra-articularly or intra-articularly;
intra-articular osteotomy allows for superior exposure of the distal humeral articular
surface. If an intra-articular osteotomy is used, it can be made either straight across the
joint or in an apex-distal chevron, entering the joint at the bottom of the curve. Protec-
tive retractors or gauze should be placed within the joint to avoid articular damage to
the humerus. The osteotomy should be completed with an osteotome to avoid remov-
ing a kerf (saw blade’s width of cartilage). At the conclusion of the case, the osteotomy
is usually repaired with a tension band construct.
VII. Goals of Treatment
The clinician should aim for restoration of painless elbow with acceptable function.
This includes anatomic reconstruction of the articular surface, restoration of the overall
distal humeral architecture, and providing fixation stable enough to allow early motion
and minimize immobilization time.
VIII. Treatment Methods
A. Nonoperative
Several reports have shown good results using bracing for extra-articular injuries, with
good union rate and functional results. Treatment of intra-articular fractures nonop-
eratively has been historically referred to as the “bag of bones” technique. Prior to the

advent of modern fixation systems, this was the preferred treatment for comminuted
fractures due to the inability to maintain rigid fixation. However, when compared to
modern fixation, conservative treatment yields typically poor results for displaced intra-
articular fractures. One may consider nonoperative treatment in either minimally dis-
placed intra-articular fractures or in patients with comorbidities precluding operative
fixation. However, in the vast majority of patients, including many geriatric patients,
operative intervention should be considered as the treatment of choice for intra-artic-
ular fractures to preserve motion and postoperative function. This includes either fixa-
tion or total elbow arthroplasty (TEA).
B. External Fixation
External fixation has limited use in the definitive fixation of distal humeral fractures.
While certainly playing a role in temporization of open fractures or in polytraumatized
patients, static external fixation should generally otherwise be avoided. Occasionally,
in severely comminuted fractures or persistent instability following ORIF, a hinged
fixator may be added to provide additional stability while still allowing for mobilization.
Should external fixation be utilized, the pins should be placed through formal incisions,
and not percutaneously, to avoid injury to the nearby neurovascular structures, particu-
larly, the radial nerve.
C. Internal Fixation/Plating
1. AO principles. Under AO technique, the physician should identify the articular
fragments and reconstruct the articular surface. The articular fragments should
be provisionally fixed with K-wires or Steinmann pins. These wires should be
placed in subchondral position to avoid interference with further hardware
placement. After the articular surface is pinned together, it should then be tem-
porarily fixed to the shaft with wires. After confirming appropriate restoration of
humeral geometry, definitive fixation should then be carried out, either utilizing
lag screws and plates, or preferably, plate-and-screw constructs.
2. Plate selection. The plates selected for use should be strong enough to not con-
tribute to failure of fixation. Options include 3.5 mm reconstruction plates,
compression plates, or precontoured plates. Use of 1/3 tubular plates is associ-
ated with up to 50% complication rate including nonunion and plate breakage;
their use is to be avoided. The use of locking plate technology may be beneficial
in the setting of osteoporotic bone or significant comminution. It should be
noted that plate placement may be a more important variable than plate type or
locking screw use in determining construct stiffness. Regardless of the type of
plate selected, the medial and lateral plates should end at different levels of the
humerus to avoid creation of a stress riser proximally.
3. Plate placement. There is debate as to the optimal placement of distal humeral
plates, either in a medial/posterior-lateral (90/90) or a medial/lateral configura-
tion (parallel). Biomechanical studies suggest contoured parallel plates are either
equivalent to or stiffer than 90/90 configuration for distal transcondylar frac-
tures. If parallel plating is used, the plates should be angled anteriorly to engage
the articular fragments. The lateral plate should be placed more posteriorly to
avoid impinging on the extensor origin and LCL insertion.
D. Total Elbow Arthroplasty

In the older, low-demand patient, consider use of a TEA, particularly when comminu-
tion precludes osteosynthesis or in patients with preexisting elbow arthritis. Closed

fractures or Grade I open fractures can be treated with acute arthroplasty; TEA is
contraindicated on Grade II or III open fractures or infected elbows. In the younger,
high-demand patient, linked arthroplasty is destined to fail. Instead, the physician
should consider interposition resurfacing after fracture union. This can be performed
with cutis graft (either autograft or allograft), fascia lata, or Achilles allograft. Although
there may be a future role for distal humeral hemiarthroplasty or newer unlinked pros-
theses, further studies are required.
IX. Post-op Management
At the conclusion of the case, the physician should consider use of a drain to prevent
hematoma accumulation. The patient should be placed in a well-padded splint at 50 to
60 degrees of flexion. This protects soft tissues and decreases tension on the wound, as
well as decreasing ability of patient to lean on elbow (and fixation).
Active and passive ROM should be started as early as fixation allows, ideally within
3 to 5 days postoperatively. Because initiation of motion is based upon construct rigid-
ity, one should consider nonoperative treatment if the nature of the fracture precludes
rigid fixation and immobilization for greater than 2 weeks is needed.
X. Outcomes
Outcomes are dependent on both fracture characteristics as well as fixation techniques.

Recent studies have shown 84% to 88% good and excellent outcomes with modern
fixation methods. Patients with painful elbows are more likely to report decreased func-
tional ratings and perceived disability. The presence of radiographic arthrosis does not
necessarily correlate to a poor clinical outcome. It is important to note that many, if not
most, patients will have mild persistent physical impairment, particularly loss of motion
(typically terminal extension and supination) and strength.
Jupiter showed that AO C3 fractures (articular and metaphyseal comminution)
had a higher rate of poor outcomes and nonunions compared to C1 and C2 fractures.
XI. Complications
A. Stiffness
Stiffness may be due to prolonged immobilization, capsular contracture, or angular
malunion. Many patients will lose terminal extension; loss of functional motion is less
common. While prolonged immobilization leads to stiffness, this stiffness may be pref-
erable to loss of fixation, with a secondary procedure for contracture release arguably
more predictable than revision fixation or corrective osteotomy.
B. Failure of Fixation
Failed fixation should be treated with early reoperation if fragments displace into an
unacceptable position. If fracture alignment is maintained, one may consider tempo-
rary cast immobilization or reoperation. Late loss of fixation should alert the clinician
to the possibility of infection, which should be included in clinical decision making.
Adjunctive fixation or structural bone grafting may be required at the time of reopera-
tion depending on bone quality.

C. Nonunion
Nonunion of distal humerus fractures typically occurs at the supracondylar fracture
line. If a well-aligned and healed articular surface is present and sufficient bone stock
remains, the nonunion can be treated with revision ORIF and autogenous bone graft.
If the remaining bone stock precludes fixation, or if arthritis is present, TEA should be
considered in an appropriate patient.
D. Olecranon Osteotomy Nonunion

This is a rare complication, with up to 6% incidence reported in the literature. It should
be treated with revision fixation with bone grafting.
E. Symptomatic Hardware
Patients may experience irritation from subcutaneous hardware, particularly in slim
patients and at the olecranon, where the overlying soft tissue envelope is thin. After
the fracture is healed and matured, consideration can be given to hardware removal. It
should be noted that hardware removal is not without risks, notably lack of symptom
resolution and risk of refracture.
F. Ulnar Neuropathy
This complication may be due to the initial injury, intraoperative manipulation, inad-
equate release with transposition, impingement on bone or hardware, or postoperative
fibrosis. Accurate documentation of the neurologic status of the limb both pre-oper-
atively and post-operatively is essential. Neurolysis may improve the condition, but
permanent deficits may persist.
G. Heterotopic Ossification
The incidence of heterotopic ossification ranges from 0% to 49% in the literature, and
is dependent on a variety of comorbidities and variables. Regardless, the treatment is
excision and capsular release after the HO is mature. The use of Radiation Therapy
(XRT) or indomethacin following excision should be considered.
XII. Special Fractures
A. Capitellum/Coronal Shear
The treating clinician must have a high degree of suspicion to identify these fractures, as
their presence affects surgical approach, fixation methods, and outcomes. Intra-articular
visualization and anatomic reduction are essential for an acceptable outcome. Coronal
shear fractures or fractures of the capitellum can be treated with anatomic reduction
and fixation with headless screws or buried threaded wires. Occasionally, fragment exci-
sion can be utilized, depending on fracture pattern and fragment size. These fractures
have a high rate of complications, including AVN, stiffness, and loss of motion.
B. Significant Absence of Articular Surface

In cases where significant portions of the articular surface are either absent or unrecon-
structable, iliac crest bone graft, either structural or nonstructural depending on the
size of the defect present, can be used to reconstruct the “spool” of the distal humerus.
Allograft use can be considered, but is associated with a higher risk of infection. The
addition of interposition arthroplasty for joint resurfacing as a staged procedure may
be of benefit.

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Nerve
17
John Elfar, Jason M. Petrungaro,
Richard M. Braun, Christine J. Cheng, Ranjan Gupta,
Adam LaBore, and Jeffrey E. Wong
Electrodiagnostic Testing
I. Introduction
Electrodiagnostic testing is a commonly ordered set of electrophysiologic tests optimally

utilized as an extension of the surgeon’s history and physical examination. The objective
of testing is to confirm the presence or absence of neuropathy as a cause of the patient’s
complaint. Testing evaluates for nerve entrapment or compression, demyelinating pro-
cesses, and diseases that cause axonal loss in sensory and motor nerves. Testing also
evaluates for disease at the neuromuscular junction and myopathies, but these processes
are generally not managed by a hand surgeon and will not be discussed.
II. Definitions
A. Stimulator—Device used to provide electrical stimulation to the tested nerve.

B. Pick-up—An electrode placed to detect a sensory or motor nerve response to
the stimulus. These can be discs of various styles adhered to the skin surface, or
rings placed around a digit.
C. Distal peak latency—Most often reported with sensory nerve studies, it is
defined as the time in milliseconds (ms) from the stimulation of a nerve to the
peak of the waveform.
D. Onset latency—Most often reported with motor nerve studies, it is defined as
the time in milliseconds (ms) from stimulation of a nerve to the onset of the
compound motor action potential (CAMP).
E. CMAP—The waveform generated by a sum of all motor unit responses in mus-
cle to stimulation of a peripheral nerve.
F. Sensory nerve action potential (SNAP)—The waveform generated by the
depolarization of a sensory nerve in response to stimulation of that nerve.
G. Conduction velocity—The calculated speed of stimulus transmission across a nerve
segment, in meters/second. This is most often reported with motor nerve studies.
H. Conduction block—Observed in conditions of acquired demyelination, it
refers to a decrement of decrease in the CMAP amplitude and/or area under
the CMAP waveform when a nerve is stimulated proximal to the demyelinated
segment. If the lesion is proximal, distal nerve stimulation demonstrates normal
action potential size. The decrement required for this diagnosis is always 20%
or more compared to the distal segment, but there is increasing evidence that a
50% decrement in area under the waveform is more reliable.
I. Conduction velocity slowing is more common than conduction block, and
can be observed without meeting the absolute criteria for a true conduction
294

Chapter 17 • Nerve 295
block. Velocity slowing is generally limited to compression and/or a segmental

demyelinating process.
J. Electomyography (EMG)—Also referred to as “Needle EMG,” is performed by
inserting a needle electrode into a muscle belly and observing for evidence of abnor-
malities in muscle membrane depolarization. Abnormalities can be observed at mus-
cle rest (abnormal spontaneous activity, such as positive sharp waves, fibrillations, or
fasciculations), or in voluntary motor unit morphology and recruitment patterns.
K. Motor unit—A motor unit is composed of all muscle fibers innervated by a
single nerve fiber.
L. Temporal dispersion—The time over which a waveform occurs in response to
a stimulus. It reflects the spread of signals reaching the electrode from slow and
fast conducting fibers. Temporal dispersion is another parameter of segmental
conduction evaluation, with an increase reflecting abnormality.
M. H wave—Analagous to a reflex arc, the H wave value is not utilized in upper
extremity studies. A stimulus causes an orthodromic sensory response to be sent
to the spinal cord, which responds with an orthodromic motor response back to
the recording electrode.
N. F wave—This study is performed by stimulating a peripheral motor nerve and
sending an antidromic motor response to the spinal cord followed by an orthodro-
mic motor response to the recording electrode. It is useful to evaluate very proxi-
mal nerve involvement in peripheral neuropathies and in brachial plexopathies.
(H and F waves are known as “late responses.”)
O. Neurapraxia—Describes an injury to a nerve in which the entire structure of the
peripheral nerve is left intact, but conduction is temporarily impaired.
P. Axonotmesis—Describes an injury to a nerve involving axonal disruption
within the supporting structures (which are left intact) of the nerve.
Q. Neurotmesis—Describes an injury in which the entire nerve is disrupted.
R. Wallerian degeneration—Degeneration of the axon that has become detached
from the neuron cell body, as in axonotmesis or neurotmesis injuries.
S. Positive sharp waves—Spontaneous electrical activity in a muscle that occurs
relatively early in the period following denervation of the muscle studied with
needle EMG.
T. Fibrillations—Spontaneous activity that occurs later in the period following
denervation of the muscle studied with needle EMG.
U. Fasiculations—Spontaneous activity that indicates chronic denervation of a
muscle studied with needle EMG. These can be seen clinically as well, whereas
fibrillations can only be seen electrically.
V. Complex repetitive discharges—Spontaneous activity that indicates chronic
denervation of a muscle studied with needle EMG.
W. Polyphasic motor units—Describes the morphology of voluntary motor units
after an axonal loss has occurred followed by reinnervation of the motor unit
studied via needle EMG.
X. Recruitment—The pattern of motor unit activation that occurs when a subject
activates a muscle. Recruitment can be diminished in any case of nerve conduc-
tion impairment.
II. Anatomy
The peripheral nerves most often involved in problems presenting to the upper extrem-
ity subspecialist include

A. Suprascapular nerve (C5/6, upper trunk)

B. Long thoracic nerve (C5/6/7, upper and middle trunk)
C. Musculocutaneous (C5/6, lateral cord)
D. Radial (C5/6, posterior cord)
E. Axillary (C5/6, posterior cord)
F. Median (primarily C8/T1, also C7, lateral and medial cords)
G. Ulnar (C8/T1, medial cord)
III. Electrophysiology
A. The purpose of the nerve is to transmit motor impulses from the anterior horn
cell to muscle, and from the peripheral sensory receptor to the spinal cord. The
axonal membrane is electrically active, dependent on both its passive qualities
and the active sodium-potassium pump, which maintains the resting membrane
electrical gradient.
B. Axonal membranes contain voltage-dependant sodium channels. Current
applied to the membrane depolarizes them and results in the opening of the
sodium channels, causing an influx of sodium into the nerve. Anytime depo-
larization occurs beyond a threshold above the resting membrane potential an
action potential is created, propagating depolarization along the axonal mem-
brane and producing a neural impulse.
C. Conduction velocity depends on the diameter of the axon and its myelination.
Depolarization propagates quickly between myelinated segments of the nerve,
speeding conduction by occurring only at point intervals without myelin called
the nodes of Ranvier (saltatory conduction). Depolarization also occurs at the
neuromuscular junction.
D. Muscle membrane physiology is complex. Important to electrodiagnostic evalu-
ation is the fact that muscle membrane stability is dependent on the integrity of
the neuromuscular junctions of all the motor units in a muscle. Disruption of
this connection between nerve and muscle results in predictable changes in mus-
cle membrane stability and motor unit morphology. These changes are observ-
able on needle EMG.
IV. Pathophysiology
From the discussion of electrophysiology, it is easy to comprehend the pathophysiology

of neuropathy. Conduction can be impaired or blocked by direct pressure on the nerve,
demyelination, or axonal loss. Axonal disruption results in the impairment of impulse
propagation, disruption of the neuromuscular junction (resulting in muscle membrane
destabilization and impaired motor units).
V. Common Entrapment Neuropathies and Basic Electrodiagnostic

Strategy for Each
A. Suprascapular nerve
1. Compression most commonly occurs at the suprascapular notch (affecting the
supraspinatus and infraspinatus) or at the spinoglenoid notch (affecting
the infraspinatus only).

2. Stimulation is performed at Erb point or the supraclavicular fossa and

onset latencies are recorded at the supraspinatus and infraspinatus. Needle
EMG of these muscles is performed to determine the presence and severity
of denervation.
3. An entrapment neuropathy at the suprascapular notch results in prolonged
latencies to both muscles. An entrapment neuropathy at the spinoglenoid
notch results in prolonged latencies to the infraspinatus only.
B. Axillary nerve
Not usually affected by intrinsic compression, axillary neuropathy is usually
imposed by blunt trauma or by a stretch injury. A conduction study can be
performed by stimulating the nerve superior to the clavicle and evaluating the
onset latency of the CAMP. Needle EMG abnormalities limited to the deltoid
and teres minor, but sparing other posterior cord–innervated muscles confirm
this diagnosis. Weakness of the axillary-innervated muscles without evidence of
denervation generally carries an excellent prognosis.
C. Musculocutaneous nerve
Entrapment by the coracobrachialis muscle may occur, and neuropathy can
also follow heavy exercise. Musculocutaneous nerve palsy is also seen follow-
ing anterior glenohumeral dislocation, although it is less frequent than axillary
nerve palsy. Needle EMG demonstrates denervation in the biceps, brachialis,
and coracobrachialis. An abnormal lateral antebrachial cutaneous sensory study
can be helpful in corroborating the diagnosis especially when compared to the
contralateral/unaffected limb.
D. Antebrachial cutaneous nerves
1. Lateral antebrachial cutaneous nerve—The peak latency can be prolonged,
and the action potential amplitude can be diminished. It is recommended
that the comparison study be made to the contralateral limb.
2. Medial antebrachial cutaneous nerve and posterior antebrachial cutaneous
nerve neuropathies are not typically identified as mononeuropathies; but
rather in association with other conditions such as brachial plexopathy.
3. Stimulation of the lateral antebrachial cutaneus nerve and medial antebra-
chial cutaneus nerves is performed at the lateral and medial antecubital arm.
Surface electrodes are used to evaluate peak latencies, SNAP amplitudes, as
well as action potential morphology.
E. Radial nerve
1. The nerve is susceptible to direct injury or extrinsic compression at the spiral
groove, or where the radial nerve crosses from posterior to lateral at the lateral
intermuscular septum.
2. Posterior interosseus nerve entrapment can occur anywhere along the “radial
tunnel” including
a) the arcade of Frohse,
b) the radial recurrent vessels,
c) the supinator, or
d) the tendon of the ECRB
3. Compression of the nerve at or distal to the supinator can result in compres-
sion neuropathy of the terminal branches, producing a variety of wrist/digit
extensor deficit patterns. Needle EMGs of the affected muscles are useful in
diagnosis.
4. Radial motor nerve conduction study is performed by stimulating the nerve
proximal to the spiral groove, at the lateral arm distal to the spiral groove,

and in the forearm. A needle or surface electrode picks up the stimulation

response, most often at the most distally innervated muscle, the extensor
indicis proprius.
5. Sensory study of the radial nerve can be performed by placing a surface
electrode over the first web space and stimulating the nerve in the lateral
forearm.
F. Median nerve
There are two commonly encountered sites of median nerve compression:
at the elbow between the two heads of the pronator teres or at the carpal
tunnel.
1. Pronator syndrome occurs when the median nerve is entrapped while pass-
ing through the two heads of the pronator teres. It can be associated with
muscle hypertrophy, trauma, fracture, or impingement by a median artery.
A fibrous band can also occur connecting the pronator teres to the tendi-
nous arch of the FDS. In addition to tenderness to palpation at the pronator
teres, clinical features distinguishing it from carpal tunnel entrapment can
include weakness of the flexor pollicis longus and hypoesthesia over the
thenar eminence (the palmar cutaneous branch of the median nerve departs
the main fiber of the median nerve and passes above the flexor retinaculum
at the wrist located just ulnar to the tendon of FCR). The syndrome can be
mistaken for similar symptoms produced by entrapment at the ligament of
Struthers and the exceedingly infrequent humeral supracondylar process.
Any weakness of the pronator teres indicates that the entrapment likely is
above the muscle.
a) Conduction studies are useful to rule out carpal tunnel entrapment and
other causes of symptoms, although mild conduction velocity slowing
through the forearm is sometimes observed. In severe cases associated
with axonal loss, needle EMG can be helpful to establish the pattern of
denervation.
1) The median motor conduction study is performed by placing a surface
electrode at the abductor pollicis brevis and stimulating the nerve at
the wrist just proximal to the carpal tunnel (to record the onset latency)
and at the medial antecubital fossa (to calculate conduction velocity
between the two stimulation points).
2) The median sensory conduction study is performed by placing a sur-
face electrode on the second or third digits and stimulating the nerve
at the wrist, proximal to the carpal tunnel.
2. Anterior interosseous nerve syndrome occurs when this branch is entrapped
after separation from the nerve proper, usually distal to the pronator teres.
It may occur spontaneously or in association with a forearm or a supra-
condylar humeral fracture. There are no sensory deficits, but motor defi-
cits may be present in the pronator quadratus, flexor pollicis longus, and
flexor digitorum profundus (FDP) of the index and middle fingers. Nerve
conduction studies will not reveal any abnormality, but needle EMG of
the innervated muscles may reveal abnormalities confined to the nerve
branch distribution. A conduction study to measure motor latency to
the pronator quadratus using a needle pick-up can be performed, but
should be compared to the asymptomatic limb. Conduction studies of the
median nerve are otherwise performed to rule out other causes of median
neuropathy.

3. Carpal tunnel syndrome is the most commonly diagnosed median compres-

sion neuropathy. The electrodiagnostic strategy includes confirming median
neuropathy and site of entrapment at the wrist. Segmental studies across the
wrist, as well as comparing the transcarpal with palm-to-digit segments for
disproportionate proximal segment slowing confirm the location of com-
pression. Needle EMG is not usually needed to identify carpal tunnel com-
pression, but is useful to rule out cervical radiculopathy or proximal nerve
involvement, especially in the case of axonal loss. Needle EMG can also help
grade the severity of neuropathy, but is unlikely to redirect care.
G. Ulnar nerve
Like the median nerve, the ulnar nerve can be compressed around the elbow or
the wrist.
1. Ulnar compression neuropathy at the elbow occurs either posterior to the
medial epicondyle (cubital tunnel), or at the aponeurosis joining the two
heads of the flexor carpi ulnaris (FCU).
2. The ulnar nerve can also be entrapped at Guyon's canal. Compression here
is commonly caused by a ganglion, but can also be the product of ulnar
artery thrombosis or aneurysm. A lack of dorsal ulnar sensory deficit helps
differentiate entrapment here from at the elbow. If axonal loss is present, it
will spare FDP III/IV and the FCU on needle EMG (a proximal lesion can
selectively affect distal fibers, so the reverse is not true). Much less commonly,
the nerve is entrapped distal to the cubital tunnel in the forearm, before it
enters Guyon canal.
3. The goal of evaluating an ulnar neuropathy is localization and characteriza-
tion. This includes a general assessment of latencies, amplitudes, and seg-
mental conduction velocities. Important to evaluation of the ulnar nerve is
conduction across the elbow. Routinely, a single segment is assessed from
the distal axilla/medial arm across the medial epicondyle. Short segment and
inching studies can also be done to attempt identification and localization of
a subtle conduction abnormality. Similar to median nerve testing, transcarpal
segment testing can help confirm that a prolonged distal latency is due to
compression at the wrist.
4. Ulnar sensory studies are performed in a similar manner as for median sen-
sory studies, placing the surface electrodes at the fifth digit. The motor study
is performed by placing an electrode at the abductor digiti minimi (can also
be placed at the first dorsal interosseus muscle) and stimulating the nerve
at the wrist proximal to Guyon canal, distal to the cubital tunnel, and then
proximal to the cubital tunnel. Similar to median nerve studies, ulnar stud-
ies evaluate onset latency CAMP amplitudes, and conduction through the
forearm as well as across the cubital tunnel.
VI. Martin-Gruber Interconnections
An anatomical variant involving an interconnection from the median to ulnar nerves

in the forearm can be identified. It is almost always motor, often arising from the
anterior interosseus nerve. Fibers communicating from the median nerve to the
ulnar nerve innervate either median nerve–innervated (thenars) or ulnar nerve–
innervated muscles (first dorsal interosseus, adductor pollicis, and abductor digiti
minimi). Routine conduction studies demonstrate an apparent conduction block on

proximal compared to distal ulnar stimulation, due to the higher number of motor
fibers in the distal nerve that have joined from the median nerve. The number of
fibers communicating varies, causing variable conduction study changes. The
interconnection encountered most frequently can be confirmed by stimulating the
median nerve at the elbow and recording the responses with electrodes placed over
the innervated ulnar and median-innervated muscles. Stimulation of the median
nerve at the wrist records a response only from the median-innervated muscle.
VII. Grading of Severity and Determining Chronicity

of Compression Neuropathies
Grading severity of a peripheral compression neuropathy is variable and somewhat sub-

jective. Test reports should include the criteria by which a neuropathy grade is assigned.
There are gradients of severity within and between the following designations, generally
reported as follows:
A. Mild: A compression that produces evidence of conduction slowing (latency
prolongation) on sensory nerve testing, but demonstrates normal sensory ampli-
tudes and normal motor responses
B. Moderate: Evidence of sensory axonal loss and/or motor conduction slowing
(latency prolongation and/or segmental velocity slowing)
C. Severe: Evidence of motor nerve axonal loss (amplitude decrement not limited
to a proximal segmental conduction block, and/or evidence of denervation on
needle EMG)
Chronicity of an axonal neuropathy can be assessed based on the presence of conduc-
tion abnormalities and the observations made during needle EMG. In the acute phase,
the appearance of spontaneous denervation potentials can range from a few days to
4 weeks or more, depending on the distance of the tested muscle from the lesion. For
most upper extremity neuropathies, abnormal spontaneous activity can be observed by
21 days following injury date. Conduction abnormalities usually appear first, and can
be observed within a few days to a few weeks, depending on severity and location of
the injury. As recovery ensues, conduction studies may normalize depending on injury
severity; and spontaneous activity may extinguish completely, while changes in volun-
tary motor unit morphology indicate reinnervation.
Demyelinating injuries are not easily assessed for chronicity. Pure demyelinating con-
ditions often produce decrement in motor unit recruitment (correlating with weakness).
Demyelination is not associated with the presence of abnormal spontaneous activity.
VIII. Normal Values
The normal values referenced for an electrodiagnostic study depend on local standards.
Normal value ranges are generally referenced from normal population studies compris-
ing 500 or more. Normal values can be established for a particular lab by similar testing.
Because of differences in equipment used and nuance of techniques, the referenced
standards of a given lab for normal and abnormal conduction results are going to be
generally more reliable for interpreting results than those sourced elsewhere. Reference
tables from the testing lab are almost always readily available. Finally, normal values for
nerves tested are often included in the report.

IX. Limitations of Testing
Electrodiagnostic testing can be limited by several factors. First, the test requires
active patient cooperation. Although it is generally uncomfortable for the patient to
go through, it is almost always tolerable. Obesity, edema, peripheral vascular disease,
wounds/skin breakdown, surgical scarring (especially if recent), burns, fixed deformities
or contractures, casts, splints, external fixators, and the many permutations of these can
all adversely affect the test by limiting the quality and amount of data collected.
X. Sample Table from an Electrodiagnostic Test
The presentation of data from electrodiagnostic reporting varies, but is similar in con-
tent. The following are representative, and the concepts are applicable from one report
to another. The abnormal values are in bold type and explained. All other values are
considered normal from the reporting lab. The following findings indicate a median
compression neuropathy at the wrist and an ulnar demyelinating/compression neu-
ropathy at the elbow.
Explanation of Table Headers (tables are explained below):
(Table 17.1 and 17.2)
Examples of Nerve Conduction Study Tables, as Typically Seen in a Report
(Table 17.3)
Examples of Nerve Conduction Study Tables, as Typically Seen in a Report
(continued) (Tables 17.4 and 17.5)
Sample Table Reporting Needle EMG Findings (Table 17.6)
Compression Neuropathies
It is important to take note that the term “compression neuropathy” refers to a chronic
condition that has developed and persisted over time, as opposed to an acute nerve
compression associated with a traumatic event, such as compartment syndrome. The
surgeon must have an understanding of the anatomy and pathophysiology of these
conditions in order to make the correct diagnosis and proceed with the appropriate
treatment. It is also imperative that the surgeon is aware of other distinct neurologi-
cal problems that may exist in the upper extremity, which may blur the diagnostic
picture.
Both sensory and motor symptoms are observed. Sensory symptoms can include
tingling, numbness, “electric shocks,” burning, and pain. As nerve compression
progresses from mild to severe, the symptoms will typically range from occasional
paresthesias to constant numbness and anesthesia. Perception of vibration, move-
ment, and pressure are the first to be lost, and perception of pain and temperature
are the last to be lost. Motor symptoms can include weakness and progress to overt
paralysis.
The most common compressive neuropathy in the upper extremity is median nerve
compression at the wrist, or carpal tunnel syndrome, followed by ulnar nerve compres-
sion at the elbow, or cubital tunnel syndrome. Other peripheral nerve compressions in
the upper extremity are much less common.

TABLE 17-1 Sensory nerve study header 302
P-T Amp Norm P-T Norm

Site NR Peak (ms) Norm Peak (ms) (µV) Amp Site 1 Site 2 Delta-P (ms) Dist (cm) Vel (m/s) Vel (m/s)
TABLE 17-2 Motor nerve study header
Norm Onset O-P Amp Norm O-P Delta-0 Norm

Site NR Onset (ms) (ms) (mV) Amp Site 1 Site 2 (ms) Dist (cm) Vel (m/s) Vel (m/s)
Site Site of stimulation
NR Nerve stimulated
Onset (ms) Recorded for motor studies, the time (onset latency) from stimulation to onset of
waveform deflection. For sensory studies, this column represents the Peak latency.
Peak (ms)
Norm Onset (ms) These represent the normal maximum values for
these latencies, for the testing lab.
or
Norm Peak (ms)
(continued)
2/22/2010 4:17:38 PM
TABLE 17-2 Motor nerve study header (Continued)
Norm Onset O-P Amp Norm O-P Delta-0 Norm

Site NR Onset (ms) (ms) (mV) Amp Site 1 Site 2 (ms) Dist (cm) Vel (m/s) Vel (m/s)
O-P Amp (mV) These reflect the amplitudes of the motor and sensory amplitudes, respectively.
P-T Amp (µV)
Norm O-P Amp These represent the normal minimum values for these amplitudes, for the testing lab.
Norm P-T Amp
First stimulation site

Site 1
Second stimulation site

Site 2
Chapter 17 • Nerve
Delta-0 (ms) Difference in latency times between two sites of stimulation (normally distal
303
first, proximal second).
2/22/2010 4:17:38 PM
304
Dist (cm) Distance between the two sites of stimulation.
Vel (m/s) Calculated velocity of nerve conduction between two sites of stimulation.
Norm Vel (m/s) Represents the normal minimum velocity of nerve depolarization propagation, for the testing lab.
TABLE 17-3 Anti sensory summary table
Norm Peak P-T Amp Norm P-T Norm

Site NR Peak (ms) (ms) (µV) Amp Site 1 Site 2 Delta-P (ms) Dist (cm) Vel (m/s) Vel (m/s)
Left Median Acr Palm Anti Sensory (Second Digit)
Wrist 4.3* <3.8 28.7 >10 Wrist Palm 2.3 7.0 30.4
Palm 2.0 30.8
Left Ulnar Anti Sensory (Fifth Digit)
Wrist 3.3 <3.7 45.7 >15.0 Wrist Fifth 3.3 14.0 42.4 >38
digit
*A prolonged sensory peak latency indicates slowed conduction from the point of sensory nerve stimulation to the point of nerve depolarization at the pick-up
electrode.
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TABLE 17-4 Motor summary table
Norm O-P Amp Norm O-P Norm

Site NR Onset (ms) Onset (ms) (mV) Amp Site 1 Site 2 Delta-0 (ms) Dist (cm) Vel (m/s) Vel (m/s)
Left Median Motor (Abd Poll Brev)
Wrist 4.5* <4.2 11.4 >5 Elbow Wrist 3.5 19.5 55.7 >50
Elbow 8.0 11.2
Left Ulnar Motor (Abd Dig Minimi)
Wrist 3.0 <4.2 10.0 >3 B Elbow Wrist 2.8 16.5 58.9 >47
B. Elbow 5.8 9.6 B Elbow B Elbow 0.3 2.5 83.3 >47
B. Elbow 6.1 9.3 B Elbow A Elbow 2.3 8.5 37.0†
A. Elbow 8.4 2.0**
*A prolonged CMAP onset latency indicates slowed conduction from the point of nerve stimulation to the peak of the waveform (detected by the pickup electrode),
representing the sum of motor units activated by the nerve stimulation.
**A drop in CMAP amplitude of greater than 50% across a nerve segment indicates an area of demyelination causing conduction block.
(Note that the amplitudes from below elbow and wrist stimulations range from 9.3 –10.0 mV.)
†
A drop in conduction velocity across a nerve segment indicates compression and/or demyelination. (Note the velocities in the below elbow-below elbow and below
elbow-wrist segments, respectively.)
†
Represents motor conduction velocity across the elbow.
305
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TABLE 17-5 Sample waveforms of sensory and motor responses
Samples of median sensory and motor

responses
These represent median SNAP responses.

Sensory latencies are generally reported
from the peak (“P”) of the waveform.
Latencies marking the waveform onset

(initial deflection) are reported less
commonly because they are less
reliably measured.
These represent median CMAP

responses at the abductor pollicis brevis.
Motor onset (“O”) latencies are reliably

measured and reflect the response time
more accurately than the peak.
Conduction velocities are calculated in
proximal segments (e.g., elbow-wrist)
using the differences in onset latencies.
The neuromuscular junction (NMJ) is
therefore removed from the velocity
calculation as its transmission is not
part of the peripheral nerve conduction.
The NMJ is evaluated on needle emg and
with special tests.
Sample, ulnar motor study waveforms
Wrist
Below elbow stimulation 1 (distal cubital tunnel)
Below elbow stimulation 2 (proximal cubital tunnel)
Above elbow (distal axialla/medial arm)
These represent the ulnar — abductor digiti

minimi CMAP responses, stimulating the
nerve at the wrist, below the elbow and
above the elbow.
Note the severely diminished amplitude of

the last waveform. This represents a
conduction block, discussed above.

TABLE 17-6 EMG
Side Muscle Nerve Root Ins Act Fibs Psw Amp Dur Poly Recrt
Left BicepsFemS Sciatic L5–S1 Nml Nml Nml Nml Nml 0 Reduced
Left VastusMed Femoral L2–4 Nml Nml 1+ Nml Nml 0 Reduced
Left AntTibialis Dp Br Peron L4–5 Nml Nml Nml Nml Nml 0 Reduced
Left Peroneus Long Sup Br Peron L5–S1 Nml Nml Nml Nml Nml 0 Reduced
Left MedGastroc Tibial S1–2 Nml Nml Nml Nml Nml 0 Nml
Left AdductorLong Obturator L2–4 Nml Nml Nml Nml Nml 0 Reduced
Side Indicates right vs. left extremity.
Muscle Indicates which muscle is being examined.
Nerve Indicates the peripheral innervating nerve supplying the muscle tested.
Indicates the nerve roots most commonly contributing to the axons of the peripheral supplying the muscle
Root
tested.
307
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308
“Insertional Activity”—it indicates the examiner’s assessment of the muscle membrane’s response to active
Ins Act needle insertion and can be used as an indicator of muscle membrane instability. Electrical instability of
the muscle membrane usually occurs early following complete denervation.
“Fibrillations”—indicates spontaneous muscle membrane electrical activity and is a hallmark of subacute
Fibs
to chronic denervation.
“Positive sharp waves”—indicates spontaneous muscle membrane electrical activity and is a hallmark of
Psw
acute to subacute denervation.
Amplitude—measured amplitude of the voluntarily activated motor units. An increase is often observed
Amp after reinnervation subsequent to denervation occurs. A decrease is often observed with diseases of the
muscle.
Duration—measured duration, or width, of the voluntarily activated motor units. An increase is often
Dur observed after reinnervation subsequent to denervation occurs. A decrease is usually associated with forms
of myopathy.
Polyphasicity—reports the frequency that voluntary motor units demonstrate increased phasicity, another
Poly
indicator of chronic reinnervation. This does not occur in the acute phase of denervation.
Recruitment—reports the recruitment pattern of voluntary motor units. Decreased recruitment occurs with
Recrt
interruption of the muscle–nerve interface, but can increase with diseases of the muscle.
2/22/2010 4:17:40 PM
Radial Nerve
I. Radial Tunnel Syndrome
A. Description: Compression of the radial nerve in proximal forearm.

1. The radial tunnel is typically defined as the area where the radial nerve exits
between the brachioradialis and the brachialis muscles to where it runs below
the supinator muscle.
B. Etiology: Anatomic structures that compress the radial nerve near the elbow.
1. There are five commonly held to be causes (FREAS):
a) Fibrous bands
b) Radial recurrent vessels (the leash of Henry)
c) The tendinous origin of the extensor carpi radialis brevis
d) The tendinous origin of the supinator (the arcade of Frohse)
e) Within and along the distal margin of the supinator muscle
C. Signs and symptoms: Aching, pain, and weakness in the region of the lateral
elbow and forearm.
1. Patients may complain of symptoms after forceful elbow extension and/or
pronation of the forearm.
2. Workers whose jobs require this repetitive motion frequently present with
these complaints.
3. Pain is the primary symptom, and it may be referred distally along the length
of the radial nerve or up to the lateral epicondyle.
4. Weakness is typically secondary to the pain.
D. Pitfalls: Radial tunnel syndrome may be confused with lateral epicondylitis
(Tennis Elbow), which is part of the differential diagnosis, and may occur
simultaneously.
1. The two can sometimes be distinguished on physical examination:
a) In lateral epicondylitis, tenderness is felt at the lateral epicondyle of the
humerus.
b) In radial tunnel syndrome, the radial nerve is tender to palpation 6 cm
distal to the lateral epicondyle.
E. Diagnosis: Based on clinical examination.
1. The classic finding includes tenderness referred to the radial tunnel with
resisted middle finger extension, which causes radial nerve compression as
the fibrous edge of the extensor carpi radialis brevis contracts at its insertion
into the base of the third metacarpal.
2. One may also elicit pain with resisted forearm supination due to activity of
the supinator.
3. Electrodiagnostic studies are typically formed.
4. Obtain radiographs of the elbow and forearm to rule out or tumors.
5. Examine the contralateral asymptomatic arm and document reproducibility
of pain in the symptomatic arm.
F. Treatment: Definitive management is surgical in patients who fail nonoperative
management.
1. A period of initial immobilization for up to 12 weeks with splints and activity
modification can help reduce elbow extension and forearm pronation.
2. Anti-inflammatory medications may offer relief of symptoms.
3. Avoid tennis elbow straps in patients who are diagnosed with radial tunnel
syndrome because the straps may exert pressure on the radial nerve, exacer-
bating symptoms.

4. Multiple approaches have been described to release the radial tunnel:

a) Anterior approach
b) Posterior approach
c) Transmuscular brachioradialis—splitting approach
5. The goal of surgery is to release the fibrous, vascular, or musculotendinous
connections that compress the radial nerve.
G. Postoperative care: Place the patient in a bulky dressing to immobilize the arm,
making sure that the wrist is in the neutral position and the elbow is flexed. The
dressing may be removed 2 to 3 days postoperatively, and range-of-motion exer-
cises are started immediately and continued for the first month. Strengthening
exercises are started at 6 weeks.
II. Posterior Interosseous Nerve Palsy
A. Description: Compression of the radial nerve in the proximal forearm.

B. Etiology: Similar anatomic points of compression as seen in radial tunnel
syndrome.
C. Signs and symptoms: The symptoms of posterior interosseous nerve palsy
are motor, due to the fact that the muscles innervated by this nerve are
affected.
1. These include
a) Supinator
b) Extensor carpi radialis brevis
c) Extensor digitorum communis
d) Extensor carpi ulnaris
e) Extensor digiti quinti
f ) Abductor pollicis longus
g) Extensor pollicis longus
h) Extensor pollicis brevis
i) Extensor indicis proprius
2. Motor symptoms can vary from weakness of grip to paralysis of any number
of muscles that extend the fingers and the wrist.
3. Symptoms may occur acutely after trauma to the forearm, iatrogenic injuries,
or more insidiously from rheumatoid synovitis or tumors.
D. Diagnosis: Patients present with weakness or paralysis of the wrist and digital
extensor muscles.
1. A typical finding is radial deviation when the patient attempts active wrist
extension due to preservation of the extensor carpi radialis longus (ECRL)
(innervated by the radial nerve proper) and paralysis of the extensor carpi
ulnaris and extensor digitorum communis.
2. Unlike radial tunnel syndrome, electrodiagnostic studies are often diagnostic
in posterior interosseous nerve palsy, and can be used to identify the site of
compression.
3. Similar to radial tunnel syndrome, radiographs should be obtained to rule
out fractures, dislocations, or tumors of the elbow and forearm.
E. Treatment: The treatment of posterior interosseous nerve palsy is similar to that
of radial tunnel syndrome.
1. Immobilization and anti-inflammatory medications may be utilized initially.
2. Surgical intervention is decompression, as in radial tunnel syndrome.
F. Postoperative care: As in radial tunnel syndrome.

III. Radial Sensory Nerve Compression (Wartenberg Syndrome)
A. Description: Radial sensory nerve compression in the forearm.

B. Etiology: The radial sensory nerve is particularly susceptible to compression and
traction due to its superficial location in the forearm.
1. When the forearm pronates, the brachioradialis and ECRL muscle tendons
converge to compress the radial nerve as it courses from deep to superficial
locations.
a) This action can be equated to a scissorlike effect of the two muscles.
2. The nerve can also become stretched as the wrist moves from radial in exten-
sion to ulnar in flexion.
3. Specific events that have been known to compress the radial nerve include
a) Tight watchbands.
b) Pressure from handcuffs.
c) Trauma.
d) Crush injury.
e) Iatrogenic injury from placement of external fixators.
f ) de Quervain tenosynovitis causing secondary radial sensory nerve irritation.
4. Work-related causes of radial sensory nerve compression include activities
that require repetitive pronation and supination of the forearm and/or ulnar
wrist flexion.
a) Specific examples include typing, using a screwdriver, and writing with a
pen.
C. Signs and symptoms: Radial sensory nerve compression is associated with
sensory symptoms only.
1. Numbness, paresthesia, or burning along the dorsoradial forearm and hand
in the distribution of the radial sensory nerve.
2. Patients will often report symptom exacerbation when tightly pinching the
thumb and index finger or with excessive wrist movement.
D. Pitfalls: If patients describe numbness in the thumb and index finger only,
carpal tunnel syndrome may be diagnosed incorrectly. In addition, ulnar
wrist deviation typically causes shooting dorsoradial pain similar to a positive
Finkelstein test for de Quervain tenosynovitis, leading to another incorrect
diagnosis. Finally, cervical disk disease (C6 radiculopathy) should be consid-
ered, and active wrist extension evaluated and compared to the contralateral
side.
E. Diagnosis: Radial sensory nerve compression is primarily diagnosed clinically.
1. Physical examination should include and elicit a positive Tinel sign where
the radial sensory nerve exits between the brachioradialis and extensor carpi
radialis muscles.
a) These symptoms can be exaggerated by hyperpronation of the forearm.
2. It is important to distinguish radial sensory nerve compression from de
Quervain tenosynovitis, for a significant portion of patients will complain of
symptoms consistent with the latter.
a) Patients with de Quervain's disease should demonstrate normal sensation
in the dorsoradial aspect of the hand compared with patients with radial
sensory nerve compression.
b) Tinel test will be negative in de Quervain's disease.
3. Electrodiagnostic studies are only occasionally useful in diagnosing this
neuropathy.

F. Treatment:
1. Nonoperative measures include activity modification and maintenance of the
forearm in a supinated position.
a) Splinting may be attempted, but it is difficult to splint in forearm supina-
tion; therefore, a thumb spica splint may be used.
b) NSAIDs may be used to decrease inflammation.
c) Local corticosteroid injections have been shown to alleviate symptoms.
2. Surgical release of the radial sensory nerve is indicated if nonoperative man-
agement fails.
a) The operation consists of releasing the fascia between the brachioradi-
alis and ECRL muscles and removing a portion of the brachioradialis
tendon.
b) Care must be taken not to injure the overlying lateral antebrachial cutane-
ous nerve.
G. Postoperative care: Range-of-motion exercises and sensory reeducation and
desensitization of the radial sensory nerve distribution on the dorsum of the
hand begin in the first week. Strengthening exercises are started at 4 weeks, and
patients are cleared for work with no activity restrictions at 8 weeks.
Median Nerve
I. Anterior Interosseous Nerve Palsy
A. Description: Compression of the AIN branch of the median nerve in the forearm.
B. Etiology: Anatomic points of compression that have been found to contribute to
anterior interosseous nerve palsy include the following:
1. An accessory bicipital aponeurosis
2. A snapping brachialis tendon
3. Fibrous bands between the deep and superficial heads of the pronator teres
muscle
4. A tendinous band at the origin of the pronator teres muscle
5. The accessory head of the flexor pollicis longus (Gantzer muscle)
6. Aberrant radial artery branches
7. Fibrous origin of FDS
C. Signs and symptoms: Weakness and/or paralysis of the flexor pollicis longus, the
FDP of the index finger or long finger, and/or the pronator quadratus.
1. Patients often describe clumsiness when attempting fine motor skills such as
typing, writing, pinching, or buttoning a shirt
2. There is seldom any sensory loss.
D. Diagnosis: Affected patients will display hyperextension of the index finger distal
interphalangeal joint and thumb interphalangeal joint on active tip pinch.
1. This will cause an inability to make a circle by pinching the thumb and index
finger (failed “OK” sign).
2. EMG may reveal denervation of the muscles innervated by the anterior
interosseous nerve.
E. Treatment: Includes both conservative and operative interventions.
1. Nonoperative management includes splinting, rest, activity modification,
and anti-inflammatory medications for up to 6 to 9 months.
2. Definitive surgical treatment involves exploration of the median nerve in the
forearm.

a) Exposure should be from the medial elbow to the midforearm.

b) The bicipital aponeurosis and lacertus fibrosis are divided, crossing vessels
are ligated, the deep head of the pronator teres is divided, and the super-
ficial tendinous arch of the flexor digitorum superficialis is released, along
with any other crossing bands over the median nerve.
F. Postoperative care: Range-of-motion exercises should be started early including
flexion, pronation, and supination in order to prevent scarring of the median
nerve. Strengthening exercises can be started 1 to 2 months postoperatively.
II. Pronator Syndrome
A. Description: Median nerve compression in the proximal forearm.

B. Etiology: Known points of compression of the median nerve in the forearm include
1. Lacertus fibrosis
2. Ligament of Struthers
3. Pronator teres muscle
4. Flexor digitorum superficialis proximal arch
C. Signs and symptoms: Pronator syndrome results in predominantly sensory
symptoms and has few motor deficits.
1. Sensory alterations are in the median nerve distribution of the hand (some-
times including the palmar cutaneous branch distribution).
2. Patients complain of pain in the volar aspect of the forearm, especially those
workers whose jobs involve repetitive upper extremity activity.
3. Pain is exacerbated by activity and relieved by rest.
4. Other specific symptoms include
a) Numbness and paresthesias in the thumb, index finger, long finger, and
the radial side of the ring finger
b) Weakness of the thenar musculature
D. Diagnosis: Based on physical findings.
1. Physical examination will often reveal a positive Phalen and Tinel sign in the
proximal forearm.
2. Provocation tests will reproduce median nerve symptoms including
a) Resisted elbow flexion with forearm supination
b) Resisted forearm pronation
c) Resisted flexion of the flexor digitorum superficialis of the middle finger.
3. Symptoms in the median nerve distribution of the hand can be reproduced
if pressure is placed over the leading edge of the pronator teres muscle while
the forearm is maximally supinated with the wrist in a neutral position.
4. Electrodiagnostic testing is typically negative.
E. Treatment: Nonoperative and operative treatments resemble those for anterior
interosseous nerve palsy.
F. Postoperative care: As in anterior interosseous nerve palsy.
III. Carpal Tunnel Syndrome
A. Description: Compression of the median nerve in the carpal tunnel.

B. Etiology: Carpal tunnel syndrome is the most common compression neuropathy
in the upper extremity. The carpal tunnel itself is bordered ulnarly by the hamate
and triquetrum and radially by the scaphoid and trapezium. The roof of the

carpal tunnel is the transverse carpal ligament (a.k.a. the flexor retinaculum).
There are ten structures in the carpal tunnel — nine flexor tendons and the
median nerve.
1. There are many factors implicated in median nerve compression in the carpal
tunnel, and carpal tunnel syndrome can often result from one or a combina-
tion of any.
2. Some believe that certain patients are genetically predisposed to possessing a
smaller, tighter carpal tunnel.
3. High-energy or low-energy trauma can cause an acute carpal tunnel syn-
drome to develop.
4. Other causes include
a) Accessory muscles
b) Tenosynovitis of the flexor tendons
c) Hypothyroidism
d) Rheumatoid arthritis
e) Type 1 diabetes mellitus
f ) Pregnancy
g) A ganglion cyst or tumor.
5. Little clinical data exist linking repetitive motions of the hand and wrist
with carpal tunnel syndrome; however, workers on assembly lines have been
shown to be three times more likely to develop carpal tunnel syndrome than
workers in the office setting.
C. Signs and symptoms: Carpal tunnel syndrome typically presents with sensory
symptoms in the median nerve distribution of the hand, but motor symptoms
may develop late in advanced disease.
1. Sensory symptoms typically have a gradual onset, and include
a) Numbness
b) Tingling
c) Paresthesias
d) Itching in the thumb, index finger, long finger, and the radial side of the
ring finger
2. The index and long fingers are most commonly affected, followed by the
thumb and ring finger.
3. Patients will often complain that their fingers feel swollen even though no
edema is present.
4. An almost universal complaint is that the symptoms awaken the patient from
sleep.
a) This is due to the fact that many people sleep with flexed wrists.
b) Patients often need to and “shake out” the numbness and tingling in their
hand.
5. Nighttime symptoms will progress to daytime symptoms as the disease pro-
gresses.
6. Severe or untreated cases of carpal tunnel syndrome may result in the loss
of temperature sensation, loss of 2-point discrimination, and thumb
weakness.
a) The motor branch of the median nerve arises at a variable location, most
commonly at the distal aspect of the transverse carpal ligament, but can
be transligamentous or run as a separate branch with the median nerve
within the carpal tunnel. This nerve innervates the thenar musculature
(except the deep head of the Flexor pollicis Brevis (FPB) muscle).

7. Common motor symptoms include

a) Loss of grip strength
b) Difficulty forming a fist
c) Inability to grasp large objects
D. Diagnosis: Carpal tunnel syndrome is a clinical diagnosis, but electrodiagnostic
studies can be used for confirmation and delineation of the severity of nerve
compression.
1. Carpal tunnel compression test and Phalen signs are classically positive at the
wrist.
2. Patients should be asked to mimic activities that produce symptoms.
3. The wrist should be examined for discoloration, warmth, swelling, tender-
ness, and masses.
4. The fingers should be examined for sensation, and the thenar musculature
should be evaluated for any signs of wasting or weakness.
5. If there is a concern of uncontrolled medical conditions that may be contrib-
uting to the condition, laboratory studies should be obtained including
a) Blood glucose levels
b) Rheumatoid factor
c) Thyroid function tests
d) If abnormalities in these tests are discovered, the underlying medical con-
dition should be treated prior to operative treatment for carpal tunnel
as the symptoms will often improve or disappear when the underlying
medical conditions are corrected.
6. Plain films can evaluate for fractures or arthritis, and CT scan or MRI can
evaluate for mass lesions if suspected. Routine radiographic examination is
not recommended.
E. Treatment: Carpal tunnel syndrome is initially treated nonoperatively, and
therapy should begin as soon as symptoms are noted.
1. Activity modification, splinting with the wrist in a neutral position at night,
and NSAIDs are the mainstays of conservative therapy for at least 6 weeks.
2. Diuretics have been shown to relieve symptoms in some patients by decreas-
ing swelling in the carpal tunnel.
3. Corticosteroid injections may be used with varying degrees of success.
A good response to a steroid injection may be a predictor of a good response
to surgical treatment.
4. For those patients who fail conservative management or who present with
advanced carpal tunnel syndrome, surgical intervention is indicated.
a) Carpal tunnel release is one of the most common surgical procedures in
the United States.
b) There are numerous described operations to release the median nerve at
the wrist, and nearly all have good to excellent results.
1) All procedures are aimed at releasing the transverse carpal ligament.
2) It is important for surgeons to choose the approach that offers them
the best visualization of the median nerve in order to avoid iatro-
genic injury to it or its branches.
3) The procedures include the traditional open technique, smaller inci-
sion and mini open techniques, and endoscopic release.
1. A concern after carpal tunnel release is bowstringing of the flexor tendons out
of the carpal tunnel.

a) For this reason, postoperative immobilization of the wrist in neutral

position is advocated by some surgeons for up to 1 week.
2. Night splinting may be used for up to 3 weeks.
3. Long-term immobilization has been shown to be unnecessary, but some sur-
geons advocate nighttime splinting in the early postoperative period.
4. Begin range-of-motion exercises for the fingers and wrist on postoperative
day 2 or 3 in order to facilitate gliding of the median nerve and prevent adhe-
sion formation.
5. It is important to inform the patient that the relief of symptoms after carpal
tunnel release is reliable and typical. Nighttime pain and tingling typically are
relieved in a matter of days, but daytime tingling and numbness may persist
for weeks to months, and may be permanent, depending on the preoperative
condition of the nerve. Most palmar tenderness resolves by 3 months, but
pillar pain can persist for up to 1 year.
Ulnar Nerve
I. Cubital Tunnel Syndrome
A. Description: Ulnar nerve compression in the cubital tunnel, which is the post-
condylar groove of the humerus covered by a fibrous roof extending from the
medial epicondyle to the olecranon.
B. Etiology: Numerous factors have been identified that result in compression of
the ulnar nerve in the cubital tunnel.
1. Common anatomic points of compression include
a) Arcade of Struthers
b) Osborne ligament
c) Triceps fascia
d) Anconeus epitrochlearis
e) The FCU aponeurosis
f ) Deep fascia overlying the FDP muscle belly
2. Other causes of compression include
a) Subluxation of the ulnar nerve over the medial epicondyle,
b) Cubitus valgus
c) Synovial hypertrophy
d) Tumors
e) Ganglia
3. As the elbow flexes, the shape of the cubital tunnel narrows from a round to
an oval shape, causing increased pressure on the ulnar nerve.
a) This pressure is further increased with shoulder abduction and
wrist extension, resulting in ulnar intraneural pressures up to six times
normal.
4. Traction is placed on the ulnar nerve itself as the elbow flexes, causing up to
8 mm of elongation.
5. Chronic and repeated subluxation of the ulnar nerve may cause inflamma-
tion and irritation.
C. Signs and symptoms: Cubital tunnel syndrome can be associated with both
senory and motor symptoms.

1. Sensory complaints present first and include

a) Numbness and paresthesias in the ring and small fingers
b) Aching in the medial elbow and forearm
2. Motor complaints include
a) Weakness of grip and pinch
b) Loss of fine dexterity
c) Dropping objects
d) Clawing of the small and ring fingers (severe cases)
e) Intrinsic muscle atrophy (severe cases)
f ) Weakness of pinch
g) Inability to spread the fingers away from one another
h) Inability to adduct the small finger toward the ring finger
3. Prolonged resting upon the elbow while in flexion will typically cause symptoms.
4. Patients will often be awakened at night if they sleep in a position of elbow
flexion, such as arms beneath the pillow.
5. Musicians may present with complaints of loss of finger speed and stamina.
D. Diagnosis: Cubital tunnel syndrome is the second most common compression
neuropathy in the upper extremity after carpal tunnel syndrome.
1. Range of motion about the elbow should be examined, evaluating for areas of
tenderness, mass lesions, or obvious nerve subluxation.
2. A positive Tinel sign is often noted in the ulnar nerve at the cubital tunnel.
a) The test is overly sensitive and often positive bilaterally in up to 25% of
patients.
3. Provocative testing is both sensitive and specific for cubital tunnel syndrome,
and involves two maneuvers:
a) Elbow flexion with digital pressure on the ulnar nerve proximal to the
cubital tunnel
b) Flexing the elbow past 90 degrees, supinating the forearm, and extending
the wrist
c) If numbness or paresthesias occur within 60 seconds, the test is positive.
4. Many patients in the early stages of cubital tunnel syndrome complain about
sensory symptoms but will not display clear motor deficits.
a) The surgeon must be sure to perform careful sensory testing to document
and quantify progression of the disease.
b) Evaluate grip and pinch strength, check vibratory perception and light
touch with Semmes-Weinstein monofilaments, and check 2-point dis-
crimination, which will become abnormal in the advanced stages of the
disease.
5. Electrodiagnostic testing is used to confirm the clinical findings and localize
the level of compression.
6. Plain films of the elbow can help rule out bony lesions, and MRI is both
sensitive and specific for diagnosing ulnar nerve entrapment at the elbow;
however, cost is often prohibitive.
7. Differential diagnosis can include ALS, C8 radiculopathy, brachial plexopa-
thy, or Pancoast tumor.
E. Treatment: Cubital tunnel syndrome is initially managed conservatively with
nonoperative measures for up to 3 months.
1. Patients must be educated to avoid or modify positions associated with pro-
longed elbow flexion, such as sleeping, talking on the telephone, typing, and
driving.

2. Postural modifications are key, and patients should wrap a bulky towel
around their arms at night to prevent inadvertent extreme elbow flexion.
3. Multiple splinting techniques preventing elbow flexion past 45 degrees have
been shown to decrease symptoms.
4. NSAIDs may help decrease inflammation around the ulnar nerve.
5. Corticosteroid injections are not typically employed.
If nonoperative treatment has failed after 3 months and the patient has
continued symptoms along with clinical evidence of ulnar nerve sensory and
motor deficits, then surgical decompression is indicated.
6. It is important to note that there are multiple operations for cubital tunnel
syndrome, and no single procedure is universally accepted.
7. The five most common operations for cubital tunnel are as follows:
a) In situ decompression (open or endoscopic)
b) Medial humeral epicondylectomy
c) Anterior subcutaneous transposition
d) Anterior intramuscular transposition
e) Anterior submuscular transposition
8. There have been no randomized prospective studies performed to determine
which procedure has the best outcome; however, anterior submuscular trans-
position is often considered the procedure for revision surgery.
9. Whatever operation is chosen, a thorough and complete release of all critical ana-
tomic structures known to compress the ulnar nerve at the elbow is performed.
F. Postoperative care: Range-of-motion exercises should be started early to avoid
stiffness. Many patients will find comfort at night by wearing a sling for 2 to
3 weeks to prevent elbow extension. The specific operation will determine the
timing for return to work and heavy activities, with in situ decompression requir-
ing the least time and submuscular/transmuscular requiring the most.
II. Ulnar Tunnel Syndrome
A. Description: Ulnar nerve compression at the wrist.

B. Etiology: In the wrist, the ulnar nerve is compressed at Guyon canal, which is a
space containing the ulnar nerve, ulnar artery, and fat.
1. The artery typically runs radial and superficial to the nerve.
2. Boundaries of the ulnar tunnel include
a) Lateral/radial by the hook of the hamate, transverse carpal ligament, and
extrinsic flexor tendons
b) Medially/ulnar by the pisiform, FCU, and abductor digiti minimmi
c) Roof/volar by the volar carpal ligament, hypothenar fat, and the palmaris
brevis
d) Floor/dorsal by the transverse carpal ligament, pisohamate ligament, and
opponens digiti minimi.
3. Compression in Guyon canal may be caused by
a) Fractures of the hook of the hamate
b) Ganglia
c) Lipomas
d) Anomalous muscle bellies
e) Ulnar artery thrombosis
f ) Ulnar artery pseudoaneurysms

4. Of note, two classic sports injuries can cause fractures of the hook of the
hamate and compress the ulnar nerve:
a) Forcibly hitting the ground with a golf club
b) Hitting a baseball
C. Signs and symptoms: Ulnar tunnel syndrome can present with pure sensory
symptoms, pure motor symptoms, or a mix of both due to branching of the
ulnar nerve into superficial (mostly sensory) and deep (motor) branches.
1. The distal ulnar tunnel is divided into three zones and symptoms will depend
on the site of compression within the tunnel.
a) Zone I includes portion of the tunnel proximal to the bifurcation into
motor and sensory branches
b) Zone II includes the deep motor branch and surrounding structures
c) Zone III includes the superficial sensory branch and surrounding distal
and lateral structures
2. Sensory complaints always include numbness or paresthesia in the small
finger and/or the ring finger.
a) The dorsum of the hand is not involved due to its innervation by the
proximal take off of the dorsal sensory branch of the ulnar nerve.
3. Cold intolerance in the ring and small fingers may also be noted.
4. Motor complaints vary and may include
a) Intrinsic muscle weakness affecting pinch and grasp
b) Loss of hand coordination and clumsiness
c) Clawing (severe, due to preserved function of long flexors of the fingers)
5. This syndrome is often seen in workers suffering from repetitive blunt trauma
to the hand, such as carpenters or construction workers who use jackham-
mers and other power tools.
D. Diagnosis: Ulnar tunnel syndrome is diagnosed clinically and confirmed with
electrodiagnostic studies.
1. Patients may demonstrate a positive Tinel or Phalen sign over the ulnar nerve
in the wrist.
2. Evaluate and document grip and pinch strength, along with 2-point
discrimination and light touch perception.
3. Physical examination may show intrinsic muscle wasting or clawing.
4. Additional imaging studies such as plain films to evaluate for fractures, CT,
or MRI to evaluate for mass lesions, and electrodiagnostic studies are often
used when motor symptoms are noted.
E. Treatment: Includes both conservative and operative interventions.
1. Nonoperative measures can be employed if no objective sensory or motor
dysfunction is noted.
2. Operative intervention includes decompression of the ulnar nerve in Guyon
canal.
a) Care must be taken to dissect the neurovascular bundle completely,
especially the deep motor branch located deep to the leading edge of the
hypothenar muscle.
F. Postoperative care: Apply a bulky dressing to maintain the wrist in a neutral
position. Remove the dressing on postoperative day 2 or 3, and begin range-
of-motion exercises. Night splinting in a neutral wrist position can be used for
up to 2 weeks to aid in patient comfort. Strengthening exercises are started
in 4 weeks, and patients are cleared for work in 6 to 8 weeks with no activity
restrictions.

Thoracic Outlet Syndrome
I. Definition
Thoracic outlet syndrome (TOS) presents as a spectrum of disabling symptoms aris-

ing from injury to the brachial plexus and/or compromise of the subclavian vessels,
the vascular supply to the upper limb. A conventional classification into neurogenic
and vascular TOS is often compromised by symptoms caused by injury to both sys-
tems, which produces a diffuse and complex pattern of patient complaints. Traction or
direct compression of nerve trunks produces neuropathic pain, which may be reported
in a specific nerve distribution. Vascular insufficiency usually produces a more diffuse
nocicentric pain response. This combination of overlapping symptoms may result in a
patient’s history that is confusing to the physician. Nevertheless, the complex issues may
be explained by an understanding of the mechanisms that produce pain in this crowded
area of anatomy.
TOS produces neck pain, arm pain, and numbness, which is often referred to the
medial arm, elbow, or ulnar aspect of the hand. Symptoms may be associated with a
history of prior trauma, either direct or cumulative. Anatomic variations, such as cervi-
cal ribs, chest wall abnormalities, or clavicle fracture deformities predispose to neuro-
vascular compromise in the periclavicular area. Symptoms usually increase when the
arms are elevated above shoulder level. Repetitive tasks, such as putting objects on high
shelves or performing hair care, are often associated with pain and fatigue, which limits
the provocative activity.
II. Anatomy
A working knowledge of the location, structure, and associated tissue relationships of

the brachial plexus, subclavian vessels, and associated muscles and nerves of the peri-
clavicular area is essential for understanding TOS.
The structure of the plexus can be reviewed in a schematic diagram (see chapter
on brachial plexus). In normal situations, the medial cord of the brachial plexus
drapes over the first rib before the plexus descends across the axilla and into the
arm. As the roots of the plexus leave the spinal foramina, they move downward and
forward toward the anterior chest wall. In the coronal plane, the plexus lies between
the anterior and medial scalene muscles. These respiratory muscles stabilize and
elevate the rib during respiration. Rib geometry also changes from an oblique sur-
face to a more flat surface at maximum inspiration when the rib edge has a sharper
surface directed toward the nerves passing obliquely over the bone and into the
axilla.
The subclavian artery joins this crowded space as the artery passes out of the chest
and courses around the scalene muscle attachment to the first rib. The artery proceeds
behind the anterior scalene muscle attachment to the scalene tubercle of the first rib.
The neurovascular bundle then descends below the coracoid process of the scapula to
enter the axilla.
Arm abduction requires the neurovascular bundle to turn upward after passing
under the coracoid process. This may occlude the pulse as the artery is tethered behind
the scalene muscle attachment to the first rib. The artery is then acutely bent under the
coracoid during arm elevation. Arterial compression reduces blood flow to the limb
when the arm is abducted and elevated away from the frontal midline of the torso.

Arm depression may also occlude the pulse. Downward traction on the arm forces
the artery to bind on the musculotendinous attachment of the scalene muscle to the
tubercle of the first rib. This abrupt bend in the artery may produce ischemia in the
limb that is related to this postural provocation.
The examining physician may take advantage of this structural and functional
anatomy when evaluating a patient thought to have TOS.
III. Examination
Examination is performed after a reasonable history of complaints is elicited. It is not

uncommon for a patient to report that symptoms have been present for several years
and that previous evaluations and imaging studies have been considered to be within
normal limits. A prior hospital evaluation for chest pain is not an unusual history for
TOS patients.
The patient is observed in the standing position. A drooping shoulder or postural
abnormality on the symptomatic side may provide a clue suggesting scapular weakness
associated with a downward and forward sloping of the shoulder, which allows the
weight of the arm to produce a chronic stretching of the plexus. The patient may report
that the arm is more comfortable when elevated from below to bring both scapulae to
an appropriate symmetrical position. Support of the arm by the examiner may be asso-
ciated with temporary relief of symptoms as the arm is brought to a zero gravity status
associated with shoulder girdle realignment.
Gentle finger pressure along the symptomatic side of the neck will usually pro-
duce tenderness in TOS patients. Finger pressure is best applied along the posterior
border of the sternomastoid muscle about two inches above the clavicle. Tenderness to
palpation usually diminishes when pressure is applied directly over the clavicle as the
clavicle shields the plexus. Tenderness often reappears in the infraclavicular area and
may continue distally into the axilla and arm. Tenderness along the plexus may increase
with arm abduction, which stretches the nerves and with gentle forced arm depression,
which distracts the plexus and drags the subclavian artery and brachial plexus nerves
down onto the rib.
A. Neurological Exam
A standard neurological examination of the upper limb is initiated. This includes a basic
assessment of muscle group strength or presence of atrophy, sensory loss areas, dimin-
ished deep tendon reflexes for the biceps, triceps, and brachioradialis responses, and
observation of any deformities that may predispose to a plexus compression syndrome
(i.e., clavicle fractures, valgus carrying angle at the elbow, rib fractures, or evidence of
Sprengel deformity of the scapula).
B. Musculoskeletal Examination
An orthopaedic evaluation of the upper limb will include evaluation for shoulder ten-
dinitis or impaired range of joint motion at any significant level. Pressure placed on the
top of the head is a standard method to assess the presence of cervical degenerative disc
disease, which often complicates the diagnosis of TOS. This provocation may be per-
formed with the neck in flexion, neutral, and extension. Radicular pain patterns with a
positive Spurling test associated with longitudinal compression of the cervical spine will
probably require further evaluation with imaging of the neck directed toward evidence
for cervical root compression.

The presence of cervical degenerative disc disease does not rule out TOS, as
confounders are not unusual in this complex area.
C. Vascular Examination
Physical examination of the vascular system begins with an observation of the neck,
shoulder, chest wall, and arm.
Distended venous markings may suggest a Paget-Schroeder syndrome associated
with venous hypertension. Blanching of the skin with arm elevation or with simple
finger flexion and extension exercise may suggest arterial insufficiency due to obstruction
and/or vasospasm.
Provocative postural positioning may be contributory, although it is known that
normal people can often occlude the radial pulse with arm elevation.
The Adson test requires downward traction on the arm, which is held at the side.
The head is turned toward the shoulder. Pulse occlusion and reported pain or numbness
may suggest neurovascular impairment during this postural provocation.
The Wright test requires arm elevation to 90 degrees of abduction at the shoulder.
Pulse loss and pain or numbness is considered a positive test suggesting plexopathy and
circulatory compromise.
Arm abduction to 90 degrees and elbow flexion of 90 degrees associated with rapid
flexion and extension of the fingers is used as a dynamic test for TOS. Arm collapse or
severe pain within 1 to 2 minutes of exercise in this position is a positive Roos test,
suggesting neurovascular compromise in the thoracic outlet area.
IV. Laboratory Studies
A. Radiographs may provide evidence for cervical ribs, clavicular abnormalities, or

previous injuries to the ribcage. They may also provide evidence for associated
conditions, such as apical lung disease or a cervical degenerative disc.
B. Electrodiagnostic studies are usually unremarkable unless major plexus injury
has been sustained. Seror has recently published studies suggesting abnormal
conduction in the medial brachial and antebrachial cutaneous nerves associated
anatomically with the medial cord of the plexus.
Electrical studies may also be helpful in evaluating other associated conditions, such as
cervical disc disease or polyneuropathy.
In the future, electrical testing in situ during provocative positioning may produce
more information on this aspect of diagnosis.
Normal electrical studies should not negate further evaluation of the patient’s
complaints, which may be caused by conditions that do not produce abnormal elec-
trodiagnostic data. A congenial relationship between the evaluating surgeon and his/her
neurology colleague is important in managing these difficult cases.
Noninvasive vascular examination can be pursued. The exact significance of these
data is under investigation, but may hold promise in the objective identification of
vascular etiologies of this condition.
V. Imaging
Collins has produced exquisite images of the neck, brachial plexus, subclavian vessels,
and thoracic outlet anatomy. These highly specialized studies require diagnostic inter-
pretation, which may not be available in every community. Werden has introduced a

similar focus on specific programs or MRI imaging of the plexus. In the future, it is
anticipated that MRI imaging technology will be more contributory in furthering not
only images of structure but in providing information that is also dynamic and associ-
ated with contributory comment on blood flow in the limb.
MR imaging and arteriography may be used when more information regarding
blood flow is desired by the evaluating physician. A normal MRI image of the brachial
plexus may not show a structural vascular abnormality. An MR arteriogram may show
arterial occlusion when the arm is abducted; however, pulse loss with arm abduction
may occur in a normal subject with no symptoms. Passive positioning of the arm in
abduction in the MRI chamber may not adequately simulate the dynamic conditions
that produce symptoms in TOS patients.
Venography is useful in the diagnosis of Paget-Schroeder syndrome and similar
venous abnormalities.
VI. Physiological Studies
Doppler studies may be used to evaluate blood flow. These studies may explain the
disabling symptoms, which occur when the limb performs physical activity. Doppler
studies may produce objective evidence of arterial obstruction, often associated with
passive positioning of the arm. These pressure gradient studies may localize the area of
vessel obstruction. In some cases, this information or evidence suggesting vessel abnor-
mality may be helpful. However, if pulse occlusion can be readily produced with arm
abduction and then restored with allowing the arm to come to rest at the patient’s side,
this can be assumed to involve obstruction to the artery in the periclavicular TOS area
provided that all other possible sites for obstruction cannot be shown to initiate pulse
loss with postural provocation.
VII. Tissue Perfusion Studies
Selective symptom provocation of pain and/or arm collapse during finger exercise per-
formed with the affected arm abducted to 90 degrees at the shoulder can be studied
with perfusion measurement. A standard pulse oximeter securely attached to the thumb
during finger flexion-extension with the arm abducted may produce objective evidence
for ischemia in the limb. This evidence for hypoperfusion identifies a claudication pain
mechanism, which prevents the patient from continuing to perform aerobic exercise.
A normal resting pO2 of 95% or higher may drop to an abnormal level below 90%
within one minute of exercise in a TOS patient. Values of 85%, considered highly
abnormal, are not unusual in TOS patients subjected to this provocative test, which
is frequently associated with a compensatory increase in heart rate. Normal heart rate
values of about 75 bpm may increase to over 100 bpm within 1 to 2 minutes of pro-
vocative hand exercise in these symptomatic TOS patients.
VIII. Scalene Muscle Block
Selective symptom suppression associated with scalene muscle block may assist medical
decision making. It is important to place the needle into the anterior scalene muscle
and to avoid an intravascular injection. If the syringe is removed from the needle prior
to injection, movement of the needle synchronizes with respirations localizing needle

placement into the respiratory scalene muscles. A small injection of 3 to 4 cc of 1%

lidocaine may be initiated when the needle tip rests in the muscle belly. At operation,
it can be demonstrated that 1 to 2 cc of intramuscular lidocaine will result in complete
flaccid paralysis of this respiratory muscle.
Subjective improvement, noted by the patient after scalene muscle block, has been
reported by Sanders, Atasoy, and Gage as providing a good marker for patient satisfac-
tion after surgery. Objective data following scalene muscle block can be measured using
the BTE work simulation machine. Functional capacity improvement with tool use
measurements before and after scalene block serves to validate the subjective responses
generated by the patient.
The tools selected for the BTE tests should relate to the patient’s complaints at
work or with activities of daily living. We currently use three tools including repetitive
pushing and pulling on an overhead bar, a waist level challenge with pushing and pull-
ing a resisted force, and the measurement of endurance in the overhead arm and finger
flexion-extension challenge. A significant improvement in functional capacity can be
expected with a successful block in a patient who is disabled by symptoms associated
with TOS.
Sensory monofilament studies are performed before and after the block. A small
injection of this type cannot produce a brachial plexus block, but it is important to
verify absence of sensory change when doing this test.
IX. Treatment
A. Nonsurgical modalities
1. Physical therapy and conservative treatment are initiated in all patients with
TOS. Shoulder and scapular positioning and postural control are taught by a
specialized therapist and practiced by the patient. Arm support may be used
during the day if symptoms improve with pelvic band support of the limb.
Some patients are willing to accept the fact that they cannot work for any
extended period of time with their affected limb fully elevated or abducted.
2. Botox injections have been successful in providing relief of symptoms for
some patients. Jordan reported an average period of relief to be about
180 days. Botox injections may be localized with electrical studies or with
ultrasound imaging in order to confirm needle placement. Some patients
may accept subsequent consecutive blocks during periods of increased
symptoms. Botox injections into cervical and occipital muscles have also
been used to treat headache symptoms in patients with TOS. The use of
these injections may also augment an otherwise successful surgical pro-
cedure that, nevertheless, has not provided adequate relief of headache
symptoms.
1. Scalenectomy has been used to relieve the symptoms of “Scalene Anticus
Syndrome” (TOS). This has been successful, although questions have been
raised about the recurrence of pain due to scar formation after scalene exci-
sion. The procedure carries less morbidity than more extensive operations
and is considered as an acceptable surgical alternative.
2. Scalenectomy combined with brachial plexus neurolysis and first rib resec-
tion performed through a supraclavicular approach is a procedure directed
toward multiple structures that are thought to produce symptoms in TOS.

Spinal accessory nerve Sternocleidomastoid

Levator scapulae muscle
Scalenus anterior Phrenic and
accessory phrenic
Scalenus medius nerves
Scalenus posterior
Omohyoid muscle
Brachial plexus
Transverse Omohyoid fascia
cervical
Suprascapular vein
artery
Trapezius
muscle
Axillary artery
Axillary vein
Figure 17.1 Anatomy of the thoracic outlet.
The procedure is complex and requires an experienced surgeon who can

safely manage the difficult anatomy of the area (Fig. 17.1). Appropriate
patient selection and reliable surgical techniques have produced good results
with this approach.
3. First rib resection through an axillary approach has been a successful surgi-
cal option for TOS patients. Endoscopically assisted procedures have been
described. The rib resection detaches the scalene muscle attachment and
provides decompression for the subclavian artery and the brachial plexus.
Specialized tools and lighting may be required for adequate visualization and
safe excision. In the hands of experienced surgeons, the results have been
satisfactory and the risks have been minimized.
4. Pectoralis minor tendon release may be considered as an ancillary procedure
for patients with symptoms that are localized to the anterior chest wall in
the area of the palpable coracoid process of the scapula. The procedure may
be performed as a primary or secondary operation. Release of a powerful
muscle, which depresses the shoulder girdle may allow slight cephalad migra-
tion of the scapula and secondary elevation of the clavicle. In some patients,
this may be enough to reduce symptoms to a tolerable level.
X. Postoperative Care
TOS patients may benefit from a preoperative therapy program designed to teach the
patient how to exercise the shoulder during the postoperative period. A stiff shoulder,
impingement tendinitis, or elective disuse of the arm must be prevented by a reasonable
active exercise regimen to preserve motion and strength in a limb.
If pain is reduced postoperatively, a gradual reduction in medications may be initi-
ated after the operation. Headache, persistent muscle pain in the neck, or similar com-
plaints may be treated by a neurologist or pain management specialist. Botox injections
into the areas of cervical and peri-occipital muscle spasm may be helpful in controlling
residual symptoms.

XI. Risks, Benefits, and Complications
The risks, benefits, and complications of TOS surgery should be discussed with the
patient preoperatively. Injury to nerves of the plexus, the phrenic nerve to the dia-
phragm, or the long thoracic nerve may occur despite careful dissection. Small pleural
tears are not considered a complication, as the parietal pleura may be integrally related
to the first rib, which is removed.
Subclavian vessel injuries or damage to collateral vessels, such as the transverse
scapular artery, may occur despite careful dissection. These risks must be considered in
the surgical decision-making process.
Appropriate patient selection, good medical judgment, and appropriate surgical
skills may produce satisfying results for TOS patients.
Peripheral Nerve Injuries
Introduction
Peripheral nerves are heterogeneous composite structures comprised of neurons,

Schwann cells, fibroblasts, and macrophages. The neuron is a polarized cell that forms
the foundation of the nerve and consists of dendrites, the cell body, and a single axon.
The cell body contains the nucleus, cytoplasmic organelles, and a cytoskeleton com-
prised of neurofilaments and microtubules. The axon originates from a unique region
of the cell body called the axon hillock, which is the site where the action potential of
the neuron is produced. Axons project toward sites of innervation where they form syn-
apses. In doing so, information is transmitted from the neuron cell body to the target
end organ via electrochemical changes.
In the peripheral nervous system, axons are surrounded by glial cells called
Schwann cells and produce myelin. If the axonal diameter is greater than or equal
to 1 mm, each Schwann cell will wrap its plasma membrane around only one single
region of an axon and develop myelin. This myelin is composed of 70% lipid and
30% protein and functions to provide fast and efficient conduction of the action
potential propagating down an axon. Discontinuities along the length of the axon
in the myelin sheath are called nodes of Ranvier, and when the action potential
reaches a node, it depolarizes sodium channels. This rapid action potential propa-
gation down the axon from node to node occurs by a process called “saltatory
conduction.”
Peripheral nerves have connective tissue layers to provide strength and protection
to the nerve with its three layers, namely, the endoneurium, perineurium, and epineu-
rium (Fig. 17.2). The endoneurium surrounds individual axons and their associated
Schwann cells. It is composed of thin collagen strands that provide nourishment and
protection. Multiple nerve fibers form a collection of axons called a fascicle. Fascicles
are grouped and surrounded by the perineurium, which is comprised of collagen and
fibroblasts. This sheath provides the nerve with tensile strength and the fibroblasts
contribute to the formation of the blood-nerve barrier. Multiple fascicles are grouped
together and surrounded by a connective tissue layer called the internal or interfascicu-
lar epineurium. This layer cushions the fascicles within the nerve and allows them to
move freely against one another. The periphery of the entire nerve is covered by the
external or extrafascicular epineurium, which protects the entire nerve from the sur-
rounding environment.

Epineurium
Artery
Perineurium
Endoneurium
Figure 17.2 Cross section of a nerve showing the epineurium, perineurium, and
endoneurium.
Injury
I. Anomalous Interconnections
1. Variations in Median Nerve Anatomy

A. The recurrent motor branch of the median nerve has five different anatomical
variations: extraligamentous and recurrent, subligamentous, transligamentous,
origin from the ulnar border of the median nerve, and motor branch on top of
the transverse carpal ligament. These variations are depicted in Figure 17.3.
B. The median nerve can also have the following variations: high division of the
median nerve, group fascicles separated by an artery or muscle, and accessory
branch of the median nerve.
2. Riche-Cannieux Connection
A. Defined as communications in the palm between the recurrent branch of the
median nerve and the deep branch of the ulnar nerve so that the ulnar nerve
innervates the intrinsic thenar muscles.
B. Variations in this pattern have also been observed. For example, the thenar com-
mon digital nerve has been shown to connect with the deep ulnar nerve. Other
variants include connections occurring deep within the belly of the abductor
pollicis brevis or within the first lumbrical.
C. With nerve laceration injuries, motion of the thumb may be retained because of
an anomalous interconnection or partial laceration of the nerve.
D. Anomalous innervation by the ulnar nerve should be discriminated from partial
median nerve lesion by electromyography and peripheral nerve block.
3. Martin-Gruber Connection
A. Most intrinsic muscles of the hand are ulnar nerve innervated. With this connec-
tion, nerve fibers supplying the intrinsic muscles of the hand are incorporated in the
median nerve somewhere within the middle of the forearm. At times, these fibers
leave the median nerve to join the ulnar nerve (median to ulnar to ulnar muscles).

A B
C D
E
Figure 17.3 Variations in the recurrent motor branch of the median nerve. Percentages
indicate incidence of three types of variations as cited by the original Lanz article.
A: Extraligamentous and recurrent (46%). B: Subligamentous branching (31%)
C: Transligamentous course (23%). D: Originating from the ulnar border of the median
nerve. E: Motor branch on top of the transverse carpal ligament.
B. The majority of these connections are made between either the median and
ulnar nerve or the anterior interosseous and ulnar nerve.
C. Martin-Gruber connections are usually diagnosed based on changes in ampli-
tude of the compound muscle action potential in nerve conduction studies.
D. In carpal tunnel syndrome, the presence of Martin-Gruber connection can result
in sparing of the thenar muscles from denervation (median to ulnar to median
muscles). With median nerve conduction studies, it can also result in a paradoxi-
cal recording of normal proximal latencies and prolonged distal latencies.
E. The four different types of Martin-Gruber connections are depicted in Figure 17.4.

Type I Type II
M U M U
AI AI
M U M U
Type III
AI AI
M U M U
Type IV
AI AI
Figure 17.4 The four different types of Martin-Gruber connections. Type I defined
by anastomoses between the anterior interosseous and ulnar nerves. Type II defined
by interconnection between the median and ulnar nerve trunks. Type III defined by
interconnection between the branches innervating the FDP. Type IV defined by
interconnection from the median or anterior interosseous nerve joining the ulnar nerve
at two different points. M, median nerve; U, ulnar nerve; AI, anterior interosseous
nerve.

II. Neurapraxia/Axonotmesis/Neurotmesis
1. Pathophysiology of Nerve Injury

A. Acute nerve injury
1. In an acute nerve injury, transection of an axon causes the distal stump to
undergo Wallerian degeneration.
2. Axon degeneration and myelin breakdown begin at the site of injury and
progress distally. Granular disintegration of the axonal cytoskeleton is the
hallmark of Wallerian degeneration.
3. After the first day of injury, macrophages are recruited to the site where axons
are degenerating. Macrophages produce interleukin-1, which stimulates the
production of nerve growth factor (NGF) by Schwann cells. NGF is required
for regeneration of axons and myelin formation.
4. By the third day after an injury, proliferating Schwann cells in the distal
nerve organize themselves into tubes called Bands of Bugner, which support
regenerating nerve fibers from the proximal stump.
5. Proximal to the site of injury, myelinated and unmyelinated nerve fibers begin
to sprout new axons, that is, growth cones. Axons that successfully reinner-
vate the distal stump will mature. Spontaneous reinnervation when the nerve
is not in continuity usually does not occur and surgical repair is required.
B. Chronic nerve injury
1. Chronic nerve compression injuries develop over the course of weeks to months.
2. In compression injury, there is a significant Schwann cell response. Schwann
cells proliferate and undergo apoptosis without morphometric signs of axonal
injury or degeneration.
3. Schwann cells become less promyelinogenic as they decrease production of
myelin-specific proteins such as myelin basic protein and myelin-associated
glycoprotein (MAG).
a) MAG normally acts to maintain axonal architecture and Schwann cells
locally downregulate the production of MAG at the site of injury. This cre-
ates an environment conducive to axonal sprouting at the nodes of Ranvier.
b) MAG eventually returns to baseline levels, which prevents axonal sprout-
ing from continuing unabated.
c) It has been suggested that axonal sprouting is responsible for the pain that
occurs with compression neuropathies.
4. Schwann cells also upregulate regenerative growth factors such as vascular
endothelial growth factor (VEGF).
5. These responses by Schwann cells result in changes in myelin thickness,
internodal length, and the occurrence of Schmidt-Lantermans incisures.
6. There is also a gradual recruitment of macrophages to the site of injury. These
macrophages upregulate nitric oxide synthase, which results in changes to the
blood-nerve barrier.
2. Classification of Nerve Injury
A. Neurapraxia
1. Characterized by transient and temporary loss of nerve function caused by a
conduction block, without the disruption of axonal integrity.
2. The mechanism of injury most likely involves compression and local ischemia.
3. This is a reversible process. Healing may require up to 3 to 4 months, but
there is good potential for the recovery of motor and sensory function.
Surgical treatment is usually not required.

B. Axonotmesis
1. Characterized by Wallerian degeneration of axons but the Schwann cell basal
lamina, endoneurium, perineurium, and epineurium remain intact.
2. In this type of injury, the axon regenerates within its endoneurial tube and is
guided back to its target site of innervation.
3. Slowing or loss of conduction velocity distal to the site of injury is the earliest
finding, which does not occur in neurapraxia.
4. Full recovery is expected, so surgery is usually not required.
C. Neurotmesis
1. Characterized by complete disruption of the nerve and neural tube along
with elastic recoil of nerve endings.
2. The proximal end may undergo neuroma formation while the distal end
undergoes Wallerian degeneration.
3. Surgery is required. Unfortunately, optimal repair often results in minimal
functional nerve recovery in adults.
III. Lacerations
1. Epineurial Versus Group Fascicular Repair (Fig. 17.5)

A. Epineurial repair
1. Traditional method of repair for nerves that have been severed.
2. The surgeon should section the nerve ends until all signs of damage are
removed and a fascicular pattern can be observed. The goal of successful
repair is to establish continuity of the nerve with the proper rotational align-
ment so as to minimize tension.
3. Alignment can be completed either by aligning an external marker such as a
vessel on the surface of the proximal and distal nerve endings or by matching
the mirror images of the fascicular pattern in both nerve stumps.
4. Coaptation is completed with nonabsorbable sutures of 8-0 nylon for larger
nerves and 9-0 or 10-0 nylon for smaller nerves. The first suture should be
passed through the epineurium proximally and distally and then tied so that
the nerve endings barely touch each other, which ensures minimal tension at
the site of repair. A second suture is placed in the same manner. The remain-
ing epineurium is closed by halving the distance on both the anterior and
posterior aspects of the nerve.
5. If the severed nerve endings cannot be approximated with two 8-0 nylon
sutures, the tension in the injured nerve is considered excessive. In such cases,
a nerve graft should be performed.
B. Group fascicular repair
1. With a group fascicular repair, the anatomical cross-sectional appearances of
both the proximal and distal nerve stumps are examined under a microscope
to determine corresponding groups of fascicles.
2. Each group fascicle, usually three to five in the proximal nerve, is coapted
to its corresponding group fascicle in the distal nerve with two to four 9-0
nylon sutures placed through the internal epineurium and perineurium.
After group fascicular repair, the epineurium is sutured to provide additional
support and alignment.
3. This technique offers an advantage over epineurial repair if motor and
sensory group fascicles in the proximal stump are appropriately aligned to
their respective motor and sensory group fascicles in the distal stump. This

Figure 17.5. A: Traumatic nerve laceration. B: Epineurial repair C: Group fascicular

repair.
arrangement helps to reduce the chance that motor axons will be directed
down endoneurial tubes toward sensory end organs and sensory axons being
directed toward motor end plates.
4. However, group fascicular repair may also increase potential fibrosis because
it requires an increased amount of dissection in addition to more intraneural
suture material.
C. The ideal method of repair
1. No significant data or Level I evidence suggest that one technique is better
than the other. Both surgical approaches result in similar outcomes.
2. The benefits of improved fascicular matching may be outweighed by an
increased surgical manipulation, which leads to fibrosis and possible fascicu-
lar mismatch.
3. Epineurial repair may be less precise but this technique may allow a neu-
rotrophic effect to influence the direction of axonal sprouting and
growth.
4. Current recommendations depend on the nature and location of injury, the tim-
ing of nerve repair, and the identification of fascicular arrangement in the nerve.

a) Nature of the injury

1) If an acute injury results in a sharp, clean laceration, an epineurial
repair can be performed because surface landmarks can be used to
align nerve endings.
2) Epineurial technique is always used for digital nerve repair.
3) If specific motor or sensory group fascicles can be identified by
dissection of the distal nerve stump, then a group fascicular repair is
indicated.
b) Location of the injury
1) In the proximal arm, the fascicular pattern of the nerve is polyfascicu-
lar. An injury at this location would indicate epineurial repair.
2) Distally, nerves become monofascicular or oligofascicular. With such
patterns, it becomes appropriate to complete a group fascicular
repair.
c) Identification of fascicular arrangement
1) Electrical stimulation of the nerve can be used to identify proximal
sensory and distal motor group fascicles.
2) Immunohistochemistry: Carbonic anhydrase stains sensory fascicles
and acetylcholinesterase will stain motor fascicles. Theoretically, this
should improve functional outcomes.
3) Median nerve at the wrist is arranged in a predictable fassicular
pattern.
a. The thenar motor group located in the volar radial aspect of the
nerve
b. The sensory group fassicles are located ulnar and dorsal radial
4) Ulnar nerve at the wrist is arranged in a predictable fassicular pattern
a. The motor group is located in the dorsal ulnar aspect.
b. The sensory group is located in the volar radial aspect of the
nerve.
2. Association with Humeral Shaft Fractures

A. The musculospiral groove and the lateral intermuscular septum are important
landmarks on the humerus that contain the radial nerve. The radial nerve is most
susceptible to injury along the posterior aspect of the humerus at the level of the
deltoid tuberosity, and along the lateral aspect of the humerus distally where it
pierces the lateral intermuscular septum.
B. Radial nerve injuries continue to be the most common peripheral nerve injury
associated with humeral shaft fractures. Radial nerve palsies are commonly
caused by spiral fractures of the humerus but they can also occur with transverse
and oblique fracture patterns.
C. Management of a humeral shaft fracture with concomitant radial nerve injury
consists of three categories: no exploration, early exploration, or late explora-
tion.
1. No exploration
a) Closed fractures associated with immediate nerve palsy can be managed
without surgery because spontaneous recovery has been reported to occur
in about 70% of patients within 3 to 6 months.
b) Studies have proposed that many cases of radial nerve palsy associated
with humeral shaft fractures are the result of a contusion. In such cases,
surgical exploration is often unnecessary. EMG/NCV studies may be

obtained at 3 weeks following injury for baseline evaluation. They can be

repeated at 3 months to confirm reinnervation.
2. Early exploration
a) Early exploration of the nerve is indicated in the following situations:
Open fracture, vascular injury, high velocity gunshot wounds, sharp or
penetrating trauma, and significant soft tissue injury.
b) Early exploration of the nerve allows for assessment of the extent of nerve
injury.
c) During exploration, fixation of the humerus can protect the nerve from
further trauma secondary to entrapment in a fracture callus.
d) If the nerve is lacerated, surgical repair at an early stage will minimize ten-
sion, which promotes healing. If the nerve is not reparable, consideration
should be given to secondary nerve grafting or tendon transfer.
3. Late exploration
a) Late exploration may help to avoid unnecessary surgery in patients who
will recover nerve function spontaneously. Moreover, this approach
decreases the risk of surgical complications related to anesthesia, wound
infection, osteomyelitis, and neural scarring.
b) Late exploration may also create an environment more conducive to nerve
healing if the nerve needs to be repaired at a later stage. Later exploration
will allow for a more accurate determination of the zone of nerve injury.
c) If neurorrhaphy is indicated, delaying surgery will also allow the neurilem-
mal sheath to thicken, which facilitates repair.
d) One of the disadvantages of delaying surgery is scarring, which will make
exploration of the nerve more challenging.
4. Considerations
a) In patients with electrophysiological evidence of failure of reinnervation
3 months after an injury along with no clinical signs of improvement, it
may be best to proceed with surgical exploration.
b) There is no definite timetable for late exploration, but it is reasonable to
consider surgery between four to 6 months after the injury, depending on
the patient’s clinical course.
c) The time between injury and intervention is critical. Reinnervation of the
motor endplate should occur within 12 to 18 months after the injury if
function is expected to return.
Reconstruction
I. Nerve Grafting
1. Nonvascularized Autologous/Standard Nerve Grafts

A. These types of nerve grafts are generally accepted as the current gold standard
for reconstructing nerve gaps.
B. Nerve grafting is usually delayed for at least 3 weeks after the initial trauma so
that both the zone of injury and extent of neural scarring can be assessed.
C. However, early nerve grafting can be performed in cases where early soft tissue
coverage is required to cover the injured zone or if re-exploration is predicted to
be difficult or dangerous.
D. Technique

1. The proximal and distal nerve stumps are transected into thin cross sections
until a healthy fascicular pattern devoid of scarring can be properly identified.
2. In cases of early grafting, the proximal and distal stumps are trimmed gener-
ously to ensure that the repair sites are well beyond the site of injury.
3. Nerve grafts are interposed using the proximal fascicular pattern as an initial
guide. If the nerve gap is short and if the injury is located distally, it may be
possible to connect proximal fascicles to distal fascicles with cable grafts.
4. If the internal motor and sensory topography of a nerve are known, graft
reconstruction should align motor with other motor fascicles and sensory to
other sensory fascicles.
5. The graft should be reversed in orientation when it is interposed between
the proximal and distal nerve stumps so that the distal end of the graft
contacts the proximal stump of the transected nerve. This will minimize
the loss of regenerating axons that are traveling down “open branches” and
it will also help to funnel the maximal number of axons toward the distal
stump.
E. Modality matching in nerve grafts
1. Axons usually enter nerve grafts in a random arrangement and the quality of
nerve regeneration is affected by the motor or sensory modality of the nerve
graft.
2. Regenerating axons that interact with a modality-matched path are more likely
to synapse with the appropriate end organ, as is the case where motor axons
enter Schwann cell basal lamina tubes vacated by damaged motor axons.
3. Regenerating axons that are matched will grow and mature. Mismatched
axons will retract secondary to the loss of trophic support.
F. Experimental studies have shown that a pure motor nerve graft results in better
regeneration than a pure sensory nerve graft. However, harvesting pure motor
nerve grafts usually results in unacceptable donor site morbidity. Thus, sensory
nerve grafts are currently used. This forces motor axons to grow without support
until they are able to reach the distal stump of the transected nerve.
G. Other considerations
1. Donor site morbidity is another important consideration when trying to
select an autologous nerve graft. The acceptable functional deficit is usually
limited to noncritical sensation.
2. Surgical access to the donor nerve is also important because a complex expo-
sure may increase morbidity and operating time.
3. The caliber of the harvested nerve is essential because nerve grafts are able to
survive through the mechanism of longitudinal inosculation and secondary
revascularization from the surrounding tissue. Large caliber nerve grafts such
as the ulnar nerve require a vascularized graft or else it will undergo ischemia-
induced central necrosis.
2. Vascularized Nerve Grafts

A. Vascularized nerve grafts are believed to facilitate axon regeneration through
scarred wound beds and to limit central graft ischemia in larger diameter nerve
trunks. They also function as vascularized carriers for nonvascular nerve grafts.
B. Many animal studies have demonstrated the benefits of vascularized peripheral
nerve grafts. Vascularized grafts have been shown to decrease the concentra-
tion of infiltrating fibroblasts and they also support myelination, nerve fiber
diameter, and Schwann cell concentrations in rabbit sciatic nerve grafts.

C. Currently, vascularized peripheral nerve grafts have been successfully used in

neural defects exceeding 20 cm in both the upper and lower extremities. Their
use is indicated with large caliber grafts such as the ulnar nerve.
II. Conduits
1. Axon Guidance Channels

A. An axon guidance channel (AGC) is an artificial conduit interposed between the
proximal and distal nerve stumps. It can be autogenous material, such as a vein,
or synthetic material, such as a collagen or PGA-based tube. It is currently under
investigation to improve outcomes and regenerative results when compared to
the traditional autograft.
B. Less surgical trauma is encountered because the nerve stumps are placed into the
ends of the tube, which requires fewer epineurial sutures for repair.
C. AGCs help to direct axons from the proximal to distal stump without interfer-
ence from imperfectly aligned degenerating fascicles of the nerve graft. They
also minimize fibrous scar tissue, which can impede axonal regeneration.
D. After the nerve stumps are placed inside the conduit, it becomes filled with serous
fluid. This serous fluid has neurotrophic factors that affect sensory, motor, and
sympathetic neurons. It allows matrix precursors to accumulate, which results
in the formation of a coaxial, acellular fibronectin-positive and laminin-negative
matrix that serves as a scaffold for migrating cells from the proximal nerve stump.
E. Current clinical indications
1. Digital nerves (pure sensory nerve) with segmental nerve gap.
2. Segmental gaps less than 2 cm.
F. The advantages of the conduits are decreased operative time when defects
requiring nerve grafting are present. The disadvantage is the cost of the synthetic
conduit or the additional incision for harvest of an autogenous conduit.
Gun Shot Wounds and Peripheral Nerve Injury

A. Gun shot wounds (GSW) to the hand and upper extremity can cause penetra-
tion injury along with the transfer of energy into the surrounding soft tissue.
B. Each different injured tissue may require a different method of treatment. For
example, a patient with a flexor tendon injury would normally be treated with early
surgery and mobilization. However, if there is concomitant nerve injury, a period of
rest may be recommended to allow the margins of the injured nerve to delineate.
C. GSW can be classified according to energy of injury, location of injury, and type
of tissue involved.
1. Less severe injuries
a) Characterized by: Low-energy injury, distal location, and single tissue
involvement. Low-energy injuries are caused by small handguns, BB
guns, and zip guns.
b) These injuries are usually treated successfully with simple wound care and
rehabilitation. If the bullet is shattered or lodged, surgical removal may be
necessary.
2. More severe injuries
a) Characterized by high-energy injuries, proximal location, and involve
multiple tissue types. High-energy injuries are caused by high-caliber

handguns or assault rifles. These weapons are associated with a greater

velocity, which increases the amount of tissue damage.
b) These patients usually require multiple surgical interventions and long
periods of rehabilitation.
D. Gun shot injuries to the hand
1. These injuries usually create some form of peripheral nerve injury and most
of the time, sensory nerves are affected.
2. Nerve injuries have the lowest priority during emergent care of a patient
with a gunshot wound as nerves can be repaired secondarily. However, initial
deficits after the injury must be noted.
3. Peripheral nerve injury secondary to GSW may create loss of sensation, pain, and
dysesthesia. A gunshot injury affecting the nerve can also result in posttraumatic
effects such as phantom pain, causalgia, and reflex sympathetic dystrophy.
4. Patients may also experience muscle weakness or loss of muscle function if
motor nerves are impaired.
E. Gun shot injuries to the wrist
1. If the wrist is involved, the ulnar or median nerve may be damaged. Ulnar
nerve repair, or reconstruction with nerve graft, is necessary to regain motor
function. Median nerve repair, or reconstruction with a nerve graft, is neces-
sary. Reconstruction is generally performed at least 6 weeks after injury when
the extent of nerve injury can be better appreciated.
2. Gunshot wounds located at the proximal radius usually result in damage
to the posterior interosseous nerve, which innervates many of the muscles
located in the extensor compartment of the forearm. Surgical repair is also
indicated in such injuries.
F. Treatment
1. Simple nerve repair under limited tension can be completed during the ini-
tial surgery. If a clinical nerve deficit is appreciated preoperatively, it may be
beneficial to repair and reconstruct the nerve at a later time when the zone of
injury to the nerve has demarcated.
2. Some studies suggest that initial nerve grafting may be preferable to nerve
reconstruction at a later time.
3. Nerve grafts can be harvested from adjacent fingers that are not salvageable, the
medial antebrachial cutaneous nerve or the sural nerve. All of these nerves are
excellent options for nerve grafts since they are purely sensory in character.
4. Healing at the initial site of neurorrhaphy occurs within 6 weeks and axons
regenerate at a rate of 1 mm a day.
G. The major concerns in peripheral nerve injury caused by GSW are loss of sen-
sory and motor function. Recovery time is extensive; it may take over a year for
the patient to experience full improvement following injury and intervention.
Nerve Transfers
In nerve injuries where primary reconstruction or grafting is either not feasible, or is

expected to produce a poor result, nerve transfer can be used. They can restore either
sensory or motor function. Examples of nerve injury that cannot be reconstructed
include avulsion of the proximal nerve root, absence or destruction of the proximal
nerve segment, large nerve gap (>10 cm), and a long distance from the injury level
to the target motor end plates. Common clinical scenarios that might require nerve

transfer include brachial plexus injuries, proximal ulnar nerve injuries, and multiple
peripheral nerve involvement. Since a donor nerve is required, the resultant defi-
cit after nerve transfer must be weighed against the potential benefit. The muscle
or sensory function of the donor nerve will no longer be available for subsequent
reconstructive procedures such as tendon transfer, if the nerve reconstruction is ulti-
mately insufficient or fails. Although there is no widely agreed upon algorithm for
nerve transfer cases, some general principles can be used to guide surgical decision
making.
A. Nerve transfer is technically challenging and should be performed only by

the surgeon experienced with microsurgical techniques for peripheral nerve
repair. Otherwise, restoration of motor function using tendon transfer or other
methods is preferred.
B. Nerve transfer should be performed as close to the distal target as possible to
decrease regeneration time and allow earlier reinnervation. This is especially true
with motor reconstruction, since the muscle motor end plates will be perma-
nently lost around 12 to 18 months postinjury, preventing any motor recovery
despite nerve reconstruction.
C. Nerve transfer should be undertaken as soon as it can be determined that spon-
taneous recovery or nerve suture or grafting is not expected to provide func-
tional recovery. Since axonal regeneration needs to occur (~1 mm/day), the time
from injury to presentation will determine whether nerve transfer is recom-
mended. This is particularly true with motor reconstruction, but there is clinical
and laboratory evidence that early reinnervation of sensory nerves also improves
outcomes.
D. Direct end-to-end nerve suture without tension is superior to nerve grafting
because barriers to maximal axonal regrowth are limited. If direct suture is not
possible, then nerve graft may be used to assure tensionfree nerve reconstruc-
tion. End-to-side nerve suture has been described for sensory reconstruction,
but is not widely used for motor reconstruction.
E. The donor nerve must be healthy and functioning, with similar diameter and
fascicular density to the recipient nerve. Pure motor donor nerves, such as the
spinal accessory or intercostal, achieve the best results for motor reconstruction.
Synergistic function between the donor and recipient muscles improves func-
tional results. Ipsilateral nerve transfer is superior to contralateral nerve transfer,
presumably due to cortical reintegration factors.
II. Functional Assessment
Preoperative assessment of donor function and postoperative assessment of recovery are

primarily clinical. The British Medical Research Council grading system for manual
muscle testing is generally used for motor function and is listed below (Table 17.7).
Donor muscle strength of at least M4 is recommended for nerve transfer in order
to achieve useful function (M3 or greater).
For sensory recovery, the modified Highet-Zachary classification is used for
assessment (Table 17.8).

TABLE 17-7 British Medical Research Council grading for manual

muscle testing
Grade Motor Function

M0 No palpable muscle contraction
M1 Return of perceptible muscle contraction
M2 Contraction with movement in the absence of gravity
M3 Muscle function against gravity
M4 Muscle function against resistance
M5 Normal muscle strength
III. Commonly Used Nerve Transfers for Motor Restoration
A. Transfers for elbow flexion

1. Intercostal nerve transfer to biceps branch of musculocutaneous nerve
a) Usually nerves from two to four intercostal levels transferred; third and
fourth intercostal space nerves contain the most motor fibers.
b) 800 to 1,300 axonal fibers per nerve. Sensory fibers can be excluded.
c) Direct coaptation may be more likely to achieve ³M3 strength elbow
flexion strength than with interpositional nerve graft (72% vs. 47%), but
want to limit distal dissection, as 10% decrease in motor axons with each
10 cm anterior dissection of the intercostal nerve.
d) Two incisions—thorax and subclavicular plexus.
2. Partial ulnar nerve transfer to biceps branch of musculocutaneous nerve
(Oberlin transfer)
a) First described by C. Oberlin in 1994.
b) One to three motor fascicles at anterior-medial aspect of ulnar nerve cho-
sen, preferentially from extrinsic flexors (FCU) instead of intrinsics. Desired
fascicles identified by low intensity electrical stimulation intraoperatively.
TABLE 17-8 Modified Highet-Zachary classification for sensory

assessment
Grade Sensory Function

S0 No sensation
S1 Protective sensation only
S2 Some tactile sensation
S2+ Some tactile sensation, but with hypersensitivity
S3 Pain and tactile sensation present
S3+ Pain and tactile sensation present, with 2-point discrimination > 10 mm
S4 Pain and tactile sensation present, with 2-point discrimination < 10 mm

c) 1,600 axonal fibers per transfer.

d) Allows direct coaptation at distal location, very close to target motor
endplates within biceps, so potentially short time to functional restoration.
e) Used for C5, C6, and/or C7 root level injuries, with preserved C8–T1
(ulnar nerve) function.
f ) No ulnar motor deficit reported. Occasional transient ulnar sensory
dysfunction.
g) One incision at medial arm.
h) May maximize elbow flexion strength with additional partial median
nerve transfer to brachialis branch of musculocutaneous nerve.
i) If necessary, can supplement with Steindler flexorplasty 12 to 15 months
after nerve transfer to improve elbow flexion strength.
B. Transfers for shoulder abduction/flexion
1. Spinal accessory nerve (CN IX) transfer to suprascapular nerve
a) Donor usually intact, even after extensive brachial plexus injury.
b) 1,500 to 1,700 axonal fibers per nerve. Few sensory fibers included.
c) Only distal portion of nerve is transferred to preserve innervation of tra-
pezius muscle.
d) Direct coaptation to recipient nerve.
e) Incision at supraclavicular plexus with extension along anterior trapezius
border.
f ) Used alone, may achieve better (³M3 strength) shoulder abduction than
transfers that reinnervate the axillary nerve alone (92% vs. 69%).
g) Can also be used for elbow flexion (musculocutaneous nerve), but requires
interpositional nerve graft, which is less desirable.
2. Posterior triceps branch of radial nerve to axillary nerve
a) First described by S. Leechavengvongs in 2003.
b) Best used for C5, C6 root or upper trunk level injuries. If C7 or middle
trunk injured, need to check radial nerve branch function with direct
intraoperative stimulation prior to transfer.
c) Branch to long head of triceps is transferred to anterior branch of axillary
nerve distal to quadrilateral space.
d) Direct coaptation to recipient nerve.
e) Posterior incision along posterior border of deltoid muscle.
f ) Recommended as combined procedure with additional suprascapular
nerve reconstruction for maximum shoulder function.
C. Transfers for hand intrinsic function
1. Anterior interosseous nerve to motor branch of ulnar nerve or recurrent
branch of median nerve
a) Used for ulnar nerve injuries proximal to midforearm level (in adults).
b) Distal portion of nerve innervating the pronator quadratus muscle is
transferred, with preservation of the more proximal muscles.
c) 900 to 1,100 axonal fibers per nerve, which includes some sensory fibers.
d) Negligible donor deficit, with functioning pronator teres.
e) Simultaneous decompression of Guyon canal allows internal neurolysis
for isolation of ulnar motor branch recipient.
f ) Direct coaptation to recipient nerve for ulnar motor nerve reconstruc-
tion. Requires interpositional nerve graft for recurrent median motor
nerve reconstruction.
g) Requires separate reconstruction of ulnar or median sensory function.

IV. Commonly Used Nerve Transfers for Sensory Restoration
A. General considerations
1. Used to reconstruct critical areas of hand sensation (ulnar aspect of thumb,
radial aspect of index finger, and ulnar border of small finger). Loss of sensa-
tion to the dorsum of the hand is not considered disabling, so sensory recon-
struction for this region is not generally performed. Sensory nerves from
intact distributions are transferred to reconstruct injured distributions (e.g.,
median-innervated digital nerve to ulnar digit).
2. Nerve transfers not frequently indicated, since long nerve grafts for sensory
reconstruction can provide adequate sensibility, even after longer regenera-
tion time. In contrast to motor endplates, the sensory end organs (Pacinian
corpuscles, Meissner corpuscles, and Raffini bodies) remain preserved after
denervation.
3. Formal sensory re-education is required. Restored sensation may be perceived
in the donor nerve distribution, which can be bothersome to patients if corti-
cal adaptation is incomplete or fails. Donor area of anesthesia is better toler-
ated and may decrease with time due to expansion of adjacent sensory nerve
territories.
4. Younger aged patients and early nerve transfer seem to achieve better results.
5. Some described sensory nerve transfers to the hand include
a) Radial sensory nerve transfer to ulnar aspect of thumb and/or radial
aspect of index finger.
b) Ulnar digital nerve of ring finger to radial aspect of index finger.
c) Ulnar digital nerve of long finger to ulnar aspect of small finger.
d) Palmar cutaneous branch of median nerve to ulnar sensory nerve branches
to ring and small fingers.
6. End-to-end nerve coaptation is most common for sensory nerve transfers.
However, some end-to-side transfers have been described.
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Belkas JS, Shoichet MS, Midha RJ. Axonal Guidance Channels in Peripheral Nerve Regeneration.
Operative Techniques in Orthopaedics. Peripheral Nerve Repair: Current Techniques and
Basic Science. 2004;14:190–198.
Chuang D C. Nerve transfers in adult brachial plexus injuries: My methods. Hand Clin. 2005;
21:71–82.
DeFranco MJ, Lawton JN. Radial nerve injuries associated with humeral fractures. J Hand Surg (Am).
2006;31(4):655–663.
Dumitru D, Amato AA, Zwarts M. Electrodiagnostic Medicine. 2nd Ed. Hanley and Belfus;
Elsevier 2001.
Gage M. Scalenus anticus syndrome: A diagnostic and confirmatory test. Surgery. 1939;5:559–601.
Jordan SE, Machleder HI. Diagnosis of thoracic outlet syndrome using electrophysiologically
guided anterior scalene blocks. Ann Vasc Surg. 1998;12:260–264.
Kimura J. Electrodiagnosis in Diseases of Nerve and Muscle: Principles and Practice. 3rd Ed. New York,
NY: Oxford University Press; 2001.
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graphy. 4th Ed. Lippincott Williams & Wilkins; 2004.
Lee KS, et al. An anatomic study of the Martin-Gruber anastomoses: Electrodiagnostic
implications. Muscle Nerve. 2005;31(1):95–97.

Leechavengvongs S, et al. Nerve transfer to deltoid muscle using the nerve to the long head of the
triceps, part 2: A report of 7 cases. J Hand Surg. 2003;28A:633–638.
Merrell GA, et al. Results of nerve transfer techniques for restoration of shoulder and elbow
function in the context of a meta-analysis of the English literature. J Hand Surg. 2001;26A:
303–314.
Myckatyn TM, Mackinnon SE. Surgical Techniques of Nerve Grafting (Standard/Vasularized/
Allograft). Operative Techniques in Orthopaedics. Peripheral Nerve Repair: Current
Techniques and Basic Science. 2004;14(3):171–177.
Oberlin C, et al. Nerve transfer to biceps muscle using a part of ulnar nerve for C5–C6 avulsion
of the brachial plexus: anatomical study and report of four cases. J Hand Surg. 1994;19A:
232–237.
Ozkan T, Ozer K, Gulgonen A. Restoration of sensibility in irreparable ulnar and median nerve
lesions with use of sensory nerve transfer: Long-term follow-up of 20 cases. J Hand Surg.
2001;26A:44–51.
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Correlations with VHS Companion. Philadelphia, PA: Vhs/Bklt Ed. Butterworth-Heinemann;
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Sanders RJ. Thoracic Outlet Syndrome – A Common Sequelae of Neck Injuries. Philadelphia, PA: JB
Lippincott; 1991.
Wang Y, Zhu S. Transfer of a branch of the anterior interosseous nerve to the motor branch of the
median and ulnar nerve. Chin Med J. 1997;110:216–219.
Wood MB, Murray PM. Heterotopic nerve transfers: Recent trends with expanding indication.
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100 patients. Orthop Clin N Am. 1988;19:131–146.

Brachial Plexus
18
Donald A. Bae and Terry Myckatyn
I. Anatomy (Fig. 18.1)
A. The brachial plexus typically arises from the C5 to T1 nerve roots, though ana-
tomic variations are frequent. “Prefixed cords,” in which there is contribution of
C4 to the plexus, occur in up to 40% of cases. “Postfixed cords,” in which there
is contribution from the T2 nerve root, may be seen in up to 4% of patients.
B. The brachial plexus is divided into five segments: roots, trunks, divisions, cords,
and nerves. (The pneumonic “red trucks drive cats nuts” may be useful.) The
C5 and C6 nerve roots join to form the upper trunk. The C7 root continues
as the middle trunk. The C8 and T1 roots join to form the lower trunk. Each
trunk then divides to form the anterior and posterior divisions. The anterior
divisions of the upper and middle trunks coalesce to form the lateral cord.
The anterior division of the lower trunk continues on as the medial cord. The
posterior divisions of all trunks join to form the posterior cord. The terminal
nerve branches arise from these cords. The lateral cord becomes the musculocu-
taneous nerve. The posterior cord gives rise to the axillary and radial nerves. The
medial cord becomes the ulnar nerve. The median nerve arises from branches
off the medial and lateral cord (the so-called M of the brachial plexus).
C. Other nerve branches arise more proximally from the brachial plexus. Notably,
the long thoracic nerve arises from the C5 to C7 nerve roots. The suprascapular
nerve arises from the upper trunk. The lateral pectoral nerve arises from the
lateral cord. The medial pectoral, medial brachial cutaneous, and medial ante-
brachial cutaneous nerves arise from the medial cord. The thoracodorsal nerve
as well as the upper and lower subscapular nerves arise from the posterior cord.
D. During surgical approaches, the brachial plexus may be explored in the
posterior triangle of the neck (borders are sternoclidomastoid, the trapezius and
the clavicle) between to the anterior and middle scalene muscle bellies. After
dissection through the skin, platysma, and underlying fascia, the scalene muscles
may be found just posterior to the sternocleidomastoid muscle. The phrenic
nerve, typically found on the anterior surface of the anterior scalene, serves as
the “lighthouse to the brachial plexus” and may be traced proximally to its origin
from the C3 to C5 nerve roots, leading the surgeon to the C5 nerve root and
brachial plexus. The inferior belly of the omohyoid muscle is another useful
anatomic landmark; the upper and middle trunks lie superior to the omohyoid,
and the inferior trunk and subclavian vessels lie inferiorly. As the divisions,
cords, and terminal branches lie inferior to the clavicle, clavicular osteotomy or
mobilization may be needed to expose the entire plexus.
E. The ganglia lie close to the spinal cord, though the motor neuron cell body
lies within the cord itself. Therefore, “preganglionic” lesions refer to ruptures
or avulsions of the neural elements from the spinal cord. Several nerves arise
in close proximity to this area, including the sympathetic chain, phrenic nerve,
343

Spinal nerves Trunks Divisions Cords Branches
C5
Dorsal scapular nerve
C6 Upp Suprascapular nerve

er An
Po ter
ior Lateral pectoral nerve
st
er
io
r Latera
C7 Middle Anterior l Musculocutaneous
Pos nerve
terio
r Po
ste
rio Axillary nerve
r r
terio
Pos
C8 Low Radial nerve
er
Ant
erio
r Thoracodorsal nerves
Med
ial
Upper and lower
T1 subscapular nerves
Long thoracic nerve

Medial nerve
Medial pectoral nerve
Ulnar nerve
Medial brachial cutaneous nerve
Medial antebrachial
cutaneous nerve
Figure 18.1 Diagram of the brachial plexus. The arrow identifies Erb point. The
“M” of the brachial plexus is outlined in gray. (Adapted from Waters PM. Obstetric
brachial plexus injuries: Diagnosis and management. J Am Acad Orthop Surg. 1997;5:
205–214.)
long thoracic nerve, and dorsal scapular nerve, which are assessed in the evalua-
tion of these patients.
F. The brachial plexus is intimately associated with the subclavian and axillary
artery and vein throughout. The cords are named according to their location with
respect to the second portion of the axillary artery posterior to pectoralis minor.
Congenital Brachial Plexus
I. Definition
Brachial plexus birth palsy (BPBP) refers to traction or compression injury to the bra-
chial plexus sustained during birth resulting in neurological impairment and upper
extremity paralysis.
II. Epidemiology
The incidence of BPBP is estimated to be 1 per 1,000 live births. Despite advances in
obstetrics, prenatal medicine, and rising Caesarian section delivery rates, the incidence
may be increasing in more developed nations.

Chapter 18 • Brachial Plexus 345
Risk factors include

A. Macrosomia (>4,500 g)
B. Difficult or prolonged labor
C. Shoulder dystocia
D. Multiparous pregnancy
E. Vacuum or forceps assisted delivery
F. History of prior delivery resulting in BPBP
III. Classification
A. BPBP may be classified according to the character of the neurological injury or

anatomic pattern of plexus involvement. The Seddon and Sunderland classifica-
tions (e.g., neurapraxia, axonotmesis, and neurotmesis) may be used. Neurot-
mesis injuries may be described as nerve root avulsions from the spinal cord or
“preganglionic” injuries versus extraforaminal or “postganglionic” ruptures at the
root or trunk level.
B. BPBP may also be characterized based upon the nerve roots involved.
1. Classic Erb palsy refers to C5–6 involvement, typically at the level of the
upper trunk at “Erb point.”
2. A Klumpke paralysis denotes C8–T1 involvement. Total plexus involvement
may also be seen.
C. The Narakas classification system has been used to categorize typical patterns of
involvement.
1. Group I refers to C5–6 palsies (~46% of patients).
2. Group II refers to C5–6–7 involvement (~29%).
3. Group III denotes a flail upper extremity (total plexus involvement) without
an associated Horner syndrome.
4. Group IV refers to a flail extremity with Horner syndrome.
IV. Natural History
A. While limited long-term data are available, several observations can be made
regarding the natural history of BPBP with regard to the pattern and timing of
neurological recovery. The majority of BPBPs are transient, and patients who
recover antigravity biceps function within the first 2 to 3 months of life are
expected to achieve full spontaneous recovery by 1 to 2 years of age. Patients
who do not recover antigravity biceps function by 6 months of age will likely
have persistent neurological deficits and upper extremity impairment; these
patients should be considered for surgical intervention. Patients who dem-
onstrate incomplete upper trunk recovery during 3 to 6 months of age will
likely have long-standing but partial limitations in upper limb motion and
strength.
B. Patients with preganglionic or root avulsion injuries are not expected to dem-
onstrate spontaneous neurological recovery. Therefore, negative prognostic
indicators include the presence of a Horner syndrome (ptosis, miosis, and anhy-
drosis), elevated hemidiaphragm, scapular winging, and absence of trapezius
function.

V. Clinical Evaluation
A careful prenatal, perinatal, and postnatal history should be obtained on all infants
presenting for the evaluation of a possible BPBP. Particular attention should be made
regarding birth weight and initial upper limb active motion. On physical examination,
the presence or absence of a Horner syndrome should be noted. Passive joint motion
and active motor function of the entire upper limb are assessed. In infants, this exami-
nation may be challenging.
VI. Differential Diagnosis
Differential diagnosis of an infant presenting with upper extremity weakness are as

follows:
1. Pseudoparalysis is caused by a clavicle or proximal humerus fracture, osteomy-
elitis, or septic arthritis of the glenohumeral joint.
2. Other neurological conditions, such as cerebral palsy, perinatal cerebrovascular
injury, or cervical spine pathology, are present similar to BPBP.
3. Other congenital conditions, such as arthrogryposis, should be considered.
VII. Diagnostic Studies
A. Plain radiographs and/or ultrasound of the clavicle and proximal humerus may
be obtained to rule out pseudoparalysis from fracture.
B. Advanced imaging techniques (myelography, CT-myelography, and MRI) have
been used in efforts to characterize the nature of the plexus injury. Unfortu-
nately, these modalities require sedation and/or anesthesia in infants and have
imperfect sensitivity and specificity.
C. Electromyography and nerve conduction velocities also have been utilized. The
presence of normal sensory nerve conduction in the absence of motor nerve
potentials is thought to be diagnostic of a root avulsion injury (dorsal root gan-
glion is in continuity with the peripheral nerve, but not the root). However,
electrodiagnostic studies may not always be helpful in guiding treatment, as the
presence of nerve conduction does not correlate with clinically useful muscle
recovery.
D. In spite of sophisticated ancillary studies, serial physical examinations remain
the primary tool to prognosticate recovery and guide treatment.
VIII. Indications for Microsurgical Nerve Reconstruction
While controversial, current indications for microsurgical nerve reconstruction

include
1. Absence of antigravity biceps function by the age of 3 to 9 months and
2. A flail upper limb associated with a Horner syndrome at age 3 months.

IX. Principles for Microsurgical Nerve Reconstruction
Strategies of microsurgical brachial plexus surgery vary depending upon the individual
pattern of injury. While there is no universal approach to surgical treatment, the follow-
ing principles are generally followed:
Meticulous surgical exploration of the brachial plexus is required to characterize
the pattern of injury.
A. Intraoperative nerve stimulation, electrodiagnostic studies, and/or immunohis-
tochemical analysis may assist in determining the extent of plexus injury.
B. Neurolysis alone is controversial and should not be used in the setting of
avulsion injuries.
C. While theoretically appealing, neuroma excision and direct tension-free end-
to-end neurorraphy are typically not possible.
D. Traditional reconstruction is done by excision of neuroma and sural nerve graft-
ing from healthy proximal to healthy distal nerve tissue. For example, a C5–6
upper trunk rupture would be treated by neuroma excision and sural nerve
grafting from C5 and C6 roots to anterior division of upper trunk/lateral cord,
suprascapular nerve, and posterior division of upper trunk/posterior cord.
E. In addition to traditional nerve grafting techniques, neurotizations (or nerve
transfers) may be performed using the terminal branch of the spinal accessory
nerve, intercostals nerves, phrenic nerve, hypoglossal nerve, ulnar nerve fas-
cicles, and even the contralateral C7 nerve root. This is particularly useful in
avulsion injuries where there is no healthy proximal nerve stump, or in extensive
injuries in which insufficient nerve graft is available to reach all target nerves.
An established nerve transfer is the Oberlin transfer, in which some motor fas-
cicles of the ulnar nerve to the flexor carpi ulnaris (FCU) are transferred to
the terminal motor fascicles of the musculocutaneous nerve in the brachium to
reinnervate the biceps. A double fascicular transfer, as described by MacKinnon
(using motor fascicles from both the ulnar and the median nerves to innervate
both biceps and brachialis), can be utilized as well.
X. Secondary Deformities
A. Muscle imbalance leads to joint deformity in growing children. Thus, persis-

tent shoulder weakness and secondary glenohumeral joint dysplasia may be seen
in BPBP patients with incomplete neurologic recovery. There is usually weak-
ness of shoulder abduction and external rotation. Radiographically, posterior
humeral head subluxation, increased glenoid retroversion, and even formation
of a pseudoglenoid may be seen. These joint changes are progressive and may
present early in life.
B. Initial treatment is comprised of physical therapy for stretching, splinting, and/or
botulinum toxin injections to the tight or contracted muscles. In those patients
with persistent functional limitations, surgical treatment can improve shoulder
function. Indications for surgical treatment include the following: Infantile gle-
nohumeral joint dislocation, persistent shoulder internal rotation contracture,
limited shoulder abduction and external rotation, and progressive glenohumeral
joint dysplasia. Choice of surgical treatment is dependent upon the underlying
status of the glenohumeral joint.

1. For abduction and external rotation weakness in the setting of minimal or

mild deformity, latissimus dorsi and teres major tendon transfers to the rota-
tor cuff can significantly improve global shoulder function.
2. For shoulder weakness in the setting of advanced glenohumeral dysplasia,
external rotation osteotomies of the humerus may be performed to reorient
the arc of shoulder motion into a more functional range.
3. For shoulder weakness in the setting of moderate deformity, tendon trans-
fers combined with arthroscopic or open musculotendinous lengthenings of
the pectoralis major and subscapularis with glenohumeral joint reduction
improves shoulder function and may lead to joint remodeling.
Adult Brachial Plexus Injuries
I. Diagnosis
A. Clinical examination
1. Motor examination: There is significant anatomic variation among the spinal
nerves, and muscles are ultimately innervated at multiple cervical levels. The
spinal nerves are typically correlated with the following functions, and injury
is manifest as loss of these functions:
a) C5: Shoulder abduction, elbow flexion
b) C6: Wrist extension, forearm pronation and supination
c) C7: Wrist flexion/finger extension
d) C8: Finger flexion
e) T1: Finger abduction and other instrinsic hand functions
2. Sensory examination: Oftentimes, only deep densation elicited by a pinch or
deep pressure stimulus can be detected. The examination of the dermatomal
distribution of sensory loss can help determine the extent of brachial plexus
injury and the course of recovery:
a) C4: Superior shoulder
b) C5: Upper, lateral arm and inferior shoulder
c) C6: Radial forearm and thumb
d) C7: Index and long fingers
e) C8: Ring and small fingers
f ) T1: Ulnar forearm
3. Other findings
a) Horner syndrome: Injury to superior stellate ganglion in lower plexus
injury can lead to myosis, ptosis, and anhidrosis.
b) Winging of the scapula: Can occur with injury to the long thoracic nerve
causing serratus anterior dysfunction or the accessory nerve causing tra-
pezius dysfunction.
c) Vascular injuries can accompany adult brachial plexus lesions, and
peripheral pulses and blood pressures (compared to the contralateral side)
if possible should be documented.
B. Ancillary studies
1. Diagnostic imaging
a) X-rays
1) C-spine series: To identify associated c-spine injury.

2) PA and lateral of shoulder: To identify proximal humerus, clavicular,

or scapular fractures.
3) Chest x-ray: To identify scapulo-thoracic dissociation, first rib fractures,
or other associated chest wall trauma
b) CT scan: For identification of scapulothoracic and C-spine injuries
c) Myelography: Useful for identifying cervical spinal root avulsion.
d) MRI: Particularly useful for imaging postganglionic brachial plexus inju-
ries, as well as for the imaging of brachial plexus tumors.
2. Electrophysiology
a) Sensory nerve action potentials (SNAPs): For injuries proximal to the
dorsal root ganglion, the sensory axon is intact and no Wallerian degen-
eration occurs. The presence of a SNAP, therefore, confirms a pregan-
glionic lesion. SNAPs are not useful for C5 evaluation because C5
rarely provides a significant contribution to a major peripheral sensory
nerve.
b) Electromyography (EMG): In the first week after injury, EMG cannot
be used to exclude a complete nerve disruption since part of the synap-
tic apparatus remains intact. EMG is typically used to confirm complete
nerve injury starting 12 weeks after the time of injury.
II. Treatment
A. Timing
1. Immediate: Immediate or early reconstruction of brachial plexus injuries is
typically reserved for cases of penetrating trauma or immediately after tumor
resection where a clear margin is demonstrated. Treatment is typically delayed
in the absence of penetrating trauma so that the extent of potential recovery
can be assessed.
2. Delayed reconstruction.
a) The extent of injury and degree of expected recovery are more apparent.
b) Motor function is unreliably restored in proximal peripheral nerve inju-
ries due to an inability to reinnervate muscle after a delay of one year or
more. So, if a regenerating nerve is not expected to reach a muscle target
within 1 year of injury, alternate forms of reconstruction like nerve or
tendon transfers are employed.
B. Tendon transfers: Redundant or expendable function from a working muscu-
lotendinous unit is used to power a more critical function that was lost with
brachial plexus injury. These may include standard transfers for muscles inner-
vated by the radial, musculocutaneous, high ulnar and median, and axillary
nerves.
C. Nerve transfers: Redundant or expendable axons from a working peripheral
nerve are diverted to reinnervate a target previously denervated with brachial
plexus injury. One example is diverting intact ulnar nerve branches intended
for the FCU to the musculocutaneous nerve following a high (C5, C6) brachial
plexus injury. Wrist flexion is maintained by other intact muscles and nerves
while biceps flexion can be restored by reinnervating the musculocutaneous
nerve with ulnar nerve axons.

Suggested Readings
Clarke HM, Curtis CG. An approach to obstetrical brachial plexus injuries. Hand Clin.
1995;11:563–581.
Waters PM. Obstetric brachial plexus injuries: diagnosis and management. J Am Acad Orthop Surg.
1997;5:205–214.
Waters PM. Comparison of the natural history, the outcome of microsurgical repair, and the
outcome of operative reconstruction in brachial plexus birth palsy. J Bone Joint Surg Am.
1999;81:649–659.

Arthritis
19
Richard A. Bernstein, Douglas M. Sammer,
Marco Rizzo, Charles S. Day, Louis W. Catalano III,
Brian D. Adams, Karim Bakri, Seth D. Dodds,
Kevin J. Malone, Steven L. Moran, and
Christina M. Ward
Inflammmatory Arthritis
I. Seropositive
Inflammatory arthropathies include the classic seropostive arthritic variants such as

rheumatoid arthritis (RA), and those that are considered seronegative such as psoriatic
arthritis (PsA) and ankylosing spondylitis. By far, the most common form of inflam-
matory arthritis is RA.
RA is an inflammatory disease affecting about 2.1 million people in the United
States with its associated features of pain, swelling, stiffness, and loss of function in
the joints. As an inflammatory process consisting of spontaneous proliferation of the
synovial cells of joints and those lining tendon sheaths, the classic features include spon-
taneous, often symmetrical joint swelling and stiffness. This progresses to soft tissue
disruption of the supporting structures of the affected joints, overgrowth of the synovial
layer (pannus) over the articular cartilage, eventually destroying this as well. The similar,
synovial proliferative, process can occur with tendons with associated tenosynovitis,
adhesions, and eventual rupture. Both flexors and extensors can be involved.
There have been major advancements in the medical treatment of this condition,
resulting in decreased need for operative treatment. Despite this, individuals with aggres-
sive forms of the disease, nonresponsive to medical management, will continue to benefit
from surgical intervention.
A. General conditions related to the upper extremity
1. Bone quality
a) Osteopenia
b) Periarticular osteolysis
c) Bone loss
d) Auto fusion
2. Soft tissue issues relevant to surgery
a) Contractures and deformity
b) Laxity
c) Tendon issues
1) Subluxation
2) Dislocation
3) Ruptures
B. Wrist
1. Deformities
a) Radial deviation of the carpus and metacarpals, volar subluxation of the carpus
351

b) Autolysis of carpal bones, with or without partial spontaneous arthrodesis

c) Ulnar head dorsal dislocation secondary to carpal supination and
synovitis of the distal radioulnar joint (DRUJ)
d) Ruptures of the extensor tendons (caput ulnae syndrome)
2. Surgical management
a) Synovectomy alone rarely indicated
b) Limited arthrodesis: Radiolunate (Chamay)
c) Total wrist arthrodesis: The gold standard
1) Techniques of wrist fusion:
a) Pin/rod
b) Plate and screws
2) Expected results
a) High level of patient satisfaction
1) Reduction or elimination of pain in almost all patients
2) Functional impairment for fine motor tasks documented
b) Bilateral issues: Fuse both in slight extension, poor satisfaction with
flexion (perineal care) in nondominant wrist
d) Arthroplasty: Evolving technology
3. Caput ulnae syndrome
a) Ulnar head resection or arthroplasty and stabilization
b) Tendon repair or transfers (tendon fraying occurs frequently over a wide
area and repair is often not possible)
C. Metacarpal phalangeal joints
1. Pathomechanics of deformities at the metacarpophalangeal (MCP) level:
Joint destruction begins early in the disease, associated with three phases:
a) Initial proliferative phase
1) Pain, effusion
2) Synovial proliferation, angiogenesis
b) Destructive phase
1) Synovial pannus invades cartilage and soft tissue
c) Late phase (“Burnt Out”)
1) Less inflammation, replaced by fibrosis scarring and fixed deformities
2. Ulnar drift consists of both ulnar shift and ulnar deviation.
a) Normal MP joint is condylar, allows multiaxial movements, relies upon
capsule and ligaments to provide stability.
b) Synovial proliferation and destruction result in laxity of the collateral
ligaments.
c) Dorsal structures stretch.
d) Extensor hood weakened at the level of the sagittal bands, allowing ulnar
subluxation of the tendons (i.e radial sagittal bands compromised).
e) Wrist radial posturing along with wrist ulnar translocation encourages
the ulnar shift of the tendons secondary to the axial load direction that is
altered by the wrist position.
f ) Volar subluxation or dislocation occurs because of collateral ligament
weakening and with the flexors overpowering the weakened extensors.
g) Dorsal extensor mechanism and capsule stretched and rendered less
effective by dislocated position.
h) This imbalance at both levels, the joint and the extrinsic tendons results in
the ulnar drift and volar subluxation of the digits at the MP level.

Chapter 19 • Arthritis 353
3. Loss of function
a) Dependent on the extent of the deformity
b) Function can be well preserved until late
4. Deformity
a) Aesthetic appearance
b) “Declaration of having a disease”
5. Current methods of surgical management
a) Synovectomy alone
i) Synovectomy
a) Alone is rarely indicated
b) May rarely be used for a joint, which is refractory to medical
management without deformity
c) Temporary relief at most, with a 30% to 50% recurrence
b) Synovectomy with tendon relocation
ii) Synovectomy plus tendon relocation
a) May be useful for the early stages of disease, in which there is pre-
served joint cartilage and for refractory synovitis with ulnar dis-
placement of extensor mechanism
b) Technique
1) Radial arthrotomy parallel to extensor tendon
2) Separate tendon from capsule and perform synovectomy as
necessary
3) Partial or full release ulnar collateral ligament and ulnar intrin-
sic wing of extensor hood
4) Plicate radial collateral ligament (RCL)
5) Repair dorsal capsule and use “Vest over pants” repair of exten-
sor hood
6) Reinforce the repair with slip of extensor tendon through the
capsule.
c) Postoperative management
1) Dynamic extension splint for 6 weeks
2) Hand therapy
c) Joint arthroplasty
iii) Arthroplasty of the MP joints
a) Most common surgical treatment for the MP joints
b) Current implant materials include silicone, metal and plastic (poly
ethylene)
c) Surgical techniques are similar
d) Surgical exposure
1) Skin incisions can be transverse or longitudinal.
a. Longitudinal may allow better wound healing, earlier
mobilization, and preservation of dorsal venous
structures.
2) Radial paratendinous arthrotomy with release of collateral
ligaments from metacarpal head.
3) Synovectomy.
4) Trial reduction implant for sizing and need for additional soft
tissue releases.
a. Ulnar sagittal band
b. Ulnar intrinsic wing at base of proximal phalanx

c. Abductor digiti minimi release (direct visualization to avoid

ulnar digital nerve injury) at base of small finger proximal
phalanx
d. Volar plate release as needed
5) Insert definitive prosthesis, tend to larger sizes for stability and
longevity.
6) Repair RCL with correction of ulnar deformity.
7) Vest over pants repair of tendon, MCP capsule with centraliza-
tion of extensor hood and dorsal capsule.
8) Skin closure with nonabsorbable suture and splint.
iv) Soft tissue balance
a) Critical to a successful outcome
b) Attention to ulnar releases, volar releases, and correct implant siz-
ing
c) Repair of RCL
d) Protection postoperatively for 6 weeks in dynamic extension splint,
active hand therapy for active and passive range of motion (ROM)
of MP and interphalangeal (IP) joints
v) Long-term results
a) Patient satisfaction 38% at 14 years follow-up.
b) Substantial reduction in pain, improvement in function and
appearance.
c) Level 2 prospective evidence proving marked and significant
improvement for RA patients with poor baseline functioning
treated with MCP joint arthroplasty over control medical manage-
ment group at early follow up.
vi) Silicone implants: Failures occur due to
a) Fracture of implant at junction of hinge and distal stem, may not
result in clinical failure
b) Long-term stability occurs from encapsulation of the implant with
scar tissue
c) Particulate silicone synovitis
d) Stretching and deformation of the implants without fracturing sec-
ondary to reoccurrence of soft tissue imbalance
d) Joint arthrodesis
D. Interphalangeal joints
1. Bone changes
Typical of other joints in arthritis with joint destruction, deformity, and
stiffness
2. Soft tissue deformities
Swan neck and boutonnière deformities can be seen in the same hand,
different digits
3. Clinical issues
a) Despite the deformities, most are well tolerated by patients.
b) Symptoms related to stiffness, inability to grip. Pain can also be a problem
with advanced disease.
4. Management: Depending on the severity of the deformity, fixed or nonfixed
5. Options include
a) Synovectomy in conjunction with tendon procedures
b) Arthroplasty

c) Arthrodesis
Swan neck deformities and boutonnière deformities are covered in detail
in the chapter on extensor tendon chronic injuries.
II. Seronegative Arthritis
‘Seronegative’ is defined by the absence of rheumatoid factor (RF) in the blood. In some
classification schemes, any arthritis in which RF is not present is classified as seronega-
tive arthritis, including RF negative RA, osteoarthritis, infectious arthritis, gout, and
others. However, seronegative usually indicates seronegative spondyloarthropathies
including Psunatic arthritis (PsA), ankylosing spondylitis, reactive arthritis (Reiter
syndrome), and enteropathic arthritis (the arthritis of inflammatory bowel disease).
PsA is the most common seronegative spondyloarthropathy that involves the hands,
and the primary focus of this section. In addition, there is a discussion of systemic
lupus erythematosus (SLE) and scleroderma as they also commonly affect the hands.
A. Epidemiology
1. As a group, the seronegative spondyloarthropathies affect men more often
than women, although PsA affects men and women equally.
2. Like the other seronegative spondyloarthropathies, the prevalence of PsA has
a positive correlation with the prevalence of the HLA-B27 MHC class II
allele, which varies widely between ethnic groups.
3. The prevalence of psoriasis in the general population ranges from 0.1% to 3%.
4. About 7% of patients with psoriasis develop PsA.
B. Pathogenesis
1. HLA-B27 is one of many possible alleles that can occupy the “B” locus in
the major histocompatability complex on chromosome 6. The HLA mol-
ecule presents antigens to T-cells and helps launch the immune response. The
exact role of HLA-B27 in the seronegative spondyloarthropathies is not well
understood.
2. An environmental trigger is probably required to initiate the arthritis. In the
case of reactive arthritis (formerly known as Reiter syndrome), the trigger
is an extra-articular bacterial infection (Chlamydia, Salmonella, and others).
The possible role of bacterial infection in reactive arthritis is being investi-
gated, although the environmental triggers are not known.
C. Presentation
1. Ankylosing spondylitis, reactive arthritis, and enteropathic arthritis typically
have axial involvement and asymmetric oligoarticular lower extremity joint
involvement. Enthesitis and sacroiliitis are common. In addition, there are
usually extra-articular findings.
a) Reactive arthritis: Urethritis, conjunctivitis, and prior extra-articular
infection (Chlamydia, Salmonella, Yersinia, Campylobacter, or Shigella).
b) Enteropathic arthritis: Inflammatory bowel disease (Crohn or ulcerative
colitis).
2. PsA presents with cutaneous findings prior to arthritis in 85% of patients.
Of the 15% that develop arthritis first, all will eventually develop a rash or
typical nail changes (pitting or crumbling).
3. PsA has five patterns of joint involvement. These patterns often overlap, and
can change over time in a given patient.
a) Distal interphalangeal (DIP) joint arthritis
b) Arthritis mutilans of the digits (severe, aggressive polyarticular arthritis)

c) Symmetric polyarthritis indistinguishable from RA

d) Asymmetric oligoarthritis, often involving the hands
e) Spondyloarthropathy
4. Erosion of the terminal phalanges can occur at the tufts (acral osteolysis).
5. At the DIP joint, proliferation at the base of the distal phalanx combined
with erosion and tapering of the middle phalanx can result in a “pencil-
in-cup” deformity.
6. DIP ankylosis is common.
7. Aggressive osteolytic changes seen with arthritis mutilans can result in an
“opera glass hand” with collapse of the digits.
8. Psoriatic dactylitis, with fusiform swelling due to periostitis, tendonitis, and
enthesitis can occur.
9. Unlike in RA, hand deformities tend to be asymmetric.
a) The most common finger deformity is a flexion contracture of the proxi-
mal interphalangeal (PIP) joint with secondary hyperextension of the
metacarpophalangeal (MP) joint.
b) Swan neck deformities do occur, and usually initiate with a mallet
finger.
c) The MP joints tend to develop extension contractures.
d) In the thumb, MP flexion and IP extension contractures are common.
e) Wrist involvement is common.
D. Diagnosis
There are no specific diagnostic criteria for PsA. The diagnosis is made when
there is an inflammatory seronegative arthritis with axial or asymmetric
peripheral involvement, in the setting of psoriatic skin lesions or typical nail
changes.
E. Imaging
Acral osteolysis with resorption of distal phalangeal tufts, spontaneous DIP
ankylosis, and the pencil-in-cup deformity are common radiographic findings.
Sacroiliitis is also seen.
F. Nonsurgical treatment
NSAIDs are used to treat early disease, but may make cutaneous lesions worse.
Other medications similar to those used to treat RA may be used (methotrexate,
cyclosporine, sulfasalazine, gold salts, antimalarials, and azathioprine).
G. Surgical treatment
Surgical treatment of wrist and finger deformities is often necessary to treat pain
and improve function.
1. Painful PIP joint with severe articular destruction (and bone defects) or PIP
flexion deformities that are fixed can be treated with arthrodesis to relieve
pain and place the joint in a more functional position.
2. Swan neck deformities may require surgery to improve function and should
be approached like a rheumatoid swan neck deformity.
3. Silicone arthroplasty is often necessary to correct extension contractures (and
occasionally flexion contractures) of the MCP joint.
4. The DIP joints rarely require arthrodesis due to the high rate of spontaneous
ankylosis.
5. In cases of arthritis mutilans, arthrodeses with bone grafts to restore length
are required.
6. In the thumb, MP or IP arthrodesis is often necessary. Carpometacarpal
(CMC) arthritis is treated with resection arthroplasty and ligament recon-
struction to relieve pain preserve motion.

7. In the wrist, limited or complete arthrodesis is sometimes indicated for pain.

Distal ulna resection or Sauve-Kapandji procedure can be used when the
DRUJ is involved.
H. Other connective tissue diseases involving the hands
SLE and scleroderma are two common connective tissue diseases that often
affect the hands. RF is present in 20% to 30% of patients with these conditions,
although most are seronegative for RF.
1. SLE is a multisystem inflammatory disease affecting the skin, heart, lungs,
kidneys, and periarticular soft tissue. About 85% of patients have cutaneous
findings, including a butterfly rash on the face, or an erythematous macu-
lopapular rash on the palms and fingers, both of which tend to occur after
sun exposure. Patients are usually young females. SLE is more common in
African Americans than whites.
a) There are a number of changes that commonly occur in the hands.
1) Raynaud phenomenon.
2) Morning stiffness that improves with motion.
3) Symmetric hand joint involvement, with swelling and pain.
4) Hand deformities are very similar to those seen in RA (ulnar transloca-
tion of the carpus, radial deviation of the metacarpals, ulnar deviation
of the fingers, volar subluxation of the MP joints, swan-neck and bou-
tonnière deformities of the fingers). However, in SLE they are due to
soft tissue pathology only, without articular involvement.
5) X-rays do not show osseous or articular changes consistent with
arthritis.
b) Early in the disease, passively correctible deformities are best managed
with therapy and splinting to preserve function. Surgery is indicated
to improve function in patients that do not improve with nonsurgical
management.
1) Soft tissue reconstruction alone has a high failure rate.
2) In spite of a lack of articular changes, arthrodeses or arthroplasties are
often performed in combination with soft tissue reconstruction to pre-
vent recurrence.
3) Common operations include
a. Limited or total wrist arthrodesis for instability or ulnar
translocation.
b. The Darrach procedure (distal ulna resection) or Sauve-Kapandji
procedure for dorsal subluxation of the ulna and arthritis of the
DRUJ.
c. MP silicone arthroplasty combined with soft tissue reconstruction
for ulnar deviation and volar subluxation. For the thumb MP joint,
arthrodesis is preferred.
d. PIP joint arthrodesis.
2. Scleroderma is a multisystem disease that affects the skin, kidneys, heart,
lungs, and GI tract, resulting in progressive fibrosis of connective tissue. It is
more common in females than males (4:1).
a) There are three clinical patterns.
1) Diffuse scleroderma: Widespread skin hardening and multiple organ
system involvement.
2) Limited scleroderma (CREST): Skin hardening limited to hands and
face—Calcinosis, Raynaud phenomenon, Esophageal involvement,
Sclerodactyly, Telangiectasias.

3) Linear (morpheaform): Isolated small areas of skin hardening without

systemic involvement.
b) Hand symptoms and deformities are common and diverse.
1) Raynaud phenomenon is very common.
2) Fingertip ulceration and autoamputation can occur.
3) Ulceration is common over the convex surface of contractures.
4) Cutaneous fibrosis leads to contractures in the fingers and loss of
function. PIP flexion contractures with compensatory MP hyperexten-
sion are the most common deformities. Tendon rupture and skin
breakdown often occur with these contractures.
5) First web space contracture is common.
6) X-rays may show tuft resorption.
7) Cutaneous or subcutaneous calcinosis in the fingers can occur and can
be painful.
c) Therapy and splinting rarely slow the progression of the disease. Surgery is
indicated primarily to improve function and to treat nonhealing wounds
or infections, such as osteomyelitis. The decision to operate should be
made carefully, since patients with scleroderma heal poorly and are prone
to infection.
1) Nonhealing ulcerations over joints contractures may require resection
of bony prominences or arthrodesis.
2) Symptomatic calcinosis can be treated with resection, debulking, or
curettage.
3) Distal amputation may be necessary for nonhealing wounds associated
with osteomyelitis.
a. Circulation must be carefully assessed prior to surgery, particularly
distal to the middle phalangeal level.
b. Medications such as calcium channel blockers may improve distal
circulation.
4) Fixed PIP flexion deformities should be corrected with arthrodesis,
including enough bone resection to ensure adequate soft tissue coverage.
5) Fixed MP contractures are treated with resection arthroplasty. A volar
approach will allow less tension on the wound closure if it is an exten-
sion contracture.
6) First web space soft tissue release is commonly performed to improve
grasp. Thumb MP or IP fusion may improve pinch in some patients.
CMC resection arthroplasty with ligament reconstruction may be
helpful to improve thumb motion.
III. Crystalline Arthropathies
A. Definition
1. Gout is a disorder of urate metabolism that results in high levels of uric acid
in the blood, urine, and synovial fluids. Under certain conditions, urate
crystals precipitate within the joint and synovium resulting in inflammatory
arthritis.
2. Pseudogout, one manifestation of calcium pyrophosphate dihydrate (CPPD)
deposition disease, is a disorder in which CPPD crystals precipitate within
the joint or synovium resulting in acute inflammatory arthritis.

B. Epidemiology
1. Gout affects 1% to 2% of the general population, and is more common in
males and African Americans. It most commonly presents in men in their
fourth to sixth decades of life, and for women in their sixth to eighth decades.
Risk factors include age, family history, heavy consumption of alcohol, meat
or seafood, diuretic use, obesity, and renal failure.
2. Pseudogout or CPPD is common in the elderly. The prevalence of CPPD is
10% to 15% in the sixth and seventh decades, and increases to 40% in those
over 80. Risk factors include age, family history, hyperparathyroidism, and
hemochromatosis.
C. Pathogenesis
1. Hyperuricemia (serum uric acid > 6.5 mg/dL) is common and usually asymp-
tomatic. Some patients, however, with hyperuricemia can develop precipita-
tion of sodium urate crystals in the joints and soft tissues, leading to localized
inflammation. Changes in tissue pH, temperature, or hydration can affect
the solubility of uric acid and lead to crystal precipitation. Certain drugs,
notably cyclosporine, can also result in gout.
2. The pathogenesis of CPPD is not well understood. CPPD crystals are depos-
ited in and around the joint, particularly on the cartilage surfaces, resulting
in inflammation. The increased deposition of CPPD is due to high local
concentrations of calcium or pyrophosphate, and altered intracellular and
extracellular metabolism of pyrophosphate.
D. Presentation
1. The natural history of gout progresses through four clinical stages.
a) Asymptomatic hyperuricemia
b) Acute gouty arthritis
c) Intercritical gout (periods between acute attacks)
d) Chronic tophaceous gout
2. Acute gout occurs most often in the lower extremities, and is usually mono-
articular or oligoarticular.
a) The first metatarsophalangeal joint is most often involved (podagra).
b) Involvement of other joints in the feet, ankles, and knees is common.
c) Symptoms include acute severe pain, erythema, and swelling.
d) Acute attacks last about a week, but can range from a few days to a few
weeks.
e) Fever and leukocytosis may be present with acute attacks, particularly in
patients with chronic polyarticular gout.
f) Upper extremity involvement is less common than lower extremity involve-
ment, and is more frequent in older patients with underlying chronic gout. It
may involve the wrist, MCP joints, or IP joints. If acute gouty arthritis pres-
ents in the wrist, it can mimic exactly the presentation of septic arthritis.
g) Involvement of the IP joints occurs more commonly in older patients, and
is more common in women with gout. It may affect sites of prior osteoar-
thritis, and inflammation of Heberden or Bouchard nodes is often pres-
ent. This is often the presenting symptom in late-onset gout in females.
3. Chronic tophaceous gout is due to recurrent bouts of acute gout. Soft tissue
deposits of sodium monourate crystals (tophi) develop, commonly at the IP
joints in the hand and over the olecranon process. Periarticular and intraosseous
tophi cause joint destruction and deformity over time. Chronic tophaceous
gout may be punctuated by attacks of acute, often polyarticular gout.

4. Acute pseudogout causes joint swelling, pain, and erythema, and feels similar to
a gout attack. It may last from days to weeks if untreated. It is usually monoar-
ticular and most commonly involves the knee or other large joints like the hip,
shoulder, and wrist. Chronic CPPD deposition disease in the upper extrem-
ity usually presents as a chronic arthropathy, resulting in cartilage calcification
(chondrocalcinosis) and degenerative changes in the joint. It usually affects the
wrist and MCP joints symmetrically, with relative sparing of the IP joints.
E. Diagnosis
1. Gout is often diagnosed clinically, particularly if classic podagra or tophi is
present. In their absence, laboratory studies may aid in diagnosis.
a) Most patients have chronic hyperuricemia (>6.5 mg/dL), although urate
levels may be normal during an attack, or may be elevated in the absence
of gout.
b) Definitive diagnosis is made by arthrocentesis.
1) Monosodium urate (MSU) crystals are negatively birefringent under a
polarized light microscope, and are thin, long, and pointed.
2) The crystals may be intracellular or extracellular.
3) Crystals may also be identified in tophi.
4) White blood cell counts (synovial fluid) are usually in the inflamma-
tory range, from 10,000 to 20,000 WBC per mL.
2. Acute pseudogout may be suspected with the appropriate clinical presenta-
tion (acute monoarticular inflammatory arthritis, particularly of the knee),
but definitive diagnosis is made with arthrocentesis.
a) CPPD crystals are positively birefringent under a polarized light micro-
scope, and are shorter and less sharp tipped than MSU crystals.
b) Crystals may be intracellular or extracellular.
c) White blood cell counts (synovial fluid) are in the inflammatory range,
from 10,000 to 20,000 per mL.
The diagnosis of chronic CPPD deposition disease is usually made clini-
cally and radiographically, although identification of crystals may confirm
the diagnosis.
3. Septic arthritis should always be considered in the differential diagnosis, and
is discussed later in this chapter. Cell count, Gram stain, and cultures should
be preformed on all arthrocentesis specimens in cases of suspected gout or
pseudogout.
F. Imaging
Routine radiographs are not particularly useful in diagnosing acute gout or
pseudogout. They should be obtained, however, to identify chronic changes or
other pathology, and to serve as a baseline. In chronic tophaceous gout, articular
and periarticular tophi cause metaphyseal and subchondral erosions on both sides
of the joint in question, typically with sclerotic borders and overhanging margins.
Joint space narrowing and destruction are late findings. Chronic CPPD deposition
leads to chondrocalcinosis seen as dense linear calcifications at the articular surface,
and accelerated degenerative joint changes. In the wrist, a pattern of collapse simi-
lar to scapholunate advanced collapse (SLAC) is common. Other imaging modali-
ties such as CT, MRI, and ultrasound are not routinely used in the diagnosis of
acute gout or pseudogout, although their potential roles are being studied.
G. Nonsurgical treatment
A rheumatologist should be consulted to assist in the management of acute or
chronic tophaceous gout, or acute pseudogout.

1. Acute gout is treated with NSAIDs, colchicine, or corticosteroids.

a) Indomethacin (an NSAID) is traditionally used for acute gout, but cau-
tion should be used in older patients and those with compromised renal
function.
b) Colchicine is very effective in stopping an acute gout attack, although it has
many potential side effects, and caution should be used in older patients.
c) Corticosteroids are becoming more popular in the treatment of acute gout,
particularly in patients with contraindications to colchicine or NSAIDs.
They can be administered as an intra-articular injection or systemically.
2. Patients with chronic tophaceous gout or recurrent acute attacks benefit from
urate lowering (hypouricemic) drugs.
a) Probenecid is a hypouricemic drug that increases urate excretion in
the urine (uricosuric drug) thereby lowing serum levels. A side effect of
probenecid is nephrolithiasis.
b) Allopurinol is a hypouricemic drug that acts by inhibiting xanthine oxidase.
3. Joint rest, NSAIDs, and intra-articular corticosteroid injections are the pri-
mary treatment modalities for acute pseudogout. Colchicine may also be
helpful in an acute attack, but is used infrequently because of its side effects.
H. Surgical treatment
There is little role for surgery in treating acute gout or pseudogout. Surgery is
sometimes indicated in chronic tophaceous gout, or in chronic CPPD deposi-
tion disease.
1. Tophi.
a) In general, soft tissue tophi should be treated medically, due to the risk of
infection and poor healing after surgical excision.
b) Irrigation and aspiration using large-bore needles inserted through unin-
volved skin have been described, and may be used to reduce symptomatic
soft tissue tophi.
c) Osseous tophi that threaten the joint should be curetted and bone grafted.
2. Painful or unstable joints with significant articular destruction due to gout
may be treated with arthrodesis.
3. CPPD deposition disease is a common cause of SLAC-pattern degenera-
tive wrist collapse in older patients. SLAC operations such as proximal row
carpectomy (PRC) or scaphoidectomy and four-corner arthrodesis may
improve pain. Painful degeneration of the MP joints due to CPPD deposi-
tion can be treated with arthrodesis or arthroplasty.
I. Other crystalline arthopathies
A group of calcium-containing molecules called basic calcium phosphate (BCP)
crystals have been implicated in the pathogenesis of osteoarthritis. Because BCP
crystals cannot be seen under polarized light microscopy and are difficult and
expensive to accurately identify, their role in the development of osteoarthritis or
other arthritides is not well understood.
IV. Infectious Arthritis
A. Definition
Septic arthritis is commonly caused by pyogenic bacteria in the joint, usually at
concentrations greater than 100,000 organisms per mL. Less common culprits
of septic arthritis include mycobacterial and fungal organisms.

B. Epidemiology
The incidence of septic arthritis is about 0.002% in the general population. It
is more common in immunosuppressed patients and in patients with prosthetic
joints (0.05%).
C. Pathogenesis
Septic arthritis may occur as a result of direct introduction of bacteria into a joint
by a penetrating object, or by spread of an adjacent infection such as cellulitis or
osteomyelitis. More commonly, it is due to hematologic seeding.
1. In the case of direct introduction of bacteria, Staphylococcus aureus followed
by streptococcal species are the most common causative organisms. Coagu-
lase-negative Staphylococcus is the most common organism in prosthetic joint
infections. Gram-negative, anaerobic, or mixed infections occur in heavily
contaminated wounds or in immunocompromised patients.
2. Hematogenous seeding is most common in immunocompromised patients,
diabetics, dialysis patients, IV drug users, patients with endocarditis, and
patients with indwelling catheters.
3. Other common clinical scenarios include
a) Pseudomonas or Candida infections in IV drug users.
b) Salmonella infections in patients with sickle cell anemia.
c) Group B streptococcal infections in infants and children under 5 years of
age.
d) Eikenella corrodens infection in human bites (fight bites of the MCP
joint).
e) Pasteurella multocida infection from animal bites, particularly cat bites.
f ) Salmonella infection after rodent bites.
4. Rarely, atypical mycobacterial or fungal infections may occur.
D. Presentation
Patients present with acute inflammation of a single joint, including pain, edema,
erythema and loss of motion. Systemic signs and symptoms such as fever and
leukocytosis may be seen. Other risk factors such as a direct injury, IV drug use,
or an indwelling catheter may be present.
E. Diagnosis
1. History should be taken to assist in determining the source of infection.
2. Physical examination reveals severe pain with active or passive ROM and
with gentle axial loading of the joint.
3. Laboratory studies including a CBC with differential, ESR, CRP, and blood
cultures should be obtained.
4. Definitive diagnosis is made by arthrocentesis.
a) Fluid should be sent for cell count and differential, Gram stain, and cul-
tures (aerobic and anaerobic).
b) If there is enough fluid, it should be sent for crystal studies, and protein
and glucose levels.
c) If indicated, fungal and mycobacterial stains and cultures should be
ordered.
d) WBC counts range from 50,000 to 300,000 per mL. Lower counts with a
high percentage of PMNs may also suggest infection.
e) A glucose level of 40 mg/dL, or less than the fasting blood glucose
level, also suggests infection. However, synovial glucose and protein
levels are rarely helpful in diagnosis due to their low sensitivity and
specificity.

F. Imaging
Routine radiographs should be obtained and examined for foreign body, gas,
or signs of osteomyelitis. Initially radiographs show a widened joint space due
to intra-articular edema and purulence. Joint space narrowing and articular
erosions are late findings.
G. Treatment
Septic arthritis is a joint-threatening emergency, and is managed with urgent
drainage and IV antibiotics. Antibiotics are not usually initiated until fluid has
been obtained for cultures.
1. The septic joint should be treated with arthrotomy, drainage, and irrigation.
2. The joint capsule should not be completely closed, and a drain or wick
should be placed to allow for continued drainage. Articular cartilage should
not be exposed to dessication.
3. The skin should be closed very loosely or not at all.
4. Postoperative saline wet to dry dressing changes should be performed, with
TID warm soaks in dilute hydrogen peroxide or iodine solution.
5. Active and passive ROM should be initiated early on to prevent stiffness.
6. If there is no improvement within 24 hours, or if purulent drainage persists,
repeat washouts are indicated.
7. Arthroscopic washout of the radiocarpal joint is an alternative to open
drainage.
8. Empiric IV antibiotics are initiated as soon as a diagnostic aspiration has been
performed. A broad-spectrum antibiotic, which will cover Gram-positives,
Gram-negatives, and anaerobes, should be used initially. The antibiotic cov-
erage can be narrowed based on Gram stain and culture results. IV antibiotics
should be continued for 2 weeks, followed by oral antibiotics to complete a
4 to 6 week course.
V. Juvenile Idiopathic Arthritis
The International League of Associations for Rheumatology (1997) has recently

changed the classification of chronic arthritis in children under 16 years of age to
Juvenile Idiopathic Arthritis. JIA is what was classically referred to as Juvenile Rheuma-
toid Arthritis and includes other types of chronic inflammatory arthritis. Though, there
are some similarities amongst the juvenile and adult forms, the change in terminology
more accurately reflects the difference between the childhood diseases and those chronic
arthritides afflicting adults.
I. Classification
A. Systemic
B. Polyarticular
1. RF positive
2. RF negative
C. Oligoarticular
1. Persistent
2. Extended
D. Psoriatic

E. Enthesitis related
F. Other
A. Systemic
1. Incidence: 10% to 20%.
2. Mean age of onset of 5.
3. Males and females are equally afflicted.
4. RF and ANA are usually negative.
5. Many extra-articular manifestations.
a) High spiking fever
b) Anemia
c) Macrophage activation syndrome
B. Polyarticular
Involves five or more joints
1. RF negative
a) Incidence: 20% to 30%
b) Mean age of onset 3 years, early childhood
c) Females are more afflicted than males
d) ANA positive in 25%
e) Variable prognosis
2. RF positive
a) Incidence: 5% to 10%.
b) Mean age of onset late childhood, adolescence.
c) Females are more afflicted than males.
d) ANA positive in 75%.
e) Small joint involvement
1) Boutonnière deformities
2) Swan neck deformities
C. Oligoarticular
1. Incidence: 50% to 60%
2. Large joint involvement: Knee and ankle
3. Less than five joints involved during first 6 months
4. ANA positive 50%, elevated ESR
5. Subtypes
a) Persistent
1. Arthritis confined to four or fewer joints
2. Better prognosis
b) Extended
3. Arthritis of five or more joints after 6 months
4. Worse prognosis
D. PsA
2. Peak age mid childhood
3. Asymmetric arthritis
4. Musculoskeletal involvement
a) Knees and ankles
b) PIP, DIP and tendon sheaths
c) Sausage digits
5. Extra-articular
a) Rash
b) Nail changes
c) Uveitis

E. Enthesitis Related
a) Includes ankylosing spondylitis
b) Inflammatory bowel disease associated arthritis
2. HLA-B27 associated
3. Males predominantly affected
4. Age greater than 8
5. Hallmarks
a) Pain and stiffness
b) Low back pain
c) Uveitis
6. RF and ANA negative
II. Diagnosis
A. Clinical findings
1. Hand
a) Joint swelling
b) Dactylitis
c) Nail changes
2. Orthopaedic
a) Joint swelling
b) Inflammatory lumbosacral pain
c) Sacroiliitis
3. Systemic
a) Rash
b) Fever
c) Serositis
B. Joint aspiration
1. Turbid yellow fluid
2. WBC 5,000 to 8,000.
C. Blood tests
1. ANA positive 30% to 40%
2. ESR, CRP usually elevated
3. Anemia of chronic disease.
III. Radiography
A. Periarticular soft tissue swelling

B. Juxtaarticular osteoporosis
C. Joint cartilage and bone destruction
D. Autofusion
E. Growth abnormalities (White)
1. Local
a) Secondary to localized inflammation
b) Increased local temperature
c) Secondary to immobilization
2. Systemic
a) Disease flare
b) Systemic medications such as corticosteroids

c) Can inhibit height but not skeletal maturation

d) Nutritional
3. Physeal changes
a) 50% of wrists with defects (Ansell).
b) Premature physeal closure.
c) Intercarpal joint narrowing.
d) CMC narrowing.
4. Common ulnar-sided wrist problems.
a) Shortened ulna.
b) Abnormal shortened growth of ring and small metacarpals.
IV. Generalized Signs and Symptoms
A. Acute morning stiffness

B. Joint guarding
C. Systemic symptoms
1. Fatigue
2. Irritability
3. Low-grade fever
4. Malaise
V. Hand and Wrist
A. Findings
1. Wrist:
a) Diminished wrist extension
b) Carpal and metacarpal ulnar deviation
c) Radial deviation at the MP joints
d) Accelerated epiphyseal maturation
e) Premature ossification
f ) Carpal deformities
1) Radiocarpal joint
a. Ligamentous laxity, common
Secondary to
i) Intrinsic destruction of ligaments.
ii) Loss of cartilage and bone secondary to synovitis.
iii) Can cause muscle imbalance of extensor carpi ulnaris (ECU)
versus FCU
b. Palmar subluxation of the wrist
c. Spontaneous ankylosis relatively common:
Autofusion more common than in adults.
d. Ulnar translocation of carpus
2) Midcarpal joint
a. Collapse rare
3) DRUJ
a. Synovitis
i) Pain
ii) Stiffness in pronosupination
iii) Differential epiphyseal growth

2. Thumb
a) Synovitis CMC, MP, and IP joints
b) Periostitis can lead to physeal overgrowth or tethering
c) CMC joint
1) Ligamentous laxity and dorsal subluxation
2) Adduction contracture
d) MP joint
1) Ligamentous laxity
2) Occasional rotatory deformity
3) Bony erosions, loss of volar, and dorsal support
3. Fingers
a) 50% of patients have MP and IP joint involvement
b) MP joints
1) Radial deviation at MP joints.
2) Loss of MP flexion. Etiology unclear possibilities:
a. Local swelling and periostitis
b. Tenosynovitis and decreased tendon excursion
c. Tight collateral ligaments
3) MP synovitis
c) IP joints
1) Children less than 4 years old, flexion IP joints.
2) Occasional boutonnière or swan neck.
3) Tenosynovitis, common.
Systemic subtype 60% with tenosynovitis.
4) Dorsal capsular tightness, collateral ligament shortening.
B. General management
1. Accurate diagnosis and subtyping.
2. Initiate early treatment to attempt to minimize long-term sequela.
3. Multidisciplinary approach
a) Pediatrician
b) Pediatric rheumatologist
c) Hand and orthopedic surgeon
d) Physical and hand therapist
C. Medical treatment
1. Medical treatment needs to be managed by a pediatric rheumatologist based
on the complexities of the disease and subtype. In general, anti-inflammatories
remain the initial line of treatment. Sulfasalazine and antimalarials have cer-
tain indications, and can be effective with the polyarticular form.
2. Systemic corticosteroids are still used in a vast majority of patients; how-
ever, toxicity especially growth failure needs to be factored in with their
efficacy.
3. Methotrexate is considered first-line therapy, especially in the polyarticular
forms. The TNF-alpha inhibitors are approved for use in children and has
recently changed the medical management of many patients with JIA.
4. Corticosteroid injections remain an effective means to manage localized flares in
JIA and are nonoperative options available for orthopaedic and hand surgeons.
5. Hand therapy/splinting.
Therapy by a well-trained occupational or physical hand therapist is
paramount.

a) Resting/night splints
1) Reduce pain and acute synovitis
2) Maintain position
3) Prevent contractures
b) Day splints
1) Facilitate ADL
c) Active involvement by a hand therapist
1) Monitor passive ROM
2) Work on active ROM
3) Combination splints and therapy
D. Surgical management
1. Similar to adults, principles of management:
a) Maximizing function
b) Minimizing pain
c) Retard progression of disease
2. Synovectomy
a) Although controversial, there is a role for surgical synovectomy when a
patient has failed medical management.
b) A patient with large painful joints particularly the wrist or metacarpopha-
langeal joint are indications.
c) Synovectomies adjacent to the physis may help avoid premature physeal
closure.
d) A dry nonproliferative synovitis is a contraindication to synovectomy for
it has been shown to accelerate ankylosis.
1) The goal is pain relief and an attempt to prevent physeal arrest.
2) Improvement of ROM is less predictable.
3. Digital tenosynovitis/triggering
a) Relatively common in JIA, up to 36% (Ansell)
b) Initial treatment is medical management
c) Corticosteroid injection
d) Often difference between active and passive flexion
1) Rule out tendon rupture
2) Can occur secondary to bulk of tissue in fibro-osseous canal
e) Recalcitrant cases can benefit from surgical tenosynovectomy.
1) Zigzag or midaxial incision for extensile exposure
2) Address the palm and digit, maintain A1 pulley if possible
3) Maintaining A1 pulley may diminish ulnar deviation
4) Consider resection of one slip of the sublimis
5) Consider standard carpal tunnel approach for proximal flexor teno-
synovitis
6) Swan neck and boutonnière deformities treated similar to adults
4. Extensor tenosynovitis
a) Less common in JIA than adult form
b) Surgery only when persistent and symptomatic
1) Dorsal longitudinal incision over fourth DC
2) Extensor tenosynovectomy of second through fifth DC
3) Maintain or repair extensor retinaculum to prevent bowstringing
4) Consider resection of Lister tubercle to protect extensor pollicis longus
(EPL)
5) Protect dorsal intracarpal ligaments

5. Joints
a) Thumb
1) CMC joint
a. Occasional extraosseous ligamentous reconstruction
2) MP joint
a. Consider MP fusion for functional stability
3) IP joint
a. Consider arthrodesis if unstable and painful
b) Fingers
1) MP joint
a. Dorsal synovectomy can help pain, less reliable for ROM
b. Consider partial release of collateral ligaments
c. MP arthroplasties after skeletal maturity
2) PIP joint
a. Severe PIP flexion deformity consider FDS slip resection
b. Synovectomy before severe bony erosions
c. Consider arthrodesis if unstable and painful
d. Arthroplasty nonindicated in JIA
c) Wrist
1) Wrist must be addressed before digital deformities.
2) DRUJ
a. Localized synovectomy rare, occasionally combined with radio-
carpal synovectomy
b. In severe cases, consider hemiresection arthroplasty of the distal
ulna if skeletally mature
c. Occasionally consider radial osteotomy if premature radial physeal
closure
d. Sauve Kapandji if rotational limitation secondary to ankylosis
3) Radiocarpal joint
a. Synovectomy (see above)
b. Occasionally osteotomy of autofusion mass is beneficial to place
wrist in more effective position; a closing wedge osteotomy avoids
bone graft
c. If severe translocation, consider radiolunate or radioscapholunate
fusion
d. Pan carpal fusion
e. In cases of severe deformity with laxity and instability, pancarpal
fusion is sometimes indicated
VI. Idiopathic Degenerative Arthritis
Idiopathic degenerative arthritis is commonly called osteoarthritis. This is a non-

inflammatory condition that involves degeneration of the hyaline cartilage in diar-
throdial joints. It is a condition of advanced age. In the hand, the most commonly
involved joints are the DIP joints, followed in descending order by the thumb CMC
joint, the PIP joints, and the MP joints. The presence of this condition in one joint
predicts occurrence of this condition in other similar joints of the same hand.
Radiographic appearance of idiopathic degenerative arthritis includes asymmetric
joint space narrowing, sclerosis, osteophytes, and subchondral cysts. Asymmetric joint
space narrowing can be severe and cause radial or ulnar deviation of the affected joint.

I. Trapeziometacarpal Arthritis
Basal joint arthritis is a common cause of disabling thumb pain. The diagnosis is usually
made from the history and physical examination alone. Radiographs are used to stage
the severity of the disease. Early stage disease can be treated by splinting alone; however,
reconstructive procedures aimed at providing pain relief as well as restoring thumb
motion and strength are usually necessary in the later stages.
A. Anatomy and biomechanics
The CMC joint of the thumb (trapeziometacarpal joint) comprises the articula-
tion between the trapezium and the base of the thumb metacarpal and comprises
the following fundamental components:
1. Articular surface: The trapezium and first metacarpal base have reciprocal con-
cave/convex surfaces (saddle joint). The trapezial surface is concave in an ulnar-
radial direction and convex in a dorsopalmar direction. Reciprocally, the base
of the first metacarpal is convex in an ulnar-radial direction and concave in a
dorsopalmar direction. The radius of curvature of the metacarpal base is 33%
greater than that of the trapezium leading to joint incongruity and instability.
2. Ligaments: Due to the lack of bony congruity, the TM joint relies heavily
on static ligamentous restraints. Up to 16 ligaments have been identified;
however, the major stabilizers of this joint are:
a) Palmar oblique ligament: This is also known as the deep anterior oblique
or beak ligament, is considered the primary stabilizer of the TM joint,
especially against dorsoradial subluxation in palmar abduction. This liga-
ment runs in a proximal/radial to distal/ulnar direction inserting on the
volar tubercle of the first metacarpal.
b) Dorsoradial ligament: This is a major stabilizer for dorsoradial subluxation
in adduction.
c) Dorsal expansion of the APL tendon: Is a stabilizer in supination of the
thumb.
3. Arcs of movement: The joint surface allows for biaxial movements—flexion/
extension of the CMC and palmar abduction/adduction. Capsular laxity
allows for rotation of the metacarpal on the trapezium. Combined flex-
ion, palmar abduction, and rotation allow for opposition as a third arc of
movement. The arc of movement in the normal trapeziometacarpal joint is
approximately 70 degrees for each axis.
The scaphotrapezial, scaphotrapezoid, and trapeziotrapezoid are also considered as part
of the basal joint of the thumb and can become involved in late stage disease.
B. Diagnosis
1. History: Basal joint arthritis typically presents in females 50 to 70 years old
who complain of worsening thumb pain interfering with activities of daily
living. Prevalence in postmenopausal women is reported at approximately
25%. Patients often complain that activities requiring opposition or pinch
grip such as opening jars or carrying heavy objects between the thumb and
fingers usually instigate the pain. Complaints of stiffness or pain at rest are
usually indicators of late-stage disease.
2. Physical examination: patients may show the following signs on examination:
a) Appearance: Classically reveals “squaring” or prominence at the base of
the thumb (dorsoradial subluxation secondary to ligamentous laxity and
the pull of APL on the base of the metacarpal).
b) Point tenderness at the CMC joint.

c) Grind test: Axial compression with rotation of the metacarpal on the

trapezium elicits pain; this is pathognomonic of CMC arthritis.
d) Adduction deformity: In later stages of the disease, the metacarpal adopts
an adducted posture and the patient may develop a subsequent contrac-
ture of the first webspace.
e) MCP hyperextension deformity: As a result of the final dorsal subtraction
of the metacarpal at the CMC joint, there may be a compensatory hyper-
extension deformity of the thumb MCP joint along with secondary coll-
storal ligament laxity.
f ) Functional deficit: Pinch strength is almost always diminished and func-
tional hand width is often narrowed.
g) Associated disorders: Carpal tunnel syndrome may be present in up to 28%
of patients. de Quervain tenosynovitis may be present in approximately
5% to 15%.
3. Radiographs: AP, lateral, and oblique radiographs of the trapeziometacarpal
joint can be used to confirm the diagnosis and stage the disease. A hyperprona-
tion view gives excellent visualization of both the CMC and the scaphotrapezial-
trapezoid (STT) articulations. Stress views (30 degree PA view with the patient
pressing their thumb tips together, or lateral pinch view) can help assess the
degree of joint subluxation and joint space loss. With radiography alone, only
28% of women who have features of CMC arthritis and 55% with features
of combined CMC/ST arthritis admit to symptoms, hence the importance of
clinical correlation. Radiography is necessary to stage the severity of the disease.
Eaton described a radiographic staging system, which is widely used
(Table 19.1).
TABLE 19-1 Eaton radiographic staging for thumb CMC arthritis
Stage Radiographic Characteristics

I Normal or slightly widened trapeziometacarpal joint
Trapeziometacarpal subluxation up to one third of articular
surface
Normal articular contours
II Decreased trapeziometacarpal joint space
Trapeziometacarpal subluxation up to one third of articular
surface
Osteophytes or loose bodies < 2 mm
III Decreased trapeziometacarpal joint space
Trapeziometacarpal subluxation more than one third of articu-
lar surface
Osteophytes or loose bodies ³ 2 mm
Subchondral cysts or sclerosis
IV Involvement of the scaphotrapezial joint or less commonly the
trapeziotrapezoid or trapeziometacarpal joint of the index

4. Differential diagnosis: Includes FCR tendonitis, trigger thumb, radial

sesamoiditis, de Quervain tenosynovitis, inflammatory arthritides, RA, gout,
pseudogout, gamekeeper’s thumb, radial sensory neuritis, and radiocarpal or
STT arthritis.
C. Treatment
Initially, all stages can be treated conservatively with splints, NSAIDS, and ste-
roid injections. If these measures fail, surgical treatment can be considered for
cases with severe pain and disability independent of radiographic findings. The
different types of surgical intervention are still widely debated. Nevertheless,
most still base operation on radiographic stage.
1. Stage I
a) CMC synovectomy and debridement (arthroscopic)
b) Metacarpal osteotomy
c) Ligament reconstruction (in cases of joint laxity)
2. Stage II
a) Arthroscopic debridement and tendon interposition
b) Partial trapeziectomy and tendon interposition
c) Metacarpal osteotomy
d) Total trapeziectomy
e) Total trapeziectomy with ligament reconstruction and tendon interposi-
tion (LRTI) or ligament reconstruction without interposition
f ) Trapeziometacarpal arthrodesis
3. Stage III
a) Partial trapeziectomy and tendon interposition
b) Total trapeziectomy with or without suspension or ligament reconstruction
c) Trapeziometacarpal arthrodesis
4. Stage IV
a) Total trapeziectomy with LRTI
5. Prosthetic implant arthroplasty may offer some benefits, but long-term data
are currently not available. Details of this and other surgical procedures are
discussed later in this chapter in the arthroplasty section.
II. Interphalangeal Joints
The DIP joints sustain the highest direct joint forces and are therefore subject to the
most attrition. Thus, the DIP joints are the most frequently involved in osteoarthritis,
followed by the PIP joints and the MP joints.
A. Symptoms: Pain and deformity—deformity occurs from asymmetric joint nar-
rowing with radial or ulnar deviation of the joint.
B. Examination: Tenderness with loading the joint. Heberden nodes in the DIP
joints and Bouchard nodes in the PIP joints. Mucous cysts (discussed in next
section) result from DIP joint arthritis. Joint contractures are more common in
PIP joints.
C. Treatment: Conservative treatment is recommended initially for all patients. If
these measures fail, then surgical options can be entertained.
1. DIP joints: Arthroplasty is rarely performed. Arthrodesis is the treatment of
choice. Most common complication is nonunion. Multiple types of fixation
can be used, but screw fixation yields the highest union rate. Fuse in neutral
or slight flexion of 10 to 20 degrees.

2. PIP joints
a) Arthroplasty is generally used in the ulnar digits (long, ring, and small).
Prerequisites include adequate bone stock without substantial angulation
or rotational deformity of the phalanges.
b) Arthrodesis is typically used in the index due to ulnarly directed stress
from pinch. When fusing the PIP joints, an increasing angle is used from
radial to ulnar (I, L, R, S = 40, 45, 50, 55)
III. Metacarpophalangeal Joints
A. Arthritis in the finger MP joints is rarely due to idiopathic degenerative arthritis.

It tends to occur more as a result of trauma or inflammatory conditions such as
RA and may also occur with hemochromatosis and ochronosis. In the fingers,
arthrodesis results in significant functional impairment, and so most surgeons
recommend arthroplasty. Silicone joint replacements have the most long-term
data. Newer implant materials may offer additional options.
B. Arthritis in the thumb MP joint does commonly occur, often in conjunction
with CMC arthritis. Symptoms are similar to smaller joint arthritis. In the
thumb, arthrodesis can be quite functional and is typically positioned in slight
flexion (20 to 30 degrees).
IV. Carpometacarpal Boss
This condition refers to an osteoarthritic spur or prominence that develops at the base
of the second and/or third metacarpals and usually involves the CMC joints. It is most
common in women between the third and fourth decades. These are often associated
with a small ganglion, which can confuse the diagnosis.
A. Symptoms: Painful, tender mass on the dorsum of the wrist.
B. Examination: Tender, firm, bony, palpable mass at the base of the CMC joints
that is most prominent with wrist flexion.
C. Radiographs: Shown best in “carpal boss views.” 10 and 20 degree supinated
lateral views of the carpus
D. Treatment: Excision of the carpal boss (and ganglion cyst, if present) can be
performed with saucerization of the involved CMC joint. All palpable promi-
nences should be removed such that areas of contact are lined with cartilage and
no bone-to-bone contact occurs. Results are unpredictable.
V. Mucous Cyst
These are ganglion cysts that arise from osteoarthritic DIP joints. They typically occur
between the fifth and seventh decades of life.
A. Symptoms and signs: Usually a painless, firm mass on the dorsum of the finger
at or distal to the DIP joint proximal to the eponychial fold. The initial clinical
signs may be nail deformity without a visible mass. Grooving of the nails, split-
ting, or loss of nail gloss can occur.
B. Examination: A firm, non-tender cyst that lies on one side of the extensor tendon
between the joint crease and the eponychium. Heberden nodes are common.

C. Radiographs: Osteoarthritic changes with osteophytes. Seen best on the lateral

view
D. Treatment: The cyst can be excised in any number of ways but most perform
a excision of the attenuated skin over the cyst. Extensions of these incisions
allow access to the DIP joint where the base of the cyst and associated bony
spurs can be excised. Care must be taken to avoid the nail matrix and extensor
insertion. Excising capsular tissue on the contralateral side of the extensor ten-
don makes recurrence less likely. If local skin is inadequate for coverage (e.g.,
in case of a rupture cyst), skin grafts may be used. Local rotation random-
pattern flaps, or reverse adipofascial turnback flap with a skin graft can also be
utilized.
E. Complications: If left alone, these cysts can enlarge and rupture. Because
mucous cysts communicate with the DIP joint, rupture can theoretically lead
to bacterial inoculation of the joint and septic arthritis. Thus, most recommend
excision of the cysts before rupture. Recurrence can occur but it is rare. Exci-
sion of the base of the cyst and the offending osteophyte is usually sufficient
to prevent recurrence. However, as long as the arthritic condition persists, new
ganglion formation is a possibility.
Posttraumatic Arthritis
I. Molecular Biology of Posttraumatic Arthritis
The exact incidence of posttraumatic arthritis in the upper extremity is unknown, but
Brown and colleagues found an incidence of approximately 12% in all cases of symp-
tomatic arthritis in the lower extremity.
A. The exact mechanisms of the development of posttraumatic arthritis are
unknown. Several theories exist, including:
1. Delivery of energy during the acute injury killing the chondrocytes and
disrupting articular cartilage. Initial supraphysiologic cartilage injury may
initiate apoptosis of articular chondrocytes as well.
2. Chronic or repetitive excessive mechanical stress due to joint incongruity
a) Loss of part of the articular surface or persistent displacement of articular
fragments
b) Lack of articular congruity increases shear stress and point stress on artic-
ular surfaces.
B. Theory of shear stress: Over the past decade, concerted effort has been focused
on defining the mechanism for the development of posttraumatic arthritis, using
animal models and in vitro experiments.
1. Buckwalter and Martin conducted an in vitro experiment with a special-
ized system to maintain pressure on the articular surfaces of excised human
chondrocytes. During the study, models with increased shear stress produced
reactive oxygen species leading to oxidative damage to the chondrocytes,
accelerated cell senescence, and increased apoptosis.
2. Additional basic science studies have found the addition of antioxidants,
the addition of P188 (a surfactant), and the inhibition of caspase (a protease
enzyme in the cellular apoptosis cascade) to the models of cartilage instabil-
ity provide a protective effect against the formation of radical oxygen species/
chondrocyte apoptosis. Through these mechanisms, these substances prevent

experimentally induced chondrocyte death and may have therapeutic roles

in the future.
3. It is important to note that although patients may develop articular
degeneration and manifest radiological signs of arthritis following trauma,
the presence of radiological signs does not necessarily correlate with
symptoms. Many patients are able to function well with abnormal radio-
graphs either due to low demand or high pain thresholds. Treat the patient
not the x-ray.
II. Distal Interphalangeal Joint
A. Although there are no specific data on the incidence of posttraumatic arthritis

of the DIP joint, pain is common. The DIP joint provides only 15% of the arc
of motion of the digital ray while the PIP joint provides 80%; therefore, loss
of DIP flexion does not result in significant morbidity.
B. Patients typically present with tender, enlarged DIP joints typically referred to
as Heberden nodes. Similar pathology occurring at the PIP joint is referred to
as Bouchard nodes. (An easy method to remember the differences is to look
at your hand with fingertips pointed upward and recite Head over Body for
Heberden and Bouchard, respectively.)
C. Treatment of a symptomatic DIP joint with posttraumatic arthritis typically
involves arthrodesis in 0 to 10 degrees of flexion with a headless compression
screw or K-wires. The advantages of this technique include high fusion rate,
early mobilization, and the screw does not need to be removed. The disadvan-
tages are that it is a technically difficult procedure and the screw may be larger
than the intramedullary diameter of the distal phalanx.
III. Proximal Interphalangeal Joint Arthritis
The treatment options for PIP posttraumatic arthritis include steroid injection,
fusion, arthroplasty (silicone, pyrolytic carbon, and volar plate), and vascularized joint
transfer. Silicone arthroplasty in the PIP joints is successful in relatively low demand
patients. Pyrolitic carbon implants and volar plate arthroplasty (VPA) having mixed
results are not considered uniformly successful at this time. Vascularized joint transfer
is an extreme option for joint reconstruction with only limited reports and fair ultimate
ROM.
IV. Metacarpophalangeal (MCP) Joint Arthritis
The MCP joint contributes more than both the DIP and PIP joints to the rela-
tive position of the distal tip of the digit in space. This contribution increases the
importance of maintaining relative motion at the MP joint. Similar to the PIP
joint, treatment options include steroid injection, fusion, arthroplasty (silicone),
and vascularized joint transfer. Fortunately, the incidence of MCP posttraumatic
arthritis is rare, leading to few case reports of proposed salvage treatments. Arthro-
desis is typically avoided in the MCP joints due to the relatively good results with
arthroplasty.

V. Wrist
Watson and Ryu examined over 4,000 wrist x-rays and determined that 95% of the
arthritis originates around the scaphoid: 55% from SLAC wrist, 26% from triscaphe
(scaphotrapeziotrapezoid) arthritis, and 14% from combined SLAC and triscaphe
arthritis. The remaining 5% occurs in ulnar-sided articulations associated with specific
trauma.
A. Scapho-lunate advanced collapse (SLAC) and scaphoid nonunion advanced col-
lapse (SNAC) wrist
Disruption of the normal mechanics of wrist motion due to traumatic injury
(scapholunate ligament injury or scaphoid nonunion) or through pathologic
laxity can lead to articular degeneration of the radioscaphoid and midcarpal
joints.
1. Theoretically, the radiographic incidence of SLAC wrist following complete
scapholunate ligament injury should be 100%. However, natural history
studies do not capture patients with degenerated wrists who are asymptom-
atic, leaving the true incidence and the incidence off symptomatic SLAC
wrists unknown.
a) Stages of SLAC wrist
1) Stage 1—arthrosis of radial border of radioscaphoid joint (sharpening
of the radial styloid)
2) Stage 2—progression of arthrosis to entire radioscaphoid joint
3) Stage 3—progression to include the midcarpal (capitolunate joint)
4) Stage 4—pan-carpal arthrosis (radiolunate joint spared)
b) Stages of SNAC wrist
1) Stage 1—arthritic change and osteophyte formation of radial styloid
2) Stage 2—proximal scaphocapitate joint (and radioscaphoid joint distal
to fracture of scaphoid)
3) Stage 3—midcarpal arthritis of capitolunate joint
4) Stage 4—pan-carpal arthritis, sparing radiolunate joint, and proximal
radioscaphoid joint.
c) Stage 1—Many patients are not symptomatic at this stage and can be
treated with nonoperative measures, such as splinting and steroid injec-
tion. When symptomatic for a surgical procedure, radial styloidectomy
can be performed for SLAC wrist. As the articulation of the radius and
proximal pole of the scaphoid is commonly preserved in SNAC wrist,
some authors perform excision of the distal pole of the scaphoid in early
symptomatic patients. Others consider radial styloidectomy concurrently
while performing open bone grafting and internal fixation procedures for
scaphoid nonunion.
d) Stage 2—With the progression of symptomatic arthritis, treatments focus
on limited intercarpal fusions with the goals of fusing painful arthritic
articulations while preserving as much function as possible. There are
two common treatments for stage 2 SLAC or SNAC wrist including
PRC and scaphoid excision and Capitate-Hamate-Lunate-Triquetrum
(four corner) arthrodesis. Long-term outcome data of the two proce-
dures reveals equivalent results, with similar decrease in motion and grip
strength. Less commonly used procedures include radial side fusions—
STT and scaphocapitate.

1) PRC
a. Since the radioscaphoid joint is the only diseased articulation, exci-
sion of the scaphoid eliminates the arthritis. The remainder of the
proximal row is excised, and the distal row moves well within the
lunate fossa.
b. The surgeon and patient must discuss the possibility of a more
extensive fusion in the event that additional arthritis is identified
intra-operatively. Specifically, the lunate fossa of the distal radius
and the head of the capitate should be free from disease to expect
success from a PRC. Despite this generalization, not all authors use
minor capitate degeneration as a contraindication for the PRC. If
degeneration of the head of the capitate is noted intraoperatively
(stage 3), soft tissue interposition (dorsal capsular flap) between the
head of the capitate and lunate fossa can be used.
2) Four-corner arthrodesis is another treatment option for the symptom-
atic SLAC wrist in which the scaphoid is excised and the lunate, tri-
quetrum, capitate, and hamate are arthrodesed. With scaphoid exci-
sion, this procedure addresses arthritis at the radioscaphoid joint.
Fusion of the ulnar four carpal bones addresses the capitolunate
arthritis. Success of this operation depends on a normal radiolunate
joint.
a. Obtaining fusion can be challenging. Nonunion rates of up to
20 percent, have been reported.
b. Dorsal radiocarpal impingement can result if the lunate is fused in
the extended position and can occur if the implant (particularly the
circular plates) is not adequately recessed.
c. Nonunion and dorsal impingement are complications specific to
four-corner fusion, and concern about the longevity of the surgi-
cally created radiocapitate joint is a problem with PRC. The sal-
vage procedure for a failed PRC or four-corner is total wrist arthr-
odesis or total wrist arthroplasty.
e) Stage 3—Treatment is by scaphoid excision, radial styloidectomy, and
four-corner arthrodesis. Modification of a PRC with soft-tissue interposi-
tion between the mildly degenerated capitate head and the lunate fossa is
also option.
f ) Stage 4—The definitive treatment for pan-carpal wrist arthritis is total
wrist arthrodesis or total wrist arthroplasty. With arthrodesis, grip
strength can be expected to be 72% of the opposite side with 83% of
patients achieving complete pain relief and 98% of patients achieving
primary union.
1) Several techniques of wrist arthrodesis have been described including
K-wire fixation, AO dynamic compression plate fixation, with a variety
of bone graft options including local sliding graft and cancellous bone
graft. The compression plate is most commonly used with the best
union rates. Up to 10% of patients will experience symptoms of carpal
tunnel syndrome following surgery.
2) Total wrist arthroplasty has been proposed as an alternative. Current
implants are not durable enough for higher demand patients, so indi-
cations for arthroplasty should be limited to very low demand, non-
manual laborers over 50 years of age.

B. Radiocarpal arthritis following distal radius fracture

a) Displaced intra-articular distal radius fractures may lead to degeneration
of the radiocarpal articulation. The arthritic changes are can occur from
non-anatomic reduction of the articular surfaces, resulting in altered shear
and load stresses, or may result from articular cartilage damage from the
initial injury even with anatomic reduction.
b) Radiocarpal and specifically radiolunate arthrosis may occur following
intra-articular distal radius fractures, particularly when reduction leaves
are greater than 2 mm displacement in the articular surface. In spite of
radiographic changes, not all patients will be symptomatic. Radioscaphol-
unate arthrodesis with excision of the distal scaphoid is a motion preserv-
ing procedure for radiocarpal arthritis involving the radiolunate joint.
C. DRUJ arthritis
a) Incongruity of the sigmoid fossa of the distal radius or instability of the
DRUJ following injury can lead to arthritis.
b) Resection arthroplasty: The Darrach procedure is a resection of the ulnar
head. Resections too proximal may result in an unstable distal ulnar stump
causing radioulnar impingement. Alternative methods in performing a
resection arthroplasty of the DRUJ include the matched resection (Watson
technique) and the DRUJ hemi-resection arthroplasty (Bower’s technique).
In these procedures, the ulnar seat is excised while the TFCC and ulnar
styloid are left intact. Thus, the stabilizing function of the TFCC is not
altered.
c) In an effort to retain the function of the TFCC and address the arthritis
of the DRUJ, the Sauve-Kapandji procedure was developed. In this tech-
nique, the distal ulna and radius are fused at the DRUJ and 1 cm of the
ulnar metaphysis is resected, creating a pseudoarthrosis, to allow forearm
rotation. Radioulnar impingement may still occur at the site of the distal
ulnar resection.
d) Early in the era of endoprosthetic reconstruction for arthritis, the DRUJ
was targeted for treatment. Unfortunately, the first series of ulnar head
endoprostheses were unsuccessful primarily due to the severe silicone
synovitis resulting from the implant. More recently, implant manufacturers
have begun to re-explore the possibility of DRUJ replacement with ulnar
head and linked metal and polyethylene endoprostheses.
Arthroplasty
I. Introduction
A. Arthroplasty is defined as a replacement of joint surfaces. In the finger, the

primary reason for joint replacement is painful arthritis from degeneration of
articular cartilage.
1. Osteoarthritis, posttraumatic arthritis, and inflammatory arthritis all lead to
degeneration of the articular cartilage. In simple terms, osteoarthritis is an
asymmetric wearing down of the joint surface due to a change in the biome-
chanics of joint motion.
2. Similarly, posttraumatic arthritis stems from biomechanical alterations to the
joint, either from articular surface irregularities or alignment changes.

3. Inflammatory arthritis causes autoimmune-related synovitis and symmetric

destruction of articular surfaces.
4. There is also an entity described in hand surgery as “erosive arthritis,” which
is characterized by joint space narrowing, osteophyte formation, and sub-
chondral erosions (inflammatory, but not autoimmune, in nature)
B. Indications
1. Age, occupation, typical hand activities, past medical history, type of arthri-
tis, prior finger surgery, finger function, and radiographic appearance of the
finger all play a role in the choice of arthroplasty.
a) Patient history should identify localized joint pain with finger use and
activities. In addition, the underlying type or cause of the arthritis must
be assessed. Systemic issues related to inflammatory arthritis are also con-
sidered prior to offering treatment options for finger joint arthritis.
b) Examination demonstrates localized joint tenderness, swelling, and crepi-
tus with motion. Passive and active ROM is documented and stability is
assessed.
c) Radiographs including anteroposterior and lateral views centered on the
affected joint are required.
2. Patients with debilitating finger joint pain, joint incongruity, or arthritis who
have failed non-operative management are candidates for joint replacement.
In cases of severe joint asymmetry, deformity, loss of bone stock, or ligamen-
tous instability, the treating surgeon should consider arthrodesis for definitive
management.
II. Different Types of Joint Replacement
A. Soft tissue interpositional arthroplasty

1. The most practical interpositional arthroplasty for the PIP or even the
DIP joint is a VPA. A creative treatment for confounding and challenging
fracture/dislocations of the PIP joint, VPA involves advancing the thick,
volar plate into the PIP joint to reconstruct a severely injured articular sur-
face belonging to the volar half of the base of the middle phalanx.
2. It has also proven to be a successful approach for more chronic, posttraumatic
problems (such as subluxation or malunion), and arthritis following a previ-
ous dorsal fracture/dislocation of the PIP joint.
3. Long-term follow-up from this procedure has demonstrated that PIP joint
remodeling can occur over time. Some authors have even advocated its use in
primary, idiopathic osteoarthritis of the PIP joint.
4. The greatest limitation of VPA is the stretchable length of the volar plate
itself. Typically, it can only be advanced to satisfactorily resurface the first
volar 30% to 50% of the base of the middle phalanx.
B. Silicone elastomer (silastic) arthroplasty
1. Silicone interpositional arthroplasty in the finger joints was initially devel-
oped by Swanson in the 1960s. It continues to be used frequently for replace-
ment of the MCP, PIP, and DIP joints. Currently, it is the arthroplasty to
which all newer designs are compared. Flexible silicone arthroplasty has been
demonstrated to be very effective in treating pain associated with inflamma-
tory arthritis affecting the MCP joints.
2. The technique of implantation involves resection of the proximal and distal
articular surfaces and sizing of the proximal and distal intramedullary canals.

The flexible, monobloc, silicone prosthesis provides a painless, hinged joint

replacement.
3. Functionally, the silicone elastomer replacement acts more as a joint “spacer”
than as a constrained arthroplasty. Still, the silicone “hinge” between the two
stems constrains this arthroplasty to a single center of rotation. The silicone
itself is prone to cracking or even breaking with use over time. Despite radio-
graphic failure of the silicone, patients frequently continue to enjoy painless
ROM of the joint.
4. Particulate synovitis may occur within and around the joint space as the sili-
cone degrades, causing joint swelling, inflammation, and pain.
C. Surface replacement arthroplasty
1. Different types of constrained and unconstrained resurfacing arthroplasties
have been used, many of which mimic the materials of total knee replace-
ments. Currently, metal and plastic components and pyrolytic carbon
implants are available.
2. Pyrolytic carbon resurfacing of the PIP joint is still under scrutiny in the
United States and is only usable under a Humanitarian Device Exemption.
Results from this type of PIP resurfacing are mixed.
3. On the other hand, MCP arthroplasty with pyrolytic carbon has demon-
strated durability over a 10-year follow-up period in patients with inflamma-
tory arthritis.
4. Current pyrolytic carbon implants for the PIP and MCP joints glide in an
unconstrained fashion. These new generation implants are susceptible to
breakage when excessively loaded.
III. Finger Arthroplasty: DIP, PIP and MCP Joints
A. While silicone arthroplasty has been found to be successful in the DIP joint, it
has not necessarily been identified as a more reliable procedure than DIP joint
arthrodesis.
B. Arthroplasty of the PIP joint, when successful, can dramatically improve hand
function over a PIP joint fusion. The PIP joint has been referred to the “corner-
stone” joint of finger function. When it does not move, finger function (includ-
ing grasp and precision activities) is significantly limited.
1. PIP arthroplasty is technically more demanding than MCP arthroplasty due
to challenges inherent to operative exposure of the PIP joint. The central
slip of the extensor tendon inserts on the dorsal base of the middle phalanx.
This tendon insertion and relatively short collateral ligaments prevent a wide
exposure of this joint during joint resurfacing. For proper soft tissue balanc-
ing of a PIP arthroplasty, care must be taken in protecting these structures or
precisely restoring them when released.
2. Surgical exposure of the PIP joint can be achieved from either a dor-
sal (tendon splitting, or Chamay), volar, or lateral approach. The volar
approach requires with retraction of the flexor tendon apparatus and the
volar plate, but has the advantage of initiation of post-operative motion
within 1 to 2 weeks following surgery and avoids disruption of the delicate
extensor mechanism. The lateral approach involves sectioning the radial or
ulnar collateral ligaments to enter the joint, avoiding both dorsal and volar
structures.

3. Other authors have recommended PIP arthrodesis in the radial digits and
arthroplasty in the ulnar digits, based on the asymmetric, translational load-
ing at the index finger PIP joint with key-pinch type activities.1
C. MCP arthroplasty has been the most thoroughly studied joint replacement of
the finger.
1. The technique of MCP arthroplasty is facilitated by a more straightforward
surgical approach than the PIP joint. Dorsally, the extensor mechanism may
be divided longitudinally without limitation to gain full access to both proxi-
mal and distal aspects of the joint.
2. Both silicone and pyrolytic carbon arthroplasties have demonstrated effective
pain relief over the long term.
3. Patients with inflammatory arthritis do not typically gain motion with MCP
arthroplasty, but will commonly have the arc of the MCP motion redirected
to a more functional zone (e.g., centered in an elevated and functional posi-
tion of 45 degrees of flexion rather than in a more fisted position of 60 degrees
of flexion).
IV. Complications of Finger Joint Arthroplasty
A. Infections: Adherence to sterile technique and perioperative antibiotics theoreti-

cally decreases the risks of infection in the finger just as they have proven to in
the hip and knee.
B. Instability: Especially in inflammatory arthritis where the local soft tissues are
equally affected by the joint synovitis. Careful surgical technique is required to
properly expose the articular surfaces without unintended iatrogenic injury to
adjacent soft tissues. Soft tissue balancing after the implantation of a finger joint
arthroplasty includes appropriate tensioning of the collateral ligaments, volar
capsule, flexor tendons, dorsal capsule, and extensor tendons.
C. Mechanical failure is uncommon in the finger, most likely due to the lack of load
bearing. However, some finger joints are more prone to asymmetric loading,
such as ulnar deviation of the index finger MCP and PIP joints in key pinch.
If uneven or excessive load bearing is expected, the preferred operative solution
for an arthritic finger joint is arthrodesis rather than arthroplasty. While silicone
implants may be found disrupted on radiographs, an unhinged silicone replace-
ment is not routinely symptomatic. In fact, the silicone arthroplasty may work
well as a joint “spacer” regardless of its actual condition.
D. Revision for failed finger joint arthroplasty is possible. Treatment options are
highly dependent on the specific patient and cause of failure; they include soft
tissue procedures for joint realignment, revision arthroplasty, and joint fusion.
V. Thumb CMC Arthroplasty
A. Regardless of stage at presentation, all patients should undergo a trial of conser-

vative management prior to operative intervention. This often includes all of the
following:
1. Activity modification
2. Thenar muscle strengthening
3. Anti-inflammatory medication

4. Splinting: This enforces resting the joint, which often diminishes the acute
inflammation and pain enough that an adequate level of function returns.
Typically, a short opponens splint holding the thumb in abduction (thumb
spica) is worn for 3 to 4 weeks and then weaned over a further 3 to 4 week
period. Symptomatic improvement can be expected in up to 76% of stage
I and II disease and 54% of stage III and IV disease. A shorter, thumb-
stabilizing hand splint (C-splint) can be used if the patient must continue
working.
5. Intra-articular steroid injections: These can be used to resolve ongoing syno-
vitis and accelerate pain relief during a course of splinting. Steroid injections
should not be more often than every 2 to 3 months and should be used cau-
tiously in very early stage disease as they can potentially accelerate arthritic
degeneration. When followed by 3 weeks of splinting, success rates of 40%
for subjective improvement of symptoms have been reported. Patients with
stage IV disease are unlikely to have long-term benefit from steroid injec-
tions. The technique for thumb CMC injection is discussed in Chapter 7.
B. Surgical procedures for stage I disease
The indications for surgical intervention for trapeziometacarpal arthritis are
persistent pain, instability, and decreased function refractory to conservative
therapy. The type of procedure used is dictated by the severity of disease present,
depending primarily on whether the cartilage of the CMC joint is unaffected
(stage I), or shows signs of degeneration(stages II to IV).
The surgical goal in early disease is to stabilize the joint, preventing further
subluxation and joint degeneration.
1. Volar ligament reconstruction (Eaton and Littler): Utilizes the radial half
of the FCR tendon, passed through the base of the thumb metacarpal to
stabilize the CMC joint. This is the procedure of choice for early disease
and has well-established efficacy when there is only early chondromalacia
seen intraoperatively. This technique has been reported to halt radiographic
progression of disease in up to 100% of patients at 5 years (65% at 15 years),
with complete pain relief in 72% at 5 years, and up to 50% at 15 years.
2. Thumb CMC arthroscopy: May offer less invasive therapeutic measures
including thermal shrinkage of the beak ligament or hemitrapeziectomy or
total trapeziectomy.
3. Metacarpal osteotomy: a 30-degree dorsal closing wedge osteotomy can be
used to offset the subluxing forces acting on the base of the metacarpal. This
procedure also has the benefit of correcting any adduction contracture that
may have developed. This procedure was original described for late disease,
but is only really useful for Eaton stage I disease.
C. Procedures for stage II to IV disease
For later stage disease when frank eburnation of cartilage is the cause of the pain,
there are essentially four treatment options—trapeziectomy, replacement of the
TM joint (prosthetic arthroplasty), arthroplasty techniques using tendon inter-
position (biological arthroplasty), and arthrodesis.
1. Trapeziectomy: Complete excision of the trapezium was the earliest described
surgical procedure for CMC arthritis. In most cases, trapeziectomy alone
leaves a weak and unstable thumb. Historical concerns with this procedure
include the possibility of proximal migration of the thumb metacarpal pro-
ducing painful metacarpo-scaphoid arthritis. Short-term randomized out-
come studies have not shown this to be a significant problem.

2. Trapeziectomy with ligament reconstruction tendon interposition: Several

procedures for tendon interposition arthroplasty are available. These proce-
dures consist of two surgical steps—a complete or partial trapeziectomy, and
stabilization ± interposition of tendinous tissue in the trapeziectomy void.
The different operations described for biological arthroplasty are distin-
guished by (i) the choice of tendon used to fill the trapeziectomy void and
prevent proximal migration of the metacarpal (interposition arthroplasty)
and (ii) methods used to stabilize the thumb after bony support provided by
the trapezium is lost, in essence reconstruction of the intermetacarpal liga-
ment anchoring the thumb metacarpal to the index metacarpal (suspension
arthroplasty).
a) Fascial arthroplasty (Froimson): After a standard trapeziectomy, half
of the FCR tendon is harvested and rolled up in an “anchovy” fashion
and used to fill the trapeziectomy space. There is no element of ligament
reconstruction with this procedure.
b) Burton and Pelligrini: A trapeziectomy is performed and the radial half
of the FCR tendon is then routed through the base of the thumb meta-
carpal, with the remaining length placed in the trapeziectomy void. Long-
term follow-up (9 years) reports show excellent pain relief in up to 95%
of patients.
c) Brunelli procedure: This utilizes one of the slips of the APL tendon for
the ligament reconstruction. The tendon is divided proximally, leaving
its insertion intact. It is then passed through a tunnel created in the
base of the thumb and index metacarpals and sutured to the second
and third CMC ligaments. Tendon interposition is achieved using an
“anchovy” obtained from palmaris longus graft. This ligament recon-
struction has also been advocated for use in early disease (TM joint
instability without significant radiographic findings), without perform-
ing a trapeziectomy.
d) APL suspensionplasty (Ceruso): This also uses one of the APL tendons
for the ligament reconstruction following a partial or standard trapeziec-
tomy. The APL is divided at the musculotendinous junction leaving its
insertion intact. It is then used to create a double loop tying the FCR
to the remaining APL tendon, simultaneously achieving both ligament
reconstruction and filling the trapeziectomy void with tendinous interpo-
sition.
e) Hematoma and distraction arthroplasty (Kuhns, Gray and Meals):
A standard trapeziectomy is performed followed by temporary K-wire
fixation of the thumb in a position of opposition and distraction. This
has been shown to achieve results similar to tendon interposition tech-
niques.
f ) Prosthetic arthroplasty
1) Silicone spacers (Swanson): The silicone trapezium implant was first
introduced in an effort to minimize proximal migration of the thumb
metacarpal after trapeziectomy. Most reports comparing outcomes
show results similar to tendon interposition arthroplasty in the short
term. However, silicone implant arthroplasty has fallen out of favor
with most surgeons because of the longer-term complication rate
including dislocations of the scaphoid, subluxations, silicone synovitis,
and particulate wear.

2) Trapeziometacarpal prostheses: Most TMC prostheses are ball-and-

socket joint replacements. They differ mainly in constraint, arc of
mobility and fixation (cemented or noncemented), and direction of
the neck. Utilization of the Orthosphere has been abandoned.
Constrained prostheses are more prone to loosening; however,
nonconstrained prostheses dislocate. The de la Caffiniere implant
(ball-and-socket, cemented, semiconstrained prosthesis with a straight
neck) is probably the most widely used, throughout Europe.
g) Arthrodesis: With the success of the above reconstructive techniques,
arthrodesis is now usually reserved as a salvage procedure for failed recon-
structions or for heavy laborers who wish to maintain grip strength. The
optimal position to fuse the joint is 20 degrees of radial abduction and 40
degrees of palmar abduction. This limits the thumb’s ROM (the position
may cause a problem as the patient cannot place the hand flat against a
table or in tight places, which require complete palmar abduction of the
thumb); however, patient satisfaction is usually very high and there is a
return of strong pinch grip. The complication rate, including nonunion,
is reported to be up to 35%, but many nonunions may be asymptomatic.
D. Choice of technique for stage II to IV disease: The ideal technique for CMC arthri-
tis is yet to be determined through the use of randomized prospective comparative
studies. Retrospective reviews have shown no difference in outcomes when com-
paring a trapeziectomy alone to a trapeziectomy and ligament reconstruction.
E. Thumb MP joint
When MP joint hyperextension is present, this should be addressed as it can
affect the results of the CMC arthroplasty. Depending on the degree of hyper-
extension, pinning in flexion, volar capsulodesis, and arthrodesis can all be used
effectively.
F. Postoperative care: This is similar for most of the procedures and involves CMC
and MCP joint immobilization in a thumb spica for 3 to 4 weeks, leaving the IP
joint free. Following this, the patient should undergo hand therapy to mobilize
the CMC and MCP joints and strengthen the thenar muscles.
VI. Wrist Arthroplasty
A. Background
1. Swanson designed the first widely used wrist implant in the United States,
which was a single piece silicone implant reinforced by Dacron similar in shape
and function to the silicone metacarpophalangeal implant. After portions of the
distal radius and carpus are resected, the stems of the implant are inserted into
the medullary canals of the radius and third metacarpal. Good pain relief and a
minimum 40-degree arc of wrist flexion-extension were found early, but long-
term studies revealed frequent implant breakage, declining wrist motion and,
most importantly, many patients developed silicone synovitis with osteolysis.
2. Subsequent designs used separate radial and carpal components made of
metal and polyethylene and fixed by bone cement. Various articulations were
used, ranging from highly mobile ball-in-socket designs to constrained hinge
types. Common complications of early implants included wrist imbalance
often leading to fixed ulnar deviation and flexion deformity, carpal compo-
nent loosening, and prosthetic dislocation.

3. Beginning in the 1980s, the most common total wrist implanted in the
United States was the Biaxial (DePuy Orthopedics, Inc., Warsaw, IN), which
introduced an ellipsoidal articulation that provided better joint balance and
motion than predecessors. Loosening of the cemented carpal component was
common and often associated with substantial bone loss; the implant is no
longer distributed.
4. Total wrist implants currently available in the United States include the
Maestro (Biomet), Remotion (SBI), and the UNI 2 (Integra Life Sciences).
These designs share the concept introduced by Menon for distal component
fixation using a central stem in the capitate and two adjacent screws in the
surrounding carpus.
B. Principal benefits of wrist arthroplasty
1. Preservation of some wrist motion substantially increases finger reach, which
can improve hand dexterity, especially in patients with arthritis involving
multiple upper extremity joints.
2. The motion provided by current wrist implants (∼30 degrees of flexion
and 30 degrees of extension) is sufficient for nearly all activities of daily
living.
3. Wrist arthroplasty patients reported greater ease with fastening buttons and
personal hygiene activities than wrist arthrodesis patients.
4. Most patients with a wrist arthroplasty and a contralateral wrist arthrodesis
prefer the side with the wrist arthroplasty.
5. Reported complication rates of wrist arthroplasty are comparable to arthro-
desis; however, arthroplasty has higher risks of major complications, namely,
implant loosening.
C. Indications
1. General indications for wrist implant arthroplasty are nearly equivalent to
those for other joints, that is, ideal patients have low activity demands, older
age, and disabling pain not responsive to nonoperative treatment.
2. Other motion-sparing, treatment options, such as PRC or scaphoid excision
with intercarpal fusion, are not appropriate due to arthritic involvement.
3. A patient who would otherwise require bilateral wrist arthrodesis, that is, the
patient had a previous contralateral arthrodesis.
4. Traditionally, wrist arthroplasty was most commonly used for the treatment
of RA because the patient typically has lower activity demands and fewer
treatment options. If both the hand and wrist are severely affected, the wrist
should be treated before reconstructing the hand.
5. Patients with osteoarthritis or posttraumatic arthritis can be considered for
implant arthroplasty if they meet other criteria.
6. The patient must recognize a lifetime limitation of activities consistent with
implant durability.
D. Contraindications
1. General contraindications for wrist implant arthroplasty are also nearly
equivalent to those for other joints, that is, patients with high activity
demands and younger age are not proper candidates because of the higher
risk of implant loosening.
2. Regular use of walking aides.
3. Absence of adequate wrist control, for example, wrist extensor tendon rup-
tures or radial nerve palsy.

4. Active rheumatoid disease involving the wrist evidenced by substantial syno-

vitis, hypermobility, and joint subluxation, especially if current medical treat-
ment has not been maximized.
5. Advanced deformity of the wrist, particularly if associated with substantial
bone loss and muscle-tendon unit contractures; volar subluxation with distal
radius remodeling is not a contraindication but additional techniques will be
required.
6. Poor function of the hand, which is most commonly seen in severe RA, such
that wrist arthroplasty would not provide a substantial benefit over wrist
arthrodesis.
7. Inadequate bone stock, which is most commonly found in the carpus due to
advanced rheumatoid disease or severe osteoporosis.
8. Previous carpal resections, for example, PRC, may reduce the potential for
adequate support of the carpal component.
9. Previous wrist infection.
10. Known history of recurrent sepsis.
E. Patient history
1. A detailed history is essential to determine if a patient is a proper candidate
for wrist implant arthroplasty. Previously assessed diagnoses for wrist arthritis
and possible systemic arthritis and all previous wrist surgeries provide essen-
tial information to assess contraindications. Concurrent arthritis, tendonitis,
or neuropathy involving the same extremity may exacerbate the wrist condi-
tion and overall disability. Thus, the treatment of these conditions may obvi-
ate or delay the need to treat the wrist.
2. The duration and degree of disability caused by wrist pain, weakness, and
stiffness, especially as it relates to work, avocational activities, and general
activities of daily living provides the basis for selecting treatment, especially
if the patient only has limitations with specific activities and all nonoperative
alternatives have not been tried.
3. For patients with RA, a thorough understanding of past and current disease
control is imperative. If the disease has been recently quite active or periods
of poor control were common, then risks of complications associated with
implant arthroplasty are much greater.
4. A review of current medications is necessary in planning surgery to reduce
the risks of bleeding and wound healing complications, which are increased
by some medications if not discontinued or modulated properly.
5. Although RA has traditionally been the most common indication for wrist
replacement, patients with osteoarthritis and posttraumatic arthritis are
being treated with implants more often in recent years. These patients typi-
cally have good bone quality, good muscle strength, and minimal deformity
leading to good overall early functional outcome; however they are more
likely to be engaged in stressful activities.
6. A complete and honest appraisal of the patient’s activity demands is most
important since it is a major determinant of implant durability. Because relief
of wrist pain may lead to a substantial increase in hand use, knowledge of past
activities is also necessary to have meaningful discussion of future activity
limitations.
7. Obtaining a history of diseases that increase the general perioperative
risks of surgery, such as diabetes mellitus, will allow proper preoperative
preparation.

F. Physical examination
1. Skin quality assessment is important because wound healing problems are
not uncommon in elderly and rheumatoid patients, especially those taking
steroids. Surgical scars and skin irregularities may require modification of the
operative technique.
2. Vascular compromise predisposes to reduced healing capacity and possibly
more difficult rehabilitation.
3. Neurologic conditions, particularly those caused by compressive neuropathy
or polyneuropathy, are common in patients with advance arthritis and may
only be evident on physical examination. To prevent neurologic deteriora-
tion, some conditions may require prior or concurrent treatment.
4. Sites of swelling and tenderness about the wrist typically correlate with radio-
logical changes. Evidence of arthritis involving the digits indicates more gener-
alized arthritis, which can be associated with increased postoperative swelling
and difficulties with stiffness. Measure all components of wrist motion, includ-
ing passive and active ranges, with emphasis on the painful arcs and positions.
5. The DRUJ should receive particular attention during the examination since
unrecognized arthritis of the DRUJ may well affect the overall outcome by
causing persistent ulnar-sided wrist pain.
6. Preoperative diagnosis allows for proper operative consent and better plan-
ning of its treatment. Because wrist motion and balance following a joint
replacement are highly dependent on muscle strength and tendon function,
a careful assessment of all wrist and finger motors is a key part of the preop-
erative examination. Common findings in the rheumatoid patient include
a volarly subluxed extensor carpi ulnaris tendon and weak wrist and finger
extension. Thus, if the preoperative examination is not conclusive for an
intact extensor carpi radialis brevis, which is a criterion for wrist arthroplasty,
it must be evaluated at the time of surgery.
7. Although the staging of surgery in patients with both hand and wrist arthritis
is dependent on a variety of factors, the traditional approach to reconstruct
the wrist before the hand is a typical starting point for planning overall man-
agement.
G. Expected long-term outcomes
1. Eighty to ninety-five percent of patients experience significant pain relief.
2. Most patients achieve a functional ROM (∼35 degrees each of flexion and
extension).
3. Although the longevity and durability of total wrist arthroplasty have sub-
stantially improved with the newer implants, distal component migration or
gross loosening remains a common cause for failure in high demand patients
or those with poor bone quality. Overall, revision rates for implants used dur-
ing the past 25 years vary between 5% and 25% at 5 years postoperatively.
4. More recent advances in implant design, materials, and surgical tech-
nique along with a better understanding of patient selection should lead to
improved long-term outcomes.
H. Complications
1. Delayed skin healing problems due to poor skin quality or swelling are com-
mon but rarely lead to deep infection.
2. Total wrist arthroplasty has a low incidence of infection, ranging from 0% to 6%.
3. Wrist imbalance and prosthetic instability were more common with older
designs but can still occur with newer implants due to improper surgical

technique, especially in a wrist with severe deformity. Delayed rehabilitation,

including a period of immobilization, may reduce this risk in certain patients
but decreased motion may result.
4. Early osteolysis from polyethylene wear is most common in patients with
prosthetic instability due to abnormal loading; the rates of long-term poly-
ethylene wear are unknown for total wrist arthroplasty.
VII. Elbow Arthritis and Arthroplasty
A. Anatomy and etiology

The elbow joint is comprised of three separate articulations: The ulnohumeral,
radiocapitellar, and proximal radioulnar joints. The bony anatomy, in particular
the congruence of the ulnohumeral joint, provides the majority of the stability
to the elbow. Additional stability is provided by the joint capsule, collateral
ligaments, and muscle groups originating from the medial and lateral condyles
of the distal humerus. Elbow dislocations for a more detailed description of
the static and dynamic restraints of the elbow joint are covered in detail in
Chapter 16.
1. Elbow arthritis is a relatively uncommon entity and is generally well tolerated
as the arm is not routinely used for weight bearing. When present, arthritis typ-
ically presents with pain. It can also present as stiffness, weakness, or instability.
The most common types of elbow arthritis are RA, osteoarthritis, and post-
traumatic arthritis. The etiology of the arthritis may have an impact on treat-
ment and prognosis. Workup and evaluation of the painful and arthritic elbow
should include a thorough history and radiographs of the involved elbow.
a) RA can affect the elbow in a manner similar to other joints, and because
of its systemic nature bilateral involvement is common. The ulnohumeral
joint is primarily involved with evidence of periarticular osteopenia and
ligament destruction in addition to the damage of the articular surface.
The resultant instability can alter joint mechanics and lead to further
joint damage. The radiocapitellar joint can also become quite symptom-
atic in this patient population leading to pain with forearm rotation.
b) Primary osteoarthritis of the elbow is an uncommon condition. It is typi-
cally seen in men in the third to eighth decade with a history of heavy
use of the arm. The characteristic finding is pain on terminal extension
or flexion and a resultant loss of arc of motion. Radiographs typically
reveal osteophytes around the olecranon and coronoid processes of the
ulna as well as within the olecranon and coronoid fossae of the distal
humerus. Changes at the radiocapitellar and radioulnar joints can be seen
in advanced cases. There may be also loose bodies within the joint that
may or may not be visible radiographically.
c) Posttraumatic arthritis of the elbow is most common following intra-artic-
ular fractures of the distal humerus. Findings include pain, stiffness, and
crepitance. The stiffness from the intra-articular injury can be confounded
by extra-articular contractures related to the trauma or prior surgery.
B. Treatment
The aim of all treatment options for elbow arthritis is to reduce pain and improve
function.

1. Nonsurgical management of elbow arthritis is dependent on the underly-

ing cause. Nonsteroidal anti-inflammatory medications are the mainstay of
treatment with activity modification, intermittent splinting, or bracing, and
gentle exercises to maintain ROM. Intra-articular injections with corticoster-
oids are also an option in an attempt to lessen pain. Patients with RA may
also be treated with more potent anti-inflammatory medications or disease-
modifying antirheumatoid drugs.
2. Surgical options for the treatment of elbow arthritis include synovectomy,
radial head excision, osteotomy, arthroplasty, and arthrodesis.
a) Synovectomy can be performed open or arthroscopically. It can be com-
bined with debridement of osteophytes from the olecranon and coronoid
processes and their respective fossae.
b) Radial head excision can also be performed arthroscopically or open to
address a painful radiocapitellar joint.
c) More aggressive decompression of the olecranon and coronoid fossae can
be done with a Outerbridge-Kashiwagi arthroplasty. This procedure
is ideal for the patient with primary osteoarthritis with pain from bony
impingement at the extremes of flexion and extension.
d) Interposition arthroplasty is ideal for the posttraumatic arthritic elbow.
Elbow stability and the preservation of the bony anatomy of the dis-
tal humerus and proximal ulna are essential for success. The procedure
involves reshaping of the articular surfaces of the elbow and insertion of
an interposition tissue, commonly autogenous fascia lata.
e) Arthrodesis is a salvage procedure for the elbow. Perhaps the only time
that this procedure would be recommended as a primary procedure is in
the young laborer.
f ) Total elbow arthroplasty (TEA): The indication for TEA is a painful
arthritic joint that has failed other attempts at treatment. The most com-
mon indication for TEA is advanced RA. Other emerging indications for
this procedure include distal humerus nonunions and acute fractures of
the distal humerus in the elderly patient with poor bone stock. Contrain-
dications for TEA are similar to other joints. Active infection is an absolute
contraindication. Many authors suggest that age less than 60 is a rela-
tive contraindication. Additionally, the need for the operated arm to be a
weight-bearing limb or used for heavy lifting is also a contraindication.
1) Implant designs can be classified as nonconstrained, semiconstrained,
and totally constrained.
a. Nonconstrained implants have historically shown problems with
loss of motion and elbow instability, particularly in the rheumatoid
patient.
b. Totally constrained implants have shown significant problems with
loosening as all of the forces are directed at the bone-cement inter-
face.
c. Semiconstrained implants are by far the most common type of
implant used.
Semiconstrained elbow implants act as a sloppy hinge joint. Once
the ulnar and humeral implants are coupled together they allow an
angular laxity of 5 to 10 degrees, thus the terminology of semicon-
strained. This laxity has been shown to dissipate the stress across

the joint so that it is not at all concentrated on the bone-cement

interface, which results in a lower loosening rate.
2) Results and complications
a. Clinical studies have shown success rates of approximately 90%
regardless of which brand of semiconstrained implants are used.
Patients report improved pain, motion, and strength.
b. However, given the complexity of the elbow joint, there are several
common postoperative complications that may occur.
i) Immediate postoperative issues include ulnar nerve neuritis
and wound healing problems.
ii) Late complications may include triceps insufficiency and
periprosthetic fracture. The design of the semiconstrained
implant places a lot of stress at the link between the humeral
and ulnar implants. This typically results in wear and break-
down of the polyethylene articulation. This is a common
cause for reoperation and exchange of the polyethylene
component.
iii) Instability is a common problem associated with the noncon-
strained implants but not the semiconstrained implant.
iv) Loosening is a problem frequently associated with the totally
constrained implants but not the semiconstrained.
v) Septic arthritis following TEA is a devastating complication
because the salvage of an infected joint results in a univer-
sally poor outcome. It has been reported to have an inci-
dence of roughly 10%, slightly higher than the infection
rates following prosthetic replacement of other major joints.
Contributing factors to this high rate are the relative sub-
cutaneous position of the joint and the medical comorbid-
ities of the patients. Many rheumatoid patients are treated
with strong anti-inflammatory agents that limit their ability
to fi ght a developing infection. The prosthesis must be
resected in the setting of an active infection. This results in
a stiff and contracted joint and makes staged reimplanta-
tion difficult.
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J Hand Surg. 1995;20A:965–970.

Skin and Soft Tissue
20
L. Scott Levin, Martin I. Boyer, David J. Bozentka,
Stephan G. Pill, Kodi K. Azari,
Nelson Castillo and Amit Gupta
I. Nail
A. Anatomy (Fig. 20.1)

1. The perionychium consists of the nail bed, nail fold, eponychium,
paronychium, and hyponychium.
2. The nail bed is the soft tissue beneath the nail and consists of the germinal
matrix proximally and the sterile matrix distally. The nail bed is supplied by
two terminal branches of the volar digital artery and innervated by the dorsal
branch of the digital nerve.
3. The germinal matrix extends from the nail fold to the lunula, which is a
white arc distal to the eponychium. The germinal matrix is responsible for
generating 90% of the nail plate.
4. The sterile matrix extends from the lunula to the hyponychium. It provides
adherence and adds a squamous epithelial layer to the nail plate.
5. The proximal nail fold is the most proximal extent of the perionychium and
consists of a dorsal roof and a ventral floor.
6. The eponychium is the skin covering the nail fold. It extends from the skin
on the dorsum of the nail, which is termed the nail wall, to the dorsal aspect
of the nail plate.
7. The cuticle, the nail vest, is the thin membrane that extends from the
eponychium to the nail plate.
8. The paronychium is the skin on each side of the nail.
9. The hyponychium is the junction of the nail bed and the skin at the most
distal aspect of the finger. It is a barrier to infection and has the greatest
density of lymphatics of any dermal area in the body.
B. Nail injuries
1. Many nail bed injuries are simple lacerations, although stellate lacerations,
crush, and avulsion injuries are also possible.
2. Injury to the sterile matrix causes nail deformity, and injury to the germinal
matrix can cause nail absence.
3. Nail bed exploration may necessitate nail plate removal, and lacerations can
be repaired with fine absorbable suture, such as 7-0 Chromic. If the lacera-
tion involves the nail fold, roof/floor, the nail plate should be cleansed and
replaced. Alternatively, foil or gauze can be introduced into the nail fold. An
x-ray should be obtained to rule out an underlying fracture.
4. A subungual hematoma can occur if there is disruption of the nail bed within
an intact nail plate. Bleeding into this poorly compliant space can cause
severe pain, and evacuation via nail trephination or removal may be needed
393

Figure 20.1 Nail anatomy. (From Rozenthal TD, Steinberg DR. Skin and soft tissue
defects. In: Beredjiklian PK, Bozentka DJ, eds. Review of Hand Surgery. Philadelphia,
PA: Elsevier; 2004, Figure 3-1).
to relieve symptoms. In general, drainage alone is sufficient for smaller

hematomas whereas areas greater than 50% of the nail bed are often best
treated with removal of the nail plate and repair of the underlying nail
bed injury. The removed nail should be cleansed and replaced in the nail
fold.
C. Nail deformity
1. Nonadherence is the most common posttraumatic deformity. Since the
sterile matrix produces nail cells that adhere to the undersurface of the
nail, transverse or diagonal scars of the sterile matrix can cause the nail
to loosen distal to the scar. Proximal nonadherence often results in an
unstable, painful nail. Distal nonadherence is not a problem unless dirt
buildup underneath the nail causes an infection. The scar must be resected
for correction of the deformity. The defect can either be closed primarily
or a sterile matrix graft can be applied from an adjacent area of the nail bed
or toenail bed.
2. Ridges can be caused by scar tissue under the nail bed or from an uneven
dorsal cortex. Ridging can cause distal nonadherence. Scar excision and
smoothing of the irregularity to create a flat nail bed are required to correct
the deformity.
3. A split nail can result from a ridge or longitudinal scar in the germinal or
sterile matrix. The scar is usually too wide for excision and primary repair of
the defect. Sterile matrix scars should be removed and covered with a split-
thickness nail bed graft. Germinal matrix scars require full-thickness grafts
for nail production.
4. Cornified nail bed deformities occur when the germinal matrix is removed
but the sterile matrix continues to produce keratinized material. Treatment
consists of sterile matrix excision and covering the defect with a split-thickness
skin graft (STSG).
5. Nail cysts and spikes can follow incomplete removal of the germinal matrix
after amputation of a fingertip. Cysts are formed when the germinal matrix
continues to produce nail under a closed defect. Patients present with a
painful, enlarging mass. (Spikes result when the germinal matrix remains,
leading to distal nail production.) These are commonly seen after resection

Chapter 20 • Skin and Soft Tissue 395
of an ingrown toenail. Treatment consists of removal of the cyst or spike and

complete excision of the germinal matrix.
6. Hook nail deformity is a nail with a pronounced volar curvature and occurs
when there is a loss of bony support under the nail. It is most commonly
seen after primary closure of fingertip amputation, when the nail bed is
pulled down over the distal phalanx. Acute treatment involves trimming
the nail bed back to the distal extent of the distal phalanx. Although
providing sufficient initial supports, bone grafts tend to resorb. Once a
hook nail is present, the soft tissue of the fingertip must be restored and
the nail bed transferred back to the level of the bone. This may be accom-
plished by a V-Y advancement flap, cross-finger flap, or full-thickness
skin graft (FTSG). Free vascularized toe transfers have been described to
preserve nail length, although they are associated with significant donor
site morbidity.
7. Pincer nail deformity is an abnormal curvature of the nail in a radioulnar
direction. It often gives semicircular appearance to the nail when viewed
from the distal aspect. On occasion, it will be painful along the radial or
ulnar aspects and have the appearance of an ingrown nail. Treatment can be
unpredictable, but when attempted, involves elevation of the nail matrix off
the bone and placement of a dermal graft. When successful, this will restore
the normal contour to the nail.
8. Pterygium refers to scarring of the nail fold and eponychium to the nail bed.
The nail is unable to grow at the site of scarring leading either to nail absence
or splitting. Treatment consists of freeing the dorsal roof of the nail fold from
the nail bed and either inserting a silicone sheet in this space or placing a
split thickness sterile matrix graft on the undersurface of the eponychium to
prevent rescarring. Alternatively, the eponychium can be reconstructed with
a composite graft. Pterygia can also occur within the hyponychium leading
to a painful fingertip. Treatment consists of removing the distal nail and
hyponychium and placing a STSG in its place to cause an iatrogenic nonad-
herence.
II. Introduction to Soft Tissue Coverage
1. Partial-thickness wounds can heal by re-epithelialization, since the basement

membrane remains intact and is capable of regenerating more superficial skin
layers.
2. Fibroblasts at the margins of full-thickness wounds differentiate into myofi-
broblasts, which contract to pull the skin edges together and reduce the area
for wound healing.
3. Healing of full-thickness wounds can be facilitated by reconstructive options,
including primary closure, secondary intention, skin grafting, and flap cov-
erage. The most appropriate option depends on both wound and patient
characteristics.
4. The reconstructive ladder is a method to approach wound reconstruction,
which proceeds from simple to complex (bottom of the ladder to the top):
Free tissue transfer
Distant axial pattern flaps

Distant Random pattern flaps

Local Island pattern flaps
Local axial pattern flaps
Local random flaps
FTSGs
STSGs
Secondary intention
Primary closure
5. The goals of soft tissue coverage are to provide an adequate barrier to con-
tamination, to restore sensibility, and to improve appearance.
A. Secondary intention
1. Allowing a wound to heal by secondary intention allows contraction and
gradual re-epithelialization to provide healing when primary closure is not
possible.
2. It can be used for small clean defects without exposed bone or substantial
deep tissue loss.
3. The classic description is for a defect less than 1 cm in diameter, but this can
be used for larger areas without exposed bone, tendon, or nerve.
3. It allows early joint mobilization, which can prevent contracture.
4. Since the defect heals by scar, adequate padding may not be restored and
tenderness, cold intolerance, and poor cosmesis may result.
B. Skin grafts
1. Skin grafting: The use of skin grafts includes use of split-thickness or full-
thickness grafts. Split grafts may be either meshed or unmeshed, and will suc-
cessfully cover many wounds in the extremities. Indications are for wounds
that cannot or should not be treated by primary or delayed primary clo-
sure. The wound bed must have good vascularity. Skin grafts will adhere to
muscle, paratenon, and intact periosteum. Fat can be used as a bed, but is
less predictable than the previously mentioned structures. The wound beds
must be freshened prior to grafting, which includes the removal of collinized
granulation tissue, to avoid infection and subsequent loss of the graft. Immo-
bilization is critical for successful graft healing.
a) STSG
1) The epidermis and a variable amount of dermis are harvested by an
adjustable dermatome.
2) Graft thickness can be thin (0.005 to 0.012 in), intermediate (0.012
to 0.018 in), or thick (0.018 to 0.030 in), although the most common
graft thickness is 0.012 to 0.015 in.
3) The ideal recipient site is located where wound contraction will not
lead to decreased joint mobility.
4) STSGs are particularly useful for defects on the dorsum of the hand
and fingers.
5) Although any part of the body can be used for skinn graft harvesting,
the anterolateral thigh is most commonly used donor site. The poste-
rolateral trunk and thigh can be used for thicker grafts.
6) Meshing the graft allows expansion for coverage of a large area and
allows drainage of postoperative hematoma, which enhances graft
viability.
7) STSGs have a better take than full-thickness grafts.

8) Disadvantages include an inability to restore sensibility, and the greater

tendency to contract, leading to a less attractive appearance.
b) FTSGs
1) FTSGs consist of the epidermis and the entire layer of dermis.
2) The subcutaneous fat is manually removed from the graft prior to
placing it in the defect.
3) The recipient site must be a clean vascularized bed.
4) They are particularly useful for defects on the palmar side of the hand
and fingers.
5) Common donor sites include the groin and lower abdomen for large
defects and the ipsilateral extremity for small defects (i.e. hypothenor
skin).
6) The donor site should be larger than the defect to allow for primary
contracture following harvest of the graft.
7) The donor site is typically closed primarily, thus, limiting FTSG to
smaller defects, but the donor site can be covered with a STSG.
8) Advantages include improved wound bed protection, better reinnerva-
tion potential, less wound contracture, and faster maturation.
9) Disadvantages include a higher infection rate and an overall lower
survival, in comparison to STSG.
c) Local or distant flaps
More complex wounds with exposed neurovascular or tendinous struc-
tures, bone devoid of periosteum, insufficient vascularity or poor soft
tissue beds require the transfer of well-vascularized tissue to achieve
wound closure. Rotation flaps, as isolated tissue or combination of
muscle, fascia, or cutaneous tissue, can provide vascularized tissue for an
obliteration of dead space and wound closure without tension. However,
these options may be limited because of the wound location or regional
donor site deficiencies. These include random-pattern, axial-pattern, or
island flaps.
III. Flaps
A flap is a tissue transferred from a donor site to a recipient site while maintaining its
own blood supply and is used when a defect cannot be closed primarily, should not be
allowed to heal secondarily, and cannot support a skin graft. Their donor site can be
closed primarily or covered with a STSG.
A. Skin flaps can be described by their vascular supply as random pattern or axial
pattern.
1. Random-pattern flaps receive their blood supply by small, unnamed ves-
sels from the subcutaneous or subdermal plexus. The flap is created by rais-
ing three sides and using the forth side as a pedicle. The flap length: width
ratio should not exceed 2:1 to avoid vascular compromise. The flaps may be
described by their geometric shape such as mitten (bilobed) flap, Limberg
(rhomboid) flap, semicircular rotation, bipeninsular, or simple unipeninsular
advancement.
2. In contrast, axial-pattern flaps are supplied by a single, constant vessel,
which must be preserved as a vascular pedicle along the long axis of the
flap. The area of skin supplied by the axial pedicle is called the vascular

territory. In general, axial-pattern flaps have a more substantial blood

supply than random-pattern flaps, making them more resistent to infec-
tion. In addition, the better blood supply enables the length: width ratio to
be greater than 2:1. Since the vascular pedicle must be carefully preserved,
care must be taken when thinning the flap. The flaps may be described
according to their contents, such as fasciocutaneous, muscle, musculocu-
taneous, osseous, osteocutaneous, or a composite (combination of tissue
types) flap.
B. Skin flaps can also be described by location as local, regional, or distant.
(Table 20.1)
1. Local flaps are taken from tissue adjacent to the defect. As such, they have
similar characteristics to the lost skin. Local flaps can be advancement flaps,
rotational flaps, transposition flaps, or island flaps. Ischemia at the tip of the
flap is a concern with local flaps.
a) Advancement flaps have a pedicle on the side opposite to the primary
defect.
b) Rotational flaps are random-pattern flaps that are moved laterally and
stretched to cover both the donor and recipient sites. Therefore, by defini-
tion, rotational flaps are always bigger than the defect.
c) Transposition flaps are also moved laterally, but the donor site is closed
primarily or with another graft.
d) Island flap implies an area of skin that is detached from all of its host
attachments except for its vascular pedicle.
2. Regional flaps are taken from the ipsilateral limb when local tissue is of insuf-
ficient amount or quality.
TABLE 20-1 Regional flap options for upper extremity defects
Local Flaps Regional Flaps Distant Flaps

Z-plasty Cross-finger flap Groin flap
Axial flag flap Reversed cross-finger Latissimus dorsi flap
flap
Dorsal metacarpal Innervated cross-finger
artery flap flap
Digital artery island Cross-thumb flap
flap
V-Y advancement Thenar flap
flap
Lateral V-Y Neurovascular island
advancement flap flap
Moberg flap Radial artery forearm flap Fillet flap
Ulnar artery forearm flap Scapular flap
Reversed posterior Lateral arm flap
interosseous artery flap

3. Distant flaps are taken from a site outside the ipsilateral limb. They are either
harvested as a free flap or divided at a second operative procedure.
C. Local flaps
1. Z-plasty
a) Z-plasty is a random, transpositional flap used to lengthen contractions
or scars (Fig. 20.2).
b) All limbs must be of equal length.
c) It can increase scar length by 25% with 30-degree angles, 50% with
45-degree angles, and 75% with 60-degree angles.
2. Atasoy volar V-Y advancement
a) This flap is often used for transverse fingertip amputations or amputa-
tions with more dorsal tissue loss (Fig. 20.3).
b) The skin is cut leaving the subcutaneous tissue intact for vascular
supply. The V-cut points toward the distal interphalangeal joint (DIP)
flexion crease and the distal flat edge is mobilized and pulled up over
the top.
c) The proximal V-segment of skin is closed primarily.
d) It is useful when sensation is vital, such as in musicians (Table 20.2).
e) A different flap is typically needed when the predominant tissue loss is
palmar.
3. Kutler paired lateral V-Y advancement flap
a) Similar to the Atasoy although the V-Y advancement is performed on
both sides of the digit, and the flat distal portions are sutured together in
the midline of the fingertip (Fig. 20.4).
b) Cleland ligaments must be freed dorsally, and the anterior neurovascular
supply must be protected.
c) This flap is best for transverse fingertip amputations.
d) The scar at the tip of the finger can be problematic.
4. Moberg volar advancement flap
a) This volar rectangular skin flap is based on the neurovascular bundles and
typically used for thumb pulp defects.
b) The flap is best for thumb defects, since the dorsal arterial supply is inde-
pendent of the volar supply in the thumb, making dorsal skin necrosis less
likely. Also, flexion of the interphalangeal (IP) joint is often needed for
sufficient flap advancement, and IP contracture is better tolerated in the
thumb.
c) Two midlateral incisions are made dorsal to the neurovascular bundles,
and the flap is dissected off the flexor tendon sheath and can be advanced
approximately 2.0 cm (Fig. 20.5).
d) The secondary site is closed primarily or covered with a skin graft.
e) The flap includes all the volar skin, subcutaneous tissue, and both neuro-
vascular bundles from the tip injury to the metacarpophalangeal joint.
f ) If the flap remains under tension, a proximal V-Y advancement or trans-
verse incision can be used to slightly increase advancement. This area can
be allowed to heal secondarily or covered with a FTSG on the secondary
defect.
g) The IP joint is immobilized for 10 days post-op.
h) The disadvantages of this flap are limited advancement, flexion contrac-
ture, and possible injury to the dorsal vascular branches.

A A
E F
C
B A
F
E
Figure 20.2 Z-plasty. Note

that all sides must be equal
D
in length. A. Flap design
and B. Orientation after
B rotation of flap

Figure 20.3 Atasoy volar V-Y advancement. (From Rozenthal TD, Steinberg DR. Skin
and soft tissue defects. In: Beredjiklian PK, Bozentka DJ, eds. Review of Hand Surgery.
Philadelphia, PA: Elsevier; 2004, Figure 3-4.)
5. Dorsal metacarpal artery island flap

a) The neurovascular island flap is raised from the dorsum of the index prox-
imal phalanx and is most useful for defects on the thumb, first web space,
and proximal long and ring fingers.
b) The pedicle contains the first or second metacarpal artery, veins, and
branches of the radial nerve, which are dissected distal to proximal.
c) The interosseous fascia is included in the flap, since the vessel runs deep
to this plane.
d) Doppler ultrasound can be used to identify the vessel course.
e) The flap can be raised with a proximal antegrade or reverse-flow pedicle,
based on a perforator from the common digital vessels.
TABLE 20-2 Examples of local finger flaps, non-innervated and

innervated
Non-innervated Flaps Innervated Flaps

Thenar flap V-Y advancement
Cross-finger flap Moberg volar advancement
Neurovascular island
Innervated cross-finger
Axial flag

Figure 20.4 Kutler paired lateral V-Y advancement flap. (From Klein HW. Fingertip
injuries. In: Chapman MW, ed. Operative Orthopaedics. 2nd Ed. Philadelphia, PA:
Lippincott Company; 1993, Figure 3-4.)
Figure 20.5 Moberg volar advancement flap. (From Rozenthal TD, Steinberg DR. Skin
and soft tissue defects. In: Beredjiklian PK, Bozentka DJ, eds. Review of Hand Surgery.

Figure 20.6 Axial flag flap. (From Rozenthal TD, Steinberg DR. Skin and soft tissue
defects. In Beredjiklian PK, Bozentka DJ, eds. Review of Hand Surgery. Philadelphia,
PA: Elsevier; 2004, Figure 3-3.)
f ) The reversed-flow flap can extend as far ulnar as the fifth metacarpal head
and is used for digital defects proximal to the PIP joints.
6. Axial flag flap
a) This flap is based on the dorsal digital artery or the proper digital artery
at the web space of the donor finger (Fig. 20.6).
b) The flap is raised over the dorsum of the proximal phalanx, near the inter-
digital crease.
c) The index and long fingers are the most common donor fingers.
d) The flap is very mobile and can cover palmar defects in the proximal
aspect of an adjacent digit.
e) The flap is particularly useful for coverage of defects with exposed
tendon.
D. Regional flaps
1. Posterior interosseous artery flap
a) This axial fasciocutaneous flap is elevated from the proximal dorsal fore-
arm. The vascular supply is based on reversed flow from the posterior
interosseous artery and its connection with the anterior interosseous
artery. It is used for covering dorsal hand defects.
b) The posterior interosseous artery can be found between the extensor
carpi ulnaris and the extensor digiti minimi tendons. Proximally, it can
be found deep to the anconeus along the proximal ulna and between the
supinator and the abductor pollicis longus.
c) The main perforators are found proximally, approximately one third of
the way between the lateral humeral epicondyle and the distal radioulnar
joint with the forearm in pronation.

d) The posterior interosseous artery is rotated proximal to where it connects

with the anterior interosseous artery, approximately 2 cm proximal to the
ulnar styloid.
e) An advantage of this flap is that no major artery is sacrificed.
f ) A disadvantage is that the posterior interosseous nerve branch to the
extensor carpi ulnaris limits elevation of the flap. In addition, because of
its short vascular pedicle and proximal axis of rotation, the flap is limited
to dorsal hand defects, including the first web space and dorsal metacar-
pophalangeal joints.
2. Radial forearm flap
a) The radial forearm flap is the workhorse for coverage of large soft tissue
defects of the hand forearm and elbow.
b) The flap can be used as an antegrade or retregrade pedicle flap or a free
flap. It is most commonly used as a fasciocutaneous flap, but can be har-
vested as fascia only or as an osteofasciocutaneous flap.
c) The distally based pedicle flap is rotated at the level of the radial styloid
and is dependent on an intact palmar arch and retrograde flow into the
radial artery.
d) The radial artery is located between the flexor carpi radialis and the bra-
chioradialis.
e) An Allen test is performed preoperatively to ensure that the ulnar artery
perfuses the entire hand.
f ) The secondary skin defect is often covered by a STSG.
3. Lateral arm flap
a) This is an axial, fasciocutaneous flap based on the posterior radial col-
lateral artery.
b) Its pedicle length is 7 to 8 cm and can be used for coverage around the
elbow. Coverage of hand defects is typically as free tissue transfer.
c) Harvest can lead to numbness of the posterolateral elbow due to transec-
tion of the lateral cutaneous nerve.
4. Thenar flap
a) This flap is used for palmar fingertip defects by sewing the fingertip down
into the thenar eminence.
b) The thenar flap is raised from the proximal radial aspect of the thumb
at the level of the thenar muscles proximal to the metacarpal-phalangeal
joint.
c) Care is taken to protect the radial digital nerve while raising the flap.
d) The fingertip is sewn into the flap for 2 weeks to allow neovascularization
at which time the flap may be sectioned.
e) The advantages of the flap include a thick, durable skin flap, which has a
more cosmetically acceptable donor site than a cross-finger flap.
f ) The main disadvantage includes the potential for finger stiffness in adults
due to the position of immobilization (PIP joint flexion). Therefore,
thenar flaps may be better tolerated in young patients (teenagers and
younger) in whom stiffness is less likely to be permanent. Other disadvan-
tages include donor scar sensitivity and insufficient fingertip padding.
5. Dorsal cross-finger flap
a) In this regional random pattern flap, the dorsal skin and subcutaneous tis-
sues are elevated from the paratenon of the donor digit and transferred to
the palmar surface of the involved adjacent finger (Fig. 20.7). The digits

Figure 20.7 Dorsal cross-finger flap. (From Rozenthal TD, Steinberg DR. Skin and
soft tissue defects. In: Beredjiklian PK, Bozentka DJ, eds. Review of Hand Surgery.
are held together for 2 weeks until neovascularization provides support

for the flap and allows sectioning of the pedicle.
b) The flap is useful when the palmar defect is large and oblique.
c) The paratenon of the donor finger is preserved.
d) The secondary defect requires a STSG.
e) This flap should not be used in patients with Buerger’s disease, Raynaud
phenomenon, diabetes mellitus, or any other small vessel disease.
f ) An advantage of this flap is the ability to cover large defects or those with
exposed tendon or bone.
g) The disadvantages of this flap include incomplete restoration of the fin-
gertip pad by the thin dorsal skin, a potentially unacceptable dorsal scar,
and a poorly tolerated period of immobilization, especially in children.
Stiffness of the PIP joints can be a problem due to the required immobi-
lization, but this is better tolerated than the thenar flap.
6. Reverse cross-finger flap
a) The reverse cross-finger flap is used for dorsal defects and is a modifica-
tion of the dorsal cross-finger flap.

b) The dorsal skin is reflected and an underlying subcutaneous tissue layer is

raised as a flap.
c) The native skin is then sutured back onto the donor site and the reflected
subcutaneous flap is used to cover the defect. The subcutaneous flap on
the recipient digit is then covered with a thick STSG.
d) This flap can provide a more acceptable appearance at the donor site.
7. Neurovascular island flap
a) The flap involves transfers of skin, subcutaneous tissues, digital artery and
digital nerve to a defect that requires durable skin and sensation.
b) The ulnar side of the long or ring fingers is typically used as the donor
sites because these digits have codominant digital vessels. A digital Allen
test is performed preoperatively to confirm patency of the adjacent finger’s
digital artery.
c) An extensive Bruner incision is used to mobilize a flap with its
neurovascular bundle to its midpalmar origin, and the flap is rerouted
to the defect through a subcutaneous tunnel (Fig. 20.8). The flap usually
extends from the fingertip to the PIP joint.
d) This is the best axial flap for digital amputation and can be used for severe
thumb pulp defects to maintain skeletal length.
e) It provides sensation for digital nerve or median nerve deficits.
f ) The disadvantages of this flap include donor site depression, impaired
venous drainage, loss of donor tip sensibility, and incomplete sensory re-
education in adults.
g) A modification of this flap is a homodigital flap, which involves elevation
of the skin, subcutaneous tissue, and one of the digital vessels to advance
distally and cover fingertip wounds that will not heal by secondary inten-
tion, either due to exposed structures or large size. This can be advanced
as sensate flaps with the digital nerve or the nerve can be left in place and
the digital vessel only elevated with the flap.
1) The advantage of this is the donor site is confined to the injured finger and
there is no need for immobilization as with cross-finger or thenar flaps.
2) This does sacrifice one digital artery, so the second artery must be
patient or finger necrosis can occur.
E. Distant flaps
1. Groin flap
a) This is an axial, fasciocutaneous flap used for large soft tissue defects.
b) The flap is useful when there is an incomplete carpal arch precluding the
use of forearm flaps and a lack of adequate vessels for a free flap.
c) The flap is centered 2 cm distal to the inguinal ligament and is based on
the superficial circumflex iliac artery.
d) Once the flap is elevated and sewn into a tube, the secondary defect is
primarily closed and the flap is sewn over the primary defect (hand is
sewed to the groin).
e) The flap is usually sectioned 3 to 4 weeks after placement.
f ) Its disadvantages include immobilization of the entire upper extremity in
a dependent position, which can cause edema of the hand and stiffness
throughout the entire upper extremity.
2. Latissimus dorsi flap
a) This is an axial muscle or musculocutaneous flap with a wide arc of rota-
tion around its pedicle, the thoracodorsal vessels.

Figure 20.8 Neurovascular island flap. (From Rozenthal TD, Steinberg DR. Skin and
soft tissue defects. In: Beredjiklian PK, Bozentka DJ, eds. Review of Hand Surgery.
b) In the upper extremity, it is most commonly used for coverage around

the elbow, as a functional muscle for restoration of elbow extension or
flexion, or as a free tissue transfer.
c) The secondary defect is closed primarily.
d) Disadvantages include the need to reposition the patient when harvesting
the flap and postoperative seroma formation.

IV. Free Tissue Transfer
A. Definition
1. Free tissue transplantation describes the transfer of autologous tissue from
one location in the body to another site using techniques of microvascular
surgery for small vessel anastomoses.
2. Free flaps types include an isolated tissue transfer, composite tissue transfer,
and functioning free muscle transfer. Structural tissue transfers such as vas-
cularized bone grafts or toe transplantations for hand reconstruction are also
included in this category
B. General principles
1. Free tissue transfer is generally considered for any tissue deficit that is not
amenable to closure by simpler means.
2. Free tissue transfer provides not only coverage and reconstitution of the soft
tissue envelope but can facilitate function. For the hand, elevation and early
mobilization can be achieved following injury, which decreases limb edema
and stiffness.
3. Free flaps allow the possibility of composite tissue reconstruction in a single
stage by transferring various combinations of skin, muscle, tendon, bone,
and nerve simultaneously.
4. A thorough understanding of the rationale, timing, and type or selection for
tissue transplantation is critical for successful reconstruction.
C. Free tissue selection and timing of transfer
1. Types of free tissues
a) Isolated tissue: Muscle, skin, fascia, bone, or nerve.
1) Classification of muscle flaps: Muscle types have been classified on the
basis of five patterns of muscle circulation. A muscle used for free tis-
sue transfer must be able to survive on one dominant vascular pedicle
that can support the entire muscle mass.
2) Composite tissue: Composite flaps are a combination of tissue types
and provide more than one function. Toe transplantation, which
includes vascular, neural, tendinous, osseous, and nail components as
a composite, is the best example of composite tissue transfer. Other
examples include myocutaneous (rectus abdominis or latissimus dorsi
with skin islands), fasciocutaneous (lateral arm or radial forearm),
osteocutaneous (fibula with skin island), or innervated myocutane-
ous flaps (e.g., functioning free muscle transfer, i.e., gracilis).
2. Selection of free flap
Donor site morbidity, recipient site requirements (i.e., size, anatomic loca-
tion, structural loss, dead space, presence of infection, or colonization),
length of the vascular pedicle, and anticipated aesthetic results are all fac-
tors considered for appropriate free flap selection. The use of free tissue flaps
is not always selected to cover soft tissue defects or to replace missing tis-
sue. Some instances require augmentation of an existing soft tissue envelope
insufficient in texture or quality.
a) Recipient site: The type of tissue deficiency and surfacing requirements
typically determines selection of the type of free flap, in isolation or as a
composite flap. For example, a myocutaneous latissimus dorsi flap is not
a good choice for resurfacing of the dorsal hand for secondary tendon

reconstruction because of its bulkiness and lack of donor tissue matching

the dorsum of the hand and its inability to support gliding tissue. An
isolated cutaneous flap such as a radial forearm or lateral arm flap would
be considered a better selection. A lateral arm flap, however, would not
afford enough tissue bulk to fill dead space created by aggressive debride-
ment, particularly in the lower extremity. In this case, muscle flaps may
be more effective for the treatment of osteomyelitis than cutaneous flaps
if a large hypovascular dead space is present.
b) Use of skin paddle: Incorporating a skin paddle as a composite tissue
transfer can serve multiple purposes. A skin paddle can provide necessary
soft tissue contouring and aesthetics, or it can solely function as a monitor
for flap perfusion during the postoperative period.
c) Vascular pedicle and recipient vessels: The vessel anastomosis should be
done in a “safe zone” where the recipient vessels have not been previ-
ously damaged. The concept of “zone of injury” refers to the inflamma-
tory response within the soft tissue of the traumatized limb that extends
beyond the grossly evident wound. Perivascular changes of blood vessels
within the “zone of injury” can result in an increased friability of vessels
and an increased perivascular scar tissue, which ultimately contribute to
the failure of free tissue transfers. The “zone of injury” can be avoided
with extensive proximal dissection of the recipient vascular pedicle or with
utilization of interpositional vein grafts. The condition of the recipient
pedicle (vessel wall pliability and quality of blood flow) is more impor-
tant than the distance of the recipient vessels from the wound. Angiog-
raphy frequently is used to evaluate the vasculature of the recipient site
although there is some debate on its necessity. Meticulous use of the Dop-
pler for clinical evaluation can obviate the need for routine recipient-site
angiography.
d) Intercalary bone defects: Vascularized bone flap selection should be based
on the cross section of the bone defect, the available vascular supply, and
the possible need for simultaneous soft tissue reconstruction.
3. Timing of free tissue transfer
a) General principles: Two key factors should be considered when determin-
ing wound coverage with a free flap transfer:
1) The presence of exposed vital structures:
Vital structures include vessels, nerves, joint surfaces, tendons, and
bone denuded of periosteum. These tissues will necrose rapidly if inad-
equately covered and may lose function with prolonged exposure.
2) The risk of infection:
The risk of infection increases with increased exposure time and in the
presence of tissue necrosis.
b) Trauma: Important factors related to an extremity injury that influences
the timing of definitive wound management include the general condi-
tion of the patient, bacterial status of the wound, type of fracture, types
of tissues injured, and exposed structures. In severe extremity trauma
with associated soft tissue defects and exposure of underlying struc-
tures, acute coverage of the wound by 5 to 7 days is generally accepted
as having a good prognosis. Early aggressive wound debridement and
soft tissue coverage with a free flap within 5 days have been shown
to reduce the risks of postoperative infection, flap failure, nonunion,

and chronic osteomyelitis. Some authors emphasize the importance of

radical debridement in cases of high-energy trauma and recommend
free flap coverage at the time of the initial debridement to within the
first 72 hours after injury. More recent use of the V.A.C. and Negative
Pressure Wound Therapy has allowed for more successful wound closure
after 5 days.
c) Tumor
1) Irradiated wounds are associated with a high incidence of wound
complications after tumor resection and attempted primary closure of
surgical incisions due to poor vascularity and tissue quality. Free tissue
transfer for coverage of these wounds affords improved local vascular-
ity and results in more rapid wound healing. For this reason, some
surgeons implement immediate free tissue transfer following tumor
resection in these cases with results showing decreased hospital stay,
decreased costs, decreased morbidity, and increased rate of limb salvage
with high patient satisfaction. When patients receive adjuvant therapy
consisting of chemotherapy and/or radiotherapy, the appropriate win-
dow for the timing of surgery, inclusive of tumor resection and free
tissue transfer, is determined by a multidisciplinary evaluation involv-
ing the oncologist, radiation therapist, oncologic surgeon, and micro-
surgical team.
2) Secondary limb reconstruction with free tissue transplantation can be
subdivided into two subsets:
a. Acute wound complications in the early postoperative period fol-
lowing tumor resection
b. Late (several months or years) reconstruction for chronic unstable
soft tissue, wound dehiscence, failed or infected prosthesis, or limb
growth complications
Patients who experience acute complications following sur-
gery such as skin flap necrosis may require debridement and free
flap coverage within the first or second week from surgery. Serial
debridements and continual wound inspection are possible to
allow for the demarcation of questionable areas before free tissue
transplantation. Patients who later present with impending expo-
sure of an allograft or prosthesis should have immediate debride-
ment and tissue coverage to avoid infection of the implant or
allograft.
4. Specific free flaps (Table 20.3)
5. Postoperative care and monitoring
a) General principles: Patients require adequate hydration, proper main-
tenance of body temperature, and maintenance of hematocrit. Routine
heparinization and anticoagulation are not utilized. Monitoring of free
flaps is essential. Flaps are typically monitored for a minimum of 5 days
using clinical acumen and adjunctive monitoring with devices such as an
implantable Doppler probes. The first 24 to 48 hours following surgery
are the most critical, but occasionally late free flap failures occur, so moni-
toring for 5 days is recommended. Extremities are elevated at all times to
avoid venous congestion.
b) Free flap monitoring: Many different devices and techniques have been
used with varying levels of success. Flap monitoring should ideally

TABLE 20-3 Free flap options for upper extremity coverage
Tissue
Types Flap Vascular Anatomy Notes
Fascial Radial Pedicle—radial Radial artery is
and forearm artery sacrificed.
fasciocu- Most common com-
taneous plication is due to skin
flaps graft problems at the
donor site.
Can be innervated by
the medial and lateral
antebrachial cutane-
ous nerves.
Posterior Pedicle—posterior Useful for defects on
interosseous interosseous artery dorsal hand.
(septocutane- Advantage over radial
ous perforators forearm flap is that
between ECU and a large artery is not
EDM). sacrificed.
Anastomoses Elevation of flap
between poste- limited by posterior
rior and anterior interosseous nerve
interosseous branch to ECU.
arteries at the level
of DRUJ maintain
viability.
Lateral arm Pedicle—posterior Can be used for cover-
radial collateral age after severe thumb
artery (pedicle web space contracture
length is 7–8 cm) release.
Harvest leads to
numbness in the pos-
terolateral elbow due
to transection posterior
cutaneous nerve of
forearm.
the posterior cuta-
neous nerve of the
forearm.
Ulnar artery Pedicle—Ulnodor- Cause of paresthesias
sal artery (arises in the hand following
2.5 cm proximal to flap elevation due to
pisiform) (pedicle transient ischemia of
length can be up ulnar nerve during flap
to 20 cm) elevation.
(continued)

TABLE 20-3 Free flap options for upper extremity coverage (Continued)
Tissue
Brachiora- Pedicle—anterior Can be innervated by
dialis recurrent radial the radial nerve.
artery
Temporopa- Pedicle—superfi-
rietal fascial cial temporal artery
Scapular Pedicle—circum-
flex scapular artery
Groin Pedicle—super- Superficial circumflex
ficial circumflex supply axial groin
artery flap; runs 1 in below
inguinal ligament.
Numbness in the thigh
after groin flap related
to meralgia paresthet-
ica (lateral femoral
cutaneous nerve).
Anterolat- Pedicle—Lateral Can be innervated by
eral thigh femoral circumflex the medial and lateral
artery (descending cutaneous nerves of
branch between the thigh.
rectus femoris and
vastus lateralis)
Lateral thigh Pedicle—profunda Can be innervated by
femoris artery the medial and lateral
(third perforator) cutaneous nerves of
the thigh.
Dorsalis Pedicle—anterior
pedis tibial–dorsalis
pedis artery
Muscle Latissimus Pedicle— Release of tendon
and dorsi thoracodorsal insertion has the great-
myocu- artery (pedicle est effect on the axis of
taneous length can be up rotation of a pedicled
flaps to 11.2 cm) latissimus flap.
the thoracodorsal nerve.
Vastus Pedicle—lateral Can be used as a
lateralis circumflex artery functional muscle
(proximal); transfer.
profunda femoris
artery (distal)
(continued)

Tissue
Serratus Pedicle—thora- No scapular winging
anterior codorsal artery occurs if lower slips
of the muscle are also
harvested.
Can be used as a
functioning muscle
transfer.
Can be innervated
by the long thoracic
nerve.
Rectus Pedicle—inferior Can be used as a
abdominis epigastric artery functional muscle
Tensor Pedicle—lateral transfer.
fascia lata circumflex artery
(proximal);
profunda femoris
artery (distal)
Gracilis Pedicle—medial
femoral circumflex
artery
Osseous Fibula and Pedicle—peroneal Can be transferred as
and osteocuta- artery an osteocutaneous
osteocu- neous fibula flap by fasciocutane-
taneous Iliac crest ous perforators in the
flaps and osteo- mid to distal third of
cutaneous the fibula.
iliac crest The vascularized
fibular graft remodels
and hypertrophies
more quickly than
nonvascularized
grafts.
Pedicle—super- Can be harvested as
ficial circumflex an osteocutaneous flap
artery. with iliac crest bone.
Composite Great toe, Pedicle—first In 78% of cases, the
tissue second toe dorsal metatarsal first dorsal metatarsal
flaps Toe wrap- artery artery runs super-
around ficially to the first
dorsal interosseous
muscle.
EDM, extensor digiti minimi.

be harmless to the patient, objective, applicable for all flap types, and
cost-effective. Monitors must be capable of prolonged continuous use
and must respond rapidly to changes in perfusion. Methods of monitor-
ing include clinical evaluation, direct vessel auscultation, tissue circula-
tion monitoring, and metabolic parameters.
1) Clinical evaluation: This method remains the gold standard. Clinical
assessment includes observation of skin color, temperature, capillary
refill, and bleeding characteristics. Experienced personnel are neces-
sary, and unfortunately, clinical examination is limited to the surfaces
of skin flaps and muscle flaps. Initial detrimental changes are often
subtle and may not be clinically apparent before irreversible tissue
damage has occurred.
2) Direct vessel monitoring:
a. Implantable Doppler probes are placed around the vien and artery
and used to assess flow.
b. Ultrasonic Doppler: Reflected sound waves from columns of
moving blood cells are measured.
6. Management of flap failure
a) Acute complications: The initial 48 hours are the most critical as most
complications occur during this time. Complications include arte-
rial insufficiency, venous insufficiency, hematoma, hemorrhage, and
excessive flap edema. These complications can occur alone or in any
combination.
1) Arterial insufficiency: This problem manifests as decreased capillary
refill, pallor, reduced temperature, and absence of bleeding following
pinprick. Arterial spasm, thrombosis, poor vessel quality (e.g., plaque,
small vessel disease), torsion or kinking of the pedicle, pressure on the
flap, technical error of the anastomosis, or flap tissue harvested
too large for its blood supply are all possible causes for arterial
insufficiency.
Prompt surgical intervention is required to restore blood flow.
Adjuvant pharmacologic agents used for flap salvage include vasodila-
tors, calcium-channel blockers, and anticoagulants.
2) Venous compromise: Obstructed venous outflow can be manifested
as flap cyanosis, rapid capillary refill, normal or elevated tempera-
ture, and the presence of dark blood following pinprick. Thrombosis,
torsion, or kinking of the pedicle, flap edema, hematoma, or an
excessively tight closure of tissue over the pedicle are all possible
causes for venous compromise. As microcirculatory disruption can
occur rapidly, early recognition of venous compromise is critical.
Hematoma can be drained at the bedside by the removal of limited
sutures to decrease pressure on a pedicle. Venous thrombosis will
eventually lead to arterial thrombosis, so this requires surgi-
cal exploration. Leeches can be used in the presence of venous
congestion despite a patent venous anastomosis with insufficient
outflow.
b) Management of late flap failures
1) Cause for failure: Technical and/or physiologic factors can result in
flap failure. Technical errors are most often the cause of failure, which
may include an error in flap harvest, pedicle compromise during

harvest, improper microsurgical technique, poor insetting of the flap

with resultant increased tissue tension or edema, or pedicle avulsion
from postoperative extremity motion (rare, but occurs).
2) Options for failure: Options include a second free flap transfer, delayed
debridement and skin grafting, or an amputation.
a. Second free flap: When a second free tissue transfer is consid-
ered, physiologic conditions and technical errors that lead to flap
failure must be recognized before proceeding. Additional studies
may be considered such as an arteriogram or blood coagulation
profiles.
b. Delayed debridement: On the basis of the Crane principle, the
unsalvageable free flap can be left in place as a biologic dressing or
eschar over the wound. If no infection is present, the eschar can be
left over the wound bed with the hopes of some healing with suf-
ficient granulation tissue. Ultimately, the eschar could be removed,
and with an appropriate granulation bed, the wound can be skin
grafted, obviating the need for a second free flap for wound clo-
sure. If sufficient healing of the underlying tissue is absent, then
consideration for a second flap must be considered. However, as a
word of caution, the failed flap can become a source of infection,
which can further compromise local tissues.
c. Amputation: When flaps fail in severely compromised extremi-
ties, consideration for an amputation should be given. Treatment
decisions must account for the additional morbidity of a second
free tissue transfer and the expected outcome for the salvaged
extremity when determining whether reconstruction or amputa-
tion is more favorable.
V. Replantation
Ronald Malt performed the first replantation of an entire upper limb in 1962. Komatsu
and Tamai performed the first digital replantation in 1965. With further develop-
ment of the operating microscope and microinstrumentation, replantation has become
commonplace.
Principles
Viability rates of replantation approach 90% although survival of the replanted part
does not equate function. Replantation is considered when the expected function post-
operatively will be improved over revision amputation and use of a prosthesis.
Major limb amputation involves an amputated part with skeletal muscle such as
an injury through the carpus or proximal. A minor limb amputation involves limited
skeletal muscle in the amputated part such as a digital amputation.
A. Replantation involves reattachment of a completely amputated part whereas
revascularization involves repair of an injury with some remaining soft tissue
bridge but no arterial blood supply.
B. Ischemia time
1. Replantation beyond the ischemia time leads to a no-reflow phenomenon
and survival of the part is unlikely. Acceptable ischemia time is dependent
on the level of injury and amount of muscle within the amputated part.

Replantation of a limb with skeletal muscle past acceptable ischemia time will
lead to the accumulation of toxic by-products with metabolic disturbances
including acidosis, hyperkalemia, and myoglobinuria.
2. In general, the acceptable ischemia time for major limb amputations is
less than 6 hours and for digit amputations devoid of muscle is less than
12 hours. Cooling the part to 4°C to 10°C can extend the ischemia time to
10 to 12 hours for a major limb and 24 hours for a digit.
C. Indications
1. Thumb replantation is performed if possible due to the functional impor-
tance of the digit. The replanted thumb typically has a better result than the
reconstructive alternatives.
2. Multiple digit loss will lead to significant functional compromise. The least
damaged digits should be replanted to the most functional positions.
3. Zone I injuries distal to the FDS insertion are technically straightforward and
result in improved sensation and cosmesis.
4. Almost any part in a child is replanted. If the part survives, there is a greater
chance of functional recovery than in an adult.
5. Sharp guillotine type injuries have the best prognosis and are ideal candidates.
6. Hand or proximal injury replantation leads to good results compared to the
devastating functional loss with amputation.
D. Contraindications
1. A crush or avulsion injury is a relative contraindication, which limits func-
tion and viability
2. Replantation of border digits, such as the index or small fingers, tends to
provide little improvement in function. A stiff index finger is often bypassed
by use of the long finger. Limited flexion of the small finger can lead to grip
strength weakness.
3. Amputation at multiple levels
4. Single digit amputation, particularly in zone II between FDP and FDS inser-
tion, replantation often leads to PIP stiffness and the digit is bypassed.
5. Contamination: Farm or barnyard injuries have a higher risk of infection
with systemic consequences.
6. Co-morbidities: Associated comorbidities that present significant medi-
cal risk for undergoing an extensive surgical procedure should be consid-
ered. Psychiatric factors such as a self-inflicted amputation may require
psychiatric evaluation.
7. Elderly patients will tend to have arteriosclerotic vessels. The patient popula-
tion will tend to have a greater anesthetic risk for a lengthy procedure and not
be amenable to a long rehabilitative postoperative program.
8. Major contraindications: Life-threatening injuries take precedence over replan-
tation. Prolonged warm ischemia time in a major limb replantation increases the
risk of failure and systemic metabolic disorders. Severe crush and avulsion inju-
ries that lead to extensive arterial injury are not amenable to reconstruction.
VI. Preoperative Assessment
A. Prehospital care
1. Amputated part should be cooled immediately to limit warm ischemia time.
An amputated digit should be wrapped in a saline soaked sponge and placed

in a plastic bag. The bag should be placed in ice slush to prevent frostbite of
the tissues.
2. The incomplete amputation is splinted and ice is applied. Any intact soft tissue
should not be severed since venous outflow may be present within the tissue.
B. Historical factors that should be determined include occupation, hand domi-
nance, mechanism and place of injury, time elapsed since injury, and any past
injury to the amputated part or extremity. A thorough past medical history is
obtained including the history of cardiovascular disease, peripheral vascular dis-
ease, diabetes mellitus, and smoking.
C. Physical exam should include an assessment of the condition of the patient and
amputated part. A complete systematic trauma evaluation should be performed.
Evaluate the level of injury and contamination.
1. Red line sign of the amputated digit is seen with an avulsion injury due to
traction of the neurovascular bundles. The changes are related to the linear
hematoma associated with the intimal arterial injury.
2. Ribbon sign also occurs with a traction injury as the neurovascular bundles
appear as a coiled twisted ribbon.
3. These are poor prognostic indicators.
D. Imaging studies. AP, lateral, and oblique radiographs are obtained of the ampu-
tated part and residual limb. The films are evaluated for level of injury, com-
minution, and foreign bodies. Intra-articular injuries are often treated with
arthrodesis of the involved articulation. A chest x-ray is obtained if clinically
indicated due to patient age, or history of pulmonary disease.
VII. Surgical Technique for Digital Replantation
A. Debridement. The neurovascular bundles are identified and all nonviable tissue
and foreign material debrided. Midlateral incisions are made with dorsal and
volar flaps. The sequence of structures to repair include bone, extensor tendon,
flexor tendon, artery, nerve, and vein
B. Bone shortening and fixation
1. Bone shortening of 0.5 to 1 cm will help limit tension on the vascular anas-
tomosis and ease skin repair.
2. Bone fixation with Kirschner wires (K-wires) is typically performed for digi-
tal replantation. This form of fixation limits surgical dissection and can be
performed expediently. Poor rigidity of the construct and potential soft tis-
sue injury are limitations of K-wire fixation. Alternative methods of fixation
include interosseous wiring, intramedullary fixation, and plate and screw
fixation, but these require more time to perform and increase the length of
the operation as well and the ischemia time.
C. Extensor tendon repair is performed with a nonabsorbable braided 3–0 suture.
With extensive crush injury, which precludes direct repair, alternatives include
tendon graft, or arthrodesis.
D. Flexor tendon repair is performed primarily. Two stage reconstruction 3 months
postoperatively is considered for crush and avulsion injuries rather than per-
forming an extensive dissection.
E. Arterial repair of both arteries can improve viability rate although one artery will
often suffice. The anastomosis is performed after adequate blood flow through
the proximal artery is confirmed. Inadequate flow proximally is addressed

1. Dissect the vessel further proximally to healthy tissue

2. Warm the patient including intravenous fluids
3. Hydrate the patient
4. Irrigate the vessels with a vasodilator such as papaverine.
5. Assess for metabolic causes of vasospasm such as acidosis.
F. Nerve repair is typically performed primarily after determining the appropriate
alignment. Nerve graft or conduit is considered to prevent repair under tension.
G. Vein repair: Two veins are anastomosed for each repaired artery to provide ade-
quate outflow. Vein grafts are used liberally to prevent a repair under tension. If
a vein graft is required in addition to soft tissue defect, both can be addressed by
a venous flap.
H. The skin is loosely approximated without tension or compression on the neuro-
vascular structures. Alternative options for coverage include rotational flaps, split
thickness, or full-thickness grafts.
VIII. Thumb Replantation
Thumb replantation provides unique technical difficulties. The digital arteries of the
thumb are out of the plane of the hand. Arterial reconstruction can be performed by
transposition of the radial digital artery of the index. This procedure can lead to first
web contractures. Alternatively, a vein graft is performed from the distal digital artery
of the thumb to the princeps pollicis or radial artery in the snuff box region. The distal
anastomosis can be performed prior to bone fixation.
IX. Distal Digital Replantation
Injuries distal to the DIP can be replanted but present difficulties in obtaining venous
outflow. Approximately 1 cm of dorsal skin proximal to the nail fold is needed to
obtain an adequate vein for anastomosis. There are several alternative options to
obtain venous outflow:
A. Volar veins may be repaired although technically difficult since they have a
smaller diameter and thinner walls.
B. Arteriovenous shunt: After repair of one digital artery for inflow, an anastomosis
of the other digital artery, if backflow is present, to a proximal vein occurs.
C. Nail plate removal and promote intermittent bleeding by rubbing the nail bed
with a gauze sponge every 1 to 2 hours. A continuous venous bleed is main-
tained with heparin-soaked sponges to the area. Alternatively, medical grade
leeches or a continuous heparin drip on an incision at the fingertip. The bleed-
ing is maintained for 5 to 7 days until neovascularization maintains adequate
outflow. These continuous bleeding methods often lead to blood loss requiring
transfusion.
X. Surgical Technique for Major Limb Replantation
Ischemia is critical in major limb injuries. The sequence of treatment includes Debride-
ment and fasciotomies, arterial shunting, bone shortening and fixation, arterial anasto-
mosis, venous anastomosis, nerve repair, muscle repair, and skin coverage.

A. Debridement and fasciotomies: After identification of the neurovascular struc-

tures, thorough debridement of all nonviable tissue is performed. Fasciotomies
of the forearm and hand are routinely performed to prevent compartment syn-
drome and myonecrosis.
B. Artery shunting, to limit ischemia time and muscle necrosis, is performed prior
to bone fixation. A catheter is temporarily inserted from the proximal artery to
the amputated part for immediate arterial flow.
C. Bone shortening and fixation: Approximately 4 cm of bone shortening is per-
formed at the forearm level. Bone stabilization using plate and screw fixation at
the forearm and crossed K-wires at the carpal level is performed.
D. Artery anastomosis prior to venous repair allows flushing of the metabolic
by-products of myonecrosis. The technique often leads to blood loss requir-
ing transfusion. Intermittent use of a tourniquet or intra-operative autologous
recovery system such as a cell saver (Haemonetics, Braintree, MA) can limit
blood loss.
E. Venous anastomosis of the deep and superficial vessels is performed. Vein grafts
are performed ideally out of the zone of injury to help ensure adequate soft tis-
sue coverage.
F. Neurorrhaphy is performed using an epineural repair after resecting the ends
and confirming the appropriate alignment.
G. Muscle and tendon repair is completed from deep to superficial.
H. Skin closure over the neurovascular bundles is performed allowing open areas
for drainage. Repeat debridement is often performed at 48 to 72 hours postop-
eratively. Complete closure is performed within a week.
XI. Postoperative Care
A. A noncompression dressing and splint is applied. The arm is elevated to heart

level. If there are venous outflow problems, the extremity is further elevated.
The hand is lowered for arterial inflow problems.
B. The patient is kept well hydrated. The room is maintained warm limiting drafts
and visitors. Caffeine and nicotine are restricted.
C. Anticoagulation and vasodilation are typically instituted. Options include aspi-
rin, dextran, heparin, and chlorpromazine. Factors considered for anticoagula-
tion include mechanism of injury, quality of the vessel anastomosis, and use of
vein grafts. Heparin is considered for crush and avulsion injuries and infused for
5 to 7 days. Heparin is not used in major limb replantation.
D. Frequent assessment is performed for color, skin turgor, temperature, and capil-
lary refill. Temperature probes are the most reliable quantitative assessment with
abnormal vascular supply denoted by a loss of 2°C over 1 hour or a temperature
lower than 30°C.
E. Venous congestion due to poor outflow is assessed first by ensuring a noncom-
pression dressing. Treatment options include allowing venous bleeding with nail
plate removal and placement of heparin-soaked sponges every 1 to 2 hours.
Alternatively, an incision on the tip of the digit with a continuous heparin drip
or medical grade leeches may be used for venous congestion. The leech injects
the anticoagulant hirudin to provide slow bleeding for several hours. Leeches are
continuously applied for 5 to 7 days until outflow develops. Antibiotic coverage
for Aeromonas hydrophila is continued while leech treatment is continued.

XII. Results
A. Digital replantation
1. Viability approximately 75% to 85%.
2. Injuries distal to the FDS insertion on average result in 80 degrees of PIP
range of motion. By comparison, injuries proximal to FDS insertion will
result in approximately 35 degrees of PIP motion.
Sensory recovery of 8 mm two-point discrimination for sharp injuries
and 15 mm following crush or avulsion injuries. Sensory results tend to be
better in children and more distal injuries.
B. Palm, wrist, and forearm
1. Replantation at the level of the palm and distal forearm provide better results
than amputation with the use of a prosthesis.
2. Intrinsic muscle recovery is poor. Extrinsic flexors and extensors provide
motion through the IP joints and proportionally less through the metacarpal
phalangeal joints. Weak pinch and gross grasp are expected.
3. Two-point discrimination on average is poor with adequate protective
sensation.
C. Proximal injuries
1. Proximal forearm injuries have an overall viability of 65% with most failures
related to vascular thrombosis.
2. Trans-articular elbow replantation provides good to fair functional results
with 70% to 85% survival rate. Multiple procedures are typically required.
3. Trans-humeral replantation allows recovery of elbow function, but these are
severe injuries and can be life threatening. The functional improvement from
an above elbow to a below elbow level is significant. Because of this, the use
of free tissue transfer may be performed to convert an above elbow amputa-
tion to a below elbow amputation. Survival of the limb on average is 50%
with failures related to infection and arterial thrombosis.
XIII. Pediatric
A. Almost any amputated part in a healthy child is considered for replantation.

Superior nerve and soft tissue regenerative capacity lead to better functional
results than in the adult population.
B. The success rate of replantation is lower in the pediatric population due to
increased technical difficulties with smaller vessels, higher percentage of crush
and avulsion injuries, and vasospasm from postoperative pain and anxiety.
C. With an open epiphysis, the replanted part will continue to grow. Bone short-
ening should be limited to prevent epiphysis injury. Longitudinal growth will be
approximately 80% of normal.
D. Sensory recovery is similar to that of an isolated digital nerve repair. Cold intol-
erance is uncommon in a child whereas it is typical in the adult population.
XIV. Complications
A. Arterial insufficiency.
B. Venous insufficiency manifests as congestion.

C. Infection including osteomyelitis.

D. Cold intolerance can be quite severe associated with replantation in adults. The
symptoms usually improve within 2 years, but never completely resolve.
E. Stiffness requiring tenolysis and contracture release.
F. Nonunion.
G. Abnormal sensation.
XV. Vacuum Assisted Closure Therapy
A. Background Information
Created at the Wake Forest University in the Plastic and Reconstructive Surgery
Department, the Wound V.A.C. has shown that application of subatmospheric pres-
sure to open wounds increases local blood flow, rate of granulation tissue formation,
and random-pattern flap viability, while decreasing wound bacterial counts and edema.
Although some consider the V.A.C to work as a mechanical myofibroblast, the mech-
anism by which the V.A.C. supplies these wound-healing measures remains unclear.
Wound V.A.C. therapy has led to a radical change in wound care for abdominal, lower
extremity, hand, and pressure wounds.
B. Indications
V.A.C. therapy can be used as an intermediate phase in wound closure following
debridement of infected, crushed, or chronic wounds. Its use extends to second-
degree hand burns and degloving injuries as it decreases hand edema and wound
progression. Recent development of the Wound V.A.C. GranuFoam hand dress-
ing allows for better hand molding of injuries and allows for less frequent dressing
changes for patients, compared to traditional wet-to-dry dressings. It can be also
used as a bolster over a skin graft, particularly over large grafts and areas difficult to
use a tie-over bolster.
XVI. Xenaderm
Applied to poor wound-healing areas, this ointment works on the basis of three main
ingredients: Balsum of Peru vasodilates surrounding tissues to increase blood flow and
has mild bactericidal action, Trypsin debrides surrounding necrotic tissues, and Castor
oil stimulates epithelialization acting as a skin conditioner and protector.
B. Indications
No formal studies to date demonstrate using Xenaderm ointment in the hand, but with
good healing results in sacral pressure ulcers and superficial erosion injuries of the lower
extremities. Xenaderm may be an option for nonhealing, superficial hand ulcers.
XVII. Alloderm
Harvested from cadaveric specimens, Alloderm is an acellular dermal matrix supply-
ing the biochemical and structural components of dermis: vascular conduits, basement

membrane, collagen framework, and elastin fibers. Successfully used in reconstructions

of the abdominal wall, breast, head and neck defects, and skin graftings, Alloderm is
thought to support rapid tissue revascularization and remodeling to functional host tis-
sue, all at minimal infectious risk or rejection.
B. Indications
Alloderm is a soft tissue supplement in the hand, acting as a grafting substitute in
burn patients and tissue augment in radial forearmfree flap donor site closures. Its use
in grafting minimizes/prevents the formation of additional donor site morbidity and
results in less tissue contracture, as grafts up to 0.02 in thick can be harvested with
its use.
XVIII. Integra
Integra is an dermal regeneration template composed of a cross-linked collagen and
glycosaminoglycan covered with a silicone layer. It is placed in a manner similar to a
skin graft, allowed to revascularize, at which time the silicone layer separates, and is
covered with a thin STSG.
B. Indications
In the hand, it is useful for dorsal skin coverage problems and can be used directly on
tendons void or paratenon and often avoid the need for a flap. The disadvantages are
the cost and the need for the second stage procedure.
Suggested Readings
Argenta, LC, Morykwas, MJ. Vacuum-Assisted Closure: A new method for wound control and
treatment: Clinical experience. Ann Plast Surg. 1997;38:563.
Birbeck DP, Moy OJ. Anatomy of upper extremity skin flaps. Hand Clin. 1997;13:175–187.
Boulas HJ. Amputation of the fingers and hand: Indications for replantation. J Am Acad Orthop
Surg. 1998;6:100–105.
Browne EZ, Pederson WC. Skin grafting. In: Green DP, Hotchkiss RN, Pederson WC, Wolfe SW,
eds. Green’s Operative Hand Surgery. 5th Ed. Philadelphia, PA: Elsevier; 2005.
Jones JM, Schenck RR, Chesney RB. Digital replantation and amputation: Comparison of func-
tion. J Hand Surg. 1982;7A:183–189.
Katz MA, et al. Microvascular hand surgery. In: Beredjiklian, PK, Bozentka DJ, eds. Review of
Hand Surgery. Philadelphia, PA: Sunders; 2004:155–170.
Klein HW. Fingertip injuries. In: Chapman MW, ed. Operative Orthopaedics. 2nd Ed. Philadelphia,
PA: Lippincott Company; 1993.
Lattari V, et al. The use of a permanent dermal allograft in full-thickness burns of the hand and
foot: A report of three cases. J Burn Care Rehabil. 1997;18:147–141.
Meara JG, et al. Vacuum-Assisted Closure in the treatment of degloving injuries. Ann Plast Surg.
1999;42(6):589–594.
Pederson WC, Lister GD. Skin flaps. In: Green DP, Hotchkiss RN, Pederson WC, Wolfe SW, eds.
Green’s Operative Hand Surgery. 5th Ed. Philadelphia, PA: Elsevier; 2005.
Rozenthal TD, Steinberg DR. Skin and soft tissue defects. In: Beredjiklian PK, Bozentka DJ, eds.
Review of Hand Surgery. Philadelphia, PA: Elsevier; 2004.
Saies AD, et al. Results after replantation and revascularization in the upper extremity in children.
J Bone Joint Surg. 1994;76A:1766–1776.

Sommer NZ, Brown RE. The perionychium. In: Green DP, Hotchkiss RN, Pederson WC, Wolfe
SW, eds. Green’s Operative Hand Surgery. 5th Ed. Philadelphia, PA: Elsevier; 2005.
Urbaniak JR, et al. The results of replantation after amputation of a single finger. J Bone Joint Surg.
1985;67A:611–619.
Wood MB, Cooney WP. Above-elbow limb replantation: Functional results. J Hand Surg. 1986;
11A:682–687.
Zook EG. Anatomy and physiology of the perionychium. Hand Clin. 1990;6:1–9.

Acute Vascular Injuries
of the Upper Extremity
21
James P. Higgins
Penetrating trauma accounts for over 80% of the acute arterial injuries to the upper
extremity. Blunt trauma, closed fractures, or thermal injuries can also produce acute
arterial injuries. Regardless of the etiology, accurate, rapid assessment and treatment of
these problems require a thorough understanding of the detailed arterial anatomy of the
upper extremity with a focus on both major vessels and sources of collateral perfusion.
I. Anatomy
A. Left subclavian artery originates from the aortic arch.

Right subclavian and right common carotid arteries originate from brachio-
cephalic trunk.
Clavicle is landmark for the transition of vessel name from subclavian to
axillary artery.
B. Axillary artery passes deep to the pectoralis major and minor, intimately envel-
oped by the infraclavicular brachial plexus.
Axillary artery is the source of several branches to the shoulder and thorax:
1. Thoracoacromial artery
2. Lateral thoracic artery
3. Subscapular trunk (thoracodorsal and circumflex scapular arteries)
Inferior margin of pectoralis minor muscle is landmark for the transition of
vessel name to brachial artery.
C. Brachial artery courses anterior to the intermuscular septum of the medial
brachium, initially running between the median nerve (anterior to the artery)
and the ulnar nerve (posterior to the artery). In the distal portion of the upper
arm, the median nerve passes medial to the brachial artery as they approach the
antecubital fossa.
The brachial artery supplies three major sources of collateral flow across the
elbow:
1. Deep brachial artery—passing posterior and lateral to the humerus in tandem
with the radial nerve to join the radial artery distally.
2. Superior ulnar collateral artery—passing posterior to the medial epicondyle
in tandem with the ulnar nerve to join the ulnar artery distally.
3. Inferior ulnar collateral artery—passing anterior to the medial epicondyle to
join the ulnar artery distally.
The brachial artery bifurcates in the antecubital fossa to form the radial and
ulnar arteries.
D. Radial artery courses more superficially than the ulnar artery in the proximal
forearm, coursing deep to the bicipital aponeurosis and brachioradialis, and
superficial to the biceps tendon, pronator teres, FDS, and FPL sequentially. At
the wrist, it can be located between the brachioradialis and FCR tendons.
424

Chapter 21 • Acute Vascular Injuries of the Upper Extremity 425
At the wrist, the radial artery bifurcates into a smaller volar branch and a larger
dorsal branch.
1. Volar branch passes superficial or within the APB to join the superficial
palmar arch
2. Dorsal branch courses deep to the first dorsal extensor tendon compartment
into the anatomic snuffbox and divides into two major branches.
a) The first creates the dorsal arch of the hand.
b) The second passes between the first and second metacarpal bases to sup-
ply the deep palmar arch distally.
c) The “princeps pollicis” artery to the thumb branches off the radial artery
in this region. Variability in its origin is encountered frequently.
E. Ulnar artery courses deeper in the forearm after branching from the brachial
artery, coursing deep to the pronator teres, median nerve, and FDS. Shortly after
its departure from the brachial artery, the ulnar artery serves as the source of the
common interosseous artery. The ulnar artery then migrates ulnarward along
the superficial surface of the FDP to join the ulnar nerve at the junction of the
middle and distal thirds of the forearm. The ulnar artery and nerve pass through
the distal aspect of the forearm in tandem. At the wrist, the ulnar artery can be
located deep and radial to the FCU tendon, and radial and superficial to the
ulnar nerve at the wrist. At the wrist, the ulnar artery passes into Guyon canal,
where it bifurcates. The larger superficial branch supplies the superficial palmar
arch. The smaller deeper branch (coursing in tandem with the motor branch of
the ulnar nerve) joins the deep palmar arch.
F. Common interosseous artery branches off the radial aspect of the proximal
ulnar artery. It divides into anterior and posterior branches.
1. The anterior interosseous artery travels in tandem with the anterior
interosseous nerve along the volar surface of the forearm interosseous mem-
brane (IOM).
2. The posterior interosseous artery courses through a fenestration in the IOM
and enters the dorsal compartment. It is found deep to the EDC and EDQ
muscles and superficial to the more obliquely oriented APB, EPB, EPL, and
EIP muscle bellies. Cutaneous perforators are found roughly at the junction
of the proximal third and distal two thirds.
3. At the wrist, the anterior and posterior interosseous arteries communicate a
second time via the posterior division of the anterior interosseous artery that
passes through a fenestration in the IOM. Both volar and dorsal components
create a rich network of communicating vessels at the radiocarpal level, creat-
ing small arcades designated palmar metaphyseal arch, palmar radiocarpal
arch, dorsal supraretinacular arch, dorsal radiocarpal arch, and dorsal inter-
carpal arch. These are clinically significant in two ways:
a) They are the source vessels of an expanding number of pedicled bone
grafts for the treatment of carpal pathology (fracture, nonunion, AVN).
b) They supply routes of collateral flow in the setting of injury to large ves-
sels of the forearm.
G. Superficial palmar arch—Supplied by the superficial branch of the radial artery
and the superficial (dominant) branch of the ulnar artery. Creates an arcade deep
to the palmar fascia and superficial to the median nerve and flexor tendons. This
arcade is the source of common digital arteries to web space 2 to 4, as well as
ulnar digital artery to small finger. These common digital arteries run in tan-
dem with the common digital nerves. The arteries bifurcate into proper digital

arteries designated by the aspect of the digit they supply (i.e., “ulnar digital artery
to ring finger”). The common digital nerves bifurcate more proximally in the
palm and migrate palmarly. The digital nerves are thus deep to the arteries in the
palm and superficial to the arteries in the digit.
H. Deep palmar arch—Supplied by the dorsal branch of the radial artery after it
passes from the snuffbox in the dorsum of the hand, between the bases of meta-
carpal 1 and 2, into the palmar space. This arch runs transversely at the level
of the metacarpal bases. It supplies the palmar metacarpal arteries that lie deep
to the flexor tendons and neurovascular structures. Palmar metacarpal arteries
communicate with digital arteries through communicating perforators at the
level of base and neck of the metacarpals. The deep palmar arch typically sup-
plies the digital arteries to the thumb and the radial digital artery to the index
finger. There is significant anatomic variation seen in this region of the first web
space. The term “princeps pollicis artery” has been employed to describe many
different anatomic structures, which serve as the main blood to the thumb. The
use of this term should be avoided because of this lack of agreement on its
definition.
I. Dorsal arch (AKA Dorsal Intercarpal Arch)—Supplied by the dorsal branch of
the radial artery. This supplies the dorsal metacarpal arteries and feeds into the rich
plexus of dorsal wrist small vessel connections to the interosseous arteries (see F).
Dorsal metacarpal vessels course along the fascia of the dorsal interosseous mus-
cles and feed angiosomes out to the level of the PIPJ of digits 2 to 5 and out to
the tip of the thumb. These vessels can routinely maintain viability of the entire
thumb despite injury to both digital arteries of the thumb. They cannot reliably
maintain viability of the remaining digits after similar injuries to their respective
digital vessels.
J. Proper digital arteries
1. Course dorsal (deep) to digital nerves, but volar to the midaxis of the digit.
2. Can be found dorsal to Grayson ligaments and volar to Cleland ligaments
3. One digital artery can maintain viability of the entire digit after single digi-
tal artery injury. This is due to rich arcades of communicating volar vessels
located between the palmodigital and IP flexion creases.
4. An isolated injury to a common digital artery will not result in critical isch-
emia of a digit. This is due to the anatomic relationship of the common
digital arteries supplying proper digital arteries to adjacent fingers.
5. The dominant artery for the index and middle fingers is usually the ulnar
digital artery, and the dominant artery for the ring and the small fingers is
usually the radial digital artery.
II. Diagnosis
A. The majority of acute arterial injuries occur from penetrating trauma (laceration,
gunshot wound, and puncture), although closed injuries (blunt trauma and closed
fractures) may cause acute vessel disruption or thrombosis. Vascular injuries are
designated critical if they result in inadequate perfusion to the limb threatening
viability. Noncritical vascular injuries do not demonstrate limb threatening isch-
emia because of adequate collateral circulation to maintain tissue viability.
In the setting of critical ischemia from vascular injury, immediate recon-
struction is warranted. In the setting of noncritical vascular injuries, the decision

regarding reconstruction is often made based on several factors including the

condition of the patient, concomitant injuries, and surgical resources.
1. Physical examination findings suggestive of arterial injury:
a) Active bleeding/hematoma
b) Abnormal/absent distal pulses
c) Pallor
d) Hypotension
e) Numbness in dermatome of adjacent nerve (i.e., ulnar nerve and digital
nerve)
f ) Ribbon sign on either side of the digit, signifying a traction injury to the
digital artery (seen usually in amputations)
The emergency room vascular examination of the traumatized extremity may
be difficult to interpret due to a number of factors—core temperature, skin pig-
ment, pain, prior administration of local analgesics, etc. The most misleading
factor in assessing the traumatized extremity for vascular injury can be the pres-
ence of distal pulses and/or perfusion despite more proximal arterial injury. This
can occur in the presence of adequate collateral circulation providing backflow
to the injured vessel or from wave pulses transmitting through a thrombosed
vessel. This is most often encountered in the setting of single vessel injury in the
forearm, but may also be seen in other locations of vessel injury with adequate
collateral networks (brachial artery below the deep brachial artery takeoff, com-
mon digital artery injury, and single proper digital artery injury).
B. To obtain reliable and objective information, a detailed Doppler examination is
helpful and simple. This may be performed in conjunction with the Allen test as
needed.
1. Doppler Allen test:
a) Useful in determining the patency of ulnar or radial arteries in the forearm.
b) Doppler signal is located along the course of the vessel distal to the
laceration.
c) The uninjured parallel vessel is compressed at the wrist to suppress poten-
tial retrograde flow at the site of the Doppler probe.
d) Persistence of the Doppler signal designates intact flow across the site of
injury.
e) Loss of signal suggests a more proximal disruption of the vessel.
2. The use of modalities other than Doppler probe examination has limited
utility in the setting of acute injury. Other modalities described include
a) Pulse echo ultrasonography
b) Color Doppler imaging
c) Conventional arteriography
d) MR angiography
e) CT angiography
III. Contrast Angiography
In particular, the use of contrast angiography has been widely debated. In the setting
of acute penetrating injuries, the surgeon may forgo the use of angiography as opera-
tive exploration is indicated without information yielded from arteriography, and the
site of arterial injury is known providing there is only a single-level injury to the limb.

Operative intervention is indicated in the setting of suspected arterial injury. The

routine use of preoperative angiography is contraindicated due to
– Morbidity associated with the test
– Time constraint of injury
– Expense
A. Angiography remains useful in the evaluation of a narrow subset of acute arterial
injuries:
1. Injuries where the extent of injury is unclear (sequential injuries to the same
vessel and traction injury)
2. Injuries where distal injury is suspected to be extensive or perhaps nonrecon-
structable (arterial injection injury)
3. Suspicion of noncritical injury (i.e., pseudoaneursym and intimal injury)
that could be source of future problem (i.e., embolism and thrombosis)
4. Injuries that may be treated with thrombolysis (i.e., acute hypothenar ham-
mer syndrome and acute digital artery thrombosis)
B. Angiography interpretation tips
1. In the setting of thrombosis or disruption of vascular structures, accurate
interpretation of upper extremity angiography requires a detailed under-
standing of the location and pathways of collateral vascular structures (see
“Anatomy”).
2. The increasing availability of real-time images (as compared to captured hard
copy images) greatly enhances the surgeon’s ability to estimate the extent of
injury and quality of collateral flow.
3. Communication between hand surgeon and interventional radiologist is vital
in obtaining the images pertinent to diagnosis/reconstruction (magnifica-
tion, vasodilatation, and runoff views), as well as to cooperate in therapeutic
modalities (i.e., thrombolysis).
4. Vessel injury or thrombosis may be more distal than demonstrated on
angiography. Vessels generally fill with contrast to the level of the last patent
perforator/branch, not to the level of the thrombus/injury.
5. Absence of contrast filling of structures distal to the injured structure does
not indicate diffuse thrombosis. Patent distal structures will often not fill with
contrast without a collateral vessel pathway for the contrast to reach them.
6. When having difficulty discerning the identity of a single patent large vessel
in the forearm, recall that the common interosseous artery is a branch off the
ulnar artery.
7. When having difficulty discerning the identity of a single patent palmar arch of
the hand, recall that the deep arch is supplied primarily by the large dorsal branch
of the radial artery after it passes between the bases of the first and second meta-
carpals. Also recall that the deep arch traverses the palm at the level of the base of
metacarpals 2 to 5 (proximal to the normal location of the superficial arch).
IV. Operative Exploration
A. Operative exploration is indicated in the majority of cases of suspected arterial

injury. Operative exploration may not be indicated in the setting of
1. Unstable patient or concomitant injury whereby operative exploration is
deemed too risky

2. Injury is deemed nonreconstructable (arterial injection injury with damage

extending beyond levels reconstructable)
3. Treatment with thrombolytic intervention (acute vessel thrombosis, injec-
tion injury, and frostbite)
B. Operative exploration tips
1. Make sure a clear vascular assessment is made before intervention (i.e.,
Doppler examination) so that improvement or deterioration of perfusion can
be determined after reconstruction.
2. Extensile exposure is critical to adequately assess the zone of injury and per-
mit execution of the best reconstruction possible.
3. When isolated segment of vascular injury is identified, use of noncrushing vas-
cular clamps will allow the reassessment of limb perfusion after tourniquet is
released. The need for reconstruction of this structure can then be determined.
4. Damage to the vessel intima is best assessed under microscope magnification.
Resection back to healthy vessel and liberal use of grafts to avoid repair under
tension are critical to successful reconstruction.
V. Repair or Ligate?
A. The decision to repair a damaged vessel is clear when critical ischemia is evident.
However, in the setting of apparent adequate perfusion via collateral vessels the deci-
sion is more difficult. Intra-operative indicators that perfusion is adequate include
1. Good capillary refill of fingertips
2. Audible Doppler signals at the digital tips
3. Pulsatile retrograde flow demonstrable from the distal end of the transected
vessel
4. Quantitative assessment (digital plethysmography and digital pressure read-
ings). Digital brachial index > 0.7 is indicative of adequate perfusion.
B. In the absence of adequate perfusion, repair should be pursued. Indeed, even in the
setting of adequate perfusion as determined by one of the above indicators, some
centers/surgeons may opt to repair damaged noncritical arterial injuries. Reasons
to consider reconstruction of noncritical vessel injuries are the following:
1. To attempt to avoid the development of critical ischemia in the future after
subsequent trauma or stress (hypothenar hammer syndrome and radial artery
occlusion at the wrist)
2. To attempt to decrease the risk of development of some symptoms of noncrit-
ical, yet “inadequate” perfusion that are poorly understood/measured (cold
intolerance and neural regeneration after associated nerve injury and repair)
3. To restore normal anatomy if the surgical team has the technical capability of
repairing the noncritical vessel without substantially prolonging operative time.
Even in experienced hands, the patency rate of reconstructed noncritical
vessels reported varies between 47% and 82%.
VI. Vascular Grafts
If reconstruction of the injured segment can be achieved primarily without tension,

no conduit is needed. If a significant segment of damaged, thrombosed, or aneurismal
vessel is excised and reconstruction is required, an interposition graft should be used to

avoid tension on the anastomosis. The use of a vein graft in the setting of critical isch-
emia does not increase the chance of thrombosis (as compared to primary repair).
A. Reversed vein grafts: The most common technique. Reversal is necessary to
insure that the valves permit unobstructed flow. Typical donor sites include the
volar wrist (to replace proper digital vessels), the dorsal hand/wrist (to replace
superficial arch or common digital vessels), and the greater or lesser saphenous
veins (to replace brachial, ulnar, or radial artery segments).
B. In situ vein grafts: Segments of roughly parallel coursing veins are transected
proximally and distally and anastomosed to adjacent arterial stumps to provide a
conduit for missing arterial segments. The advantage is appropriate size taper, but
disadvantages to this technique exist and include the need for ligation of branches
and disruption of valves with valvulotome to allow unimpeded antegrade flow.
C. Nonreversed vein grafts: Completely harvested veins inset in a nonreversed
fashion to take advantage of size match and taper of vessel. This technique has
similar advantages and disadvantages of in situ vein grafts.
D. Arterial grafts: Advantages are ease of handling, theoretical increased patency
rate, and appropriate size taper. Expendable arterial graft harvest sites include
thoracodorsal artery, deep inferior epigastric artery, and descending branch of
lateral circumflex femoral artery.
E. Synthetic shunts: These are commercially available conduits that may be utilized
in the setting of prolonged critical ischemia prior to presentation. They enable
the surgeon to rapidly cannulate the proximal and distal ends of the vessel and
allow temporary distal reperfusion prior to further surgical intervention.
VII. Specific Considerations for Anatomic Location of Arterial Injury
A. Brachial artery—Relationship of brachial artery laceration/thrombosis to the

takeoff of the deep brachial artery can affect the clinical picture. Injuries distal to
this branch may demonstrate adequate distal perfusion via collateral flow from
the deep brachial artery to the radial artery and posterior interosseous arteries
distally. Injuries proximal to this branch will often demonstrate critical ischemia
distally. Despite adequate collateral flow, repair of identified brachial artery inju-
ries is indicated.
B. Radial or ulnar arteries at the wrist forearm—Adequate digital perfusion is usu-
ally seen in single radial or ulnar artery lacerations due to the presence of a com-
plete deep or superficial palmar arch. In this setting, the decision to reconstruct
or ligate is made based on the patient’s medical status, associated injuries, and
the surgeon’s judgment.
C. Radial and ulnar artery injuries at the forearm/wrist—This injury may dem-
onstrate adequate distal perfusion through the interosseous arteries. More
commonly critical ischemia is evident. At least one of the vessels should be
reconstructed and perfusion reassessed. Both vessels may be reconstructed at the
discretion of the surgeon even in the setting of adequate perfusion achieved by
a single repair.
D. Superficial palmar arch (SPA)—This is the only vascular arch of the hand rou-
tinely repaired or reconstructed. Thrombosis, laceration, or avulsion of some
or all of this structure requires assessment of perfusion of each digit with the
findings/tools discussed above. Adequate distal perfusion may exist even in

the setting of complete avulsion of the Superficial palmar arch (SPA) through
collateral flow from the deep and dorsal arches. Inadequate perfusion may
require repair ranging from primary anastomosis to multiple branched graft
reconstruction with several anastomoses to distal common digital vessels.
E. Common digital arteries—Adequate distal perfusion may be maintained to
both digits supplied by the injured vessel due to blood supply from adjacent
common digital vessels to contralateral proper digital vessels.
F. Radial or ulnar digital vessels—Single digital artery injury is noncritical in the
absence of previous injury to the digit. These are routinely ligated if adequate
distal perfusion is evident.
G. Radial and ulnar digital artery injuries—These are often noncritical in the
thumb due to adequate dorsal circulation reaching the tip of the digit. These
often demonstrate inadequate perfusion in the nonthumb digits if they occur at
or proximal to the PIP join and require reconstruction.
VIII. Thrombolytic Therapy
The use of thrombolytic intervention for lower extremity vascular disease is well estab-
lished and widely employed. The use of similar techniques in upper extremity vascular
injury requires further study, but is being employed for
A. Acute ischemia due to thrombosis of discrete segment of upper extremity artery
from axillary artery to fingertip
B. Effects of embolic disease to the digits from more proximal injury
C. Arterial injection injuries
D. Arterial cannulation injuries
E. Digital frostbite
IX. Arterial Injection Injuries
Most often caused by drug abuse, iatrogenic injury, or work-related injection injuries.
These cause a devastating and often diffuse endarterits, thrombosis, and vasospasm that
result in critical ischemia of one or more digits. Assessment includes all modalities listed
above including arteriography in the hope of finding discrete segments of vessels that
may be reconstructed. Usually damage extends to the distal fingertips and reconstruc-
tion is not possible; surgical care is limited to fasciotomies if required. Nonsurgical
treatment modalities reported include
A. Thrombolytics
B. Heat
C. Heparin/dextran
D. Steroids
E. Vasodilators
X. Digital Ischemia in Critically Ill Patient on Vasopressors
These patients demonstrate inadequate distal perfusion in the setting of vasoconstric-

tion. This usually indicates preexisting vascular abnormality in the upper extremity

(i.e., incomplete arch, previously asymptomatic hypothenar hammer syndrome, or

radial artery occlusion at the wrist). Assessment of the blood flow may be performed
with handheld Doppler probe or digital pressure recordings. Often these patients are
not candidates for surgical reconstruction and non-surgical modalities are utilized to
avoid critical ischemia until the vasopressors are no longer required. These modalities
can include
A. Aspirin
B. Heat
C. IV heparin (if not contraindicated for other reasons)
D. Transcutaneous nitroglycerine ointment
E. Botulinum toxin (experimental)
F. Viagra (experimental)
XI. Indications for Compartmental Fasciotomy Distal to Vascular Injury
A. Suspicion/evidence of increased compartment pressures prior to revascularization

B. Delayed revascularization (no consensus on duration)
C. Anticipated risk of compartment syndrome after revascularization
XII. Closed Osseous Injuries Associated with Vascular Compromise

at Time of Injury or Reduction
A. Anterior shoulder dislocations

B. Supracondylar fractures in children
C. Elbow dislocations
Perfusion is reassessed after acceptable reduction and is usually restored. Operative
exploration is indicated when critical ischemia persists following reduction.
Suggested Readings
Borman KR, Snyder WH III, Weigelt JA. Civilian arterial trauma of the upper extremity. An
11 year experience in 267 patients. Am J Surg. 1984;148(6):796–799.
Fitridge RA, et al., Upper extremity arterial injuries: Experience at the Royal Adelaide Hospital,
1969 to 1991. J Vasc Surg. 1994;20(6):941–946.
Hammond DC, Gould JS, Hanel DP. Management of acute and chronic vascular injuries to the
arm and forearm. Indications and technique. Hand Clin. 1992 Aug;8(3):453–463.
Hess AV. Treatment of vascular injuries from penetrating and nonpenetrating trauma. Hand Clin.
1999;15(2):249–259.
Raskin KB. Acute vascular injuries of the upper extremity. Hand Clin. 1993;9(1):115–130.

Vascular Conditions
22
Michael Alexander McClinton
Vascular ‘conditions’ generally fall into two categories: Vascular mass or ischemia. An
estimated 10% of the U.S. population has some form of ischemia. This may be a chronic non-
limb-threatening annoyance or may jeopardize digit or limb survival. The vascular workup
determines whether immediate treatment is indicated or whether the patient may, with a
few lifestyle modifications, live with the condition. A vascular mass should be suspected any
time that a tumor overlies the course of an artery, or there are embolic symptoms at the distal
arterial tree, especially if this is unilateral. This chapter will review the anatomy, physiology,
and medical evaluation of vascular lesions, followed by the individual conditions.
I. Definitions
A. Functions of vascular system

1. Delivers oxygen and nutrition to cells
2. Core temperature maintenance
3. Removes waste products of metabolism
B. Vascular incompetence—Koman: Inadequate arterial inflow due to structural
damage to arteries, or inappropriate vascular control from nerve or hormonal
abnormality
C. Critical vascular event versus noncritical vascular event—Koman
1. Critical: Tissue death and necrosis without intervention
2. Noncritical: Collateral circulation maintains tissue viability
II. Anatomy
A. Macroarterial upper extremity vascular system (see Ch 21, Section 1.)

1. Begins at the heart and great vessels
2. Brachial artery branches just distal to the antecubital fossa
3. From that point on there are redundant vascular channels
a) Forearm: Radial, ulnar, and interosseous arteries
b) Wrist/hand: Superficial, deep palmar, and dorsal arterial arches
c) Digits: Radial, ulnar digital arteries, and digital arches
4. Superficial palmar arterial arch is complete in 80% of hands, that is, either
radial or ulnar artery can supply all digits. The deep palmar arterial arch is
complete in 97% of hands.
B. Microarterial system
1. Peripheral vascular system vessels are less than 100 μm in diameter or circum-
ference?
a) Smooth muscle in arterial wall is sensitive to circulating chemicals and
local sympathetic nerves.
b) Blood flows between arteries and veins either through nutritional capil-
lary beds or through parallel thermoregulatory AV shunts.
433

2. Only 10% of arterial flow is needed for skin viability; 90% is for temperature
regulation.
3. If blood flow is inadequate to the nutritional capillary beds, tissue ulceration,
ischemia, and necrosis may occur.
III. Blood Flow Physiology
A. Larger vessels follow laws of fluid dynamics: diameter, pressure, and

resistance
B. Critical arterial stenosis: Blood flow decreases minimally with reduction in arte-
rial diameter until a critical point, about 50%.
C. Vascular wall control: Central nervous system and local vascular control act
through nerve innervation or circulating vasoactive chemicals including
vasoconstrictors, vasodilators, and thrombolytic or thrombogenic substances.
D. Compensatory mechanisms to combat ischemia following stenosis: Arterial
dilatation, collateral vessel formation, and lowered arterial resistance secondary
to vasodilators released from the vessel endothelium.
IV. Evaluation
A. Office evaluation
1. Medical history
a) Usual complaints: Vascular mass or ischemic symptoms
b) Acute or chronic trauma including repetitive hand injury or vibration
exposure
c) Systemic illnesses: Hematologic, metabolic (diabetes), connective tissue,
and atherosclerosis
d) Medication/drug exposure especially vasoactive drugs
e) Tobacco products
2. Physical examination
a) Inspection of upper limb skin and fingernails for rash, ulcerations, splinter
hemorrhages, scars, narrowing of the nails (sclerodactyly), clubbing, and
hair pattern
b) Hand color: Pale, redness, and cyanosis
c) Temperature differences between upper limbs or between individual dig-
its
d) Masses with overlying audible bruit or palpable thrill
e) Arterial pulses at elbow and wrist
3. Allen test: Compress both arteries at the wrist, patient closes and then
opens fist, sequentially release one then the other artery. Look for time and
completeness of blood return to the digits. Longer than 6 seconds indicates
narrowing or occlusion of a wrist artery.
4. Doppler examination: Ultrasonic flowmeter measures blood flow by detecting
the changing frequency of reflected sound waves from moving red blood cells.
The output data from the Doppler are converted to audible sound waves.
Listen to wrist and palmar arch arterial sounds, then digit sounds. Occlude
sequentially radial and ulnar arteries while listening to digital sounds to
augment findings from the Allen test.

Chapter 22 • Vascular Conditions 435
5. Digital Allen test: Doppler distal pulp of a finger while occluding first the
radial and then the ulnar digital artery. Test determines if a digital artery is
occluded.
6. Additional tests
a) Echocardiogram to look for surface abnormalities in the heart that could
be the source of emboli to the upper limb (valvular vegetation, atrial myx-
oma, atrial thrombus, septal defect)
b) Blood studies primarily aimed at detecting clotting disorders and vasculitis
B. Noninvasive vascular testing
1. Greatly extends the clinician’s office evaluation
a) 97% agreement between noninvasive testing and findings from arteriog-
raphy and surgery
b) Identifies location of vascular pathology
c) Determines the severity of vascular compromise
d) Allows repeated follow-up of nonsurgical and surgical therapy
2. Segmental arterial pressure measurements
a) Single most valuable laboratory tool
b) Doppler unit and an occlusive pressure calibrated cuffs allow the mea-
surement of systolic blood pressure at any level along the extremity and
between extremities
c) Greater than 15 mm Hg difference between different extremities or
different levels on the same extremity is usually significant
d) Mean arterial pressure less than 70 mm Hg denotes ischemia
3. Digital/brachial index (DBI) standardizes the different digit arterial
measurements by dividing them by the higher of the two brachial arterial
pressures. This measurement allows standardized testing and reporting
between different persons. Normal DBI—1.0; ischemic DBI—<0.7
4. Pulse volume recording (PVR, plethysmography)
a) Volume changes in the digits correlate with arterial inflow and egress,
which is converted to an analog signal.
b) Characteristic pulse volume tracings for normal, stenotic, and occluded
vessels
c) Cold stress testing applied to the hands; then measuring PVR identifies
patients with vasospastic disease.
5. Color duplex imaging
a) Color-coded combination of Doppler signal and pulse-echo that gives an
actual image as well as flow information.
b) Compared to arteriogram, this technique is noninvasive, cost efficient,
repeatable, and portable; the images are less distinct
c) Indicated for evaluation of masses to determine whether they are vascular,
for example, wrist volar ganglion versus radial artery aneurysm
d) Can also be used to study vascular perfusion in ulnar artery thrombosis,
acute arterial trauma, and postoperative arterial repair problem
6. Skin surface temperature: Digital skin temperature measurements correlate
with total blood flow below 30° C
C. Radiologic evaluation
1. Magnetic resonance imaging (MRI)
a) Noninvasive, low risk of vascular spasm
b) Nonionizing radiation, or iodinated contrast reactions
c) Useful for evaluating congenital and acquired masses

2. Magnetic resonance arteriography (MRA)

a) Blood flow highlighted to show vessels
b) Difficult in small, stenotic, or occluded vessels
c) Gadolinium-enhanced test improves visualization of vascular structures
3. Contrast arteriography
a) Gold standard for vascular evaluation
b) Best anatomic and structural arterial detail
c) Risks with this technique preclude its use as a screening tool for extremity
ischemia
d) Generally, catheter is inserted into the femoral artery and passed through
the aorta to the great vessels and extremity arteries
e) Have radiologist use intravascular vasodilators
f ) Communication with the radiologist performing the procedure is critical
to obtain specific and accurate information
g) Begin at the great arch and proximal vessels to rule out vascular thoracic
outlet syndrome
h) Complications: Injection injury to the catheterized artery; catheter-
induced vasospasm; emboli dislodged; vasospasm distorted picture of the
distal arterial tree; intervention is possible with thrombolytics through
the catheter
V. Congenital Vascular Disorders
Definition: Confusing terminology, because “hemangioma” is often used to refer

to any vascular growth in a child. The important point is to distinguish between
a hemangioma (an involuting tumor) and venous malformation (a noninvoluting
tumor).
A. Hemangioma
1. True tumor
2. 30% visible at birth, 90% present by 4 weeks
3. Rapid growth, followed by slower growth
4. Maximum size by 10 to 12 months
5. Involution: 50% gone by 5 years and 70% by 7 years
6. More common in females indicating a possible hormonal association.
7. Evaluation: MRI can evaluate mass and determine high flow or low flow
status
8. Treatment
a) If discrete, observation for signs of regression
b) Nonsurgical Rx: Corticosteroids for large hemangiomas, those causing
high output heart failure in neonate
c) Surgical Rx: Rarely need to excise
9. Kassabach-Merritt syndrome is thrombocytopenia, often with spontaneous
bleeding due to the destruction of platelets in the hemangioma. Requires
steroids, tumor compression, or surgical excision of the hemangioma.
10. Capillary hemangioma (Port wine stain)
a) Present at birth
b) Flat, pink, circumscribed
c) Proportionate growth with child

d) May be associated with internal vascular malformations

e) Laser can be used to ablate these lesions for cosmetic reasons
B. Venous malformation
1. Most are present at birth.
2. Does not involute
3. Commensurate growth with the child. May see some growth acceleration
due to increased female hormone activity.
4. Soft, compressible mass that engorges with dependent position and flattens
with elevation
5. Diagnosis
a) Phleboliths may be seen on radiographs
b) MRI helpful in determining whether the lesion is low or high flow and its
extent
6. Treatment
a) Localized tumor may be surgically excised
b) Sclerotherapy (injection of caustic substance, e.g., ethanol)
c) Diffuse lesions are best observed, because excision is generally not cura-
tive for extensive lesions and may damage normal tissue
d) Evaluation for a coagulation defect in the child
C. Arteriovenous malformation (AVM)
1. Myriad vascular connections, large and small, between major arteries and the
venous system
2. Blood flows rapidly from the high pressure arterial to the low pressure venous
systems, that is, shunted
3. Distal extremity ischemia secondary to AVM arterial shunting is common
4. Diagnosis
a) Mass with thrill and bruit. Spontaneous bleeding may occur.
b) Distal hand/digit pain may occur
c) Puberty seems to stimulate significant growth of these tumors
d) Plain radiographs may show characteristic calcifications
e) Repeat Duplex scanning can be used to safely follow AVMs over time
f ) Arteriography demonstrates the extent of arterial enlargement and shunt-
ing
g) MRI shows the extent of the soft tissue mass
5. Treatment
a) Extremely difficult surgical problem
b) Observe unless symptomatic with cardiac, peripheral ischemia, bleeding,
or pain problems
c) Medical management: Compressive garments may control size and symp-
toms initially. Calcium channel blockers or alpha blockers may improve
blood flow and reduce ischemic pain.
d) Interventional radiologist is helpful with diagnosis and treatment of
AVM. Elective embolism may be preoperative adjunct to surgical exci-
sion, decreasing size of lesion and intraoperative blood loss. It is typically
performed 24 to 48 hours prior to surgical excision
e) Surgery for localized tumors that can be entirely excised. Larger lesions
require team approach and may require cardiopulmonary bypass to reduce
blood loss for massive AVM resection. Amputation may be ultimate
solution for recalcitrant and life-threatening tumors.

VI. Hypothenar Hammer Syndrome
Definition: Ulnar artery occlusion at the wrist is the most common occlusive disorder
of the upper extremity. Perform an Allen test during every hand examination that you
do, and you will diagnose this common vascular disorder.
A. Physiology
1. Chronic trauma to ulnar artery at its exit from Guyon canal
2. Ulnar artery covered only by palmaris brevis muscle and subcutaneous tissue
3. Hook of hamate functions like an anvil when the palm of the hand is used
like a hammer, hence hypothenar hammer syndrome
4. Chronic ulnar artery trauma may cause periadvential arterial scarring and
external compression; intimal and medial layer damage. Ulnar artery throm-
bosis or aneurysm formation may occur producing downstream emboli
B. Diagnosis
1. Laborers who use their hands as hammers, that is, carpenters, auto body shop
workers, and mechanics
2. High association with smoking history
3. Tender mass in palm, possibly pulsatile
4. Cold sensitivity or frank ischemic symptoms, especially ring and small fingers
5. Adjacent ulnar nerve symptoms from compression
6. Allen test: Reduced or no flow through ulnar artery
7. Noninvasive vascular testing confirms Allen test and demonstrates reduced
arterial pressures in the affected digits
8. Duplex and MRA studies will show arterial occlusion or aneurysm formation
9. Arteriogram outlines both radial and ulnar artery course and level of ulnar
artery obstruction. Distal palmar and digital artery outflow may also be seen.
C. Medical management
1. Cease tobacco usage. Nicotine patches may be utilized if necessary.
2. Medication: Calcium channel blockers; stellate ganglion, brachial plexus, or
local anesthetic blocks for acute critical ischemia of the digits
D. Thrombolytic therapy
1. Best if ulnar artery thrombosis is recent
2. May be used as adjunct to operative exploration and bypass to clear clot from
common and proper digital arteries
3. Given intravenously or intra-arterially (through catheter or directly into
ulnar artery during operative exploration)
4. Retevase (recombinant t-PA), streptokinase, and urokinase generate plasmin,
which has fibrinolytic activity
5. Bleeding complications, up to 10%, can occur anywhere in the body
E. Operative treatment
1. Excision of aneurysmal or thrombosed segment without reconstruction = Leriche
sympathectomy
a) Removes source of downstream emboli
b) Surgical sympathectomy
2. Arterial repair
a) Must resect to undamaged artery proximal and distal to thrombosed or
aneurysmal area
b) Ulnar artery aneurysms may be amenable to direct arterial repair after
resection if they are small

3. Arterial reconstruction
a) Most commonly a gap between the proximal and distal arterial segments
exists after excision of the damaged segments.
b) Vein grafts are harvested from the same arm or a leg (lesser saphen-
ous vein, dorsal foot vein) slightly longer than the defect, reversed, and
sutured between the remaining proximal and distal arterial segments with
the use of the operating microscrope.
c) Recently interest has been generated for the use of arterial grafts to bridge
arterial defects. Cardiac surgeons have used arterial grafts for coronary
artery bypass with improved patency rates.
F. Postoperative management
1. Critical arterial repairs and grafts require close monitoring to detect early
occlusion. Early return to the OR can salvage at least 50% of arterial
repairs.
a) Changes in color, turgor, Doppler signal, and temperature of the extrem-
ity demand further investigation and possible return to the OR.
b) More sophisticated techniques may be used for monitoring arterial
repairs. These include an implantable Doppler that detects changes
in flow directly at the anastomosis. Pulse oximetry has also been
utilized.
2. Controversy exists concerning the best, if any, choice of postoperative antico-
agulant therapy or use of vasodilators. There is no clear evidence that any of
these include patency rates. Choices include
a) Aspirin 80 to 300 mg/day
b) Dextran low molecular weight 10%
c) Low dose heparin therapy
d) Calcium channel blockers
VII. Radial Artery Thrombosis
A. Radial artery can be thrombosed at two specific sites:

1. Dorsal radial artery at or just distal to the anatomic snuffbox
a) Thumb and index finger are primarily ischemic
b) Medical management is not usually successful
2. Thenar hammer syndrome
a) Thrombosis of the palmar radial artery from repetitive trauma
b) Relatively new entity
c) Thumb and index finger are most often symptomatic
1. Excision of thrombosed segment
2. Reconstruction is similar to that for the ulnar artery
VIII. Arterial Aneurysms
Definition: Permanent localized vessel wall dilatation of 50% or greater above the
normal arterial wall diameter. Two aspects of causation: Arterial wall weakness, and
mechanical stress secondary to chaotic arterial blood flow. Ulnar artery is the most
common site for true and false aneurysms of upper extremity. Aneurysm presence may
be heralded by downstream emboli.

A. True aneurysm
1. All three layers of arterial wall involved
2. Blunt trauma to the artery with resultant gradual vessel wall dilation
3. Diagnosis
a) Duplex accurately shows this lesion
b) Noninvasive vascular testing demonstrates whether the aneurysm is
occluded and the condition of the downstream digital artery blood flow
4. Treatment
a) We recommend excision of the aneurysm before embolization occurs.
b) End-to-end repair may be possible after aneurysm excision.
c) Repair or reconstruction, rather than simple arterial ligation, is recom-
mended if the DBI with noninvasive vascular testing is less than 0.7 in
affected digits.
B. False aneurysm
1. Follows full thickness arterial wall injury with bleeding after penetrating
trauma or a chronic arterial cannulation injury. Blood becomes encapsulated
creating pulsatile hematoma and out-pouching of the arterial wall.
2. Diagnosis
a) Mass is palpable along the course of an artery. May be pulsatile.
b) Intermittent bleeding is often reported by the patient after penetrating
trauma and aneurysm formation
c) Duplex scanning
d) Arteriography for structural detail
3. Treatment
a) Excision of the aneurysm.
b) Arterial ligation/repair/reconstruction as indicated.
c) Percutaneous injection of thrombin, to cause the aneurysm to occlude
and disappear, has been reported recently. Check with your vascular
surgery colleagues.
C. Digital artery aneurysm
1. Diagnosis
a) Soft tissue mass of a finger or thumb, nonpulsatile
b) Often unsuspected as an aneurysm before exploration
c) Transverse but not longitudinal movement of the tumor on preoperative
examination
2. Treatment: Excision with or without repair/vein graft, if the involved artery
is critical for digit survival
D. Mycotic aneurysm
1. Caused by hematogenous or local arterial wall infection.
2. Virtually all are now the result of intravenous drug abuse.
3. Think of this condition when a cutaneous infection overlies the course of a
peripheral artery, to avoid inadvertent incision and drainage into an arterial
structure.
4. Treatment: Excision of the infected segment with/without arterial bypass.
IX. Arteritis/Systemic Conditions
Definition: A diverse group of diseases that provoke acute or chronic inflammatory

changes in walls of small, medium, and large arteries. Usually, this is one facet of a

widespread disease process and systemic symptoms, for example, fever, arthralgias,
weight loss, and skin lesions may be present.
A. Diagnosis
1. Laboratory studies include
a) Sedimentation rate
b) Immunoglobulin screening
c) Connective tissue disease screening
2. Early identification of the specific disease is crucial, because critical organ
systems may also be affected
B. Buerger disease (thromboangiitis obliterans)
1. Inflammatory occlusive disease of small-sized and medium-sized arteries and
veins.
2. Smoking history.
3. Onset before age 50 years.
4. Arterial lesions distal to the elbow and knee with migratory phlebitis.
5. No other arteriosclerotic risk factors except smoking.
6. Noninvasive vascular testing indicates the location and degree of arterial
obstruction and ischemia.
7. Arteriography usually is necessary to determine arterial out flow feasibility of
bypass.
9. All nonsurgical therapy begins with the cessation of cigarette smoking. If
smoking does not stop, additional therapy will not be successful.
10. Surgical therapy includes
a) Arterial bypass if feasible.
b) If direct bypass is not possible, indirect or salvage methods include arte-
rialization of the venous system (reversal of flow) by joining the distal
dorsal venous network to the brachial artery; or microvascular omental
transfer that is inserted beneath the dorsal forearm and hand skin for
indirect revascularization.
C. Diabetes mellitus
1. Diabetes is a common source of lower extremity ischemia but less often a
cause of upper limb arterial disease.
2. Calcification of arterial walls may preclude arterial bypass.
D. Atherosclerosis
1. Atheroslerosis is usually seen in the proximal left upper limb subclavian and
axillary level or lower limb and much less frequently in the hand.
2. Distal hand and digit symptoms are usually due to embolization from the
proximal vessels.
3. Comparison of brachial pressures from each side, looking for more than
20 mm Hg difference, will demonstrate proximal vascular occlusion.
4. Reduced radial artery pulse on the affected side.
5. Bruit is audible over the subclavian artery.
6. Repair is usually undertaken by general vascular surgeons.
E. Additional arteriopathies
1. Connective tissue disorders, for example, lupus erythematosis, rheumatoid
arthritis, and scleroderma, result in digital ischemia when antigen-antibody
complexes are deposited in the vessel walls. These complexes cause external
fibrosis and intimal damage with thrombosis.

2. Ischemia may be the result of release of tumor-related antigens. Ask patients

with undiagnosed ischemia whether they have a malignant process, and
search for this in older patients even in the absence of a tumor history.
3. Sepsis is another cause of ischemia and digit loss secondary to released
endotoxins.
4. Newborns are prone to thrombotic and embolic disease because of a poorly
developed fibrinolytic capacity. Thrombolytic therapy may be effective in
these small patients.
5. Less common causes of arteritis include giant cell arteritis, Wegener granulo-
matosis, polyarteritis nodosa, and Takayasu arteritis.
6. Calcific vascular disease, as seen in patients with end-stage renal disease, often
require end stage reconstructive efforts, such as arterialization of the venous
system or free omental transfer.
X. Vasospastic Disease (Raynaud’s Syndrome)
Definition: Episodic attacks of small vessel constriction in the distal extremities in

response to cold or emotional stress. No etiology is implied.
A. Evaluation
1. Complete medical history looking for blood disorders and drug exposure
2. Smoking history
3. History of repetitive or vibration work trauma or frostbite
B. Testing
1. Noninvasive vascular testing with cold stress demonstrates inappropriate
vasoconstriction with cold exposure.
2. If occlusive arterial disease is suspected, arteriography will demonstrate struc-
tural integrity of the vessels.
XI. Primary Vasopastic Disease (Raynaud’s Disease)
Definition: Vascular system is structurally intact without fixed obstruction; therefore,

no ulceration, gangrene, or digit loss is seen.
A. Medical treatment
1. Avoidance of cold stress
2. Calcium channel blockers are the drugs of choice
a) Prevention of calcium influx into smooth muscle interfering with
vasospasm from sympathetic nerve stimulation.
b) Nifedipine 30 to 60 mg per day in a long-acting form.
3. Tricylcic antidepressants (Elavil) and serotonin reuptake inhibitors (Prozac,
Paxil, Zoloft) have been helpful in decreasing sympathetic tone and in
treatment of the frustration and depression associated with chronic severe
vasospastic conditions.
4. Consider aspirin in patients with a likelihood of vascular thrombosis.
5. Prostoglandins have been used for digit-threatening disease.
6. Botox is a new addition to medical management
a) Smooth muscle paralysis-vessel dilation—the actual mechanism of action
is under investigation at the time of this publication, but is different from
the effects on skeletal muscle.

b) Onset of effect is almost immediate, as opposed to several days when used

in skeletal muscle.
c) Repeated injections are needed, possibly every 3 months.
B. Surgical management: Surgical sympathectomy at hand or digit level (see below).
XII. Secondary Vasospastic Disease (Raynaud’s Phenomenon)
Definition: Structural arterial damage secondary to underlying connective tissue disease

process
A. Evaluation
1. Noninvasive vascular testing with cold stress and local anesthetic blockade
analysis determines the severity of ischemia and potential benefit of sym
patholytic procedures.
2. Obtain an arteriogram on patients with digit-threatening secondary vasos-
pastic disease to determine whether they are candidates for revascularization
procedures such as arterial bypass.
3. Prognosis depends on degree of arterial obstruction.
B. Medical treatment
1. Medical management is similar to that used for primary vasospastic disease
2. Botox has been helpful for about three months per treatment
3. May not help obstructive conditions
C. Surgical management
1. Cervicothoracic sympathectomy: Benefit may be temporary
2. Leriche sympathectomy (arteriectomy)
a) If collateral flow exists, the thrombosed segment is removed and no bypass
is needed.
b) Excision of the arterial segment interrupts the sympathetic fibers.
3. Peripheral sympathectomy
a) Initially, individual digital level sympathectomy performed (Flatt, Wilgis)
b) Now radial, ulnar, and palmar level sympathectomy carried out for
multiple digit disease (Koman)
c) Koman has demonstrated sympathectomy can increase percentage of
nutritional blood flow without increasing total blood flow
d) Palmar and/or digital sympathectomy: may be used as an adjunct to
improve healing after digital amputation
4. Arterial bypass with vein grafting: Best option for patients with occlusive
disease and vasospasm if sufficient outflow present
Suggested Readings
Koman LA, et al. Vascular disorders. In: Green DP, Hotchkiss RN, Pederson WC, Wolfe SW,
eds. Green’s Operative Hand Surgery. Philadelphia, PA: Elsevier Churchill Livingstone; 2005;
2:2265–2313.
McClinton MA, Wilgis EFS. Ischemic conditions of the hand. In: Mathes SJ, Hentz VR, eds.
Plastic Surgery. Philadelphia: WB Saunders; 2006;7:791–822.
Mulliken JB, Glowacki J. Hemangiomas and vascular malformations in infants and children:
A classification based on endothelial characteristics. Plast Reconstruct Surg. 1982;69:412.
Upton J, Marler JJ, Pap SA. Vascular disorders: Arteriovenous malformations. In: Berger RA,
Weiss A-PC, eds. Hand Surgery. Philadelphia, PA: Lippincott Williams & Wilkins; 2004;2:
1615–1642.

Osteonecrosis
23
Raymond S. Fryrear and Steven L. Moran
I. Introduction
Avascular necrosis (AVN) is defined as cellular death of bone components due to

interruption of the blood supply. This results in eventual bone collapse, joint destruc-
tion, pain, and loss of joint function. AVN is associated with numerous conditions
and usually involves the epiphysis of long bones, such as the femoral head, humeral
head, and the femoral condyles, but the small bones of the wrist can also be affected,
including the lunate, scaphoid, and capitate.
II. Etiology
AVN within the hand and wrist is often idiopathic, with no antecedent trauma or iden-
tifiable cause; however, several risk factors have been identified for the development of
AVN in long bones and these include:
A. Corticosteroids: The most common proposed mechanism of AVN due to corti-
costeroid use is related to mobilized lipids from the liver that occlude end arteries
in the bone. While the risks of long-term steroid use have had the most investiga-
tion, there are numerous case reports of short-term corticosteroid use resulting
in AVN. The endogenous overproduction of corticosteroids, which occurs in
Cushing syndrome, may also predispose to the development of osteonecrosis.
B. Collagen vascular disorders: Conditions such as rheumatoid arthritis, sclero-
derma, SLE, and dermatomyositis can produce a vasculitis, which can lead to the
occlusion of arteries and arterioles resulting in the disruption of bone blood flow.
Treatment of these diseases usually includes the regular use of corticosteroids
placing these patients at a higher risk of AVN.
C. Alcoholism: Chronic alcoholism and associated fatty liver disease are thought to
increase the incidence of fat emboli, which may, in turn, lead to the development
of AVN. The femoral head is the most common location for this to occur.
D. Sickle cell disease: The sickle-shaped cells in this disease can result in small ves-
sel thrombosis and bony infarcts. When AVN occurs in patients with sickle cell
disease, it usually occurs in bones that are actively participating in hematopoiesis.
E. Other proposed causes of AVN may include Caisson disease, a condition where
nitrogen bubbles are released out of solution from cells and result in embolism
production. Gout has also been reported as a risk factor for AVN with approxi-
mately 30% of patients with gout experiencing some form of AVN.
III. Pathogenesis
The pathogenesis of osteonecrosis is commonly divided, artificially, into four different

phases: the avascular phase, the revascularization phase, the repair phase, and the deformity
phase. Histological and radiographic changes are associated with each of these phases.
444

Chapter 23 • Osteonecrosis 445
A. Avascular phase: This first step in the process of osteonecrosis begins with an infarc-
tion to a section of the bone. This infarction typically takes place within fatty marrow
adjacent to the subchondral cortex of the bone. The infarction at the subchondral
portion of the bone leads to bone loss. As the subchondral bone becomes necrotic,
the overlying cartilage hypertrophies as it attempts to convert itself to bone.
The radiographic changes that correspond to this first phase are often minimal.
Osteopenia or subtle soft tissue changes may be appreciated. The osteopenia is
not due to the infarction itself, but hyperemia surrounding the involved area as
well as synovitis and increased osteoclastic activity.
B. Revascularization phase: Increased osteoclastic and osteoblastic activities are
seen during this stage. Radiographs may show areas of lucency and sclerosis.
Increasing cell death beneath the articular surface results in fragmentation and
collapse of the overlying cortex.
C. Repair phase: The repair phase actually begins when revascularization begins.
There is a variable degree of reconstitution and healing that is dependent upon
1. The degree of blood loss and cell death in the initial insult
2. The patient’s immune system and healing response
3. Whether the joint is weight bearing versus nonweight bearing
D. Deformity phase: The deformity phase is highly variable and site specific. It is
also dependent upon ongoing loading to the bone (weight-bearing areas show
increase in deformities).
IV. AVN in the Hand and Wrist
AVN is most frequently found in the scaphoid, lunate, and capitate. Isolated ischemia
of the other carpal bones is exceedingly rare.
A. AVN of the scaphoid (Preiser’s disease)
In 1910, Preiser described an osteitis of the scaphoid, which was distinct from
that seen in scaphoid fractures. Preiser’s disease is defined as AVN of the scaphoid
occurring in the absence of trauma and/or prior wrist procedures; where at least
80% of the scaphoid shows radiographic changes. This definition allows one
to distinguish Preiser’s disease from AVN of the scaphoid, which is the direct
result of fracture, most commonly proximal pole fracture. The etiology has been
loosely linked to collagen vascular disease, steroid therapy, and repetitive trauma.
This condition has also been reported in children.
1. Clinical presentation and diagnosis
Patients may present with pain within the snuff box, synovitis, or general-
ized wrist pain. Radiographs typically show sclerosis within the scaphoid,
and there is often fragmentation of the proximal articular surfaces. MRI is
valuable for identifying early cases as well as the extent of avascularity. Nor-
mal marrow elements produce high-intensity signals on T1-weighted images.
Avascularity or marrow edema will lead to alterations in these signals. Preiser’s
disease may be graded according to its radiographic and MRI appearance.
a) Stage I: Normal radiographs with a positive bone scan or avascularity on
MRI
b) Stage II: Increased density in the proximal pole on plain radiographs with
generalized osteoporosis
c) Stage III: Fragmentation of the proximal pole on plain radiographs, with
or without pathologic fracture

d) Stage IV: Carpal collapse with osteoarthritis

Kalainov has also described a classification system, which grades the
scaphoid’s avascular status as generalized (Type I) or segmental vascular
impairment (Type II). The differentiation between global ischemia and
segmental ischemia is made with MRI. Those patients with Type II dis-
ease, or localized ischemia, have a more favorable clinical outcome.
2. Treatment
The treatment of Preiser’s disease remains controversial. Multiple treatment
options have been suggested including observation, silicone replacement,
arthroscopic debridement, proximal row carpectomy, and scaphoid excision
with four-corner fusion. The two largest series reported on the treatment if Pre-
iser’s disease includes the use of silicone replacement and proximal row carpec-
tomy. Procedures that attempt to preserve the scaphoid and reverse the effects of
AVN are limited to vascularized bone grafting. Salvaging the scaphoid requires
that the cartilaginous shell of the bone remain intact and the radiocarpal and
midcarpal joints must be free of any arthritic changes. Vascularized bone grafts
from the dorsal distal radius have been reported with some success; however,
equally successful results have been reported with proximal row carpectomy.
Given the lack of reliable treatment options, in the absence of severe pain and
disability a conservative approach may be warranted and should certainly be
discussed with the patient prior to embarking on salvage surgery.
B. AVN of the lunate (Kienböck’s disease)
In 1910, Robert Kienböck described AVN of the lunate. Kienböck’s disease is most
commonly observed in patients from 20 to 40 years of age. The loss of blood sup-
ply to the lunate has been attributed to primary blood vessel occlusion, ligament
trauma, and to single or multiple fractures resulting in secondary vascular impair-
ment. The exact cause of Kienböck’s disease is still the topic of much debate but
the leading theories for the development of Kienböck’s disease are listed below.
1. Ulnar variance
In 1928, Hultén published a study noting that 18 of 23 patients with
Kienböck’s disease had an ulna negative variance at the distal radioulnar joint
(the distal articular surfaces of the ulna was found to be proximal to the
articular surface of the radius on zero rotation PA radiographs). Only five
patients with Kienböck’s disease showed a neutral or zero variant (ulnar neu-
tral), and an ulna-plus relationship was absent from all patients with AVN of
the lunate. Other authors have further verified a relationship between nega-
tive ulnar variance and Kienböck’s disease. Why ulnar variance would cause,
or be associated with the development of Kienböck’s disease is still an area
of speculation. In contrast to the above-mentioned studies, D’Hoore exam-
ined 125 normal wrists and 52 wrists of patients with Kienböck’s disease
and was unable to show a significant association between ulnar variance and
Kienböck’s disease. The association between ulnar variance and Kienböck’s
disease may also be ethnically biased, as studies from Japan have noted that a
negative ulnar variance occurs with equal frequency in the general population
and in patients with Kienböck’s disease.
2. Lunate morphology
In 1966, Antuña Zapico noted an association between the shape of the
lunate and the length of the ulna. He described a Type I lunate, seen in
the ulnar-minus wrists, as having a proximal apex or crest. Types II and III
lunates were rectangular or square and were found to occur with an ulnar

neutral or ulnar positive wrist. Lunate shape may result in a greater potential
for bone fatigue and stress fracture under loads. Fragmentation was more
frequent seen in Type I lunates. Other studies have noted that the ulna-minus
wrists provided poor “coverage” for the lunate. Wrists that are ulnar minus
often have a large portion of the lunate, which extends ulnarly beyond the
radial origin of the TFCC; such a condition may result in the uneven stress
through the bone, with the radial half of the lunate being the most suscep-
tible to compression. A study of load stresses on the lunate has added support
to this theory.
3. Distal radius morphology
Studies have shown that the radial inclination can have an effect on loads
seen within the lunate during wrist motion. Radial inclination has been
shown to be flatter in patients with Kienböck’s disease. In addition, there are
multiple case reports linking Kienböck’s disease with other risk factors for
AVN including disease processes such as lupus, scleroderma, carpal coalition,
sickle cell disease, and corticosteroid use.
4. Clinical presentation and diagnosis
Patients present with pain in the wrist area that is usually aggravated by wrist
motion or gripping. Because of the intracapsular location of the lunate, swell-
ing may be minimal. Tenderness is generally present on the dorsum of the
wrist just distal and ulnar to Lister’s tubercle. There may be pain with axial
loading of the third digit. If presentation is late, stiffness or decreased range
of motion of the wrist may be the only complaint. Carpal tunnel symptoms
and extensor tendon rupture may be present in significant cases. Kienböck’s
disease can occur in skeletally immature patients.
The diagnosis is usually made by x-ray; however, radiographs may appear
normal in the early stages of the disease. If strongly suspected, one should
proceed to MRI or bone scintigraphy. Care must be taken when interpreting
MRI images of the lunate; as ulnolunate impaction can also produce signal
changes similar to those seen in Kienböck’s disease. In cases of ulnar impac-
tion, the signal changes within the lunate are limited to the ulnar aspect. (In
addition, patients with ulnar impaction present with an ulnar positive or neu-
tral wrist.) Most cases of Kienböck’s disease present late where fragmentation
or sclerosis is easily identified on plain radiographs. Late fragmentation of the
lunate results in disruption of the scapholunate and lunotriquetral ligaments.
In such cases, radiographs will show the scaphoid in a rotated in a palmar
flexed position while the triquetrum rotates into extension. The net effect is
one of progressive loss of carpal height and generalized wrist arthrosis.
5. Clinical staging
Radiographic findings may be used to classify the progression of Kienböck’s
disease. The 4 stage grading scale was originally proposed by Stahl and later
modified by Lichtman. The staging system is useful for both discussing treat-
ment options and charting disease progression (or regression) after interven-
tion. Staging is based on the appearance of the lunate on plain x-rays.
a) Stage 0: MRI changes within the lunate or abnormality on the bone scan
with normal x-rays negative. This stage was not in the original grading
system, but with the advent of bone scans and MRI it has become pos-
sible to identify changes that precede radiographic Stage I.
b) Stage I: There is a linear compression fracture within the lunate, but the
remaining bony architecture is normal.

c) Stage II: The density within the lunate is abnormal, but there is no
evidence for significant lunate or carpal collapse.
d) Stage III: The lunate shows signs of collapse. Stage III is often separated
into
1) Stage IIIA, without carpal collapse (i.e., carpal height is normal,
radioscaphoid angle is less than 60 degrees, after Goldfarb et al.,
2006).
2) Stage IIIB, with carpal collapse (diminished carpal height and a
radioscaphoid angle greater than 60 degrees).
e) Stage IV: Extensive osteoarthritic changes are present.
6. Treatment
Treatment for Kienböck’s disease is extremely varied, and most everything
seems to improve symptoms. Until the exact etiology of the disease process
is established, no true consensus will be reached on treatment. In general,
there are four issues to consider when deciding on treatment for Kienböck’s
disease:
a) The stage of involvement (Stage IV disease usually precludes any attempt
at lunate preservation)
b) The patients ulnar variance (patients who are ulnar positive or ulnar neu-
tral are not good candidates for a radial shortening)
c) The patient’s age and level of hand function
d) The presence or absence of arthritis at other joints in the wrist
The most common treatments are listed below:
a. Nonoperative treatment
Tajima surveyed 80 wrists with Kienböck disease seen during a 42-year
period and noted no appreciable difference in the end results of non-
operative versus surgical treatment. Contrary studies, however, have
noted that nonoperative management is associated with eventual
radiographic progression of the disease and carpal collapse.
b. Lunate replacement
Silicone replacement of the lunate was the most popular; unfortu-
nately these implants deteriorated producing particulate synovitis
within the wrist, often resulting in pancarpal degeneration. Other
implant materials such as Vitallium and acrylic have also been used,
but long-term success has not been reported.
c. Intercarpal arthrodesis.
A variety of intercarpal arthrodesis has been performed including
capitate-hamate, scaphotrapezial-trapezoid, and scaphocapitate
arthrodesis. All of these procedures are designed to unload the lunate.
All procedures have met with some measure of success.
d. Lunate unloading procedures.
Multiple procedures have been designed to decrease the forces passing
through the lunate in an attempt to unload the bone and
prevent further collapse. These procedures can be summarized as either
changing the relative height or inclination of the radius and those that
change the shape of the capitate.
i) Radial shortening. Shortening the radius unloads the lunate and
produces beneficial changes in radiocarpal height due to the
proximal displacement of the origin of the radiocarpal ligaments

after the shortening. Studies have revealed that 2 mm of

shortening produces some evidence of lunate decompression.
This procedure, while only applicable in those patients with a
preoperative ulnar minus variance, has been shown to increase
wrist motion, grip strength, and produce signs of revasculariza-
tion within the lunate.
ii) Capitate shortening. Capitate shortening decreases the load on the
lunate by 66%, but increases scaphotrapezial load by 150%. This
procedure is often combined with a capitohamate fusion.
iii) Angular osteotomy of the distal radius. Watanabe and others have
recommended a radial closing wedge osteotomy to unload the
lunate in patients with ulna-neutral wrists. Decreased radioulnar
inclination of the distal radial articular surface unloads the lunate,
placing an increased load through the scaphoid. The greatest clini-
cal and biomechanical improvements have been observed with
wedge resections of 5 to 10 degrees.
e) Lunate revascularization
As with Preiser’s disease, attempts have been made to augment the vascu-
larity of the lunate, in an attempt to reverse the AVN. Revascularization
can occur through direct and indirect means.
a. Vascularized bone graft for Kienböck’s disease. In 1979, Hori et al.
reported their experience with implantation of a dorsal metacarpal
arteriovenous pedicle into the lunate as treatment for Kienböck’s dis-
ease. Free vascularized tricortical iliac bone grafts and pronator pedicle
grafting have also been proposed to treat Stage II and III disease.
b. Radial metaphyseal decompression. This technique is felt to produce
hyperemia within the carpus, which may aid in lunate revascularization.
f ) Salvage procedures
If the lunate itself is beyond repair, some form of wrist salvage procedure
must be employed to stabilize the wrist and reduce pain.
a. Proximal row carpectomy may be performed if the capitate and lunate
fossa are free of arthritic changes.
b. Denervation of the wrist has been advocated for the management of
advanced Kienböck’s disease; however, its long-term beneficial results
are not predictable.
c. Total wrist arthodesis is reserved for the most severe cases.
d. Total wrist arthroplasty is reserved for low demand patients.
C. AVN of the capitate
The capitate is at risk of AVN because the proximal pole is entirely intra-articular
and the bone’s blood supply enters through a distal pedicle; thus fractures through
the waist of the capitate result in a high incidence of AVN within the proximal
pole. Other cases of AVN within the capitate have been attributed to ligamen-
tous laxity, steroid use, and repetitive wrist extension. The natural history of
capitate AVN appears to be one of progressive collapse with variable symptoms.
Verification of the vascular status of the bone may be made with MR imaging.
AVN may be classified into one of three types as described by Milliez.
1. Type I: AVN involving the proximal portion only (the most common)
2. Type II: AVN involving the distal portion
3. Type III: AVN involving the entire capitate.

Treatment options have included bone grafting with vascularized or nonvascularized

bone grafts, midcarpal fusion, and capitohamate arthrodesis.
Diagnosis of capitate fractures and capitate AVN requires a high degree of
suspicion. Pain may be vague and physical examination may reveal little tender-
ness except that present dorsally directly over the capitate head. MRI is often
helpful in making this diagnosis. If the physician makes the diagnosis of a
capitate fracture, he or she should thoroughly inspect the MRI and radiographs
for additional carpal fractures or ligamentous injury. Approximately 50% of
capitate fractures will be associated with concomitant ligamentous and bony
injures within the wrist.
D. AVN of the Metacarpal Head (Dieterich’s Disease)
AVN of the metacarpal head may occur following trauma, systemic Lupus ery-
thematosus, and steroid use; it may also result idiopathically. The long meta-
carpal head is most commonly reported site of occurrence but cases involving
the metacarpal base have also been reported. The disease process is seen more
commonly in males and may occur anytime from preadolescence into adult-
hood. Treatment includes observation, subcortical decompression, curettage and
bone grafting, and arthroplasty. Spontaneous resolution of the AVN has also
been reported.
E. AVN of the Phalanges (Thiemann’s Disease)
Thiemann, in 1909, described a teenage boy with progressive enlargement of the
proximal interphalangeal (PIP) joints of the fingers due to AVN of the proximal
phalanx. Thiemann’s disease is a rare form of AVN affecting the PIP and DIP
joints. This disease process usually occurs in the second decade of life. The typical
presentation is an initial painless swelling of the PIP joint with eventual develop-
ment of pain and deformity. The etiology is not fully understood but this disease
does have a genetic component with an autosomal dominant inheritance pattern
being noted in many series. Sporadic cases have been reported and tend to occur
in males. Pathological changes within the bone are consistent with avascular
osteonecrosis.
Radiographically, irregularity of the epiphyses of the phalanges occurs espe-
cially in the middle fingers. The bones appear broadened, sclerotic, and frag-
mented and may exhibit a medial and lateral osseous excrescence. Eventually
joint space narrowing late osteoarthrosis is often seen; however, many cases will
resolve spontaneously with joint preservation following physeal closure. Addi-
tional conditions that may accompany Thiemann’s disease include Legg-Calve-
Perthes’s disease, bipartite patella, and endocrine abnormalities such as thyroid
enlargement and diabetes mellitus; however, a definitive association has not been
verified. Differential diagnosis includes trauma, infection, thermal injuries, and
juvenile chronic arthritis. Treatment is palliative for most cases, while severe
cases may require arthodesis or arthroplasty.
Suggested Readings
Goldfarb CA, et al. The Lichtman classification for Kienböck’s disease: an assessment of reliability.
J Hand Surg (Am). 2003;28(1):74–80.
Herbert TJ, Lanzetta M. Idiopathic avascular necrosis of the scaphoid. J Hand Surg. 1994;19B:
174–182.
Illarramendi AA, Schulz C, De Carli P. The surgical treatment of Kienbock’s disease by radius and
ulna metaphyseal core decompression. J Hand Surg. 2001;26A(2):252–260.

Kalainov DM, et al. Preiser’s disease: Identification of two patterns. J Hand Surg. 2003;28A:
767–778.
Moran SL, et al. Vascularized bone grafts for the treatment of Kienbock’s disease: A ten-year
experience. in 57th annual meeting of the ASSH. 2002. Phoenix, Arizona, October 4.
Tsuge S, Nakamura R. Anatomical risk factors for Kienböck’s disease. J Hand Surg. 1993;
18B:70–75.
Watanaba K, et al. Biomechanical analysis of radial wedge osteotomy for the treatment of
Kienböck’s disease. J Hand Surg. 1993;18A:686–690.

Dupuytren’s Disease
24
Ghazi M. Rayan
Dupuytren disease (DD) is a fibroproliferative disorder that afflicts primarily the hands
with the development of pathologic tissue that originates from existing normal palmar
fascial structures. The etiology is unknown, the pathology is diverse, and diagnosis can
be difficult in the early stages. The treatment can be challenging, and there is potential
for recurrence. The prognosis is variable depending on the patient’s diathesis or degree
of genetic predisposition.
I. Fascial Anatomy
The palmar fascial complex (Fig. 24.1) of the hand has five components: the radial,
ulnar, and central aponeuroses, the palmodigital fascia, and the digital fascia.
A. The radial aponeurosis has four components:
1. The thenar fascia
2. The thumb pretendinous band
3. The distal commissural ligament
4. The proximal commissural ligament
B. The ulnar aponeurosis consists of three components:
1. The hypothenar muscle fascia
2. The pretendinous band to the small finger
3. The abductor digiti minimi soft tissue coalescence
C. The central aponeurosis is a triangular fascial layer. The apex is located at the
proximal aspect and the fibers extend distally and are oriented longitudinally,
transversely, and vertically.
1. The longitudinal fibers fan out as pretendinous bands of the three central
digits.
2. The transverse fibers make up the natatory ligament located in the distal
part of the palm and the transverse ligament of the palmar aponeurosis
(TLPA), which is located proximally and gives origin to the septa of Leg-
ueu and Juvara. The TLPA distal radial extent is the proximal commissural
ligament.
3. The vertical fibers of the central aponeurosis are the minute vertical bands of
Grapow and the septa of Legueu and Juvara. The vertical bands are numer-
ous, small, strong, and scattered along the palmar fascial complex, and are
most abundant in the central aponeurosis. There are eight vertical septa of
Legueu and Juvara (one along the radial aspect and one along the ulnar aspect
of each finger) (Fig. 24.2), forming seven compartments: four flexor septal
canals that contain the flexor tendons and three web space canals that contain
the common digital nerves and arteries and the lumbrical muscles.
D. The palmodigital fascia is a confluence of several retinacular structures located
between the palm and digits, the most important of which is the spiral band that
connects the palmar and digital fascial structures.
452

Chapter 24 • Dupuytren’s Disease 453
Digital
fascia
NL
Palmodigital
fascia
CA
UA RA
Ulnar aponeurosis (UA) Radial aponeurosis (RA)
Central aponeurosis (CA) Natatory ligaments (NL)

Figure 24.1 An illustration of the five components of the palmar fascial complex.
E. The digital fascia components surround the neurovascular structures, and con-
sist of Grayson ligament volar, Cleland ligament volar, and the lateral digital
sheet of Gossett.
II. Pathology
Dupuytren nodules and cords are pathognomonic of DD. In DD, normal fascial
bands become diseased cords. Typically, these cords progressively shorten, leading to
joint and soft-tissue contractures. These shortened cords cause joint deformity, and
the long-standing flexion deformity leads to contracture of the capsuloligamentous tis-
sue and attenuation of the dorsal gliding structures causing flexion contractures of the

Figure 24.2 An illustration of the septa of Legueu and Juvara*.
metacarpophalangeal and proximal interphalangeal joints. There are many pathologic

structures encountered in DD.
A. Microcords are the diseased Grapow vertical bands. They lead to skin thicken-
ing, which is one of the earliest manifestations of DD. These can mimic callus
formation and make diagnosing early disease difficult.
B. Skin pits are small-depressions in the palmar skin surface. They are pathogno-
monic of DD and develop from the superficial fibers of the pretendinous band
that became diseased, pulling on their attachments into the dermis.
C. The pretendinous cord develops from the pretendinous band and is the cord
most frequently seen in DD. It is responsible for flexion deformity of the meta-
carpophalangeal joint.
D. The vertical cord is the diseased septa of Legueu and Juvara, which is located between
the flexor tendon sheath and neurovascular bundles. Its presence may be responsible
for the associated stenosing tenosynovitis that is encountered with DD.
E. The spiral cord has four origins:
1. The pretendinous band
2. The spiral band
3. The lateral digital sheet
4. Grayson ligament
This cord is encountered most often in the small finger. Initially, the cord spi-
rals around the neurovascular bundle, but as it contracts, the cord straightens
and the neurovascular bundle spirals around the cord, displacing proximally,
superficially, and toward the middle of the digit. This distorted anatomy of the
neurovascular bundle renders it at risk during surgery.

F. The natatory cord develops from the natatory ligament, converting the u-shaped
web-space fibers into a v shape and producing contracture of the second, third,
and fourth web spaces.
G. The central cord is an extension of the pretendinous cord from the palm into the
digit. It courses in the midline and attaches into the flexor tendon sheath near
the proximal interphalangeal joint or the periosteum of the middle phalanx. It
causes proximal interphalangeal joint contracture.
H. The lateral cord is a digital cord that originates from the lateral digital sheet
and attaches to the skin or to the flexor tendon sheath near the Grayson liga-
ment. The lateral cord typically leads to contracture of the proximal interpha-
langeal joint, but can cause flexion contracture of the distal interphalangeal
joint.
I. The abductor digiti minimi cord is also known as the isolated digital cord. It
originates from the abductor digiti minimi tendon and inserts on the ulnar side
of the base of the middle phalanx, but it may attach on the radial side, causing
contracture of the distal interphalangeal joint.
J. The commissural cords on the radial side of the hand have a proximal compo-
nent, which originates from the proximal commissural ligament, and a distal
component, which is the diseased distal commissural ligament. Both of these
cords cause contracture of the first web space.
K. The isolated digital cord (Strickland) displaces the neurovascular bundle cen-
trally after crossing from the base of the proximal phalanx to the flexor sheath
or the periosteum overlying the middle phalanx. It is located most commonly in
the small finger.
L. The thumb pretendinous cord originates from the thumb pretendinous band
and causes flexion deformity of the thumb metacarpophalangeal joint.
M. Extensive palmar fascial complex disease affects multiple palmar and digital reti-
nacular structures, including the longitudinal and transverse fibers with wide-
spread disease in the palm.
III. Clinical Presentation
A. The incidence and prevalence of DD are influenced by geography, gender, and

age. Men are more likely to have the disease than women, and the overall inci-
dence increases with age. The disease is very common among descendants of
the Celts and Whites of Northern Europe. It is common in Scandinavia, Great
Britain, Ireland, Australia, and North America. It is uncommon in southern
Europe and South America and rare in Africa and China.
B. DD is associated with diabetes and is related to alcohol consumption, smoking,
hypercholesterolemia, and infection with human immunodeficiency virus. The
etiology of DD remains controversial with inflammation, neoplasia, and genetics
implicated as causative factors. There is strong evidence that genetic predisposi-
tion is an important factor in the etiology as there is a clearly increased incidence
among relatives of patients with DD, and there have been reports of identical
twins with the disease. The disease seems to have an autosomal dominant mode
of transmission with variable penetrance.
C. The disease can be classified into three phases:
1. Phase I (early phase) consists of skin changes with the loss of normal archi-
tecture and formation of skin pits.

2. Phase II (intermediate phase) consists of the development of nodules and

cords.
3. Phase III (late phase) results in joint and tissue contractures.
D. Advanced contracture of the metacarpophalangeal or proximal interphalangeal
joints will compromise hand function and make it difficult for the patient to per-
form fine motor activities or place the hand in a pocket or glove. Typically, the
disease is progressive, bilateral, with more than one digit involved, and ectopic
manifestations may be present such as involvement of the feet and male genitals.
The ring finger is the most commonly involved digit, followed in order of fre-
quency by the small, long, and index fingers and the thumb. Patients with early
onset, strong family history, or multiple digital involvement, with severe and
rapidly progressive disease are considered to have strong Dupuytren diathesis.
E. Non-Dupuytren disease is a clinical condition that is similar but should not
be confused with DD. Classic DD occurs mostly in Whites, whereas non-
Dupuytren disease occurs mostly amongst other ethnic groups. Non-Dupuytren
disease patients have no family history and the condition is unilateral, usually
involving a single digit, and often follows trauma such as wrist and hand frac-
tures and surgery. The condition is nonprogressive and does not cause digital
contracture. Patients with non-Dupuytren disease do not need surgical treat-
ment, and the condition can spontaneously improve.
F. In addition to non-Dupuytren disease, benign soft-tissue changes can mimic
early DD, and certain aggressive processes can be mistaken for established DD.
Examples of these are the skin thickening from friction and epithelioid sarcoma.
Nodules in DD should be distinguished from occupational thickening, hyperk-
eratosis, and callus formation.
IV. Treatment
A. Nonoperative treatment
Observation is appropriate for non-Dupuytren disease and indicated for a
patient who has static DD with minimal contracture and without compromise
of function. Steroid injection of Dupuytren nodules has been used to suppress
the disease. Enzymatic fasciotomy using injection of trypsin, hyaluronidase, and
lidocaine followed by forcible extension of the digit was also described. Collage-
nase as well as gamma-interferon injections have been described as nonoperative
treatment methods for DD. Radiation therapy was also used in early stages of
DD to minimize disease progression and avoid surgery. High recurrence rate is
reported with many of these modalities and additional scientific studies on all
these unconventional methods are needed.
Surgery is the most widely used and conventional treatment of advanced DD.
Flexion contracture of the metacarpophalangeal joint more than 30 degrees and
flexion contracture of the proximal interphalangeal joint of 10 to 15 degrees
that interfere with function and, in the presence of a well-developed cord, are
indications for surgical treatment. Treatment of metacarpophalangeal joint con-
tractures is more predictable than that of proximal interphalangeal joint contrac-
tures. The various surgical techniques for treating DD include
1. Percutaneous fasciotomy (scalpel or needle) was first used by Astley Cooper
and has been advocated for palmar cords in older patients. In severe cases,
this technique may be useful as a preliminary procedure.

2. Segmental aponeurectomy is done through multiple small incisions that are

created in the palm and digits, and segments of diseased tissue are excised
without removal of all tissue.
3. Partial, regional, or limited fasciectomy remains the most predictable, con-
ventional and widely used technique among hand surgeons today. Partial fas-
ciectomy is the excision of the diseased tissue only and preserving uninvolved
areas of the palmar fascial complex.
4. Dermofasciectomy and skin grafting are indicated for especially severe cases
and recurrent disease. This technique has not shown evidence of recurrence
beneath the graft.
5. Extensive fasciectomy is indicated for widespread involvement of the palmar
fascial complex and is done through a transverse or U-shaped palmar incision.
6. Total fasciectomy was intended as a prophylactic procedure for removal of
the entire palmar fascia including uninvolved tissue. This procedure is not
recommended because of its great morbidity.
Regardless of the surgical treatment modality used, patients with strong diathesis
have a higher recurrence rate and incidence of postoperative complications and a
less favorable prognosis when compared to patients with weak diathesis.
V. Rehabilitation
The goal of postoperative care is to allow for wound healing and early digital range of
motion in both flexion and extension. Splinting in full finger extension and comfort-
able wrist position is utilized following the release of proximal interphalangeal joint
contracture if residual flexion deformity is present. A forearm-based thermoplastic
splint is fabricated if long-term splinting is necessary. Gentle active and passive digital,
thumb, and wrist joint range of motion exercises are initiated, with emphasis on finger
extension and intrinsic stretching. Hand elevation is important for edema control and
compressive gloves can be used in cases of severe edema and for scar compression. Fol-
lowing initial wound healing, regaining full composite flexion becomes a priority while
continuing to focus on maintaining or achieving full finger extension. Exercise sessions
are increased hourly to achieve full range of motion. The extension splint is used at
night and as needed during the day, to maintain full extension.
Progressive strengthening and reconditioning program is implemented between
4 and 6 weeks. Return to light or moderate work activities is allowed by 8 weeks with
progression to full duty and heavy work by 12 weeks. Occasionally, prolonged splinting
is indicated in cases of residual flexion of PIP joint and can be maintained for several
weeks postoperatively. Night extension splinting with a scar conformer is continued up
to several months if necessary.
VI. Complications
A. Intraoperative complications
1. Nerve injury: Digital nerves may be partially or completely transected dur-
ing open or percutaneous surgery. The spiral cords that contribute to MP
and PIP contracture displace the digital neurovascular bundles in a proximal,
superficial, and midline direction. This places the bundles at risk especially
when operating near the level of the MP flexion crease. It is recommended to
identify the neurovascular bundles proximally in the palm before dissecting
distally. If lacerated, digital nerves should be primarily repaired.

2. Vascular injury: Digital blood supply may be compromised due to vessel lac-
eration (similar to nerve laceration) or due to spasm or stretch of the arteries
when significant contracture is corrected. When facing vascular compromise
without vessel laceration, conservative measures are employed first (warm
the room above 76°F, cover the digit in warm, wet gauze, warm the patient,
and 20% lidocaine or papaverine may be applied to the vessel). If necessary,
a systemic heparin bolus or dextran may be given. When unsuccessful, digits
may need to be kept in a resting flexed posture if that restores blood flow.
Uncommonly, digital vessels are explored, tortuosities corrected, adventitia
stripped, and potentially vein grafted to bypass injured segments.
3. “Buttonhole” in skin flaps: Often occurring without negatively impacting
outcomes, the vascularity of skin flaps should be assessed after tourniquet
deflation. If a skin flap is poorly vascularized despite conservative measures
above, the portion of skin may require excision and local skin advancement
or grafting for closure.
B. Early postoperative complications
1. Hematoma: This can be minimized by achieving hemostasis with a bipolar
cautery, use of wound drains, or leaving portions of incisions open.
2. Swelling: Diffuse digital swelling is best addressed by release of tight dress-
ings, elevation, digital exercises, and Coban wrapping.
3. Infection: Postoperative infection is treated with antibiotics, surgical debride-
ment, and loose skin closure according to the severity of the infection.
4. “Flare”: Pain syndromes can complicate Dupuytren surgery and have been
linked to carpal tunnel syndrome and acute flexor tenosynovitis. Identi-
fiable etiologies are to be surgically addressed while that without clear
cause may be treated similar to other cases of sympathetically mediated pain
syndromes.
5. Wound dehiscence: Open wounds that expose flexor tendons or neurovas-
cular structures will require coverage while those in the palm are generally
amenable to healing by secondary intention.
C. Late postoperative complications
1. Recurrence: Revision Dupuytren surgery may be necessary for some patients.
However, this surgery becomes increasingly technically challenging given
prior incisions and scar tissue obscuring normal anatomy. Patients, especially
those with more aggressive disease should be aware of the chance for recur-
rence of disease.
2. Digital pseudoaneurysm: This is an uncommon complication that may result
from trauma that weakens the arterial wall of the digital vessel.
Suggested Readings
Boyer MI, Gelberman RH. Complications of the operative treatment of Dupuytren’s disease.
Hand Clin. 1999;15:161–166.
Heuston JT. The control of recurrent Dupuytren’s contracture by skin replacement. Br J Plast Surg.
1969;22:152–156. Medline.
McFarlane R, Botz J, Cheung H. Epidemiology of surgical patients. In: McFarlane RM,
McGrouther DA, Flint MH, eds. Dupuytren’s Disease: Biology and Treatment. New York, NY:
Churchill Livingstone; 1990:201–213.

Rayan GM. Dupuytren disease: Anatomy, pathology, presentation, and treatment. J Bone Joint
Surg (Am). 2007;89(1):189–198.
Rayan GM. Nonoperative treatment of Dupuytren’s disease. J Hand Surg (Am). 2008;33(7):1208–
1210.
Rayan G, Moore J. Non-Dupuytren’s disease of the palmar fascia. J Hand Surg (Br) 2005;30:551–
556. Medline.
Tubiana R, et al., eds. Dupuytren’s Disease. London, England: Martin Dunitz; 2000.

Tumors
25
Ed Athanasian
I. Benign Soft Tissue Tumors
A. Ganglion cysts
1. Definition
Ganglion cysts are the most common soft tissue masses in the hand. These
lesions can be thought of in simple terms as a herniation of joint or tendon
sheath synovial fluid outside the normal confines of the articular capsule or
tendon sheath. These balloonlike structures are attached to the capsule or
tendon sheath by a stalk. This can be narrow or broad based. The “stalk” can
behave as if it has a one-way valve or a two-way valve. This concept helps to
explain the variation in the size of ganglion cysts. At times, these lesions pro-
gressively enlarge in size. At other times, they can enlarge and then decrease
in size. The cyst wall is comprised of fibrous tissue and does not have a true
endothelial lining. Some ganglion cysts may arise from degenerated ligament
as can be seen with dorsal carpal ganglion cyst arising from the scapholunate
interosseous ligament. Common types of ganglion cysts include dorsal carpal
ganglion cysts, volar carpal ganglion cyst, retinacular cyst arising from ten-
don sheath, and mucous cysts, which represent a specialized form of ganglion
cyst arising from the distal interphalangeal (DIP) joint. Ganglion cysts can
arise from any joint in the hand.
2. Pathogenesis
a) Mucous cysts arise at the DIP joint and extend dorsally or peripherally.
On occasion they can be subungual. These are felt to arise in association
with osteoarthritis, and osteophytes have been felt to be a significant fac-
tor contributing to their development. The excision of associated osteo-
phytes is important during treatment in an effort to reduce recurrence
risk.
b) Retinacular cysts may arise spontaneously, following tendon sheath injec-
tion, and following repetitive digit flexion against resistance. These cysts
most commonly arise in close proximity to the A1 pulley but can be seen
further distally.
c) Dorsal carpal ganglion cysts commonly arise in association with the sca-
pholunate interosseous ligament. Mucoid degeneration of the ligament
has been implicated as a source for the cysts.
d) Volar carpal ganglion cysts tend to arise radially in association with the
extrinsic radio carpal ligaments or the scapho-trapezialtrapezoid ligament
and can abut or even surround the radial artery.
Each type of ganglion cyst tends to arise in a common and predictable
location. When suspected ganglion cysts are seen in unusual locations, the
460

Chapter 25 • Tumors 461
initial differential diagnosis should include alternate lesions including solid

neoplasms.
a) Mucous cysts tend to arise dorsally at the level of the DIP joints. This is usu-
ally seen in the setting of osteoarthritis and Heberden nodes may be present.
The overlying dorsal skin may be thinned. There can be spontaneous clear
drainage. Nail deformity can be seen in the form of grooving if the lesion
affects the germinal matrix or dorsal nail fold. The lesions are firm and usu-
ally not tender. Infection can be seen following spontaneous drainage.
b) Retinacular cysts tend to arise palmarly in line with the proximal aspect of
the flexor tendon sheath. These lesions are firm. They tend to be relatively
small and often less than 5 mm. They can be central or eccentric. These
lesions can be tender on deep palpation and patients frequently report
pain with direct contact when gripping such as when holding a hammer.
c) Dorsal carpal ganglion cysts tend to arise somewhat radial to midline in
the region of the lunate capitate articulation or scapholunate articulation.
These lesions are variable in size. Wrist flexion may assist in the identifica-
tion of lesions and allow easier palpation. Pain may radiate distally along
the course of the finger extensors and symptoms can be accentuated by
resisting digit extension. Pain may be made worse with active wrist exten-
sion and on occasion there may be limitation of active and passive wrist
extension. These lesions typically transilluminate. If transillumination is
not possible, alternate diagnoses should be considered. A positive Watson
scaphoid shift test is usually present on examination.
d) Volar carpal ganglion cysts tend to arise in close proximity to the radial
artery just proximal to the volar wrist flexion crease. These lesions are
usually firm. Transillumination will help delineate the lesion and identify
the course of the radial artery. Aspiration typically yields thick gelatinous
clear or straw-colored fluid, which on occasion might be blood tinged.
4. Radiographs
Plain x-rays of mucous cysts will frequently demonstrate dorsal osteophytes
and osteoarthritis. Radiographs of retinacular cysts as well as dorsal and volar
carpal ganglion cysts are most commonly normal. On occasion arthritis can
be seen in association with these lesions. MRI is generally not indicated when
history and physical examination are consistent with ganglion cyst. On occa-
sion occult dorsal carpal ganglion cysts can be better delineated by MRI or
ultrasound. If a solid lesion is suspected, MRI may be useful.
5. Treatment
a) Mucous cysts
When lesions are small, asymptomatic, and not spontaneously draining
observation is reasonable. Many patients simply wish to be assured that
they do not have a solid tumor or malignancy. Large or symptomatic
lesions may be aspirated; however, recurrence is frequent. Mucous cysts
may be excised surgically although there is a substantial risk of recurrence
as the underlying cause (osteoarthritis) remains. While marginal excision
with debridement of osteophytes may be effective, simple excision of the
base of the lesion at the level of the joint with joint debridement is also a
very effective means of treating these lesions and appears to have a lower
risk of skin and wound healing problems. Skin coverage is typically not
required with the latter method.

b) Retinacular cysts
Small asymptomatic or minimally symptomatic lesions may be observed
as long as physical examination findings are characteristic. Symptomatic
central lesions may be aspirated in the office under local anesthesia with
occasional recurrence. Eccentric lesions may be in close proximity to the
digital vessels and nerves and may not be amenable to aspiration in the
office. These lesions may be excised under local anesthetic in the form of
marginal excision.
c) Dorsal carpal ganglion cysts
Asymptomatic lesions may be observed assuming physical examination
findings strongly support the diagnosis of dorsal carpal ganglion cyst.
These lesions should clearly transilluminate on examination. If this is not
the case, further evaluation is necessary. Treatment alternatives include
aspiration either in the office floor under ultrasound guidance. Recur-
rence may exceed 50% following aspiration. There is no clear benefit to
the injection of corticosteroid, which on occasion may be associated with
skin depigmentation and fat atrophy. Open marginal excision may be
considered for multiple recurrent lesions with anticipated recurrence risk
of approximately 5%. Recent studies have suggested that arthroscopic
excision of dorsal carpal ganglion cysts may be an alternative effective
means of treating these lesions.
d) Volar carpal ganglion cysts
Asymptomatic lesions can be observed. Symptomatic lesions can be
treated similar to the dorsal counterpart, although the close proximity of
the radial artery increases the risk of complications, including the devel-
opment of a psuedoaneyrysm if the radial artery is injured. Open excision
with identification of the radial artery generally results in low recurrence
and minimal complications. Prior to excision, an Allen test should be
performed to determine patency of the radial artery and arterial filling of
the hand through the ulnar artery.
B. Giant cell tumor of tendon sheath
Giant cell tumor of tendon sheath is the most common soft tissue solid neo-
plasm that arises in the hand. Its pathogenesis has not been clearly defined.
Multinucleated giant cells and hemosiderin laden macrophages are typically seen
on histological assessment. These lesions arise in close proximity to joints. There
can be direct extension into adjacent joints and ligaments. This may play a role
in local recurrence following marginal excision. Most commonly, these lesions
are firm and nodular. There is also a diffuse variant, which tends to spread proxi-
mally along flexor tendon sheaths and appears to be associated with a higher risk
of local recurrence.
These lesions arise in close proximity to the proximal interphalangeal (PIP)
and DIP joints but may be seen anywhere in the hand. Lesions may arise in
association with the flexor tendon bursa in the palm. Rarely symptoms of
nerve compression can be seen. The nodules can be quite firm and are typi-
cally not tender. The nodule may move with digit motion when adherent to
tendons. These lesions do not transilluminate.
2. Radiographs
Giant cell tumor of tendon sheath is most commonly not visible on x-ray.
Approximately 5% of lesions can cause a pressure erosion and sclerotic reaction

on adjacent bone. There are rare but well-described examples of direct bony
invasion mimicking a more aggressive process. MRI typically demonstrates
a nodular lesion with decreased signal seen in association with hemosiderin.
The diffuse variant may mimic a proliferative synovitis with decreased signal.
On ultrasound, they appear as solid, homogeneous hypoechoic masses with
detectable internal vascularity
3. Treatment
The standard treatment for giant cell tumor of tendon sheath is marginal
excision. The potential for a different neoplasm including a malignant tumor
must be considered prior to proceeding with marginal excision of these
lesions. This is particularly true for lesions arising in the carpal tunnel. The
risks of soft tissue contamination in the event of a diagnosis of malignancy are
great. During excision of a giant cell tumor of tendon sheath most commonly
the lesion will have a Brown/yellow xanthomatous appearance, which is char-
acteristic. If the lesion is in close proximity to a joint, careful inspection of
the joint may demonstrate extension deep to the volar plate or in the region
of the collateral ligaments. Local recurrence can be seen in approximately
30% of patients with reports of recurrence ranging from 5% to 50%.
II. Benign Bone Tumors
A. Enchondroma
1. Definition
Enchondroma is a benign cartilaginous neoplasm. It is the most common
primary bone tumor which arises in the hand. It is most commonly seen in
the proximal phalanx and metacarpal. These lesions can grow very slowly
and may distend the cortex resulting in weakness and subsequent pathologic
fracture. Most lesions are identified either incidentally when x-rays are done
for another reason or following pathologic fracture. Greater degrees of cel-
lular atypia can be seen with enchondroma’s arising in the hand as compared
to central locations on the body. Malignant degeneration to chondrosarcoma
is rare but well described. While Ollier disease has been called “multiple
enchondromatosis,” it is clearly a distinct entity with more aggressive clini-
cal, radiographic, and histological findings.
Again, most lesions are found incidentally or following pathologic fracture.
On occasion patients may present with distention of the bone and rarely
tenderness on deep palpation. Soft tissue mass is not typical of enchondroma
but may be seen with Ollier disease. Typically, findings are limited in the
absence of fracture.
3. Radiographs
Plain x-rays most commonly will demonstrate a lytic lesion with well-defined
borders. There may be marginal sclerosis. There can be distention of the cor-
tex and thinning of the cortex. The classic matrix has stippled calcifications;
however, purely lytic lesions may be seen in association with a more myxoid
stroma histologically. MRI will commonly demonstrate a lobular contour,
cortical thinning, and distention. Frank bone destruction is not commonly
seen, and should raise the suspicion of a more aggressive process such as
chondrosarcoma.

4. Treatment
Observation may be considered for those lesions identified incidentally
with characteristic radiographic appearance, which does not predispose the
patient to a substantial risk of pathologic fracture. Interval surveillance is
prudent and patients must be told of the potential for malignant degen-
eration even though this is small. Curettage may be advocated for symp-
tomatic lesions, those lesions causing substantial cortical weakness, or in
the setting of prior pathologic fracture. Bone grafting with the patient’s
own bone or allograft bone would seem prudent when there is concern
for subsequent pathologic fracture. Outcomes appear to be similar whether
autogenous or allograft bone is used. Some have advocated simple curettage
alone as adequate treatment; however, healing appears to be slower. There
are limited data regarding the role for bone substitutes. In the setting of
acute pathologic fracture, superior results have been reported when treat-
ment is delayed until after union has occurred and patients have recovered
motion. This would assume that there is no fracture deformity requiring
correction. In the setting of substantial deformity, immediate surgery may
be indicated.
B. Giant cell tumor of bone
1. Definition
Giant cell tumor of bone is a destructive primary bone neoplasm, which his-
torically has been classified as a benign process; however, it has the potential
to metastasize and is best classified as a low-grade malignancy. Approximately
2% of giant cell tumors of bone rise in the hand exclusive of the distal radius.
Lesions of the distal radius account for the third most common site of presen-
tation. This lesion is slightly more common in women and most commonly
occurs early in the fourth decade of life. Histological examination demon-
strates numerous large giant cells with multiple nuclei, which have similar
characteristics to the surrounding stroma.
Pain and swelling are the most common patient complaints. Less commonly,
a patient will present with pathologic fracture. Physical examination find-
ings may include swelling, warmth, dark red discoloration, tenderness, and
limitation of range of motion.
3. Radiographs
Plain x-rays are the most specific test in trying to develop a differential diag-
nosis. Lesions are typically centered in the epiphysis but may be seen in the
metaphysis in skeletally immature patients. These lesions are typically lytic
but may have pseudotrabeculation. The borders of the lesion are typically
less well defined than most benign lesions. Marginal sclerosis is not typically
seen. There may be cortical destruction with soft tissue extension. Lesions
are commonly graded using the Campanacci system. Grade 1 lesions are
confined to the bone and do not distort, distend, or perforate the cortex.
Grade 2 lesions distend or distort the cortex but do not extend beyond it.
Grade 3 lesions destroy the cortex and extend into the surrounding soft
tissues.
4. Treatment
Lesions suspicious for giant cell tumor of bone should be biopsied through
an approach that will allow immediate intralesional treatment based on fro-
zen section analysis or allow staged wide excision.
a) General principles

Grade 1 and 2 lesions in most long bones are treated intralesionally with
curettage and the use of adjuvants. There is some controversy regarding
the most effective adjuvants. The use of a high-speed mechanical burr
has been advocated to extend the zone of curettage. Argon beam laser
coagulation of the endosteal cavity may also extend the zone of curettage.
The application of phenol or cryosurgery with the use of liquid nitrogen
has also been advocated. Packing of the treated cavity with methyl meth-
acrylate bone cement has also been advocated as a means of reducing
local recurrence risk and improving the ability to detect local recurrence
following intralesional treatment. Local recurrence seems to be higher
following curettage and bone grafting only. Grade 3 extremity long bone
lesions with very limited cortical perforation at times may be treated
intralesionally as noted above. If there is extensive soft tissue extension
or limited bone stock, wide excision and reconstruction may be the most
appropriate treatment. Reconstruction can be done by means of vascular-
ized or nonvascularized bone grafting or the use of dental prostheses.
b) Specific locations
Lesions specifically arising in the hand appear to have a more aggressive
behavior. Intralesional treatment of lesions arising in the hand is associ-
ated with an unacceptable risk of local recurrence and is generally not
advocated. There is limited data supporting the use of curettage and cryo-
surgery for hand lesions.
1) Phalanx
Wide excision of phalangeal lesions is often best accomplished by ray
amputation.
2) Metacarpal
Metacarpal lesions are also often best treated with ray amputation. On
occasion wide excision and reconstruction may be appropriate.
3) Carpus
Carpal lesions are best treated with wide excision and reconstruction.
4) Distal radius
Grade 1 and 2 distal radius lesions may be treated with curettage and
adjuvants. Grade 3 lesions are often best treated with wide excision
and reconstruction often in the form of intercalary wrist arthrodesis or
articular allograft reconstruction. There is recent data to support
intralesional treatment of grade 3 lesions of the distal radius with cor-
tical perforation limited to a single plane.
All patients with giant cell tumor of bone require systemic staging
at the time of diagnosis and prolonged periodic surveillance to rule out
local recurrence or metastasis. Late recurrence beyond five years is well
described.
C. Glomus tumor
1. Definition
Glomus tumor is a benign vascular lesion, which is known to occur in the nail
bed or in close proximity to the nail bed. Patients will commonly complain
of exquisite pain with contact or cold exposure. Such complaints should raise
the clinical suspicion for this diagnosis.
The patient can often localize the lesion precisely by pointing to it with a pen
tip and marking the site of maximal pain. On occasion dark red or bluish
discoloration may be seen; however, frequently there is no visible finding.

Rarely broadening of the nail can be seen with long-standing or large lesions.
Cold immersion on occasion may reproduce symptoms.
3. Radiographs
Plain x-rays are typically normal; however, on occasion pressure erosion of
the dorsal cortex of the distal phalanx could be seen. MRI may be helpful
if specific finger coil equipment is available and vascular sequences are per-
formed. MRI may also be helpful in the detection of local recurrence.
4. Treatment
Suspected lesions are best assessed using magnetic resonance imaging. Precise
measurements are required preoperatively to localize lesions, which are not
clinically visible and allow precise nail bed incision placement. Nail removal
is typically required. Longitudinal incision of the sterile matrix may allow
access to lesions, which have been marginally excised. This is followed by nail
bed repair and replacement of the nail.
III. Malignant Bone Tumors
A. Chondrosarcoma
1. Definition
While chondrosarcoma has been reported to be the most common malig-
nant bone tumor arising in the hand it remains rare. These are cartilaginous
tumors, which may arise primarily or in the setting of malignant transforma-
tion of a benign cartilage lesion such as enchondroma. Chondrosarcoma is
most commonly low grade when it arises in the hand. Metastatic risk appears
to be less than 10% and may correlate with histological grade.
Patients typically present with a slowly growing mass. Pain may or may not be
present. Lesions are typically firm and nontender. Large lesions may restrict
range of motion. On occasion rapidly growing lesions may be painful and
tender on examination.
3. Radiographs
Lesions may be lytic or have a stippled calcified matrix. Ring-shaped calcifi-
cations may be seen. Bone destruction may be seen. MRI will demonstrate
signal characteristics of cartilage.
4. Treatment
Wide excision in the form of ray amputation has been advocated for phalanx
and metacarpal lesions. Recent reports of small numbers of patients support
the concept of intralesional treatment of curettage and bone grafting for low-
grade chondrosarcomas. Local recurrence may be more frequent; however,
this approach has been advocated due to the very low risk of metastasis.
B. Osteogenic sarcoma
1. Definition
Osteogenic sarcoma is relatively rare in the hand. This is a primary bone-
forming neoplasm. It may arise primarily or in the setting of a prior benign
lesion. Lesions may be low grade or high grade. The risk of metastasis cor-
relates with histological grade.
Patients may present with a slow or rapidly growing mass. More rapidly
growing lesions may be painful. Lesions are typically firm and tender. Range
of motion may be decreased.

3. Radiographs
Plain x-rays may demonstrate a blastic, lytic, or mixed appearance. Bone
destruction may be seen. There may be substantial edema seen on MRI.
4. Treatment
Biopsy proven lesions are best treated with wide excision. Phalanx and meta-
carpal lesions are usually best treated with ray amputation. Rarely wide exci-
sion achieving negative margins may be appropriate. Low-grade lesions are
most commonly treated with surgery only. High-grade lesions have a sub-
stantially higher risk of metastasis and are best treated with systemic chemo-
therapy and long-term surveillance.
C. Ewing sarcoma
1. Definition
Ewing sarcoma is extremely rare in the hand. This is a highly malignant small
blue round cell tumor. It is usually seen in the first or second decade of life.
It is readily confused with infection.
Physical examination findings may suggest infection; there may be redness,
swelling, tenderness, and even fever. Soft tissue mass may be present.
3. Radiographs
Plain x-rays may demonstrate a lytic destructive process with a moth-eaten
appearance to the bone. Soft tissue mass may be apparent. MRI may demon-
strate extensive soft tissue edema.
4. Treatment
Ewing sarcoma is a highly malignant tumor and requires systemic chemo-
therapy. Local control may be achieved by wide excision in the form of ray
amputation. Primary radiation without surgery may also be effective in pro-
viding local control; however, radiation in the hand is associated with sub-
stantial morbidity.
D. Acral metastasis
1. Definition
The most common sources of metastasis to the bones of the hand include
primary lung and breast cancer. Multiple histologies have been reported.
Prognosis correlates with the primary lesion; however, metastasis to the
hand is typically seen late in the course of disease and survival may be lim-
ited. The exception is metastatic renal cell carcinoma where long-term sur-
vival may be seen following aggressive treatment of solitary metastasis to
the hand.
There is no well-defined physical examination profile for acral metastasis.
Swelling, pain, tenderness, and pathologic fracture may be seen. Range of
motion may be limited. Physical findings may mimic those of osteomyelitis
of the distal phalanx or septic arthritis of the DIP joint.
3. Radiographs
Most commonly lesions are lytic, destructive, and permeative. Soft tissue
mass may be present.
4. Treatment
Patients with acral metastasis often have limited long-term survival. Treat-
ment is usually directed at palliation but often will require wide excision or
amputation. On occasion radiation may be considered primarily or as an
adjuvant. Treatment decisions are based in the context of the primary disease
and expected survival.

IV. Malignant Soft Tissue Lesions
A. Soft tissue sarcomas

1. Definition
Soft tissue sarcomas are primary malignant soft tissue neoplasms, which
are thought to arise from primitive mesenchymal cells. These are relatively
uncommon in the hand. The most common histological subtypes seen in
the hand include epithelioid sarcoma, synovial sarcoma, malignant fibrous
histiocytoma, and malignant peripheral nerve sheath tumors. These lesions
have the potential to metastasize. Epithelioid sarcoma, angiosarcoma, clear
cell sarcoma, and rhabdomyosarcoma are known to metastasize to lymph
nodes, with most others metastasizing via the hematogenous route. The risk
of metastasis is predicted by histological grade, size, and depth of the primary
lesion.
Soft tissue sarcomas most often present as slow-growing painless lesions. Syn-
ovial sarcoma on occasion may be painful. More rapid growth may be seen
on occasion. These lesions are commonly confused with presumed ganglion
cysts or lipomas.
3. Radiographs
Plain x-rays are most commonly normal; however, soft tissue calcifications
may be seen with all soft tissue sarcomas and are well described for synovial
sarcomas. On occasion, pressure erosion of the bone may be seen. MRI is an
extremely useful tool for delineating the extent of soft tissue involvement.
Signal characteristics will not often differentiate between different histologi-
cal subtypes.
4. Treatment
The most important aspect of treatment is clinical suspicion prior to per-
forming biopsy. Marginal excision of a lesion, which is presumed to be benign
results in extensive soft tissue contamination and may limit limb or hand
salvage options at definitive treatment. Soft tissue sarcomas are best treated
with wide excision through negative margins. If negative margins cannot be
achieved through wide excision or if wide excision will result in significant
functional impairment, amputation of some form may be the best treatment.
Radiation may be used as an adjuvant for high-grade lesions greater than
5 cm in size. Patients with soft tissue sarcomas require systemic staging with
CAT scan assessment of the chest. The role of Sentinel lymph node biopsy
for epithelioid sarcoma, clear cell sarcoma, angiosarcoma, and rhabdomyo-
sarcoma is currently under investigation. Patients require long-term surveil-
lance. Those patients with high-grade lesions greater than 10 cm in size or
systemic metastasis are candidates for chemotherapy.
B. Cutaneous malignancies
1. Squamous cell carcinoma and basal cell carcinoma
a) Definition
Squamous cell carcinoma and basal cell carcinoma are skin cancers,
which may be seen in the hand later in life. Risk factors may include
sun exposure or viral infection. These lesions have a relatively low risk of
metastasis; however, on occasion lymphatic metastasis may be seen, more
commonly with squamous cell carcinoma.

b) Physical examination
Change in skin color, texture, or discrete lesions or nodules may be seen.
Suspected lesions may be biopsied with a skin punch tool commonly used
by dermatologists or by incision or excisional biopsy.
c) Radiographs
Plain x-rays are typically normal except with advanced disease where there
may be involvement of bone such as the distal phalanx. MRI may be
helpful with very large lesions with associated soft tissue mass for bone
extension. Systemic staging with CAT scan may be helpful for assessing
the lung or lymph nodes.
d) Treatment
Small lesions may be treated in conjunction with a dermatologist. Topical
treatment or micrographic surgery on occasion may be indicated. Large
lesions may be best treated by wide excision. On the dorsum of the hand,
soft tissue coverage in the form of skin grafting may be required. Nail
bed excision and skin grafting consider primary nail bed lesions. At times
DIP disarticulation may be the most appropriate treatment for fingertip
lesions. Sentinel lymph node biopsy may be indicated for long-standing
or ulcerated lesions or the setting of palpable lymphadenopathy. Long-
term follow-up is required.
2. Melanoma
a) Definition
Melanoma is the third most common skin cancer, but the most aggres-
sive with the highest rate of metastasis. Risk factors include previous sun
exposure and particularly a history of sunburns. They are more common
in fair-skinned individuals and rarely seen in African Americans (with the
exception of the acral lentiginous type).
Melanomas typically present as an asymptomatic pigmented lesion and
may develop from a preexisting nevus. The appearance consists of asym-
metrical lesion with irregular borders and diameter greater than 6 mm.
c) Radiographs
Plain radiographs are normal and there is not a routine use for other
imaging studies.
d) Treatment
The initial treatment is aimed at establishing the diagnosis. A full thick-
ness excisional or (incisional if the lesion is large) biopsy is needed to
determine the thickness of the lesion and appropriate treatment. Shave
biopsies should be condemned as it will not allow adequate determina-
tion of thickness and treatment results could be compromised. Mela-
noma in situ can be treated with excision with a 5-mm margin. Thin
melanomas (<1 mm thickness) can be treated with a 1-cm margin, while
intermediate and thick lesions should be treated with 2-cm margins and
will require skin grafting or flap closure in the upper extremity. Sentinel
lymph node biopsy is recommended for all intermediate thickness lesions
and many thick lesions to determine the presence of regional disease.
A full metastatic workup is required including routine blood work and
CT scans of the chest, abdomen, and pelvis. A positive sentinel lymph
node biopsy will require completion lymphadenectomy and these patients
may benefit from adjuvant therapy.

Long-term follow-up is required by both the surgeon and the medical

oncologist.
3. Subungual lesions
a) Definition
Lesions appearing under the nail plate should raise suspicion for a malig-
nant lesion, with squamous cell carcinoma and melanoma being the most
common.
Any pigmented lesion, which does not grow with the nail plate should
be biopsied when in question. There are some ethnic groups, particu-
larly from the Mediterranean region, which have pigmented lesions under
multiple nails and in multiple family members, and these do not need
treatment.
c) Radiographs
Plain radiographs will be normal, unless the lesion is large and has eroded
into the distal phalanx, in which case, cortical changes may be noted
along the dorsal aspect of the distal phalanx.
d) Treatment
The first step is again, establishing a tissue diagnosis. For small lesions,
this may involve removal of the nail plate and an excisional biopsy. Larger
lesions may require a full thickness incisional biopsy. Invasive squamous
cell carcinoma typically requires amputation at the DIP joint level while
melanoma typically requires more aggressive treatment with middle pha-
lanx or PIP joint amputation in conjunction with sentinel lymph node
biopsy. If the sentinel lymph node is positive, completion lymphadenec-
tomy is indicated and possible adjuvant therapy. As with the cutaneous
malignancies, long-term follow-up is required.
Suggested Readings
Athanasian E. Bone and soft tissue tumors. In: Green DP, Hotchkiss RN, Pederson WC,
Wolfe SW, eds. Green’s Operative Hand Surgery. 5th Ed. Philadelphia, PA: Elsevier; 2005:
2211–2264.
Chung K. Skin tumors. In: Green DP, Hotchkiss RN, Pederson WC, Wolfe SW, eds. Green’s
Operative Hand Surgery. 5th Ed. Philadelphia, PA: Elsevier; 2005:2192–2210.
Cohen T, et al. Subungual melanoma: Management considerations. Am J Surg. 2008;195(2):
244–248.
Plate AM, et al. Tumor like lesions and benign tumors of the hand and wrist. J Am Acad Orthop
Surg. 2003;11:129–141.
Plate AM, Steiner G, Posner MA. Malignant tumors of the hand and wrist. J Am Acad Orthop
Surg. 2006;14:680–692.

Infections
26
Thomas R. Hunt III, Christopher Robert,
Michael Makary, and Alexander M. Marcus
Treatment to successfully eradicate hand infections consists of incision and drainage,

debridement of devitalized tissues, immobilization and elevation, and antibiot-
ics. Tetanus status should be updated and once cultures are obtained, the patient
should be placed on empiric antibiotics chosen based on the expected patho-
gen causing the disease process. The antibiotics are then adjusted according to the
results of the cultures and sensitivities. Soaking the hand following surgical drain-
age will aid in keeping the wound open and decrease the reaccumulation of purulent
exudates.
Patient’s medical issues should be accounted for in the treatment of hand infec-
tions. In general, the same organisms that are encountered in the general popula-
tion cause hand infections seen in immunocompromised patients. However, the
course of disease is much more virulent. Patients who are immunosuppressed from
transplants or diabetes may require amputations to control the infection and tis-
sue necrosis. Gram-negative and polymicrobial infections are more common in
this population. Fluctuations in blood glucose are common and should be treated
aggressively.
II. Deep Space Infections
In order to recognize and treat deep space infections, it is essential to understand the
anatomy of the potential spaces of the hand and their relationship to each other. Urgent
drainage, thorough irrigation, intravenous antibiotics, elevation, and immobilization
are the critical components of successful management. The wound should be packed
open and 1 to 2 days later soaks and rehabilitation are initiated.
A. Midpalmar Space
A midpalmar space infection usually follows penetrating trauma or contiguous spread from
a long, ring, or small finger septic flexor tenosynovitis. As with other deep space infec-
tions in the hand, marked dorsal hand swelling may divert the examiner’s attention away
from the palm, the true site of the infection. The mid-palm is swollen, with loss of the
normal palmar concavity in addition to tenderness and erythema. Passive motion of the
involved digits causes pain. Debridement can be performed through transverse or oblique
longitudinal incisions.
B. Thenar Space
In addition to erythema, tenderness, and swelling, patients present with palmar abduc-
tion of the thumb. Passive thumb adduction and opposition exacerbate the pain.
Palmar, dorsal, and combined incisions for drainage have been described. Release of the
471

thenar space may require both volar and dorsal incisions to completely drain the dumb-
bell abscess. Incisions parallel to the web commissure should be avoided to prevent web
space contracture.
C. Hypothenar Space
The hypothenar space is located ulnar to the midpalmar space, and is composed of the
hypothenar muscles surrounded by their enveloping fascia. Hypothenar space infec-
tions are less common than other deep space infections in the hand.
D. Parona Space
Parona space is the potential space bounded by pronator quadratus, digital flexors,
flexor pollicis longus, and a vertical band of fascia radial to flexor carpi ulnaris and the
ulnar neurovascular bundle in the distal forearm. This space becomes infected by spread
from either the radial or ulnar bursa and provides the “bridge” for the development of
a horseshoe abscess. A tender, erythematous fullness is palpable at the volar wrist crease
level. Signs and symptoms of septic flexor tenosynovitis of the thumb or small finger
and radial or ulnar bursa infection are likely. Symptoms of median nerve irritation are
frequently present. Incisions used for decompression are placed to protect the median
nerve and its palmar cutaneous branch and to maintain adequate postoperative soft
tissue coverage. (an extensile Carpal Tunnel Release (CTR) incision made across the
wrist flexor crease, centered just ulnar to the palmaris longus and radial to the hook of
the hamate).
E. Dorsal Subaponeurotic Space

The dorsal subaponeurotic space is contained by the extensor tendons and fascia dor-
sally and the interosseous muscles and metacarpals palmarly. Infection involving this
space is typically secondary to dorsal penetrating injuries of the hand. In contrast to
other deep space infections, dorsal subaponeurotic space infections are accompanied by
significant soft tissue swelling. Dorsal longitudinal incisions over the second and fourth
metacarpals are used for drainage.
III. Bacterial Infections
A. Cellulitis
Cellulitis is a soft tissue bacterial infection that must be differentiated from an
abscess. It presents with the four cardinal signs of inflammation—rubor,
calor, dolor, and tumor. It is also important to know that cellulitis in the
hand may occur secondary to septic arthritis or osteomyelitis. When aspi-
rating a joint in search of infection, placement of the needle through
an area of cellulitis should be avoided as this could potentially seed the
joint.
1. Diagnosis is usually made on physical examination. Results of laboratory
studies such as sedimentation rate and C-reactive protein level, though not
always elevated, can sometimes be used to follow the course of treatment.
Most frequently, cellulitis results from trauma to the skin and subcutaneous
tissues. Other causes include chronic ulceration, lymphedema, and derma-
titis. Group A beta-hemolytic streptococcus is the most common causative
organism followed by Staphylococcus aureus.

Chapter 26 • Infections 473
2. Treatment of primary cellulitis includes antibiotics, elevation, and

immobilization. If the organism and its sensitivities are known, antibiotics
are directed accordingly. Otherwise, coverage for both Staphylococcus and
Streptococcus is needed. For mild, early cases, oral antibiotics are adequate.
Oral antibiotics of choice are dicloxacillin and cephalexin. Clindamycin or
erythromycin can be used for penicillin-allergic patients. If improvement is
not noted within 48 hours or if the infection is more severe, intravenous
antibiotics (cefazolin or vancomycin for penicillin-allergic patients) are initi-
ated. If the area of cellulites does not resolve with antibiotics, the treating
physician must rule out a localized fluid collection, or abscess. Ultrasound
and MRI may be useful adjuncts to clinical examination. The patient is
observed closely in the hospital and the possibility of a deeper infection is
again considered. Once resolution is noted, oral antibiotics are given for 7 to
10 more days.
B. Subcutaneous abscess
A subcutaneous abscess typically occurs after a puncture wound or in response
to a retained foreign body.
1. Diagnosis—Clinical findings include those described for cellulitis as well as
an area of fluctuance.
2. Treatment involves incision and drainage of the localized abscess and removal
of any foreign material. Cultures are obtained before antibiotic administra-
tion, and the wound is packed open to encourage continued drainage. The
hand is immobilized and elevated. The packing is removed 12 to 24 hours
after incision and drainage, and whirlpools, soaks, or moist to dry dressing
changes are begun. The wound is allowed to close by secondary intention if
no vital structures are exposed. Delayed primary closure can be performed
once the infection is eradicated. Depending on infection severity, either oral
or intravenous antibiotics are initiated. The most common causative organ-
ism is S. aureus. A first-generation cephalosporin is the antibiotic of choice.
If the puncture wound occurred in a farm setting (or other contaminated
environments), penicillin is added to cover clostridia. In diabetic patients and
intravenous drug users, the organisms most commonly involved are Strepto-
coccus and Staphylococcus. In addition to the first-generation cephalosporin,
Gram-negative coverage (gentamicin) must be provided.
C. Osteomyelitis
Osteomyelitis in the hand typically results from an open fracture. The frequency
ranges from 1% to 11% and is highly dependent on the degree of damage to
the soft tissue envelope. Less frequently, bone infections are iatrogenic, caused
by procedures such as open or percutaneous stabilization of closed fractures and
placement of external fixator pins. On occasion, direct spread from a local soft
tissue or joint infection or hematogenous spread from a more distant source can
cause a bone infection. Bone infections may occur more commonly in patients
with peripheral vascular disease or systemic illnesses such as diabetes, immune
compromise, and intravenous drug or alcohol abuse.
1. Diagnosis
Symptoms include persistent or recurrent swelling, erythema, pain, and
sometimes drainage. Erythrocyte sedimentation rate, C-reactive protein level,
and white blood cell count may be elevated. C-reactive protein level is more
reliable than erythrocyte sedimentation rate for following the response to
treatment. Radiographic changes include osteopenia and periosteal reaction.

These findings are usually not apparent at the initial presentation. They tend
to appear 2 to 3 weeks after the development of symptoms. A sequestrum
may be seen late. Sequential technetium-gallium scans and labeled white
blood cell scans, such as indium-labeled leukocyte scans, are helpful in mak-
ing the diagnosis. Magnetic resonance imaging may help define the presence
and extent of the infection.
2. Treatment
a) Antibiotics are sometimes used alone to treat osteomyelitis in its earliest
stages.
b) Most commonly, successful treatment is predicated on effective surgical
debridement combined with intravenous antibiotics. If a sequestrum is
present, all necrotic bone must be debrided. Antibiotic coverage is aimed
initially at the most common organism, S. aureus (or another pathogen if
the history indicates). It is then tailored according to culture results and
clinical response. Once initial clinical improvement is documented, anti-
biotics are continued for 4 to 6 weeks on an outpatient basis, usually with
a peripheral intravenous catheter. Normalization of the C-reactive protein
level, wound status, and type of infecting organism are used to determine
the length of antibiotic treatment.
c) In the case of an infection associated with acute fracture with internal
fixation in place, the fixation is maintained as long as the construct is
stable and the fracture has not yet united. The internal fixation may be
exchanged, or alternative fixation such as external fixation may be pro-
vided if the implant is not functional.
d) If osteomyelitis develops in a healed fracture, the implant is removed and
necrotic bone debrided. The goals of surgical management are to remove
all necrotic tissue, eradicate dead space, provide healthy soft tissue cover-
age, obtain fracture healing, and restore function.
e) After the infection has been eliminated, reconstruction of bone defects
may be required. Defects less than 1.5 cm may be treated by cancellous
bone grafting. Larger defects and those critical for structural stability may
require corticocancellous bone grating after debridement or as a staged
procedure. Staged reconstruction uses an antibiotic-impregnated polym-
ethylmethacrylate spacer to fill dead space and provide local antibiotic
infiltration. The second-stage reconstruction of the bone defect is consid-
ered when there is no evidence or persistent infection, which in general is
4 to 6 weeks after the first stage.
D. Septic arthritis
As in other joints, septic arthritis in the hand can have permanent, detrimental
effects if untreated. Cartilage destruction is mediated by bacterial toxins and
enzymes produced primarily by the bacteria as well as the synovial and reticu-
loendothelial cells. Further damage occurs as the joint pressure increases, imped-
ing synovial blood flow. A joint infection may be caused by direct trauma as well
as by local or hematogenous spread. In an adult, hematogenous spread most
frequently occurs in an individual already weakened by systemic disease.
1. Diagnosis
a) Patients with a septic joint complain of pain that is significantly aggra-
vated by joint motion. Swelling, erythema, joint tenderness, and severe
pain with active and passive motion, as well as with axial loading, are
classic findings on physical examination.

b) Joint aspiration is used to confirm the infection and obtain cultures.

There is usually more fluid present than would normally be expected,
and the aspirate is cloudy and thick.
1) Fluid analysis indicates more than 50,000 white blood cells with an
increased percentage of polymorphonuclear lymphocytes (>75%).
2) Decreased glucose levels (40 mg less than the fasting blood glucose
level).
3) The presence of bacteria on Gram stain.
4) The fluid should be examined for crystals to rule out gout and
pseudogout. However, the presence of crystals does not preclude a
simultaneous septic process.
c) Radiographs may reveal a foreign body or associated bony injury. In the
early stages of an infection, radiographs may show a widened joint space.
Late changes include loss of joint space due to the cartilage destruction.
d) S. aureus is the most common organism isolated in septic arthritis of the
hand and wrist followed by Streptococcus species. In pediatric patients,
Haemophilus influenzae should also be considered, but is rare since the
advent of routine immunization.
e) The most common cause of atraumatic septic arthritis among patients
younger than 30 years and sexually active is Neisseria gonorrhoeae. The
disease is four times more common in women than in men and typically
begins with a low-grade fever, chills, and migratory polyarthralgias. A true
septic monarticular arthritis develops in less than 50% of patients with
early symptoms.
2. Treatment
a) Nongonococcal septic arthritis must be surgically decompressed urgently
in order to protect the integrity of the joint. The joint is thoroughly irri-
gated, necrotic tissue is debrided, and either the wound is left open or a
drain is placed. A second look with repeat irrigation and debridement
is often required at 48 hours. Serial joint aspiration is not an effective
method of treatment for septic arthritis in the joints of the hand.
b) Adequate irrigation can be accomplished arthroscopically for wrist joint
infections. However, more severe infections are best eradicated using an
open arthrotomy. The radiocarpal joint is approached dorsally in the
interval between the third and fourth compartments. After irrigation and
debridement, the grossly contaminated wound is left open to heal by sec-
ondary intention. If there is little concern for recurrent infection, the
wound may be loosely closed to prevent articular desiccation.
c) The metacarpophalangeal (MCP) joints are approached and drained
through a dorsal longitudinally oriented incision to the side of the exten-
sor tendon. The sagittal band is incised and the joint capsule is opened.
On occasion, the sagittal bands may be retracted distally to expose the
dorsal MCP capsule. In this way, the sagittal bands are left intact and
no suturing is required to maintain stability of the long extensor during
MCP joint flexion).
d) The proximal interphalangeal (PIP) joint may be decompressed through
a dorsal incision between the lateral band and the central slip. The central
slip must be protected to prevent the loss of PIP extension and a bouton-
niere deformity. Alternatively, the PIP joint may be drained through a
midaxial incision and the joint is entered through the collateral ligament.

e) The distal interphalangeal joint may be drained through a dorsal approach,

incising the capsule adjacent to the terminal tendon while protecting the
extensor mechanism to prevent a mallet deformity. Alternatively, a midax-
ial incision may be performed as for the PIP joint. The thumb MCP and
interphalangeal joints are approached in a similar fashion.
f ) Whirlpools, in combination with gentle range-of-motion exercises, and
moist to dry dressing changes are started 24 hours after surgery. If a drain
rather than an open wound accomplishes postoperative drainage, it is
often left in place for 48 hours. The splint is discontinued as the joint
pain decreases with range of motion.
g) Empiric antibiotics covering the common Gram-positive organisms are
administered, unless circumstances indicate another likely pathogen.
Typically, a first-generation cephalosporin or clindamycin are started after
obtaining cultures and then antibiotics are tailored to the specific culture
results once available. Intravenous antibiotics should be used until there
are signs of clinical improvement. Intravenous or oral antibiotics are con-
tinued for another 2 to 4 weeks.
h) Arthritis caused by N. gonorrhoeae is usually treated nonsurgically. Intra-
venous ceftriaxone is the first line of therapy, sometime accompanied
by joint aspirations. After initial clinical improvement, oral antibiotics
are used for an additional 7 to 10 days, depending on the severity of the
infection.
E. Necrotizing fasciitis
Necrotizing fasciitis is a severe, life-threatening, and limb-threatening infection
of soft tissues often stemming from a small laceration or other minor insult to the
extremity. Patients who abuse intravenous drugs or alcohol are included in the
at-risk population. A single organism, usually Group A beta-hemolytic strepto-
coccus, is identified in approximately 50% of cases. S. aureus and anaerobes may
also be present.
1. Diagnosis
a) The infection is extremely painful and rapidly progressive.
b) It is characterized by poorly demarcated erythema, marked nonpitting
edema, and shiny skin.
c) Within a few days of onset, occlusion of the vessels supplying the skin
results in patches of skin discoloration and bullae. At that point, necrotiz-
ing fasciitis begins to spread rapidly, over a period of just hours, dissecting
along fascial planes, and liquefying fat. Dissection along normally tough
fascial planes in the digit is possible as well.
d) Because skin and muscle are not primarily involved, the infection may
extend well beyond the apparent zone of injury.
e) Typical signs of infection may not be obvious early, although an increased
white blood cell count is common. As the infection develops, systemic
effects occur, including disseminated intravascular coagulopathy and
shock.
f ) The diagnosis should be quickly suspected in patients with extreme pain,
clinical examination findings consistent with cellulitis, and hemodynamic
instability. Radiographs may reveal gas in the involved soft tissues.
2. Treatment
a) Treatment is predicated on prompt recognition, early administration
of antibiotics, and radical surgical debridement. Fibrinous and necrotic

tissue, liquefied subcutaneous fat and watery, and foul-smelling fluid

(“dishwater pus”) are characteristic surgical findings.
b) Antibiotics should be started immediately, even before culture specimens
are taken. Empiric antibiotics must include coverage of Gram-positive
organisms (cephalosporin), Gram-negative organisms (gentamicin), and
anaerobes (penicillin).
F. Gas gangrene
Gas gangrene, or myonecrosis, is usually caused by a clostridial species, most
often Clostridium perfringens. This infection often begins with an open wound
associated with a significant amount of devitalized tissue, as might occur after a
severe crush injury. Dirty wounds, especially resulting from a farm injury, that
are prematurely closed are at particular risk.
1. Diagnosis
a) The skin becomes edematous and bronze, and blebs and hemorrhagic
bullae develop.
b) Gram stain of the characteristic serosanguineous drainage reveals spore-
forming Gram-positive rods with central clearing.
c) Pain increases quickly as the infection spreads, often within hours.
d) Palpation of the soft tissues reveals crepitence caused by subcutaneous
gas. This gas may be visible on radiographs. Septic shock can develop in a
short period of time and death can follow rapidly in the absence of rapid
surgical intervention.
2. Treatment
a) Wounds must be properly cleansed, with removal of all devitalized tissue,
and left open to drain.
b) Antibiotic prophylaxis is required for crush injuries associated with tissue
necrosis and open fractures.
G. Diabetic gangrene
1. Nonclostridial gangrene occurs most commonly in patients with diabetes. At
greatest risk are those diabetic patients with renal failure and an arteriovenous
fistula. These infections are generally polymicrobial.
2. Treatment of established gangrene involves surgical debridement and broad-
spectrum antibiotics tailored appropriately when the causative organisms are
identified (fungal cultures are always obtained). Amputation is sometimes
necessary to eliminate the infection or because the remaining tissue does not
allow a functional digit.
H. Paronychia
1. Paronychia is an infection beneath the eponychial fold. Disruption of the
barrier between the nail and the underlying tissues usually results from mani-
cures, artificial nails, hangnails, or nail biting. The infection begins dorsal to
the nail and may spread superficially around the nail to the other side (run-
around lesion), or it may progress volar to the nail, spreading to involve the
pulp (see “Felon”).
2. Effective treatment for early cases includes warm soaks and oral antibiot-
ics. Drainage provides more definitive treatment and is performed when an
abscess is noted. Under local anesthesia, the eponychial fold is separated from
the nail in an atraumatic fashion. If a subungual abscess is noted, the involved
portion of the nail is removed (usually <25%) after it is carefully separated
from the underlying matrix by a small elevator. The area is fully decom-
pressed and irrigated. Incisions in the eponychial fold are rarely required and

should be avoided. A sterile dressing is applied, sometimes with a thin slip

of gauze to allow egress of purulent material. The next day, the dressing is
removed and soaks are begun, followed by dry, sterile dressing changes.
3. Chronic paronychial infections that are not responsive to antibiotics and nail
plate removal can be treated by marsupialization of the skin proximal to the
eponychial fold and allowing the wound created to heal secondarily.
I. Felon
1. A felon is a subcutaneous abscess in the fingertip. The fingertip is composed
of a series of fascial septa running from the distal phalanx to the skin. These
fascial bands define the poorly compliant compartments. An infection in this
small, closed space results in the rapid development of pain. Felons often fol-
low a puncture wound or a severe paronychia. The most common causative
organism is S. aureus.
2. In the earliest cases, elevation, warm soaks, and oral antibiotics are effective.
Surgical drainage is indicated when an abscess is evident. If the infection is
“pointing” on the volar surface, an oblique incision directly over that area
on the digital pad is most effective. Alternatively, a midaxial longitudinal
incision on the ulnar side of the index, long, and ringer fingers and on the
radial side of the small finger and thumb can be used. Branches of the digital
nerve are avoided while the pad is decompressed with a fine clamp or scis-
sors by disrupting the fibrous septa so that all the small compartments of the
fingertip are decompressed. After irrigation, the wound is packed open and
antibiotics are started. A protective splint is placed over the distal digit. The
next day, the packing is removed and soaks are begun.
J. Septic flexor tenosynovitis
Purulence within the flexor tendon sheath is one of the most dreaded hand infec-
tions. If left untreated, it can affect the precise gliding mechanism of the digit
and cause tendon necrosis and rupture. S. aureus is the most common organism
isolated with a penetrating injury as the most common etiology. Hematogenous
spread can occur in gonococcal infections.
1. Diagnosis
Diagnosis is based on clinical criteria, specifically
a) Kanavel four cardinal signs:
1) Fusiform swelling of the digit
2) Resting flexed posture of the digit
3) Pain to palpation along the flexor sheath
4) Pain with passive extension of the digit
b) Because contiguous spread is not uncommon, the anatomic relationship
of the flexor sheaths to deep spaces of the hand should be kept in mind in
treating these infections. The small finger flexor sheath becomes the ulnar
bursa proximally, and similarly, the thumb flexor sheath is contiguous with
the radial bursa. The radial and ulnar bursae communicate at the level of the
wrist in 50% to 80% of patients, often resulting in a “horseshoe abscess.”
2. Treatment
a) Very early cases (<24 hours) can be treated nonoperatively with elevation,
immobilization, intravenous antibiotics, and close observation.
b) If improvement is not noted in 12 to 24 hours, surgical decompression
is required. Two incisions are generally required, one oblique incision at
the level of the distal palmar crease and a longitudinal midaxial incision
at the level of the distal joint.

c) The sheath is copiously irrigated in a flow-through manner from proximal

to distal.
1) On occasion, adequate irrigation of the sheath cannot be performed
in this fashion because of loculation of pus or technical difficulties.
2) In these cases, the midaxial incision is extended proximally and the
sheath is fully exposed. The sheath is incised between the A2 and
A4 pulleys.
d) If flow-through irrigation is achieved, a continuous postoperative irriga-
tion system can be used. An angiocatheter is threaded into the sheath
through the proximal incision, checked for ease of irrigation, and unfet-
tered egress of the fluid. It is then sutured in place. A small Penrose
drain is advanced into the tendon sheath through the distal incision to
help maintain adequate outflow. Sterile intravenous tubing connects the
angiocatheter with a three-way stopcock. Fluff dressings are then applied
with a resting hand splint. A bag of fluid and a syringe are attached to the
remaining two ports of the stopcock. Postoperatively, 15 to 20 mL of fluid
is flushed through the system four to six times per day for 48 hours. This
may cause patient discomfort and require instillation of local anesthetics.
This process is often difficult to accomplish and generally adequate irriga-
tion can be achieved in the OR.
e) Next, the splint is removed in favor of whirlpools two to three times per
day and functional rehabilitation.
K. Collar-button abscess
Patients with a collar-button or web space abscess present with abducted digits
and pain, swelling, and erythema in the web space. This abscess forms from a
distal palmar callus, blister, or fissure (often in laborers) or spreads from an infec-
tion in the proximal part of the finger. Because this infection is both volar and
dorsal, two incisions are frequently needed. A transverse incision in the interdigi-
tal space causes web space contracture and should be avoided.
L. Atypical bacterial infections
The most commonly encountered atypical infection is from Mycobacterium
marinum and often presents with pain and swelling with the clinical appearance
of tenosynovitis. There is often a prolonged incubation period following expo-
sure, delaying development of symptoms, and subsequent diagnosis. Because the
diagnosis is not usually evident, patients often present to multiple physicians
and have multiple failed treatment regimens. These infections are commonly
seen following aquatic exposure, but patients may not recall an inciting injury.
Because the organism grows at lower temperatures (30°C to 32°C), these infec-
tions are limited to the extremities. Tissue biopsy is required for diagnosis and
must be cultured on Lowenstein-Jensen medium at 30°C to 32°C. Treatment
involves prolonged course of antibiotics, often using a multidrug regimen.
IV. Fungal Infections
Fungal infection in the hand may be broadly categorized into cutaneous, subcutaneous,
and deep space or systemic forms.
A. Cutaneous
Cutaneous lesions involve the skin or nails.
1. Onychomycosis (tinea unguium) is a relatively common infection of the
nail caused by dermatophytes such as Trichophyton rubrum and C. albicans.

Individuals whose hands are constantly moist or wet are most susceptible.
Early in the infection, there is a thickening of the paronychium progressing
to nail thickening, cracking, discoloration, and sometimes softening with
eventual nail disintegration. This infection may be confused with nail defor-
mities caused by psoriasis or vitamin deficiencies.
2. Potassium hydroxide preparation of nail scrapings can confirm the diagnosis.
3. Treatment consists of topical or oral antifungal agents. Unfortunately, ony-
chomycosis is often refractory to treatment and has a high recurrence rate.
In refractory cases, when the whole nail is involved or when a secondary
bacterial infection is present, the nail is removed and oral antifungal agents
are used. Antibacterial medication is added if needed. Cure rates range from
57% to 80%.
B. Subcutaneous
1. Sporotrichosis is a subcutaneous infection caused by Sporothrix schenckii.
The infection is found predominantly in people who work with plants,
particularly roses. The rose thorn introduces the organism into the subcuta-
neous tissues. The initial papulonodular lesion ulcerates, and the infection
spreads through lymphatic drainage. Regional lymph nodes enlarge and may
ulcerate.
2. Diagnosis is made by fungal culture.
3. Treatment consists of a saturated solution of potassium iodide. Itraconazole
can also be used and is effective against lymphocutaneous disease. Even
without the characteristic skin symptoms, sporotrichosis can become a deep
infection and spread to bones and joints.
C. Deep/systemic
Deep fungal infections are usually coccidiomycosis, blastomycosis, or histoplas-
mosis. Opportunistic infections include aspergillosis, candidiasis, mucormyco-
sis, and cryptococcosis. The route of inoculation is usually through the lungs
with subsequent hematogenous spread. Treatment consists of amphotericin B
and surgical debridement.
V. Viral Infections
A. Herpetic whitlow
1. Caused by herpes simplex virus types 1 and 2, this infection is usually seen
on the fingertips of young children or medical or dental personnel exposed
to orotracheal secretions.
2. Herpetic whitlow is characterized by vesicles (without pus) that coalesce into
bullae, unroof, and then ulcerate, followed by epithelialization. Systemic
symptoms of fever, malaise, and lymphadenopathy are sometimes present.
This painful infection begins 2 to 14 days after exposure and runs a self-
limited course over several weeks. The patient is considered contagious until
the lesions have healed. Immunosuppressed patients will experience a more
prolonged course. These patients often require antiviral medication to resolve
the infection. Recurrences are induced by a number of precipitants, especially
stress, be it psychological or physical. Some patients may experience a pro-
drome of pain or paresthesias in the involved digit.
3. Diagnosis is made by physical examination, culture of the fluid within the
vesicles, analysis of the tissue with Tzanck smear, and rise in antibody titers.

4. The treating physician can easily confuse herpetic whitlow with a paronychia
or felon. Herpetic whitlow subsides within weeks without specific medical
or surgical therapy and debridement can cause a secondary bacterial infec-
tion. Herpes simplex infection is the most common infection in the hand in
human immunodeficiency virus–positive patients.
B. Warts
Common warts (verruca vulgaris) and flat warts (verruca plana) are caused
by human papillomaviruses. Common warts appear as a painless, raised, gray
mass with an irregular surface. Treatment is usually sought for cosmetic reasons.
Although it is uncommon, physicians should look for signs of deeper spread or
malignant transformation. Treatment of patients with normal immune function
is observation or topical therapies such as keratolytic agents.
VI. Bites
Infections related to animal and human bites are covered in Chapter 33.
VII. Postoperative Infections
A. Infections are uncommon after elective hand surgery. When they do occur, they
are typically caused by Gram-positive organisms. Presentation is typically 3 to
7 days after surgery. The literature does not support the routine use of antibiotic
prophylaxis in clean, elective hand procedures that last less than 2 hours.
B. The antibiotic chosen for prophylaxis should cover the organisms commonly
involved in postoperative infections (S. aureus and Staphylococcus epidermidis)
and have a low morbidity and expense. First-generation cephalosporins are
favored for this purpose. Clindamycin or vancomycin is commonly used for
patients allergic to cephalosporins or penicillin.
VIII. Infections in Post-traumatic Wounds
The literature does not support the routine use of prophylactic antibiotics in healthy
patients with uncomplicated soft tissue wounds without bone, joint, or tendon involve-
ment that are effectively treated acutely. The rate at which traumatic wounds become
infected is dependant on injury factors such as the type and number of organisms intro-
duced at the time of injury, the anatomic location of the wound, and the complexity of
the injury. A wound with a high degree of tissue devitalization is more likely to become
infected.
IX. Mimickers of Hand Infections
A. Crystalline arthropathy
1. Gout and pseudogout are inflammatory arthropathies that may have a clini-
cal presentation similar to that of septic arthritis. Involved joints are pain-
ful, erythematous, swollen, and diffusely tender. Differentiation is based
on past medical history, radiographs, and arthrocentesis. The patient may
have had similar “attacks” in the past, involving the metatarsophalangeal

joint of the great toe or other joints. Chondrocalcinosis is sometimes seen

on radiographs, especially in the region of the triangular fibrocartilage of the
wrist with pseudogout. The white blood cell count in the joint is moderately
elevated, rarely reaching levels consistent with septic arthritis. Joints involved
are frequently arthritic.
2. Therapy for crystalline arthropathy includes splinting, anti-inflammatory
agents and if needed colchicine for symptomatic treatment until the acute
episode subsides.
B. Pyogenic granuloma
1. These lesions present as red, friable masses that frequently penetrate through
the skin and can be prominent and dramatic in appearance. Pyogenic granu-
loma may form in response to a penetrating wound or a retained foreign
body.
2. Treatment by cauterization with silver nitrate is frequently effective. Surgical
excision is curative.
C. Pyoderma gangrenosum
1. This process is associated with several systemic diseases, such as ulcerative
colitis and Crohn disease. It presents as a small, painful ulcer that expands
and undergoes central necrosis.
2. Treatment includes biopsy, topical or systemic steroids, and evaluation/treat-
ment of the systemic disease.
D. Neoplasia
Metastatic lesions in the hand can present with pain, inflammation, ulceration,
and a radiographic appearance similar to that seen with an infection.
E. Acute calcific tendinitis
This condition may be confused with an infection because of its findings of
erythema, edema, pain, and occasional fever. The onset of symptoms is acute
and pain is often localized over the tendon or ligament that contains the calcium
deposit. The diagnosis is confirmed by centering the radiograph on the region of
maximum tenderness. The most common site is the pisiform. Calcific tendinitis
is self-limited and resolves without treatment.
Suggested Readings
Abrams RA, Botte MJ. Hand infections: Treatment recommendations for specific types. J Am Acad
Orthop Surg. 1996;4:219–230.
Barbieri RA, Freeland AE. Osteomyelitis of the hand. Hand Clin. 1998;14:589–603.
Louis DS, Jebson PJL. Mimickers of hand infections. Hand Clin. 1998;14:519–529.
Murray PM. Septic arthritis of the hand and wrist. Hand Clin. 1998;14:579–587.
Neviaser RJ. Closed tendon sheath irrigation for pyogenic flexor tenosynovitis. J Hand Surg.
1978;3:462–466.

Compartment Syndromes
27
Fraser Leversedge
I. Definition
A. A condition in which interstitial tissue pressures within an osteofascial compart-

ment are elevated to sustained, nonphysiologic pressures.
B. Compartment syndrome may be considered as incipient, acute, late (delayed
diagnosis), chronic/exertional, or from extrinsic compression such as from a
constricting cast or splint.
II. Pathophysiology
A. In general, increasing pressure within a confined space will compromise the

circulation and function of its contents.
B. The law of Laplace determines the equilibrium about the vessel wall:
Pi – Po = T/R
where Pi is the pressure inside vessel
Po is the pressure outside vessel
T is the vessel wall tension
R is the radius of vessel
C. Local blood flow (LBF) is determined by the following equation:
LBF = (Pa – Pv)/R
where Pa is the arterial pressure
Pv is the venous pressure
R is the local vascular resistance
D. Progressive pathologic alteration in compartmental physiology is described below:
Increased compartment pressure
¯
Venous outflow obstruction
¯
Increased capillary permeability
¯
Increased intracompartmental pressure
¯
Decreased arterial perfusion
¯
Decreased tissue oxygenation
¯
Reversible ischemia
¯
Irreversible ischemia
483

III. Pertinent Anatomy
Multiple osteofascial compartments have been described for the upper extremity (below);
however, subcompartmentalization of these compartments, such as the flexor digitorum
profundus within the volar forearm compartment, has been observed clinically.
A. Brachium/arm (Fig. 27.1)
1. Deltoid (anterior, middle, and posterior subcompartments)
2. Anterior compartment
3. Posterior compartment
B. Antebrachium/forearm (Fig. 27.2)
1. Dorsal compartment (superficial & degs)
2. Volar compartment (superficial & degs)
3. Mobile wad
C. Hand (Fig. 27.3)
1. Carpal tunnel/distal ulnar tunnel
2. Thenar compartment
3. Hypothenar compartment
4. Dorsal and palmar interosseous compartments
5. Digit
IV. Compartment Syndrome: Etiology
A. There are many potential etiologies for the condition of compartment syndrome,
including
1. Fracture or soft tissue injury (trauma)
2. Prolonged limb compression
Figure 27.1 Cross-sectional illustration demonstrating the compartments of the upper

arm. (Reprinted with permission. Copyright 2009: Leversedge FJ, Goldfarb CA, and
Boyer MI.)

Chapter 27 • Compartment Syndromes 485
Figure 27.2 Cross-sectional illustration demonstrating the compartments of the

forearm. (Reprinted with permission. Copyright 2009: Leversedge FJ, Goldfarb CA,
and Boyer MI.)
Figure 27.3 Cross-sectional illustration of the compartments of the hand. (Reprinted

with permission. Copyright 2009: Leversedge FJ, Goldfarb CA, Boyer MI.)

3.
Arterial injury
4.
Reperfusion injury
5.
Snakebite injury
6.
Electrical burns
7.
Hematologic disorders
8.
Infections
9.
Iatrogenic: excessive tourniquet ischaemia
a) Limb lengthening
b) Closure of fascial defects
c) Constrictive cast/splint/dressing
d) Complications of intraoperative positioning
e) Intermittent, exercise induced
B. Remember: Compartment syndrome can develop in the presence of an open wound.
V. Diagnostic Considerations
A. History of injury
1. Consider both intrinsic (intracompartmental bleeding/swelling) and extrin-
sic (tight cast or dressing) factors, which may elevate intracompartmental
pressures.
2. External compression, such as from a constricting cast or splint, can contrib-
ute to the elevation of intracompartmental pressure.
B. Clinical evaluation
1. Compartment syndrome, or an incipient condition, is primarily a clinical
diagnosis although objective testing may be confirmatory.
2. Six “P”s are considered in the diagnostic evaluation of compartment syndrome:
a) Pain with passive stretch
b) Increased pressure of the affected compartment on palpation
c) Paraesthesias
d) Paralysis
e) Pallor
f ) Pulselessness
Of these six Ps, only the first is seen in compartment syndrome but not
in cases of arterial insufficiency.
3. Evaluation should include inspection for swelling/dysvascular changes, pal-
pation of swollen/tense compartments, and assessment for neurological
dysfunction and pain out of proportion for injury.
4. A predictable progression of neurological dysfunction has been described:
a) Subjective numbness.
b) Hypaesthesias to light touch/pinprick.
c) Motor weakness.
d) Anesthesia.
5. When evaluating a patient for compartment syndrome, the examination
can be difficult as patients exhibit a range of pain responses to injury such
as fractures. However, those with compartment syndrome will nearly uni-
versally describe unrelenting pain that is not improved by loosening dress-
ings, elevation, or pain medication. Manual compression of the involved
extremity will identify tense swelling (this may be less obvious with

increasing subcutaneous fat). Gently moving digits distal to the injury

will be poorly tolerated. At that time or beginning shortly after the com-
plaints of pain, patients describe subjective paresthesias distally in distri-
butions of nerves coursing through effected compartments. Compartment
syndromes should be diagnosed before paralysis, pallor, and pulselessness
occur.
C. Differential diagnosis
1. Arterial insufficiency: Paraesthesias, paralysis, pallor, pulselessness but no
pain on passive stretch.
2. Acute carpal tunnel syndrome: Paraesthesias in the median nerve distribution
following distal radius fracture.
3. Nerve laceration: Paraesthesias, paralysis but these are confined to a single
nerve distribution and generally do not have excessive swelling or pain on
passive stretch.
Late findings in a missed compartment syndrome include a history of
increased pain in the extremity that has resolved with the limb now demonstrat-
ing more “woody” or firm swelling with paraesthesias/paralysis. These findings
should be correlated with the timing of the injury and sequence of complaints to
determine if decompression is of any potential benefit or will place the patient
simply at increased risk for infection.
D. Objective testing/manometry
1. Various methods of intracompartmental tissue pressure measurement have
been proposed including
a) Needle manometry
b) Indwelling wick catheter
c) Slit catheter
d) Stryker hand-held manometer
2. Needle manometry, through an infusion technique as described by Rene-
man and subsequently detailed by Whitesides, is simple and does not rely on
electronic gauges, although the method is simplified using an arterial line
setup.
3. As compartment syndrome is a dynamic condition, a definitive diagnostic
pressure threshold has not been determined. There are several proposals for
consideration:
a) more than 40 mm Hg
b) within 20 mm Hg of diastolic blood pressure
c) more than 30 mm Hg
d) within 30 mm Hg of DBP (atraumatic) or: within 40 mm Hg of DBP
(traumatized tissue)
4. Normal tissue pressures: 0 to 12 mm Hg
5. Tissue pressures, within the same compartment, may vary significantly with
measurements obtained as close as 4 to 5 cm in both normal and traumatized
limbs.
6. Indications for objective testing/manometry include patients for whom
a clinical examination is difficult or is not practical. This group includes
patients who are
a) Uncooperative or unreliable (the pediatric patient).
b) Unresponsive patients (obtunded or sedated patients).
c) Patients with neurological deficit(s) attributable to other conditions.

VI. Treatment
Recognition of compartment syndrome necessitates emergent surgical decompres-

sion of the involved compartments. Prophylactic fasciotomies may be indicated for
patients with conditions presenting a high risk for the development of compartment
syndrome.
Perioperative considerations include the following:
A. Preoperative management
1. Recognition of emergent condition
2. Remove external sources of limb compression
3. Position limb at the level of the heart
4. Medical resuscitation
5. Monitor for myonecrosis (myoglobinuria and renal dysfunction)
6. Antibiotics and tetanus update should be routine
7. The utilization of anticoagulants or antiplatelet agents should be reassessed
B. Surgical management
1. Timeliness of treatment is imperative to maximize ultimate outcomes
2. Incision planning is critical for secondary wound closure and reconstruction
3. Incisions should be placed to maximize soft tissue viability and the potential
for coverage of vital neurovascular structures (Figs. 27.4 and 27.5).
4. Fasciotomies of the primary compartments are critical for decompression.
Decompression of subcompartments and epimysiotomy have been demon-
strated to improve tissue viability.
5. Adequate debridement of devitalized structures is imperative
Volar
Volar ulnar
Figure 27.4 Incision placement for standard volar surgical approaches for forearm
compartment decompression. (Courtesy: American Society for Surgery of the Hand.)

Figure 27.5 Incision placement for a standard dorsal surgical approach for compartment
decompression of the forearm and hand. (Courtesy: American Society for Surgery of
the Hand.)
6. Primary skin closure following decompression is contraindicated as

re-elevation of intracompartmental pressure occurs.
7. Fractures should be stabilized as a part of the initial surgical procedure.
8. Specific considerations include the following:
a) Forearm
1) Volar incision begins proximal to the elbow.
2) Typically, a Henry or McConnell approach is used.
3) The lacertus fibrosus is released.
4) Volar decompression includes carpal tunnel release (pneumatic tour-
niquet control for carpal tunnel release is helpful).
5) The pronator quadratus and deep flexors are released as well.
6) Longitudinal, dorsal incision should extend distally to the level of the
musculotendinous junction, usually at the mid- to distal one-third
forearm.
7) The extensor retinaculum is preserved.
8) Following release of the volar compartments, the mobile wad of three and
the dorsum of the forearm are reassessed for tightness before release.
b) Hand
1) Carpal tunnel decompression is routine.
2) Two dorsal, longitudinal incisions are made; one between the index
and long and the second between the long and ring finger metacarpals
for access to the interosseous muscles (Fig. 27.6 B,C).
3) Fibrous septae separate the dorsal and palmar interossei; adequate
decompression of each is accomplished by meticulous circumferential
dissection about the finger metacarpals.
4) The thenar muscles are released via a longitudinal incision along the
radial aspect of the thumb (Fig. 27.6 A).
5) Hypothenar muscles are released via an incision along the ulnar hand
(Fig. 27.6 D).
6) The adductor pollicis muscle may be released via an incision perpen-
dicular to the skin crease of the thumb-index web space of the first web
space (Fig. 27.6 E).
c) Digits
1) Decision to release digital compartments is clinical.
2) This may be necessary following thermal injury.
3) Midaxial incision on ulnar aspect of index, long and ring fingers;
midaxial incision on the radial aspect of thumb and little fingers
(Fig. 27.7).

C B
Dor. interossei C
B Dor. interosseous
fascia
A Hypothenar
muscles
Vol. interossei
Thenar
muscles Ad. pollicis
Figure 27.6 Incision placement for standard surgical approaches for compartment
decompression in the hand. (Courtesy: American Society for Surgery of the
Hand.)
C. Postoperative care
1. Minimize swelling.
2. Functional splinting may reduce stiffness/contractures.
3. Return to OR for repeat debridement and wound reassessment is indicated
at approximately 48 hours following initial surgical treatment.
4. Multiple, repeat surgical debridements may be indicated prior to consider-
ation of wound closure/definitive wound reconstruction.
D. Delayed wound closure/reconstruction
1. Wound closure ± reconstruction with split thickness skin grafting is often
completed over several return visits to the operating room. Emphasis is
placed on coverage for vital neurovascular structures initially.

Trans. ret. lig. Cleland’s lig.

Skin
Trans.
retinacular Incision
lig.
Cleland’s lig.
Grayson’s lig. Neurovascular

bundle
B
Figure 27.7 Incision placement for midaxial surgical approaches for digital
compartment decompression. (Courtesy: American Society for Surgery of the Hand.)
2. Delayed excision of skin graft(s) are often possible at more than 6 months
from surgical wound reconstruction.
E. Postoperative therapy
1. Range of motion (ROM) for the involved extremity should be instituted
early, particularly for independent tendon gliding to minimize adhesions/
stiffness/contracture. Gentle ROM may be started during hospitalization.
F. Compartment syndrome: Late/delayed diagnosis
1. At a point in which reversible ischaemia is no longer present due to a delay in the
diagnosis of compartment syndrome, surgical debridement may not be indicated
in the subacute phase due to the greater risk of secondary wound infection.
2. Tissue debridement may be considered for neurolysis or for delayed recon-
struction with tendon transfers as appropriate.
Suggested Readings
DeFelice A Jr, Seiler JG III, Whitesides TE Jr. The compartments of the hand: An anatomic study.
J Hand Surg. 1998;23A:682–686.
Havig MT, Leversedge FJ, Seiler JG III. Forearm compartment pressures: An in-vitro analysis of
open and endoscopic assisted fasciotomy. J Hand Surg. 1999;24A:1289–1297.
McCarthy DM, et al. A cadaveric and radiologic assessment of catheter placement for the
measurement of forearm compartment pressures. Clin Ortho Rel Res. 1995;312:266–270.

Leversedge FJ, Goldfarb CA, Boyer MI. Primus Manus – A Pocketbook of Hand and Upper Extrem-
ity Anatomy. Lippincott Williams & Wilkins. In Press.
Naidu SH, Heppenstall RB. Compartment syndrome of the forearm and hand. Hand Clin.
1994;10(1):13–27.
Seiler JG III, et al. Intracompartmental pressure measurements in the normal forearm. J Ortho
Trauma. 1993;7:414–416.
Whitesides TE Jr, Heckman MM. Acute compartment syndrome: Update on diagnosis and man-
agement. J Am Acad Orthop Surg. 1996;4:209–218.

Injection Injuries
28
Martin I. Boyer
A. Definition: The inadvertent introduction under pressure of paint, grease, oil, or

other liquid into the fingers or the hand leading to local superficial and deep tis-
sue necrosis, vascular and neurological embarrassment, and an urgent/emergent
need for surgical assessment and treatment.
High-pressure injection injuries of any liquid (organic, inorganic, or water
soluble) is an indication for an emergent surgical consultation for the consider-
ation of possible incision, drainage, debridement, and irrigation. These surgical
treatments may need to be repeated several times over a short period of time
(sometimes daily) in order to achieve adequate wound toilet. Following debride-
ment, provision of soft tissue coverage in the form of either skin grafts or flaps
(local or distant) may be necessary.
B. Pathogenesis
1. Both local pressure effects on tissue perfusion and direct tissue destruction
from the noxious injectate are etiologic in tissue destruction. A secondary
inflammatory reaction to the presence of paint or lubricating oils injected
under high pressure has been cited as well in ongoing tissue damage.
2. Patients at their job less than 6 months are represented highly in this group
of patients
C. Factors related to outcome
1. Injection into fingers do more poorly than injections into the palm.
2. Paint injections do more poorly than oil or grease injections.
3. Volume of injectate may be related to a poorer outcome.
4. Early surgical treatment may not necessarily lead to improved outcome
(Gelberman), although Stark has suggested that interval between injury and
surgical treatment was a “major factor” in ultimate result.
5. Patients’ function is eventually better if amputations (when required) are
carried out earlier in the course of treatment.
D. Use of steroids: Although advocated by some, there is no evidence-based support
for its widespread use.
E. Radiography
1. Mandatory.
2. Injectate is often not radio-opaque.
3. Plain radiographs cannot be counted upon to fully appreciate deep tissue
involvement or location of the injectate.
F. Physical examination
1. Small puncture wound often at the tip of the index or middle finger.
2. Wound may express injectate.
3. Variable amount of swelling in finger, palm; related to injectate (paint
and lubricating oils are more inflammatory) and time elapsed since
injection.
4. Injected material may extend down flexor sheath into palm.
493

5. Evaluate median nerve sensation for injections into the palm, thumb, index,
middle, or ring fingers; evaluate ulnar nerve for injections into the ulnar side
of the hand and small finger.
6. Gross ulnar artery or radial artery involvement is uncommon.
7. Small entry wound in a patient who presents early following injection may
belie the injury severity and lead to delay in diagnosis and treatment.
G. Treatment
1. Wide exposure of the injected area through extensile exposures (either mid
lateral or Bruner).
2. Debridement of all dead and devitalized tissue while attempting to preserve
longitudinal neurovascular structures of the digit as well as A2 and A4 pulleys
if possible.
3. Surgical excision of all foreign material and granulomata.
4. Irrigation of all exposed tissues with saline by gravity only (use of pulse lavage
irrigation is discouraged in this situation).
5. Release of the carpal canal if appropriate; release of Guyon canal if appropriate
6. Loose wound closure only (coverage of gliding tissues and neurovascular ele-
ments only).
7. Antibiotics should be given prophylactically (empiric suggestion, not evi-
dence based).
8. Tetanus status should be assessed (Td intramuscular injection if uncertain
immunization status over preceding ten years; tetanus antitoxin for prophy-
laxis after injury in nonimmune or partial immune persons may be given
3,000 to 5,000 units subcutaneously or intramuscularly).
H. Compartment syndrome
1. If suspected and confirmed by IM pressure assessment, then surgical decom-
pression of the finger, the compartments of the hand (thenar, hypothenar,
adductor, and interosseous), as well as carpal tunnel, Guyon canal, and fore-
arm as necessary
I. Postoperative care
1. Keep all gliding tissues moist (hydrocolloid gels such as IntraSite work well).
2. Frequent debridement and return to the operating room.
3. Provision of a stable durable soft tissue cover (Full Thickness Skin Graft
(FTSG), local pedicle, or island pedicle flaps can work well in the finger if
vascular embarrassment has been minimal; flag flaps or cross finger flaps also
can be utilized) is performed when serial debridements completed.
4. Early active, active assist, and passive range of motion stressing tendon glid-
ing, and digital edema control.
I. Epinephrine Injection
A. Phentolamine digital block recommended following inadvertent epinephrine

injection into finger (5 mg in 9 cc of NS)
B. Repeated administration q30 minutes until ischemia resolves
C. If no reversal of ischemia, angiogram with intra-arterial reserpine
D. If intra-arterial reserpine is ineffective, surgical incision, and lidocaine and
papaverine applied to ressel exterior.
E. If phentolamine is unavailable, terbutaline is used instead (1 mg in 10 cc of NS
proximally; 1 mg in 1cc NS for persistent distal ischemia.

Extravasation Injuries
29
Martin I. Boyer
A. Definition: The infiltration into the subcutaneous and/or deep tissues by fluids
administered usually through an intravenous cannula. It is most frequently asso-
ciated with chemotherapeutic agents, phenytoin, or intravenous contrast dye.
B. Pathogenesis
1. Direct cytotoxicity
2. Osmolar rupture
3. Vasopression, or cationic cellular toxicity
4. Mechanical compression
5. Secondary bacterial infection
C. Early treatment
1. Controversial
2. Expectant (ice and elevation)
3. Local injection of hyaluronidase 1,500 IU followed by flush with NS through
multiple small incisions over the affected area
4. Topical free radical scavengers (dimethylsulfoxide plus topoisomerase-2
inhibitor desrazoxane IV)
5. Topical corticosteroids
6. Goal of treatment is to mitigate against skin loss directly over gliding tissue
by local elimination (as much as possible) of the cytotoxic agent
D. Specific agents
1. Doxorubicin (Adriamicin), Epirubicin, and other vesicants (compounds that
cause tissue blistering)
a) Persists in tissue for 28 days or greater.
b) Fluorescein useful for evaluating extent of infiltration.
c) Complete removal of agent necessary because cell death and autolysis do
not deactivate drug and cell necrosis can continue for weeks.
d) Multiple remedies/antidotes tried; degree of functional loss related to age,
delay in diagnosis and treatment and location of infiltration.
e) For nitrogen mustards, aspiration of vesicant through the IV needle, fol-
lowed by local injection of isotonic sodium thiosulphate within 24 hours
of the extravasation.
2. Vinca alkaloids (antimicrotubule agents/mitotic inhibitors such as Vinorel-
bine, Vincristine and Vinblastine).
a) Similar treatment to vesicants.
3. Taxoids (yew tree–derived anticancer agents: Docetaxel and Paclitaxel)
a) Paclitaxel (Taxol) requires hyaluronidase injection; docetaxel might not
require hyaluronidase
b) Natural history of reported cases treated by ice, elevation, and topical
corticosteroids
c) Desquamation usually by 3 weeks
495

4. Phenytoin
a) High pH (alkaline), precipitates easily and endothelial irritant
b) Risk of purple glove syndrome if infusion rate exceeds 25 mg/minute
c) Can see severe thrombotic reaction on the histopathology of amputation
specimens
d) Greater than 33% “hand mortality”
5. IV contrast dye
a) Surgical evacuation and irrigation if greater than 20 mL
b) Preoperative x-ray can help in localizing infiltrate
6. Saline
a) Unless compartment syndrome is suspected, these can usually be man-
aged nonoperatively
7. Calcium gluconate (in neonates)
a) Expectant management of cutaneous calcimosis
b) Treatment with 2% EDTA (calcium chelator) soaks has been recom-
mended
c) Often sequellae resolve after three months
E. Surgical treatment
1. Irrigation and debridement, possible use of hyaluronidase, extravasant
specific pharmacological therapy.
2. Provision of a stable durable soft tissue cover.
3. Over the dorsum of the hand in cancer patients, posterior interosseous flap
or reverse pedicle radial forearm flaps (as opposed to STSGs or free tissue
transfers) with primary donor site closure are preferred.

Frostbite
30
Kodi K. Azari and Roee E. Rubinstein
Frostbite encompasses a spectrum of cold injury to tissues, ranging from temporary

tissue cooling to freezing and crystallization of intracellular and extracellular fluids. In the
absence of wind, frostbite injuries are associated with ambient temperatures below −2°C.
The extent of tissue damage is related to factors such as the duration of cold exposure,
the wind chill effect, altitude, and the rate of heat loss (influenced by various homeostatic
mechanisms). The fingers, toes, nose, and ears are most commonly affected.
I. Epidemiology
Frostbite poses a continual threat to individuals who participate in outdoor winter

activities and mountaineering, as well as those with inadequate shelter and poor judg-
ment due to extremes of age or mental impairment. A number of factors have been
correlated with frostbite risk as well as severity of injury.
A. Environmental factors
1. Not surprisingly, the ambient temperature, as well as the duration over
which tissues are exposed to it, has a strong environmental influence on tissue
surface temperature and thus can initiate frostbite injury. Thus, the skin and
its circulation are generally affected first. Opposing the effect of ambient cold
temperatures on the extremity skin is heat generated from the deeper tissues,
whose effect is proportional to the muscle mass of the extremity. Thus, hands
are particularly vulnerable due to their distance from the body core as well as
their relatively large surface area and small muscle mass.
2. Water and moisture can conduct heat 25 times faster than air, and because
of this, wet and windy environmental conditions (particularly when moisture
is in contact with the skin) amplify the effect of the ambient temperature and
accelerate heat loss.
3. There is evidence from human and animal studies that subjects can adapt
to relatively cold climates with prolonged exposure, and that this acclima-
tion is protective in the face of intermittent extreme cold exposure. One
putative mechanism for this acclimatization, observed in Alaskan Eskimos, is
increased peripheral blood circulation, particularly in the hand.
B. Host factors
1. Although young age is not associated with immature homeostatic function,
frostbite is more common in healthy children compared to healthy adults.
A majority of frostbite injuries in children are preventable and attributed to
improper clothing and lack of supervision during outdoor activity. Further-
more, frostbite most often affects the fingers and hands of children, while
adults more often suffer from cold injury to the toes and feet.
2. The risk of these injuries is further increased by
a) Mental illness and
b) Low socioeconomic status, which are in turn associated with
497

c) Poor hygiene
d) Unemployment and
e) Substandard living conditions
f) Alcohol abuse is a strong risk factor, in part due to the vasodilatory
effect of alcohol consumption and consequent loss of core body heat
3. Vasoconstrictive processes, from static vasoocclusive atherosclerosis (primar-
ily in the lower extremities) to vasospastic phenomena such as Raynaud dis-
ease (upper extremities), represent significant risk factors for frostbite as well.
4. The severity of the injury is furthermore affected by dependency, body posi-
tion, presence of open wounds, and constrictive clothing.
II. Pathophysiology
Vogel and Dellon described the injury pattern of frostbite in distinct phases. Familiarity
with these mechanisms is important to the understanding of therapeutic measures in
the acute postinjury period.
A. Cooling and freezing
1. There is intermittent cold-induced peripheral vasodilation, together with
transient arteriovenous shunting in the extremity. This is known as the
“hunting response,” a physiologic strategy to rewarm an extremity at the
cost of core body temperature.
2. However, if prolonged cold exposure leads to hypothermia (35°C), the
response becomes dampened, sacrificing the extremity to preserve life.
3. Tissue freezing begins with crystallization of the extracellular water, leaving
behind a relatively hypersomolar extracellular solution.
4. This alteration in osmotic balance induces fluid shifts out of cells. Destruc-
tion of cells thus occurs through dehydration as well as mechanical trauma
from expanding crystals.
B. Rewarming
1. Extracellular ice crystals begin to melt, creating a hypoosmolar interstitium.
Resultant fluid shifts cause cells to swell or lyse. Endothelial cell damage pre-
dominates first, creating leaky capillaries vessels, and significant edema. Cellular
injury increases exponentially with repeated cycles of freezing and rewarming.
2. This cycle of cell injury causes progressive tissue damage. This is medi-
ated by the release of high local levels of prostaglandin and thromboxane
A2, which increase platelet and leukocyte adhesiveness and further constricts
blood vessels. The resultant increase in blood viscosity leads to thrombosis,
peripheral circulatory failure, and ischemic necrosis of the frostbitten tissue.
Thromboxane levels have been shown to correlate with the extent of tissue
necrosis from frostbite.
C. Resolution
Dependant upon the extent to which the tissue has been damaged prior to diag-
nosis and rewarming, as well as the clinical management of the injured tissues.
III. Evaluation
A. Clinical examination
The clinical evaluation of frostbite injuries aims to determine the extent, or
depth, of soft tissue damage. A thorough history must include an assessment

Chapter 30 • Frostbite 499
of comorbid conditions as well as the duration of cold exposure. Similar to burn

injuries, the extent of tissue injury is often difficult to discern at the initial evalu-
ation, and time is needed for nonviable tissues to clearly demarcate or “declare
themselves.” A particularly difficult challenge is the timely diagnosis of damage
to the bones of the hand. Clinical examination and close follow-up remain the
mainstays of the evaluation of frostbite, but several other diagnostic modalities
are available (Table 30.1).
B. Ancillary studies
1. Plain radiography—changes are variable, and may appear weeks to months
after the injury
a) Osteopenia (detectable after 4 to 10 weeks, may resolve by 6 months
postinjury)
b) Osteolytic lesions of the articular surfaces of small joints (detectable after
6 to 8 months)
c) Periosteal reaction
d) In children, phalangeal growth retardation or deformity may be noted
after 12 to 24 months (due to fragmentation or premature partial/com-
plete fusion of epiphyseal growth plates)
2. Triple-phase bone scan
Technetium bone scans have been shown to correlate with the final extent of
tissue damage from frostbite months before it becomes clinically apparent.
One study demonstrated clinical reliability within 48 hours of admission,
and that positive uptake correlated with eventual healing. This modality is
employed frequently today within the first several days after injury, in order
to assess the microcirculation of both bone and soft tissues.
3. Magnetic resonance imaging (MRI/MRA)
This modality permits the direct visualization of occluded blood vessels
and injured soft tissues. It is useful in establishing a clear demarcation of
TABLE 30-1 Clinical examination and classification
Superficial Deep
First degree Second degree Third degree Fourth degree
(partial skin (full-thickness (full-thickness (freezing extends
freezing) skin freezing) skin and to muscle,
subcutaneous tendon, bone)
tissue freezing)
Edema Edema Edema Little edema
Erythema and Erythema Blue-gray Initially mottled,
hyperemia discoloration deep red, or
(skin necrosis) cyanotic
Absence of Blistering with clear Violaceous and No blisters
blisters or fluid-containing hemorrhagic
necrosis vesicles blisters
±Desquamation Desquamation of Desquamation of Becomes dry,
after several blisters and blisters and for- black, and
days formation of eschar mation of eschar gangrenous

nonviable tissues before one becomes clinically evident; however, further

studies are needed to define radiographic features predictive of necrosis. The
cost of magnetic resonance studies is high, but MRI/MRA may confer a
substantial savings by guiding early surgical intervention and averting severe
infections and long hospital stays.
4. Thermography
Because it may take months before a clear line of tissue demarcation
becomes clinically evident, this modality is currently being investigated as
a potential aid in establishing early the junction of viable and nonviable
tissues.
5. Angiography
Angiograms have been used to delineate the extent of vascular compromise
after cold injury, as well as to detect neovascularization and collateral cir-
culation to the injured tissues. Clinical usefulness is controversial and case
dependent.
IV. Treatment
A. Prehospital care
1. Priority: Protect extremity from mechanical trauma
2. Do not initiate any rewarming at the scene unless definitive treatment is
available as repeated freeze-thaw cycles cause exponential increases in cellular
damage.
B. Hospital care
1. A measurement of core temperature is a critical first step in hospital care of
frostbite. All cold and wet clothing must be removed. Further treatment of
the extremity should not be undertaken until the core temperature reaches
above 35°C. At this temperature, the “hunting response” resumes, and the
peripheral circulation is again granted access to the warmer core. A paradoxi-
cal decrease in body temperature may result from the return of cold extremity
blood.
2. Rewarming of the extremity proceeds by rapid thawing, but excessive heat
should not be used.
3. In the acute period, therapies are aimed at maximizing the viability of the
involved tissues and minimizing infections.
4. The Heggers-Robson protocol should be adopted as follows:
a) Measurement of core temperature, while protecting involved extremity
from mechanical injury.
b) Core warming measures initiated first (warm IV fluids, blankets, etc.) in
setting of hypothermia. Multisystem evaluation proceeds as per trauma
protocol.
c) When core temperature is stably above 35°C, affected extremities are
rapidly rewarmed in circulating warm water (40°C to 42°C) for 15 to
30 minutes.
1) Patients presenting more than 24 hours after injury are not
rewarmed.
d) Tetanus prophylaxis and analgesics are administered.
e) A course of penicillin (500,000 units, IM, every 6 hours) is given until
edema resolves.

Chapter 30 • Frostbite 501
f ) ±Triple-phase technetium-Tc99m bone scan.

g) Debridement of blisters and application of topical aloe vera every 6 hours.
Wounds are dressed with moist, nonocclusive dressing and coverted to a
dry dressing when wounds are no longer draining.
h) Affected extremities are elevated.
i) Unless medically contraindicated, ibuprofen, 12 mg/kg/day, is pre-
scribed.
j) Hydrotherapy is performed daily.
k) Early ambulation is encouraged with regular physical therapy and/or
occupational therapy, which may require prolonged courses for rehabili-
tation.
C. Conservative therapies
1. Aloe vera cream is now widely used on frostbite wounds, because it is a
potent inhibitor of thromboxane A2. Other medical therapies that inhibit
the arachidonic acid metabolites (prostaglandin and thromboxane) present
in frostbite wounds are also beneficial. These include aspirin and nonsteroi-
dal anti-inflammatory agents (NSAIDs), such as ibuprofen.
2. Blood-thinning agents such as dextran, heparin, and urokinase have shown
variable benefits in frostbite wounds, and are not routinely used at the pres-
ent time.
3. Administration of thrombolytic agents, such as tissue plasminogen activator,
has shown that early administration can save digits and limit the extent of
amputations. This pharmacologic technique is still being assessed critically,
however.
D. Surgical care
1. Debridement/amputation should be delayed until viable tissue can be reli-
ably differentiated from nonviable tissues, usually 1 to 2 months after the
injury.
2. Only in the setting of uncontrolled infection should early debridement be
undertaken.
3. Amputations should be conservative in the absence of infection (the tissues
usually heal well due to hyperemia), and should be staged if purulence or wet
gangrene is noted.
4. For wounds that have required skin grafting, pressure therapy with elastic gar-
ments and/or silicone sheets can be employed for 6 months to improve scars.
Spacers to minimize web space contractures in the hand are also useful.
5. Surgical and chemical sympathectomies have been shown in human and ani-
mal studies to hasten tissue recovery and decrease tissue loss. Furthermore,
there may be long-term benefits, including decreased risks of vasospasm, cold
sensitivity, and peripheral neuropathy. Currently, the role of sympathectomy
in the setting of frostbite remains controversial.

Thermal Injuries
31
Kodi K. Azari, Christine Fisher,
and Galen S. Watchman
I. Definition/Introduction
Thermal injury to the upper extremity and hands remains a common clinical event.
The severity of injury ranges from mild to catastrophic, and recovery from burn injuries
must take into consideration functional as well as aesthetic outcomes. The cornerstones
of upper extremity burn care are early excision and stable soft tissue coverage, splinting,
early mobilization, and concerted rehabilitation.
II. Epidemiology
The upper extremity is involved in 89% of burns, with 1% of the population of Western
countries sustaining a burn injury each year. One fourth of these patients will require
medical care.
III. Anatomy
The dorsum of the hand is more likely to be involved in explosive or flame injuries
while the palmar surface is more likely to be involved in friction burns and electrical
injuries. The location of the burn wound is significant in the severity of the injury. The
thin and mobile skin on the dorsum of the hand facilitates direct thermal effects on
the tendons, blood vessels, and joints directly below the surface. The glabrous skin on
the palmar surface of the hand has a thick epidermis and subcutaneous fat layer with
a dense arrangement of fibrous septa connecting to the deep fascia to provide shock
absorption and frictional stability.
IV. Pathophysiology
A. The duration of heat exposure and the temperature of the heat source determine
the severity of a burn.
B. Thermal injury to the skin leads to protein denaturation, blood vessel coagula-
tion, and increased capillary permeability, thus creating zones of necrosis, stasis,
and impaired circulation.
C. Burns of 20% or more total body surface area (TBSA) result in generalized
edema and swelling of nonburned tissues.
D. Fluid shifts from the intravascular to interstitial spaces cause edema, which can
decrease perfusion.
E. Inadequate fluid resuscitation can lead to the conversion of zones of stasis to
necrosis. Elevated tissue pressures due to swelling or constriction by circumfer-
ential full thickness burns can cause neurovascular injury to a limb.
502

Chapter 31 • Thermal Injuries 503
F. Approximation of surface area of body burned: Head 9%, anterior chest and
abdomen 18%, posterior chest and abdomen 18%, each arm 9%, each leg 18%,
and genitalia 1%.
V. Evaluation
The evaluation of thermal injuries is based on the extent and severity of soft tissue
injury. The extent of the injury may not be clear early as it is often difficult to determine
the depth of the burn. All burned patients must be fully evaluated for concomitant
systemic injuries and aggressively resuscitated. Referral to a specialized burn center has
been well defined by the American Burn Association.
A. American burn association criteria for transfer
1. Partial thickness to full thickness burns greater than 20% TBSA in patients
10 to 50 years old.
2. Partial thickness to full thickness burns greater than 10% TBSA in patients
less than 10 years of age or greater than 50 years of age.
3. Full thickness burns greater than 5% TBSA in patients of any age.
4. Partial or full thickness burns to hands, feet, face, eyes, ears, perineum, geni-
talia, and major joints.
5. High-voltage electrical injuries, including lightning.
6. Chemical burns.
7. Any patient with burns or concomitant trauma (e.g., fracture) in which
the burn injury poses the greatest risk of morbidity or mortality. When the
trauma poses a greater immediate risk, the patient may be treated initially in
a trauma center until stable before transfer to a burn center.
8. Inhalational injury.
9. Circumferential burns to extremities or chest.
10. Patients with preexisting medical conditions that make burn resuscitation
and recovery more difficult or present a risk of mortality (diabetes, chronic
obstructive lung disease, and coronary artery disease).
11. Hospitals without qualified personnel or equipment for care of burn-injured
children.
12. Patients with burns who will require special social, emotional, or long-term
rehabilitative support. (This includes cases involving suspected child abuse,
substance abuse, etc.)
Clinical evaluation of the burned extremity remains the most important
tool. It may be difficult to assess the true depth of injury, and serial examina-
tions over several days may be required to determine the level of demarcation
of devitalized tissues.
B. Thermal injury is best described by the layer of tissue involved
1. Superficial (first degree) burns involve the epidermis only, are erythematous
in appearance, painful to the touch, and are best treated with topical care only.
2. Partial thickness (second degree) burns involve the entire epidermis and
the dermis to varying depths.
a) Superficial partial thickness burns are usually pink, moist, and painful;
they will heal spontaneously in 2 to 3 weeks and are best treated conser-
vatively.
b) Deep partial thickness burns are characterized by a dry, mottled pink
to white appearance with variable sensation. Early excision and grafting

are necessary for burns of this depth to avoid prolonged healing and
minimize the risk of hypertrophic scar formation.
3. Full-thickness (third degree) burns extend below the dermis. The skin may
appear pale-white and waxy to leathery brown. These burns are painless, and
require excision and grafting as all dermal elements have been lost.
4. Fourth-degree burns have been described as burns that include deeper struc-
tures such as bone or tendon.
VI. Treatment
The burned patient must be fully evaluated for systemic injuries and triaged to a burn
center if necessary.
A comprehensive history of the injury is essential to correct diagnostic and thera-
peutic decision making. Knowledge of the mechanism of the burn and the circum-
stances surrounding the injury can help the health care provider estimate the severity
of the burn.
Thorough documentation of the initial injury is important, including measure-
ment of the size of the burn and definition of the likely depth of the burn, includ-
ing the presence and severity of associated injuries. Photographic documentation is
valuable.
A. The burn should be washed with copious lukewarm water and scrubbed with
antibacterial soap.
B. Tissue perfusion
1. Evaluate tissue pressures and burn wound severity to assess the need for
emergent operative treatment by initial escharotomy. Early escharotomy of
full-thickness burns is advocated. The wound receives a skin graft or flap for
coverage, or a temporizing dressing is applied. Unnecessary death of normal
tissue may be prevented by aggressive use of early escharotomy.
2. Circumferential eschars are initially incised prophylactically to allow for
the inevitable early swelling that occurs. Patients become edematous due to
aggressive fluid resuscitation and progressive local inflammation that affect
the burn wound.
3. Late effects of circumferential partial thickness burn wounds, such as scar
contracture, cause compression neuropathies or deform underlying struc-
tures and impair their function. Zigzag incisions or digital midlateral inci-
sions help prevent scar contractures, which can be especially problematic on
the mobile joints and web spaces of the hand.
4. Circumferential burns in the upper extremity can cause decreased tissue per-
fusion and threaten limb viability.
5. Although not common in thermal burns, compartment pressures may be
elevated and require fasciotomy. This is, however, common with electrical
burns.
a) Indications for fasciotomy include objective measurements such as elevated
compartment pressures and clinical findings suggestive of tissue compres-
sion. Measurements of tissue compartment pressures are an especially
valuable tool when evaluating patients who have altered mental status.
b) Objective measurements of compartment pressure of more than 40 mm
Hg or tissue pressure within 30 mm Hg of diastolic pressure indicate an
emergent need for fasciotomy. In awake and oriented patients, a pressure

Chapter 31 • Thermal Injuries 505
greater than 30 mm Hg itself is not used as an absolute indication but

is considered with any clinical evidence of nerve compression, that is,
tingling, increased pain, decreased sensation, or vessel compression. The
clinical signs of increased compartment pressure in the face of a thermal
injury include
1) Evidence of nerve compression
2) Onset of paresthesias (early sign)
3) Decreased sensation or increased pain
4) Increased muscle turgor to palpation and cool temperature of the
limb
5) Decreased peripheral pulse (late sign)
C. Splinting and initiation of early hand therapy prevent the development of an
intrinsic minus posture in the severely burned hand, resulting in the claw defor-
mity. Scarring and fibrosis leave the wrist flexed, the MCP joints hyperextended,
the PIP and DIP joints flexed, the thumb adducted into the palm, and the
thumb IP hyperextended. The anticlaw (intrinsic plus) position prevents con-
tracture deformity. Hand splints should be applied on the day of injury, custom-
ized by the occupational therapists from thermoplastic material. Early motion is
initiated if burns over the PIP joints are superficial. The hand should be relatively
immobilized for a longer period if the thin skin over the PIP joints is deeply
burned, as disruption of the central extensor mechanism will result in a bouton-
niere deformity. Severe hand burns may require temporary pinning of the MCP
joints in flexion and the IP joints in extension to prevent the development of the
intrinsic minus deformity. This is especially helpful when the patient has other
injuries and cannot actively participate in early therapy.
VII. Wound Care
A. After initial evaluation, daily dressing changes should be initiated. Each day the
wounds are copiously irrigated and cleansed, silver sulfadiazine and nonstick
dressings are applied, and nonocclusive dressings cover the area. Splints are reap-
plied to prevent contractures.
B. The extent of a partial thickness burn becomes evident and the wound demar-
cates over time.
C. Tangential excision and split-thickness skin grafting is complete within the first
5 days after burn injury.
1. Most grafts are meshed elsewhere in the body; however, unmeshed split-
thickness grafts or full-thickness grafts should be considered in the hand to
minimize postoperative contracture.
2. Palmar burns may not require grafting due to its thickness and the intrinsic
healing ability that is unique to glaborous skin. However, dorsal burns fre-
quently require grafting.
D. Excision under tourniquet control combined with the use of epinephrine-soaked
sponges limits blood loss.
E. Integra is a proprietary dermal substitute that can be useful in dorsal hand burns.
It is applied and allowed to revascularize over a two- to three-week period and
then a thin split-thickness skin graft is applied. This theoretically allows better
tendon gliding and ultimately motion, but there are not any studies to confirm
this. It does make the coverage more durable and less prone to breakdown.

F. Postoperative splints are employed to prevent contracture with operative dress-

ings generally being removed in 3 to 5 days, and grafted areas are kept moist with
petroleum-based ointments and nonadherent dressings.
VIII. Rehabilitation
A. After successful grafting, aggressive hand therapy with focus on early active
motion and motion of all joints is employed.
B. When the patient has acceptable range of motion and control of extremities,
splints may be discontinued.
C. Therapy should be continued until scars are supple and range of motion is
maximized.
D. Custom-fitted compressive elastic garments are useful, as are Silicone gel
sheeting and massage to soften scars and to reduce their bulk.
IX. Secondary Reconstruction
After the initial wounds have healed, management of postburn deformities can be
addressed several months to years after injury. Scars should be supple and range of
motion maximized with therapy by a hand therapist before secondary surgery is con-
sidered. Correction of postburn contractures can utilize full-thickness skin grafts,
Z-plasties or W-plasties, local, distant, or free flaps.
Suggested Readings
Burnsurgery.org. [online].
Donelan, M. Principles of burn reconstruction. In: Thorne CH, Beasley RW, Ashton SJ, Bartlett
SP, Gurtner GC, Spear SL. Grabb and Smith’s Plastic Surgery. 6th Ed. Philadelphia, PA.
Lippincott Williams & Wilkins; 2006.
Germann G, Philipp K. The burned hand. In: Green DP, Hotchkiss RN, Pederson WC, Wolfe
SW, eds. Green’s Operative Hand Surgery. 5th Ed. Philadelphia, PA: Elsevier; 2005.

Chemical Poisoning
and Exposures
32
Kodi K. Azari and Roee E. Rubenstein
Chemical burns comprise a group of devastating injuries. Their management requires

expertise, especially in the acute injury period when interventions to minimize the
extent of tissue damage must be implemented. The knowledge of the specific properties
of the offending agent is important to obtain the most optimal result.
There are over 25,000 known products, which can cause a chemical burn as a result
of topical exposure, and these agents are extremely diverse. Although more than 60% of
hospital admissions for chemical injuries are work related, exposures to harmful chemi-
cals may also occur in household settings. These injuries have significant occupational
morbidity, and some patients are not able to return to their jobs. Individuals working in
the landfill industry are most susceptible to chemical exposures with industrial cleaners
and paper manufacturers following closely behind. Extravasation injuries may occur in
with chemotherapeutic and radiological contrast dyes and although often self-limiting,
can create significant tissue loss.
Despite a relative paucity of literature on the subject, hand surgeons commonly
see chemical burns as the digits are one of the most common locations of chemical
burns.
I. Pathophysiology
A. Chemical burns of the hand, like thermal burns, usually cause damage that is
limited to the skin. However, some chemical agents may continue to be active at
the site of injury, causing assiduous destruction to the tissues even after the spill
has been cleaned, and without immediate pain.
B. Determinants of the extent of tissue damage include the part of the body exposed,
the nature and concentration of the chemical agent, the volume of substance in
contact with the skin, the comorbid condition of the skin and patient, with the
most important being the duration of contact between the skin and the noxious
chemical.
C. Most chemical burns are the result of exposure to either acidic or alkaline
agents.
1. Acid chemicals erode through the skin’s protective stratum corneum, causing
fluid shifts and cellular dehydration, damaging cell membranes, and coagula-
tion necrosis. The damage can progress and spread until the agent is lavaged
away, sufficiently diluted, or neutralized. Significantly, damaged tissue retains
sufficient buffering capacity for acids to limit the depth of tissue damage
sustained.
2. Alkali burns are more dangerous than acid burns. They are clinically more
latent, and often victims do not sense the burn until the exposure is pro-
longed. Furthermore, these burns are considered “hygroscopic” because
protein-bound alkali molecules are highly reactive and lipophilic, achieving
easy tissue penetration by combining with membrane elements to form fatty
507

soaps. The damaged tissues have a limited capacity to buffer alkalis, the
wound milieu remains basic, and the reactions can continue for days with
extensive and deep tissue destruction known as liquefaction necrosis.
II. Evaluation
The evaluation of a patient who presents with a chemical injury begins with a focused
history, including the duration of exposure, the time elapsed since the accident, the spe-
cific chemical if known, the location(s) (often there are several), and comorbid skin and
systemic conditions (such as open wounds, diabetes, and peripheral vascular disease).
III. Management
The management strategy is much the same as that for thermal, electrical, and cold
injuries. The involved extremity should be elevated, immobilized, and monitored for
neurovascular status at regular intervals. A tetanus booster should be administered
appropriately upon presentation. The critical first step is to arrest the chemical process
that is creating the burn.
A. Termination of the injurious process: The first goal of treatment is the immediate
dilution or neutralization of the substance if possible.
1. Immediately after the chemical exposure, the patient should be removed
from the injurious chemical agent; including removal of all contaminated
clothing.
2. Copious and continuous water lavage, which aims to dilute the chemical
agent and decrease the chemical load to the tissue, is the appropriate treat-
ment for most chemical contact accidents. It should be performed for at least
1 to 2 hours for acid burns, and up to 12 hours for alkali burns. Further-
more, it should be initiated immediately, as any delay of treatment may allow
destruction of the epidermal barrier. Time should not be wasted looking for
specific antidotes until water lavage is in progress (with few exceptions,
discussed below).
3. Once the specific agent has been identified, neutralizing substances can be
administered. Regarding endpoints of neutralization, surface tissue pH mea-
surements can be made, but they do not provide information regarding the
deeper tissues. Furthermore, the abatement of a patient’s pain is not always
reliable due to the ability of some substances, such as phenols, to demyelinate
nerves and create an anesthetic wound.
B. Specific toxic substances and neutralizing agents
1. Phenol is widely used in industrial cleaning agents, explosives, plastics, and
even cosmetics. It is not water soluble, and thus cannot be diluted with water
lavage. It should be removed from the skin and tissue with mineral oils such
as glycerol or polyethylene glycol.
2. Hydrofluoric acid has many industrial applications and is a potent toxin that
easily penetrates the skin, particularly the nail bed, and causes severe pain.
Treatment consists of high-volume water lavage followed by specific fluoride-
binding agents such as subdermal injections of 10% calcium gluconate and
intravenous calcium solutions.
3. Cement contains the alkali lye, or calcium oxide, whose pH is 12.9. Because
it usually causes little or no pain, and is hygroscopic, it achieves diffuse

Chapter 32 • Chemical Poisoning and Exposures 509
penetration when left untreated for hours. Early detection, followed by

copious irrigation with soap and water, or vinegar (acetic acid) is paramount
for successful treatment. Unfortunately, cement burns usually present as a
full-thickness and poorly healing wound, requiring more complex recon-
structive procedures.
4. White phosphorus is highly lipophilic and fat soluble, and its tissue penetra-
tion is enhanced by topical oil-based substances. These substances should
thus be avoided, and treatment should consist of water lavage and debride-
ment of remaining solid phosphorus particles. A dilute solution of copper
sulfate causes a mild chemical reaction, which may be helpful in identifying
solid particles of phosphorus.
C. Exceptions to early water irrigation, such as hydrochloric acid, sulfuric acid, and
elemental sodium, potassium, and lithium, require specific neutralizing agents
prior to copious lavage.
1. Hydrochloric acid, a reducing agent found in industrial cleaners, can be fur-
ther ionized by water irrigation, leading to additional heat release and tissue
damage. Magnesium hydroxide, copper solutions, liquid soap, or soda
lime can be used to neutralize the acid prior to water lavage.
2. Sulfuric acid (found in car batteries) can produce extreme heat and “explode”
upon contact with water lavage. Magnesium hydroxide, copper solutions,
liquid soap, or soda lime can be used to neutralize the acid prior to water
lavage.
3. Elemental sodium, potassium, and lithium can spontaneously ignite with
water irrigation, resulting in superimposed thermal injury to the tissues.
Mineral oil should be applied to neutralize these substances when their pres-
ence is suspected.
D. Subacute management
1. Once lavage and neutralization are achieved, attention is focused on pro-
tecting the exposed tissues and damaged skin from infection. This requires
vigilant and meticulous wound care, including debridement of blisters, bul-
lae, and necrotic tissue, which may be contaminated. Nail plates should be
removed if there is any concern that chemicals have contacted the nailbed,
as the nail plate may render adequate lavage and neutralization of the under-
lying bed impossible. Topical antibiotics should be applied frequently, and
creams (such as silver sulfadiazine) may be superior to ointments, which
may obstruct the flow of wound drainage and systemic antibiotics should be
administered as well.
2. When the depth of the burn is evident, partial-thickness injuries can
be managed conservatively with dressing changes, while full-thickness
burns should be excised followed by early grafting. Occlusive dressings
should be avoided so that wound drainage can flow freely. Compromise of
deeper tissues may produce defects that require local or microvascular flap
reconstruction
3. Assessment of the neurovascular status of the extremity is imperative, as
inflammation and edema associated with chemical burns place the extremity
at risk for compartment syndrome.
a) Extremities should be elevated at all times to control edema and splinted
in the “position of safety” to minimize the risk of joint contractures.
b) Nonsteriodal anti-inflammatory agents may be beneficial in decreasing
inflammation and swelling.

c) Fasciotomy should be performed in cases with increased compartment

pressures or with high clinical suspicion, as the consequences of not
releasing the compartments can be devastating.
d) Removable splints facilitate frequent examination of the thin soft tissues
overlying the proximal interphalangeal joints, and close monitoring of
this area may prevent damage to the central slip resulting in a bouton-
niere deformity. Early soft tissue coverage of exposed tendon and joints is
recommended.
e) Early motion is encouraged to prevent postinjury stiffness, except in
cases where the dorsal soft tissues overlying the interphalangeal joints are
severely damaged.

Bite Wounds
33
Kodi K. Azari and Nelson Castillo
I. Human Bites
A. Background information
Epidemiological studies demonstrate that the hand suffers over 80% of human
bites, with the average victim being a male in his twenties. Human bites to the
hand account for 25% to 30% of hand infections annually, and over 42 species
of bacteria have been cultured from the human mouth. Although most bites are
intentionally inflicted as the result of altercations, etiologies of child abuse or
domestic violence must be considered.
B. Pathogenesis
1. Most commonly, a clenched hand strikes a tooth, resulting in potential direct
damage to overlying skin, subcutaneous tissues, extensor tendons, muscles,
and bone; secondarily, bacterial inoculation of the extensor tendon mecha-
nism, bone, and joint space can occur. Following injury, extension of the
hand allows for proximal migration of inoculated bacterium, as the extensor
mechanism returns to its resting position.
2. A gnawing-type bite mechanism to an open hand results in a crush com-
ponent that can appear to have limited hand tissue involvement, but with
limited dorsal skin thickness over superficially placed extensor tendons, sig-
nificant damage can occur. Open hand injuries can also effect damage to the
palmar surface of the hand, with skin and subcutaneous tissue loss, but with
the palm’s thicker, glaborous skin, and densely adherent fascia, less involve-
ment of the hands’ blood supply, flexor tendon mechanism, musculature,
and skeleton is seen.
C. History/physical examinations
1. Though a full history should be obtained at the time of patient interview,
the mechanism of injury, position of the hand at the time of injury, and
patient-specific conditions such as tetanus immunization and immunosup-
pressed states (steroids, diabetes, cancer, and HIV) play a large role in focused
workup of the bitten patient.
2. Physical examination should include full vascular, neurological and musculo-
tendinous evaluation. Cutaneous physical examination manifestations can
range from a single puncture-type injury, to large avulsed flap segments, each
carrying the possibility of significant short-term and long-term sequelae, the
most common of which is infection.
3. Hand infections develop as the result of a bacterial inoculum and the inabil-
ity to clear the infection in the hand tendons and deeper structures. Hand
infections can range from a mild cellulitis to a paronychia/eponychial infec-
tion, to significant purulent tenosynovitis or necrotizing fasciitis.
4. Involvement near joint spaces can result in the development of septic arthritis
with cartilaginous and bony destruction; therefore, all injuries near joints,
511

especially the metacarpo-phalangeal joint, should be managed as if the joint

is involved until effectively ruled out. Wound extension to accurately identify
tendinous injuries may be needed.
D. Laboratory exams
Differential diagnosis of patient complaints and physical examination findings
will guide laboratory examinations. Uncomplicated cellulitis does not require
blood-work, but ascending cellulitis unresponsive to oral antibiotics or demon-
strating lymphangitic spread should have a CBC to track white blood cell count,
and blood cultures to rule out bacteremia. Drainage of any fluid collection
should have both aerobic/anaerobic culture and sensitivity studies performed in
order to assist with antibiotic therapy.
E. Radiology examinations
Initial plain film x-rays are useful to rule out any concomitant osseous injury or
foreign bodies; if patients develop infectious complications, x-rays can be use-
ful baselines for osteomyelitis workup, or identification of bony destruction in
septic arthritis.
F. Treatments
1. The incidence of human hand bites far exceeds the number that receives
medical attention. Most bites to the hand should be treated as a contami-
nated wound and treated with irrigation and appropriate debridement.
2. Bite wounds should be allowed to close by secondary intention.
3. The patient’s tetanus immunization status should be updated as warranted
4. For complicated bites involving more than simple skin and subcutaneous
tissue injury, therapy then becomes injury directed: Skeletal integrity needs
to be restored following identification of fractures, control or repair of vas-
cular and neural injuries, and repair or debridement of musculo-tendinous
injuries.
5. Infectious complications are addressed by presentation: Eikenella, Bacteroides
and other anaerobic bacteria are often discussed with human hand bites, but
Staphylococcus and Streptococcus species comprise the most common causes of
hand infections.
6. Complicated cellulitis, or failure of initial oral antibiotic coverage, will require
hospital admission for IV therapy (cefoxitin/ampicillin-sulbactam). Parony-
chia, eponychia, abscesses, and suppurative tenosynovitis, require incision,
drainage, and irrigation of the fluid collections.
7. Septic arthritis and osteomyelitis require incision for culture and irrigation,
or bony curettage, followed by culture-specific antibiotics to suppress or clear
the infection.
G. Additional complications
Tissue contracture, necrotizing fasciitis, and HIV/HepB/HepC transmission.
II. Animal Bites
Annual incidence is 3 to 6 million cases, accounting for 1% of all emergency
department visits. The vast majority of these bites result from domestic animals
that are known by the victim. Dogs account for approximately 80% and cats
account for approximately 10%. Dog bites typically will result in crushing and
avulsion injuries, while cats produce puncture wounds. Both canines and felines

Chapter 33 • Bite Wounds 513
have over 100 disease-producing organisms in their oral flora, and an infected
bite from either most commonly results from a mixed aerobic and anaerobic
bacterial inoculation.
B. History/physical examinations
Though a full history should be obtained at the time of patient interview, addi-
tional key animal-specific history elements should include the following: The
type of animal, whether the attack was provoked or unprovoked, and the cur-
rent location of the animal for potential observation and testing for rabies. Key
human-specific history elements should include the following: Immunosup-
pressed states (steroids, diabetes, cancer, and HIV) and tetanus immunization
status.
Physical examination is performed in the same manner as for human bites.
C. Laboratory examinations
For infectious complications of animal bites, all purulent secretions and sites of
active infection should have both aerobic and anaerobic culture and sensitivities
performed. As for human bites, degree of infection and the health status of the
patient should guide the need for CBC and blood cultures.
D. Radiology examinations
Initial plain film x-rays are useful to rule out any concomitant bony fracture or
foreign bodies; if patients develop infectious complications, x-rays can be use-
ful baselines for osteomyelitis workup, or identification of bony destruction in
septic arthritis. A “soft tissue” window radiograph may assist in the identification
of retained tooth fragments.
E. Treatments
1. Surgical management for animal bites is the same as for human bites.
2. Infectious complications are addressed by presentation and commonly
known
a) Dog (Staphylococcus, Streptococcus, Pasteurella canis, Eikenella, Bacteroides,
and Capnocytophaga canimorsus) and
b) Cat (Pasteurella multicoda, Staphylococcus, Streptococcus, Propionibacterium,
and Bacteroides) pathogens.
3. Most animal bites obtain broad-spectrum antibiotics (amoxicillin-clavulanate)
for the increased propensity toward infection, especially seen in cat bites.
F. Complications
Rabies, sepsis, osteomyelitis, and septic arthritis.
G. Animal bites
1. Snakes—The ability to identify the snake permits rapid institution of therapy
as it distinguishes venomous from nonvenomous bite etiologies.
a) Up to 75% of snakebites are venomous, and in general, venomous snakes
tend to have triangular-shaped heads and elliptical pupils. In the United
States, the Crotalidae family of snakes causes 99% of snakebites.
b) Equine-derived antibody antivenin, or sheep-derived antigen-binding frag-
ment (CroFab), is the standard of care for venomous snakebites but must
be given with caution as allergic reactions may occur with administration.
c) Tetanus status must be addressed and updated as warranted.
d) If envenomation is known, patients should be monitored for at least
12 hours, noting extent of wound erythema for infectious potential,
and circumference of arm for compartment syndrome; laboratory
examinations focus on coagulation status, as a disseminated intravascu-
lar coagulation picture can arise with hemotoxic venom. Other potential

complications from envenomation that should be accurately monitored

include rhabdomyolysis and nephrotoxicity.
2. Skunk/bat/raccoon—Collectively contributes 90% of rabies transmission
cases in the United States. Patients suffering bites should be started on rabies
vaccination for postexposure prophylaxis.
III. Insect Bites—Spiders
Approximately 3,000 spider species exist in North America, few are large enough
or contain enough poison to threaten humans. The most dangerous spiders to
humans include the following: Black widow spiders (Southwest United States),
brown/fiddlebacked (recluse) spiders (South-Central United States), and funnel-
web spiders (mostly in Southeast Australia).
B. History/physical examinations
Though a full history should be obtained at the time of patient interview, focused
identification of the spider is of key importance. Physical examination will typi-
cally demonstrate one or two separate portals of entry at the site of the suspected
bite. One of the three possible reaction types may develop at the bite site:
1. Local inflammation (including necrotic lesions)—local redness and a ten-
der nodule
Brown spiders can produce necrotic lesions 15 to 36 hours after initial
bite, with a local blister that opens and produces a crater, taking months to
heal leaving permanent scarring.
2. Systemic reactions-fever, myalgias, fatigue, lymphadenopathy, mild coagul-
opathy
The brown recluse spider can also produce viscerocutaneous loxoscelism,
a severe intravascular hemolytic syndrome that can result in death. The black
widow can induce latrodectism, a condition characterized by severe muscle
spasms, nausea, and vomiting, hematuria, hemolytic anemia, and autonomic
activation: dizziness, sweating, tachypnea, tachycardia, etc.
3. Allergic reactions ranging from urticaria to anaphylaxis
Tarantulas are not aggressive, rarely bite, and their bites result in non-
necrotic lesions, but sensitization to the tarantula’s hairs can result in an ana-
phylactic reaction.
C. Laboratory examinations None are required.
D. Radiology examinations None are required.
E. Treatments
1. Treatment begins with local wound care, including appropriate irrigation
and debridement of the wound of all bite sites.
2. Tetanus immunization should be updated.
3. In cases of large (>2 cm) necrotizing cutaneous lesions, systemic corticoster-
oids should be given for 5 to 7 days and the area debrided once ulceration
develops; dapsone can be used to limit the extent of local necrosis, but patients
should be screened for glucose-6-phosphate dehydrogenase deficiency as
hemolytic anemia can occur in this population.
4. As systemic symptoms are varied for spider bites, supportive therapy is
directed at the involved organ system, but antivenom should be administered
for any black widow bite demonstrating systemic symptoms.

Chapter 33 • Bite Wounds 515
5. Patients with known allergic reactions to insect bites should have an EpiPen
available for severe systemic reactions, and receive full allergy therapy, includ-
ing H1 and H2 blockade.
F. Complications Necrotizing soft tissue loss.
G. Other insects
1. Mosquitoes: Worldwide, mosquito bites and their transmission of disease
result in 1 out of 17 deaths. In the United States, mosquito bites result in ery-
thematous, pruritic reactions that can last 2 to 7 days, though some disease
transmission can still be present (West Nile).
2. Ticks: Recognized cause of allergic reactions and infectious disease trans-
mission. Lyme disease is produced by Borrelia burgdorferi, a spirochete, and
transmitted by the Ixodes tick. The Dermacentor tick is responsible for the
transmission of Rocky Mountain Spotted Fever.
3. General therapy of these insect bites lies with symptomatic control of pruritis
and local edema. Albeit rare, systemic signs of insect bites must be treated
rapidly, with possible epinephrine use in cases of anaphylaxis.
Suggested Readings
Fradin MS. Mosquitoes and mosquito repellents: A clinician’s guide. Ann Intern Med.
1998;128:931.
Talan DA, et al. Bacteriologic analysis of infected dog and cat bites. N Engl J Med. 1999;340(2):
85–89.

III Other Conditions

Dermatologic Conditions
34
Lynne Cornelius and Kara Nunley
Careful examination of the skin and nails is an important part of the physical
examination of the hand. Skin lesions can provide important clues to the diagnosis
of systemic conditions, which can affect the joints. In addition, skin disease can affect
wound healing and surgical outcomes. This chapter will cover basic clinical features
and treatment of common cutaneous conditions, which the hand surgeon is likely to
encounter and be called on to recognize.
I. Eczema (Fig. 34.1)
A. Hand eczema is a common cause of discomfort and disability. It is most

common in atopic individuals, but many patients experience the onset of symp-
toms in adulthood and have no prior history of eczema.
B. Hand eczema is characterized by erythema and scaling of the palms. The
involved areas may be hyperkeratotic and crack easily. Patients often complain
of pruritus and/or pain from fissures.
C. Pompholyx, or dyshidrotic eczema, is a form of hand eczema that presents with
deep-seated vesicles on the lateral fingers and hands.
D. The clinical features of hand eczema overlap with contact dermatitis. It is
important to perform a careful history and consider patch testing to evaluate for
environmental allergens or irritants that could be exacerbating the condition.
Figure 34.1 Chronic hand eczema in a patient with atopic dermatitis. Lichenification and
hyperlinearity are evident on the palm. (From Goodheart HP. Goodheart’s Photoguide of
Common Skin Disorders. 2nd Ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2003.)
519

520 Section III • Other Conditions
E. First-line treatment involves topical steroids depending on the severity of dis-

ease. Topical steroids may be used with occlusive dressings for limited time peri-
ods to increase their penetration and efficacy. Patients who are not responsive to
topical treatment may require treatment with short courses of oral prednisone
or steroid-sparing agents.
F. Skin care is essential to decrease the severity and frequency of flares. Patients
should apply thick creams or ointments (i.e., petroleum jelly) as often as pos-
sible throughout the day and particularly after washing hands. Gloves should
be worn for all wet work. Alcohol-based hand sanitizers should be avoided in
favor of mild soaps. It is important to instruct patients that this is a chronic
condition and emphasize that these measures are an important part of their
treatment.
II. Contact Dermatitis (Fig. 34.2)
Allergic contact dermatitis is caused by a delayed-type (type IV) hypersensitivity

reaction. It occurs 24 to 48 hours after re-exposure to an allergen.
A. Irritant contact dermatitis is a nonspecific inflammatory reaction and may occur
on first exposure to a chemical.
B. Acute lesions are erythematous, edematous plaques, which may become vesicu-
lar. Scaling and lichenification characterize chronic lesions.
C. Pruritus is a prominent symptom.
D. Contact dermatitis often involves the dorsal hands. This may help to
differentiate it from hand eczema, which is generally confined to the palmar
surface and lateral edges of the hand.
E. In a recent study, the compounds most commonly implicated in allergic con-
tact dermatitis of the hand were quaternium-15, formaldehyde, nickel sulfate,
fragrance mix, thiuram mix, balsam of Peru, carba mix, neomycin sulfate, and
bacitracin.
Figure 34.2 Contact dermatitis. This eczematous dermatitis on the dorsa of the hands was
caused by exposure to lanolin. (From Goodheart HP. Goodheart’s Photoguide of Common
Skin Disorders. 2nd Ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2003.)

Chapter 34 • Dermatologic Conditions 521
F. Patients with suspected contact dermatitis should be referred to a dermatologist

for patch testing if an etiologic agent cannot be identified by history.
G. Topical steroids are the mainstay of treatment. Patients must also be educated to
avoid all substances containing the causative chemical, if one can be identified.
Short course oral steroids tapered over 2 to 3 weeks may be necessary to manage
severe flares.
III. Psoriasis (Figs. 34.3–34.6)
A. Psoriasis is a Th1-mediated immunologic disorder that results in an abnormal

increase in the rate of keratinocyte proliferation.
B. It classically manifests as well-demarcated erythematous plaques with thick,
silvery scale. On the hands, it may present with palmar scaling and hyperkerato-
sis that is difficult to distinguish from eczema. Psoriasis can also present pustules
on the palms and soles.
C. Patients may have localized disease limited to the hands or hand involvement
in the context of generalized disease. Other common sites for psoriasis are the
extensor elbows and knees, scalp, and nails. Typical lesions in these areas can help
distinguish psoriasis from eczema.
D. Nail changes in psoriasis include onycholysis, pigmentary changes that resemble
oil spots, subungual debris, and pitting. These changes can resemble onychomy-
cosis.
E. Approximately 10% to 30% of patients with psoriasis will have some degree of
associated arthritis.
Figure 34.3 Psoriasis. This patient’s lesions are symmetric. She also has similar plaques
on her feet. (From Goodheart HP. Goodheart’s Photoguide of Common Skin Disorders.
2nd Ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2003.)

Figure 34.4 Psoriasis. This is the pustular variant of psoriasis. (From Goodheart HP.
Goodheart’s Photoguide of Common Skin Disorders. 2nd Ed. Philadelphia, PA: Lippincott
Williams & Wilkins; 2003.)
Figure 34.5 Psoriatic arthritis. “Sausage finger deformity” of the distal interphalangeal
joint. Note onycholysis. (From Goodheart HP. Goodheart’s Photoguide of Common Skin
Disorders. 2nd Ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2003.)

Figure 34.6 Psoriatic arthritis (“arthritis mutilans”). This patient has severe psoriatic arthritis
with marked deformities and subluxations of the small bones of the hands. Note also the
characteristic onycholysis on the nails. (From Goodheart HP. Goodheart’s Photoguide of
Common Skin Disorders. 2nd Ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2003.)
F. Treatment depends on the extent of cutaneous disease and the presence of

arthritis.
G. Topical treatment options for limited disease include the following:
1. Topical steroids
a) Superpotent topical steroids can be used on the thicker skin of the palms
and soles for acute flares.
b) Once the disease is controlled, topical steroids can be used intermit-
tently alternating with calcipotriene or tazarotene to decrease the risk of
atrophy.
c) Oral steroids may cause severe flares of psoriasis when discontinued, and
they should be avoided in most cases.
2. Calcipotriene
a) Vitamin D analogue
b) Helps to regulate keratinocyte differentiation
c) May work synergistically with topical steroids.
3. Tazarotene
a) Topical retinoid
b) Helps to regulate keratinocyte differentiation
4. Phototherapy
a) Both UVB and psoralen with UVA (PUVA) are effective
b) For disease limited to the hands and feet, topical psoralen followed by
UVA treatments can be effective. This avoids the side effects of oral
psoralen and decreases UV exposure to uninvolved areas.
c) Full body UVB or oral PUVA may be good options for patients with
extensive disease who have contraindications to other systemic therapies.

H. Systemic treatment options for more extensive disease or disease with associated
arthritis include the following:
1. Systemic retinoids
2. Methotrexate
3. Cyclosporine
4. Biologic agents
a) Etanercept, adalimumab, and remicade are TNF-alpha blockers. Etan-
ercept and adalimumab are injectable medications that can be self-
administered by patients. Remicade is given as an infusion.
b) Efalizumab is an injectable medication, which binds CD11a and blocks
T-cell activation.
c) Alefacept is an injectable medication, which binds CD2 and blocks T-cell
activation.
d) All of the biologic agents produce some degree of immunosuppression.
IV. Verruca Vulgaris (Fig. 34.7)
A. Warts are caused by human papillomavirus (HPV) infection and the

resultant induction of keratinocyte proliferation. Numerous HPV subtypes
cause cutaneous warts. HPV 2 and 4 are most frequently found in lesions
on the hands.
B. Lesions are papules with a rough, hyperkeratotic surface. Thrombosed capillaries
can cause the appearance of black dots within the lesion. Warts disrupt dermato-
glyphics, whereas these lines are preserved in callouses.
Figure 34.7 Verruca vulgaris. This young boy has multiple common warts. (From
Goodheart HP. Goodheart’s Photoguide of Common Skin Disorders. 2nd Ed. Philadelphia,
PA: Lippincott Williams & Wilkins; 2003.)

C. Warts are most common in children. HPV enters the skin through areas of
minor trauma. Nail-biters and those involved in wet work or other activities,
which can cause skin breakdown are at higher risk for developing warts. Immu-
nosuppressed patients are also more likely to develop warts.
D. Diagnosis is most often based on clinical characteristics. It is important to keep
in mind that other neoplasms including squamous cell carcinoma, verrucous
carcinoma, and epithelioid sarcoma can mimic warts. Therefore, lesions that
are atypical in appearance or fail to respond to treatment should be biopsied to
confirm the diagnosis.
E. Treatment of warts is often difficult and all modalities may require repetitive
application to be effective. Periungual lesions may be particularly challenging to
eradicate. Treatment options include the following:
1. Salicylic acid
a) Topical keratolytic
b) Available over the counter
2. Cantharidin
a) Topical blistering agent
3. Cryotherapy with liquid nitrogen
a) Causes blistering and tissue necrosis
b) Over-the-counter freezing agents do not reach the same temperatures as
liquid nitrogen (-196°C) and may not be as effective
4. Squaric acid
a) Topical sensitizer.
b) Induces allergic contact dermatitis and local immune response.
c) Useful in children or patients with numerous lesions who cannot tolerate
cryotherapy.
5. Intralesional candida
a) Causes local immune response
6. Intralesional bleomycin
a) May be used in lesions that have been recalcitrant to multiple therapies
b) Risks include pain, Raynaud phenomenon, allergic reaction, and tissue
necrosis
V. Actinic Keratoses (Fig. 34.8)
A. Actinic keratoses are precancerous lesions that result from ultraviolet damage.
B. It is estimated that approximately 3% to 5% of actinic keratoses will develop
into squamous cell carcinomas if left untreated.
C. Lesions are erythematous, scaly papules that occur in sun-exposed areas includ-
ing the dorsal hands, forearms, scalp, and face.
D. Risk factors for the development of actinic keratoses include a history of
extensive sun exposure, older age, fair skin, and immunosuppression. Patients
with actinic keratoses are at higher risk for all nonmelanoma skin cancers and
should be educated about photoprotection.
E. Individual lesions are most often treated with liquid nitrogen cryotherapy. This
causes blistering and epidermal necrosis with destruction of the dysplastic cells.
F. For patients with numerous lesions, therapies, which can treat an entire area
of skin at once may be preferable. Options for this type of “field therapy”
include 5-fluorouracil, a topical chemotherapy, and imiquimod, a topical

Figure 34.8 Actinic keratosis actinic keratoses are superficial, flattened papules covered
by a dry scale. Often multiple, they may be round or irregular, and are pink, tan, or
grayish. They appear on sun-exposed skin of older, fair-skinned persons. Though
themselves benign, these lesions may give rise to squamous cell carcinoma (suggested
by rapid growth, induration, redness at the base, and ulceration). Keratoses on face
and hand, typical locations, are shown. (Source of photo: Sauer GC. Manual of Skin
Diseases. 5th Ed. Philadelphia, PA: JB Lippincott; 1985.)
immunomodulator. Both of these treatments require repeated application over

several weeks and are accompanied by significant redness and irritation dur-
ing treatment. Photodynamic therapy, in which application of photosensitizing
medication is followed by a short exposure to blue light, is another form of field
therapy that is coming into increasing use.
G. Any lesions that do not respond to treatment must be biopsied to rule out
malignancy.
VI. Lichen Planus (Fig. 34.9)
A. Lichen planus is a T-cell-mediated inflammatory disorder.

B. It is characterized by violaceous, flat-topped papules with a white, reticulated
surface. Lesions commonly appear on the volar wrists and dorsal hands as well
as the trunk and shins.

Figure 34.9 Lichen planus. Flat-topped, violaceous, polygonal papules on the flexor
wrists are present. There are active and resolving lesions. Note the postinflammatory
hyperpigmentation. (From Goodheart HP. Goodheart’s Photoguide of Common Skin
C. Pruritus may be severe.

D. Nail involvement occurs in 5% to 10% of patients and may manifest as
longitudinal ridging, onycholysis, and pterygium formation.
E. Oral and genital involvement are common and all patients should be carefully
evaluated for mucosal disease.
F. Diagnosis is made based on clinical appearance or by skin biopsy.
G. Lichen planus is idiopathic in the majority of cases. An association with hepati-
tis C has been documented, and hepatitis screening in newly diagnosed patients
may be advisable.
H. Lichenoid drug eruptions may be very similar in appearance to idiopathic lichen
planus. They have been associated with antimalarial agents, beta-blockers, cap-
topril, thiazides, and numerous other drugs. A careful medication history is
important to identify any potential inciting agents.
I. Treatment options for mild disease include topical steroids and oral antihista-
mines. More severe cases may require treatment with oral steroids, oral retin-
oids, or phototherapy.
VII. Granuloma Annulare (Fig. 34.10)
A. Granuloma annulare is a benign inflammatory condition of unknown etiology.

B. It is characterized by erythematous papules, which may spread peripherally
to produce annular plaques with an elevated, indurated border and depressed
center.
C. Lesions tend to occur on the extensor surfaces of extremities and are often
found on the dorsal fingers and hands. This can have a similar appearance to
Dupuytren diathesis, but it is a different entity.
D. Children and young adults are most commonly affected.

Figure 34.10 Granuloma annulare. This lesion is a typical annular plaque with central
clearing. (From Goodheart HP. Goodheart’s Photoguide of Common Skin Disorders.
2nd Ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2003.)
E. Diagnosis is made based on typical clinical appearance or skin biopsy.

F. More than 50% of lesions will resolve spontaneously within two years; however,
recurrence is common.
G. Many cases are asymptomatic and do not require treatment. If treatment is
desired, topical steroids may be effective for small lesions. Large or recalcitrant
lesions should be treated with intralesional steroids.
VIII. Connective Tissue Diseases
A. Multiple connective tissue diseases have cutaneous manifestations that can

involve the hands. Identification of these signs should prompt referral to a der-
matologist or rheumatologist for further evaluation.
B. Dermatomyositis
1. Gottron papules: Violaceous papules located over the knuckles
2. Periungual telangectasias
3. Ragged cuticles
4. Raynaud phenomenon
5. Mechanic’s hands: Hyperkeratotic plaques and fissuring of the palms and
fingertips
C. Subacute cutaneous lupus erythematosus (SCLE)
1. Scaly papules and annular plaques in a photodistributed pattern
2. Unlike dermatomyositis, SCLE usually spares the knuckles
D. Systemic lupus erythematosus
1. Erythema and edema of the fingertips
2. Red lunulae
3. Periungual telagectasias

E. Scleroderma
1. Early—edema of the hands and fingers
2. Late—sclerodactyly with telescoping fingertips, skin induration, and
decreased mobility
3. Periungual telangectasias
4. Digital ulcerations
F. Raynaud phenomenon
G. Antiphospholipid syndrome
1. Digital ulcerations
IX. Pyogenic Granuloma (Fig. 34.11)
A. Pyogenic granulomas are benign vascular proliferations that may occur

spontaneously or after minor trauma.
B. They present as rapidly growing, friable, and red-purple vascular papules or
nodules often on the palm or periungual areas.
C. The development of multiple pyogenic granulomas has been associated with
medications including isotretinoin, antiretroviral drugs, and chemotherapeutic
agents.
D. Treatment is by excision or shave removal followed by destruction of the base
with curettage and/or electrocautery. Failure to fully ablate the base of the lesion
may result in recurrence.
E. All lesions should be sent for histological examination to rule out amelanotic
melanoma and other tumors, which may have a similar clinical appearance.
Figure 34.11 Pyogenic granuloma. This patient has a typical dusky red nodule with
a collarette of skin. (From Goodheart HP. Goodheart’s Photoguide of Common Skin

Figure 34.12 Neutrophilic Dermatosis.
X. Neutrophilic Dermatosis of the Dorsal Hands (Fig. 34.12)
The definition of this disorder is evolving. Many cases previously reported as

atypical pyoderma gangrenosum or localized Sweet syndrome would now be encom-
passed within this classification.
A. Similar to pyoderma gangrenosum and Sweet syndrome, it is an inflammatory
condition characterized by a neutrophilic infiltrate. Most authors believe that it
can be considered a distinct clinical variant of these diseases.
B. The clinical presentation is variable and may include erythematous, edematous
plaques, pustules or vesicles, and nodules with ulceration. As implied by the
name, lesions tend to be restricted to the dorsal hands.
C. Cases have been reported in association with hematologic malignancy and
inflammatory bowel disease, disorders often seen with Sweet syndrome or pyo-
derma gangrenosum. The frequency of underlying disease in this condition has
not been well elucidated.
D. Diagnosis is made by skin biopsy. Tissue cultures should be sent to rule out
infection.
E. Treatment options include prednisone, dapsone, and steroid-sparing immuno-
suppressants.
XI. Clubbing (Fig. 34.13)
A. Clubbing is characterized by enlargement of the terminal phalanx accompanied

by increased curvature of the nail and obliteration of Lovibond angle, the angle
between the dorsal surface of the distal phalanx and the nail plate.
B. There are three types of clubbing.
1. Idiopathic clubbing may occur as an autosomal dominantly inherited trait.
2. Clubbing may be associated with a genetic syndrome, most often pachyder-
miperiostosis.

Figure 34.13 Clubbing of the fingers in clubbing, the distal phalanx of each finger is
rounded and bulbous. The nail plate is more convex, and the angle between the plate and the
proximal nail fold increases to 180 degrees or more. The proximal nail fold, when palpated,
feels spongy or floating. Causes are many, including chronic hypoxia from heart disease or
lung cancer and hepatic cirrhosis. (Source of photo: Habif TP. Clinical Dermatology: A Color
Guide to Diagnosis and Therapy. 2nd Ed. St. Louis, MO: CV Mosby; 1990.)
3. Clubbing may occur secondary to an underlying disease, including

a) Pulmonary disease—Lung cancer, cystic fibrosis, idiopathic pulmonary
fibrosis, sarcoidosis, empyema, and pulmonary metastases
b) Gastrointestinal disease—Ulcerative colitis and Crohn’s disease
c) Hepatic disease—Cirrhosis
d) Cardiac disease—Cyanotic congenital heart disease, conditions with left-
right shunting
e) Thyroid disease
f ) Malignancy
C. Identification of clubbing on physical examination should prompt an evaluation
for an underlying etiology.
XII. Onychomycosis (Fig. 34.14)
A. There are four major types of onychomycosis:

1. Distal subungual onychomycosis
a) Presents as a thickened nail with white-yellow discoloration, subungual
debris, and onycholysis
b) Most often caused by Trichophyton rubrum
2. White superficial onychomycosis
a) Characterized by chalky, white patches on the surface of the nail plate
b) Most often caused by T. mentagrophytes
3. Proximal subungual onychomycosis
a) Characterized by white discoloration at the proximal nail fold
b) Most often caused by T. rubrum or T. megninii
c) Usually seen in HIV positive patients

Figure 34.14 Onychomycosis of the nail plates.
4. Candida onychomycosis
a) Characterized by white discoloration of the nail plate and onycholysis,
often accompanied by chronic paronychia
B. Pseudomonas can also cause nail infections characterized by onycholysis and
green discoloration of the nail plate.
C. Diagnosis may be made by fungal culture or by submitting a nail clipping for
histological evaluation and GMS stain. Fungal culture takes several weeks, but
is less costly and provides identification of the involved organism. Histological
evaluation can provide results in several days. It is the most sensitive diagnostic
technique, and it can be helpful in cases where there is a high clinical suspicion
but fungal culture is negative.
D. Topical therapies are usually ineffective in eradicating fungal infections in the
nail. However, they are useful in preventing the spread of the infection to the
surrounding skin. Patients who do not desire or are not candidates for oral
medications should still be treated with a topical antifungal such as terbinafine,
econazole, thymol, or cicloprox. The most commonly used oral therapy is terbi-
nafine. Fingernail infections should be treated for 8 weeks and toenail infections
should be treated for at least 12 weeks. Itraconazole and fluconazole are also
effective alternatives. After completing oral therapy, patients should be main-
tained on a topical antifungal to prevent reinfection.
E. Other conditions including trauma, psoriasis, lichen planus, and eczema can
cause onychodystrophy. Therefore, a diagnosis of onychomycosis should be
substantiated by culture or histopathological evaluation before initiating oral
treatment.

Medicolegal Principles
35
Charles Carroll VI and David S. Wellman
The physician-patient relationship is an implied contract under law and serves as the
foundation of the physician’s role in patient care. Thus, understanding the legal context
of medicine is imperative for any practicing surgeon. Further, the litigious aspect of
practicing medicine is continually on the rise; since 1975, malpractice costs have risen
11.5% annually, and the total costs of the malpractice system reached $29.4 billion in
2005. On average, an orthopaedic or hand surgeon can now expect to be a defendant
in two lawsuits during his or her career.
Most medical-legal cases, including malpractice, personal injury, and workers’
compensation, fall under tort law. Tort law deals with civil wrongs that violate relation-
ships bound by implied contract. As the physician-patient relationship is a type of implied
contract, negligence and breach of the implied contract fall under laws of tort, which are
dictated by statutes and previous court opinions. In these cases, the role of the physician
falls into two major categories: physician as defendant and physician as witness.
In the practice of medicine, physicians strive to be teachers and knowledgeable
healers. We are taught to be caring and compassionate. We aim to please and heal.
Unfortunately, we are not trained in medical school or residency to interface effectively
with the law. After delivering appropriate care, we may be called to testify as a treating
physician. Often this will be for a patient who has been injured and has filed litigation
after the accident for payment of medical expenses and damages. An orthopaedist/
hand surgeon/therapist may be called to recount our care, and we may be asked to offer
opinions concerning permanent damages and causalty. We function as an expert in
these situations based on our knowledge, experience, and training. The plaintiff or the
defense may call us. In either case, we are functioning as an expert witness.
We may be asked to see a patient or review records for a law firm. This may be
workers compensation matter or a personal injury claim and may involve the plaintiff
or the defense. In this scenario, we are serving as a controlled expert witness.
Medical malpractice continues to be an important issue in the United States. Many
states are in a form of crisis as claims continue to plague the practicing orthopaedist.
Premiums continue to rise, and there is loss of practicing orthopaedists in some states.
The cost of malpractice premiums continues to be of great concern. An important part
of the malpractice process is the use of expert witnesses to establish the presence of an
action that constitutes malpractice. Expert witnesses assess the presence of damages to
the plaintiff/patient and can provide advice as to whether there has been a breach of the
standard of care. The process of litigation in a state or Federal Court relies on expert
witness testimony in the process of finding of facts. Physicians can and must play an
important role as an impartial expert or as an expert in their own defense.
I. Physician as Defendant
The most stressful role a physician can play in the legal system is one of a defendant in
a medical liability case.
533

A. Most lawsuits against physicians fit into three major categories: negligence,
improper informed consent, or physician abandonment.
1. Negligence
The most common claim against a physician is negligence, or not practicing
according to the accepted standard of care. In a court of law, the standard of
care is generally accepted as the “skill, knowledge, expertise, and experience”
that a practicing physician in that specialty would possess and employ in a
similar situation and location. While state law dictates the specific definition,
every state has a similar interpretation. To successfully argue a negligence
claim in court, a patient must prove that
a) The physician owed the patient a duty.
b) The physician breached the duty.
c) The breach led directly to injury.
d) The injury caused legally recognizable damages.
As discussed below, the patient must rely on other physicians to establish the
elements of his or her claim.
2. Improper informed consent
Formal informed consent involves a discussion with the patient regarding the
potential risks and benefits of the proposed procedure, alternative treatments
available, and risks of refusing treatment. Legally, it is acceptable to provide a
thorough, but not necessarily exhaustive, list of all complications that a rea-
sonable person in a similar situation would consider important. If a physician
performs a procedure according to the classic description and a recognized
complication arises that was discussed during the informed consent phase of
preoperative planning, the physician cannot be held liable in court.
A patient must be able to understand the information presented, be
capable of decision making, and be allowed to make a decision voluntarily.
While capacity to consent is a legal standard, physicians typically make deci-
sions regarding the ability to consent. In a situation where determining com-
petence is not straightforward, it is advisable to obtain physician consult for
a second opinion. If the patient is determined to be incompetent, physicians
should know their particular state’s laws regarding who can legally provide
informed consent.
In a review study of malpractice cases claiming improper informed con-
sent, Bhattacharyya et al. found the risk of malpractice claims was signifi-
cantly increased if the informed consent discussion was performed on the
wards or in the preoperative holding area. The study also concluded that mal-
practice claims were significantly decreased if documentation of the informed
consent discussion existed in the office notes.
3. Physician abandonment
Physician abandonment claims arise when patient in need of treatment has
care terminated by physician without proper notification or assistance in find-
ing a new treating physician. A 1935 court ruling in Utah advises physicians
to “give the patient sufficient notice so that the patient can procure other
medical attention if he desires.” In orthopaedic and hand surgery, failure
to provide proper follow-up is both a common claim citing abandonment
and a leading cause for overall malpractice claims. Premature discharge from
the hospital as well as improper discharge instructions also fall under aban-
donment. Proper and thorough documentation of discussions with patients

Chapter 35 • Medicolegal Principles 535
regarding follow-up, transfer of care, and termination of service is needed for

defense against abandonment claims.
B. Preparing for role of defendant
Given the current litigious dynamic of practicing medicine, young physicians can
assume they will be involved in at least one court case in their career, whether as
witness or as defendant. Understanding the legal system is an important step in self-
protection as it aids the young physician to take steps in practice to guard against
lawsuit and protect professional credibility when asked to serve as a witness.
As the burdens of malpractice suits include a major time commitment, an
insult to professional integrity, and potential financial loss, it is prudent for phy-
sicians to employ proven strategies to reduce the likelihood of being sued.
1. Personal interaction
The quality of the doctor/patient relationship has been shown to affect the
prevalence of malpractice claims. At an administrative level, malpractice attor-
neys recommend returning telephone calls personally as well as reviewing test
results and specific treatment recommendations directly with patients. This
avoids the common complaints that patients have regarding the amount of
personal interaction with their doctors. Offices should be arranged so that
appointments are not overbooked and patients are not left frustrated in the
waiting room.
2. Addressing errors
Physicians should develop a plan on addressing mistakes and medical errors
early in practice. Acknowledgement of error, as well as an appropriate apol-
ogy, can be made without admission of liability. Prompt, honest disclosure
may even reduce malpractice claims. The time spent formally addressing
patients regarding mistakes is miniscule compared to the time spent prepar-
ing for a malpractice court case.
3. Thorough documentation
All office notes should be complete and legible, and all interactions with
patients must be documented, both in the office and over the phone. The
timing of documentation is also important: Operative reports completed
months after the procedure suggest that certain pertinent facts about the case
may have been forgotten. All changes to a note must be made so that the
original is still legible, and corrections or changes to a note should not occur
after a lawsuit has been filed. Plaintiff ’s attorneys specifically seek this infor-
mation and use it effectively to discredit defense counsel arguments. Good
documentation habits from the onset of establishing a practice will eliminate
the need for reactionary revisions in your documentation methods.
4. Defensive medicine
As doctors move to protect themselves from lawsuits, defensive practice
behaviors have become more prevalent. A recent study analyzed the behavior
of doctors practicing within certain high-risk fields (including orthopaedics)
and found that 93% admit practicing defensive medicine. The majority of
orthopaedic surgeons surveyed described ordering more tests than medically
indicated in order to provide assurance. The study also found 57% of ortho-
paedic surgeons report avoiding caring for certain patient populations because
of potential liability. These practices only add to the overall financial burden
of the legal environment on the health care industry. Physicians must learn to
practice comprehensive care without overburdening the health care system.

5. Communication
The most effective risk management tool is communication. Every orthopaedist
and hand surgeon should take the time to develop and institute a program of
effective communication with each patient. An effective communicator is an
active listener who asks open-ended questions in a pleasant and nonjudgmental
manner. A connection should be made with each patient. An effective physician
will carefully assess the role of the disease process in the whole patient. With
effective communication and teaching of the patient, one can practice good
medicine and minimize malpractice claims. Strive to work as a team with each
patient, and take a genuine interest in their problem. A patient who finds that
their physician is interested, competent, and personable is less likely to sue their
physician.
II. Physician as Witness
Both young and established physicians should familiarize themselves with the statutes
of their home state, as they will likely be approached during their career to participate
as a witness. Preparing for expert witness testimony involves close communication with
the participating attorneys and an understanding of state law. As described in this chap-
ter, state laws dictate specific aspects of testimony, and the physician will be expected to
adhere to the particular state’s regulations.
As a defendant, one should be thorough in their review of the chart, hospital
records, and any other applicable information. A pertinent review of the medical litera-
ture is essential. Be careful to consider any staff member who may have been present
and may remember the case, as their testimony could be very helpful. Set the time aside
for review and preparation. The depositions can be long. Trial testimony and watching
the trial will be very stressful. Spend the time with attorneys and be ready for any occur-
rence. Rely on loved ones and family for mental support but maintain the privacy of the
patient. Eat well, try to sleep, and exercise in preparation for the matter. Try to maintain
a positive attitude, and move on mentally when it is over.
1. Physician as an expert witness
In many jurisdictions, court cases based on medical information above the
level of understanding of the layperson require expert testimony. As a jury
of laypeople decides liability for most medical-legal cases, they must become
knowledgeable of the standard of care in each case. Thus, the parties rely
on physicians outside the case to act as expert witnesses. Since professional
journals and textbooks are rarely considered completely authoritative, a prac-
ticing physician is brought in to interpret the data and offer an opinion based
on medical literature and his or her professional experience. Both plaintiffs
and defendants are encouraged, expected, and often required to provide
expert witness testimony to support their cases.
Standards for whom can provide expert testimony differ across states. The
general prerequisite for giving testimony is being a licensed practitioner famil-
iar with the issues in question. Many states employ a locality rule, in which
a physician must practice in or be familiar with the community in which the
defendant practices. How loosely this is interpreted differs based on the state.
For example, in 2001 a Louisiana appellate court did not allow testimony
from a physician who could not demonstrate having practiced in Louisiana or

a similar demographic as the defendant. Regardless of the specific definition, a

trial judge will interpret the state’s law and decide if the proposed witness can
testify based on if the medical facts of the case are within the proposed physi-
cian’s area of expertise and if testimony will help the jury reach a decision.
Expert witness testimony is further complicated when a physician of
a particular specialty offers opinions regarding a separate specialty. This is
called crossover testimony. It is legal to testify in an area of medicine outside
one’s designated specialty; the court will determine if the issue in question
deals with a particular area of expertise, whether or not expert witness is
needed, and whether the witness is qualified. In 1988, an Idaho court opin-
ion addressed crossover testimony by stating: “It is the scope of the witness’
knowledge and not the artificial classification by title that should govern the
threshold question of admissibility.”
Serving as an expert witness is not an easy assignment. One faces judg-
ment from the defendant, the jury, and the medical community in which he
practices. In one survey of judges, 79% of respondents questioned witnesses’
impartiality, and 57% considered witnesses “hired guns.” Many physicians
are uncomfortable with such stereotypes and avoid the role of the expert wit-
ness, creating what one author calls a “conspiracy of silence.” As our court
system remains the main source for medical policing, expert witnesses are a
necessary part of that process. As long as standards and laws are rigorously
followed, one does not compromise ethics or the community of physicians in
providing qualified, informed expert testimony.
When one is approached to be a possible expert witness, it requires a
moment of reflection and introspection before making a decision as to whether
one will take on the commitment. You must first consider what is your interest
or motivation. The first issue: Are you a defendant who has a different set of
issues to consider than a controlled witness? After that, one must able to define
why they will participate. Are you interested in learning about this process and
are looking to get experience? Are you interested in teaching the law about issues
in medicine from a constructive viewpoint? Do you have an interest in the inter-
face of law and medicine? Is your interest financial in nature? The most impor-
tant issue is whether you are qualified to assume the role as an expert witness.
a) Definition of an expert witness
An expert witness is defined in the Federal Rules of Evidence in Rule 702.
The rule reads as follows: “If scientific, technical, or other specialized
knowledge will assist the trier of fact to understand the evidence or to
determine a fact in issue, a witness qualified as an expert by knowledge,
skill, experience, training, or education may testify thereto in the form of
opinion or otherwise, if
– The testimony is based upon sufficient facts or data.
– The testimony is the product of reliable principles and methods.
– The witness has applied the principles and methods reliably to the facts
of the case.
An expert has the exception to the requirement to testify to the facts
rather than opinions.
This exception allows an expert to formulate opinions and to testify
about them in written or verbal form. Experts are qualified to draw inferences
from facts that a jury could not by virtue of their lack of expertise. The expert
is not required to have firsthand knowledge of the facts or the issues at hand.

1) Types of expert witnesses

A physician can function in a number of roles as an expert. The
establishment of a claim requires that a physician reviews the case and
establishes that the claim has merit. There has to be a duty that the
treating physician owes the patient when a doctor-patient relationship
has been established. The duty must have been breached by an action
that can be considered as a violation of a standard of care. There has
to be a causation of the action as it relates to the issues involved in the
claim. The causation can be factual (“but for”) or a substantial factor
(“proximate cause”). The expert also has to establish the damages to
the plaintiff in the form of economic and noneconomic damages.
Physician’s can act as an expert in the following manner:
– Nondisclosed consulting expert
– Plaintiff expert
– Defense expert
– Physician as an expert for himself/herself
– Court-appointed expert
Each of these roles can play a critical part in the litigation process.
a. As a nondisclosed expert, one may advise an attorney, insurance
company, or a patient as to the nature of the claim and the presence
or absence of merit in a malpractice action. As a treating physician
who may work as a nondisclosed expert, one has to be aware of
their fiduciary duty to their patient and to not disclose information
that can violate the doctor-patient privileged relationship or the
HIPAA act of 1996.
b. The plaintiff ’s expert will advise and testify on behalf of the
plaintiff to establish the merit and causality of the actions in ques-
tion. This expert will also establish the violation of the standard of
care and the presence of damage to the plaintiff. Professional fees
for this service will be paid by the plaintiff.
c. The expert for the defense will testify on behalf of the physician or
other party that has been named in the suit or claim. This expert
will attempt to refute merit, causality, any violation of the standard
of care, or the presence of damages. The defense pays all profes-
sional fees. The plaintiff or defense expert may rely on records,
deposition testimony, medical literature, and their own knowledge.
An examination of the plaintiff may or may not be required.
d. The physician as a defendant can also act as an expert for himself
or herself. Although the defendant physician is sitting on the “hot
seat,” he or she can be qualified to act as an expert for himself or
herself in addition to the outside retained or controlled witness.
The defendant physician has examined and treated the patient. He
or she also will have the training knowledge and experience to assist
the jury of peers in the finding of fact. This role can be critical in
the defense of a malpractice claim and should not be ignored.
e. A court-appointed expert has been brought in by the court to assist
in the education of the jury and to assist the jury in the finding of
fact. This expert has not been retained by either party and is to be
impartial. A physician in this role functions as an educator and has
not offered opinions at the request of the plaintiff or the defense.

This expert may appear voluntarily or at a rate determined in

discussion with the court.
2) Are you qualified?
To be able to function as an expert, one must be qualified. You must
have knowledge and training, which can be obtained in medical school,
residency, fellowship, and further continuing medical education.
Experience in practice is also necessary to be qualified. Teaching at an
academic medical center can also add to your qualifications but is not
essential. Publications can also be helpful, but make sure your opinions
match what you have written (or have new thoughts and possibly data
available); if you are going to offer an opinion, which contradicts what
you have published, it can become an issue at deposition or trial.
It is important to consider the case. It should deal with issues
relevant to orthopaedic surgery. The case may deal with issues involv-
ing subspecialty orthopaedics such as hand surgery, spine surgery,
tumor surgery, pediatrics, or foot and ankle surgery. The expert will
have to be ready to answer questions about their qualifications as it
applies to orthopaedic surgery or one of the subspecialties. A case
involving other medical fields can be considered, but the issues about
which the orthopaedic expert offers opinion must relate to the field,
knowledge, training, and experience of the expert.
There are other issues to consider that are more person or expert
specific. Do you have the time to be an expert witness? Do you speak in a
clear and concise fashion? Can you speak to an audience? Can you handle
the possible pressure of testimony? Do you posses the panache to perform
as an expert witness? Most importantly, are you prepared to tell the truth,
the whole truth, and nothing but the truth: So Help You God?
III. Expert testimony
A. Rules of testimony as a testifying expert

As a controlled testifying expert, an orthopaedic surgeon can be called to offer
opinions relative to the case to assist the jury in their deliberation relative to the
issues at hand. As the trier of fact, the jury may need assistance in their education
and understanding of the pertinent medical issues. The physician is to function
as an educator and not an advocate.
As an expert for the plaintiff, one will be called to offer opinions that may
be in support of the theses of the case as presented by the patient and their legal
counsel. As an expert for the defense, one will be called to offer opinions that
will support the theses of the defense team of defendants and attorneys. In either
case, the testifying physician must remember that he or she is not the attorney,
judge, or jury. The physician must not act as an advocate and should be aware
of any personal bias relative to the matter at hand that might alter the expressed
opinions. The opinions must have a basis. The first basis can be direct observa-
tion from treatment given or from a solicited medical examination. The medical
records and deposition testimony related to the case can be part of the basis for
opinions. A physician’s education, training, and experience can also be part of
the bases. The medical literature can also be a source of basis. When a paper or
piece of literature is cited, the expert should be thorough in their review of that

literature as there may be questions asked about less relevant material to test their
understanding in cross-examination. In addition, one must be aware of conflicting
literature. A source that is used must be carefully chosen, as the deposition record
from one case may be brought forth if you offer a different opinion on the same
issue at a later time to discredit the testimony on the basis of being inconsistent or
contradictory. The testimony should not be based solely on the personal opinion
of the physician, as that can be speculative in nature, and a speculating physician
is an anathema to the court. Two case have set precedent relating to admissibility
of an opinion in court or in deposition testimony. In Frye versus United States,
the precedent was set that opinions had to be generally accepted within the rele-
vant scientific community to be admitted into evidence. An innovative procedure
had to be published in a peer-reviewed journal. These rules apply in many state
and local jurisdictions. In Daubert versus Merrell Dow Pharmaceuticals, Inc., the
precedent set that the trial judge must assess validity, reasoning, and methodology
when considering the admissibility of a specific opinion. The judge will require
the separation of junk science from evidence-based medical testimony. This dates
to 1993 and is the standard in the United States Federal Court. A Daubert chal-
lenge to an expert physician’s testimony will require the physician to produce
the medical literature that is relevant to the opinion and four years of records rela-
tive to the physician’s experience in the role as an expert witness. These principles
are starting to appear in the courts of many states, and should be considered when
deciding to present testimony outside of one’ place of practice.
B. Preparation for testimony
The key concept in expert witness testimony is preparation. One can never be
too prepared. A thorough review of the patient chart must be completed. For-
mulate a time line of events, procedures, testing, and the outcome of the medical
care. Review all of the care as it may be pertinent to the final disposition of the
patient that can play a prominent role in the determination of any permanent
damages to the patient or plaintiff. All available deposition testimony must be
reviewed and analyzed. Opinions of experts must also be reviewed as part of the
prepared opinions and in the context of their deposition testimony. Any writ-
ten notes that are prepared during this review process are subject to discovery
at the time of the discovery. Discussions and letters written above and beyond a
medical report are also subject to discovery. As a defendant though, a physician’s
verbal discussion with his or her personal attorney(s) may be subject to attorney-
client privilege. Unless the attorney is representing a testifying expert in the mat-
ter of the discovery deposition, any verbal discussions are subject to discovery.
An examination of the plaintiff or patient may be necessary and should be
requested as needed by the expert. That report will be discussed at the time of the
discovery deposition or in evidence deposition or trial as indicated. Prior to any
deposition testimony of the expert, opinions will have to be formulated and com-
municated in writing to all parties with appropriate time for all to prepare any
direct or cross-examination. As the testifying expert, one should be thoroughly
familiar with the opinions and the bases for each opinion in the reviewed mate-
rial and the body of medical knowledge. As an examining or treating physician,
an opinion may be based on direct observation, but that will not be the case with
most retained experts who have only written material to review. The opinions
will be prepared with the attorney, but the physician should be comfortable with
the wording of their opinions. The opinions must be presented before the end
of the time set aside for discovery by the trial court. Proper timing will prevent

opinions from becoming inadmissible by a judge at the time of a motion to limit

the presentation of the opinions. Appropriate time should be set aside for a com-
prehensive review and for preparation for testimony. A knowledge deficit can be
exploited in a well-prepared cross-examination by an opposing attorney. While
taking the adequate time for preparation, one will become very familiar with the
basis of their opinions, which will be probed during the discovery deposition. As
part of proper preparation, the testifying expert should be aware of deadlines for
discovery and trial. Any conflicts must be identified and discussed early in the
process to prevent problems and possible sanctions as they might apply.
Proper time must be allocated for meetings, calls, depositions, and trial. A
busy practicing physician will have to mesh patient care and testimony to prevent
the problems that can arise with improper scheduling. The medical team that
supports the physician must be aware of deadlines, dates, and potential trial com-
mitments as a lack of planning of a schedule can present significant issues to a
physician with angry patient or attorneys who face rescheduling at short notice.
C. Deposition testimony
There are two forms of deposition testimony.
1. The discovery deposition is the initial opportunity for an expert physician to
testify. The opposing attorney will be given the opportunity to verbally solicit
and discuss the opinions that have been derived relative to the case and the
issues at hand. Each opinion will be explored and examined. The attorney
who retained the expert may ask questions as well. There may be redirected
examination after the initial phase. The length may be 2 or more hours.
2. This deposition segues into an evidence deposition or trial testimony. If an
expert is unable to be presented in trial, a verbal or videotaped deposition
may be requested and played to the jury with editing.
It is essential to be prepared for a discovery deposition. One must know
the records and the previous testimony. The expert should be prepared to state
their opinions and the basis for the opinion. Appropriate time must be taken for
review and meetings before the deposition to allow for necessary preparation.
The trial testimony or evidence deposition is set by the information presented in
the discovery deposition. All parties have the right to know an expert’s opinions
and bases prior to the trial. It would be unusual for an expert not to be deposed
in discovery by opposing counsel. Opinions expressed at an evidence deposition
or trial must be consistent with the discovery deposition or they will potentially
be inadmissible. New opinions cannot be presented at an evidence deposition or
trial without proper discovery.
A testifying physician must be well prepared and set aside appropriate time
for preparation and meetings and calls with the retaining attorney. The direct
examination will commence and will be followed by cross-examination. A redi-
rected examination can follow clarifying information in the cross-examination.
The scope of the redirected examination deals with the material presented only
in the segment of testimony that occurred immediately prior to keep the scope of
questioning narrow. One must listen to the questions carefully and ask for clari-
fication as needed. If one cannot understand a question, then one should state
that to make sure that the answer given reflects an understanding of the question
asked. One should listen to a question and break up compound questions as
needed. One should answer in a clear and succinct fashion. An answer should
be embellished only where necessary. As a retained expert, the physician should
expound where indicated and consult with the retaining attorney as to where one

should expound or answer succinctly. Questions must be answered in an honest

and sincere fashion. Opinions should be stated without bias. The retained expert
should maintain a pleasant demeanor and answer the question that was asked. Be
prepared for any deposition. Basis must be known. Opinions must be considered
and the expert must be ready for any and all questioning about their opinions.
D. Trial testimony
A trial can be a fascinating and taxing experience. One must be thoroughly pre-
pared to discuss their opinions and bases in front of all parties, a judge, and
potentially a jury. The expert should dress neatly and remain polite to all parties.
It is the courtroom of the presiding judge and that should never be forgotten.
Maintain privacy in and out of the courtroom. One must take the appropriate
time to prepare and confer with the attorneys who have retained the expert.
Opinions and bases must be known and new opinions cannot be expressed on a
general basis. Opinions should be consistent with those expressed in discovery.
Answer questions in a sincere and honest fashion. Eye contact should be main-
tained with the attorneys and jury. Argumentative, intentionally comical, and
nonresponsive experts may not be of any help or value. Remember that an oath is
taken at deposition and trial to tell the whole truth and nothing but the truth.
E. Closure of a case
A testifying expert should attempt to end on a positive note. One should quietly
exit and be pleasant. One should converse with the retaining attorney at the end
to discuss the testimony and accept praise or criticism as indicated. A bill should
be submitted with realistic fees. Reimbursement for work as an expert witness
can be subject to examination in a deposition or trial. A potential expert must
remain qualified by experience and education. After retiring from active practice,
a potential expert may be disqualified after several years. One must be realistic in
their estimation of themselves when it comes to being qualified.
F. Conclusion
A good expert will be honest and prepared. He or she should be available, affable,
and able to speak and work on their feet under pressure. Mistakes in testimony
are often due to poor preparation and offering new and previously unknown
opinions. One must answer the questions and have a basis for the opinions.
Being prepared can minimize the risk of the unexpected question or tactic to
shake an expert. Carefully listen to the questions and state “I do not understand
the question” as indicated. Poor testimony can be harmful to the retaining party
and may open the expert to legal and professional sanction. In summary, be pre-
pared. The most important thing to remember is to be honest. You will be under
oath to provide the truth and nothing but the truth.
Authors Disclaimer:
Neither author has a law degree. Consult an attorney as necessary. This informa-
tion should be used for advisory and educational purposes only. The information
does not reflect on any position of the American Society for Surgery of the Hand.
IV. Physician as Treating Physician
The most likely role that most orthopaedic surgeons will play in the process of litiga-
tion is the role of a treating physician. In that context, one is functioning as a healer
and is not a defendant. One has to keep in the forefront of their mind that they
have established a doctor-patient relationship. The testimony will be based on their

treatment and direct observation of the patient, the care provided, and the outcome
of the care. Much of the testimony will be a presentation of factual information that
should be contained in the medical chart. As part of that process, the treating physi-
cian has a fiduciary responsibility to the patient and must consider and represent the
interests of that patient. Opinions may be solicited beyond the scope of the factual
information, and the orthopaedist should be ready to answer or state that they do
not have an opinion where that may apply. The rules of discovery and HIP PA rules
must be observed by the treating physician. The attorney for the patient may have
unrestricted access to the physician under the law, but the defense attorney may
not. The orthopaedist and their staff should be aware of the local rules of discovery
to prevent inappropriate release of information verbally or in writing. The defense
attorneys may be required to subpoena all records and may be able to speak with
the treating physician at the time of a discovery or subsequent evidence deposition.
All opinions should be based on a reasonable degree of medical or surgical certainty.
The opinions should be based on scientific precedent and fact. Opinions should not
be based only on the thoughts of the treating physician, which can be speculative
in nature. As the field of evidence-based medicine continues to grow, one should
consider opinions that have roots in evidence-based medicine. As a treating physi-
cian, one must be aware of external pressures. A patient may place subtle or obvious
pressure to push the treating orthopaedist to support the opinions of the patient or
the legal team representing them. Any expressed opinion should be carefully thought
out. One should refrain from an off-the cuff opinion or comment that can present
as a communication challenge at a later date. A treating physician may want to con-
sider having legal counsel at a discovery deposition, evidence deposition, or at trial
to represent their personal interests when one is testifying as a treating physician in
a malpractice action.
Suggested Readings
2006 Update on U.S. Tort Cost Trends. 2006. Towers and Perrin. 31 Dec. 2007 http://www.
towersperrin.com/tp/getwebcachedoc?webc = TILL/USA/2006/200611/Tort_2006_FINAL.pdf.
Bhattacharyya T, Yeon H, Harris MB. The medical-legal aspects of informed consent in orthopaedic
surgery. J Bone Joint Surg Am. 2005;87(11):2395–2400.
Clark v Prenger, 760 P.2d 1182 (Idaho 1988).
Daubert v. Merrell Dow Pharmaceuticals, 509 U.S. 579 (1993).
Fed. R. Evid. 702 (2000).
Frye v. United States, 293 F. 1013 (D.C. Cir. 1923).
Gould MT, et al. An analysis of orthopaedic liability in the acute care setting. Clin Orthop Relat
Res. 2003;407:59–66.
Hoffman PJ, Plump JD, Courtney MA. The defense counsel’s perspective. Clin Orthop Relat Res.
2005;433:15–25.
Jerrold L. The role of the expert witness. Surg Clin North Am. 2007;87(4):889–901.
Nichols JD. Lawyers advice on physician conduct with malpractice cases. Clin Orthop Relat Res.
2003;407:14–18.
Ricks v Budge, 64 P.2d 208, 211–212 (Utah 1937).
Roberts v Warren, 782 So.2d 717 (Louisiana 2001).
Shuman DW, Whitaker E, Champagne A. An empirical examination of the use of expert witnesses
in the courts: II. A three-city study. Jurimetrics. 1994;34:193–208.
Studdert DM, et al. Defensive medicine among high-risk specialist physicians in a volatile
malpractice environment. JAMA. 2005;293(21):2609–2617.
Suk M, Udale AM, Helfet DL. Orhopaedics and the law. J Am Acad Orthop Surg. 2005;13(6):
397–406.

Workers’ Compensation
36
Paul F. Nassab
Workers’ compensation laws vary from state to state. These laws are generally governed
by the state departments of labor and provide both rights and obligations to employers
and employees alike. They may be found on state Web sites.
The workers compensation system was developed to provide protection for both
the employee and the employer. The system is set up as a “no fault” system in order to
provide the employee with medical care, cover lost wages, and provide for potential
future lost wages from an injury.
The system mandates that employers meeting specified requirements self-insure
their workers, provide Workers Compensation Insurance through a third party, or pay
into a state-funded program. The employer, in return, is protected from lawsuits as
payment does not constitute an admission of guilt. The United States Department of
Labor Web site, http://www.dol.gov/index.htm, provides a clear overview of each state’s
requirements and exceptions.
Several federal acts exist and serve to protect federal employees. The federal
government, through the Federal Employees Compensation Act (FECA) and the Fed-
eral Employer’s Liability Act, provides similar benefits for federal employees and those
involved in interstate commerce. U.S. Post Office employees and railroad workers
are examples of employees so governed. Merchant Mariners are covered by the Jones
Act and the Longshore and Harbor Workers’ Compensation Act provides workers’
compensation to specified employees of private maritime employers.
The workers compensation process begins with the Occupational Disease or
Injury, which is defined as an identifiable disease or injury arising with or without
human fault out of and in the course of the employment. The physician is often the
person who decides whether an injury is to be considered as work related. The employee
receives compensation only when the surgeon makes such a determination.
How does one make a determination of causation in cases where an injury
cannot be directly correlated to an event at work? Szabo writes that “causality of
a disorder is established based on systematic reviews of the available evidence pro-
vided by epidemiologic studies supported by biomechanical and biologic laboratory
experiments” (Szabo, 2006). Medical literature fails to provide clear and convinc-
ing evidence for the association of many upper extremity complaints and the work
environment.
In vivo animal studies have shown changes at the cellular level, structural
reorganization, inflammatory cell migration, and even necrosis with high repetition
and low force activities (Backman et al., 1990;). Is this “biological evidence” suffi-
cient to diagnose an injury, disease, or disorder as a work-related event? The treat-
ing physician must use the knowledge of a patients’ work environment, tasks,
the disease, psychosocial status, and literature that either supports or refutes the associa-
tion to make a determination on the causation of the injury.
Workers must report an injury to their supervisor. The supervisor, through perhaps
an occupational medicine physician, will assess the injury and determine whether to
544

Chapter 36 • Workers’ Compensation 545
treat the patient under workers compensation. If so, the injury must be reported to the
state department of labor, which tracks these injuries.
The employer is obligated to clearly state and post a policy. The employer is also
obligated to provide safety devices and rules to protect the employee. If an injury occurs
and the employee failed to use the safety devices or follow the safety rules, his benefit
is reduced.
The derived benefit has several forms: Medical expenses, lost wages, and per-
manent impairment. All medical expenses are paid for by the compensation system
(self-insured, private insurance, or state fund). The employee is compensated for lost
work if he or she is disabled. States have different waiting periods before reimbursement
for lost salary can begin. The monetary benefit, with a few state exceptions, is two thirds
of their salary. Patients are often able to do “light duty” and often can collect their salary
with restrictions set forth by the doctor.
The American Medical Association Publication, Guides to the Evaluation of
Permanent Impairment, 4th Ed, defines an impairment as a condition that interferes
with the performance of activities of daily living. “Disability,” though is different,
and is defined as “an alteration of an individual’s capacity to meet personal, social, or
occupational demands” and occurs as a result of impairment. The impairment will be
essentially the same for a given injury, while the degree of disability may differ substan-
tially from patient to patient for the same injury. Therefore, the term impairment is
more accurate and should be used. The treating surgeon often performs an impairment
rating for the employee once he or she has reached his or her maximal medical improve-
ment or MMI. States vary on how this impairment is calculated.
The financial settlement, based upon the impairment rating, often terminates the
workers’ compensation case. Each state determines the monetary award based upon
the impairment rating. The employee may have hired an attorney to help guide him
through the process. The burden of proving entitlement falls upon the employee. While
their client’s best interest is always paramount, an attorney’s compensation is frequently
tied to the settlement. States regulate the financial compensation an attorney can receive
in a compensation case as a percentage of the award.
Suggested Readings
American Medical Association. Guides to the Evaluation of Permanent Impairment. 4th Ed.
Chicago, IL: American Medical Association; 2006.
Backman C, Boquist L, Friden J, et al. Chronic Achilles Paratenonitis with tendinosis: an experi-
mental model in the rabbit. J Orth Res 1990;8:541–547.
Szabo RM. Determining causation of work-related upper extremity disorders. Clin Occup Environ
Med. 2006;5(2):225–234.

Clinical Trials and Hand
Surgical Literature
37
Brent Graham
Overview
a) The main concern with any type of scientific report is the presence of bias in the
study.
b) Bias may enter into a study at many different levels: Sample, the intervention or
observation of interest, the methods of measurement, the statistical analysis, the
interpretation of the findings.
c) Selection of the study sample is often the most obvious and important source
of bias. Samples of convenience drawn from a particular setting, such as an aca-
demic institution or subspecialty clinic, are unlikely to be representative of the
general population of interest, especially if the sample is small.
d) Various study designs attempt to address the issue of bias in the study sample by
assigning a control group.
e) In the uncontrolled case series, which remains the most common sample
reported in the hand surgery literature, there is an implied historical con-
trol although making comparisons to other series in the literature is often
inappropriate.
f ) A study can be blinded to the provider of care and or the patient. A “blinded”
study is a study wherein the evaluator does not know which group the patient or
variable being examined is in. A “double blinded” study is one wherein neither
the patient nor the evaluator knows which treatment was given, or whether one
was given at all (dependant on study design).
I. Hierarchy of Clinical Research Designs
A. Randomized control trial

1. Advantages
a) Controls for both known and unknown biases by randomly assigning
eligible patients to treatment groups
b) Comparison of results is usually very intuitive and clear
c) Gold standard for defining evidence
d) Can establish cause and effect relationships
2. Disadvantages
a) Cost; primarily related to needs for data collection/security and the time
required to recruit enough participants into the study
b) Generalizability may be poor because study sample does not necessarily
resemble the patient population of interest
c) Answers only the question posed by the study
546

Chapter 37 • Clinical Trials and Hand Surgical Literature 547
Randomized controlled trials are most effective when the time required to
ascertain the result is relatively short. Interventions that may require a lengthy
period before the outcome is known are difficult to study with a randomized trial
because costs may become substantial.
B. Cohort
Cohort designs are used to establish associations between exposures and out-
comes by identifying samples with and without exposure to factors of interest
and then following through time to observe an outcome.
1. Advantages
a) Feasibility, especially for the study of rare exposures unless the outcome
requires a long time to be identified
b) Useful for studying occupational exposures
2. Disadvantages
a) Confounding; the samples are not randomly chosen so spurious associa-
tions may be seen if the sample is somehow nonrepresentative
b) Can only identify associations, not cause and effect
Beware the retrospective cohort represented as a prospective cohort study! The
measurements made on the sample may not be of adequate quality if the cohort
was assembled for another purpose and then secondarily studied for the current
question.
C. Cross-sectional study
All measurements are made at once in a sample drawn from the population of
interest; distribution of variables within the sample may allow conclusions to be
made about various associations.
1. Advantages
a) Feasible; since all measurements are made at one time, costs are
relatively low.
2. Disadvantages
a) Can only identify associations, not cause and effect
D. Case control
In contrast to the cohort study, the case control starts with the outcome and
then works backward to identify exposures of interest in the sample and
in a control group matched to the study sample for important confounding
variables.
1. Advantages
a) Feasible; because the samples sizes are relatively small and the outcome
has already taken place, costs related to acquiring the data are usually
small.
b) Effective for studying rare occurrences.
c) Results are usually expressed as an odds ratio, which is easily understood
by users of the study.
2. Disadvantages
a) Predictor variables are often measured retrospectively leading to bias.
b) Can only identify associations, not cause and effect.
c) Because the process is controlled by the investigator, the selection of con-
trols may be biased; should have at least two (or more) controls for each
case although this is rarely done in the hand surgery literature.
E. Decision analysis
This approach models a clinical condition and systematically evaluates the
expected utility of various decisions about testing, therapy, etc. Informs clinical

policy about a particular condition but does not necessarily provide any insight
into the treatment of an individual.
1. Advantages
a) Feasible; does not always require the collection of data from patients but
may use data from the literature.
b) Transparent; users may be able to fully replicate the model because inves-
tigators are obligated to fully define all the variables.
c) Flexible; sensitivity analysis reveals the variables that are most influential
over the decision regarding the most desirable strategy. This may provide
insights into the problem that would not be evident in an experimental
design like a randomized trial.
2. Disadvantages
a) Measures the utility, or preference for a given health state or outcome,
which may not be fully intuitive to clinician
F. Health services research
Sometimes called “outcomes research,” this type of approach involves the analy-
sis of data obtained for another purpose, frequently billing information for large
health care aggregates like Medicare.
1. Advantages
a) Large volumes of data available for analysis.
b) Usually the studies are inexpensive because the data have already been
collected.
c) Can provide interesting insights into the process of care.
2. Disadvantages
a) Can only identify associations, not cause and effect
b) Usually more effective as a method for the generation of new hypotheses
rather than the answering of specific research questions
Although only a prospective study design can demonstrate cause/effect relation-
ships, these are often prohibitively expensive. A substantial body of lower-level
evidence that identifies a strong and consistent association may be almost as
convincing. It is now common and required by many of the journals to state the
level of evidence of the publication along with the abstract (Table 37.1).
II. Framing a Research Question
Whether planning a clinical research study or evaluating clinical research reported in the
literature, it is useful to consider the characteristics of an appropriate research question.
Think of the research question as FINER if it meets these criteria:
Feasible
Interesting
Novel
Ethical
Relevant
These are the questions reviewers and editors should be asking themselves when
evaluating manuscripts submitted for publication. Stated another way: Is it new? Is it
true? Does it matter?
A. A few points about statistical analysis
In almost all instances, there are a variety of approaches that can be conceivably
utilized to analyze data collected in a clinical research study. However, there is
often one strategy that is most meaningful, explanatory, and simple.

TABLE 37-1 Levels of evidence for primary research questiona
Types of Studies
Prognostic Studies— Economic and Decision
Therapeutic Studies— Investigating the Effect of Diagnostic Studies— Analyses—Developing
Investigating the Results of a Patient Characteristic on Investigating a an Economic or
Treatment the Outcome of Disease Diagnostic Test Decision Model
Level I High-quality randomized con- High-quality prospec- Testing of previously Sensible costs and alter-
trolled trial with statistically signifi- tive studyd (all patients developed diagnostic natives; values obtained
cant difference or no statistically were enrolled at the same criteria in series of con- from many studies;
significant difference but narrow point in their disease with secutive patients (with multiway sensitivity
confidence intervals ≥80% follow-up of enrolled universally applied refer- analyses
patients) ence “gold” standard)
Systematic reviewb of Level-I Systematic reviewb of Systematic reviewb of Systematic reviewb of
randomized controlled trials (and Level-I studies Level-I studies Level-I studies
study results were homogeneousc)
Level II Lesser-quality randomized con- Retrospectivef study Development of diag- Sensible costs and alter-
trolled trial (e.g., <80% follow-up, nostic criteria on basis of natives; values obtained
no blinding, or improper random- consecutive patients (with from limited studies;
ization) universally applied refer- multiway sensitivity
ence “gold” standard) analyses
Prospectived comparative studye Untreated controls from a Systematic reviewb of Systematic reviewb of
randomized controlled trial Level-II studies Level-II studies
Systematic reviewb of Level-II Lesser-quality prospective
studies or Level-I studies with study (e.g., patients enrolled
inconsistent results at different points in their
disease or <80% follow-up)
Chapter 37 • Clinical Trials and Hand Surgical Literature
Systematic reviewb of
Level-II studies
549
(continued)
2/22/2010 9:35:09 PM
TABLE 37-1 Levels of evidence for primary research questiona (Continued)
550
Prognostic Studies— Economic and Decision

Therapeutic Studies— Investigating the Effect of Diagnostic Studies— Analyses—Developing
Investigating the Results of a Patient Characteristic on Investigating a an Economic or
Treatment the Outcome of Disease Diagnostic Test Decision Model
Level III Case-control studyg Case-control studyg Study of nonconsecutive Analyses based on
patients (without consis- limited alternatives and
tently applied reference costs; poor estimates
“gold” standard)
Retrospectivef comparative studye Systematic reviewb of Systematic reviewb of
Section III • Other Conditions
Level-III studies Level-III studies

Systematic reviewb of Level-III
studies
Level IV Case seriesh Case series Case-control study No sensitivity analyses
Poor reference standard
Level V Expert opinion Expert opinion Expert opinion Expert opinion
a
A complete assessment of the quality of individual studies requires critical appraisal of all aspects of the study design.
b
A combination of results from two or more prior studies.
c
Studies provided consistent results.
d
Study was started before the first patient enrolled.
e
Patients treated one way (e.g., with cemented hip arthroplasty) compared with patients treated another way (e.g., with cementless hip arthroplasty) at the same
institution.
f
Study was started after the first patient enrolled.
g
Patients identified for the study on the basis of their outcome (e.g., failed total hip arthroplasty), called “cases,” are compared with those who did not have the
outcome (e.g., had a successful total hip arthroplasty), called “controls.”
h
Patients treated one way with no comparison group of patients treated another way.
Source: This chart was adapted from material published by the Centre for Evidence-Based Medicine, Oxford, UK. For more information, please see www.cebm.net.
2/22/2010 9:35:09 PM
Chapter 37 • Clinical Trials and Hand Surgical Literature 551
1. The main consideration is the research question, which should have clearly
and unequivocally identified a primary objective and the way in which
that is to be measured. The appropriate statistical analysis flows from this
measurement.
2. Establish whether or not this variable is continuous and normally
distributed.
3. Nonnormally distributed variables require the use of nonparametric tests that
include assumptions about the data that render the tests more conservative.
4. Noncontinuous data (ordinal, nominal categorical) require specific treatment
with tests designed for the analysis of these variables.
Some of these ideas are summarized in Table 37.2.
B. Common pitfalls
1. Regression modeling should be thought of as a method of predicting an out-
come from a series of predictor variables. Even though this is its primary
function, it is often used in a hypothesis-testing mode to evaluate the com-
parative importance of the various predictor variables. The main concern
with this idea is that models constructed on small or in other ways, nonrep-
resentative samples may not validate new samples because of “overfitting” to
a biased sample. Conclusions drawn on the basis of this kind of model may
not be accurate.
2. The large majority of clinical research studies published in hand surgery jour-
nals are uncontrolled case series. Authors are only able to make very limited
conclusions based on observations made in this kind of study. Beware of any
TABLE 37-2 Statistical tests for comparing independent groups

and paired samples
Number of Groups If the Groups are

Data for Comparisons Independent Paired Samples
Continuous
Normal 2 Student’s t test Paired t test
Non-normal 2 Mann-Whitney U test Wilcoxon signed
rank test
Normal 3 or more Analysis of variance Repeated
measures analysis
of variance
Nonnormal 3 or more Kruskal-Wallis test Friedman test
Ordinal 2 Mann-Whitney U test Wilcoxon signed
rank test
3 or more Kruskal-Wallis test Friedman test
Nominal 2 Fisher exact test McNemar test
3 or more Chi-square test Q test
Survival 2 or more Log-rank test Conditional
logistic regression
Source: Adapted from Kocher MS, Zurakowski D. Clinical epidemiology and biostatistics: A primer
for orthopaedic surgeons. J Bone Joint Surg. 2004;86A(3):607–620.

definitive statements that are not clearly backed up by the data presented in
the paper.
3. In a hypothesis testing strategy, the most dominant statistical analysis used
by authors of clinical research papers, the “p-value” should be understood
to indicate that should a statistically significant difference be identified, the
probability that this is an incorrect conclusion (i.e., there actually is not a dif-
ference) is, by convention 5%, hence “p < 0.05.” This assumes that only one,
or at most a few, tests are being performed. Where multiple tests are being
performed, the actual p value of any one of these tests is no longer 0.05 but
in reality 1−0.95n, where n is the number of pairwise comparisons made. For
example, if five comparisons are made, the p value for each of those compari-
sons is not 0.05 but actually about 0.23. A correction to the critical threshold
for identifying “statistical significance” should be done where multiple com-
parisons are made.
4. Many papers in the literature that seek to make comparisons fail to recognize
that their samples may have inadequate power to make the intended com-
parison. Where a comparison fails to demonstrate a statistically significant
difference, there are at least two possible reasons: There is no difference; there
is a difference but the size of the sample studied to evaluate the parameter of
interest was not sufficiently large to demonstrate the difference that exists.
Sometimes this is a function of choosing the wrong outcome measure, one
that is either insensitive to the outcome of interest or does not measure it
with the precision necessary so there is a lot of variation in the outcomes that
are observed. This should be considered in the planning stages of any study
so that if no difference is observed there can be a reasonable probability that
this means that there probably is not a difference to be found. The standard
for this is a probability of 80%. Methods of estimating the sample size neces-
sary for meeting this requirement are found in most standard texts on clinical
research methods including the ones listed at the end of this chapter.
5. One must keep in mind that statistical significance dos not always correlate
with clinical significance. In other words, the findings of a study may reach
statistical significance, the clinical difference is not important.
Statisticians should be consulted for their input during the planning
stages of a study, not at the analysis stage!
Suggested Readings
Bailar JC, Mosteller F. Guidelines for statistical reporting in articles for medical journals. Ann Int
Med. 1988;108:266–273.
Hulley SB, Cummings SR. Designing Clinical Research. 2nd Ed. Baltimore, MD: Williams &
Wilkins.
Kocher MS, Zurakowski D. Clinical epidemiology and biostatistics: A primer for orthopaedic
surgeons. J Bone Joint Surg. 2004;86A(3):607–620.
Petrie A. Statistics in orthopaedic papers. J Bone Joint Surg. 2007;88B(9):1121–1136.

Psychological Factors
38
David C. Ring and Ana-Maria Vranceanu
I. Overview
If disease is defined as a pathophysiological process, and illness as a human being’s

experience of that process, then one can readily appreciate the psychological, sociologi-
cal, and behavioral aspects of illness behavior. Contrast on the one hand the placebo
effect, where the patient’s wellness is derived from the meaning they invest in a given
treatment rather than that treatment’s efficacy or effectiveness, with secondary gain,
where—mindfully (malingering) or mindlessly—the patient derives benefit from their
illness. Also, consider the substantial variation in disability (what the patient perceives
they cannot do) for a given degree of impairment (or objective decrease in physical
function such as diminished motion or sensation). For instance, contrast examples of
two patients with operatively repaired diaphyseal forearm fractures: The athlete whom
you struggle to keep off the field until the fractures are healed and the patient who
claims they cannot work even a year after injury with near normal objective function.
Some of the psychosocial aspects of illness—such as secondary gain—are intuitive
and obvious to the surgeon, while others are not. Surgeons, as a rule, tend to see ill-
ness as mechanically based and physically correctable. Combine this with the current
stigmatization associated with psychological illness and its treatment, along with our
society’s tendency to dichotomize between the cognitive and physical aspects of illness
(e.g., “It’s all in your head”), and it can be counterintuitive, unfamiliar, and even offen-
sive to consider some of the less obvious psychosocial aspects of illness behavior. The
majority of these illness concepts are most evident in the treatment of pain, particularly
chronic pain.
Evidence is growing with respect to illness throughout the body, and chronic pain
in particular, that psychological distress (depression/anxiety), ineffective coping skills
(catastrophizing), and heightened illness concern (health anxiety/hypochondriasis)
determine a patient’s complaints and disability as much as, if not more than, objective
pathophysiological processes. But this is just putting fancy names to aspects of illness
behavior that surgeons see every day.
A. The patient with a flat affect and disproportionate pain who complains that he
or she sleeps poorly, is inactive, watches television all day, and is afraid to return
to the job that injured him or her is likely experiencing elements of depression
and anxiety.
B. Talk to the patient who gets a stiff swollen hand during recovery from a distal
radius fracture and you will find that pain sends a very strong danger alarm to
their mind that they cannot modulate and the sense of trouble is exacerbated by
negative illness misconceptions such as “the pain means I’m causing damage,”
“the pain will never go away,” and “I’ll never be able to do the things I enjoy”
among other thoughts captured under the concept of pain catastrophizing.
C. Finally, consider the patient with vague, diffuse, disabling arm pain who does
not feel the expected sense of relief and wellness when the examination and
553

diagnostic tests are reassuringly normal—they are convinced that something

is seriously wrong with them, and your best efforts consistently fail to reassure
them.
These patients tend to puzzle us. We feel uneasy with these patients. We feel inad-
equate, ignorant, and challenged. As result, the first patient (A) gets labeled as a malin-
gerer, the second (B) is diagnosed with “chronic regional pain syndrome,” and the final
patient (C) gets test after test until someone applies a diagnosis and—at worst—surgery
is elected in a context where surgery can only do harm and any positive result may be
due to the placebo effect.
It is probably best to trust feelings of uneasiness—no matter the combination of
ignorance, limited technical skill, or difficulty in understanding a patient’s illness at
their root. Our diagnoses and diagnostic tests are not as precise as we would like, and a
large percentage of the surgeries that we do—particularly for pain—have not been ade-
quately tested against simpler treatments or placebos. Perhaps the best reason to learn
to trust uneasy feelings and look for their source is that depression, catastrophizing, and
heightened illness concern, when recognized, are highly responsive to treatment. Given
the substantial psychosocial influences on arm illness, one hopes that we will eventually
treat arm illnesses in multidisciplinary teams that include behavioral medicine special-
ists as they do in many spine centers and chronic pain programs. Until that time the
surgeon may not be able to provide or even suggest psychological treatments, but they
can be honest about their puzzlement and unease, any disconnect between impairment
and disability, disproportionate nonanatomical complaints, and what is healthy about
the arm. All this should be done in a context that conveys empathy and legitimizes the
patient’s illness, no matter the proportion that is biological and the portion that is psy-
chosocial/behavioral. This will make it easier for other members of the patient’s health
care team—their primary care doctor in particular—to help address the psychosocial-
behavioral aspects of the illness.
II. Communication Skills
A. Empathy
Do not interrupt.
1. Use open-ended questions. Let the patient tell their story.
2. Communicate interest and empathy with body language.
3. Summarize the problem, using the patient’s words. The patient will feel
“heard.”
4. Legitimize the illness by repeating the patient’s concerns. Do not agree or
disagree with the patient’s concerns, just restate them in a way that legitimizes
them.
5. Introduce options, follow patient preferences. You should talk less than the
patient. The patients should feel like they are getting what they need from you.
a) Asking permission is a powerful way to show respect. “Can I describe
what the surgery involves?” “If it’s alright with you, I’d like to ask some
specific questions about your pain.”
6. Expressions such as “I really admire how well you manage with this” or
“This must be difficult for you” can help to make deposits into the patient’s
emotional bank account. Find something interesting about the patient, or
something that you have in common—a way to make a connection. Building
this connection and rapport with the patient will help you when you do not

Chapter 38 • Psychological Factors 555
say something as well as you would have liked or when you have to deliver
difficult advice.
B. Hope
1. Realize that the patient has often placed all of their hope in you, the surgeon,
the “fixer of problems.” It is very appealing to see illness as mechanical and
fixable. Patients are often looking for the “quick fix, miracle cure,” and sur-
geons have the reputation for being able to provide this, or to “cut the pain
out,” so to speak.
2. If you as the surgeon say, “I don’t know what’s wrong,” or “There’s nothing
I can do for you” you may leave the patient with no hope.
3. When patients lose hope they can become upset. If their upset is expressed as
anger, it may be directed at you.
4. Instill and preserve hope: “I have seen many cases like yours. This might take
longer than expected, but let us make a plan as to how to move forward with
this.” Provide thorough explanation of symptoms and treatment option. This
will increase patient’s confidence in your skills and will help patients feel that
you listen and care.
C. The emotive power of words
Instead of “I don’t know” or “I’m confused,” say “I’m puzzled.”
1. Instead of “This is going to be challenging,” say “I think we need to take a
creative approach.”
2. Instead of “There’s nothing I can do for you,” say “we need to be sure that we
consider all possibilities.”
3. Instead of “Don’t be worried,” say “I hope I can put you at ease.” Instead of
“You’re not in danger” say “You are safe.” Double negatives do not work, the
patient will hear “worried” or “danger” and become more anxious.
4. Orthopaedic surgeons have made particularly poor word choices for some of
the illnesses that we treat:
a) Most “tears” (e.g., rotator cuff, TFCC) are actually degenerative defects
or lesions. Calling them tears implies that an injury occurred resulting in
damage that needs to be repaired—which is not the usual situation.
b) Speculation about “overuse” is in most cases overstated and not well sup-
ported by scientific data, but the concept of overuse validates the catastro-
phizing patient’s fears and encourages their illness behavior. Admonitions
to work to the pain but not beyond or concerns that one can “overdo it”
are similarly counterproductive in the catastrophizing patient.
c) The best approach is to always choose your words and illness concepts
carefully. As health care providers, we are obligated to promote the most
positive, optimistic, enabling, practical, confidence-building illness con-
cepts consistent with scientific data.
III. The Multidisciplinary Approach
A. An appreciation that all illness is biopsychosocial will go a long way toward

diminishing the stigmatization associated with the cognitive/emotional aspects
of recovery.
B. When patients recovering from injury are uneasy about their exercises, ask them
to slow down time and tell you the story that flashes across their mind automati-
cally and intuitively when they feel the pain.

1. This story typically features elements of catastrophizing that make it difficult

for them to work with the pain.
2. Discuss positive experiences with pain such as the pain associated with mus-
cle stretches or the pain after a workout, as means of putting patients at ease
with their pain and helping them see that pain is not always “dangerous.”
Reframing pain from “bad” to “good” or neutral will help patients adhere to
their exercise regiment.
3. If this does not help them reorient and feel more confident and at ease with
the exercises, then it may be useful to point out that their uneasiness is based
on misconceptions that can be unlearned. If they are interested, cognitive
behavioral therapy can help. Normalizing the situation and discussing how
many people have trouble with pain and difficulties with exercises, but that
they can learn skills (via cognitive behavioral therapy) that would help them
recover quicker and have a better quality of life in doing so, may make
patients more open to thinking in a more flexible, comprehensive manner.
WARNING: Successful communication of these concepts is based upon
an emotional connection with the patient and successful demonstration of
empathy. These are “developing skills” for most surgeons.
C. An empathetic, supportive discussion of these issues sometimes leads a patient
to have insight into how personal matters, psychological distress, and coping
styles are hindering recovery. Such insight may help the patient be more open to
behavioral therapies.
IV. Specific Psychiatric Disorders in the Hand
A. Malingering versus somatoform disorder

1. Surgeons are relatively familiar with secondary gain and outright malinger-
ing, but they are not as quick to recognize increased health anxiety/hypo-
chondriasis/heightened illness concern.
2. Patients with somatoform disorders have more subtle and less familiar needs
from illness.
B. Posturing is often a somatic expression of psychological distress
1. Clenched fist/finger syndrome.
C. Self-injury
1. Factitious lymphedema—look for signs of a constriction band on the upper
arm.
2. Secrétan’s—classically self-inflicted repeated dorsal hand trauma, but the area
of trauma may vary.
3. Wound manipulation/nonhealing ulcers
V. Reaction to Injury and Disease in the Hand
A. Depression/anxiety
1. Occurs on a spectrum, not all or none (e.g., major depression)
2. Increases perceived pain and disability
3. Most common worldwide health problems
4. Exacerbates disability associated with other chronic diseases
5. Fosters avoidance of pain

Chapter 38 • Psychological Factors 557
6. Preinjury depressive symptoms sensitize patient to more severe depression

and posttraumatic stress disorder
7. Treatable
a) Medications
b) Cognitive behavioral therapy
B. Catastrophizing
1. Intuitively thinking the worst. Magnifying the pain, feeling helpless when
in pain, ruminating on the pain experience. Pain becomes the center of ones
life.
2. A “strong pain alarm.”
3. Ineffective coping skills and negative illness misconception.
4. Increases perceived pain and disability.
5. Hinders exercises, recovery, and resumption of normal activities.
C. Heightened illness concern/health anxiety (hypochondriasis)
1. Also a spectrum and not all or none
2. Patient difficult to reassure
3. Convinced there is something seriously wrong in spite of reassuring informa-
tion from health care providers and diagnostic tests
4. Strongly associated with pain intensity and disability in nonspecific (idio-
pathic) arm pain
VI. The Psychology of the Surgeon
A. God syndrome
1. “I can do it,” “I can fix it.”
2. Surgeons are stereotypically overconfident to the point of arrogance
3. Inadequate humility in the face of the limitations of modern medicine
B. Psychological factors are contagious—transference
1. Surgeons may become anxious, depressed, and fearful of the worst possibility
around patients with these types of illness behavior.
2. Surgeons may associate intense pain complaints with more intense pathol-
ogy, in spite of scientific evidence that greater complaints result largely from
psychosocial issues.
C. Secondary gain—“care and trust” supplanted by “suspicion and deceit”
Suggested Readings
Branck, WT, Malik TK. Using windows of opportunity in brief interviews to understand patient
concerns. JAMA. 1993; 269:1667–1668.
Charon RC. Narrative medicine: A model for empathy, reflection, profession and trust. JAMA.
2001;286(15):1897–1902.
Flor H, Fydrich T, Turk DC. Efficacy of multidisciplinary pain treatment centers: A meta-analytic
review. Pain. 1992;49:221–230.
Turk DC, Gatchel R. Approaches to Pain Management: A Practitioners Handbook. 2nd Ed.
New York, NY, The Guilford Press; 1999:360 pp.
Turk DC, Swanson KS, Tunks ER. Psychological approaches in the treatment of chronic pain
patients when pills, scalpels and needles are not enough. In review. Can J Psychiatry.
2008;3:213–233.

Splinting
39
Rebecca von der Heyde and Patricia M. Paytner
I. Chronic Pain Syndromes
Chronic Regimal Pain Syndrome (CRPS) I/II

A resting hand splint in the position of function provides support to the hand, wrist,
and thumb and limits painful motion. The splint is worn as needed between exercise
and functional activities. A circumferential night splint, preferably of a soft material,
can provide positive pressure and facilitate pain management. When pain is controlled,
low force dynamic splinting can be used to increase joint range of motion.
II. Flexor Tendons
A. Flexor Tendon Repair in Zones I to V

A dorsal-based synergistic wrist splint is recommended following flexor tendon repair in
zones I to III (Fig. 39.1). The MP joints are positioned in more than 60 degree flexion,
with the PIP and DIP joints in full extension. The wrist is immobilized in 20 degrees of
flexion, but is allowed up to 30 degrees extension during place and hold exercises initi-
ated within 2 to 3 days following surgery. The combination of wrist and digital motion
as afforded by this protocol produces high excursion/low force rehabilitation. Repairs in
zones IV and V are managed using a traditional, dorsal blocking splint. Splints are worn
at all times for the first 4 to 6 weeks.
III. Extensor Tendons
A. Mallet Finger
A static DIP extension splint is worn at all times for 6 to 8 weeks to facilitate scarring of the
terminal tendon to the distal phalanx (Fig. 39.2). The fabrication of at least two splints is
suggested to allow the application of a dry splint after showering to prevent maceration.
B. Boutonniere and Pseudoboutonniere Injuries

Injuries to the central slip are managed using finger-based PIP extension splints, worn
at all times for 6 to 8 weeks. The inclusion of DIP flexion exercises while in the splint
will facilitate dorsal translation of the lateral bands.
C. Sagittal Band Rupture

A hand-based, MP extension splint (P1 blocking splint) immobilizes and aligns the MP
joint in full extension and neutral ab/adduction (Fig. 39.3). Active motion of the PIP
and DIP is allowed while in the splint. Buddy taping to the finger on the involved side
is permissible for partial tears and in later stages of healing to control active motion.
558

Chapter 39 • Splinting 559
Figure 39.1 Synergistic splint for flexor tendon repair.
Figure 39.2 DIP extension splint for mallet finger.
D. Proximal Zones
A dynamic MP extension assist splint allowing 30 degrees of active MP flexion is the
preferred method of treatment following extensor tendon repairs in zones V to VII
(Fig. 39.4). This protocol facilitates distal glide of the healing tendon to decrease adhe-
sion formation. These injuries can also be treated more conservatively using a forearm-
based, static MP extension splint; however, theses splints have been demonstrated as less
effective in preventing extensor lags. Splints are worn at all times for the first 4 weeks.

Figure 39.3 Hand-based MP extension/P1 blocking splint.
Figure 39.4 Dynamic MP assist/extension splint.
E. Chronic Boutonniere Deformity

Dynamic PIP extension splints are utilized to increase joint mobility in the patient with
a chronic boutonniere. These splints can be fabricated in various ways; however, excel-
lent prefabricated options are also available.
F. Chronic Swan Neck Deformity

Oval splints are fabricated to decrease PIP hyperextension and reinforce the volar plate
(Fig. 39.5). In addition, silver ring splints can be custom ordered for the patient to
provide an attractive, long-term option.
G. Yoke
A controlled active motion splint used for extensor tendon rehabilitation that places
the affected digit in relative extension when compared to the adjacent uninjured digits,
eliminating the force of extension across the tendon repair.

Figure 39.5 Oval splint.
IV. Tendinopathy
A. de Quervain Tenosynovitis
A forearm-based thumb spica splint with the IP joint free is fabricated to decrease
the combined motions of thumb flexion/adduction and wrist ulnar deviation. The
splint is worn for 6 to 8 weeks to decrease pain and inflammation of the first dorsal
compartment. As immobilization of the thumb often decreases function, positioning of
the thumb in palmar abduction to ensure opposition to the index and long will increase
compliance with splint wear.
B. Trigger Finger
Hand-based P1 blocking splints (Fig. 39.3) have been suggested to control active trigger-
ing. Blocking of the MP joint should be tested to determine symptom relief prior to splint
fabrication. If successful, splints are worn for 6 weeks to decrease tendon inflammation.
C. Intersection Syndrome
A forearm-based thumb spica splint with the wrist positioned in slight extension and
the thumb IP joint free is fabricated to decrease irritation of the muscles of second dor-
sal compartment. The splint is worn for 6 to 8 weeks to decrease repetitive wrist motion
and inflammation of the radial wrist extensors.
D. ECU Tendonitis
A wrist cock-up splint is recommended to decrease pain and inflammation. An ulnar
gutter splint that does not encompass the fingers is an additional option if pressure over
the ulnar head does not provoke pain. Splints are typically worn for 6 to 8 weeks during
functional tasks.
E. FCR Tendonitis
A wrist-resting splint in a neutral position (Fig. 39.6) provides relief to the patient with
FCR tendonitis. Splints are typically worn for 6 to 8 weeks during functional tasks.

Figure 39.6 Wrist resting splint in a neutral position.
F. Tennis Elbow
A prefabricated counterforce brace is postulated to reduce force production of the ECRB
during wrist extension. Static wrist cock-up splints can also be fabricated in severe cases
to maintain the wrist in an extended position and rest the affected musculature. A 6 to
8 week course of splinting is recommended.
G. Golfer’s Elbow
A wrist-resting splint in a neutral position (Fig. 39.6) is suggested for the patient with
pain and symptoms at the medial epicondyle. Splints are donned during functional
tasks to decrease repetitive motions for 6 to 8 weeks.
V. Tendon Transfers
The goal of postoperative splinting following tendon transfers is to maintain both

muscles in a shortened, protected position. For example, a brachioradialis to FPL
transfer would require a long arm posterior splint with the elbow in flexion and the
forearm in pronation. A dorsal blocking splint positioning the wrist and thumb
in flexion would be attached distally. Typical immobilization of the transfer is 4
weeks, followed by progressive neuromuscular re-education and tendon transfer
training.
VI. Stiffness
Finger, Thumb, Wrist, and Elbow

Serial static, static progressive and dynamic splints can be fabricated or custom ordered
for the patient who has decreased joint mobility in any joint from the elbow distal.
These splints should be implemented following adequate healing of bony and soft tissue
structures and closely monitored with goniometric measurement, resulting in at least
10 degrees of progress per week. Typical wearing schedules focus on a low-load, long
stretch in multiple intervals throughout the day.

Figure 39.7 Ulnar gutter splint.
VII. Fractures and Dislocations: Hand
A. Distal Phalanx
A static DIP extension splint is applied to ensure fracture stability. Splints are worn at
all times for 4 to 6 weeks.
B. Middle Phalanx
A finger-based extension splint immobilizing both the PIP and DIP joints is fabricated
for support and protection. Early active motion of PIP and DIP joints reduces edema
and maximizes tendon glide. Splints are worn at all times between exercises.
C. Proximal Phalanx
A hand-based P1 block is fabricated with the MP joint in full extension to provide
support to the proximal phalanx (Fig. 39.3). The maintenance of PIP joint mobil-
ity, including avoidance of flexion contractures, is of vital importance. Gliding of
both the extrinsic flexors as well as the extensor mechanism also contributes to
positive outcomes. The splint is removed for exercise, including progressive MP
flexion, and can be modified to position the MP in greater degrees of flexion as
healing occurs.
D. Metacarpal
Distal fractures of the ring and small metacarpals, including the head and neck, are
commonly splinted using an ulnar gutter (Fig. 39.7) with the wrist in slight exten-
sion and the digits in an intrinsic plus position. More proximal fractures of the shaft
and base, as well as stable fractures of the neck can be efficiently splinted using a

Figure 39.8 Metacarpal cuff splint.
metacarpal cuff (Fig. 39.8). The metacarpal cuff allows active motion of the wrist and
MP joints while in the splint, increasing tendon glide of the extrinsic digit extensors.
Both splints are worn for 4 to 6 weeks, or until the fracture is adequately healed.
E. Intra-articular Carpometacarpal Fracture/Dislocation
A traction splint is fabricated to distract and align the bony fragments and to allow
controlled, active motion. The fabrication of this splint requires a longitudinal k-wire
or pin placed intra-operatively for the application of rubber band traction. Accurate
fabrication requires close collaboration between surgeon and therapist, including an
x-ray to ensure proper traction and alignment during motion.
VIII. Fractures and Dislocations Wrist
A. Carpometacarpal/Carpus
A wrist-resting splint in a neutral position (Fig. 39.6) is used to immobilize carpometa-
carpal (CMC) and carpal fractures/dislocations in the central and ulnar aspects of the
wrist. For those injuries to the thumb or radial carpal bones, a forearm-based thumb
spica is recommended. Splints are worn at all times for 4 to 6 weeks and discontinued
upon recognition of stability and healing. Scaphoid fractures are often immobilized for
a greater length of time due to circulatory issues that impede healing.
B. TFCC/DRUJ
A Munster splint limits rotation of the forearm and is indicated for 6 to 8 weeks fol-
lowing injury to the TFCC or DRUJ. Following DRUJ dislocation, immobilization is
determined by the position in which the joint is most stable on clinical examination.
A long arm posterior splint, immobilizing the elbow in a position of comfort, can also
be employed (Fig. 39.9).
C. Distal Radius and Ulna
A fracture of the distal radius or ulna is commonly immobilized using a wrist-resting
splint in a neutral position (Fig. 39.6). Clamshell, or circumferential splints, can be
used for complex cases. Splints are typically worn 4 to 6 weeks.

Figure 39.9 Long arm posterior splint.
IX. Fractures and Dislocations: Elbow
A. Radial Head
During surgery, stability of the elbow is evaluated in flexion and extension with the fore-
arm in pronation, neutral, and supination. Stable repairs are immobilized in extension,
whereas repairs with residual instability are splinted at 90 degrees of elbow flexion and
the forearm position that produced optimal stability for 4 to 6 weeks. Gentle active
motion is initiated on the first postoperative day.
B. Simple Elbow Dislocation/Fractures of the Proximal Ulna, Olecranon, or

Distal Humerus
A prefabricated, soft elbow immobilizer is often applied postoperatively as a more com-
fortable option than a thermoplastic splint. Alternatively, a long arm posterior splint
with the elbow positioned at 90 degrees and the forearm in neutral can be fabricated
(Fig. 39.9). Protective splinting is maintained for 4 to 6 weeks, with gentle active
motion initiated within the first week.
X. Nerve
A. Carpal Tunnel Syndrome

A wrist resting splint in a neutral position (Fig. 39.6) is custom-fit for use at night. The
purpose of the splint is to avoid positions that provoke pain and symptoms of median
nerve compression. The splint can also be used during functional tasks to maintain the
wrist in a neutral position. Splints are worn for 4 to 6 weeks followed by reassessment
of symptoms.

Figure 39.10 Hand-based thumb spica splint.
B. Cubital Tunnel Syndrome

An elbow extension splint is applied to the volar aspect of the forearm to decrease
tension on the ulnar nerve. The splint is worn at night and during the waking hours
as needed. A prefabricated elbow pad can also protect the ulnar nerve from external
contact. Symptoms are reassessed after 4 to 6 weeks.
C. Submuscular Ulnar Nerve Transposition

A long arm posterior splint with the elbow positioned at 90 degrees and the wrist and
forearm in neutral (Fig. 39.9) is fabricated within the first postoperative week. Gentle
active motion is initiated at the elbow, limited to −30 degrees extension. Wrist and forearm
motions are delayed until 3 weeks postoperatively, and the splint is worn for 4 to 6 weeks.
D. Median Nerve Palsy

A hand-based thumb spica splint (Fig. 39.10) is fabricated to substitute for the loss of
opposition as produced by the thenar musculature. The splint is worn during functional
activities.
E. Ulnar Nerve Palsy

An anticlaw splint positions the MP joints of the ring and small fingers in flexion,
allowing the extrinsic extensors to translate force through the extensor mechanism,
producing PIP and DIP extension. The splint is worn during functional activities
and passive exercises are completed to maintain MP flexion and IP extension of the
digits.
F. Radial Nerve Palsy

An MP extension assist splint (Fig. 39.4) is fabricated to compensate for the absence of
extension in the wrist, digits, and thumb. Alternatively, a simple wrist cock-up splint

can be fabricated to maximize grasp, with relaxation used for the release of objects from
the hand. Both splints are worn during functional activities.
XI. Arthritis
A. Rheumatoid
1. Wrist
A resting wrist splint that maintains the MP joints in extension can provide
alignment and stability to the patient with a zigzag deformity. This splint is
worn on an as needed basis for support and pain relief.
2. MP
From a conservative perspective, multiple prefabricated and custom
hand-based splints can be offered to the patient demonstrating ulnar drift at
the MP joints. The purpose of an ulnar drift splint is to gently pull the MP
joints toward neutral abduction. These splints are worn throughout the day
to maximize joint alignment.
3. Digits/swan neck deformity
Oval splints are fabricated to decrease PIP hyperextension and reinforce the
volar plate (Fig. 39.5). In addition, silver ring splints can be custom ordered
for the patient and provide an attractive, long-term option.
B. Idiopathic Degenerative
1. Thumb CMC
Conservative management of thumb CMC osteoarthritis can be accomplished
with a thumb spica splint, either hand based or forearm based, although the
hand-based splint is better tolerated. Neoprene splints provide some support
and allow a greater degree of freedom than the orthoplast splints. Splints
are worn for 4 to 6 weeks during functional tasks and supplemented with
stretching of the adductor pollicis in the web space.
C. Arthroplasty
1. PIP
A digital extension splint is fabricated and active motion is initiated at the
sixth postoperative week. Lateral forces are carefully monitored during strap-
ping of the splint and any interventions for edema management. The splint
is worn between exercises for 4 to 6 weeks.
2. MP
A dynamic MP extension assist splint is applied following MP joint arthro-
plasty. Gentle MP flexion and extension are allowed within the splint, guided
by traction in a radial direction. A resting pan can be attached to the splint
for nightwear; this can be coupled with antirotational strapping as needed.
The splints are worn at all times for 6 weeks.
3. CMC
Following CMC arthroplasty of the thumb, a forearm-based thumb spica splint
is applied and early, gentle motion is initiated with a focus on circumduction of
the CMC joint. The splint is worn between exercises for 4 to 6 weeks.
4. Elbow
A long arm posterior splint with the elbow positioned in 90 degree flexion
(Fig. 39.9) is fabricated for daytime use. A static extension splint is also fab-
ricated to be donned at night. The patient begins active-assisted flexion and
gravity-assisted extension during the first postoperative week.

XII. Replantation
The goal of splinting following replantation is to maintain the affected joints in a mid-
range position while avoiding tension or compression on arterial and venous repairs.
A functional resting hand splint provides a safe position for immobilization following
replantation and can be fabricated using soft straps with a large surface area.
XIII. Dupuytren Release
Following Dupuytren release, the goal of splinting is to maximize extension of the MP

and IP joints. The goal of therapy, in comparison, is to maintain a balance between
accomplishing maximal extension while maintaining functional flexion. A forearm-
based splint, which provides a gentle stretch toward extension at the wrist and digits
is optimal, and can be fabricated either dorsally or volarly. With a dorsal approach, a
greater stretch can be affected and maceration is less likely to occur in the palmar area.
The splint is worn at all times between exercises for the first 3 to 4 weeks, then slowly
weaned to night use depending on extension outcome. The night splinting can be con-
tinued for up to 6 months.
Suggested Readings
Chow JA, et al. A comparison of results of extensor tendon repair followed by early controlled
mobilization versus static immobilization. J Hand Surg (Br). 1989;14(1):18–20.
Evans RB, Hunter, JM, Burkhalter WE. Conservative management of the trigger finger: A new
approach. J Hand Ther. 1988;1:59–68.
Lieber RL, et al. Wrist and digital joint motion produce unique flexor tendon force and excursion
in the canine forelimb. J Biomech. 1999;32(2):175–181.
Meyer NJ, et al. Modeled evidence of force reduction at the extensor carpi radialis brevis origin
with the forearm support band. J Hand Surg. 2003;28(2):279–286.
Weiss S, et al. Prospective analysis of splinting the first carpometacarpal joint: An objective,
subjective, and radiographic assessment. J Hand Ther. 2000;13(3):218–226.

Surgical Instrumentation
40
Beth Paige
Bone Excision/Shaping (Fig. 40.1a and 1b)
A. #1 Bone Curette str Codman 23-1044
Fig. 40.1a
569

B. #2 Bone Curette str Codman 23-1045
Fig. 40.1b
C. #3 Bone Curette str Codman 23-1046

D. Marquardt Bone Rongeur 8˝ cvd-dbl action Aesculap FO520R
• Leur-Friedmann Rongeur 5¾˝ cvd-single action Aesculap FO409R.
• Both Rongeurs have thinner jaws, which allow better biting in small tight
areas. The double action gives the surgeon a stronger bite. Both of the
rongeurs bite range is 2 to 3 mm.
• There are different lengths of curettes: hand and spinal—both seen below. Surgeon’s
preference when dealing with length. Codman does carry both lengths.
Fig. 40.1c,d

Chapter 40 • Surgical Instrumentation 571
Fig. 40.1c,d
Clamps (Fig. 40.2)
A. Ochsner (Kocher), straight Aesculap BH443R

• The Ochsner clamp is great for grasping bone and pulling.
B. Allis Clamps Aesculap EA015R
• The Allis clamp is good for grasping tendons and is considered to be relatively
atraumatic (nontissue damaging).
Fig. 40.2a,b

Fig. 40.2a,b
C. Kelly Clamps (Peons) Aesculap BH443R
Fig. 40.2c

Fig. 40.2c
D. Right Angle Mixer Clamp Jarit 140-218

• This Right Angle clamp is a Mixer clamp. The Mixer clamp allows for the
more aggressive 90-degree angle and a fine tip.
Fig. 40.2d

Fig. 40.2d
E. Mosquito Clamp, cvd Aesculap BH120R

F. Mosquito Clamp, str Aesculap BH121R
Fig. 40.2e,f

Fig. 40.2f,e
Forceps (Fig. 40.3)
A. Micro-Adsen Forcep w/teeth Aesculap BD520R

B. Adsen Forcep w/teeth Aesculap BD511R
Fig. 40.3a,b,c

C. Adsen Forcep w/o teeth Codman 30-1185

• The Micro-Adsen forcep has a more delicate (finer) tip than that of regular
Adsen forceps, and the neck of the forceps is thinner and longer. The body of
the Micro-Adsen is also longer than the regular Adsen forcep. Smooth jawed
forceps are needed to grasp implants without scratching the surface of the
implant.
• Micro-Adsen Forcep w/teeth
• Adsen Forcep w/teeth
• Adsen Forcep w/o teeth
Fig. 40.3c,b,a

Fracture and Periosteal Manipulation (Fig. 40.4)
A. Freer Elevator Jarit 285-380

B. Kleinert Kutz Elevator Jarit 400-290
C. Dingman Periosteal Elevator V. Mueller RH2744
Fig. 40.4c,a,b
Fig. 40.4c,a,b

Fig. 40.4c,a,b
D. Penfield Dissector Jarit 285-368

E. Bone Hook Synthes 319.39
F. Dental Hooks (tracheal) Aesculap BT103R
Fig. 40.4f,e,d

Knife Handles (Fig. 40.5)
A. #3 Knife Handle Aesculap BB074R

B. Beaver Handle Beaver K3
Fig. 40.5
Mallet (Fig. 40.6)
A. Mallet 7½˝ 9oz Miltex 19-794
Fig. 40.6

Pliers/Cutter (Fig. 40.7)
A. Wire Cutter Jarit 215-530

B. Pliers Millennium 48-253
Fig. 40.7a,b
Retractors (Fig. 40.8)
A. Army-Navy Retractors Aesculap BT041R

• Army-Navy retractors are used for medium to deep retraction.
B. Hohmann Retractor 8 mm Synthes 399.19
• Hohmann retractors are used to retract tissue away from the bone during
drilling and plating.
C. Hohmann Retractor 6 mm Synthes 399.18
Fig. 40.8a
Fig. 40.8c,b

D. Myerding Finger Retractor-short, teeth Millennium M52-122

E. Myerding Finger Retractor-long, teeth Millennium M52-118
F. Myerding Finger Retractor-short, blunt Millennium M52-124
G. Myerding Finger Retractor-long, blunt Millennium M52-116
• These retractors are great retractors because they prevent retractor holder
fatigue and allow their hands to be further away from the field while the dif-
ferent lengths allow shallow or deep retracting.
Fig. 40.8d,e,f,g
Fig. 40.8e,f,d,g

H. Senn Retractor 6½˝ Aesculap BT008R

I. Ragnell Retractor 6˝ Aesculap BT004R
• Ragnell retractors are good for retracting close to a nerve because of the blunt
tips and the varying depth of retraction. Senn retractors are good for retrac-
tion thick tissue with its sharp teeth without slipping.
Fig. 40.8h,i
Fig. 40.8h,i

Fig. 40.8h,i
Fig. 40.8h,i

J. Joseph Skin Hook—double prong Aesculap OL620R

K. Joseph Skin Hook—single prong Aesculap OL623R
• Skin Hook retractors retract the superficial skin at the beginning incision.
Fig. 40.8j,k
Fig. 40.8j,k

L. Gelpi Retractor 5¼˝ Aesculap BV996R

M. Weitlaner Retractor blunt Aesculap BV073R
• Gelpi and Weitlaner retractors allow for retraction without hands in field,
Gelpi retractors are usually used for shallow retraction while Weitlaner retrac-
tor is used for deep and longer incisions.
Fig. 40.8l,m
Fig. 40.8l,m

Scissors (Fig. 40.9)
A. Tenotomy Scissors, black handled Wexler KM35-194

B. Iris Scissors, cvd-sharp Jarit 360-101
• These scissors are for dissecting depending on surgeon’s preference. The
Tenotomy scissors allows for narrow tip dissection but as tissue moves down
the jaws tissue is dissected more without any extra hand movements.
Fig. 40.9a,b
Fig. 40.9b,a
C. Strabimus Scissor, str-blunt Jarit 360-130

• The small Strabimus scissors are used to cut suture-only!
D. Mayo Scissor, str Aesculap BC547R
• The Mayo scissors can be used to cut suture but most useful for cutting
dressings.

Fig. 40.9c
Fig. 40.9c
Fig. 40.9d,e

E. Bandage Scissor Aesculap MB223R

• The Bandage scissor is used to cut off the drapes.
Fig. 40.9d
Fig. 40.9e

Suction Tip (Fig. 40.10)
A. Frazier & Fr. Suction Tip Aesculap MD125
Fig. 40.10
Towel Clips (Fig. 40.11)
A. Edna Towel Clips (non-penetrating) Aesculap BF461R

B. Penetrating Towel Clip Aesculap BF431R
• Edna towel clips are used to secure cords and things to the drapes but the
Penetrating towel clip secures the towel around the tourniquet just prior to
the sterile drape application.
Fig. 40.11b,a
Fig. 40.11b,a

Webster Needle Holder (Fig. 40.12)
A. Webster Needle Holder TC 5˝, smooth Sklar 21-1650

• This needle holder with its smooth jaws allows the surgeon to manipulate the
suture needle in different positions without having to regrasp with hand or
forceps.
Fig. 40.12

Bone Grafting and Bone Graft
Substitutes
41
Drew R. Engles and Andrew J. Schoenfeld
While the majority of osseous injuries can be treated with either immobilization or
surgical stabilization, there is a specific subset of injuries or conditions that require
supplemental bone grafting. These include instances where there is actual bone loss
(i.e., open fractures), relative bone loss (i.e., impacted distal radius fractures), or
loss of sufficient bone quality (i.e., osteonecrosis). Bone resection for tumors or
osteomyelitis can also result in significant actual bone loss with varying degrees of
structural compromise. In order to address these insufficiencies, bone graft or bone
graft substitutes are employed. Initially, simple techniques relying on cortical and
cancellous autografts were employed. Today, the field has now expanded to encom-
pass the use of allografts, synthetic ceramic-based and collagen-based matrices,
demineralized bone matrix (DBM) and even vascularized bone grafts. Recently, the
use of purified recombinantly manufactured human osteoinductive growth factors,
known as bone morphogenetic proteins (BMPs), has also become common in the
clinical realm. The science and rationale behind the utilization of the various types
of bone graft and bone graft substitutes commonly employed in hand surgery will
be discussed.
I. Basic Science
A. Basic properties. All bone grafts and bone graft substitutes have inherent proper-
ties vital to their performance and function in the clinical realm. These include
osteoconductivity, osteoinductivity, osteogenic potential as well as individual
structural properties.
1. Osteoinduction. Proteins signal local mesenchymal stem cells to differentiate
into cells capable of producing bone. Recruitment and differentiation of cells
are controlled by matrix-derived growth factors.
a) BMP-2, -4 and -7 are members of the transforming growth factor (TGF)-
b superfamily. Undifferentiated perivascular mesenchymal cells are the
targets for BMP.
b) Fibroblast growth factors are angiogenic factors important in neovascular-
ization and wound healing.
c) Platelet-derived growth factor.
d) Insulinlike growth factor II stimulates type I collagen production, cartilage
matrix and osseous formation.
2. Osteoconduction. A substance’s three-dimensional structure facilitates
the ingrowth of perivascular tissue, capillaries, and osteoprogenitor cells,
ultimately enabling bone ingrowth/ongrowth.
a) Osteoconduction is a property of cancellous bone grafts, DBM, and
synthetic bone graft substitutes.
b) Pore size of osteoconductive grafts plays a vital role in facilitating bone
ingrowth. Optimal pore size is 150 to 500 mm.
591

3. Osteogenic potential includes the ability to synthesize new bone through

cells present in the graft or derived from the host.
a) Osteoblasts, osteocytes, and undifferentiated mesenchymal stem cells.
b) Cortical and cancellous grafts both possess cells that can survive trans-
plantation and form new bone at the graft site.
4. Structural properties include the ability of the graft to confer initial strength
and/or immediately resist tensile/compressive forces at the graft site.
a) Free vascularized cortical grafts are biomechanically superior to nonvascu-
larized cortical grafts for 6 months after transplantation.
b) Autologous cortical bone provides structural support initially; this
becomes more limited during the resorption phase.
c) Calcium phosphate cement provides structural support and remodels
according to Wolff law.
d) Cancellous bone graft and DBM provide minimal structural integrity.
e) Ceramics must be shielded from loading forces due to their brittle
nature.
B. Types of graft
1. Autograft harvested from the patient
a) Can be vascularized, nonvascularized, cortical, cancellous, corticocancel-
lous, or osteochondral.
2. Allograft—harvested from a human donor
a) Can be cortical, cancellous, corticocancellous, or osteochondral.
3. Xenograft is harvested from another species (usually porcine or bovine).
C. Graft preparation
1. Autografts are harvested from the same patient in whom they will be used.
Harvesting autografts involves a risk of infection and fracture at the donor
site. There is increased operative time and surgical cost. In addition, there is
a potential for increased surgical blood loss, postoperative pain, and lengthier
or requisite hospital stay.
2. Allografts are harvested from cadaveric donors.
a) Frozen or freeze-dried (lyophilization) tissue decreases antigenicity and
limits the risk of disease transmission. Frozen bone retains the greatest
biomechanical strength. Freeze-dried bone grafts are weak in torsion and
bending.
b) Osteoprogenitor cells are destroyed but osteoconductive properties
remain. Disease transmission (HIV and HCV) remains a potential risk,
although with a statistically low likelihood. Due to strict donor screening,
tissue testing, and preparation techniques, there are only two documented
cases of HIV transmission in more than 3 million tissue transplants. Both
cases occurred with the transplantation of unprocessed, fresh-frozen
allografts.
D. Limitations
1. Most studies regarding the efficacy of bone graft and bone graft substitutes
are nonrandomized in which efficacy cannot be proven.
2. There are no studies directly comparing the performance of osteoconductive
bone graft substitutes.
3. The method of allogeneic graft preparation influences clinical performance.
4. Expense—All bone graft substitutes incur an expense and indiscrimi-
nate use, without proper indications, can result in gratuitous health care
expenditures.

Chapter 41 • Bone Grafting and Bone Graft Substitutes 593
E. Bone graft impairment

1. Smoking inhibits cellular proliferation and causes vasoconstriction, which
inhibits bone healing and graft consilidation. Several studies have indicated
that smoking increases the risk of tibial pseudoarthrosis by as much as 40%.
It also increases time to union, and incidence of infection.
2. Systemic steroids inhibit progenitor cell differentiation down the osteoblastic
pathway.
3. NSAIDs inhibit prostaglandin formation, decreasing blood flow, and delay-
ing graft resorption.
4. Malnutrition. Calcium and phosphorous deficiencies are associated with
delayed formation of new bone.
II. Autograft
A. Autologous cancellous bone

1. Commonly harvested from the iliac crest, distal radius, olecranon, tibial
metaphysis (proximal or distal), and calcaneus.
a) Indicated for nonunions with less than 5 to 6 cm of bone loss or as filler
for bone cysts or bone voids.
b) Contraindicated in situations where structural integrity of the graft is
required.
c) Iliac crest provides twice the volume of bone graft as either the distal
radius or the olecranon.
2. Does not provide significant structural support, but acts mainly as an osteo-
conductive graft with some (theoretical) osteoinductive potential, achieving
optimal strength at 6 to 12 months.
3. Easily revascularized and rapidly incorporated at the graft site. The process
occurs through osteointegration, whereby the graft unites with pre-existing
osseous structures and is remodeled along lines of stress.
B. Autologous cortical bone
1. Sources include the iliac crest, rib, and fibula.
2. Provides immediate structural support.
3. Incorporated by a process of creeping substitution.
a) Demonstrated most significantly at the graft-host bone interface.
b) Process leads to an initial loss of biomechanical strength at 6 weeks of
implantation.
4. No difference in the biomechanical strength of vascularized and nonvascular-
ized cortical grafts at 6 months.
C. Bone marrow aspirate
1. Osteogenic and osteoinductive. Contains osteoblastic stem cells, BMPs,
cytokines, and other growth factors.
2. Harvested in aliquots of 2.5 to 3 cc per site.
3. Can be injected into sites of nonunion.
4. Can also be combined with all available allograft and synthetic osteoconduc-
tive materials to recreate a more favorable fracture-healing environment.
D. Vascularized bone grafts
1. Major advantage of vascularized grafts is the preservation of circulation,
resulting in improved strength, healing, and response to stress.
a) Free vascularized bone grafts rely on microvascular anastomoses to
recipient site arteries and veins.

b) Pedicle grafts are rotated about their blood supply to an adjacent

graft site.
2. Increased likelihood of bone healing. A more rapid union and bone hypertro-
phy occur in response to applied stress.
3. Can restore longitudinal growth by the inclusion of a growth plate, increased
local blood flow, reconstruction of composite tissue loss, and revasculariza-
tion of necrotic bone.
4. Indications
a) Segmental bone defects larger than 6 to 8 cm.
b) Persistent nonunion after conventional treatment.
c) Dysvascular or necrotic bone.
d) Scarred, previously infected or irradiated soft tissue bed.
e) Congenital pseudoarthrosis.
5. Carpal vascularized bone grafts are used to treat scaphoid fractures, pseudo-
arthroses, and Kienbock disease.
a) Dorsal distal radial graft based on the 1,2 intercompartmental supraret-
incular artery (1,2 ICSRA) of Zaidenberg. Used for scaphoid nonunions,
but not for other carpal nonunions due to a limited arc of rotation.
b) Dorsal distal radial graft based on the 2,3 intercompartmental supraret-
incular artery (2,3 ICSRA). The blood supply is from the distal anas-
tamosis with the dorsal intercarpal arch. It has an arc of rotation that
reaches the entire proximal carpal row and is used in Kienbock disease or
proximal scaphoid nonunions.
c) Dorsal distal radial graft based on the 5 + 4 extensor compartment
artery (4 + 5 ECA). The blood supply is via the retrograde flow from
the intercarpal arch. After ligation of the posterior interosseous artery, a
“Y-” shaped bifurcation essentially doubles the length of the pedicle. This
allows an arc of rotation reaching anywhere in the carpus.
d) Volar distal radial graft based on a pronator quadratus pedicle. The blood
supply is based off of either the anterior interosseous artery or the radial
artery depending on whether the pronator is harvested via lateral or
medial release. Its use is limited since insetting requires exposure through
the critical volar carpal ligaments.
e) Pisiform graft based on the deep volar and dorsal carpal branches of the
ulnar artery.
E. Specific hand surgery applications
1. Intercalated wedge grafting for scaphoid nonunions that have progressed to
carpal collapse or “humpback” deformity. A wedge-shaped or trapezoidal-
shaped graft is inserted volarly to correct malalignment.
a) Fisk used the radial styloidectomy for graft.
b) Fernandez used iliac crest bone graft fixed with internal fixation.
2. Matti-Russe procedure for scaphoid nonunion without osteoarthritis or car-
pal malalignment. Two corticocancellous grafts are placed in a saucerized bed
of viable bone within the scaphoid.
a) Iliac crest harvesting is preferred by Russe. Cylindrical bone graft is har-
vested using bone trephine biopsy forceps. Simple harvest technique
decreases morbidity. Graft placement and fixation can be done with
arthroscopic/fluoroscopic assistance as described by Slade.
b) Radial metaphyseal donor site can yield corticocancellous or cancellous
grafts.

c) Radial styloidectomy provides 1 to 1.5 cc of cancellous bone.

d) Recent reports suggest that some scaphoid nonunions, without exten-
sive sclerosis or cavitation, can be treated with percutaneous compression
screw fixation alone.
F. Technique for harvesting commonly used autogenous bone grafts
1. Iliac crest
Bone graft (either corticocancellous or cancellous) is harvested from the iliac
crest through an oblique incision over the anterior aspect of the crest that
begins posterior to the anterior superior iliac spine. The intermuscular plane
between the gluteus medius and the external oblique muscle of the abdomen
is developed, and the Sharpeys fibers attaching the gluteus muscle to the outer
table of the pelvis is detached using an osteotome or a Cobb elevator. The ilia-
cus muscle is elevated easily off the inner table, as it does not attach to the inner
table via Sharpeys fibers. Homan retractors are used to provide retraction and
exposure, and iliac crest bone is harvested using both straight and curved 1/2
in osteotomes. Following harvest, local hemostasis is provided with Gelfoam
(Pharmacia and UpJohn, Kalamazoo, MI) and a layered closure is done.
2. Distal radius
For harvest of the distal radius bone graft, one of the three approaches is uti-
lized. The most frequently used is through a dorsal incision over Lister tuber-
cle, and between the second and third dorsal compartments. The tubercle is
excised using an osteotome, and morsellized graft is removed from the radius
metaphysis using a large curette. Another approach to the radial metaphysis
is through the base of a radial styloidectomy. Again, a large curette is used so
that useable pieces of metaphyseal bone can be obtained. A final approach
has been taught by Kleinman, in which a radial approach to the metaphysis
of the distal radius is made at the base of the styloid and the bone is exposed
after incising the tendinous insertion of brachioradialis. An advantage of this
approach is that the BR insertion can be closed following harvest in order
to control hemostasis. A potential difficulty with this approach is in neuritis
or injury of the terminal branches of the radial sensory nerve or the lateral
antebrachial cutaneous nerve.
III. Allograft
A. Morselized and cancellous allografts

1. Osteoconductive and provide limited biomechanical support.
2. Indications similar to those for autologous cancellous bone.
3. Osteoclast-mediated resorption with host bone synthesized along the allograft
scaffold. Incomplete resorption is expected as some allograft remains trapped
within the new host bone.
B. Cortical allografts
1. Indications similar to those for autologous cortical bone.
2. Lack of vascularization results in a weaker graft compared to cortical
autografts of the same size and anatomic location.
3. Incorporation occurs via appositional bone formation.
C. (Allogeneic) DBM
1. Formed by acid extraction of bone, leaving behind a composite of collagen,
noncollagenous proteins, and BMPs.

a) Available as freeze-dried powder, crushed granules or chips, gel, or paste.

b) Each batch of DBM is obtained from a single human donor.
2. Acts as an osteoconductive and possibly osteoinductive, bone graft.
a) Provides a scaffold for osteoprogenitor cells to invade and may stimulate
mesenchymal stem cells to differentiate into osteoblasts.
b) Osteoinductive capability based on the presence of BMPs.
c) Provides no biomechanical support although it is suitable for filling con-
tained defects and cavities.
3. Most successful grafts may be a composite of DBM and autologous bone
marrow stabilized with internal or external fixation.
4. Different batches of DBM may have different potencies due to the wide
variety of donors used to supply grafts.
IV. Bone Graft Substitutes
A. General indications
1. Indicated for filling bone defects that are not essential to stability.
a) Poor biomechanical properties.
b) Must be used in conjunction with internal or external fixation for
stability.
c) Primary clinical application includes filling contained bone defects or
restoring areas of bone loss in joint depression fractures or periarticular
regions.
2. Contraindicated in children with open growth plates, in fractures with asso-
ciated vascular trauma and in the presence of osteomyelitis.
B. Collagen-based matrices
1. Xenografts formed of type I bovine fibrillar collagen combined with
hydroxyapatite and tricalcium phosphate (TCP).
a) TCP is quickly resorbed, librating calcium and phosphate ions.
b) Hydroxyapatite acts as a scaffold, promoting bone ingrowth.
2. Can be used as a surface onlay graft for cortical deficiency or in the event of
significant periosteal loss.
3. Poor mechanical properties preclude use in metaphyseal regions.
C. Coralline hydroxyapatite
1. The skeleton of Goniopora coral is converted from calcium carbonate to
hydroxyapatite in an industrial process.
2. Osteogenic cells, along with vascular and fibrous tissues, propagate along the
coral’s porous ultrastructure, ultimately creating lamellar bone in a process
similar to that of autogenous bone graft incorporation.
a) Bone ingrowth occurs in 25% to 47% of the coralline graft.
b) Coralline hydroxyapatite is poorly resorbed.
3. The strength of the graft is proportional to the amount of osseous ingrowth.
At implantation, coralline graft is slightly stronger than cancellous bone.
4. Recommended use within one month of original fracture, which optimizes
the potential for successful bone ingrowth.
D. Calcium phosphate
1. Injectable paste of phosphate and inorganic calcium. It forms dahllite, which
is a carbonated apatite similar to the mineral phase of bone.
2. Hardens in-situ and cures by crystallization.

3. Highest mechanical compressive strength of any osteoconductive bone

graft substitute with a compressive strength four to ten times higher than
cancellous bone.
4. Provides immediate and continuous strength when utilized with adjacent
hardware.
a) Some preparations can be augmented with hardware before or after
implantation.
b) Gradually remodeled in a process similar to normal bone remodeling,
which is associated with cutting cones and osteoclastic activity.
5. Studies have demonstrated that the use of calcium phosphate provides better
stability at the fracture site and may allow accelerated rehabilitation, range
of motion, and weight bearing. Useful in elderly patients with osteoporo-
sis and in patients with questionable compliance regarding weight-bearing
restrictions.
E. TCP
1. Composed of 39% calcium and 20% phosphorous by weight.
a) Scaffolding with 90% interconnectivity
b) Pore size ranging from less than 1 to 1,000 mm. 75% of pores range from
100 to 1,000 mm, optimizing bone ingrowth.
2. Biomechanical properties similar to cancellous bone.
3. Undergoes resorption through osteoclast-mediated dissolution and fragmen-
tation over 6 to 24 months.
a) TCP is partially converted to hydroxyapatite, which is degraded slowly.
b) Estimated resorption rate of 10% per month.
c) Resorption rate is 10 to 20 times faster than hydroxyapatite.
d) Degradation process of TCP is unpredictable
4. Ultimate resultant bone volume produced is always less than the volume of
TCP resorbed.
F. Calcium sulfate
1. Available in a powder or pellet form. Mixed with solution for form moldable
shapes or create an injectable paste.
2. Compressive strength similar to cancellous bone.
3. Most rapidly resorbed of all the osteoconductive graft substitutes.
a) Resorbs within 4 to 12 weeks.
b) Resorption is theorized to increase local tissue acidity, resulting in the
demineralization of adjacent bone and the release of matrix-bound BMPs
providing a secondary osteogenic potential.
4. Recommended as an autograft extender or for combination with antibiotics
if the concern for infection is present.
V. Combined (Composite)
A. Composite grafts
1. The combination of materials that includes osteogenic or osteoinductive
materials along with an osteoconductive scaffold.
2. Manufactured. Type I bovine collagen matrices combined with hydroxyapa-
tite and TCP.
3. Surgeon prepared.

a) Bone graft extenders. The combination of any type of allograft or synthetic

substitute with autogenous bone graft to increase volume.
b) The addition of bone marrow aspirate to DBM or allograft. The use of a
bone marrow aspirate with DBM slurry, in combination with internal or
external fixation, may be one of the most successful types of composite
graft. This limits graft site morbidity but optimizes osteoconductive and
osteoinductive properties.
VI. Recombinant Technology
A. BMPs. Members of the TGF-b superfamily that exhibit autocrine and paracrine
effects in vivo.
1. Only exert their effect on cells that exhibit type I and II BMP receptors
(serine/threonine kinase receptor). Population of target cells expressing appro-
priate receptors must be present in order for BMPs to exert their effects.
2. Influence cell differentiation at a dosage range of 1 to 100 ng/mL. Current
BMP formulations deliver 50 times this amount to target graft sites.
3. Recombinant human BMPs are approved by the FDA for clinical use in a
limited number of settings.
a) BMP-2 on a collagen carrier.
b) BMP-7 osteogenic protein 1.
Suggested Readings
Bishop AT. Vascularized bone grafting. In: Green DP, Hotchkiss RN, Pederson WC, Wolfe SW,
eds. Green’s Operative Hand Surgery. 5th Ed. Philadelphia, PA: Elsevier; 2005:1777–1811.
Bruno RJ, et al. Bone graft harvesting from the distal radius, olecranon, and iliac crest: A quantita-
tive analysis. J Hand Surg. 2001;26:135–141.
Finkemeier CG. Bone-grafting and bone-graft substitutes. J Bone Joint Surg Am. 2002;84:
454–464.
Gitelis S, Brebach GT. The treatment of chronic osteomyelitis with a biodegradeable antibiotic-
impregnated implant. J Orthop Surg. 2002;10:53–60.
Hak DJ. The use of osteoconductive bone graft substitutes in orthopaedic trauma. J Am Acad
Orthop Surg. 2007;15:525–536.
Khan SN, et al. The biology of bone grafting. J Am Acad Orthop Surg. 2005;13:77–86.
Ladd AL, Pliam NB. Use of bone-graft substitutes in distal radius fractures. J Am Acad Orthop
Surg. 1999;7:279–290.
Muschler GF, Nakamoto C, Grauer JN. Bone healing and grafting. In: Vaccaro AR, ed. Ortho-
paedic Knowledge Update 8. Rosemont, IL: American Academy of Orthopaedic Surgeons;
2005:29–37.
Younger EM, Chapman MW. Morbidity at bone graft donor sites. J Orthop Trauma. 1989;3:
192–195.

Examination of the Severely
Injured Hand
42
David J. Bozentka
Hand injuries account for 5% to 10% of all emergency room visits in the United States.
Hand and upper extremity trauma involve a wide range of injuries. The severely trau-
matized hand is a life-changing event that can lead to a completely dysfunctional limb.
A systematic evaluation of the extremity allows a thorough assessment of the extent of
the trauma and prevents neglecting less obvious injuries. After staging the injury and
reviewing patient and injury-related factors, an individualized treatment plan is deter-
mined to permit the optimal functional result. This section will review the evaluation
and initial management considerations for mutilating hand injuries. It will discuss the
development of a logical comprehensive treatment plan.
I. Definitions
A. Structural systems
The structural systems of the hand include bone, joint, nerve, extrinsic flexor
and extensor tendon, intrinsic muscles, arterial system, venous outflow, skin,
and nail bed.
B. Isolated injury
An isolated injury involves a single structural system at one location. A flexor
tendon laceration and a closed fracture are examples. A noncomplicated skin
wound is not considered a relevant wound; therefore, a type I open fracture is
considered an isolated injury.
C. Combined injuries
1. Combined injuries involve two or more relevant structural systems at a par-
ticular region. For example, a flexor tendon laceration with a digital nerve
injury or an open fracture with extensor tendon damage would be considered
combined injuries. In addition, by definition mutilating hand wounds are
combined injuries.
2. Multiple interactive functional restraints to healing lead to unique dif-
ficulties in postoperative management and poorer prognosis in combined
injuries compared to isolated injuries. Combined injuries require twice as
many procedures and have a higher complication rate. Time off from work is
4.7 times longer and permanent disability is more significant when compared
to isolated injuries.
II. Initial Evaluation
Regardless of the severity of the injury, the first priority is patient survival followed
by limb survival, limb function, and integration back to vocational and avocational
activities. The energy involved in these severe hand injuries often lead to other visceral
injuries.
599

A. Patients with unstable conditions

1. A primary survey is performed to identify and treat those injuries that can
lead to early death. The mnemonic ABCDE is used for a systematic approach
to the trauma patient. In this survey, the airway, cervical spine, breathing, cir-
culation, neurological disability, and circumferential exposure of the patient
are addressed.
2. The subsequent secondary survey involves a head-to-toe evaluation to inven-
tory all injuries sustained. Life-threatening injuries are treated prior to limb-
threatening injuries.
3. Hypotension related to blood loss due to open injuries including arterial
injury is treated with appropriate fluid resuscitation. Adequate intravenous
access is required to maintain hemodynamic stability.
4. Active bleeding due to major arterial injury is initially controlled by direct
pressure just proximal to the area of injury. In addition to limiting blood loss,
this localized area of compression allows collateral blood flow to maintain
limb viability. Attempting to blindly clamp bleeding vessels in the emergency
room often leads to further nerve or tendon injury and is contraindicated.
Tourniquets are used if there are no other means of controlling blood loss.
Ischemia related to tourniquets is a common cause for amputation of the
injured arm. A blood pressure cuff or surgical tourniquet elevated to 250 mm
Hg is used temporarily. Makeshift tourniquets using thin straps are discour-
aged due to the associated high edge pressures that can lead to further soft
tissue injury. Major arterial injuries require urgent surgical treatment.
5. A clean dressing and splint are applied to the extremity. The splint will pro-
vide pain relief and limit blood loss by temporarily stabilizing the bone and
soft tissues.
6. Once the patient is stabilized, a more thorough history and examination are
completed.
7. Placement of a nasogastric tube into the stomach and a catheter into the
urinary bladder are carried out, and supplemetal oxygen is provided. Cardiac
monitors are placed, and a peripheral oxygen saturation probe may be uti-
lized. Radiographs of the cervical spine, chest, and pelvis are performed.
B. Patients with stable conditions
After ruling out more severe injuries or following stabilization of the unstable
patient a more extensive history and physical examination are performed.
1. History
a) Age
b) Hand dominance
c) Occupation
d) Mechanism of injury: Significant crush, blast, and avulsion injuries tend
to lead to greater damage related to shearing, stretching, and contusion
of the tissues. The zone of injury must be considered in addition to the
extent of the external skin wound. A crush lesion dominates the mecha-
nism of injury for the severely traumatized hand with a more extensive
injury in general than sharp or guillotine type injuries. The mechanism of
the traumatic event will determine the “zone of injury,” wound vascularity,
healing potential, and zone of scarring and in turn determine prognosis.
e) Location or environment in which the injury occurs is documented. Agri-
cultural injuries will have different bacterial contamination than a household
injury altering the recommendation for antibiotic and tetanus prophylaxis.

Chapter 42 • Examination of the Severely Injured Hand 601
f ) Symptoms in the other extremities and proximal to the hand injury are
queried to aid in the diagnosis of occult injuries.
g) Prior injury and preinjury functional status of the extremity are noted in
addition to avocational activities.
h) Time of injury including duration of warm and cold ischemia time is
determined.
i) Management of the injury in the field and facilities prior to transfer is
established.
j) Smoking history: Smoking is associated with a greater risk of nonunion
and vascular disease increasing the risk of complications.
k) Tetanus status is documented and updated.
l) Last oral intake is determined prior to surgical treatment.
m) Past medical history should investigate for major illness including periph-
eral vascular disease, diabetes, or other immune-compromising processes.
Presence or absence of sickle cell disease is assessed in African-American
patients.
n) Review of systems: Factors such as loss of consciousness, chest pain, short-
ness of breath, etc., are reviewed.
The hand surgeon’s initial evaluation of the severely injured hand may be
limited due to pain, deformity, and patient anxiety. The priority is to clas-
sify the extent of the known injury and identify occult injuries. A systematic
evaluation of the entire extremity is performed. The vigilant examiner must
not let the severe traumatic injury divert their attention away from other less
obvious injuries. Specific attention must be given to other potential local,
regional, or systemic injuries.
a) Inspection
1) Much of the examination does not require touching the patient. Often
merely observing the hand one can determine extent of the injury.
2) In the normal resting position of the hand, the fingers lie in a position
of increasing flexion from the index to small fingers. Loss of the nor-
mal resting flexion cascade of the digits may be related to flexor tendon
injury or metacarpal and phalangeal fractures.
3) With flexion of the fingers, assess for rotational deformity. Evaluate for
overlap of the digits. The planes of the nail plates when viewed distally
should be congruent.
4) Color and turgor of the digits provide information regarding the
vascularity.
b) Vascular status—The ischemic hand or digit requires emergent care.
1) Capillary refill should be less than 3 seconds after compressing the nail
plate.
2) Pulses are palpated including brachial, radial, and ulnar arteries
3) If possible an Allen test at the forearm is performed to evaluate radial
and ulnar artery patency. A digital Allen test may be performed at the
base of each finger to determine patency of the digital vessels. Recall
that the “dominant” arterial supply to each digit tends to be from the
“interior” artery (ulnar digital artery for the index and middle fingers,
and radial digital artery for the ring and small fingers).
4) A portable Doppler may be required to assess the vascular system.

c) Skin
1) Assess the extent and location of lacerations and skin loss. Document
areas of skin contusion, abrasion, and questionable viability.
2) Lacerations should be measured and inspected for full thickness injury,
which increases the likelihood of tendon injury.
3) Location and extent of edema of the extremity are noted. Swelling may
be related to fracture or soft tissue injury.
d) Neurologic—Nerve function should be documented prior to the infiltra-
tion of local anesthetic.
1) Sensation is examined by light touch and two-point discrimination.
Intact light touch does not preclude a subtle nerve injury. Normal
static two-point discrimination is 5 mm or less.
2) Motor
a. Manual muscle testing is performed as pain and deformity allow.
Muscle strength is graded 0 to 5.
b. The integrity of each flexor and extensor tendon in the region of
trauma is assessed. A partial tendon injury is suspected when pain is
associated with resistance testing of a tendon that is in-continuity.
e) Skeletal and joint
1) Integrity: Each bone is palpated documenting pain, abnormal motion,
and crepitation.
2) Gross alignment, angular and rotational deformities are documented.
Accurate range of motion of the extremity is often difficult to deter-
mine due to limitations related to pain.
C. X-rays
After the patient is stabilized, x-rays are obtained with orthogonal biplanar views
of the injured region. X-rays of the injured digit should be obtained without
overlap of the other digits to adequately evaluate fracture and joint displacement.
Radiographs of any amputated part are also obtained to assess bony anatony.
III. Initial Treatment
A. Reduction of dislocated joints and realignment of fractures can improve perfu-

sion of the injured part.
B. Never complete an incomplete amputation or discard an amputated part until it
is determined that replantation is precluded. Even the smallest soft tissue bridge
may have an intact vein, which could determine the outcome of the replanta-
tion. Even if a part is considered not replantable, it can be used as a spare part
for reconstruction of other injured areas of the hand.
C. A sterile dressing and temporary splint are applied to the extremity for the
stabilization of fractures, soft tissues and comfort.
D. Broad-spectrum antibiotics to cover suspected antimicrobials are started as soon
as possible following the injury. The environment in which the injury occurs
is determined. Industrial and farm injuries will lead to greater contamination.
Staphylococcus aureus is the most common infecting organism of open hand frac-
tures. Gram-negative infections are less common but occur in agricultural envi-
ronment. A first-generation cephalosporin is used following home or industrial
trauma. An aminoglycoside is added for agricultural, lawn, and garden injuries.
E. Ensure that tetanus prophylaxis is updated.

IV. Development of a Treatment Plan
Following the history, physical and x-ray evaluation, the hand surgeon stages the injury
and determines prognosis. A logical treatment plan is developed, which is individual-
ized dependent on patient and injury-related factors. The required surgical instruments
and implants are determined and the operating room is prepared.
A. Grading of each injured system provides an assessment of prognosis
1. Open fractures are graded according to Gustilo. The grade of injury is depen-
dent on size of the wound, periosteal stripping, and vascular injury (Fractures-
Chapters 13-14).
2. Flexor and extensor tendon lacerations are graded according to the zone
of injury. Flexor tendon injuries in Zone II have the poorest prognosis
(Tendons-Chapter 10).
B. Patient-related factors will affect treatment plan
1. Determine if the patient will be able to medically tolerate the length of sur-
gery and multiple surgeries typically required for the reconstruction of a
combined injury.
2. The dominant hand injury is often treated more aggressively to maintain
function than the nondominant extremity.
3. Socioeconomic factors play a role in allowing a patient to undergo lengthy
rehabilitation often lasting over 1 year.
4. Assess special vocational and avocational needs of the patient.
5. The child’s role in society is not yet determined. Salvaging anatomy and
length is often indicated.
C. Injured part–related factors
1. Determine if the basic functions of gross grasp, release, and pinch be
regained.
2. System approach
a) There is a relationship between nerve and arterial function. Inability to
establish nerve or arterial function results in a digit with poor sensation
and cold intolerance.
b) Flexor tendons injured in Zone II have the poorest prognosis.
3. Anatomic approach
a) The impairment is increased with the involvement of greater number of
digits and more proximal injury. Length preserving salvage procedures are
considered to improve prosthetic fitting for multiple digit and proximal
injuries.
b) Emphasis should be made to preserve thumb function and length.
c) An index finger that has limited sensibility or stability will be bypassed by
the patient. Amputation of the index finger or ray does not significantly
alter power grip and opposition function is transferred to the middle
finger.
d) The ulnar digits require adequate range of motion for power grip. It is
important to maintain MP and PIP range of motion of the ring and small
fingers.
e) Long and ring finger amputations distal to the FDS insertion have little
functional deficit. Loss of these digits proximal to the middle of the proxi-
mal phalanx may lead to small objects falling out of the hand. In this
setting, consider ray amputation and adjacent ray transfer.

4. Determine if a useless part can be used for other areas for reconstruction – spare
parts.
D. The determination to replant or revascularize the injured part must be made
early and is dependent on several factors (Replantation—Chapter 20).
1. Level of injury: Zone II injuries and multiple levels of injury are unfavorable
for replantation. Zone I, multiple digits, thumb, wrist or proximal injuries
are considered for replanation.
2. Gross contamination of the wound is less likely amenable for replantation
3. Mechanism of injury will determine the zone of tissue damage. Avulsion
injuries with a wide zone of injury have a poorer prognosis.
4. Ischemia time limits for digital amputation in general are 6 hours of warm
and 12 hours of cold ischemia time.
5. Associated injuries and other medical conditions may preclude the length
of time required for these procedures. Arteriosclerotic vessels are limiting
factors.
6. Physiologic age of the patient (as a measure of the patients’ general state of
health) and functional needs of the patient are considered.
E. Factors to be considered when contemplating between replantation and ampu-
tation: On average, patients undergoing replantation will be out of work for
7 months; 50% will regain protective sensation; and 50% of range of motion
will be obtained. Approximately 60% will need greater than two operations and
the medical costs will be 5 to 15 times greater than amputation.
V. Preoperative Surgical Considerations
A. Skeletal system
1. Bone fixation providing a rigid construct allowing postoperative mobiliza-
tion should be considered. Options include K-wires, plate and screws, and
interosseous wiring. External fixation is considered for severe comminution,
bone loss, and extensive soft tissue loss. Fluoroscopy is used intraoperatively
at the time of fixation.
2. Bone grafting: Cortico-cancellous graft is used for segmental defects. Can-
cellous graft is used for metaphyseal defects following reduction. Autograft,
allograft, and bone substitutes are options to be considered.
3. Arthroplasty or arthrodesis is occasionally required for the severely trauma-
tized joint.
B. Vascular: Temporary vascular conduits such as carotid catheters may be placed to
limit ischemia and allow bone fixation prior to revascularization. Direct arterial
repair is often difficult in avulsion and crush injuries and vein grafts are used
liberally. Operating microscope will be needed for the vascular and nerve repair.
C. Nerve: Nerve grafts are considered for segmental nerve defects to prevent a direct
repair under tension. Sural nerve graft is commonly harvested although alterna-
tives include the terminal branch of the posterior interosseous nerve or ante-
brachial cutaneous nerves branches. Smaller defect less than 3 cm is considered
for synthetic nerve conduits. Primary nerve grafting of acute defects is rarely
performed.
D. Tendon: If primary tendon repair is not feasible, graft for flexor and extensor
tendon reconstruction may be required. Palmaris longus and Plantaris are most

commonly used for tendon reconstruction. Silastic rods should be available for
possible staged tendon reconstruction.
E. Skin: An aggressive debridement of all necrotic tissue is performed. Follow-
ing debridement, pulse lavage irrigation is used for severely contaminated
wounds. The reconstructive ladder for soft tissue coverage is considered for
defects. Options include skin grafts, local, regional, and distant flaps. Biologic
skin substitutes may be used for temporary coverage (Skin and soft tissue—
Chapter 20).
VI. Specific Injury Pattern
A. Exploded hand syndrome has been described as an entity in which a perpendicu-

lar crushing force to the hand leads to specific clinical findings:
1. Skin failure at the webspace or glaborous border.
2. Atypical usually longitudinal fracture patterns of the tubular bones.
3. Axial carpal dislocations.
4. Extensive compromise of the interosseous musculature with extrusion
through the skin injury at the webspaces.
5. Evolving compartment syndrome.
6. Treatment requires each component of injury to be addressed including skin
and soft tissue, bone, and neurovascular injury.
VII. Complications
A. Compartment syndrome
Compartment syndromes may occur about the hand, forearm, and arm. The
diagnosis is made clinically. Pain may be out of proportion to the extent of the
injury. The compartments are swollen, tense, and tender. A hand or forearm
compartment syndrome is suspected in a patient with pain on passive flexion and
extension of the fingers. Late findings include paresthesia, pallor, and paralysis.
An abnormality in the pulse pressure rarely occurs solely due to a compartment
syndrome. Compartment pressure measurements provide additional diagnostic
information. (See Chapter 28—Compartment syndrome section.) Acute carpal
tunnel syndrome is a form of compartment syndrome and should be treated
with urgent decompression of the median nerve.
B. Infection rate has been reported to be as high as 48% following mutilating hand
injuries. It is difficult to predict an infection or the infecting organisms with
cultures at the time of presentation.
C. Stiffness is to be expected with these severe combined injuries. Extensive occupa-
tional therapy is required with the use of dynamic and static progressive splints.
Often staged joint contracture release and tenolysis are required to improve
functional range of motion.
D. Nonunion: The extensive devascularization with periosteal stripping and muscle
necrosis associated with these injuries leads to a greater risk of nonunion.
E. Rhabdomyolysis is associated with muscle necrosis from prolonged ischemia
with release of by-products following revascularization. These by-products
include potassium, lactic acid, myoglobin, and creatinine phosphokinase. Asso-
ciated complications include cardiac arrhythmias and nephropathy. To limit this
effect, discarding 250 to 500 mL of venous blood following arterial repair is

considered in major limb revascularization. Treatment includes hydration,

diuresis, intravenous bicarbonate to alkalinize the urine, antibiotics (PCN is first
line medication) and dialysis.
F. There are a wide range of psychological reactions that can occur following these
devastating injuries. Psychological support should be available soon after the
injury to promote strategies for positive adjustment.
Suggested Readings
Buchler U, Hastings HI. Combined injuries. In: Operative Hand Surgery. Green, DP, ed. Vol. 2.
New York, NY: Churchill Livingstone; 1993:1563–1585.
Graham T. The exploded hand syndrome: Logical evaluation and comprehensive treatment of the
severely crushed hand. J Hand Surg. 2006;31A:1012–1023.
Hoffman R, Adams B. Antimicrobial management of mutilating hand injuries. Hand Clin.
2003;19(1):33–39.
Neumeister M, Brown R. Mutilating hand injuries: principles and management. Hand Clin.
2003;19(1):1–15.
Seiler JI. Essentials of Hand Surgery. Philadelphia, PA: Lippincott Williams & Wilkins; 2002.
Tomaino M. Treatment of composite tissue loss following hand and forearm trauma. Hand Clin.
1999;15:319–333.
Zachary S, Peimer C. Salvaging the “unsalvageable” digit. Hand Clin. 1997;13(2):239–249.
A systematic approach to the severely injured upper extremity is reviewed. Preoperative and
surgical considerations are discussed.

IV Appendix

Definitions of Hand Surgery
Terminology
43
Kimberly L.Z. Accardi and Warren C. Hammert
I. Fracture Eponyms/Classification
Bado classification Classification of Monteggia fractures (proximal ulna

fracture) based upon direction of the radial head
dislocation.
Barton fracture A partial-articular distal radius fracture in which the dor-
sal or volar rim of the distal radius is displaced with the
hand and wrist.
Bennett fracture A non-comminuted, intra-articular fracture of the base of
the thumb metacarpal. The metacarpal is displaced radi-
ally, proximally, and dorsally by the APL. The volar frag-
ment is held in place by the anterior oblique ligament.
Boxer fracture Fracture of the fifth metacarpal neck with apex dorsal
angulation.
Colles fracture Metaphyseal fracture of the distal radius in which the
distal fragment is dorsally displaced, dorsally angulated,
radially shifted, and shortened.
Gamekeeper thumb Chronic instability of the thumb MP joint secondary to
rupture of the ulnar collateral ligament (UCL). Often
incorrectly used to describe and acute rupture of the
thumb MCP joint UCL.
Galeazzi fracture Fracture of the distal shaft of the radius with disruption
of the distal radioulnar joint (DRUJ).
Jersey finger Traumatic avulsion of the terminal FDP tendon, result-
ing in inability to actively flex the DIP joint.
Monteggia fracture Fracture of the proximal ulna (not olecranon) in associa-
tion with a radial head dislocation.
Rolando fracture A comminuted, intra-articular fracture of the base of the
thumb metacarpal.
Salter-Harris classification Classification system used to describe physeal fractures in
the skeletally immature population, delineating the frac-
ture’s involvement of the metaphysis, epiphysis, and physis.
Seymour fracture A physeal fracture of the distal phalanx. There is an asso-
ciated nail bed injury and the nail matrix may become
interposed within the physis, preventing reduction of the
fracture segments. The nail plate is displaced dorsal to
the eponychial fold that suggests the presence of this eas-
ily missed open fracture.
Smith fracture An extra-articular fracture of the distal radius with volar
angulation or volar displacement of the hand and wrist.
A reverse Colles fracture.
609

610 Section IV • Appendix
Stener lesion Associated with an UCL injury of the thumb MCP joint.
The UCL is displaced superficial to the adductor aponeu-
rosis, preventing healing. It is an indication for operative
treatment.
II. AVN Eponyms
Kienbock’s Avascular necrosis of the lunate

Panner’s Avascular necrosis of the capitellum. Also known as Little
Leaguer elbow
Preiser’s Avascular necrosis of the scaphoid
III. Anatomy Terminology—Nail
Eponychium Thin membrane that extends onto the dorsum of the nail
and gives the nail its “shine.”
Germinal matrix The proximal portion of the nail matrix. This is the area
where nail growth is initiated.
Lunula The white crescent visible through the nail plate. Its distal
extent marks the beginning of the sterile matrix.
Paronychium Skin lateral to the nail plate.
Perionychium Nail bed complex.
Nail fold The depression into which the nail fits proximally. The
ventral floor is composed of the germinal matrix.
Nail plate The hard portion of the nail complex (the nail itself ).
Sterile matrix The distal portion of the nail matrix. This area is respon-
sible for nail adherence.
IV. Anatomy Terminology—Finger
Central slip The portion of the extensor tendon that inserts on the
base of the middle phalanx and is responsible for the
extrinsic component of PIP joint extension.
Check ligaments The proximal extensions of the PIP joint volar plate.
When a flexion contracture develops at the PIP joint,
these may be termed as “check-rein” ligaments as they
tighten and contribute to the contracture.
DIP Distal interphalangeal joint.
Extensor apparatus The elaborate confluence of the extrinsic extensor tendon
and intrinsic extensor tendons that control MCP, PIP,
and DIP joint motion.
Lateral bands The distal tendonous portion of the interossei, which
combine with the lateral slips of the extrinsic extensor
tendon to form the conjoined lateral bands. These con-
tribute to DIP joint extension
MCP/MP Metacarpal phalangeal joint
Oblique retinacular ligament Structure which passes volar to the PIP axis of rotation and
dorsal to the DIP axis of rotation serving to synchronize

Chapter 43 • Definitions of Hand Surgery Terminology 611
extension of the two joints. Extension of the PIP tightens

this ligament, which augments DIP extension.
Phalanges (P1, P2, and P3) P1 refers to the proximal phalanx; P2 refers to the middle
phalanx; and P3 the distal phalanx.
PIP Proximal interphalangeal joint.
Sagittal bands The proximal part of the extensor apparatus which cen-
tralizes the extensor tendon over the MCP. It attaches to
the extensor tendon and wraps around the base of the
proximal phalanx, inserting on the volar plate. It contrib-
utes to proximal phalanx extension at the MCP joint by
“lifting” the proximal phalanx when the extrinsic exten-
sor tendon contracts.
Transverse retinacular lig Structure at the level of the PIP joint (similar to the sagit-
tal band at the MCP joint), which attaches to the exten-
sor tendon and the volar plate and functions to prevent
dorsal shift of the lateral bands when the digit is extended.
Attenuation contributes to Swan neck deformity.
Triangular ligament A structure that joins the lateral bands at the level of the
middle phalanx. It prevents volar subluxation of the lat-
eral bands during PIP joint flexion. Attenuation contrib-
utes to Boutonnière deformity.
Volar beak ligament The anterior oblique ligament of the thumb carpometa-
carpal (CMC) joint. It originates on the trapezium and
inserts on the volar beak of the base of the thumb meta-
carpal. This ligament prevents dorsal subluxation of the
thumb CMC joint. Often felt to be the primary stabilizer
of the thumb CMC joint.
Volar plate Thickening of the volar joint capsule with proximal exten-
sion at the level of the MCP, PIP, and DIP joints; it pre-
vents dorsal subluxation and hyperextension. The proximal
extensions known as the check ligaments at the PIP joint.
V. Anatomy Terminology—Hand/Wrist
Basal joint Carpometacarpal joint of the thumb. Also referred to as

the CMC joint.
Distal palmar flexion crease Volar flexion crease, which marks the cutaneous level of
the MCP joints.
Juncturae tendinum The tendinous connections between the EDC tendons
to the individual digits. When a tendon laceration occurs
proximal to the juncturae, the MCP can still be actively
extended through the adjacent tendon connection via the
juncturae albeit with pain and some weakness.
TFCC Triangular fibrocartilage complex. This is the soft tissue
stabilizing structure of the DRUJ. It is comprised of the
dorsal and volar distal radioulnar ligaments, a central disc
with attachments to the fovea and the ulnar styloid, the
meniscal homolog, ulno-carpal ligaments, and the sheath
of the ECU tendon.

VI. Deformities/Positions—Finger
Bouchard nodes Dorsal osteophytes at the proximal interphalangeal joint

(osteoarthritis)
Boutonnière deformity Position of the finger in which the DIP joint is hyperex-
tended and the PIP joint is flexed
Extension lag A condition in which a joint lacks full active extension,
but can be passively extended
Flexion contracture A condition in which the finger lacks full active and pas-
sive extension
Heberden nodes Dorsal osteophytes at the distal interphalangeal joint
(osteoarthritis)
Lumbrical plus Parodoxical extension of the finger at the PIP joint with
attempted flexion. This occurs secondary to proximal
retraction of the FDP tendon, creating increased tension
on the lumbrical muscle
Mallet finger Position of the finger in which the DIP joint is flexed and
can not be actively extended secondary to disruption of
the terminal extensor tendon
Swan neck Position of the finger in which the DIP joint is flexed and
the PIP joint is hyperextended
VII. Deformities/Positions—Hand
Claw hand A sign of intrinsic weakness of the hand manifested by

flattening of the palmar arch, MCP hyperextension, and
PIP and DIP flexion which occurs secondary to ulnar
nerve dysfunction.
Intrinsic plus Position of the hand with the MCP joints (safe position)
flexed and the PIP and DIP joints extended. This mini-
mizes stiffness as the MCP collateral ligaments are maxi-
mally stretched.
Intrinsic minus Position of the hand with the MCP joints extended and
the PIP and DIP joints flexed
VIII. Tendon Terminology
Quadregia effect Difficulty with full flexion of the digits secondary to

imbalance in the length of the individual FDP tendons
due to their common muscle belly. This can occur when
a flexor tendon is sutured too tight following primary
repair, a tendon graft or amputation revision.
Tenodesis The posture of the fingers or hand, secondary to the
normal tension on the tendons, which occurs with wrist
motion (the digits will flex with wrist extension and the
digits will extend with wrist flexion.
Synergy The reciprocal relationship between the flexor and exten-
sor tendons used in normal motions (digital flexion is

synergistic with wrist extension and digital extension is

synergistic with wrist flexion).
Stenosing tenosynovitis Also known as trigger finger; a thickening of the flexor
tendon and/or tendon sheath causing a catching of the
tendon as it passes through the A1 pulley.
Flexor tenosynovitis A bacterial infection involving the space between the
tendon and tendon sheath. Kanavel signs assist in the
diagnosis.
IX. Congenital/Pediatric Terminology
Epiphysis The region of bone between the physis and the joint
Metaphysis The region of bone between the physis and diaphysis
Physis Growth plate
Pre-axial Refers to the radial side of the hand
Post-axial Refers to the ulnar side of the hand
Polydactyly Extra digits
Syndactyly Digits joined with either soft tissue (simple) or bone
(complex)
Symbrachydactyly A congenital deformity of the hand in which the fingers
are not developed longitudinally; however, nail remnants
are present. This is an “atypical” cleft hand
X. Brachial Plexus Terminology
Erb Palsy Brachial plexus injury involving the C5 and C6 nerve

roots; characterized by waiter’s tip position of the upper
extremity (shoulder internally rotated, elbow extended,
wrist flexed).
Erb point The part of the upper plexus in which the C5 and C6
roots join
Horner syndrome Ptosis, miosis (pupil constricted), and anhydrosis. May
be associated with a lower plexus insult (C8–T1) at
the root level or apical lung tumor (Pancoast tumor).
It is a poor prognostic sign for spontaneous recovery of
function.
Klumpke palsy Brachial plexus injury involving the C8 and T1 nerve
roots
Pre-ganglionic Refers to injury to the brachial plexus that occurs proxi-
mal to the dorsal root ganglion. Afferent fibers remain
intact (as sensory axons are in continuity with the cell
body in the dorsal root ganglion) while efferent fibers
undergo wallerian degeneration.
Post-ganglionic Refers to injury to the brachial plexus that occurs distal
to the dorsal root ganglion. Afferent and efferent fibers
undergo degeneration.

XI. Bone Healing Terminology
Delayed union Failure of a fracture to heal within an expected time (often

6 months is used)
Nonunion Failure of a fracture to heal
Malunion Malalignment of healed fracture
XII. Nerve Terminology
Axontomesis Nerve injury involving disruption of axons, but not the

epinurinum
Demyelination Loss of myelin sheath cover; slows conduction of a nerve
Denervation Loss of innervation or signaling to an end target
Endoneurium Tissue that surrounds each axon
Epineurium Tissue that surrounds the nerve and provides substance
between the fascicles
Nerve graft Transplantation of a nerve from its anatomic site to another
site; involves transection of the donor nerve proximally
and distally, then transfer to the recipient site. Example:
Use of sural nerve to address a brachial plexus injury
Nerve transfer Transfer of a portion of a functioning nerve to a site that
lacks innervation, maintaining the proximal connection
of the donor nerve. Example: Oberlin transfer to obtain
elbow flexion in cases of upper brachial plexus injury,
transfering motor fascicles of the FCU to the motor
branch to the biceps
Neuroma A group of regenerating nerve fibers, which fail to reach
distal targets or end organs
Neuroma in continuity A collection of disorganized nerve fibers within an intact epi-
nurial sheath. This occurs following a nerve injury with dis-
ruption of axons in which the proximal sprouting nerve fibers
fail which fail to connect to the distal targets (nerve ends) .
Neurapraxia Nerve injury in which there is stretching, but no disrup-
tion of the continuity of the nerve
Neurotmesis Nerve injury in which there is complete transection of
the nerve, resulting in demyelination and distal wallerian
degeneration
Perineurium Tissue that surrounds each fascicle
XIII. Carpal Instability Terminology
Carpal instability Refers to instability pattern which occurs within a carpal

dissociative (CID) row (examples include SL and LT interosseous ligament
injuries)
Carpal instability Refers to instability pattern between carpal rows or
non-dissociative (CIND) between the carpus and the distal radius (examples
include midcarpal instability, volar carpal subluxation,
and capitate-lunate instability)

DISI Dorsal intercalated segment instability. Lunate extension

as visualized on lateral radiograph. This typically results
from disruption of the scapholunate interosseous
ligament.
Lunate dislocation Final stage of perilunate dislocation, which occurs as the
carpus resumes its position on the distal radius and the
lunate is pushed volarly secondary to disruption of dor-
sal radiocarpal ligament from the lunate. Radiographic
appearance of a “spilled teacup”
Perilunate dislocation Disruption of the intercarpal ligaments causing dissocia-
tion of the carpal bones from the lunate. The carpus is
typically displaced in a dorsal direction while the lunate
remains in the lunate fossa of the radius.
SLAC wrist Scapholunate advanced collapse—arthritic pattern which
develops over time following unrepaired scapholunate
interosseous ligament disruption
SNAC wrist Scaphoid non-union advanced collapse – arthritic pat-
tern which develops over time following scaphoid non-
union (similar to that seen in SLAC wrist)
VISI Volar intercalated segment instability. Lunate flexion as
visualized on lateral radiograph. This typically results
from disruption of the lunatotriquetral interosseous
ligament.
XIV. Hand/Wrist Examination
Bouvier test An examination in a patient with ulnar nerve dysfunc-

tion to determine the ability to actively extend the PIP by
blocking MP hyperextension
Boyes test An examination for chronic rupture of the central slip
Durkin test An examination for carpal tunnel syndrome; also called
compression test
Elson test An examination for acute rupture of the central slip
Finkelstein test An examination for de Quervain tenosynovitis
Grind test An examination for diagnosis of arthritis at the thumb
CMC joint
Kleinman shear test An examination for lunatotriquetral instability (LT shear
test)
Phalen test An examination for carpal tunnel syndrome
Provocative maneuver A physical examination designed to elicit symptoms of a
pathologic condition
Tinel sign Tingling sensation, which occurs while tapping on a
nerve. This is used in the diagnosis of compression
neuropathies, nerve regeneration, or the diagnosis of
neuromas
Watson test An examination for scapholunate instability (scaphoid
shift test)

XV. Infection
Felon Bacterial infection of the pulp of the distal fingertip

Horseshoe abscess Bacterial infection which tracks along the radial and ulnar
bursae of the hand, forming a horseshoe-shaped swelling
on the volar aspect of the hand providing potential spread
of infection between the small finger and the thumb.
Paronychia Bacterial infection centered in the soft tissue around the
nail plate.

Index
Page numbers in “italics” denote figures; those followed by “t” denote tables.
A index finger, 60–61

Acid burns, 508 middle and ring finger, 61
Acral metastasis, 467 small finger, 61
Actinic keratoses, 525–526, 526 Analgesics
Adult brachial plexus injuries (see also hepatotoxicity, 38
Brachial plexus) narcotics, 37
diagnosis, 348–349 Anesthesia
ancillary studies, 348–349 bier block, 34
clinical examination, 348 brachial plexus
treatment, 349 sensory and motor blockade, 29t
AGC (see Axon guidance channel) single-shot block durations, 30t
Alcoholism, 444 emergency room blocks, 33–34
Alkali burns, 507–508 fingertip, 33
Allen test, 434 lateral antebrachial cutaneous nerve
Alloderm, 421–422 (LABC), 33
Allograft median nerve
demineralized bone matrix, 595–596 anatomy, 30–31, 30t
morselized/cancellous/cortical, 595 elbow, 31
Allopurinol, 361 wrist, 31
American Medical Association Publication, radial nerve
545 anatomy, 32–33
Amputations elbow and wrist, 33
adverse outcomes ulnar nerve
cold intolerance, 63 anatomy, 31–32
lumbrical plus finger, 62–63 elbow, 32
neuroma management, 62 wrist, 32
phantom pain, 63 Aneurysm, true/false, 440
quadrigia, 62 Animal bites, 513–514
digital Anterior interosseous nerve palsy, 312–313
distal interphalangeal (DIP) joint, 60 Anterior/Henry exposure, 257
distal phalanx, 59 Antibiotics, 36–37
metacarpophalangeal (MP) joint, 60 Anticholesterol medications, 40–41
middle phalanx, 60 Antihypertensives, 40
proximal phalanx and PIP joint, 60 Antiplatelet medication, 41
functional objectives, 58 AO classification, 279
management principles Arteriovenous malformation (AVM), 437
bone, 59 Arthritis
neurovascular bundle, 58 arthroplasty
soft tissue, 59 complications of, 381
tendons, 58–59 define and indications, 378–379
thumb, 59 DIP, PIP, and MCP, 380–381
multiple digits, 61 and elbow arthritis, 388–390
post operative management, 62 thumb CMC, 381–384
proximal, 61–62 types of, 379–380
ray wrist arthroplasty, 384–388
617
Boyer_Index.indd 617 2/22/2010 8:59:01 PM

618 Index
Arthritis (Continued) principles, 46

idiopathic degenerative arthritis, 369 thumb carpometacarpal (CMC),
carpometacarpal boss, 373 46–48, 47
interphalangeal joints, 372–373 ulnar collateral ligament (UCL),
metacarpophalangeal joints, 373 thumb, 48
mucous cyst, 373–374 wrist
trapeziometacarpal, 370–372, 371t diagnostics, 49–53, 50
infectious therapeutics, 53–57
definition, 361 uses, 48
diagnosis and epidemiology, 362 Aspirin, 39
imaging, 363 Autograft, 593–595
pathogenesis and presentation, 362 Avascular necrosis (AVN), 440, 444, 614
treatment, 363 (see also Osteonecrosis)
inflammmatory Avascular phase, 445
crystalline arthropathies, 358–361 AVM (see Arteriovenous malformation)
infectious arthritis, 361–363 AVN (see Avascular necrosis)
juvenile idiopathic arthritis (see Axon guidance channel (AGC),
Juvenile idiopathic arthritis) 336
seronegative arthritis, 355–358 Axonotmesis, 295, 331, 614
seropositive, 351–355
posttraumatic arthritis
distal interphalangeal joint, 375 B
MCP joint arthritis, 375 Bacterial infections
molecular biology of, 374–375 cellulitis, 472–473
proximal interphalangeal joint collar-button abscess, 479
arthritis, 375 diabetic gangrene, 477
wrist, 376–378 felon, 478
splinting, 571 gas gangrene, 477
Arthrography, 24 necrotizing fasciitis, 476–477
Arthroplasty osteomyelitis, 473–474
complications of, 381 paronychia, 477–478
define and indications, 378–379 septic arthritis, 474–476
DIP, PIP, and MCP, 380–381 septic flexor tenosynovitis,
and elbow arthritis 478–479
anatomy and etiology, 388 subcutaneous abscess, 473
treatment, 388–390 tenosynovitis, 479
thumb CMC, 381–384 Bado classification, 609
types of Barton fracture, 609
silicone elastomer (silastic), Basal cell carcinoma, 468–469
379–380 Bennett fracture
soft tissue interpositional, 379 definition, 609
surface replacement, 380 hand, fractures and dislocations,
wrist arthroplasty, 384–388 206
Arthroscopy Bite wounds
general principles animal bites, 512–514
equipment and general guidelines, human bites, 511–512
44–46, 45 insect, spiders, 514–515
setup, 44 mosquito and ticks, 515
hand Bone graft
idiopathic MCP joint synovitis, 48 allograft

Index 619
demineralized bone matrix, 595–596 definition, 613

morselized/cancellous/cortical, 595 tendon transfers, 166–168
autograft Brachial plexus birth palsy (BPBP), 344,
autologous cancellous/cortical bone, 348 (see also Brachial plexus)
593 Brunelli procedure, 383
bone marrow aspirate, 593 Buerger disease, 441
hand surgery applications, 594–595
harvesting techniques, 595
vascularized bone grafts, 593–594 C
basic science Calcific tendinitis, 482
graft preparation and types, 592 Calcium phosphate, 596–597
impairment, 593 Calcium pyrophosphate dihydrate
limitations, 592 (CPPD), 358–361
properties, 591–592 Calcium sulfate, 597
composite, 597–598 CAMP (see Compound motor action
recombinant technology, 598 potential)
substitutes, 596–597 Cancellous allografts, 595
Bone healing, 614 Candida onychomycosis, 532
Bone tumors Capitate, AVN, 449–450
benign Capitellum/Coronal shear, 292
enchondroma, 463–464 Carpal instability
giant cell tumor, 464–465 dissociative (CID), 614
glomus, 465–466 non-dissociative (CIND), 614
malignant Carpal tunnel syndrome, 313–316
acral metastasis, 467 Carpometacarpal (CMC), thumb
chondrosarcoma, 466 anthroscopy
Ewing sarcoma, 467 complications, 47–48
osteogenic sarcoma, 466–467 procedure, 47
Bouchard nodes, 612 setup/portals, 46, 47
Boutonniere deformity, 121–123 Carpometacarpal (CMC) boss, 373
definition, 612 Carpometacarpal (CMC) joints, 209–210
Bouvier test, 615 Cellulitis, 472–473
Boxer fracture, 609 Cerebral palsy, 153–156
Boye test, 615 Chemical poisoning and exposures,
Brachial plexus 508–509
adult brachial plexus injuries Chondrosarcoma, 466
diagnosis, 348–349 Chronic boutonniere deformity, 564
treatment, 349 Chronic extensor tendon disorders
anatomy, 343–344, 347 boutonniere deformity, 121–123
congenital chronic ECU rupture, 127–129
classification, 345 chronic EDC ruptures, 131–133
clinical evaluation, 346 chronic EPL rupture, 125–127
definition, 344 chronic rupture EDQ
diagnostic studies, 346 anatomy, 129–130
differential diagnosis, 346 clinical problems and physical
epidemiology, 344–345 examination, 130
microsurgical nerve reconstruction, definition, 129
346–347 etiology, 130
natural history, 345 treatment and complications, 130–131
secondary deformities, 347–348 swan—neck deformity, 123–125

620 Index
Chronic pain syndromes (CRPS) autonomic dysfunction, 82

(see Complex regional pain bone scans, 82
syndrome (CRPS)) endurance test, 84
Claw hand, 612 isolated cold stress test, 82–83
Clinical research designs laser doppler fluximetry (LDF), 83
hierarchy pseudomotor function evaluation, 84
case control, 547 signs and symptoms, 82
cohort designs, 547 vital capillaroscopy, 83–84
cross-sectional study, 547 incidence and prevalence, 80
decision analysis, 547–548 natural history, 81–82
health services research, 548, nociceptive and neuropathic pain, 79
553t–554t pain
randomized control trial, 546–547 anatomy and physiology, 80
question framing criteria definition, 79
common pitfalls, 551–552 pathognomonic marker, 79
statistical analysis, 548, 551, 555t splinting, 562
Clubbing, 530–531, 531–532 staging and severity, 84
Cocaine, 35 synonyms, 80
Colchicine, 361 treatment, 91
Cold intolerance, 421 late management, CRPS, 91
Collagen vascular disorders, 444 management choices, 85–90, 85t–89t
Collar-button abscess, 479 psychotropic therapy and prevention
Colles fracture, 609 methods, 90–91
Compartment syndrome surgical and ablative therapies, 90
definition, 483 types, 79
diagnostic considerations Compound motor action potential
clinical evaluation, 486–487 (CAMP), 294
differential diagnosis, 487 Computed topography (CT), 24–26
history, injury, 486 Congenital brachial plexus (see Brachial
objective testing/manometry, plexus)
487–488 Congenital/pediatric, 613
etiology, 484–486 Connective tissue diseases, 528–529
injection injuries, 494 Contact dermatitis, 520, 520–521
pathophysiology, 483 Coralline hydroxyapatite, 596
pertinent anatomy Coronoid fractures
antebrachium/forearm, 484, 485 anatomy, 264–266, 265, 268–269, 272
brachium/arm, 484, 489 classification, 269–270, 271, 273
hand, 484, 485 clinical evaluation, 270
severely injured hand examination, 605 complications, 273
treatment incidence, 269
postoperative care and therapy, management
490–491 nonoperative, 272
preoperative management, 488 ORIF, 272
surgical management, 488–490, osseous and ligament injuries, 270
493–491 surgical approach, 272
Complex elbow instability (see Proximal outcome, 272–273
radius) rehabilitation, 272
Complex regional pain syndrome (CRPS) Corticosteroids, 38, 444
classification, 84 CPPD (see Calcium pyrophosphate
diagnosis/clinical presentation dihydrate)

Index 621
Crystalline arthropathies onychomycosis, 531–532

definition, 358–359 psoriasis, 521–524
diagnosis, 360 pyogenic granuloma, 529, 529
epidemiology, 359 verruca vulgaris, 524–525, 524
hand infections, 481–482 Dermatomyositis, 528
imaging, 360 Dermofasciectomy, 457
nonsurgical treatment, 360–361 Diabetic gangrene, 477
pathogenesis, 359 Dieterich disease, 450
presentation, 359–360 Differential diagnosis
surgical treatment, 361 acute loss, active digital motion, 76
Cubital tunnel syndrome clunking wrist, 76
description, 316 complex regional pain syndrome, 76
diagnosis, 317 dorsal hand mass, 76
etiology, 316 dorsal wrist pain, 73–74
postoperative care, 318 numbness and tingling, 74–76
signs and symptoms, 316–317 radial-sided wrist pain, 72–73
treatment, 317–318 ulnar-sided wrist pain, 71–72
Cyclooxygenase (COX) Digital amputations, 59–60
corticosteroids inhibition, 38 Digital artery aneurysm, 440
nonsteroidal anti-inflammatory drugs, 39 Digital stiffness
evaluation, 172–173
pathoanatomy
D DIP joint, 171
DBI (see Digital/brachial index) extensor mechanism, 171–172
de Quervain syndrome flexor tendons, 172
injection, 67, 67–68 MP joint, 170
splinting, 565 PIP joint, 170–171
tendinopathy, 135–136 skin, 172
Deep space infections treatment
dorsal subaponeurotic, 472 nonoperative, 173
hypothenar, 472 splinting method, 173–176
midpalmar, 471 Digital/brachial index (DBI), 435
parona, 472 Disease modifying antirheumatic drugs
thenar, 471–472 (DMARDs) (see Rheumatoid)
Defensive medicine, 535 Distal humerus fractures
Deformity phase, 445 anatomy, 264–266, 265
Demineralized bone matrix (DBM), bicondylar fractures fixation, 287–289
595–596 classification, 286–287
Demyelination, 614 complications, 291–292
Denervation, 614 epidemiology, 286
Dermatitis, 520, 520–521 outcomes, 291
Dermatologic conditions patient evaluation, 286
actinic keratoses, 525–526, 526 post-op management, 291
clubbing, 530–531, 531–532 special fractures, 292
connective tissue diseases, 528–529 treatment goals and methods
contact dermatitis, 520, 520–521 external fixation, 290
eczema, 519, 519–520 internal fixation/plating, 290
granuloma annulare, 527–528, 528 nonoperative, 289–290
lichen planus, 526–527, 527 total elbow arthroplasty, 290–291
neutrophilic dermatosis, 530, 530 Distal interphalangeal (DIP) joint, 375

622 Index
Distal palmar flexion crease, 611 Elbow stiffness, fractures and dislocations
Distal phalanx, 563 anatomy of, 178–179
Distal radioulnar joint (DRUJ) cause, 179
anatomy, 241 classification, 179
arthritis, 378 coronoid fractures, 264–266, 268–273
dislocation/subluxation, ECU tendon, distal humerus fractures, 264–266,
241–242 286–292
dorsal ulnar dislocation, 242 evaluation, 179–180
instability, 242–244 functional anatomy, 265
volar ulnar dislocation, 242 capsuloligamentous components, 264,
Distal radius fractures 266
anatomy, 244–245 musculotendinous components, 266
classification, 245–246, 249t nerve relationships, 266
complications, 248–249 osseous components, 264
functional classification scheme, 246–247 management
pathogenesis, 245 nonsurgical treatment, 180
physical examination, 247 surgical treatment, 181–185
radiography, 245 olecranon fractures, 264–266, 278–281
treatment, 247–248 proximal radius and ulna injuries, 285,
Distal subungual onychomycosis, 531 273, 282
Distal ulna injuries radial head fractures, 264–266,
anatomy, 249 273–278
distal radius fractures, 254 simple elbow dislocations
examination, 249–253 anatomy, 264–266, 265
imaging, 253 definition, 266
isolated ulnar fractures, 253–254 evaluation and initial treatment,
pediatric considerations, 254–255 267–268
Doppler allen test, 427 incidence, 267
Dorsal intercalated segment instability postreduction management, 268
(DISI), 615 results, 268
Dorsal subaponeurotic space infections, 472 Elson test, 615
Dorsal/thompson exposure, 256–257 Embryology
DRUJ (see Distal radioulnar joint) congenital anomalies, 5–6
Dupuytren disease (DD) early limb formation, 3–4
clinical presentation, 455–456 later events, limb development
complications, 457–458 myogenesis, 5
fascial anatomy, 452–453, 458 peripheral nerves, 5
pathology skeletogenesis, 4–5
cords, 454–455 vasculogenesis, 5
joint/soft-tissue contracture, 453–454 limb identity, 4
rehabilitation, 457 Enchondroma
treatment definition, 463
nonoperative, 456 physical examination, 463
surgical, 456–457 radiographs, 463
Durkin test, 615 treatment, 464
Endoneurium, 614
Epicondylitis
E pathologic anatomy, 141
ECU tendonitis, 565 physical examination, 141
Eczema, 519, 519–520 presentation, 140–141

Index 623
radiology, 141 Flaps, skin and soft tissue

treatment distant
conservative, 141–142 groin, 406
operative, 142–143 latissimus dorsi, 406–407
Epinephrine injection, 494 local flaps
Epineurial vs. group fascicular repair, atasoy volar V-Y advancement, 399,
331–333, 332 400–401, 406t
Epineurium, 614 axial flag, 403, 408
Epiphysis, 613 dorsal metacarpal, 401, 403
Eponychium, 610 Kutler paired lateral V-Y advancement,
Erb palsy, 613 399, 402
Essex-Lopresti lesion, 259–260 Moberg volar advancement, 399, 402
Etodolac, 39 Z-plasty, 399, 400
Ewing sarcoma, 467 location, 398, 403–399
Expert witness, physician random/axial pattern, 397–398
definition of, 537 regional
qualification, 539 dorsal cross-finger, 404–405, 410
testimony, 539–542 lateral arm, 404
types of, 538–539 neurovascular island, 406, 407
Exploded hand syndrome, 605 posterior interosseous artery, 403–404
Extensor apparatus, 610 radial forearm, 404
Extensor carpi ulnaris tendonitis, 137–139 reverse cross-finger, 405–406
Extensor tendons thenar, 404
acute injuries Flexion contracture, 612
anatomy, 115–117, 116 Flexor carpi radialis tendonitis, 139–140
rehabilitation, 120 Flexor tendon injuries, acute
zones of injury, 117–120 anatomy
splinting FDS and FDP, 96, 97
boutonniere/pseudoboutonniere zones, 95, 95
injuries, 562 examination, 97–98, 98
chronic boutonniere deformity, 564 partial tendon laceration, 105
chronic swan neck deformity, 564, 565 pediatric patient, 108
mallet finger, 562, 563 rehabilitation
proximal zones, 563, 564 principles, 105–106
sagittal band rupture, 562, 564 programs, 106–108
yoke, 564 segmental tendon defects, 104–105
Extravasation injuries, 495–496 zone I, 98–99, 99
Ezetimibe, 40 zone II, 99–101, 101–102
zone III injuries, 102
zone IV injuries, 103
F zone V injuries, 103–104
False aneurysm, 440 Flexor tendons, splinting, 562, 563
Fascial arthroplasty, 383 Flexor tenosynovitis, 613
FCR tendonitis, 565, 566 Forearm (see Fractures and dislocations)
Federal Employees Compensation Act Fractures and dislocations
(FECA), 544 elbow (see Elbow stiffness, fractures and
Federal Employer’s Liability Act, 544 dislocations)
Felon, 478, 616 eponyms/classification, 609–610
Fibroproliferative disorder, 452 forearm
Finkelstein test, 615 anatomy, 255–256

624 Index
Fractures and dislocations (Continued) skin paddle, 409

compartment release, 257–258 trauma, 409–410
open fractures, 259 tumor, 410
operative exposures types of, 408
radius, 257 vascular pedicle and recipient vessels, 409
ulna, 256 specific free flaps, 416t–418t
refracture, 260 Frostbite
treatment, 258 epidemiology, 497–498
hand evaluation methods, 498–500
distal phalanx fractures, 186–188, pathophysiology, 498
187, 192 treatment, 500–501
MCP dislocations, 212–214 FTSG (see Full-thickness skin graft)
metacarpal fractures, 201–205 Full-thickness skin graft (FTSG), 395, 397
middle phalanx shaft fractures, 189 Fungal infections, 479–480
open fractures/antibiotics, 186
proximal interphalangeal joint, 189–196
proximal phalanx, 196–201 G
thumb extra-articular metacarpal base Galeazzi fracture, 259, 609
fracture, 212 Gamekeeper thumb, 609
ulnar carpometacarpal joints, 210–212 Ganglion cysts
interosseous membrane definition, 460
anatomy, 260–261, 264 pathogenesis, 460
biomechanics, 261–262 physical examination, 460–461
pathology, 262 radiographs, 461
splinting treatment
elbow, 562, 567 dorsal carpal ganglion cysts, 462
hand, 558, 560–561, 563, 566–568 mucous cysts, 461
wrist, 558, 561–568 retinacular cysts, 462
wrist volar carpal ganglion cysts, 462
carpal kinematics, 217–218 Gas gangrene, 477
carpus anatomy, 216–217 Germinal matrix, 393, 610
distal radioulnar joint, 238, 241 Giant cell tumor
distal radius fractures, 241–246, 246t bone, 464–465
distal ulna injuries, 246–249 tendon sheath, 462–463
radiocarpal dislocations, 230–228 Glomus tumor, 465–466
scaphoid fracture and fracture non- Golfer’s elbow, medial epicondylitis,
union, 218–227, 224, 225t, 227t 566, 566
triangular fibrocartilage, 229–237, Granuloma annulare, 527–528, 528
232t, 230–231, 233–235, 239t Grind test, 615
ulnar carpometacarpal joints, 210–212 Gun shot wounds (GSW), 336–337
Free tissue transfer
definition, 408
flap failure, management of, 414–415 H
general principles, 408 Hand
postoperative care and monitoring, anatomy, 7–11, 611
410–414 arthroscopy
selection and timing idiopathic MCP joint synovitis, 48
general principles, 409 thumb carpometacarpal (CMC),
intercalary bone defects, 409 46–48, 47
recipient site, 408–409 ulnar collateral ligament, thumb, 48

Index 625
deformities/positions, 612 postoperative, 481

examination, 615 post-traumatic wounds, 481
Heart failure medications, 41 viral
Heberden nodes, 612 herpetic whitlow, 480–481
Hematoma and distraction arthroplasty, warts, 481
383, 458 Inflammmatory arthritis (see Arthritis)
Herpetic whitlow, 480–481 Injection
Horner syndrome, 613 injuries, 493–494
Horseshoe abscess, 616 techniques
Human bites, 511–512 carpal tunnel, 65, 66
Humeral shaft fractures, 333–334 CMC thumb injection, 67, 67
Hypothenar space infection, 472 de Quervain syndrome injection, 67,
67–68
intersection syndrome, 68, 68
I radiocarpal/scapholunate injection,
Idiopathic degenerative arthritis, 571 68, 69
(see Arthritis) setup, 65
Imaging methods, hand and wrist trigger injection, 69, 69
arthrography, 24 trigger thumb injection, 70, 70
computed topography (CT), 24–26 ulnocarpal injection, 70, 70
magnetic resonance imaging (MRI), 26–28 Injuries
radiograph (see Radiograph, wrist/hand) chemical burn, 507–510
Indomethacin, 361 extravasation, 495–496
Infections injection, 493–494
bacterial thermal
cellulitis, 472–473 anatomy, 502
collar-button abscess, 479 definition, 502
diabetic gangrene, 477 epidemiology, 502
felon, 478 evaluation methods, 503–504
gas gangrene, 477 pathophysiology, 502–503
necrotizing fasciitis, 476–477 rehabilitation, 506
osteomyelitis, 473–474 secondary reconstruction, 506
paronychia, 477–478 treatment, 504–505
septic arthritis, 474–476 wound care, 505–506
septic flexor tenosynovitis, 478–479 Insect bites
subcutaneous abscess, 473 mosquito and ticks, 515
tenosynovitis, 479 spider, 514–515
bites (see Bite wounds) Insulin
deep space type I diabetics, 41–42
dorsal subaponeurotic, 472 type II diabetics, 42
hypothenar, 472 Integra, 422
midpalmar, 471 Interosseous membrane (IOM), 260–262
parona, 472 Interphalangeal joints, 372–373
thenar, 471–472 Intersection syndrome, 136–137, 565
fungal IOM (see Interosseous membrane)
cutaneous, 479–480
deep/systemic, 480
subcutaneous, 480 J
general principles, 471 Jersey finger, 609
hand, 481–482 Juncturae tendinum, 611

626 Index
Juvenile idiopathic arthritis MCP joint arthritis, 375

classification Medial collateral ligament (MCL), elbow
enthesitis related, 365 joint, 264
oligoarticular, 364 Median nerve palsy, 570, 570
polyarticular, 364 Medicolegal principles, physician as
PsA, 364 defendant
systemic, 364 categories, 534–535
diagnosis, 365 defendant role, 535–536
hand and wrist deposition testimony, 541–542
findings, 366–367 expert testimony
general management, 367 case closure, 542
medical treatment, 367–368 deposition, 541–542
surgical management, 368–369 preparation, 540–541
radiography, 365–366 rules, 539–540
signs and symptoms, 366 trial, 542
expert witness role
definition, 537
K qualification, 539
Ketorolac, 39 testimony, 539–542
Kienböck’s disease types, 538–539
clinical presentation and diagnosis, 447 treating physician role, 542–543
clinical staging, 447–448 Melanoma, 469–470
definition, 610 Metacarpal cuff splint, 563–568, 568
distal radius morphology, 447 Metacarpal fractures, hand
lunate morphology, 446–447 base, 205
treatment, 448–449 diagnosis, 201–204
ulnar variance, 446 shaft, 204–205
Kleinman shear test, 615 thumb extra-articule, 212
Klumpke palsy, 613 Metacarpal head (see Dieterich
disease)
Metacarpophalangeal (MP) joint, 356,
L 369, 373
Lateral collateral ligament (LCL), elbow Metaphysis, 613
joint, 264 Microsurgical nerve reconstruction,
Lichen planus, 526–527, 527 346–347
Lumbrical plus, 612 Middle phalanx, 563
Lunate (see Kienböck disease) Midpalmar space infection, 471
Lunate dislocation, 615 Monteggia fracture, 259, 609
Lunula, 393, 610 Morselized allografts, 595
Motor restoration nerve transfers
elbow flexion, 339
M hand intrinsic function, 340
Magnetic resonance imaging (MRI), hand Oberlin transfer, 339–340
and wrist, 26–28 shoulder abduction/flexion, 340
Mallet finger, 562, 563, 612 Mucous cyst
Mangled hand (see Severely injured hand examination and complications,
examination) 373–374
Martin–Gruber interconnections, soft tissue tumors, 461
299–300 symptoms and signs, 373
Mayo classification, 279 treatment, 374

Index 627
Mycotic aneurysm, 440 peripheral nerve injuries

Myogenesis, 5 anomalous interconnections, 327–328,
331, 329
cross section, 326, 327
N lacerations, 331–334, 332
Nail neurapraxia/axonotmesis/neurotmesis,
anatomy, 393, 394, 610 330–331
fold, 186, 610 radial nerve
plate, 188, 610 posterior interosseous nerve palsy,
Narcotic analgesics 310
administration routes, 37 radial sensory nerve compression,
medication regimens, 37–38 311–312
natural and synthetic medications, radial tunnel syndrome, 309–310
37 reconstruction
Necrotizing fasciitis conduits, 336–337
diagnosis of, 476 nerve grafting, 334–336
treatment of, 476–477 splinting
Needle manometry, 487 carpal tunnel syndrome, 566, 569
Neoplasia, 482 cubital tunnel syndrome, 570
Nerve, 614 median/ulnar/radial nerve palsy, 564,
electrodiagnostic test 570, 570–571
anatomy, 295–296 submuscular ulnar nerve transposition,
antebrachial cutaneous nerves, 297 570
anti sensory, 301, 307t thoracic outlet syndrome
axillary nerve, 297 anatomy, 320–321
definitions, 294–295 definition, 320
electrophysiology, 296 examination, 321–322
EMG, 301, 310t–311t imaging, 322–323
limitations of, 301 laboratory studies, 322
Martin–Gruber interconnections, physiological studies, 323
299–300 postoperative care, 325
median nerve, 298–299 risks, benefits, and complications,
motor nerve study, 301, 306t 326
motor summary, 301, 308t scalene muscle block, 323–324
musculocutaneous nerve, 297 tissue perfusion studies, 323
normal values, 300 treatment, 324–325, 328
pathophysiology, 296 transfers
radial nerve, 297–298 functional assessment, 338, 342t
sensory and motor responses, general principles, 338
waveforms, 301, 309t motor restoration, 339–340
sensory nerve study, 301, 305t sensory restoration, 339–340
severity and chronicity, 300 ulnar nerve
suprascapular nerve, 296–297 cubital tunnel syndrome, 316–318
ulnar nerve, 299 ulnar tunnel syndrome, 318–319
graft, 334–336, 614 Neurapraxia, 295, 330–331
median nerve Neuroma, 614
anterior interosseous nerve palsy, Neurotmesis, 295, 331, 614
312–313 Neutrophilic dermatosis, 530, 534
carpal tunnel syndrome, 313–316 Nonsteroidal anti-inflammatory drugs
pronator syndrome, 313 (NSAIDs), 38–39

628 Index
O cross section, 326, 327

Oblique retinacular ligament, 610–611 and GSW, 336–337
Olecranon fractures lacerations, 331–334, 332
anatomy, 264–266, 265 neurapraxia/axonotmesis/neurotmesis
fracture classification and injury classification of, 330–331
patterns, 279 pathophysiology of, 330
initial evaluation, 278–279 tendon transfers, 148–153
mechanism and associated injuries, 278 Phalanges, 615 (see Thiemann disease)
treatment options, 279–281 Phalen test, 615
Onychomycosis, 479–480 Pharmacology
diagnosis, 532 analgesics
topical therapies, 532 hepatotoxicity, 38
types, 531–532 narcotics, 37
Open reduction and internal fixation antibiotics
(ORIF) (see Specific fracture type) cell wall synthesis inhibition, 36
Oral antihyperglycemic agents DNA metabolism interference, 37
type I diabetics, 41–42 membrane permeability, 36
type II diabetics, 42 ribosomal inhibition, 37
Osteoconduction, 591 anticholesterol medications, 40–41
Osteogenic sarcoma, 466–467 antihypertensives, 40
Osteoinduction, 591 antiplatelet medication, 41
Osteomyelitis corticosteroids, 38
diagnosis of, 473–474 heart failure medications, 41
treatment of, 474 insulin and oral antihyperglycemic
Osteonecrosis agents
etiology, 444 type I diabetics, 41–42
hand and wrist type II diabetics, 42
capitate, 449–450 local anesthetics, 35–36
lunate (Kienböck disease), 446–449 nonsteroidal anti-inflammatory drugs
metacarpal head (Dieterich disease), 450 (NSAIDs), 38–39
phalanges (Thiemann disease), 450 rheumatoid medications
scaphoid (Preiser disease), 445–446 leflunomide, 40
pathogenesis, 444–445 methotrexate and TNF-a, 39
Outerbridge-Kashiwagi arthroplasty, 389 thyroid medication, 41
Physician-patient relationship, 533
Polydactyly, 613
P Posterior interosseous nerve
Palmar fascial, 452–453, 458 palsy, 310
Panner’s disease, 610 Posterolateral rotatory instability, 266
Parona space infection, 472 Posttraumatic arthritis (see also
Paronychia, 477–478, 610, 616 Arthritis)
Percutaneous fasciotomy, 456–457 mechanisms of, 374
Perilunate dislocation, 615 shear stress theory, 374–375
Perionychium, 610 Preiser disease
Peripheral nerve injuries (see also Nerve) clinical presentation and diagnosis,
anomalous interconnections 445–446
Martin–Gruber connection, 327–328, definition, 610
329 treatment, 446
median nerve anatomy, 327, 328 Primary vasopastic diseas (see Raynaud
Riche–Cannieux connection, 327 disease)

Index 629
Probenecid, 364 R
Pronator syndrome, 313 Radial aponeurosis, 452, 453
Prosthetics, 63 Radial head excision and arthroplasty, 276
Provocative maneuver, 615 Radial head fractures
Proximal interphalangeal (PIP) joint, 356, anatomy and biomechanics, 264–266,
372–373, 375, 380–381 265, 273, 273–274
Proximal phalanx, 563 classification, 274
Proximal radial ulnar joint (PRUJ), 256, clinical evaluation, 274–275, 277–278
259, 264 complications, 277
Proximal radius incidence, 274
morphology, 273, 278 management, 275–276
and ulna injuries, complex elbow outcome, 277
instability, 282 rehabilitation, 277
anterior/transolecranon fracture surgical approach, 276–277
dislocations, 284 Radial nerve palsy, 564, 570–571
classification and injury pattern, 283 Radial sensory nerve compression,
clinical evaluation, 283 311–312
complications, 285 Radial tunnel syndrome, 309–310
functional anatomy, 264–266, 265 Radiocarpal dislocations
ligamentous injury, 283–284 anatomy, 230
mechanism of injury, 282–283 classification and treatment, 231
posterior monteggia fracture, 284–285 diagnosis, 231
Proximal subungual onychomycosis, 531 examination, 231
PRUJ (see Proximal radial ulnar joint) radiographs, 231
Psoriasis Radiograph, wrist/hand
arthritis, 522–523, 526–527 anterior-posterior (AP) and posterior-
pustular variant, 521–522, 525–526 anterior (PA) views, 11–14, 12–14
pustular variant of, 521–522, 525–526 carpal tunnel view, 22–23, 22–23
systemic treatment, 524 clenched fist AP view, 23–24, 23–24
topical treatment, 523 lateral view, 14–16, 15–17
Psoriatic arthritis (PsA), 354–356, 364 lateral view and CMC joint, 16–18, 18
Psychiatrics oblique and pronated oblique view, 19,
disorders, 556 19
factors, 416 Roberts view, 16, 17
Psychological factors scaphoid view, 20, 20
communication skills, 554–555 supinated oblique view, 20–22, 21
illness, 553–554 Ray amputations
multidisciplinary approach, 555–556 index finger, 60–61
psychiatric disorders, 556 middle and ring finger, 61
reaction to injury/disease small finger, 61
catastrophizing, 557 Raynaud disease, 442–443
depression/anxiety, 556–557 Replantation
hypochondriasis, 557 contraindications, 416
surgeon psychology, 557 digital, surgical technique for, 417–418
Pyoderma gangrenosum, 482 distal digital, 418
Pyogenic granuloma, 482, 529, 533 indications, 416
ischemia time, 415–416
major limb, surgical technique for,
Q 418–419
Quadregia effect, 612 principles, 415

630 Index
Replantation (Continued) Sensory nerve action potentials (SNAPs),

revascularization, 415 294, 349
thumb, 418 Sensory restoration nerve transfers, 341
Retinacular cysts, 462 Septa of Legueu and Juvara, 452, 454
Revascularization, 415 Septic arthritis, 474–476
Rhabdomyolysis, 605–606 Septic flexor tenosynovitis, 478–479
Rheumatoid Seronegative arthritis
arthritis, 351, 354, 356, 372, 565, 571 diagnosis, 356
extensor tendon ruptures, 165–166 epidemiology, 355
flexor tendons, 166 imaging, 356
medications nonsurgical treatment, 356
leflunomide, 40 pathogenesis, 355
methotrexate and TNF-a, 39 presentation, 355–356
principles, 164–165 rheumatoid factor, 355
splinting, 571 SLE, 357–358
Rolando fracture, 609 surgical treatment, 356–357
Seropositive arthritis
bone quality, 351
S interphalangeal joints, 354–355
Sagittal bands, 611 metacarpal phalangeal joints
Salter-Harris classification, 609 deformity, 353
Scaphoid bone long-term results, 354
anatomy, 218 loss of function, 353
classification, 219 MP joints, arthroplasty of,
evaluation, 218–219 353–354
fracture nonunion pathomechanics of, 352
axial carpal dislocations, 230 silicone implants, 354
carpal instability, 221–222 soft tissue balance, 354
diagnosis, 222–223 surgical management, 353
imaging techniques, 223–225, 224, 225t synovectomy, 353
lunotriquetral dissociation, 227–229, synovectomy plus tendon relocation,
229t 353
midcarpal instability, 229–230 ulnar shift and deviation, 352
perilunate dislocation, 229 soft tissue issues, 351
proximal pole, 220 wrist, 351–352
radiographic characterisation, 220 Severely injured hand examination
scapholunate dissociation (SLD), complications
226–227, 227t compartment syndrome, 605
symptomatic fracture, 220–221 rhabdomyolysis, 605–606
trauma, 220 definitions, 599
treatment, 219–220 initial evaluation
Scaphoid nonunion advanced collapse stable conditions, 600–602
(SNAC), 376–378, 615 unstable conditions, 600
Scapholunate advanced collapse (SLAC), X-rays, 602
360, 376–377, 615 initial treatment, 602
SCLE (see Subacute cutaneous lupus preoperative surgical considerations
erythematosus) nerves, 604
Scleroderma, 529 skeletal system, 604
Secondary vasospastic disease skin, 605
Segmental aponeurectomy, 457 tendon, 604–605

Index 631
specific injury pattern, 605 Skin grafting, 396–397

treatment plan development SLAC (see Scapholunate advanced
injury-related factors, 603–604 collapse)
patient-related factors, 603 SLE (see Systemic lupus erythematosus)
Seymour fracture, 609 Smith fracture, 609
Sickle cell disease, 444 SNAC (see Scaphoid nonunion advanced
Silicone spacers, 383 collapse)
Skeletogenesis, 4–5 SNAPs (see Sensory nerve action
Skin and soft tissue potentials)
alloderm, 421–422 Soft tissue coverage, 395–402 (see also Skin
complications, 420–421 and soft tissue)
coverage, 395 Soft tissue tumour
secondary intention, 396 benign
skin grafting, 396–397 ganglion cysts, 460–462
digital replantation, surgical technique giant cell tumor, tendon sheath,
for, 417–418 462–463
distal digital replantation, 418 malignant lesions
flaps (see also Flaps, skin and cutaneous, 468–470
soft tissue) soft tissue sarcomas, 468
distant, 406–407 Spider bites (see Insect bites)
local, 399–403, 400–408 Spinal cord injury
location, 398–399, 403t anatomy, 156–157, 161t
random/axial pattern, 397–398 epidemiology, 156
regional, 403–406, 407 historical review, 157
free tissue transfer surgical planning, 158
definition, 408 tendon transfer surgery
general principles, 408 IFSHT group level, 159–161
selection and timing, 408–415, intrinsic reconstruction, 161–162
416t–418t level, 158–159
integra, 422 Splinting
major limb replantation, surgical arthritis, 565, 569, 571
technique for, 418–419 chronic pain syndromes (CRPS), 562
nail Dupuytren release, 572
anatomy, 393, 394 elbow fractures/dislocations, 569, 569
deformity, 394–395 extensor tendons
injuries, 393 boutonniere/pseudoboutonniere
pediatric, 420 injuries, 562
postoperative care, 419 chronic boutonniere deformity, 564
preoperative assessment, 416–417 chronic swan neck deformity,
replantation 564, 565
contraindications, 416 mallet finger, 562, 563
indications, 416 proximal zones, 563, 564
ischemia time, 415–416 sagittal band rupture, 558, 564
principles, 415 yoke, 564
revascularization, 415 flexor tendon repair, 558, 563
results, 420 hand fractures/dislocations, 563–568,
thumb replantation, 418 564, 567–568
vacuum assisted closure therapy, nerve, 569–571
421 carpal tunnel syndrome, 566, 569
xenaderm, 421 cubital tunnel syndrome, 570

632 Index
Splinting (Continued) knife handles, 573, 588

median/ulnar/radial nerve palsy, 564, mallet, 574, 578
570, 570–571 pliers/cutter, 574, 579
submuscular ulnar nerve transposition, retractors, 575–577, 576–579, 584
570 scissors, 581–582, 585–588
replantation, 572 suction tip, 578, 583
stiffness, 566 towel clips, 583, 588, 590
tendinopathy, 564, 565–566, 566 webster needle holder, 589, 590
tendon transfers, 566 Swan—neck deformity
wrist fractures/dislocations, 566, clinical problems, 124
568–569, 569 complications of treatment, 125
Split-thickness skin graft (STSG), 394, definition, 123, 612
396 etiology, 123–124
Sporotrichosis, 480 physical examination, 124
Squamous cell carcinoma, 468–469 treatment, 124–125
Stener lesion, 610 Symbrachydactyly, 613
Stenosing tenosynovitis, 613 Syndactyly, 613
Sterile matrix, 393, 610 Synergy, 612–613
Stiffness Systemic lupus erythematosus (SLE),
digital 355–358, 528
evaluation, 172–173
pathoanatomy, 170–172
treatment, 173–176 T
elbow TEA (see Total elbow arthroplasty)
anatomy, 178–179 Tendinopathy
cause, 179 de Quervain syndrome, 135–136
classification, 179 epicondylitis, 140–143
evaluation, 179–180 extensor carpi ulnaris tendonitis,
management, 180–185 137–139
splinting flexor carpi radialis tendonitis,
finger/thumb/wrist/elbow, 566 139–140
wrist intersection syndrome, 136–137
evaluation, 177 splinting, 565–566
treatment, 177–178 trigger digits, 133–135
Stroke Tendon, 612–613
hemiplegia, 162 biology
patient evaluation, 162–163 flexor tendon healing, 93
surgery, hemiplegic upper extremity, growth factors, 94
163–164 wound healing, 93–94
STSG (see Split-thickness skin graft) extensor tendon, chronic disorders
Subacute cutaneous lupus erythematosus boutonniere deformity, 121–123, 122
(SCLE), 528 chronic ECU rupture, 127–129
Subcutaneous abscess, 473 chronic EDC ruptures, 131–133
Subungual lesions, 470 chronic EPL rupture, 125–127
Surgical instrumentation chronic rupture EDQ, 129–131
bone excision/shaping, 569 swan—neck deformity, 123–125
clamps, 571–572 extensor tendons, acute injuries
forceps, 575–576, 590 anatomy, 115–117, 116
fracture and periosteal manipulation, rehabilitation, 120
571–572, 576, 578 zones of injury, 117–120

Index 633
flexor tendon injuries, acute pathophysiology, 502–503

anatomy, 95, 95–97, 97 rehabilitation, 506
examination, 97–98, 98 secondary reconstruction, 506
flexor tendon rehabilitation, 105–108 treatment
partial tendon laceration, 105 lukewarm water/antibacterial
pediatric patient, 108 soap, 504
segmental tendon defects, 104–105 splinting and initiation, 505
zone III injuries, 102 tissue perfusion, 504–505
zone IV injuries, 103 wound care, 505–506
zone of injury, 98–102, 101–102 Thiemann disease, 450
zone V injuries, 103–104 Thoracic outlet syndrome (TOS)
flexor tendon injuries reconstruction anatomy, 320–321
pulley reconstruction, 114–115 definition, 320
rupture repair, 109 examination
tendon grafts, 110–114 musculoskeletal, 321–322
tenolysis, 110 neurological exam, 321
tendinopathy vascular, 322
de Quervain syndrome, 135–136 imaging, 322–323
epicondylitis, 140–143 laboratory studies, 322
extensor carpi ulnaris tendonitis, physiological studies, 323
137–139 postoperative care, 325
flexor carpi radialis tendonitis, risks, benefits, and complications, 326
139–140 scalene muscle block, 323–324
intersection syndrome, 136–137 tissue perfusion studies, 323
trigger digits, 133–135 treatment, 324–325, 328
transfers Thromboangiitis obliterans (see Buerger
brachial plexus, 166–168 disease)
cerebral palsy, 153–156 Thumb carpometacarpal joint
peripheral nerve, 148–153 anatomy, 205–206
principles, 145–148 comminuted intra-articular fractures, 206
rheumatoid, 164–166 dislocations, 206–208
spinal cord injury, 156–162 metacarpal fractures, 206
stroke, 162–164 Thyroid medication, 41
thermal injury, 566 Tinel sign, 615
Tennis elbow, lateral epicondyles, 309 TOS (see Thoracic outlet syndrome)
Tenodesis, 612 Total elbow arthroplasty (TEA), 389
Tenosynovitis, 479 Transverse ligament of palmar aponeurosis
Testimony, medicolegal (TLPA), 452, 454
deposition, 541–542 Transverse retinacular lig, 611
preparation for, 540–541 Trapeziometacarpal
rules, 539–540 arthritis
trial, 542 anatomy and biomechanics, 370
Thenar space infection, 471–472 diagnosis, 370–372, 371t
Thermal injuries treatment, 372
anatomy, 502 prostheses, 384
definition, 502 Triangular fibrocartilage
epidemiology, 502 anatomy, 232–234, 233–237
evaluation method complex (TFCC), 256, 262, 611
American burn association criteria, 503 diagnosis
tissue layers, 503–504 arthroscopy, 236–238

634 Index
Triangular fibrocartilage (Continued) definition, 440

classification, 238, 241 diabetes mellitus, 441
examination, 234–235 diagnosis, 441
history, 234 blood flow physiology, 434
imaging methods, 235–236, 239–237 congenital vascular disorders
joint levelling, 240 arteriovenous malformation (AVM), 437
treatment, 238–240, 242t hemangioma, 436–437
differential diagnosis, 232 venous malformation, 437
Tricalcium phosphate (TCP), 597 definitions, 433
Trigger digits, 133–135 hypothenar hammer syndrome,
Tumors 438–439
benign noninvasive vascular testing, 435
bone, 463–466 office evaluation, 434–435
soft tissue, 460–463 primary vasopastic disease, 442–443
malignant radial artery thrombosis, 439
bone, 466–467 radiologic evaluation, 435–436
soft tissue lesions, 468–470 secondary vasospastic disease, 443
vasospastic disease, 442
Vascular grafts, 429–435
U Vascular injuries, acute
Ulnar anatomy
aponeurosis, 452, 453 axillary and brachial artery, 424
carpometacarpal joints deep palmar arch, 426
anatomy, 210 dorsal arch, 426
dislocations, 210–212 interosseous artery, 425
collateral ligament (UCL), thumb, 48 left subclavian artery, 424
nerve palsy, 570 proper digital arteries, 426
tunnel syndrome radial artery, 424–425
description, 318 superficial palmar arch, 425–426
diagnosis, 319 ulnar artery, 425
etiology, 318–319 arterial injection injuries, 431
postoperative care, 319 arterial injury anatomic location,
signs and symptoms, 319 430–431
treatment, 319 compartmental fasciotomy distal,
Upper extremity vascular injuries indications for, 432
(see Vascular injuries, acute) contrast angiography, 427–428
diagnosis, 426–427
digital ischemia, 431–432
V operative exploration, 428–429
Vascular conditions repair, 429
anatomy thrombolytic therapy, 431
macroarterial upper extremity vascular time of injury/reduction, 432
system, 433 vascular grafts, 429–430
microarterial system, 433–434 Vascularized bone grafts, 593–594
arterial aneurysms, 439–440 Vascularized nerve grafts, 335–336
arteritis/systemic conditions Vasculogenesis, 5
additional arteriopathies, 441–442 Vasoconstrictive process, 498
atherosclerosis, 441 Vasospastic disease (see Raynaud
Buerger disease (thromboangiitis syndrome)
obliterans), 441 Verruca vulgaris, 524–525, 524

Index 635
Viral infections portals, 49, 50

herpetic whitlow, 480–481 radiocarpal joint, 51–52
warts, 481 setup, 51
VISI (see Volar intercalated segment DRUJ arthritis, 378
instability) examination, 615
Volar beak ligament, 611 radiocarpal arthritis, 378
Volar carpal ganglion cysts, 462 SLAC and SNAC, 376–378
Volar intercalated segment instability therapeutic
(VISI), 615 debridement, 53–54
Volar plate, 611 distal ulna resection, 55–56
dorsal carpal ganglion excision, 56
intra-articular fractures, 56–57
W scaphoid fractures, 57
Wallerian degeneration, 295
triangular fibrocartilage complex
Wartenberg syndrome (see Radial sensory
(TFCC) repair, 54–55
nerve compression)
Warts, 481, 524, 524–525
Watson test, 615
White superficial onychomycosis, 531 X
Workers compensation laws Xenaderm, 421
American Medical Association X-ray
Publication, 545 anterior-posterior (AP) and posterior-
benefits, 545 anterior (PA) views, 11–14, 12–14
FECA, 544 lateral view, 14–16, 15–17
occupational disease/injury, 544
Wrist and arthroscopy
anatomy, 611
diagnostics Z
distal radioulnar joint (DRUJ), 53 Zancolli lasso, 150–151, 162
midcarpal joint, 52 Z-plasty, 112, 184, 399, 400

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ASSH Manual

Martin I. Boyer, MD, FRCS(C)

Boyer_FM.indd i 2/22/2010 10:19:14 PM

Two Commerce Square

Library of Congress Cataloging-in-Publication Data

Boyer_FM.indd ii 2/22/2010 10:19:16 PM

To my past, present, and future fellows,

To my wife, for her patience and support,

Boyer_FM.indd iii 3/8/2010 7:20:12 PM

Section I General Concepts

6. Amputations and Prosthetics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .58

7. Techniques of Injections. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .65

8. Differential Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .71

Section II Specific Conditions

10. Tendon . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .93

11. Tendon Transfers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .145

12. Stiffness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .170

Boyer_FM.indd v 8/21/2012 8:17:48 PM

13. Fractures and Dislocations: Hand . . . . . . . . . . . . . . . . . . . . . . . . . . .186

14. Fractures and Dislocations: Wrist. . . . . . . . . . . . . . . . . . . . . . . . . . . .216

15. Fractures and Dislocations: Forearm . . . . . . . . . . . . . . . . . . . . . . . . .255

16. Fractures and Dislocations: Elbow . . . . . . . . . . . . . . . . . . . . . . . . . . .264

17. Nerve. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .294

18. Brachial Plexus. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .343

19. Arthritis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .351

20. Skin and Soft Tissue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .393

21. Acute Vascular Injuries of the Upper Extremity . . . . . . . . . . . . . . . . .424

22. Vascular Conditions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .433

23. Osteonecrosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .444

24. Dupuytren’s Disease. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .452

25. Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .460

26. Infections. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .471

27. Compartment Syndromes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .483

28. Injection Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .493

29. Extravasation Injuries. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .495

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30. Frostbite . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .497

31. Thermal Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .502

32. Chemical Poisoning and Exposures . . . . . . . . . . . . . . . . . . . . . . . . . .507

33. Bite Wounds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .511

Section III Other Conditions

35. Medicolegal Principles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .533

36. Workers’ Compensation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .544

37. Clinical Trials and Hand Surgical Literature. . . . . . . . . . . . . . . . . . . .546

38. Psychological Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .553

39. Splinting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .558

40. Surgical Instrumentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .569

41. Bone Grafting and Bone Graft Substitutes. . . . . . . . . . . . . . . . . . . . .591

42. Examination of the Severely Injured Hand . . . . . . . . . . . . . . . . . . . .599

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Kimberly L.Z. Accardi, MD, CPT, MC, Robert M. Baltera, MD

Karim Bakri, MD Martin I. Boyer, MD

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David J. Bozentka, MD James Chang, MD

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George S.M. Dyer, MD Jeffrey A. Greenberg, MD, MS

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Michelle A. James, MD Adam LaBore, MD

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Michael Makary, MD, MBA Paul F. Nassab, MD

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David C. Ring, MD, PhD John G. Seiler III, MD

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